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Handbook for
Physical Therapists
Acute Care
Handbook for
Physical Therapists
Second Edition
Jaime C. Paz, M.S., P.T.
Assistant Clinical Specialist, Department of Physical
Therapy, Northeastern University, Boston; Adjunct
Faculty Member, Department of Physical Therapy,
Simmons College, Boston; Adjunct Physical Therapist,
Care Group Home Care, Belmont, Massachusetts
UTTERWORTH
E I
An Imprint of Elsevier
-&
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v,,, tIle E1scner hOlnepage (hup IIw',\'W elsevier COIll). by selecting 'CUSlOIII('f Snppon'
;uld then' Oblrurung Pc:mUSSlOI1S'
Every effort has been made to ensure that the drug dosage schedules within this text
are accurate and conform to standards accepted at time of publication. However, as
treatment recommendations vary in the light of continuing research and clillical
experience, the reader is advised to verify drug dosage schedules herein with informa
tion found on product information shee[S. This is especially true in cases of new or
infrequently used drugs.
Recognizing the importance of preserving what has been written, Bunerworth
Heinemann prints its books on acid-free paper whenever possible.
Contents
Contributing Authors
Contributing Artists
Preface
Acknowledgments
1.
Cardiac System
ix
XI
XIII
xv
1
Seall M . Col/ills
2.
Respiratory System
89
3.
Musculoskeletal System
159
4.
Nervous System
259
Michele P. West
5.
Oncology
331
Susan Polich
6.
363
7.
435
8.
Gastrointestinal System
501
jaime C. Paz
9.
Genirourinary System
557
jamie C. Paz
10.
Infectious Diseases
605
VIlI
CONTENTS
11.
Endocrine System
649
Jaime C. Paz
12.
Organ Transplantation
697
745
Michele P.West
I -B.
749
Michele P.West
D.
763
ill-A.
ill-B.
Mechanical Ventilation
811
Sean M. Collins
ill-G.
829
Jaime C .Paz
IV.
Pharmacologic Agents
839
Effects of Anesthesia
871
Michele P. West
VI.
Pain Management
877
Jaime C.Paz
YD.
Amputation
887
Postural Drainage
897
Michele P. West
lX.
Functional Tests
901
921
Michele P.West
Index
925
Contributing Authors
IX
CONTRIBUllN G AlITHORS
Contributing Artists
XI
Preface
XIII
XIV
PREFACE
Clinical Tips appear throughout each chapter. These helpful hints are
intended to maximize safety, quality, and efficiency of care. These clin
ical rips are suggestions from the editors and contributors that, from
clinical experience, have proved to be valuable in acclimating thera
pists to the acute care setting.
Appendices provide information to complement topics presented in
the cha pters.
It is important to remember that all of the information presented in
this book is intended to serve as a guide to stimulate independent critical
thinking within the spectrum of medical-surgical techniques and trends.
Developing and maintaining a rapport with the medical-surgical team is
highly recommended, as the open exchange of information among pro
fessionals is invaluable. We believe this new edition of Acute Care
Handbook (or Physical Therapists can enhance the clinical experience
by providing valuable information while reviewing charts, preparing for
therapy intervention, and making clinical decisions in the acute care
setting.
j.p.
M. P. \\7.
Acknowledgments
xv
XVI
ACKNOWLEDGMENTS
Acute Care
Handbook for
Physical Therapists
1
Cardiac System
Sean M. Collins
Introduction
PHYSICAL
THERAPISTS
Structure
The heart and the roots of the great vessels ( Figme 1 - 1 ) occupy the peri
cardium, which is located in the mediastinum. The sternum, the costal
cartilages, and the medial ends of the third to fifth ribs on the left side of
the thorax create the anterior border of the mediastinum. It is bordered
inferiorly by the diaphragm, posteriorly by the vertebral column and ribs,
and laterally by the pleural cavity (which contains the lungs).' Specific
cardiac structures and vessels and their respective functions are outlined
in Tables 1 - 1 and 1-2.
Note: The mediastinum and the heart can be displaced from their
normal positions with changes in the lungs secondary to various dis
orders. For example, a tension pneumothorax will shift the mediasti
num away from the side of dysfunction (see Chapter 2 for further
description of pneumothorax ).
Function
The cardiovascular system must adjust the amount of nutrient and oxy
gen rich blood pumped out of the heart (cardiac output [CO]) to meet
the wide spectrum of daily energy (metabolic) demands of the body.
CARDIAC SYSTEM
Sinus Node
=, Pulm", Art,,,,
...->''',w''' Branch
Branch -/---<
Branches
Right Coronary
Art,,>,
Inferior Vena CO'"
--J+PostcnOf Dcscmdlng
Art,,,,
".,1:;..
;; =-
____
Pulmonary Artery
Left Atrium
Ldt Main
Coronary
Artery
lsI
Diagonal
Branch
Left Venuicle
2nd Diagonal
Branch
\r--#o+-- Left
Anterior
Descending Artery
Apical
Branches
Figure 1-1. Anatomy of the right coronary artery and Jeft coro,wry artery,
including left maiu, left auterior descending, and left circumflex coronary
arteries. (Reprinted with permissioll (rom R C Becker. Chest Pain: The Most
Common Complaints Series. Boston: Butterworth-Heinemann, 2000;26-28.)
Table
1-1.
Structure
Description
Function
Pericardium
and trauma
Endocardium
Right atrium
tissue
Heart chamber
Tricuspid
valve
Atrioventricular valve
and ventricle
Hearr chamber
systole
Right
circulation
ventricle
Pulmonic
valve
Left atrium
Heart chamber
Mitral valve
Atrioventricular valve
and ventricle
Left ventricle
Heart chamber
Aortic valve
lation
left ventricle and aorta
CARDIAC SYSTEM
Description
Function
Chordae
tendineae
Tendinous attachment of
atrioventricular valve
cusps to papillary
muscles
Muscle that connects
chordae tendineae to
floor of ventricle wall
Papillary
muscle
Description
Function
Aorta
Primary artery from the left ventricle that ascends and then
descends after exiting the heart
Superior
vena cava
Inferior
vena cava
Pulmonary
artery
AarrE CARE
THERAPISTS
Cardiac Cycle
B lood flow throughout the cardiac cycle depends on circulatOry and
cardiac pressure gradients. The right side of the heart is a low
pressure system with little vascular resistance in the pulmonary arter
ies, whereas the left side of the heart is a high-pressure system with
high vascular resistance from the systemic circulation. The cardiac
cycle is the period from the beginning of one contraction, starting
with sinoatrial (SA) node depolarization, to the beginning of the next
contraction. Systole is the period of contraction, whereas diastole is
the period of relaxation. SystOle and diastOle can also be categorized
into atrial and ventricular components:
1.
Atrial diastole is the period of atrial filling. The flow of blood is
directed by the higher pressure in the venous circulatory system.
2.
Atrial systole is the period of atrial emptying and cOntraction. Initial emptying of approximately 70% of blood occurs as a
result of the initial pressure gradient between the atria and the ventri
cles. Atrial contraction then follows, squeezing our the remaining
30%.3 This is commonly referred to as the atrial kick.
3.
Ventricular diastole is the period of ventricular filling. It initially
occurs with ease; then, as the ventricle is filled, atrial contraction is neces
sary to squeeze the remaining blood volume into the ventricle. The
amount of stretch placed on the ventricular walls during diastOle,
referred to as left ventricular end diastolic pressure (LVEDP), influences
the force of contraction during systOle. ( Refer to description of preload in
the section Factors Affecting Cardiac Output.)
4.
Ventricular systole is the period of ventricular contraction.
The initial contraction is isovolumic (meaning it does nOt eject blood),
which generates pressure necessary to serve as the catalyst for rapid
ejection of ventricular blood. The left ventricular eiectiOlt fraction
(EF) represents the percent of end diastOlic volume ejected during sys
tOle and is normally approximately 60%. 3
Cardiac Output
CO is the quantiry of blood pumped by the heart in 1 minute. It can
also be described relative to body mass as the cardiac index, the
CARDIAC SYSTEM
amount of blood pumped per minute per square meter of body mass.
Regional demands for tissue perfusion (based on local metabolic needs)
compere for systemic circularion, and roral CO adjusts ro meet these
demands. Adjustment ro CO occurs with changes in hearr rate (HR)
(chronotropic) or stroke volume (SV) (inotropic). Normal resting CO
is approximarely 4-8 liters per minute, and normal cardiac index is
approximately 2.5-4.0 liters per minute per meter'' (with a resting HR
of 70 beats per minute [bpml, resring SV is approx imately 71 ml/beat).
The maximum value of CO represents the functional capacity of the
circulatory system to meet the demands of physical activity.
CO (liters per minute)
H R (bpm)
SV (liters)
Preload
Preload is the amount of tension on the ventricular wall before it con
tracts. It is related ro venous return and affects SV by increasing left
ventricular end diastolic volume as well as pressure and therefore con
traction J This relationship is explained by the Frank-Starling Mecha
nism and is demonstrated in Figure 1-2.
Frank-Starli/lg Mechanism
The Frank-Starling mechanism defines the normal relationship
between length and tension of the myocardium,s The greater the
stretch on the myocardium before systole (preload), the stronger
the ventricular contraction. The length-tension relationship in
skeletal muscle is based on the response of individual muscle
fibers; however, relationships between cardiac muscle length and
tension co nsist of the whole heart. Therefore, length is considered
in terms of volume; tension is considered in terms of pressure. A
greater volume of blood returning to the hearr during diastole
equates ro greater pressures generated initially by the heart's con
tractile elements. Ultimately facilitated by elastic recoil, a greater
volume of blood is ejected during systole. The effectiveness of this
mechanism can be reduced in pathologic situations.4
Afterload
Afterload is the force against which a muscle must contract to ini
tiate shortening.s Within the ventricular wall, this is equal to the
QO
S)'mpithtuc Tant
utecholaminn
S1"Olk SWill of tIM Myocudl".:
Tht lour bns prowk an eumple of
how tbt contrxtiIt .It of Iht
myocanJl\lDI InfluIonca Iht
rNtiondUp bftWftft LVEDV and
vmtritWM pmornwn.
foror.FftqUftlC)' Relation
"""".
" ....,.
AnoDa/Hyptrc:&pnlal
"""""
l.osIof MyocardIum
lnlnnlit
'"
'"
z
"
"
o
..
Elutldty 01 MyocardJum
upKity of Ventrkwn
0._
.....
'"
J:
-<
,...
i
......
of Myocard.i...
we
I_
V_ Rttum
Atnal Contribution ID
VmlriNL1r filII,.
(Atnal Kid:J
Figure 1-2. Factors affecting left ventricular function. (Adapted from E Braunwal. J Ross, E Somlenblick. et al. Mechanisms of
Contraction of the Normal and Faili,lg Heart {2nd ed}. Boston: Little, Brown, 1 976.}
CARDIAC SYSTEM
tension developed across its wall during systo le. The most promi
nent fo rce contributing to afterload in the heart is SP, specifically
vascular compliance and resistance. BP affects aortic valve opening
and is the most obvious load enco u ntered by the ejecting ventricle.
An example o f afterload is the amount of pressure in the aorta at
the time of ventricular systo le.3
-A::;::-:;--
Sinoatrial ___
node
Atrioventricular
node
Bundle of His
Area 1
Rtpa"of
--+/1-----'<'<\
---------
ventricular discharge
Q wave
--4h
Area2
Secondpart of
T
Q S
ventricular discharge
10
Netlral lnptlt
The SA node has its own inherent rate. Neural input can, however,
influence HR, H RV, and contractility through the autonomic nervous
system.Js
Parasympathetic system (vagal) neural input generally decelerates
cardiac function, thus decreasing HR and contractility. Parasympa
thetic input travels through the vagus nerves. The right vagus nerve pri
marily stimulates the SA node and affects rate, whereas the left vagus
nerve primarily stimulates the AV node and affects AV conduction.J,8
Sympathetic system neural input is through the thoracolumbar
sympathetic system and serves to increase HR and augment ventricu
lar contractility, thus accelerating cardiac function.3
Endocrine Input
In response to physical activity or stress, a release in catecholamines
increases HR, contractility, and peripheral vascular resistance for a
net effect of increased cardiac function.' Refer to Table 1-3 for the
cardiac effects of hormones.
Local Input
Tissue pH, concentration of carbon dioxide (C0 ), concentration of oxy
2
gen (02) and metabolic products (e.g., lactic acid) can affect vascular
'
tone.' During exercise, increased levels of CO , decreased levels of 0
2
2'
decreased pH, and increased levels of lacric acid ar the tissue level dilate
local blood vessels and therefore increase CO distribution to thar area.
Cardiac Reflexes
Cardiac reflexes influence H R and contractility and can be divided
into three general categories: baroreflex (or pressure), Bainbridge
reflex (or stretch ), and chemoreflex (or chemical reflexes).
CARDIAC SYSTEM
Table
1-3.
1t
Hormone
Primary Site
Stimulus
Cardiac Effect
Norepinephrine
Adrenal
medulla
Adrenal
medulla
Kidney
Stress/exercise
Vasoconstriction
Stress/exercise
Coronary artery
vasodilation
Vasoconstriction,
increases blood
volume
Potem vasoconstriaor
Epinephrine
Angiotensin
Vasopressin
Bradykinin
Histamine
Posterior
pituitary
Formed by
polypeptides in
blood when
activated
Throughout
tissues of
body
Atria of heart
Adrenal
cortex
Tissue damage
Increased atrial
stretch
Angiotensin II
(stimulated) by
hypovolemia
or decreased
renal perfusion
Vasodilation,
increased capillary permeabiliry
Vasodilation,
increased capillary permeability
Decreased blood
volume
Increases blood
volume, kidneys
excrete more
potassium
Source: Data from AC Guyton.JE Hall. Textbook of Medical Physiology (9th cd). Philadelphia: Saunders, 1996.
12
Coroltary Perfusiolt
For a review of the major coronary arteries, refer to F igure I - I . Blood
is pumped to the large superficial coronary arteries during ventricular
systole. At this time, myocardial contraction limits the flow of blood
to the myocardium; therefore, myocardial tissue is actually perfused
during diastole.
Systemic Circulatiolt
For review of the primary anatomic structures and distribution of
the systemic circulation, refer to F igure ] -4. Systemic circulation is
affected by roral peripheral resistance (TPR), which is the resis
tance to blood flow by the force created by the aorta and arterial
system. Two factors that contribute to resistance are ( 1 ) vasomotor
tone, in which vessels dilate and constrict, and (2) blood viscosity,
in which greater pressure is required to propel thicker blood. Also
called systemic vasClilar resistaltce, TPR and C O influence blood
pressure ( B P ) .3 This relationship is ill ustrated in the following
equation:
BP
CO xTPR
CARDIAC SYSTEM
13
//6
7"'-_
Anenes
Liver Circulation
Intestinal Circulation
Figure
Cardiac Evaluation
Patiellt History
In addition to the general charr review presented in Appendix I-A,
pertinent information about patients with cardiac dysfunction that
should be obtained before physical examination includes the
following' 1 0-12 :
Presence of chest pain (see Appendix X for an expanded
description of characteristics and etiology of chest pain)
14
1.
Location, radiation
Physical inactivity
Obesity
Body mass index
>30 kglm'
Abdominal obesity (waist
hip ratio)
Men >40 in.
Elevated triglycerides
Small LDL parricles
Elevated homocysteine
Elevated lipoprotein (a)
C-reactive protein
Fibrinogen
Elevated inflammatory
markers
CARDIAC SYSTEM
15
Clinical Tip
When discussing angina with a patient, use the patient'S
terminology. If the patient describes the angina as "crush
ing" pain, ask the patient if he or she experiences the
crushing feeling during treatment as opposed to asking the
patient if he or she has chest pain.
o The common medical record abbreviation for chest
pain is CPo
Physical Exam;1Iatio1l
Observation
Key components of the observation portion of the physical examina
tion include the following7:
1.
2.
3.
Respiratoty rate
4.
Signs of trauma (e.g., paddle burns or ecchymosis from car
diopulmonary resuscitation)
5.
Presence of jugular venous distention, which results from
the backup of Auid into the venous system from right-sided CHF
(Figure 1-5)
a. Make sure the patient is in a semirecumbent position (45
degrees).
b. Have the patient turn his or her head away from the side
being evaluated.
c. Observe pulsations in the internal jugular neck region.
Pulsations are normally seen 3-5 em above the sternum. Pul-
16
CaroHd artery
Pulses for circulation quaty, HR, and rhythm (Table 1-5, Figure 1-6)
Clinical Tip
When palpating HR, counting pulses for 1 5 seconds
and multiplying by 4 is sufficient with normal rates and
rhythms. [f rates are faster than 1 00 bpm or slower than
60 bpm, they should be palpated for 60 seconds. If the
rhythm is irregularly irregular (e.g., during atrial fibrilla
tion) or regularly irregular (e.g., premature ventricular
contractions [PVCs]), auscultation of heart sounds should
be performed to identify the apical HR for a full minute.
CARDIAC SYSTEM
t7
Degree
Description
o
1+
Absent pulse
Diminished pulse
2+
Normal pulse
3+
Moderately increased
4+
Markedly increased
(boundlllg)'
No pulse-no circulation
Reduced stroke volume and ejec
tion fracrion, Increased vascular
resistance
Normal resting conditions, no
pathologies
Slightly increased stroke volume
and ejection fraction
Increased stroke volume and ejec
tion fraction, can be diminished
with vasoconstriction
Pulse Abnormalities
Abnormality
Palpation
Description
Pulsus
alternans
Bigeminal
pulses
Pulsus
paradoxus
Corrigan's pulse IS a houndmg pulse viSible in the carotid artery rhat occurs with aor
lIC rcgurgltallon.
Source: Data from SL Woods, ES SivaraJian-Froelichcr. S Underhill-Morzer (eds). Car
dlac NurSi ng (4th cd). Philadelphia: Lippincott, 2000.
18
Brachial Pullse---I/I.jrll
1\\ 1foK+--
Popliteal Pulse
(posterior knee)
CARDIAC SYSTEM
19
Degree
Description
Trace
2+ Mild
Slighr
0-{}.6
1+
3+ Moderare
4+ Severe
EID
em
em
1.3-2.5 em
0.6-1.3
B)ood Pressure
BP measurement with a sphygmomanometer (cuff) and ausculta
tion is an indirect, noninvasive measurement of the force exerted
against the arterial walls during ventricular systole (systolic blood
pressure [SBPJ) and during ventricular diastole (diastolic blood
pressure). BP is affected by peripheral vascular resistance (blood
volume and elasticity of arterial walls) and CO. Table 1-7 lists
normal BP ranges. Occasionally, BP measurements can only b e
performed o n certain limbs secondary ro the presence o f condi
tions Stich as a percutaneous inserted central catheter, arteria-
Age 8 yrs
Agel2 yrs
Adulr
Borderline
hypertension
Hypertension
Normal exer
cise
Systolic
Diastolic
111m Hg
95-'135 mm Hg
100- 140 mm Hg
140-150 mm Hg
52-85
mm Hg
Increases during rime and wirh
increased load or intensity
> 100 mm Hg
,,) O mm Hg
85-1 14
>150
mOl Hg
mm Hg
60-90 mm Hg
90-100 mm Hg
58-88
20
3.
4.
Place the bell of the stethoscope gently over the brachial arrery.
7.
Re-inflare rhe cuff to 30-40 mm Hg greater rhan the value in
srep 5. Then slowly deflare rhe cuff. Cuff deflation should occur at
approximately 2-3 mm Hg per second.1 3
8.
Listen for the onset of tapping sounds, which represents blood
flow returning to the brachial arrery. This is the systolic pressure.
9.
As the pressure approaches diastolic pressure, the sounds will
become muffled and in 5-10 mm Hg will be completely absent. These
sounds are referred to as Korotkoff's sounds (Table 1_8). 12.1 3
Clinical Tip
CARDIAC SYSTEM
21
Sound
Indicates
Systolic pressure (blood stans to flow
through compressed artery).
Sounds increase in
inrensity with a
distinct tapping
Sounds become muf
ned
Disappearance
22
0-Supine
Sitting
Standing
Auscultation
Evaluation of heart sounds can yield information about the patient'S
condition and tolerance to medical treatment and physical therapy
through the evaluation of valvular function, rate, rhythm, valvular
compliance, and ventricular compliance.4 To l isten to heart sounds,
a stethoscope with both a bell and a diaphragm is necessary. For a
review of normal and abnormal heart sounds, refer to Table 1-9.
The examination should follow a systematic pattern using both the
bell (for low-pitched sounds) and diaphragm ( for high-pitched
sounds) and should cover all auscultatory areas, as illustrated in
CARDIAC SYSTEM
23
Location
Description
5 1 (normal)
All areas
52 (normal)
All areas
53 (abnormal)
Best appreciated
at apex
54 (abnormal)
Best appreciated
at apex
Murmur
(abnormal)
Over respective
valves
Pericardia I
friction rub
(abnormal)
TIlird or fourth
inrercostal
space, anrerior
axillary line
Source: Data from LS Bickley. Bate's Guide to Physical Examination and Hisfory
Taking 17th cd). Philadelphia: Lippincott, 1999.
24
Pulmonic Area
Aortic Area
Figure 1-8. Areas for heart sound auscultation. (Drawn by Barbara Cocanour.
Ph.D., University of Massac/msetts, Loweff. Departmel1l of Physical Therapy.)
Clinical Tip
Always ensure proper function of stethoscope by tapping
the diaphragm before applying the stethoscope to the patient.
Rubbing the stethoscope on extraneous objects can add
noise and detract from true examination.
Auscultation of heart sounds over clothing should be
avoided, because it muffles the intensity of both normal
and abnormal sounds.
If the patient has an irregular cardiac rhythm, HR
should be determined through auscultation (apical HR).
To save time, this can be done during a routine ausculta
tOry examination with the stethoscope's bell or diaphragm
in any location.
CARDIAC SYSTEM
25
Holter Monitoring
Holter monitoring is 24- or 48-hour ECC analysis. This is per
formed to detect cardiac arrhythmias and corresponding symp
toms during a patient'S daily activity. 12 Holter monitoring is
different than telemetric monitoring because the ECC signal is
recorded on a tape, and the subsequent analysis follows from this
recording.
Indications for Holter monitoring include the evaluation of syn
cope, dizziness, shortness of breath with no other obvious cause, pal-
26
Wave/Segment
Duration
(sees)
Amplitude (mm)
Indicates
P wave
PR interval
<0. 1 0
0 . 1 2-1).20
1-3
Isoelectric line
QRS complex
0.06-1).10
ST segment
0.12
25-30
(maximum)
-1/2 co +1
QT interval
( QT c)
0.42-1).47
Varies
T wave
0.16
5-10 mm
Atrial depolarization
Elapsed time between atrial
depolarization and ven
tricular depolarization
Ventricular depolarization
and atrial repoiariz3tion
Elapsed time between the
end of ventricular depo
larization and the begin
ning of repolarization
Elapsed time between the
beginning of ventricular
repoiarization and the
end of repolarization
(QT c is corrected for
heart rate)
Ventricular repolariz3rion
Sources: Data from RS Meyers (ed). Saunders Manual of Physical Therapy Practice.
Philadelphia: Saunders, 1 995; B Aehlen (ed). ACLS Quick Review Study Guide. St.
Louis: Mosby, 1 994; and D Davis (ed). How to Quickly and Accurately Mast'er ECG
Interpretation (2nd ed). Philadelphia: Lippincott, 1992.
CARDIAC SYSTEM
27
Clinical Tip
Some hospitals use an activity log with Holter monitor
ing. If 0, be sure to document physical therapy interven
tion on the log. If there is no log, be sure to document time
of day and intervention during physical therapy in the
medical record.
The use of cellular phones, although usually prohibited
in any hospital, is especially prohibired on a telemetry
unit. The cellular phone may interfere with the radio fre
quency transmission of the signal.
28
Elevated white blood cell Counts can indicate that the body is fight
ing infection, or they can occur with inflammation caused by cell
death, such as in M I. Erythocyte sedimentation rate (ESR), another
hematologic test, is a nonspecific index of inflammation and is com
monly elevated for 2-3 weeks after MIP Refer to Chapter 6 for more
information about these values.
Coagulation Profiles
Coagulation profiles provide information about the c10rting time of
blood. Patients who undergo treatment with thrombolytic therapy
after the initial stages of MI or who are receiving anticoagulant ther
apy owing to various cardiac arrhythmias require coagulation profiles
ro moniror anticoagulation in an attempt to prevent complications,
such as bleeding. The physician determines the patient's therapeutic
range of anticoagulation by using the prothrombin time (PT), partial
thromboplastin time, and international normalized ratio.17 Refer ro
Chapter 6 for details regarding these values and their significance to
treatment.
Patients with low PT and partial thromboplastin time are at higher
risk of thrombosis, especially if they have arrhythmias (e.g., atrial
fibrillation) or valvular conditions (mitral regurgitation) that produce
stasis of the blood. Patients with a PT greater than 2.5 times the refer
ence range should not undergo physical therapy because of the poten
tial for spontaneous bleeding. Likewise, an international normalized
ratio of more than 3 warrants asking the physician if treatment
should be withheldP
Blood Lipids
Elevated total cholesterol levels in the blood are a significant risk
factor for atherosclerosis and therefore ischemic heart disease. 29
Measuring blood cholesterol level is necessary ro determine the risk
for development of atherosclerosis and to assist in patient educa
tion, dietary modification, and medical management. Normal values
can be adj usted for age; however, levels of more than 240 mg/dl are
generally considered high, and levels of less than 200 mg/dl are con
sidered normal.
A blood lipid analysis categorizes cholesterol into high-density
lipoprotiens ( HDLs) and low-density lipoproteins (LDLs) and pro
vides an analysis of triglycerides.
HDLs are formed by the liver and are considered beneficial because
they are readily transportable and do nOt adhere to the intimal walls
CARDIAC SYSTEM
29
Clinical Tip
Cholesterol levels may be falsely elevated after an acute
MI; therefore, pre-infarction levels (if known) are used to
guide risk factor modification. Values will not return to
normal until at least 6 weeks post-M!.
Biochemical Markers
After an initial myocardial insult, the presence of tissue necrosis can
be determined by increased levels of biochemical markers. Levels of
biochemical markers, such as serum enzymes (creatine kinase [CK),
lactate dehydrogenase [LDHJ) and proteins (myoglobin, troponin I
and T), can also be used to determine the extent of myocardial death
and the effectiveness of reperfusion therapy, In patients presenting
with specific anginal symptoms and diagnostic ECG, these biochemi
cal markers assist with confirmation of the diagnosis of an M I (Table
1 -1 1 ) . Enzymes play a more essential role in medical assessment of
the many patients with nonspecific or vague symptoms and inconclu
sive ECG changes, 30 Such analysis also includes evaluation of isoen
zyme levels as wel1,31 Isoenzymes are different chemical forms of the
same enzyme that are tissue specific and allow differentiation of dam
aged tissue (e,g" skeletal muscle vs, cardiac muscle),
CK (formally called creatille phosphokinase) is released after cell
injury or cell death. CK has three isoenzymes. The CK-MB isoenzyme
is related to cardiac muscle cell injury or death, The most widely used
30
Enzyme or
Marker
Isoenzyme
Creatine kinase
(CK)
CK-MB
Lactate
dehydrogenase
LDH-I
Troponin T
(cTnT)
Troponin I
(cTnl)
Myoglobin
Normal
Value
55-7 1
IU
0-3%
1 27 1U
14-26%
<0.2 g/
liter
d . 1 pg/
liter
3 1-80
ng/ml
Onset
of Rise
(hrs)
Time of
Peak Rise
Return to
Normal
3-6
1 2-24 hrs
24-48 hrs
4-8
1 2-24
1 8-24 hrs
72 hrs
72 hrs
5- 1 4 days
24-72
2-4
3-4 days
24-36 hrs
1 0- 1 4 days
10-14 days
2-4
24-36 hrs
1 0- 1 4 days
1-2
6-9 hrs
24-36 hrs
Sources: Data from RH Christenson, HME Azzazy. Biochemical markers oC Ihe acute
coronary syndromes. Clin Chern 1 998;44: 1855-1 864; and AK Kratz, KB Leq:md
Rawski. Normal reference laboratory values. N Engl ] Med 1 998;339: 1 063-1072.
CARDIAC SYSITM
31
rises with muscle and renal failure.JO These newer markers are emerg
ing as sensitive and cardiac specific clinical indicators for diagnosis of
MI and for risk stratification.
Myoglobil1 is an O,-binding heme protein in both cardiac and skele
tal muscle. Although myoglobin is good for identifying acute MI in the
early stages, skeletal muscle origin needs to be ruled out. One mecha
nism of ruling out skeletal muscle damage is a rise in carbonic anhy
drase. Carbonic anhydrase only rises with skeletal muscle damage, and
irs rise is early, very similar ro myoglobin. Some have advocared a rario
of myoglobin and carbonic anhydrase to diagnose acute MI .I 2
LDH is also released after cell injury or death. LOH has five isoen
zymes. LOH-I is specific for cardiac muscle injury. Testing for LOH-l
is valuable for determining myocardial injury in patients admitted a
few days after the initial onset of chest pain, because it takes approxi
mately 3 days to peak and may stay elevated for 5- 1 4 days .'7
Clinical Tip
Physical therapy geared toward testing functional
capacity or increasing rhe patient's activity should be with
held until CK-M B levels have peaked and begun to fall.
It is best to await the final diagnosis of location, size,
and rype of MI before active physical therapy treatment.
This allows for rest and time for the control of possible
post-MI complications.
32
I)HYSICAL TI-IERJWISTS
Contrast Echocardiograph
The ability of the echocardiograph to diagnose perfusion abnor
malities and myocardial chambers is improved by using an intra-
CARDIAC SYSTEM
33
34
Acute pericarditis
Unstable angina
Decompensated CHF
Acute illness
CARDIAC SYSTEM
35
Metabolic
EquivaJenrs
(METS)
52.5
49.5
45.5
42.0
38.5
35.0
15
14
13
12
11
10
3 1 .5
28.0
24.5
21.0
7
6
17.5
14.0
5
4
10.5
7.0
Functional
Tasks
l
j
Treadmill:
Bruce PrOtocol
3Min Stages
(mph/elevation)
Bike Ergometer:
for 70 kg of
Body Weight
(kr/min)
4.2/16.0
1,500
1,350
1,200
3.4114.0
1,050
j ogg g
900
750
2.5112.0
1J
r
1 .7/10.0
Stalr
climbing
600
w k g
(level
Surf e)
450
300
150
Sources: Data from Amencan Heart Association, Comminee on Exercise. Exercise Testing
rc se
and Traimng of Apparently Healthy Individuals: A Handbook for Physicians. Dallas, 1972;
and GA Brooks, TO Fahey, TP Whlre (eds). Exe i
Its Applications (2nd ed). Mountain View, CA: Mayfield Publishmg, 1 996.
36
Clinical Tip
Synonyms for exercise tests include exercise tolerance test
and graded exercise test.
CARDIAC SYSTEM
37
Clinical Tip
After catheterization, the patient is on bed rest for
approximately 4-6 hours when venous access is performed
or for 6-8 hours when arterial access is performed.12
The sheaths are typically removed from the vessel 4-6
hours after the procedure, and pressure is applied con
stantly for 20 minutes following sheath removal.'2
The extremity should remain immobile with a sandbag
over the access site to provide constant pressure to reduce
the risk of vascular complications. 1 1
38
Angiography
Angiography involves the injection of radiopaque contrast material
through a catheter to visualize vessels or chambers. Different tech
niques are used for different assessments 1 2 : Aortography is used to
assess the aorta and aortic valve. Coronary arteriography is used ro
assess the coronary arteries. Pulmonary' angiography is used to assess
the pulmonary circulation. Ve/ltriculography is used to assess the
right or left ventricle and AV valves.
Elecrrophysiologic Studies
EPSs are performed to evaluate the electrical conduction system of the
hearr. '2 An electrode catheter is inserted through the femoral vein
into the right ventricle apex. Continuous ECG monitoring is per
formed both internally and externally. The electrode can deliver pro
grammed electrical stimulation to evaluate conduction pathways,
formation of arrhyrhmias, and the automaticity and refractoriness of
cardiac muscle cells. EPSs evaluare the effectiveness of antiarrhyrhmic
medication and can provide specific information about each segment
of the conduction system.' 2 [n many hospitals, these studies may be
combined with a therapeutic procedure, such as an ablation proce
dure (discussed later in this chapter, in the Management section). Indi
cations for EPSs include the following l 2:
CARDiAC SYSTEM
AV or intraventricular block
Unexplained syncope
39
Clinical Tip
Patients undergoing EPS should remain on bed reSt for 4--6
hours after the test.
Pathophysiology
40
CARDIAC
SYSTEM
41
Ml/Wall
Affecred
Possible
Occluded
Coronary
Artery
Anterior MY
anterior left
ventricle
Left coronary
Inferior MU
inferior left
venrricle
Right coro
nary (RCA)
Anterolateral
Mllantero
lateral left
ventricle
Anrerosepral
Mllsepral
region
berween left
and right
ventricles
Posterior Mll
posterior
heart
Right venerieu
lar MI
Lefr anterior
descending
(LAD), cir
cumnex
LAD
Transmural M l
(Q-wave MI)
Subendocar
dial MI
(non-Q
wave MI)
Possible Complications
Left-sided CHF, pulmonary edema, bun
dle branch block, AV block, and ven
tricular aneurysm (which can lead to
CHF, dysrhythmias, and embolism)
AV blocks (which can result in bradycar
dia) and papillary muscle dysfunction
(which can result in valvular insuffi
ciency and eventually CHF)
Brady or rachyarrhythmias, acute ventric
ular sepral defecr
RCA, circum
flex
RCA
Any artery
Any artery
....
N
OutMI
Delefmined by
Biochemical
M.mn
Ifpatierlllw:
",""", CO
No Rest
"""M
No Noaurnal
"""M
May be oonsid0=4:
lDw Riu I Stable
0.,.
TlvomboIytic Thc:npy Of
RevascularbauOQ procedures while in
"dR.
>-
'"
I'
i::
J:
"
g'"
IfpaDmIIlal:
Ifpatient bas:
.......,. .....
PAP >20mmHO
S3 GoIIop
H",....,....
"""""' Sf aw.g.,
""""'"
compIicatiol'lJ and;
HoWoMI
No bcbernic pWI
SIIbIe Rhythm
NoCHP
No Heart Block
HcmodyrwuicaUy
......
MI)'bc:
Low RisklSUibIe
Prior MI
"'-y be oonsidered:
Hip Rw - f\st1hcr Medical
Wort-Up
Mly UI:IdI::r:to
NoniJ!va5I."
StralTm or
C......,
Anmogaphy
Ulu&lly
Dl5Chuged III 12
CABO;
Uncomplicakd
die 4-7 days
Horpil&lization
IOdacftuerisJr:
and atabilix
for-Klirit)'
MD IDII)'
dlc:l4-4
"""' _ ..
OUI.,.rimt manqcmml
RCCllnull iJc:hcnua
CHF
Hypocensloa
""",...
Heart block
May be considefeld:
HiJh RiKICompIica&cdlUnst.ble
incNde. calheterizarion.
Treatma'li ml)' Include IOIDI:;
farm ofwioo.
o
,.
J:
-<
CARDIAC SYSTEM
43
Clinical Tip
(ST) depression, on a patient's ECG, of approximately
1-2 mm is generally indicative of ischemia.
ST elevation is generally indicative of myocardial injury
or infarction.
.... Figure 1-9. Possible clinical course of patients admitted with chest pain.
(CABC
electrocar
diogram that shows elevatioll of the ST segment.) (Data from American Col
lege of Cardio/ogy/Americall Heart Associatioll. 1999 Update: ACCIAHA
guidelines for the manageme11t of patiellls with acute myocardial infarction:
executive summary and recommendations. Circulation 1 999; 1 00: 1 016-1 030;
American College of Cardiology/American Heart Association. ACCIAHA
guidelines for the management of patients with acute myocardial infarction. J
Am Coli Cardiol 1 996;28:1328-1428; alld American College of Cardio/ogy/
American Heart Association. ACCiAHA guidelines for the management of
patients with ltltstable angina and Ilon-ST segment elevation myocardial
infarctioll. J Alii Coli CardioI 2000;36:971-1 048.)
44
2.
Regurgitation, the back flow of blood through the valve,
occurs wirh incomplete valve closure.
3.
Prolapse involves enlarged valve cusps. The cusps can
become floppy and bulge backward. This condition may progress
to regurgitation.
Over time, these disorders can lead to pumping dysfunction and,
ultimately, heart failure.
Refer to Table 1 - 1 4 for common valvular heart diseases and a
description of their signs and symptoms.
Heart Fail"re
Hearl (ailllre, a decrease of CO, can be caused by a variety of cardiac
pathologies. Because CO is not maintained, life cannot be sustained if
heart failure continues without treatment. Heart failure results in the
congestion of the pulmonary circulation and, in certain cases, even the
systemic circulation. Therefore, it is commonly referred to as CHF. The
CARDIAC SYSTEM
45
Symptoms
Signs
Aortic
stenosis
Chronic aortic
regurgitation
Acute aortic
regurgitation
Rapid progression of
symptoms of left ven
tricular failure, pulmo
nary edema, angina.
Mitral
stenosis
Symptoms of pulmonary
vascular congestion
(dyspnea, orthopnea), If
patienr develops pulmo
nary hyperrension
(which can cause
hypoxia, hypotension),
he or she may have
angina, syncope.
Symptoms of pulmonary
vascular congestion,
angina, syncope, farigue.
Rapid progression of
symproms of pulmonary
vascular congesrion.
Most commonly asymptom
aric, fatigue, palpiration.
Chronic
mitral
regurgitation
Acute mitral
regurgitation
Mitral valve
prolapse
46
Cardiomyopathy
Dysfunction
Description
Dilated
Systolic
Hypertrophic
Diastolic
Restrictive
Systolic and
diastolic
Etiologic Classification
Etiology
Examples
Etiology
Examples
Inflammatory
Viral infarction,
bacterial
infarction
e1enium defi
ciency, diabe
res mellitus
Carcinoid fibro
sis, endomyo
cardial fibrosis
Cardiac trans
plant rejection,
methyldopa
Hypertrophic Car
diomyopathy,
Duchenne's
muscular dys
trophy
Idiopathic hyper
trophic cardi
omyopathy
Infiltrative
Sarcoidosis, neoplastic
Hemaco
logic
Toxic
Physical
agents
Miscella
neous
acquired
Ischemic
Metabolic
Fibroplasric
Hypersensiriviry
Generic
Idiopathic
CARDIAC SYSTEM
47
Symptoms
Signs
Acute peri
carditis
Constrictive
pericarditis
Chronic peri
cardial effu
sion (without
tamp<made)
Pericardial
tamponade
ECG = electrocardiogram.
Sources: Data from Sl Woods, ES Sivarajian-Frocl icher, S Underhill-Morzer (cds). Car
diac Nursing (4th ed). Philadelphia: Lippincotf, 2000; and MD Cheidin, M Sokolow,
MB Mcilroy. Clinical Cardiology (6th cd). Norwalk, CT: Appleton & lange, 1993.
48
Sign s
Dyspnea
Tachypnea
Paroxysmal nocrurnal dyspnea
Onhopnea
Cough
Fatigue
1 996;76:520.
CARDIAC SYSTEM
49
Objective Assessmentb
No objective evidence of
cardiovascular disease
Objective evidence of
minimal cardiovascular
disease
Objective evidence of
moderately severe car
diovascular disease
Objective evidence of
severe cardiovascular
disease
F""cliu".,l cap,JClty refers to subjective symptoms of the paflenr. This aspect of the
classification is idenncal lo the New York Heart Association's Classification.
"Ob;ectwe ,lssessmem was added to the claSSification system by the American 'Ieart
Assouauon In 1 994. II refers 10 measurements such as electrocardiograms, stress tests,
ech()(ardiogram. and radiologic Images."l
50
Management
CARDIAC SYSTEM
51
3.
Directional coro/wry atherectomy can be performed by
inserting a catheter with a currer housed at the distal end on one
side of the catheter and a balloon on the other side . 1 2 The balloon
inflates and presses the cutter against the atheroma (plaque). The
cutter can then cut the atheroma and remove it from the arterial
wall. This can also be performed with a laser on the tip of the
catheter. Rotational ablation uses a high-speed rotating bur coated
with diamond chips, creating an abrasive surface. This selectively
removes atheroma due to its inelastic properties as opposed to the
normal elastic tissue. 1 2 The debris emitted from this procedure is
passed into the coronary circulation and is small enough to pass
52
Clinical Tip
Refer to the Diagnostic and Laboratory Section's discus
sion for precautions after a catheterization procedure.
Transmyocardial Revascularization
[n transmyocardial revascularizarion, a catheter with a laser tip creates
transmural channels from patent coronary arteries into an area of the
myocardium that is thought to be ischemic. It is intended for patients
with chronic angina who, due to medical reasons, cannot have angio
plasty or CABG. Theoretically, ischemia is reduced by increasing the
amount of oxygenated blood in ischemic tissue. Angiogellesis (the
growth of new blood vessels) has also been proposed as a mechanism
of improvement after this procedure. Although therapists should expect
improvements in functional capacity with decreased angina, the
patient's risk status related to CAD or left ventricular dysfunction does
not change.46 Postcatheterization procedure precautions, as previously
described, will apply after this procedure.
Coronary Artery Bypass Graft
A CASG is performed when the coronary artery has become com
pletely occluded or when it cannot be corrected by PTCA, coronary
arrhrecromy, Or stenting. A vascular graft is used to revascularize the
myocardium. The saphenoll s vein and the left internal mammary
artery are commonly used as vascular grafts. CABG can be per
formed either through a median sternotomy, which extends caudally
from JUSt i nferior to the suprasternal notch to below the xiphoid
process and splits the sternum longitudinally, or through a variety of
minimally i nvasive incisions.1 2
A minimally invasive technique that is being used for CASG
includes a CASG with a median sternoromy but without coronary
CARDIAC SYSTEM
53
Clinical Tip
To help patients understand this concept, inform them
that a gallon of milk weighs approxminately 8.5 lb.
Ablation Procedure
Catheter ablation procedures are indicated for supraventricular tachycar
dia, AV nodal re-entrant pathways, atrial fibrillation, atrial flurrer, and
some patients with cerrain types of ventricular tachycardia. 12 The proce
dure anempts to remove or isolate ectopic foci in an attempt to reduce
the resultant rhythm disturbance. Radiofrequency ablation uses low
power, high-frequency AC current to destroy cardiac tissue and is the
most effective technique for ablation.12 After the ecropic foci are located
under fluoroscopic guidance, the ablating catheter is positioned at the site
to deliver a current for 10-60 seconds.
Clinical Tip
S4
Clinical Tip
If the pacemaker does not have rate modulation, low
level activity with small increases in metabolic demand is
First Symbol
Pacing Location
Second Symbol
Sensing LOC3[ion
Third Symbol
Response to Pacing
0 = None
A = Arrium
N = None
A = Atrium
0 = None
I = Inhibited
V = Ventricle
T = Triggered
D = Dual
Dual
Dual
Ventricle
Fifth Symbol
Antitachyarrhythmia
Function
0 = None
S = Simple
programmable
M = Multiprogrammable
C = Communicating
R = Rate modulacion
0 = None
P = Pacing
S
Shock
D = Dual
detection of stimulus produces an immediate stimulus in the same chamber; Simple programmable
D = Dual
Fourth Symbol
Programma b i l i ry/
Modulation
program
Source: Adapted from AD Bernstein, AJ Camm, RD Fletcher, er al. The NASPElBPEG generic pacemaker code for anribradyarrhythmia and
adaptive pacing and anritachyarrhythmia devices. PACE 1987;1 0:795.
Q
:;
-<
'"
'"
56
For example,
Training SBP ( 1 80 - 120)(10.6 for lower
limit] [0.8 for upper limitJ) + 1 20
=
Training SBP
1 56-1 68 mOl Hg
CARDIAC SYSTEM
57
Value Repiacemell(
Valve replacement is an acceptable method for treatment of valvular
disease. Patients with mitral and aortic stenosis, regurgitation, or
both are the primary candidates for this surgery. Like the CABG, a
median sternotomy is the route of access to the heart. Common valve
replacements include mitral valve replacements and aortic valve
replacements. Prosthetic valves can be classified as mechanical ( bileaf
let and tilting disc valves are commonly used) as well as biological
valves (derived from cadavers, porcine, or bovine tissue),
Mechanical valves are preferred if the patient is younger than 65
years and i s already o n anticoagulation therapy (commonly due to his
tory of atrial fibrillation or embolic cerebral vascular accident). The
benefit of mechanical valves is their durability and long life.' 2 Mechan
ical valves also tend to be thrombogenic and, therefore, require life
long adherence to anticoagulation. For this reason, they may be
contraindicated in patients who have a history of previous bleeding
related problems, wish to become pregnant, or have a history of poor
medication compliance. These patients may benefit from biological
valves since there is no need for anticoagulation therapy. Biological
valves may also be preferred in patients older than 65 years of age.t 2
Postoperative procedures and recovery from mitral valve replacement
and aortic valve replacement surgeries are very similar to CABG, ll
Dyllamic Cardiomyoplasty
Dynamic cardiomyoplasry uses the latissimus dorsi muscle to provide
a muscular assist to the left ventricle during systole for patients with
dilated cardiomyopathies." The latissimus dorsi is detached distally,
moved forward, and wrapped around the left ventricle. The latissimus
dorsi is mechanically paced to contract with cardiac contraction. It
takes approximately 1 2 weeks for transformation of the latissimus
dorsi's contractile structure to correspond to cardiac requirements,
and patients may not receive benefit for 2-3 months ' Moving the
latissimus dorsi may restrict the thorax and result in atelectasis, which
needs to be addressed in postoperative physical therapy intervention.
This procedure is reserved for patients with end-stage heart failure
who have limited treatment options.4 In light of the marginal benefits
and high postoperative mortality rates, the cominued use of dynamic
cardiomyoplasty has recently been questioned "
58
Cardiac Transplantation
Cardiac transplantation is an acceptable intervention for rhe rreat
ment of end-stage heart disease. A growing number of facilities are
performing heart transplantation, and a greater number of physi
cal therapists are involved in the rehabilitation of pre- and POSt
transplant recipients. Physical therapy intervention is vital for the
success of heart transplantation, as recipienrs have often survived a
long period of convalescence both before and after surgery, render
ing them deconditioned. In general, heart transplant patients are
immunosuppressed and are without neurologic input to their
heart. These patients rely first on the Frank-Starling mechanism to
augment SV and then on the catecholamine response to augment
both H R and SV. The reader is referred to Chapter 12 for informa
tion on heart and heart-lung transplantation.
Cardiac Medications
Cardiac medications are classified according to functional indica
tions, drug classes, and mechanism of aerion. Cardiac drug classes
are occasionally indicated for more rhan one clinical diagnosis.
CARDIAC SYSTEM
59
60
Effecrs
Central nervous
system
Cardiac system
Gastrointestinal
system
Premature atrial and/or ventricular conrracrions, paroxysmal supravenrricular tachycardia, ventricular tachycar
dia, high degrees of atrioventricular block, venrricular
fibrillarion
Nausea, vomiting, diarrhea
Anriarrhythmic Drugs
Antiarrhythmic drugs attempt to normalize conduction of the cardiac
elecrrical sysrem .'o These drugs are classified in rhe following manner
according to their mechanism of action:
Class
Antihypertensive Drugs
Antihypertensive drugs attempt to assist the body in maintenance of
normotension by decreasing blood volume, dilating blood vessels,
preventing constriction of blood vessels, preventing the retention of
sodium, or a combination of these.
Medication classes successful in achieving these goals include
the fol iowi ngSo:
CARDIAC SYSTEM
61
Lipid-Lowering Drugs
Lipid-lowering drugs attempt to decrease lipid levels. They are usually
prescribed in combination with a change in diet and exercise habits
(see Appendix Table lV_22).5o Medications successful in lowering
lipid levels are the following:
Anion exchange resin
Nicotinic acid
Probucol
Fish oils
Coals
The primary goals in treating patients with primary or secondary car
diac pathology are the following'''
Assess hemodynamic response in conjunction with medical or sur
gical management during self-care activities and functional mobility
62
CARDIAC SYSTEM
63
Relative Indications
That the Patient Is Unstable and
Treatment Should Be
Modified or Withheld
Resting heart rate > 100 bpm
Hypertensive resting BP (syscolic
> 160 mm Hg, diascolic >90 mm
Hg)
Hypotensive resting BP (systolic
<80 mm Hg)
Myocardial infarction or exten
sion of infarction within the pre
vious 2 days
Ventricular eccopy at rest
Atrial fibrillation with rapid ven
tricular response at rest (HR
> 100 bpm)
Uncontrolled metabolic diseases
Psychosis or other unstable psycho
logical condition
heart rate.
Sources: Data from LP Cahalin. Heart failure. Phys Ther 1 996;76:520; MH Ellestad.
Stress Testing: Principles and Practice (4th cd) Philadelphia: FA Davis, 1 996; and NK
Wegener. Rehabilitation of the Patient with Coronary Heart Disease. In RC Schlant,
RW Alexander (cds), Hurst's the Heart (8th cd). New York: McGraw-Hili, 1994;1 227.
done to make the patient stable (i.e., medical treatment may stabilize
this response). Additionally, the therapist should find the level of func
tion that a patient could perform with a stable response. However, at
times, patients will not be able to be stabilized to perform activity. I n
these cases, physical therapists need to determine whether a condition
ing program would allow the patient to meer the necessary energy
demands without becoming unstable. Proceeding with therapy at a
lower level of activity is based on the premise that conditioning will
improve the patient'S response. The cardiac system suppOrts the body in
its attempt to provide enough energy to perform work. Often, becom
ing stronger-increased peripheral muscle strength and endurance
will reduce the demands on the heart at a certain absolute activity
....
....
Det
t:
rm
bchcmk Con
d
l
li
ON
IadIemk Sympto....
STSeamc:n1 Chanp
Onsel of or lnoe.ued F of
Ventrkula. Ectopy (Stop Rx II > IO/min..",.
baomes .,...p
... tom.tic or 8P Motu
......
amtpromised)
Unlfoat PVC. bKnme MuJtiIoal PVC.
0nJf!t tlfSigN ofCHF (5ft Table 1.17)
Syltollc 8100d Pn!t.sure Dropo> 10 mm He
.... ...
Cy;..-a
""ph<>-
Nasal Flaring
1ncrea.M'd UN of Aa:euory MWlCieoI 01
Respl11on
...
...
..
-------
UnNr Inert
In .fiR and Systolic 8P
.....
....
.......... ....
_....-l
NOTE.: St.oble may Include
lnaellSed n!$plnototy note, heart rale,
bloQd p"-, and Rf'E. Hown.
with tlw 5U1bleraponH.
<Oem,. indkate the patlI'5
-
b
e
a
m .ympICmUtio;or BPbt>mel;
compromlMd)
Unlfonl PVC'. become Mullifoo;al PVC.
0.-. of5lsn- 0'0-11' (Sft Table 1.17)
Sy.tolk Iood J>res.ure Dropf > 10 mm He
DIutoIIc IItood f'TeM
Incn-uea or
Drcno
>IO mm Ha
......
...
.....
..
Diaphorftlt. Pallor. ConftWon
In.cn&M:d IU'1i. deplte no o:hangn In vital
""
bcNrnlc SyrnptOlN
Sf I Changes
...
"'"ph<>
.....
N....
I.. F\a.ri.na
U""(>ftyM\OIIdft c>f
Rapitiltion
Figure 1 - 1 0. Determination of stable liS. unstable responses to activity/exercise. rBP blood pressure; CHF congestive heart
failure; HR heart rate; PVC premature ventricular contraction; RPE rating of perceived exertion; Rx Ireatmetlt.)
=
-=
8
o
'"
(l
"
"
:i!
CARDIAC SYSTEM
.,..
...
.....
....
..
...
--..
.
,
I--W."""" ,I
_ .. _----
.....
_ Vbllrp a..-
-.-- --=--==y
1--I'T -wot...
--_..... .._100
f.
_
DIoooI LI_.
.. _ ua. _ ...... LL -,.
--.. 01. .....- .... _
\1"'"""'
.... -
_.,.....- ..-t
-_00 __.... .....
...... ...._....".-,
... --.-
...,.-
65
...--", ...
--.,..,.. ......
_____
-.vr c-Tall
...
...
..
....... _ Itl\I M
D U
....... ... __ .. ... PfI""I w....
"" ......
..... .... "" ....
....... ... po_ ...u..& '" -.pi .. ......".
....
.......,. Of ,.- _ r.oN. _
,"NIIM ...,
,,
........... ..
. __ .SoI.
r
..... QoIr.
-""""
...
...
...
... ..
-.
...-..,... .. ...
. .
..
..... ...
66
lows the warm-up period. Very often in the acute care hospital, this con
ditioning phase is part of the patient'S functional mobility training. With
patients who are independent with functional mobility, an aerobic-based
conditioning program of walking or stationary cycling may be used for
conditioning. Finally, a cool-down or relaxation phase of deep breathing
and stretching ends the physical therapy session.
Listed below are various ways to monitor the patient'S activity tolerance.
1.
HR: H R is the primary means of determining the exercise
intensity level for patients who are not taking beta-blockers or who
have non-rate-responsive pacemakers.
There is a linear relationship between HR and work.
In general, a 20- to 30-beat increase from the resting value dur
ing activity is a safe intensity level in which a patient can exercise.
If a patient has undergone an exercise stress test during the hospi
tal stay, a percentage (e.g., 60--80%) of the maximum HR achieved
during the test can be calculated to determine the exercise intensity.52
2.
BP: Refer to the cardiac assessment section regarding BP measurements and Table 1-6 for BP ranges. Examples of a disproportionate
response to exercise are a systolic pressure decrease of 10 mm Hg below
the resting value, a hypertensive systolic response of more than 1 80 mm
Hg, or a hypertensive diastolic response of more than 1 1 0 mm Hg."
I f the patient is on a pacemaker that does nor have rare modula
tion, BP response can be used to gauge intensity. Please refer to the
Procedures section for the discussion on pacemakers.
CARDIAC SYSTEM
67
I O-Point Scale
o Nothing at all
0.5 Very, very slight
1 Very slight
2 Slight
3 Moderare
4 Somewhar severe
5 Severe
6
7 Very severe
8
9 Very, very severe
(almost maximal)
1 0 Maximal
8
9 Very light
10
1 1 Fairly light
12
13 Somewhar hard
14
15
Hard
16
Very hard
18
19 Very, very hard
20
17
3.
Borg's Rating of Perceived Exertioll (RPE) is depicted in
Table ] -22. Borg's RPE scale was initially proposed in 1 962 and has
evolved today to be the classic means of objectively documenting sub
jective feelings of exercise intensity.
This scale can be easily used to monitor exercise intensity for the
purpose of exercise prescription in a variety of patient populations.
It is the preferred method of prescribing exercise intensity for a
patient taking beta-blockers.
68
5.
Heart sounds: Refer to the section on Auscultation and Table
1-9 for normal and abnormal heart sounds.
The onset of murmurs, S3 heart sounds, or S4 heart sounds dur
ing treatment may be detected and could indicate a decline in car
diac function during activity. This finding should be brought to the
attention of the nurse and physician.
6.
Breath soul/ds: Refer to Chapter 2 for a discussion of lung
auscultation and the interpretation of breath sounds.
7.
fCC rhythm: Refer to the section on ECC and the section
Rhythm and Conduction Disturbance.
CARDIAC SYSTF1
69
Clinical Tip
Patients should be encouraged to report any symptom(s),
even if they think it is trivial.
References
I.
2.
3.
4.
5.
6.
7.
8.
9.
1 0.
I I.
1 2.
70
CARDIAC SYSTEM
71
32. Fisher EA, Stahl JA, Budd JH, Goldman ME. Transesophageal eohoear
diography: procedures and clinical application. J Am Coli Cardiol
1 99 1 ; 1 8: 1 333-1348.
33. Ellestad MH (cd). Stress Testing: Principles and Practice (4th ed). Phila
delphia: FA Davis, 1 996.
34. Perez JE. Current role of contrast echocardiography in the diagnosis of
cardiovascular disease. Clin Cardiol 1 997;20:13 1-138.
35. Bellardmelli R, Geordiou 0, Prucaro A. Low dose dobutamine echocar
diography predicts improvement in functional capacity after exercise
training in patients with ischemic cardiomyopathy: prognostic implica
tions. J Am Coli Cardiol 1 998;31 (5): I 027- 1 034.
36. American Heart Association, Committee on Exercise. Exercise Testing
and Training of Apparently Healrhy Individuals: A Handbook for Physi
Cians. Dallas, 1 972.
37. Brooks GA, Fahey m, White TP (eds). Exercise Physiology: Human
Bioenergetics and Its Applications (2nd ed). Mountain View, CA: May
field Publishing, 1 996.
38. Noonan V, Dean E. Submaximal exercise testing: clinical applications and
interpretation. Phys Ther 2000;80:782-807.
39. American College of Cardiology/American Heart Association. 1 999
update: ACOAHA guidelines for the management of patienfs with
acute myocardial infarction: executive summary and recommendations.
Circulation 1 999; I 00: 1 0 1 6- 1 030.
40. American College of Cardiology/American Heart Association. ACa
AliA guidelines for the management of patients with acute myocardial
infarction. J Am Coli Cardiol 1 996;28: 1 328-1428.
4 1 . American College of Cardiology/American Heart Association. ACC/
AliA guidelines for the management of patients with unstable angina
and non-Sf segment elevation myocardial infarction. J Am Coli Cardiol
2000;36:97 1 - 1 048.
42. Cahaltn LP. Heart failure. Phys Ther 1 996;76:520.
43. American Heart Association. AHA MedicaUScientific Statement. 1 994
Revisions to Classification of Functional Capacity and Objective Assess
ment of Patients with Diseases of the Heart. Dallas: American Heart
Association, 1 994.
44. Defre KM, Iioimes DR, Holudrov R, et al. Incidence and consequences
of periprocedural occlusion. Circulation 1 990;82:739.
45. Lirlak F. Margilis J, Cumins R. Excimer laser coronary (ECLA) registry:
report of the first 2080 patients. J Am Coli CardioI 1992;1 9:276A.
46. Humphrey R, Arena R. Surgical innovations for chronic heart failure
in the context of cardiopulmonary rehabilitation. Phys Ther 2000;
80,61-69.
47. Bernstein AD, Carnm AJ, Fletcher RD, er al. The NASPElBPEG generic
pacemaker code for antibradyarrhythmia and adaptive pacing and anti
tachyarrhythmia devices. PACE 1 987; 1 0:795.
48. Sharp cr, Busse EF, Burgess JJ, Haennel RG. Exercise prescription for
patients with pacemakers. J Cardiopulm Rehabil 1 998;18:421-43 1 .
49. Hayward MP. Dynamic cardiomyoplasty: time to wrap it up? IEdito
riall. Heart 1 999;82:263.
72
Appendix 1 -A
...,
..
ECG Characteristics
Supraventricular
tachycatdia
Atrial flutter
Common Causes
PT
Rheumatoid heart
disease (RHD),
mitral valve pro
lapse, cor pulmo
nale, digitalis
wxicity.
Mitral stenosis,
CAD, hyper
tension.
Atrial fibrilla
tion (A F)
Consideration
g
'"
m
Z
c
"
'"
;;;
:i!
Premature atrial
contractions
Sources; Data from B Aehlert. ACLS Quic.k Review Srudy Guide. St. Louis: Mosby. 1993; and EK Chung. Manual of Cardiac Arrhythmias. Bos
ton: Butterworth-Heinemann, 1 986.
2
o
"
()
-<
>
=ll
!Z
o
x
>
"
'"
"
'"
>
Name
ECG Characteristics
Common Causes
PT Considerations
Agonal rhythm
Near death
Do not creat.
Ventricular tachycardia
(VT)
Multifocal VT (rorsades de
poimes)
1::
J:
>
g
"
o
"
Of
J!
Ventricular fibrillation
Idioventricular rhythm
CAD
In normal individuals,
secondary to caffeine,
smoking, emotional dis
turbances; CAD, MI,
cardiomyopathy, MVP,
digitalis toxicity
cardiac output; MI
;:
>
,.
x
:>
'"
'"
ECG Characteristics
Common Causes
PT Considerations
Junctional escape
rhythm
Junctional tachycar
dia
Sources: Data from 8 Aehlert. ACLS Quick Review Study Guide. St. LoUIS: Mosby, t 994; and EK Chung. Manual of Cardiac Arrhythmias.
Boston: Butterworth-Heinemann, t 986.
"
00
g
'"
'"
'"
:t
>
Z
c
'"
'"
i!1
r
i
>
"
;!
N3me
ECG ChJracrcristics
Common Causes
PT Considerations
brst-degree AV block
Anterosepral MI
CHF
Second-degree AV block
type I (Wenkebach,
Mobltz I)
Second-degree AV block
type II (Mobitz II)
Third-degree AV block
(complete heart
block)
AV = amoventricubr; ClIF
ventricular rarc.
myocardial infarction .
Sources: Data from B Aehlen. ACLS Quick Review Study Guide. St. Louis: Mosby, 1 994; and EK Chung. Manual of Cardiac Arrhythmias. 80s
tOn: Bunerwonh-Heinemann, 1 986.
('
>'"
;;
;:
>
"
x
,;.
....
'D
Appendix 1 -B
82
Figure 1-8.2. Atrial {lutter. Note regular rhythm (P waves) but vemriwfar
rhythm depends on CONduction pattern. (\Vith permission fr011l M \Valsh, A
Cmmbie, S RevelC),. Nurse PractitioNers: Clinical Skills and Professional
Issues. Boston: Butterworth-Heinemann, 1 993;95.}
83
Figure I-B.3. Atrial fibrillation. Note the irregular rhythm alld absence of
normal P waves. (With permission from M Wafsh, A Crumbie, S Reveley.
Nurse Practitioners: Clinical Skills and Pro(essional Issues. Boston: Butter
worth-Heinemann, 1 993;95.)
84
Figure I-B.S. Ventricular ectopy with refractory period afterward. (\Vith per
missioN from M \Valsh, A Crumbie, S Reveley. Nurse Praclltioners: Clinical
Skills and Professional Issues. Boston: Butterworth-Hememallll, 1 993;97.)
"
o
;;
('
'"
"
>
:g
z
o
><
Figure 1-8.6. Sinus rhythm with premature ventricular contractions. (\Vith pennissio1t from EK Chung. Manual of Cardiac
Arrhythmias. Boston: Butterworth-Heinemann, 1 986; 1 02.)
,
=
00
,,,
86
87
88
D
Figure 1-B.8 (A-D). Continued.
Clinical Tip
F E V FVC, and the FEVj/FVC ratio are the most commonly interpreted PFT values. These measures represent
the degree of airway patency during expiration, which
affects airflow in and out of the lung.
Predicted normal values for a person's given age, gender, and height will be provided in the PFT report for reference to the person's actual PFT result.
p
3
Musculoskeletal System
Michele P. West and James J. Gaydos
Introduction
An understanding of musculoskeletal pathology and medical-surgical
intervention is often the basis of physical therapy evaluation and treat
ment planning for patients with acute orthopedic impairments. The pri
mary goal of the physical therapist working with a patient in the acute
care setting is ro initiate rehabilitative techniques that foster early restora
tion of maximum functional mobility and reduce the risk of secondary
complications. The objectives for this chapter are to provide the following:
1.
culoskeletal system
2.
3.
4.
159
160
5.
6.
Musculoskeletal Examination
The initial evaluation of a patient with orthopedic dysfunction is
invaluable to clinical management in the acute care setting. Physical
therapy intervention for the patient with orthopedic impairments typ
ically occurs postoperatively or after an injury is managed by the
medical-surgical team.
Patie1lt History
In addition to a standard medical review (see Appendix I-A), informa
tion pertaining to the patient'S musculoskeletal history should include
the following:
injury, or surgery
MUSCULOSKELETAL SYSTEM
161
History of falls
with activity
the hospital
Paill
Musculoskeletal pain quality and location should be determined
subjectively and objectively. Use a pain scale appropriate for the
patient's age, mental status, and vision. Note if pain is constant or
variable, and if movement or position increases or decreases the
pain. Refer to Appendix VI for more detailed information on pain
assessment and management.
Obseroatio11
A wealth of information can be gathered by simple observation of the
patient. This includes
162
General appearance
Clinical Tip
Skin Integrity
The patient'S skin integrity should be inspected in general for edema,
discoloration, bruising, or scars. If there is traumatic injury, care
fully inspect the skin at the level of and distal to the injury. Note any
lacerations or abrasions. If the patient has recently had surgery,
observe the location, direction, and quality of incision(s}. Note any
pressure sores or potential for such. Refer to Chapter 7 for further
discussion of skin integrity evaluation.
MUSCULOSKEU:.iAL SYSTEM
163
Clinical Tip
Pressure sores from prolonged or increased bed rest after
trauma or orthopedic surgery can develop in anyone,
regardless of age or previous functional abilities. Inspect
the uninvolved extremity for skin breakdown too.
Palpatio1l
Palpate skin temperature to touch, capillary refill, and peripheral
pulses at the level of or distal to injury or the surgical site. Refer to
Chapter 6 for further discussion of vascular examination. A discus
sion of special tests is beyond the scope of this text; however, the ther
apist should perform special testing if results of the interview or
screening process warranr further investigation.
the upper and lower extremities are listed in Tables 4-7 and 4-8,
respectively. Dermatomal innervation is shown in Figure 4-6.
The sequencing of the upper- and lower-quarter screen is as
follows2:
1.
proximal to distal and beginning at the spinal level and moving dis-
164
Deep
Root
Mymome
Dermatome
Tendon Reflex
CI
Cervical rmation
No innervation
None
C2
Shoulder shrug
Posterior head
None
C3
Shoulder shrug
Posterior neck
None
C4
Shoulder shrug
Acromioclavicular joint
None
C5
Shoulder abduction
Lateral arm
C5,6
Elbow flexion
C6
Wrist extension
Biceps
None
Brachioradialis
C7
C8
Finger abduction
Triceps
middle finger
Palmar distal aspect of
None
litde finger
Medial forearm
None
2.
distally, as above.
3.
Clinical Tip
MUSCULOSKELETAL SYSTEM
165
Nervc
Root
Myorome
Dermarome
Reflex
L1
Hip flexion
None
Hip flexion
None
L3
Knee extension
None
Patellar
with L4
L4
Knee extension
tendon
with L3 and LS
L4,S
Ankle
LS
Great toe
None
dorsiflexion
extension
51
Ankle plantar
flexion
Posterior
tibialis
Achilles tendon
166
Shoulder
Flexion/extension
0-18010-60
Abduction
0-180
Internal/external rotation
0-7010-90
Elbow
Flexion
0-150
Forearm
Pronation/supination
0-8010-80
Wrist
Flexionlextension
0-8010-70
Hip
Flexion/extension
0-120/0-30
Abducrion
0-45
Internal/external rotation
0-4510-45
Knee
Flexion
0-135
Ankle
Dorsiflexion/plantar flexion
0-2010-45
Clinical Tip
MUSCULOSKELETAL SYSTEM
167
the patient may feel (e.g., "Your foot will throb a little
when you lower it to the floor.").
Because orthopedic injuries can often be the final result of other
medical problems (e.g., balance disorders or visual or sensory impair
ments), it is important that the therapist take a thorough history, per
form a musculoskeletal screen, and critically observe the patient's
functional mobility. Medical problems may be subtle in presentation
but may dramatically influence the patient's capabilities, especially with
new variables, such as pain or the presence of a cast. Collectively, these
factors lead to a decreased functional level.
Clinical Tip
It may be the physical therapist who first appreciates an
additional fracture, neurologic deficit, or pertinent piece of
medical or social history. Any and all abnormal findings
should be reported to the nurse or physician.
Diagnostic Tests
The mOSt commonly used diagnostic tests for the musculoskeletal sys
tem are listed in the following sections. These tests may be repeated
during or after a hospital stay to assess bone and soft tissue healing
and disease progression, or whether there is a sudden change in vas
cular or neurological status postoperatively.
Radiography
More commonly known as x-rays or plain films, radiographic photo
graphs are the mainstay in the detection of fracture, dislocation, bone
loss, or foreign bodies or air in tissue. Sequential x-rays are standard
intra- or postoperatively to evaluate component position with joint
arthroplasty, placement of orthopedic hardware, or fracture reduc
tion. X-rays may also detect soft tissue injuries, such as joint effusion,
tendon calcification, or the presence of ectopic bone.'
Computed Tomography
Computed tomography (CT) is the diagnostic test of choice for the
evaluation of conical bone in certain circumstances. For fracture and
168
MUSCULOSKEU-rAL SYSTEM
169
Clinical Tip
Fracture Management
Types of Fracture
The analysis and classification of fracture reveal the amount of energy
impacted on bone and the potential for secondary injury, and direct
fracture management. Fractures can be described according to the
followings:
1.
2.
170
segmental; 4
(1
transverse; 2
oblique; 3
1995;22.)
MUSCULOSKELETAL SYSTEM
4.
171
5.
172
Figure 3-2. Techniques of if/temal fixatiofl. A Plate af/d six screws for trans
verse or short oblique fracture. B. Screws for [ollg oblique or spiral fracture.
c. Screws for long butterfly fragment. D. Plate and screws for short butterfly
fragment. E. Medullary nail for segmental fracture. (\Vith permission from
PC Beare, JL Myers [eds[. Adult Health Nursing [3rd edt. St. Louis: Mosby,
1 998; 1243.)
Complicatio/IS of Fracture
MUSCULOSKELETAL SYSTEM
173
Unfavorable
Early mobilization
nancy
Younger age
Vitamin deficiency
Good nutrition
Osteoporosis
Infection
Irradiated bone
Severe soft tissue damage
Distraction of fracture fragments
Severe comminution
Bone loss
Multiple fracture fragments
Disruption of vascular supply to bone
Avascular necrosis
Corticosteroid use
Comparrment syndrome
Incisional infection
Shock
174
Post-traumatic arthritis
Osteomyelitis
AVN
MUSCULOSKELETAL SYSTEM
175
Figure 3-3. Examples of ullstable pelvic fractures include (A. 8. and C) verti
cal shear (Malgaigne) fractures involving ischiopubic rami and disruption of
all ipsilateral sacroiliac joint, he they fA) throughout the ioint itself, (B)
through a (racture of the sacral wing, or (e) through a (racture on the iliac
bone. D. Straddle (rac/ures, involving all four ischiopubic rami, E. Bucket
handle fractures, involving all ischiopubic ramus and contralateral sacroiliac
joint. F. Dislocations invo{/Jing one or hoth sacroiliac joints and the symphy
sis pubis. (With permission from LN McKinnis /ed). Fundamentals of Ortho
pedic Radiology. Philadelphia: FA Davis, 1997:225.)
Acetabular Fracture
Acetabular fracture occurs when a high-impaCt blunt force is trans
mitted at one of four main points: the greater trochanter, a flexed
knee, the foot (with the knee extended), or the posterior pelvis." The
exact location and severity of the fracture (Figure 3-4), with or with
out dislocation, can depend on the degree of hip flexion and exten
sion, abduction and adduction, or internal and external rotation at
the time of injury." Acetabular fractures are highly associated with
multiple injuries and shock. Common immediate and early complica
tions associated with acetabular fracture include retroperitoneal
176
Hip Dislocatioll
Hip dislocation is the result of a high-velocity impact force and can
occur in isolation or with a femoral or acerabular fracture. The
majority of hip dislocations occur in a posterior direction, and ante
rior dislocations are rare.16 A patient with a posteriorly dislocated
hip has a limb that is shortened, internally rotated, and adducted in
slight flexion.'7 An anteriorly dislocated hip appears adducted and
externally rotated.16
Management of hip dislocation without fracture includes closed
reduction under consciolls sedation and muscle relaxation followed
MUSCULOSKELETAL SYSTEM
177
Clillical Tip
178
Figure 3-5.
3, 4
Clinical Tip
The uninvolved leg or a single crutch can be used to
assist the involved lower leg in and out of bed .
The patient should avoid rotation of and pivoting on
the lower extremity after intramedullary rod placement, as
microrotation of the intramedullary rod can occur and
place stress on the fixation device.
MUSCUtOSKELHAL SYSTEM
179
I
I
II
(I subcapltai; 2 transcervi
4 m/ertrocballleric; .5 subtrochanteric.) (With per
missi(J1l (rom A U",11I1, K JOlles /cds/. emergency Orthopaedics and Trauma.
cdi;
b,1S()Cervica/;
Patellar Fractllre
A patellar fracture results from direct trauma to the patella from a fall,
blow, or MVA (e.g., dashboard injury). The knee is often flexed during
injury, as the patella fractures against the femur. Patellar fracture may
also occur from sudden forceful quadriceps comracrion, as in sports or
180
MUSCULOSKELETAL SYSTEM
Type 1
Type 4
Type 2
Type 5
181
Type 3
TypeS
fractures (i.e., pilon fractures) are the result of high vertical loading
forces, such as with parachuring accidents, falls from heights, sport
ing injuries, and MVAs.23 Often, long axis compression throughout
the proximal lower extremity can cause associated tibial plateau frac
ture, hip dislocation, or acetabular fracture.
Ankle fractures commonly result from torque caused by abnormal
loading of the talocrural joint with body weight. Fractures may be
simple, involving avulsion of a portion of the distal fibula, or com
plex, involving rhe enrire morrise (trimalleolar fracture) with disrup
tion of the syndesmosis. Fracture severity depends on the degree of
foot inversion or eversion in relation to the subtaiar joint ar the time
of injury.23 Stability of the ankle depends on joint congruity and liga
mentous inregrity. Complications associated with ankle fractures arc
182
MUSCULOSKELETAL SYSTEM
183
II
Figure 3-8. Odontoid peg (ractllres. Type I (raetllres o( the upper third o( the
peg. Type II (raetllres at the ;1I/letioll o( the peg with the body o( C2. Type III
(raetllres esselltially o( the body o( C2 at the base o( the peg. (With permis
sion from A Unwin, K Jones /eds/. Emergency Orthopaedics and Trauma.
Boston: Buttertuorth-Heillemamt, 1 995;85.)
184
Figure 3-9.
Clinical Tip
MUSCULOSKELETAL SYSTE.M
185
Upper Extremity
Shoulder Girdle Fractures
186
Clinical Tip
When the patient is lying supine, placing a thin pillow
or folded sheet under the upper arm will help maintain
neutral alignment and reduce pain.
Getting in and out of bed on the opposite side of an
upper arm fracture is usually more comfortable for the
patient.
187
B
Figure 3-10. A. hacture of the medial epIcondyle. Note the "lnar nerve nuts
ImmedIately posterior to the fracture. B. The brachial artery is at risk lit
supracondylar fractures. (W"tl1 permISSIon from A Ullwm, K Jones reds).
Emergency OrthopaedIcs and Trauma. Boston: Butterworth-Hememann,
1995;126.128.)
188
1."
f.
I
MUSCULOSKEU:.IAL SYSTEM
189
Clinical TIp
For patients who have concurrent lower- and upper
extremity injuries and require the use of a walker or
crurches, a platform attachment placed on the assistive
device will allow weight bearing ro occur through the
upper extremity proximal to the wrist.
Metacarpal alld Phalallgeal Fractllres
190
Joint Arthroplasty
Joint arthroplasty, the surgical reconstruction of articular surfaces
with prosthetic components, is indicated to restore function and
motion to a joint that is affected by degenerative arthritic changes."
Total joint arthroplasty is reserved for the individual with pain that is
no longer responsive to conservative measures, such as anti-inflamma
tory medication, restriction or modification of activity, exercise,
weight loss, or the use of an assistive device. This surgery is elective in
nature and can be unilateral or bilateral. The incidence of bilateral
total j oint arthroplasties, simultaneous or staged, being performed in
the acute care setting has increased in recent years. Bilateral joint
arthroplasty has been established to be a safe procedure that reduces
total rehabilitation time and hospital length of stay, thus decreasing
medical costs and length of debilitation of the patient.35
Joint arthroplasty provides patients and caregivers with a predict
able postOperative course in the acute orthopedic care setting. For this
reason, there are high expectations for these patients to achieve spe
cific short- and long-term functional outcomes. The following sec
tions provide basic surgical information and clinical techniques and
suggestions for the acute care physical therapist.
Hip Arthroplasty
Hip arthroplasty involves the replacement of the femoral head, the
acetabulum, or both with prosthetic component . A hip arthroplasty
i s most commonly performed on patients with severe hip arthritis
(degenerative or rheumatoid), AVN, hip infection, or congenital dis-
MUSCULOSKELETAL SYSTEM
191
Table 3-5. Hip Disorders That May Require Tara I Hip Arthroplasty
Degenerative arrhritis (hyperrrophic or osteoarrhritis)
Rheumaroid arthritis
Arraumatic avascular necrosis
Imrapelvic prorrusio acetabuli"
Congeniml subluxation or dislocation
Post-traumatic disorders (femoral neck, trochameric, or acetabular
fractures)
Failed reconstructive procedures (femoral osteotomy, arthrodesis, or
resurfacing)
Metabolic disorders (Paget'S disease, Gaucher's disease, or sickle cell
anemia)
Fused hip or ankylosing spondylitis
Infectious disorders (tuberculosis and pyogenic arthritis)
Bone tumors
Neurologic disorders (cerebral palsy and Parkinson's disease)
Chronic progression of thc femoral head into rhe acetabulum and pelvis.
Source: Adapted from JW llarkcss. Arthroplasry of Hip. In ST Canale (cd), Campbell's
Operarive Orthopaedics, Vol. 1 (9th cd). 51. Louis: Mosby, 1998.
orders. Refer to Table 3-5 for a complete list of hip disorders that may
require hip arthroplasty.
The 1110st common type of hip arthroplasty, a total hip arthroplasty
(THA), is the replacement of both the femoral head and the acetabu
lum with a combination of metal (titanium or cobalt alloys) and poly
ethylene components ( Figure 3-13). Technology and research have
introduced new materials for the weight-bearing components, such as
ultra-high-molecular-weight polyethylene and ceramic-on-ceramic and
metal-on-metal implants; however, long-term survival of such compo
nents is not yet known.36
The acetabular and femoral components may be tmcentenled or
cemented. Uncemenred components are commonly used in the
younger, active patient, as well as in a patient with a revision THA
involving a failed cememed prosthesis. The uncemented components
have areas of porous coated metal on the surface that may be treated
with a biochemical agent, hydroxyapatite, to promote bony ingrowth
for improved fixation.'7 Press-fit prostheses are also being used and
have heavily textured surfaces that achieve fixation through interfer
ence or interlocking of bone and metal surfaces." Use of uncemented
192
Figure 3-13.
.\tUSCULOSKEU:,IAL SYSTEM
193
Figure 3-14. Mcuhfied bIpolar CliP. Polyetbylene CLIP IS placed over bead, and
the" the metal cup IS pressed over It. polyetbylene Imer is locked m metallic
cup, and bead is locked In socket of polyethylene liner. EntIre cup moves lvith
femoral head as olle lIlIIt, so cup canllot assume valglls or varus fixed posi
tiol1. Metal bead ca" rotate HI plastIC socket m aXIS of neck. CliP mllst be used
witb the femoral prostheSIS designed to fit properly mto plastic liner. (Wllh
permisS/oll (rom JIV Harkess. Arthroplasty o( Hip. In AH Crenshaw [edj,
Cmllpbd/'s OperatIve OrthopaedIcs, Vol.
Table 3-6. Surgical Approaches and Precaurions for Toral Hip Anhroplasry"
Surgical
Approach
Precnutions
Posterolateral
(most common)
Lnteral
AnterolMeral
194
incision made in the muscle mass and joint capsule for exposure of
the hip during surgery. Consequently, the hip remains at risk for dislo
cation until these structures are well healed, edema is reduced, and
the surrounding musculature is strengthened. Signs of dislocation
include excessive pain with motion, abnormal internal or external
rotation of the hip with limited active and passive motion, and short
ening of the Iimb.40
Medical complications that may occur after THA include nerve
inj ury, vascular damage and thromboembolism that can cause pulmo
nary embolism, myocardial infarction, and cerebral vascular accident.
Complications pertaining to the implant can include fracture, asepric
loosening, osteolysis, heterotopic ossification, and infection.43
Physical Therapy Intervention after Hip Arthroplasty
Early physical therapy intervention is focused on functional mobility,
patient education about movement precautions during activities of
daily living (ADLs), ROM, and strengthening of hip musculature.
Physical therapy may assist in preventing complications, such as
atelectasis, blockage of the intestines because of decreased peristalsis
secondary to anesthesia ( postoperative ileus), and D VT. Early mobili
zation improves respiration, digestion, and venous return from the
lower extremities. Patients should be educated about these risks to
assist in prevention of secondary complications.
The priority of treatment is to achieve safe functional mobility
(i.e., bed mobility, transfers, and ambulation with assistive devices)
to maximize independence and functional outcome. Patient educa
tion is an important aspect of physical thera py. The physical thera
pist should educate the patient about movement precautions while
encouraging use of the operated limb with functional activities.
Verbal and tactile clieing may assist a patient in precaution mainte
nance; failure to do so may result in hip dislocation. The therapist
should educate the patient that movement of the operated hip can
decrease postoperative pain and stiffness.
MUSCULOSKELETAL SYSTB1
195
Clinical Tip
All peripheral innervations, dermatomal and myoto
mal, should be assessed on initial examination, with
emphasis on the femoral nerve that innervates the quadri
ceps and the sciatic nerve that innervates the peroneals.43
Neuropraxia of the femoral nerve can occur secondary to
compression from surgical instrumentation and edema. A
knee immobilizer may be necessary to provide stability if
the quadriceps lacks adequate strength and stabiliry for
ambulation. If the peroneals are affected, resulting in a
footdrop on the affected side, a custom-fit ankle-foot
orthosis may be indicated for the patient to optimize gait.
o
The use of a knee immobilizer reduces hip flexion by
maintaining knee extension. This can be helpful in pre
venting dislocation in patients who are unable to maintain
posterior hip precautions independently.
o
Instruct the patient to avoid pivoting on the operated
extremity when ambulating. Instead, the patient should
turn by taking small steps and flexing the knee of the oper
ated leg to clear the toes. To maintain movement precau
tions, the patient is encouraged to turn away from the
operated limb.
196
Klfee Arthroplasty
\1USCUlOSKHFTAL SYSTEM
197
compartment.
198
Figure 3 16. A.
MUSCUlOSKELI;rAL SYSTEM
199
Source: Adaprcd from JL Guyron. Anhroplasry of Ankle and Knec. In ST Canale ( cd),
Campbell's Oper:ltive Orrhop:lcdics, Vol. I (9th cd). $(. LOllis: Mosby, 1998.
200
Clinical Tip
MUSCULOSKE.LETAL SYSTE.M
201
202
Shoulder Arthroplasty
Total shoulder arthroplasty (TSA) is indicated for patients with severe
MUSCULOSKELE.TAL SYSTEM
Figure 3-17.
203
204
Clinical Tip
A shoulder CPM can be ordered by the surgeon and
applied postOperatively or for home use to assist with
ROM and to prevent formation of adhesions.
The physical therapist should initiate a consult for
occupational therapy to instruct the patient on ADLs,
especially if the patient'S dominant arm is affected.
l\.lUSCULOSKELETAL SYSTEM
205
206
MUSCULOSKELETAL SYSTE.M
207
208
Figure 319.
MUSCULOSKELETAL SYSTEM
209
Clinical Tip
210
MUSCULOSKt::LI:.'AL SYSTEM
21 t
Indication
Procedure
Discectomy or
Herniated nucleus
microdiscecromy
Laminecromy
pulposus (HNP)
Spinal stenosis or
nerve root com
pression
Foraminotomy
Spinal stenosis,
HNP, or multiple
pression
Carpectomy
Multilevel stenosis,
spondylolisthesis
compression
Spinal fusion
Segmental instabil
ity, fractures,
tis
"'These procedures may be performed in any area of [he spine when indicated. The
approach may be anterior, posterior, or posterolateral.
Sources: Adapted from GW Wood. Lower Back Pain and Disorders of lntervenehral
Disc. In ST Canale (cd), Campbell's Opcrarive Onhopacdics, Vol. 1 (9th ed). St. Louis:
Mosby, 1998; and JJ Regan. Endoscopic Spinal Surgery Anterior Approaches. In jW
Frymoyer (cd), The Adult Spine Principles and Pracrice (2nd cd). New York: Lippin
cott-Raven, 1 997.
212
Figure 3-20.
MUSCULOSKELETAL SYSTEM
213
Clinical Tip
For surgical procedures with an anterior approach, the
patient should be given a splinting pillow and educated in
its use to promote deep breathing and coughing. A corset
can be use to aid patient comfort with activity.
214
o
Rolling walkers are useful to promote a step-through
gait pattern and decrease stress on the spine caused by lift
ing a standard walket. Patients should progress to a cane
or no assistive device to promote upright posture.
o
If an iliac crest bone graft is harvested through a second
incision, a patient may complain of increased pain at the
surgical site. Ice can decrease swelling at the donor site.
With this rype of graft, a patient wiiJ likely need an assistive
device to increase safery with ambulation and decrease pain.
o
If interbody fusion cages are used, the patient should be
encouraged to sit in a chair as soon as possible to increase
compression on the cage and promote bone ingrowth. Sit
ting time can be unlimited according to patient comfort.56
o
Patients who have undergone spinal fusion should be
educated about the adverse effect that cigarette smoking
has on the success of fusion.' The health-care team
should emphasize smoking cessation, or the patient should
be given the appropriate resources to assist with this task.
o The physical therapist should always check orders for
braces used by the surgeon and any other restrictions on
activity. Braces are usually worn when the patient is out of
bed. If necessary, a surgeon may limit raising the head of the
bed. Reverse Trendelenburg (putting the whole bed at a 45degree angle, with head up) can assist with patient ADLs.
o Treatment should be coordinated with the administra
tion of pain medication. Patients should be educated i n
relaxation techniques or breathing exercises to help man
age their pain. The physical therapist should also be aware
of any psychosocial factors that can interfere with patient
recovery. If necessary, consult the psychiatric or chaplain
services to assist with a patient'S coping skills.
Skin breakdown or decubitus ulcer formation of the immobilized limb over high-pressure areas (See Pathophysiology of
Wounds in Chapter 7)
Infection of traction pin sites or osteomyelitis
Compartment syndrome
MUSCUlOSKEU:,'TAl SYSTEM
235
236
53. Saltzman CL, Mclff TE, Buckwalter JA, Brown TO. Toral ankle replace
ment revisited. j Orthop Sports Phys Ther 2000;30(2) ,56-67.
54. Tattevin P, Cremieux AC, Porrier P, et al. Prosthetic joint infection:
When can prosthesis salvage be considered? Clin Infect Dis 1999; 2 9
(2 ) ,292-295.
55. Westrich GH. Salvati EA, Brause B. Postoperative Infection. In JV Bono,
jC McCarthy, TS Thornhill, et al. (eds), Revision Total Hip Arthro
plaSty. New York, Springer-Verlag, 1999;371-390.
56. Wood GW. Lower Back Pain and Disorders of Intervertebral Disc. In ST
Canale (ed), Campbell's Operative Orthopaedics, Vol. 3 (9th ed) . Bos
ron, Mosby, 1998; 3 014-3092.
57. Findlay GF, Hall BI, Musa BS, et al. A 1O-year follow-up of the outcome
of lumbar microdiscecromy. Spine 1998;23(10),1168-1171.
58. Miyakoshi N, Abc E, Shimada Y, er al. Ourcome of one-level posterior
lumbar interbody fusion for spondylolisthesis and postoperative inter
vertebral disc degeneration adjacenr to the fusion. Spine 2000;25(14) :
1837-1842.
59. Sandhu HS. Anterior lumbar interbody fusion with osteoinductive
growth facrors. Clin Orthop 2000;3 71,56-60.
60. Zeegers WS, Bohnen LMLj, Laaper M, Verhaegen MjA. Artificial disc
replacement with the modular type SB Charin! III: 2 -year results in 50
prospectively Studied patients. Eur Spine j 1999;8,21(}"'217.
61. Cinocti G, David T, Posracchini F. Results of disc prosthesis after a min
imum follow-up period of 2 years. Spine 1996; 2 1(8),995-1000.
62. Glassman SO, Anagnost SC, Parker A, et al. The effect of cigarette
smoking and smoking cessation on spinal fusion. Spine 2 000;25(20):
2 608-2615.
63. Philips BB. General Principles of Arthroscopy. In ST Canale (ed), Camp
bell's Operative Orthopaedics, Vol. 2 (9th cd). St. Loui" Mosby,
1998;1453-1469.
64. Norberg FB, Field LD, Savoie FH. Repair of the rorator cuff, mini-open
and arthroscopic repairs. Clin Sports Med 2000;19(I P7-97.
65. Minas T, Peterson L. Chondrocyte transplantation. Operative Tech
niques Orthop J997; 7(4P2 3 -3 3 3 .
66. Bentley G, Minas T. Treating joint damage in young people. BMJ
2000;320(7249) ,1585-1588.
67. Bryant GG. Modalities for Immobilization. In: AH Maher, SW
Salmond, TA Pellino (eds), Orthopaedic Nursing (2nd ed). Philadelphia,
Saunders, 1998;2 96-3 2 2 .
68. Stills ML, Christensen K . Management o f Extremity Fractures: Princi
ples of CaSting and Orthotics. In MM Lusardi, CC Nielsen (eds),
Onhotics and Prosthetics in Rehabilitation. Boston: Burrerwonh
Heinemann, 2000;291-306.
69. Tumbarello C. Acute Extremity Compartment Syndrome. J Trauma
Nurs 2000;7,3(}"'36.
70. Dubuisson We. Nursing Management of Adults with Musculoskeletal
Trauma. In PG Beare, jL Myers (eds), Adult Health Nursing (3rd ed). St.
Louis, Mosby, 1998; 1228-1231.
71. Zimmer Traction Handbook : A Complete Reference Guide to the Basics
of Traction. Zimmer, Inc., 1996.
Note: This appendix was created as a guide for the physical thera
pist-these tables are not all-inclusive. Specific fracrure classification
systems are used only if they are universal or very commonly used;
otherwise, fractures are listed by general type such as nondisplaced or
displaced, closed or open, or stable or unstable. The authors encour
age the therapist to consult other resources for specific fracture pat
terns or eponyms not described here. T he weight-bearing starus is
provided as an estimate in the setting of a localized fracture; there
fore, be sure to follow physician mandated orders for weight-bearing,
Table 3-A.1. Young Classification, Management, and Physical Therapy Intervention for Pelvic Ring Fractures
Fracture Type
Management Options
External fixation
Anterior ORIF
PWB
Hip and disca) joint ANAROM
Lower-extremity exercise
External fixation
Posterior percutaneous pinning
Anterior and posterior ORIF
Sympromatic pain management
B
Functional mobility NWB or rOW
ut of bed
o
sfer
ed
to
ally
tran
limit
(usu
only) on the least-involved , ide
j:;
:r
>
z
"
'"
o
"
..-
N
'"
00
External fixation
Anterior and posterior ORIF
External fixation
Anterior and posterior ORIF
AlAAROM acrive/ac[ive-3ssistive range of motion; APC anteroposterior compression; LC lateral compression; PWB panisl weight
bearing; NWB = non weight bearing; ORIF = open-reduction imernal fixation; 511 = sacroiliac joint; mWB = touch-down weight bearing;
WBAT weighr bearing as tolerated.
Sources: Adapted from HG Cryer, EJohnson. Pelvic Fracrures.In DV Feliciano, EE Moore, KL Marrox (eds), Trauma (3rd ed). Stamford, CT:
Appleton & Lange, 1996;640; and data from AR Burgess, ALJones. Fractures of the Pelvic Ring. In CA Rockwood, DP Green, RW Bucholz,
JD Heckman (cds), Rockwood and Green's Fracrures in Adults (4th ed), Philadelphia: Lippincon-Ravcn, 1996.
=
1:;
r-
r-
x
w
,.
N
w
'"
Table 3-A.2. Management and Physical Therapy Intervention for Acetabular Fractures
Fracture Type
Stable (displacement of <2-5
Management Options
mm
in the
Closed reduction
large ante
Percutaneous pinning
Open reduction internal fixation
(may involve trochanteric osteot
omy if posterior wall fracture)
Total hip arthroplasty
PWB partial weIght beanng; ROM range of motion; TOWB touch-down weight bearing.
The patient m3y have hip dislocation precautions if the acetabular fracture IS associated with hip dIslocation.
Sources: Data from TG DIPasquale, RJ NOWinSki. The Acute Care and Evaluation of Acctabubr Fractures. In M Bosse, JF Kellam, TJ Fisher, P
Tomena (cds), Orthopaedic Knowledge Update: Trauma (2nd ed). Rosemont,IL: American Academy of Orthopaedic Surgeons. 2000; and M
Tile. Fractures of the Acetabulum. In CA Rockwood. Dr Green. RW Bucholz, JD Heckman (cds), Rockwood and Green's Fractures in Adults
(4th cd). Philadelphia: Lippincott-Raven, 1996.
=
'"
....
o
>
()
;;
iE
'"
o
"
J:
:;I
24 t
Options
Garden I (impacted,
Closed reduction
incomplete
and percutane
fracture)
ous pinning
Closed reduction
and spica casr
Garden II (complete
Closed reduction,
fracture witheur
displacement)b
internal pin
fixation
or NWB (spica)
NAAROM exercises
(Iimired by pain)
Lower-extremity strengthening
Functional mobility PWB
NAAROM exercises
(Iimired by pain)
ORIF
Lower-extremity strengthening
ORIF
ORIF
Unipolar or bipolar
arthroplasty
or WBAT, NAAROM
exercises and strengthening,
usual l y with posterior hip
precaurions
242
Physical Therapy
Fracture Type
Options
Intervention
fixation
(CRIF)
ORIF
ORIF
osteotOmy
and bone
grafting
Distal LE strengthening
Bipolar
exercise
arthroplasty
Subtrochanteric, Russell
Taylor type LA (single
fracture line extends from
ORIF
1M rod
See Intertrochanteric,
Evans rype I, above
ORIF
1M rod
See Intertrochanteric,
Evans type I, above
ORIF/OHS
1M rod
See Intertrochanteric,
Evans type I, above
ORIFfDHS
Bone grafting
Functional mobility
NWBorTOWB
Gentle hip ROM exercise
Distal LE strengthening
exercise
243
Management Options
Intervention
1M rod
Functional mobility
NWB,TDWB,or
ORIF
WBAT
Gende ROM exercise
Closedj comminuted,
impacted, or both
Functional mobiliry
NWBorTDWB
1M rod
Lower extremity
ORIF
exercise if on bed
rest
Open; comminuted
and displaced
nuted, impacted, or
ate or delayed
both, above
wound closure
Short-term skeletal
traction on bed rest
External fixation
1M rod
244
Options
Supracondylar;
extra- articular,
simple,
NAAROM exercise
nondisplaced
Supracondylar;
extra-articular,
displaced, or
comminured
articular,
close monitoring
nondisplaced
Unicondylar; intraarticular,
displaced
245
Management
Fracture Type
Options
Inrercondylar;
Long-term traction
Functional mobility
intra-articular
ORIF
Cast brace if less
stable fixation
achieved
Management Options
Intervention
Nondisplaced
Closed reduction
Functional mobility
PWBor WBAT
Avoid strong straight
extension
Displaced (simple
vertical or trnns-
verse fracture)
full extension
Continuous passive
Illorion
Comminuted
246
Table 3-A.7.
Continued
Physical Therapy
Fracture Type
Management Options
Intervention
Partial patellectomy
See Nondisplaced,
above, in regard to
menr remains) or
quadriceps
Management Options
Intervention
Nondisplaced
Closed reduction
Functional mobility
Cast-brace immobilization
or postoperative knee
brace
Ligament repair (if appli
cable)
TDWB or PWB
AAROM exercise,
continuous passive
morion to knee joint,
or both
247
Physical Therapy
Fracture Type
Management Options
Imervention
Displaced; single
External fixation
Functional mobiliry
condylar or
split compres
sion fracrure
NWB ,mWB , or
ORIF
Cast-brace application or
posroperarive knee brace
PWB
AAROM exercise,
continuous passive
morion to knee joint,
or both
Displaced;
impacted, or
severely
comminuted
bicondylar
fracture
extremity exercise if on
cable
bed rest
Immobilization brace
248
Management Options
Closed; minimally
Closed reduction
displaced
PWB, or WBAT
Quadriceps strengthening
Edema management
Closed; moderately
displaced
Closed; severely
displaced,
comminured,
or borh
External fixation
Temporary calcaneal
traction [Q allow for
soft tissue healing
ORIF
Open
External fixation
with or without; NWB = non weight bearing; PWB = parrial weight bearing; ROM =
range of motion; TOWB = touch-down weight bearing; WBAT weight bearing as tol
erated.
Physical Therapy
Fracture Type
Options
Intervention
Distal tibial;
Closed reduction
closed,mini
mally displaced
Distal tibial;
closed,moder
ately displaced
ORIF
Short leg cast
249
Medical-Surgical
Physical Therapy
Fracture Type
Options
Intervention
Distal tibial;
Temporary calcaneal
closed, severely
displaced
traction
External fixation
ORIF
Lower-extremity isomet
riCS
Neutral ankle positioning
Proximal joinr strengthening
Edema management
External fixation
Ankle; closed,
nondisplaced
Closed reduction
Short leg cast or walk
ing cast
Closed reduction
placed, multi
ORIF
Edema management
fracture, or both
Cast application or
Proximal lower-extremity
other immobilization
strengthening exercise
method dependenr on
degree of edema
Ankle; open
placed, multifracture,
or delayed wound
or both, above
closure
Tracrion
External fixation
ORIF
NWB = non weight bearing; ORJF = open-reduction inrernal fixarion; PWB = p artia l
weight bearing; ROM = range of morion.
Source: Data from WB Geissler, AK Tsao, JL Hughes. Fracrures and Injuries of rhe
Ankle. In CA Rockwood, Dr Green, RW Bucholz, JD Heckman (cds), Rockwood and
Green's Ff3crurcs in Adults (4rh cd). Philadelphia: Lippincott-Raven, 1996.
250
Management Options
Intervention
Calcaneal; extra-
Closed reduction
Functional mobility
articular, minimally
displaced
NWB
SLC
Proximal lower-extremity
strengthening and
ROM exercise
Edema management
Ank le/forefoot exercise as
per physician and type
of immobilization
device
Calcaneal; avulsion
Closed reduction
ORIF
SLC
Sk eletal traction
Immediate or delayed
SLC
Calcaneal; open
very severe
articular, minimally
ate or deJayed
displaced, above
wound closure
Skeletal traction
External fixation
251
Physical Therapy
Fracrure Type
Management Options
lnrervention
Forefoot; minimally
Closed reduction
Functional mobility
displaced
Percutaneous pinning
SLC or walking cast
NWB,PWB ,or
WBAT, dependent
on exact location
and severity of frac
ture
Proximal lower
extremity strength
ening and ROM
exercise
Edema management
Forefoot; moderate or
severe displacement,
with fragmentation
or angularion
Forefoot; open
ORJF
Percutaneous pinning
displaced, above
SLC
See Forefoot; minimally
See Calcaneal;
open, above
displaced, above
ORIF
NWB = non weight bearing; ORIF open-reduction internal fixatioll; PWB = partial
weight bearing; ROM range of motion; SLC short leg cast; WBAT weight bearing
as tolerated.
'"For calcaneal fractures, cast application may not be in the neutral ankle position to
protect the fracture site from strong ankle muscle contractions.
Source: Data from JD Heckman. Fractures and Dislocations of the Foot. In CA Rock
wood, DP Green, RW Bucholz, JD Heckman (cds). Rockwood and Green's Fractures in
Adults (4th cd). Philadelphia: Lippincon-Raven, 1996.
=
252
Management Options
Intervention
Hangman's fracture,
or bilateral pedicle
fracrure of axis IC I )
Type I-no angulation and <3 mm
displacement of
C2 on C3
Type 11->3 mm
displacement of
C2 on C3
Type !lA-minimal
displacement and
possible)
Posterior open reduc
tion and halo vest
or CT-3 fusion for
type 11\
logroll precautions
Posture and body
mechanics training
Therapeutic exercise and
active-assisted/passive
range of motion depcn
dent on neurologic
IIlJury
Balance and scapular
exercises for the patient
in a halo vest
significant angu
lation of C2
Type III-full uni
or bilateral facet
dislocation
Odontoid process
fracture
Type l-<lblique
avulsion fracture
vest, amerior or
odontoid
posterior C1-2
Typc II-fracture of
the neck of the
odontoid
Type 1I1-fracture
extending ro the
C2 vertebral body
253
Physical Therapy
Fracture Type
Management Oprions
Intervention
Cervical collar
Functional mobility
wedge) fracture-
mechanics training
Cervical collar
(stable, isolated) or
laminal fracture
Management Options
Intervention
Spinous process,
Cervicothoracic or
rransverse process,
thoracolumbar
laminar, or facet
orrhosis
fracture (stable,
logroll precaurions
PoSture and body
mechanics training
isolated)
254
Management Options
Intervention
(axial compression)
fracture-unstable
Thoracolumbosacral
orthosis
Anterior/posterior
decompression and
transverse process,
laminar, or facer
fracrure (stable,
isolated), above
reconstruction :t:
bone grafting
Multidirectional frac
Anterior/posterior
decompression and
involvement and
fusion
facet dislocarion
unstable
Thoracolumbosacral
orthosis
with or without.
Source: Data from AR Vaccaro, K Singh. Thoracolumbar Injuries: Nonsurgical Treat
ment. DC Kwok. Thoracolumbar Injuries: The Posterior Approach. In Orthopaedic
Knowledge Update: Trauma (2nd ed). Rosemont, IL: American Academy of Ortho
paedic Surgeons, 2000.
:!: =
Management Options
Intervention
Proximal humeral;
Closed reduction
Functional mobility
displaced, one-part
Sling immobilization
NWB
Pendulum exercises and
passive range of
motion per
physician
Elbow, wrist, and hand
range-of-morion
exercises
Edema management
255
Physical Therapy
Fracture Type
Management Options
Intervention
Proximal humeral;
displaced, two-part
percutaneous
displaced, one-parr,
pinning
above
ORIF
Intramedullary rod
Sling immobilization
Proximal humeral;
displaced,
three-part
ORIF
Hemiarthroplasty
Proximal humeral;
displaced, four-part
Transcutaneous reduc
tion with
displaced, three-part,
fluoroscopy
above
Percutaneous pinning
ORIF
Comminution of
humeral head
Humeral shaft; closed,
minimal
displacement
Hemiarthroplasty
Sling immobilization
Closed reduction
Sling, hanging arm
cast, or functional
brace
256
Table 3-A.14.
Continued
Physical Therapy
Fracture Type
Management Options
Intervention
ORIF
displaced with
angularion
Humeral shaft; open
Intramedullary nails
Long arm spline
irrigation and debride-
closed, minimal
displacement, above
See Humeral shaft;
mentwith immediate
closed, minimal
or delayed wound
displacement, above
closure
External fixation
ORIF
257
Management Options
Intervention
Olecranon; closed,
Functional mobility
nondisplaced
elbow in midflexion
NWB
Initiation of elbow active
assisted range of
motion in pain-free
range per physician
Distal and proximal joint
active range of motion
Edema management
Olecranonj closed,
ORIF
ORIF
displaced
Olecranon; closed,
comminured
Radial head; closed,
nondisplaced, above
nondisplaced, above
Immobilization
Closed reduction
non-, or minimally
with early
displaced
immobilization
Hemaroma aspirarion
Sling or short-term
splint
Radial head; closed,
displaced
short-term splinting
nondisplaced, above
if range of motion
(ROM) adequate or
ORIF if ROM inad
equate
Partial or total radial
head excision
Radial head; closed,
comminuted
ORIF with
immobilization
nondisplaced, above
:t
bone grafting
with or without; NWB = non weight bearing; ORfF open-reduction internal fixation.
Source: Dala from RN Hotchkiss. Fractures and Dislocations of the Elbow. In CA
Rockwood, DP Green, RW Bucholz, JD Heckman (eds), Rockwood and Green's Frac
tures in Adults (4th ed). Philadelphia: Lippincott-Raven, 1996.
%=
258
Management Options
Intervention
Shaft fracture of
Functional mobility
radius or ulna
casting, or casting
alone if
nondisplaced
ORJF (if displaced)
with functional
brace
Distal radius;
extra-articular
NWB
Distal and proximal
range-of-morion
exercises
Edema management
See Shaft fracture, above
percutaneous
pinning
Sugar-tong splint
or c:ast
ORIF:t: functional
brace
Distal radius;
intra-articular
ORJF
movemenr if patient
percutaneous
pinning
Arthroscopic con
trolled internal
fixation
Distal radius;
illtra-articul:ar,
external fixation
comminuted
ORIF
Bone grafting
Splinr
4
Nervous System
Michele P. West
Introduction
The nervous system is linked ro every system of the body and is
responsible for the integration and regulation of homeostasis. It is
also involved in the action, communication, and higher cortical
function of the body. A neurologic insult and its manifestations
therefore have the potential ro affect multiple body systems. To
safely and effectively prevent or i mprove the neuromuscular, sys
temic, and functional sequelae of altered neurologic status in the
acme care setting, the physical therapist requires an understanding
of the neurologic system and the principles o f neuropathology. The
objectives of this chapter are ro provide the following:
1.
A brief review of the structure and function of the nervous
system
2.
An overview of neurologic evaluation, including the physical examination and diagnostic tests
3.
A description of common neurologic diseases and disorders, including clinical findings, medical and surgical management,
and physical therapy interventions
259
260
Protective Mechanisms
The brain is protected by the cranium, meninges, ventricular system,
and blood-brain barrier.
Cranium
The cranium encloses the brain. It is composed of eight cranial and
14 facial bones connected by sutures and contains a pproximately
85 foramen for the passage of the spinal cord, cranial nerves
(CNs), and blood vessels.' The cranium is divided into rhe cranial
vault, or calvaria (the superolateral and posterior aspects), and the
cranial floor, which i s composed of fossae (the anterior fossa sup
POrtS the frontal lobes; the middle fossa supports the temporal
lobes; and the posterior fossa supports the cerebellum, pons, and
medul la).2
NERVOUS SYSTEM
261
....... """'.
-""" ..
MlClIO'ML",., I'OITCltmlAL
GnU)
.....
.........
Inlemal
C".M.-+O
B
Figure 4-1. A. Medial (midsagittal) view of a hemisected brain. (\Vith permis
sion from S Gilman, S W Newman ledsJ. Manter and Gatz's Essentials of
Neuroanatomy and Neurophysiology [7th edJ. New York: Oxford University
Press, 1987;9.) B. Horizontal section of the cerebrum showing the basal gan
g[ia. ( With permission from RJ Love. we Webb [eds[. Neuro[ogy for the
Speech-Language Pathologist [4th ed]. Boston: Butte nvorth- Heinemaml,
2001 ;38.)
'"
Lobe of
Cerebrum
Frontal
lobe
Structure
Function
Dysfunction
Precentral gyrus
Supplementary
motor area
Prefrontal pole
Paracentral
lobule
Broca's a rea
Parietal
lobe
Postcentral gyrus
Parietal pole
>
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"
"
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>
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r
-l
>
Wernicke's area
Temporal
lobe
Optic radiation
GustatOry cortex
Visual tract
Perception of taste
Superior
temporal gyrus
(audicory
cortex)
0: Appreciation of language
Middle and
inferior
tern poraI gyri
Wernicke's area
i::
<
.....
'"
w
N
'"
....
Occipital
lobe
o
Structure
Dysfunction
Function
>
Optic radiation
Visual tract
Striate and
parastriare
cortices
dominant, ND
"
'"
J:
>
Z
"
o
"
nondol11inant.
Sources: Data from KW Lindsay, I Bone, R Callander (eds). Neurology and Ncurosurgery Illustrated (2nd cd). Edinburgh, UK: Church.1l
"
Livingscone. 1991; S Gilman. SW Newman (cds). Manrer and Gaez's Esscmials of Clmical Neuroanatomy and Neurophysiology (7th ed).
=t
i'i
>
r
CO
Anatomy and Physiology (5th ed). San Francisco: Benjamin-Cummings, 200t; and L Thelan, J Davic, M Lough (eds). Cnncal Care Nursing:
Diagnosis and Managemcll( (2nd cd). Sr. Louis: Mosby, 1994.
i'"
!:'
Table 4-2. Structure, Function, and Dysfunction of the Diencephalon, Brain Stem, and Cerebellum
Brain Structure
Substructure
Function
Dysfunction
Thalamus
Cortical arousal
Integrative relay station for all
ascending and descending
motor stimuli and aU ascending
sensory stimuli except smell
Memory
Altered consciousness
Signs and symptoms of i ncreased
ICP
Contralateral hemiplegia,
hemiparesis, or hemianesthesia
Altered eye movement
Hypothalamus
Mamillary bodies
Optic chiasm
Infundibulum (stalk) connects
to the pituitary gland
Forms inferolateral wall of third
ventricle
Diencephalon
13
5<
N
'"
'"
N
'"
'"
Substructure
Function
Dysfunction
Pineal body
Posterior commissure. striae
medulla res, habenular nuclei
and commissure
Dysfunction unknown
Subthalamus
Substantia nigra
Red nuclei
Pituitary
Contralateral hemiparesis or
hemiplegia and hemianesthesia
Contralateral hemiparesis or
hemiplegia and hemianesthesia,
altered consciousness and
respiratory pattern, cranial
nerve palsy
Epithalamus
Internal capsule
n
>
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'"
Brain stem
Midbrain
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n
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0
0
'"
'"
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-<
1)
>
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>
Pons
Medulla
Anterior lobe
Medial portion
Lateral portion
Posterior lobe
:erebellum
Z
m
'"
iii
N
'"
"
ADH
N
a..
co
Substructure
Function
Dysfunction
Flocculus nodule
antidiuretic hormone; eN
intracranial pressure.
Sources; Data from KW Lindsay, I Bone, R Callander (cds). Neurology and Neurosurgery Illustrated (2nd ed). Edinburgh, UK: Churchill
Livingstone, 1991; S Gilman, SW Newman (cds). Manter and Gatz's Essentials of Clinical Neuroanaromy and Neurophysiology (7th ed),
Philadelphia: FA Davis,
1989; JA Kiernan
(ed). Introduction to Human Neuroscience. Philadelphia: Lippincott, 1987; EN Marieb fed). Human
Anatomy and Physiology (5th ed). San Francisco: Benjamin-Cummings. 2001; and L Thelan, J Davie, M Lough reds). Critical Care Nursing:
Diagnosis and Managemenr (2nd ed). St. Louis: Mosby.
1994.
8;;!
n
>
'"
'"
:t
>
15
1')
o
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Ci
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or
:im
s:
NERVOUS SYSTEM
269
Meninges
The meninges are three layers of connective tissue that cover the brain
and spinal cord. The dura marer, rhe outermost layer, lines the skull
(periosteum) and has four major folds (Table 4-3). The arachnoid, the
middle layer, loosely encloses the brain. The pia mater, the inner layer,
covers the convolutions of the brain and forms a portion of the chor
oid plexus in the ventricular system. The three layers create very
important anatomic and potential spaces in the brain, as shown in
Figure 4-2 and described in Table 4-4.
Ventricular System
The ventricular system nourishes the brain and acts as a cushion
by increasing the buoyancy of the brain. It consists of four ventri
cles and a series of foramen, through which cerebrospinal fluid
(CSF) passes to surround rhe CNS. CSF i s a colorless, odorless
solution produced by rhe choroid plexus of all ventricles. CSF cir
culares in a pulse-like fashion through the ventricles and around
the spinal cord with the beating of ependymal cilia rhar line the
ventricles and intracranial blood volume changes that occur with
breathing and cardiac systole] The flow of CSF under normal con
ditions, as shown in Figure 4-3, is as follows4:
Falx cerebelli
Tentorium cerebelli
Diaphragm sellae
Source: Data from JL Wilkinson (ed). Neuroanatomy for Medical Srudents (3rd ed).
Oxford, UK: Butterworth-Heinemann,
1998.
270
Figure 4-2. Coronal section o(cranial meninges showing a venous sinus and
dural (old. ( With permission from PA Young, PH Young. Basic Clinical Nell
roallatomy. Phi/adelphia: \Vil/iams & \Vi/kills, 1997;8.)
to
Subdural space
Subarachnoid space
NE.RVOUS SYSTE.M
271
Fourth veolflcle
Foramen olluschka
Foramen 01 Magendle
Figure 4-3. The velltricular system of the brai". Arrows indicate the ciratla
liol1 of cerebrospinal fluid from the site of formatioll in the choroid plexus to
the site of absorptioll ill the villi of the sagittal 5;11115. (\Vith permission from J
Bogouss/avsky, M Fisher /edsJ. Textbook of Neurology. Bostol1: Blitterworth
Heillemallll, 1998;656.)
272
around, these cells. The blood-brain barrier is absent ncar the hypo
thalamus, pineal region, anterior third ventricle, and floor of the
fourth ventricle.3
Circulation
The brain reccives blood from the internal carotid and vertebral arter
ies, which are linked together by the circle of Willis, as shown in Fig
ure 4-4. Each vessel supplies blood to a certain part of the brain
(Table 4-5). The circulation of the brain is discussed in tcrms of a sin-
---'tj:.--"'''' rnlernal
carotid art
CIrcle 01 WilNs
& associated veins
NERVOUS SYSTEM
273
Artery
Anterior circulation
Internal carotid artery
(ICA)
Posterior circulation
Vertebral artery
Basilar artery
Posterior inferior
cerebellar artery (PICA)
Anterior inferior
cerebellar artery (AICA)
1995; and KL Moore (cd). Clinically Oriented Anaromy (2nd cd). Baltimore:
1985.
274
ACUTE CARE
HANDBOOK FOR
PHYSICAL THERAI)ISTS
site. The superior sagittal sinus and sinuses located in the dura and
scalp then drain blood into the internal jugular vein for return to the
heart.
Spinal Cord
The spinal cord lies within the spinal column and extends from the
foramen magnum to the first lumbar vertebra, where ir forms the
conus medullaris and the cauda equina and attaches to the coccyx
via the filum terminale. Divided into the cervical, thoracic, and
lumbar portions, it is prorected by mechanisms similar ro those
supporting the brain. The spinal cord is composed of gray and
white matter and provides the pathway for the ascending and
descending tracts, as shown in cross section in Figure 4-5 and out
lined in Table 4-6.
Ulftlar
i:!aCortiooSPlflai (l
RubrOlf)lnal Tract
An1
HomofGrayMaMIW
vestibulospinal Trac1
-+-1-,'
Px
...<
<).,
-'
. 0:: "(
/1
1
C;
" G..-,
S ecaJ
Post SPft)Cereoeiar Trac1
C
,'\.
;;>
'Y
s.cr.I
...
AnI
Spmocerebellar Tracl
ASCENDING
PATHWAYS
Figure 4-5. Cross-section of the spinal cord. (Ant. :; anterior; Lat. :; lateral; Post. :; posterior.) ( With permission from RJ Love,
we Webb ledsl. Neurology for the SpeechLanguage Pathologist 14th edl. Bosto", BuHerlVorth-Hei"ema"". 2001 ;44.)
N
....
v.
276
Function
Fasciculus
gracilis
Fasciculus
cuneatus
Laceral
spinothalamic
Ventral
spinocerebellar
Dorsal
spinocerebellar
Lateral
corticospinal
(pyramidal)
Anterior
corticospinal
(pyramidal)
Rubrospinal
(extra
pyramidal)
Tectospinal
(extra
pyramidal)
Vestibulospinal
(extra
pyramidal)
"Sensory tracts ascend from the spinal cord; motor tracts descend from (he brain
(0
the
spinal cord.
Sources: Data from S Gilman, SW Newman (cds). Mamer and Gatt's Essenrials of Clin
ical Neuroanatomy and Neurophysiology (7th ed). Philadelphia: FA Davis, 1989; and
EN Marieb (cd). Human Anatomy and Physiology (5th cd). San Francisco: Benjamin
Cummings, 2001.
NE.RVOUS SYSTEM
277
Spinal RoO[
Innervation
Dorsal scapular
C5
Supmscapular
C5 and C6
Supraspinatus, infraspinatus
Lower
subscapular
C5 and C6
Teres major
Axillary
C5 and C6
Radial
Ulnar
C8 and T I
Median
Pronator teres, flexor carpi radialis, palmaris longus, flexor digirorum super
ficialis and profundus, flexor pallicis
longus, pronaror quadratus, abductor
pollicis brevis, opponens pollieis,
flexor pollicis brevis, first and second
lumbricals
Musculo
cutaneous
Source: Data from FH Nencr (cd). Arias of Human Anaromy. Summit Ciry, NJ: CIBA
GEIGY Corporation, 1989.
Neurologic Examination
The neurologic examination is initiated on hospital admission or in
the field and is reassessed continuously, hourly or daily, as necessary.
The neurologic examination consists of patient history; mental status
examination; viral sign measurement; vision, motor, sensory, and
coordination testing; and diagnostic resring.
278
Spinal Root
Innervation
Femoral
L2, U, and L4
Iliacus
Psoas major
Sartorius
Pecrinous
Rectus femoris
Vastus lateral is, intermedius, and medialis
Articularis genu
Obturator
Sciatic
Biceps femoris
Adductor magnus
Semitendinosus
Semimembranosus
Tibial
Gastrocnemius
Soleus
Flexor digitorum longus
Tibialis posterior
Flexor hallucis longus
Common
peroneal
Patietlt History
A detailed h istory, initially taken by the physician, is often the most
NERVOUS SYSTEM
279
Spinal Root
Innervation
Trapezius
Spinal accessory
C3 and C4
Phrenic
Diaphragm
Long thoracic
Serratus anterior
Medial pecroral
Lateral pecroral
Pectoralis major
Thoracodorsal
C 7 and C8
Latissimus dorsi
Intercostal
Corresponds ro nerve
root level
External intercostals
Internal intercosrals
Levatores costarum longi
and brevis
Iliohypogastric and
ilioinguinal
LI
Transversus abdominus
Internal abdominal
oblique
Inferior gluteal
Gluteus maximus
Superior gluteal
Source: Data from FH Netter (cd). Arias of Human Anatomy. Summit City, NJ: eIBA
GEIGY Corporation, 1989.
In addition to the general medical record review (see Appendix 1A), questions relevant to a complete neurologic history include the
following:
280
Vlnuall)tlal
UM of
limb
upper
Figure 4-6. Dermatome chart based 0" embryologic segments. (\vith permis
sion from CD Maitland /ed/. Vertebral Manipulation /5th edt. Oxford, UK:
Butterworth-Heinemallll, 1986;46.)
NERVOUS SYSTEM
281
Observation
Data that can be gathered from close or distant observation of the
patient include the following:
Body position
Eye movement(s)
Clinical Tip
The therapist should correlate these observations with
other information from the chart review and other health
care team members ro determine (1) if the diagnosis is con
sistent with the physical presentation, (2) what rypes of
commands or tone of voice to use, ( 3 ) how much assis
tance is needed, and (4) how to prioritize the portions of
the physical therapy evaluation.
282
Completely awake.
Aware of all stimuli.
Able to interact meaningfully with clinician.
Lethargic or
somnolent
Obtundent
Difficult to arouse.
Requires constant stimulation for all activities.
Confused.
Stuporous
Coma
Delirium
Dementia
Sources: Data from RL Strub, FW Black (cds). Mcntal Status Examination in Neurolo!,'Y
(2nd cd). Philadelphia: FA Davis, 1985; and F Plum, J Posner (cds). The Diagnosis of
Scupor and Coma (3rd cd). Phil3delphia: FA Davis, 1980.
NERVOUS SYSTEM
283
Clinical Tip
284
Response
Eye opening (E)
Spontaneous: eyes open without stimulation
To speech: eyes open to voice
6
5
4
Nil: no vocalization
Source: Data from B jennen, G Teasdale (cds). Management of Head Injuries. Phibdel
phia: FA Davis,
198 I .
score (i.e., E + M
signifies coma.10
Clinical Tip
Calculation of the GCS usually occurs at regular intervals.
The GCS should be used to confirm the type and amount
of cueing needed to communicate with a patient, deter
mine what time of day a patient is most capable of partici
pating in physical therapy, and delineate physical therapy
goals.
NERVOUS SYSTEM
285
Cognition
Cognitive testing includes the assessment of attention, orientation,
memory, abstract thought, and the ability to perform calculations or
conStruct figures. General intelligence and vocabulary are estimated
with questions regarding history, geography, or current events. Table
4- 1 2 lists typical methods of testing the components of cognition.
Definition
Task
Ability to artend to a
specific stimulus or task
Repetition of a series of
numbers or lerrers
Spelling words forward and
backward
Orientation
Ability to orient to
person, place, and time
Memory
Immediate recall
Short-term memory
Long-term memory
Calculation
Construction
Ability to construct a
two- or three-dimen
sional figure or shape
Abstraction
Ability to reason in an
abstract rather than a
literal or concrete
fashion
Inrerpret proverbs
Discuss how two objects are
similar or different
Judgment
Ability to reason
(according to age and
lifestyle)
fO
Physical Examina
286
Emotional State
Emotional State assessment entails observation and direct question
ing to ascertain a patient's mood, affect, perception, and thought
process, as well as to evaluate for behavioral changes. Evaluation of
emotion is not meant to be a full psychiatric examination; however,
it provides insight as to how a patient may complete the cognitive
portions of the mental status examination. I I
Clinical Tip
It is important to note that a patient's culture may affect
particular emotional responses.
Clinical Tip
The physical therapist should be aware of and use, as
appropriate, the speech-language pathologist's suggestions
for types of commands, activity modification, and posi
tioning as related to risk of aspiration.
The physical therapist is often the first clinician to
notice the presence or extent of speech or language dys
function during activity, especially during higher-level
tasks or those activities that cause fatigue. The physical
therapist should report these findings to other members of
the health care team.
NERVOUS SYSTEM
287
Vital Sig1ts
The brain is the homeostatic center of the body; therefore, vital
signs are an indirect measure of neurologic status and the body's
ability to perform basic functions, such as respiration and tempera
ture control.
Blood pressure, heart rate, respiratory rate and panern (see Table
2-3), temperature, and other vital signs from invasive monitoring (see
Appendix III-A) are assessed continuously or hourly to determine
neurologic and hemodynamic stability.
Clinical Tip
The therapist should be aware of blood pressure parameters
determined by the physician for the patient with neurologic
dysfunction. These parameters may be set greater than nor
mal to maintain adequate perfusion to the brain or lower
than normal to prevent further injury to the brain.
Cranial Neroes
CN testing provides information about the general neurologic status
of the patient and the function of the special senses. The results assist
in the differential diagnosis of neurologic dysfunction and may help in
determining the location of a lesion. CNs I through XII are tested on
admission, daily in the hospital, or when there is a suspected change
in neurologic function (Table 4 - 1 3 ) .
Vision
Vision testing is an important portion of the neurologic examination,
because alterations in vision can indicate neurologic lesions, as illus
trated in Figure 4-7. In addition to the visual field, acuity, reflexive,
and ophthalmoscopic testing performed by the physician during C N
assessment, the pupils are further examined for the following:
N
00
00
Nerve/Origin
Purpose
How to Test
SignslSymproms of impairment
Sense of smell
Anosmia
,.
\?
'"
m
J:
,.
z
"
Blindness
g'"
"
'"
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!j
r
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!i!,.
Pupil (onstricflon
Visual focuslllg
Diplopia
Head nit to unaffected side
Weakncss in depression of
ipsilateral adducted eye
Sensation of face
hrdm
Mastication
z
'"
"
i
Ipsilateral deviation of opened
Jaw
5i
-<
;:
...
00
'"
N
'"
0
Purpose
How to Test
SignS/Symptoms of Impairment
Cornea I reflex
Jaw jerk""
Autonomic innervation of
lacrimal and salivary
glands
Vestibular branch: sense of
equilibrium
>
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()
>
'"
'"
J:
>
z
"
Diplopia
Convergent strabismus
Ipsilateral abductor paralysis
Paralysis of ipsilateral upper
and lower facial muscles, loss
of lacrimation, dry mouTh,
loss of taste on ipsilateral
two-thirds of tongue.
15
0
'"
d
'"
n
>
r
:i
'"
'"
>
<q
Vertigo, nystagmus,
disequilibrium, neural
deafness
Gag reflex
Motor and proprioception
of superior pharyngeal
muscle
Autonomic innervation of
salivary gland
Taste (posterior one-third of
tongue)
Blood pressure regulation
Swallowing
Proprioception of pharynx
and larynx
Parasympathetic inner
vation of hearr, lungs, and
abdominal viscera
-<
N
'D
tv
'"
tv
Purpose
How to Test
Signs/Symptoms of lmpairment
eN
cranjal nerve.
R3rd)' tested.
Sources: Data from KW Lindsay, I Bone, R Callander (eds). Neurology and Neurosurgery Illustrated (2nd cd). Edmburgh, UK: Churchill
Livingstone, 1991; EN Marieb ted). Human Anatomy and Physiology (5th ed). San Francisco: BenjaminCummings, 200 1 ; RJ love, we Webb
(eds), Neurology for the Speech-Language Parhologist (4th cd). Boston: Burterworth-Heinemann, 200 I ; and adapted from PA Young, PH
Young (cds). Basic Clinical Neuroanatomy. Baltimore: Williams & Wilkins, 1997;295-297.
>-
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'"
r
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NERVOUS SVSfEM
293
0
() C)
() ()
() ()
() ()
Figure 4-7. Visual pathway with lesion sites and resulting visual field defects.
The occipital lobe has been cut away to show the medial aspect aNd the cal
carine sulci. ( With permission from RJ Love, we Webb leds/. Neurology for
the Speech-Language Pathologist 14th ed/. BoStOl1: Butterworth-Heinemann,
2001 ; 1 03.)
294
Clinical Tip
Motor Fill/chon
The evaluation of motor function consists of strength, tone, and reflex
testing.
Strength Testing
Strength is the force output of a contracting muscle directly related to
the amount of tension that it can produce. IS Strength can be graded in
the following ways in the acute care setting:
Graded 0-5/0-
Graded functionally
NERVOUS SYSTEM
295
Clinical Tip
Muscle Tone
Muscle tOne has been described in a multitude of ways; however, neither
a precise definition nor a quantitative measure has been determined.16 It
is beyond the scope of this chapter to discuss the various definitions of
rone, including variants such as clonus and tremor. For simplicity, muscle
tone is discussed in terms of hyper- or hypotonicity. Hypertollicity, an
increase in muscle contractility, includes spasticity (velocity-dependent
increase in resistance to passive stretch) and rigidity ( increased agonist
and antagonist muscle tension) secondary ro a neurologic lesion of the
CNS or upper motor neuron system. 17 Hypotollicity, a decrease in mus
cle contractility, includes flaccidity (diminished resistance to passive
stretching and tendon reflexes)1 7 from a neurologic lesion of the lower
mOtor neuron system (or as in the early Stage of spinal cord injury [SCrl).
Regardless of the specific definition of muscle tone, clinicians agree that
muscle tone may change according to a variety of facrors, including
stress, febrile state, pain, body position, medical status, medication, eNS
arousal, and degree of volitional movement. I S
Muscle tone can be evaluated i n the following ways:
296
to
stretch
Spinal Level
Normal Response
Biceps
CS
Elbow flexion
Brachioradialis
C6
Elbow flexion
Triceps
C7
Elbow extension
Patellar
L4
Knee extension
Posterior tibialis
L5
Achilles
Sl
Plantar flexion
NERVOUS SYSTEM
297
Response
Inrerpretation
0
1+
No response
Abnormal
Low normal
2+
Active response
Normal
3+
Brisk response
H igh normal
4+
Abnormal
Clinical Tip
The numeric results of DTR resting may appear in a stick
figure drawing in the medical record. The DTR grades are
placed next to each of the main DTR sites. An arrow may
appear next to the stick figure as well. Arrows pointing
upward signify hyper-reflexia; conversely, arrows pointing
downward signify hyporeflexia.
298
Sensation
Sensation testing evaluates the abiliry ro sense lighr and deep rouch,
proprioception, temperature, vibration sense, and superficial and deep
pain. For each modality, the neck, trunk, and extremities are tested bilat
erally, proceeding in a dermaromal pattern. For more reliable sensation
resring results, rhe parient should look away from rhe area being tesred.
Table 4-16 outlines rhe method of sensarion resting by stimulus.
Superficial pain
Deep pain
Light touch
Proprioceprion
Vibrarion
Temperacure
Stereognosis
Two-poinr
discriminarion
Graphesrhesia
Double
simultaneous
stimulation
Sources: Data from KW Lindsay, I Bone, R Callander (cds). Neurology and Neurosurgery
lIIustr:ned (2nd cd). Edinburgh, UK: Churchill Livingstone, 1991; S Gilman, SW New
man (cds). Manter and Gatt's Essentials of Clinical Neuroanatomy and Neurophysiology
(7th ed). Philadelphia: FA Davis, 1 989; and JV Hickey (cd). The Clinical Practice of Neu
rological and Neurosurgical Nursing (4th ed). I)hiladelphia: Lippincon, 1 997.
NERVOUS SYSTEM
299
Clinical Tip
Before completing the sensory examination, the physical
therapist should be sure that the patient can correctly iden
tify stimuli (e.g., that a pinprick feels like a pinprick).
Coordination
Although each lobe of the cerebellum has its own function, cootdina
tion tests cannot truly differentiate among them. Coordination tests
evaluate the presence of ataxia (general incoordination), dysmetria
(overshooting), and dysdiadochokinesia (inability to perform rapid
alternating movements) with arm, leg, and trunk movements, as well
as with gait.8 The results of each test (Table 4- 1 7) are described in
tetms of the patient's ability to complete the test, accuracy, tegularity
of rhythm, and presence of tremor."
Another test is the prol1ator drift test, which is used to qualify loss
of position sense. While the patient is sitting or standing, he or she
flexes both shoulders and extends the elbows with the palms upward.
The patient is then asked to close his or her eyes. The forearm is
observed for 1 0-20 seconds for ( 1 ) pronation or downward drift,
which suggests a contralateral corticospinal lesion, or (2) an upward
or sideward drift, which suggests loss of position sense H
Diagnostic Procedures
A multitude of diagnostic tests and procedures is used to evaluate, dif
ferentiate, and monitOr neurologic dysfunction. Each has its own
cost, accuracy, advantages, and disadvantages. For the purposes of
this text, only the procedures most commonly used in the acute care
setting are described.
X-Ray
X-rays can provide anterior and lateral views of the skull that are
used to assess the presence of calcification, bone erosion, or fracture,
especially after head or facial trauma or if a tumor is suspected. Ante
rior, lateral, and posterior views of the cervical, thoracic, lumbar, and
sacral spine are used to assess the presence of bone erosion, fracture,
300
AClrn CARE
II:\NDBOOI(
fOR I'IIYI)ICAI
Till' ItAl'I')l,
Method
Upper extremity
Finger to nose
Supination and
pronation
Tapping
Arm bounce
Rebound phenome
non
Lower extremity
Heel to shm
Tapping
Romberg test
Gait
Source: Dat:l from KW l.mdsay, J Bone, R C:lllandcr (cd! . f\!curolngy and Ncurmur
gcry Illustrated (2nd cd). Edinburgh, UK: Churchill LlvmgslOnc, 1 99 1 .
NERVOUS SYSTEM
301
Computed Tomography
I n computed tomography (CT), coronal or sagittal views of the head,
with or without contrast media, are used to assess the density, dis
placement, or abnormality ( location, size, and shape) of the cranial
vault and fossae, cortical sulci and sylvian fissures, ventricular system,
and gray and white matter. CT is also used to assess the presence of
extraneous abscess, blood, calcification, contllsion, cyst, hematoma,
hydrocephalus, or tumor. "2J CT of spine or otbits is also available.
Head CT is the preferred neuroimaging test for the evaluation of
acute cerebrovascular accident (CVA), as it can readily distinguish a
primary ischemic from a primary hemorrhagic process and thus deter
mine the appropriate use of tissue plasminogen activator (tPa) ( see
Appendix IV)."
Doppler Flowmetry
Doppler f/owmetry is the use of ultrasound to assess blood flow.
Transcranial Doppler Sonography
Transcrallial Doppler sOllography (TCD) involves the passage of
low-frequency ultrasound waves over thin cranial bones (temporal)
or over gaps in bones to determine the velocity and direction of
blood flow in the anterior, middle, o r posterior cerebral and basilar
302
Digital-Sttbtractiolt Altgiography
Digital-subtraction angiography (DSA) is the computer-assisted
radiographic visual ization of the catotids and cetebral vessels with
a minimal view of background tissues. An image is taken before
and after the injection of a contraSt medium. The first picture is
"subtracted" from the second, a process that creates a highlight of
the vessels. Digital-subtraction angiography is used to assess aneu
rysm, AVM, fi s tu l a, occlusion, or stenosis. It is also used in the
operating room (i.e., television display) to examine the integrity of
anastomoses or cerebrovascular rcpairs. 1 4,2]
Cerebral Altgiography
Cerebral angiography involves the radiographic visualization (angio
gram) of the displacement, patency, stenosis, or vasospasm of intra
or extracranial arteries after the injection of a radiopaque contrast
medium via a catheter (usually femoral). It is used ro assess aneurysm,
AVMs, or intracranial lesions as a single procedure or in the operating
room to examine blood flow after surgical procedures (e.g., after an
aneurysm c1ipping). '4
Clinical Tip
Patients are on bed rest with the involved hip and knee
immobilized for approximately 8 hours after cerebral
angiography to ensure proper healing of the catheter inser
tion site.
NE.RVOUS SYSTEM
303
Lumbar PUllcture
A lumbar puncture (LP) is the collection of CSF from a needle placed
into the subarachnoid space below the Ll vertebra, usually between
L3 and L4. The patient is placed in a side-lying position with the neck
and hips flexed as much as possible (to open the laminae for the best
access to the subarachnoid space). Multiple vials of CSF are collected
and tested for color, cytology, chlorine, glucose, protein, and pH. The
opening and closing pressures are noted. LP is used to assist in the
diagnosis of autoimmune and infectious processes, and, in certain cir
cumstances, it is used to verify subarachnoid hemorrhage (SAH). L P
provides access for the administration o f spinal anesthesia, intrathecal
anribiotics, or for therapeuric CSF removalYL2J
Clinical Tip
Headache is a common complaint after an LP secondary
to meningeal irritation or CSF leakage. A patient may be
placed on bed rest for several hours after an LP to mini
mize upright positioning, which increases headache. Other
short-term complications of LP include backache, bleeding
at the needle site, voiding difficulty, and fever.
Electroellcepbalograpby
Electroencephalography is the recording of electrical brain activity,
using electrodes affixed to the scalp at reSt or sleep, after sleep depri
vation, after hyperventilation, or after photic stimulation. Brain
304
Evoked Pote"tials
Evoked potentials are electrical responses generated by the stimula
tion of a sensory organ. A visual evoked potential is measured using
electrodes that are placed over the occipital lobe to record occipital
cortex activity after a patient is shown nashing lights or a checker
board pattern. Visual evoked potentials are used to assess optic neu
ropathies and opric nerve lesions. A brain stem auditOry evoked
response is measured using electrodes that are placed over the vertex
to record CN V I I I, pons, and midbrain activity after a patienr listens
to a series of clicking noises through headphones. Brain stelll auditOry
evoked responses are used to assess acoustic tumors, brain stem
lesions in multiple sclerosis (MS), or brain srem function (in comatOse
parienrs). A somatosensory evoked potential is measured using elec
trodes over the contralateral sensory cortex after the median or poste
rior tibial nerve is electrically stimulated. Somatosensory evoked
potentials are used to assess SCI, cervical disc disease, sensory dys
function associated with MS, or parietal cortex rumor.1423
Myelography
Myelography uses x-ray to show how a contraSt medium nows
through the subarachnoid space and around rhe vertebral column
NERVOUS SYSTEM
305
after the removal of a small amount of CSF and the injection of dye
via LP. It is used ro assess bone displacement, disc herniation, cord
compression, or tumor. 14,2j
Clinical Tip
Depending on the rype of dye used, a patienr may have
positioning restrictions after a myelogram. I f water-based
dye was used, the patient should remain on bed rest with
the head of the bed at 30 degrees for approximately 8-24
hours, because the dye may cause a seizure if it reaches the
cranium. If an oil-based dye was used, the patienr may
have to remain in bed with the bed flat for 6-24 hours.
Additionally, the patient may experience headache, back
spasm, fever, nausea, or vomiting, regardless of the type of
dye used B
Pathophysiology
1.
Location. TBI may involve damage to the cranium only, the
cranium and brain structures, or brain structures only. Frequently,
head trauma is categorized as ( 1 ) closed (protective mechanisms are
maintained), (2) open (protective mechanisms are altered), ( 3 ) coup
(the lesion is deep to the site of impact), (4) conrrecoup (the lesion is
opposite the site of impact), or (5) coup-contrecoup (a combination
of coup and contrecoup).
2.
Extent. TBI may be classified as primary (in reference to the
direct biomechanical changes in the brain) or secondary (in refer
ence to the latent intracranial or systemic complications that exacer-
306
bate the original injury). The terms focal and diffuse are often used
to describe a specific or gross lesion, respectively.
3.
Severity. In addition to diagnostic tests, TBI may be classified according to cognitive skill deficit and GCS as mild ( 1 3- 1 5),
moderate ( 9 - 1 2), or severe (3-8 ) .
4.
Mechanism o f injury. The two mechanisms re ponsible for
primary TBI are acceleration-deceleration and rotation forces. These
forces may be of low or high velocity and result in the compression,
traction, or shearing of brain structures.
Secondary brain injury occurs within minutes to hours of the trau
matic primary injury and is characterized by inflammatory, vascular,
and biomolecular abnormalities. These changes include the release of
cytokines and a disruption of the blood-brain barrier, which causes
the development of vasogenic (extracellular) brain edema; impaired
cerebral autoregulation and ischemia in the setting of hypoxia and
hypotension; tissue acidosis and an influx of electrolytes, which
causes cytotoxic (intracellular) brain edema; and the loss of neurons,
glial cells, and presynaptic terminals from neurochemical and oxygen
free radical reactions. 17.18
Table 4- 1 8 defines the most common types of TBI and describes
the clinical findings. The management of these conditions is discussed
later in General Management and in Table 4-2 1 .
2.
Mechanism of injury. SCI may result from blunt or penetrating injuries. Blunt forces include ( I ) forward hyperOexion, causing the
discontinuity of the posterior spinal ligamenrs. disc herniation, and
NERVOUS SYSTEM
307
Definition
Clinical Findings
Cerebral
concussion
Cerebral
contusion
Cerebral
laceration
Diffuse
axonal
injury
IDAI)
308
Definition
Clinical Findings
Epidural
hematoma
(EDH)
Subdural
hematoma
(SDH)
Intracere
bral
hematoma
(ICH)
NERVOUS SYSTEM
Injury
309
Clinical Findings
Definirion
May also arise as a compli
carion of hypertension or
delayed bleeding with
progression of blood into
the dural, arachnoid, or
ventricular spaces.
Sources: Data from JV Hickey (ed). The Clinical Practice of Neurological and Neuro
surgical Nursing (4th ed). Philadelphia: Lippincon, 1997; and SA Mayer, LP Rowland.
Head Inj ury. In LJ> Rowland (ed). Merrirr's Neurology ( I Orh cd). Philadelphia: Lippin
can,
B
Incomplete-The preservation of sensory function without
motor function below the neurological level and includes 54-5.
=
310
C
Incomplete-The preservation of motor function below the
neurological level. Muscle function of more than half of key mus
cles below this level is less than 3/5 .
=
D
Incomplete-The preservation of motor function below the
neurological level. Muscle function of at least half of key muscles
below this level is less than 3/5.
=
Clinical Tip
If, during physical therapy intervention, a patient
Mechanism of Injury
Description
Central cord
Hyperextension injury, or as
a result of tumor, rheuma
toid arthritis, or syringo
myelia
Anterior cord
Brown-Sequard
Sources: Data from DA Buckley, MM Guanci. Spinal cord trauma. Nurs Clin North Am
of Neurological and Neurosurgical Nursing (4[h cd). Philadelphia: Lippincorr,
1997.
8
:;;
-<
312
Clinical Tip
A patient who has received tPA is at risk for intracranial hem
morhage or bleeding from other sites and requires strict blood
pressure control during the first 24 hours of infusion." Physi
cal therapy is usually nor initiated during this time frame.
NERVOUS SYSTEM
313
314
Asymptomatic
II.
Moderate to severe headache, nuchal rigidity, without
neurologic deficit
111.
IV.
V.
NERVOUS SYSTEM
315
Ventricular Dysfunction
Hydrocephalus
Hydrocephalus is the acute or gradual accumulation of CSF, causing
excessive ventricular dilation and increased JCP. CSF permeates
through the ventricular walls into brain tissue secondary to a pressure
gradient. There are twO rypes of hydrocephalus:
I.
Noncommtlllicatillg (obstrucrive) hydrocephalus, in which there
is an obstruction of CSF flow within the ventricular system. There may be
thickening of the arachnoid villi or an increased amount or viscosity of
CSF. This condition may be congenital or acquired, often as the result of
aqueduct stenosis, tumor obstruction, abscess, or cyst, or as a complica
tion of neurosurgery.4
2.
Communicating hydrocephalus, in which there is an obstruction in CSF flow as it interfaces wirh the subarachnoid space. This
condition can occur with meningitis, after head injury, with SAH, or
as a complication of neurosurgery.2
Hydrocephalus may be of acure onset characterized by headache,
altered consciousness, decreased upward gaze, and papilledema.s
Management includes treatment of the causative factor if possible, or
ventriculoperitoneal (VP) or ventriculoatrial (VA) shunt.
316
Clinical Tip
If it is known that a patient has a CSF leak, the therapist
should be aware of vital sign or position restrictions before
physical therapy intervention. If a CSF leak increases or a
new leak occurs during physical therapy intervention, the
therapist should stop the treatment, loosely cover the leak
ing area, and notify the nurse immediately.
Seizure
A seizure is a phenomenon of excessive cerebral cortex activity with
or without loss of consciousness. The signs and symptoms of the sei
zure depend on the seizure locus on the cortex (e.g., visual hallucina-
NERVOUS SYSTEM
317
318
Clinical Tip
Establish the seizure history, including prodrome or aura
(if any), for the patient with a recent seizure or epilepsy by
either chart review or interview to be as prepared as possi
ble to assist the patient if seizure activity should occur.
SYllcope
Syncope is the transient loss of consciousness and postural tOne sec
ondary to cerebral hypoperfusion, usually accompanied by bradycar
dia and hypotension." Syncope can be any of the following43:
NERVOUS SYSn:M
319
NCI/roill(ectiol/s Diseases
320
Guillain-Barre Syndrome
Guillain-Barre syndrome (GBS), or acute inflammatory demyelinat
ing polyradiculopathy, is caused by the breakdown of Schwann cells
by antibodies." There is an onset of paresthesia, pain (especially of
the lumbar spine), symmetric weakness (commonly proximal fol
lowed by distal, including the facial and respiratory musculature),
and autonomic dysfunction approximately 1-3 weeks afrer a viral
infection. GBS is diagnosed by history, clinical presentation, CSF
sampling ( increased protein level), and EMG studies (which show
decreased motor and sensory velocities).' Once diagnosed, the
patient with GBS is hospitalized because of the potential for rapid
respirarory muscle paralysis.4S Functional recovery varies from full
independence to residual weakness that takes J 2-24 months to
resolve." GBS is fatal in 5% of cases.'s The management of GBS
may consist of pharmacologic therapy (immunosuppressive agents),
plasma exchange, intravenous immunoglobulin, respiratory sup
port, physical therapy, and the supportive treatmenr of associated
symptoms (e.g., pain management).
Multiple Sclerosis
MS is the demyelination of the white maner of the CNS and of the
optic nerve, presumably an autoimmune reaccion. MS is categorized
by onset and progression as relapsing-remitting (clearly defined
relapses with full recovery or with residual deficit), primary progres
sive (occasional plateaus in disease progression and only temporary
improvements), secondary progressive (initial relapsing-remitting fol
lowed by disease progression with or without relapses or plateaus), or
progressive relapsing (progressive from onset with acute relapses,
with or without full recovery) J4
MS typically occurs in 20- to 40-year-olds and in women more
than men. It is diagnosed by history (the onset of symptoms must
occur and resolve more than once), clinical presentation, CSF sam
pling ( increased myelin protein and immunoglobulin G levels), and
by M R I (which shows the presence of two or more plaques of the
CNS).' These plaques are located at areas of demyelination where
lymphocytic and plasma i nfiltration and gliosis have occurred. Signs
and symptoms of the early stages of MS may include focal weak
ness, fatigue, diplopia, blurred vision, equilibrium loss (vertigo), and
urinary incontinence. Additional signs and symptoms of the larrer
stages of MS may include ataxia, paresthesias, spasticity, sensory
deficits, hyper-reflexia, tremor, and nysragmus.44 The management
NERVOUS SYSTEM
321
General Management
322
B
Figure 48. Herniat toll syndromes depIcted. tntracramaJ shIlts from supraten
toriaJ lesions. A. N ormal locatIo" of structures. B. Vanous hermatloll sy,,
dromes are demonstrated. I . Cmgulate gyrus is hermatmg under falx cerebrt.
2. Temporal lobe is hermatmg dowtlluard through the te"torial notch.
J. CompressIon of contralateral cerebral peduncle IS seen. 4. Downward d,s
placement of bram stem through tentorial notch ;s a central herniatIOn syn
drome. ( W ,th permlsS/on (rom PC Beare, lL M)'ers {eds{. Adllit Health
NI/rsmg {3rd ed{. Pllliodelpl"a , Sal/llders, 1 998;919.}
NERVOUS SYSTEM
323
Early
Late
Level of
consciousness
Confusion, restless
ness, lethargy
Coma
Pupil appearance
Vision
Moror
Contralateral paresis
Abnormal posturing
Bilateral flaccidity if
herniation has occurred
Vital signs
Additional
findings
Headache, seizure,
cranial nerve palsy
Source: D:1(:I from JV Hickey. Thc Clinical Practice of Neurological and Neurosurgical
NurSIng (41h cd). Philadelphia: Lippincott, 1997.
324
Treatment
Blood pressure
Osmorherapy
Mechanical
ventilation
Cerebrospinal
fluid drainage
Sedation/paral ysis
Positioning
Environment
Seizure control
Temperature
control
Routine aggressive hyperventilation is no longer used for the control of elevated ICP.
Hyperventilarion can contribute to secondary brain injury because of a rebound
increase in cerebral blood flow and volume in response to a decreased cerebrospinal
fluid pH.
Source: Data from
2000;20, 18-27.
NERVOUS SYSTEM
325
Phamtacologic Therapy
A multitude of pharmacologic agents can be prescribed for the patient
with neurologic dysfunction. These include anticonvulsant agents (see
Appendix Table IV.5), osmotic diuretics (see Appendix Table lV.26),
adrenocorricosteroids (see Appendix Table lV. I ), skeletal muscle relax
ants (see Appendix Table lV.28), and anti parkinsonian agents (see
Appendix Table IV.9). Additional pharmacologic agents for medical
needs include antibiotics (e.g., for infection or after neurosurgery), anti
hypertensives, thrombolytics, anticoagulants, chemotherapy and radia
tion for CNS neoplasm, stress u lcer prophylaxis (e.g., after SCI), pain
control, and neuromuscular blockade.
Neurosurgical Procedures
The most common surgical and nonsurgical neurologic procedures
arc described below (see Ta ble 3 - 8 for a description of surgical
spine procedures and Appendix I II-A for a description of ICP mon
itoring devices).
Allellryslll clippillg. The obliteration of an aneutysm with a surgical
clip placed at the stem of the aneurysm.
Bllrr hole. A small hole made in the skull with a drill for access to the
brain for the placement of ICP monitoring systems, hematoma
evacuation, or stereotactic procedures; a series of burr holes is
made before a craniotomy.
Cralliectomy. The removal of incised bone, usually for brain (bone
Aapl tissue decompression; the bone may be permanently removed
or placed in the bone bank Or temporarily placed in the subcutane
ous tissue of the abdomen (to maintain blood supply).
Crallioplasty. The reconstruction of the skull with a bone graft or
acrylic material to restore the protective properties of the scalp and
for cosmesis.
Cralliotomy. An incision through the skull for access to the brain for
extensive intracranial neurosurgery, such as aneurysm or AVM
repair or tumor removal; craniotomy is named according to the
area of the bone affecred (e.g., frontal, bifrontal, frontotemporal
[ pterional], temporal, occipital).
326
Clinical Tip
NERVOUS SYSTEM
327
Take extra time to observe and assess the patient with neuro
logic dysfunction, as changes in neurologic status are often very
subtle.
A basic knowledge of the factors rhat a ffect ICP and the ability
to modify treatment techniques or conditions during physical ther
apy intervention for the patient wirh head rrauma, afrer intracra
nial surgery, or other pathology interfering with intracranial
dynamics is necessary for patient safety.
328
References
1 . Marieb EN (ed). Human Anaromy and Physiology. Redwood Ciry, CA:
Benjamin-Cummings, 1 989; 1 72.
2. Moore KL. The Head. In KL Moore (cd), Clinically Orienred Anaromy
(2nd ed). Balrimore: Williams & Wilkins, 1 985;794.
3. Wesrmoreland BF, Benarroch EE, Daube JR, et al. (eds). Medical Neuro
sciences: An Approach to Anatomy, Pathology, and Physiology by Sys
rems and Levels (3rd ed). New York: Little, Brown, 1986; 1 07.
4. Young PA, Young PH (eds). Basic Clinical Neuroanatomy. Baltimore:
Williams & Wilkins, 1 997;251-258.
5 . Marieb EN (ed). Human Anaromy and Physiology. Redwood Ciry, CA:
Benjamin-Cummings, 1 989;375.
6. Wilkinson JL (ed). Neuroanatomy for Medical Srudents (3rd ed).
Oxford, UK: Burterwonh-Heinemann, 1 998j 1 89-200.
7. Goldberg S (cd). The Four-Minute Neurological Exam. Miami: Med
Masrer, 1 992;20.
8. Lindsay KW, Bone I, Callander R (cd). Neurology and Neurosurgery
Illustrated (2nd cd). Edinburgh, UK: Churchill Livingstone, 1 99 1 .
9. Plum F, Posner J (cds). The Diagnosis of Srupor and Coma (3rd cd).
Philadelphia: FA Davis, 1 980; 1 .
10. Jennett B, Teasdale G (eds). Management of Head Injuries. Philadelphia:
FA Davis, 1 9 8 1 ;77.
1 1 . Strub RL, Black FW (eds). Mental Status Examination in Neurology
(2nd ed). Philadelphia: FA Davis, 1 985;9.
1 2. Love RJ, Webb WG (eds). Neurology for rhe Speech-Language Patholo
gist (4th ed). Boston: Butterwonh-Heinemann, 2001 ;205.
1 3 . Specrer "'VI. The Pupils. In HK Walker, WD Hall, JW Hursr (cds), Clin
ical Methods: Te History, Physical, and Laboratory Examinations (3rd
ed). Boston: Butterworth, 1 990;300.
'14. Hickey ]V. The Clinical Pracrice of Neurological and Neurosurgical
Nursing (4th ed). Philadelphia: Lippincott-Raven Publishers, 1 997.
1 5 . Kisner C, Colby LA. Therapeutic Exercise Foundations and Techniques
(3rd ed). Philadelphia: FA Davis, 1 996;57.
16. Katz RT, Dewald J, Schmir BD. Spasticity. In RL Braddon (ed). Physical
Medicine and Rehabilitarion (2nd ed). Philadelphia: Saunders, 2000;592.
17. Victor M, Ropper AH. Moror Paralysis. In M Victor, AH Ropper (cds),
Adam and Victor's Principles of Neurology. New York: McGraw-Hili,
200 I ;50-58.
1 8 . O'Sullivan SB. Motor Control Assessment. In SB O'Sullivan, TJ Schmitz
(eds). Physical Rehabilirarion: Assessment and Trearment (3rd cd). Phil
adelphia: FA Davis, 1 998; 1 1 5.
1 9 . Charness A. Gathering the Pieces: Evaluation. In A Charness (ed),
SrrokelHead Injury: A Guide ro Functional Outcomes in Physical Ther
apy Management. Rockville, MD: Aspen, 1 986; 1 .
20. Swartz MH. The Nervous System. In M H Swaru, W Schmitt (cds),
Textbook of Physical Diagnosis History and Examinarion (3rd ed). Phil
adelphia: Saunders, 1 998;529.
NERVOUS SYSTEM
329
330
5
Oncology
Susan Polich
Introduction
332
Definitions
The terms neoplasm, tumor, and cancer are currently used inter
changeably. Neoplasm means "new growth" and applies to any
abnormal mass of tissue which exceeds the growth of normal tissue,
grows at the expense of itS host, and persists even after the stimulus to
grow is removed. The term /1I1110r originally applied to the swelling
caused by inf1mmation but now refers only to a new growth. Cancer
is the layperson's term for all malignant neoplasms.''''
Normal cells change in size, shape, and type, known collectively as
dysplasia, if the proper stimulus is provided. Hyperplasia refers to an
increase in cell number. Metaplasia is the change of one cell type to
another. Hyperplasia and metaplasia can be reversible and normal
or persistent and abnormaI.1,2,4
Neoplasms, or persistent, abnormal dysplastic cell growth, are
classified by cell type, growth pattern, anatomic location, degree of
dysplasia, tissue of origin, and their ability to spread or remain in the
original location. Two general classifications for neoplasm are benign
and malignant. Bellign tumors are usually considered harmless and
slow growing and have cells that closely resemble normal cells of
adjacent cissue. However, chese benign tumors may occasionally
become large enough to encroach on surrounding tissues and impair
their function. Malignant neoplasms, or malignant tumors, grow
uncontrollably, invading normal tissues and causing destruction to
surrounding tissues and organs. Malignant neoplasms may spread, or
metastasize, to other areas of the body through the cardiovascular or
lymphatic system. '-5
Tumors may also be classified as primary or secondary. Primary
rumors are the original tumors in the original location. Secondary
tumors are those metaStases that have moved from the primary site.4
Nomenclature
ONCOLOGY
333
Benign
Malignant
Surface epithelium
Papilloma
Carcinoma
Adenoma
Adenocarcinoma
Epithelium
Fibroma
Fibrosarcoma
Cartilage
Chondroma
Chondrosarcoma
Bone
Osteoma
Osteosarcoma
Smooth muscle
Leiomyoma
Leiomyosarcoma
Striated muscle
Rhabdomyoma
Rhabdomyosarcoma
Nerve tissue
Glioma
Glial
Meninges
Meningioma
Meningeal sarcoma
Retina
Retinoblasroma
Lymphoid tissue
Lymphoma!
lymphosarcoma
Bone marrow
White blood cells
Leukemias
Plasma cells
Multiple myeloma
Source: With permission from S Baird (ed). A Cancer Source Book for Nurses (6th cd).
The causes, or etiologies, of neoplasm are often divided into two cate
gories, external or environmental and generic. There are risk factOrs
that are thought ro predispose a person ro cancer. Most cancers proba
bly develop from a combination of facrors. The most common etiolo
gies can be found in Table 5-2. Risk facrors can be found in Table 5-3.
Signs and symptOms of cancer are most often due to rhe tumor's growth
and invasion of surrounding tissues. The American Cancer Society has
the acronym CAUTI ON for several common signs of cance:
334
1999.
0;
ONCOLOGY
335
High-Risk Factors
Heavy smoker, older than age 40 yrs
Smoked one pack per day for 20 yrs
Started smoking at age 15 or before
Smoker working with or near asbestos
Breast
Lump in breast
Nipple discharge
History of breast cancer
Filmily history of breast cancer
Benign breast disease
High-far diet
Nulliparous or first child after age 30 yrs
Early menarche or menopause
Colon/rectum
Uterine
Skin
Oral
Ovary
336
Table 5-3.
Continued
Cancer Sire
Prosrare
High-Risk Factors
Increasing age
Occuparions relaring to the use of cadmium
Family hisrory
Sromach
or
salred foods
Source: Wirh permission from S Baird (ed). A Cancer Source Book for Nurses (6rh ed).
Arbma: American Cancer Society, 1991 ;32.
Diagnosis
ONCOLOGY
337
Description
Biopsy
Blood rests
Marker
Cancer
Prostate disease
Carcinocmbryonic
Colon cancer
antigen
Prostaric-acid
Prosrate cancer
phosphatase
Srool guaiac
Alpha-fcroprorein
CAI2S
Ovarian cancer
CA19-9
Colon cancer
CAU-3
Stool guaiac
Sigmoidoscopy
Colonoscop}'
Mammography
Radiography
Magnetic resonance
colonoscope.
calcification in breast tissue.
imaging and
computerized
axial romography
Bone scan
Pap smear
Sputum cytology
Bronchoscopy
flexible bronchoscopy.
CA
c:trboh),dratc :tntigcn.
338
Management
Not all cancers are curable. Physicians may therefore foclls treatment
on quality of life with palliative therapies rather than on curative
therapies. Four major treatment options include:
Chemotherapy
tlllllor
ONCOLOGY
339
Grade IV
moderately differentiated.
tic) that the cell of origin is difficult or impos
sible to determine.
Surgery
Surgical intervention is determined by the size, location, and type of
cancer, as well as the patient's age, general health, and functional sta
tus. The following are the types of general surgical procedures for
resecting or excising a neoplasm:
340
Clinical Tip
Radiation
High-ionizing radiation is used to destroy or prevent cancer cells from
growing furrher, while minimizing the damage to surrounding healthy
tissues. Radiation therapy reduces the size of a tumor to allow for
resection surgically, to relieve compression on structures surrounding
the tumor, and to relieve pain (by relieving compression on pain-sensi
tive structures). Reducing the size of a tumor with radiation therapy
may also help to reduce the need for a large resecrion, amputation, or
complete mastectomy.7
Radiarion may be delivered via supervolrage radiotherapy (tele
therapy) or by planting radioactive marerial near the rumor (seeding
or brachytherapy). Radiation destroys cells in its path; therefore, spe
cial consideration is given to irradiating as little normal tissue as pos
sible. Teletherapy uses variolls methods, such as linear acceleration
and modifying-beam wedges, to permit greater localization.' Seeding
may destroy all surrounding tissues, including healthy tissue. Radio
active seeds are implanted for several days, then removed.
ONCOLOGY
341
Clinical Tip
Chemotherapy
The overall purpose of chemotherapy is to treat or prevent meta
sratic disease and reduce the size of the tumor for surgical resection
or palliative care. Patients may receive single agents or a combina
tion of agents. Chemotherapy can be performed preoperatively and
postoperatively. Chemotherapy is usually delivered systemically, via
intravenous or cenrral lines, bll[ may be directly injected in or near a
tumor. Patients may receive a single or multiple rounds of chemo
therapy over time to treat their cancer and to possibly minimize side
effects. Side effects of chemotherapy include nausea, vomiting,
342
"cancer pain," and loss of hair and other fast-growing cells, includ
ing platelets and red and white blood cells.
Different types of chemotherapeutic agents have different mechanisms
of action. Alkylating agents and nitrosoureas inhibit cell growth and divi
sion by reacting with DNA. Antimetabolites prevent cell growth by com
peting with metabolites in production of nucleic acid. Plant alkaloids
prevent cellular reproduction by disrupting cell mitosis.12
Chemotherapeuric agents are listed in Appendix IV, Tables rV-IS.A-H.
Clinical Tip
ONCOLOGY
343
Biotherapy
Hormonal therapy and immunotherapy also play an important role in
managing cancer. Hormonal therapy includes medically or surgically
eliminating the hormonal source of cancer (e.g., orchiectomy,
oophorectomy, or adrenalectomy) or pharmacologically changing
hormone levels.'' Immunotherapy includes enhancing the patient'S
immune system and changing the immune system's response to the
cancer, most commonly with recombinant growth factors, such as
interferon-alpha or interleukin.
Hormonal therapy is most commonly used to treat breast and
prostate cancer. Some breast tumor cells contain estrogen in their
cytoplasm (estrogen-receptor positive). Use of antiestrogens, such as
tamoxifen, may keep the tumor from enlarging or metastasizing.
344
Cancers can invade or affect any organ or tissue in the body. The fol
lowing is a description of various cancers in each body system.
Pulmonary Cancers
Cancer can affect any structure of the pulmonaty sysrem. The cOlTlmon
types of lung cancer are squamous cell carcinoma, adenocarci1loma,
small cell carcinoma, and large cell carcinoma.6.7 Symptoms associated
with these include chronic cough, dyspnea, adventitious breath sounds
(e.g., wheezing, crackles), chest pain, and hemoptysis.'
Nonsurgical techniques, such as x-ray, computerized axial
romography, and positron emission tomography, can be lIsed to
stage lung cancer." Table 5-7 describes pulmonary cancer sites and
Surgical Procedure
Pleura
Pleurecromy
Portion of pleura
Rib
Rib resection
Portion of rib
Trachea n.nd
Trachea
bronchi
reconstcuction
Lung
Excision of
Sleeve resection
Pneumonectomy
lobec(Qmy
Wedge cesection
ONCOLOGY
345
Clinical Tip
Musculoskeletal Cancers
Tumors of bone are most commonly discovered after an injury or
fracture or during a medical work-up for pain. Some tumors in the
bone or muscle may arise from other primary sites. Common primary
tumors that metastasize to bone include breast, lung, prostate, kidney,
and thyroid tumors.17 Treatment of musculoskeletal tumors can
include radiation, chemotherapy, amputation, arthroplasty (joint
replacement), and reconstruction using an allograft (cadaver bone).
Types of primary orthopedic cancers are described in Table 5-8.
Although not all metastases to bone cause pathologic fractures,
surgical intervention can be used for a patient with a bone metastasis
because of the risk of pathologic fracture. These procedures may
346
Type of Tumor
Osteosarcoma
Chondrosarcoma
Fibrosarcoma
Rhabdomyosarcoma
(Ewing's sarcoma)
Adul"
Adul"
Children and adolescents
Common Site of
Tumors
Distal femur, proximal
tibia
Commonly metastasize
to lung
Pelvis or femur
Femur or tibia
Trunk. pelvis, and long
bones
Clinical Tip
Breast Cancer
Breast cancer, although more prevalent in women, is also diagnosed in
men to a lesser extent. It may be discovered during routine breast
examinations or mammography. Common surgical procedures for the
treatment of breast cancer are listed in Table 5-9.
ONCOlOGY
347
Tissues Involved
Radical l11<lsrccmll1Y
or local wide
eXCISion
ReeoIl!)trlIetion-i111piall(5
Rcconsrrunion-l11u.,clc nap
rrnn!)fcr
Clinical Tip
348
Clinical Tip
ONCOLOGY
349
Excision
Uterus
Hysterectomy
Ovary
Ovaries and
OVIducts
Prosrate
Testes
Toral abdominal
hysterectomy
Subcocal abdominal
hysterectomy
Oophorectomy
Bilateral salpingooophorectomy
Radical prosratecmmy
Orchiectomy
Surgical Intervention
Excision
Stomach
Subtotal gastrectomy
Near-wtal gastrectomy
Total gastrecromy
Gastroduodenosromy
Gasrrojejunostol11 y
Colon
Rectum
Hemicolectomy
Anterior or low-anterior
resection
Abdominal perineal
resection
350
Hepatobiliary Cancers
Primary liver tumors can arise from hepatic cells, connective tis
sue, blood vessels, or bile ducts. Primary malignant liver carcino
mas are almost always associated with cirrhosis. Benign liver
tumors are associated with women taking oral contraceptives.
Most benign liver tumors are asymptomatic.
Hepatic adenomas (benign hepatic cell tumors) are highly vas
cular, and patients carry the risk of hepatic rupture. Hepatomas,
or malignant hepatic parenchymal cell tumors, are closely associ
ated with male gender, excessive ethanol use, hepatitis B, and hep
atitis C. Treatment is usually with chemoembolization or tumor
resection. Patients with a small, nonmetastasizing hepatoma may
be [rea ted with liver transplantation. Untreated hepatoma has a
very poor prognosis. Five-year survival rates for treated tumors are
15-45%.7
Cancer of the biliary tract is usually found during surgery for
another biliary disease or when metastasizing to other organs,
particularly [he liver. Treatment is by surgery, but prognosis is
poor.
In both hepatic cancer and biliary cancer, laboratory values are
used to diagnose, prognose, and monitor the course of treatment.
Liver function tests may include bilirubin, aspartate aminotrans
ferase (AST), alanine aminotransferase (ALT), lactate dehydroge
nase (LDH), gamma-glutamyltransfer.se, alkaline phosphatase,
coagulation factors, and serum proteins.
Surgical interventions for the hepatobiliary system are outlined
in Table 5-12.
Surgical Intervention
Excision
Pancreas
Whipple procedure
Liver
Segmental resection
$uhsegmental
resection
ONCOLOGY
351
Clinical Tip
Any patient with hepatic adenoma must be cautioned to
avoid lifting heavy objects or performing maneuvers thar
increase intra-abdominal pressure.
Pancreatic Callcer
Hematologic Cancers
352
Cells Involved
Lymphocytes
Stem cells
Granulocytes
Lymphocytes
Nodal involvemenr
Spread
Extranodal involvement
Hodgkin's Lymphoma
Non-Hodgkin's
Lymphoma
ONCOLOGY
353
Distribution of Disease
I
II
III
IV
Source: Adapred from Carbone PP. Kaplan HS, Musshoff K, er 31. Report of rhe Conlfllir
tcc on Hodgkin') Disease Sraging Classificarion. Cancer Res 1971 ;31 (11): 1860--1861.
Clinical Tip
Platelet counts and hematocrit should be assessed to deter
mine a safe level of activity or exercise. See Bone Marrow
Transplant in Chapter 12 for specific guidelines.
354
Multiple Myeloma
Multiple myeloma is a malignancy of plasma cells, which are derived
from B-lymphocytes (B-cells), and are responsible for creating antibod
ies. The disease is characterized by the tumor's arising in the bone mar
row of Aat bones and the infiltration of the myeloma cells into the bone
and, eventually, other organs. These malignant cells produce a single
type of antibody that may increase the viscosity of the blood. Classi
cally, the disease produces bone pain and decreased number of normal
hematOlogic cells (e.g., red blood cells, white blood cells, and platelets).
The disease has a slow progression. Most persons affected with
multiple myeloma have an asymptOmatic period that can last lip to 20
years. I Bone pain, usually the first symptom, occurs when the
myeloma cells have destroyed bone. Lesions created in the bone by
the malignant cells can cause pathologic fractures, especially in the
vertebral bodies. As further bone is destroyed, calcium and phospho
rus are released, causing renal stones and renal failure.I. 2.7
Amyloidosis may occur in patients with multiple myeloma. Depo
sition of this glycoprotein in tissues may cause them to become hard
and waxy.
Myeloma is treated with chemotherapy, biotherapy, radiation, and
bone marrow transplantation. No treatment is curative.
Clinical Tip
Head, neck, and facial cancers involve the paranasal sinuses, nasal
and oral cavities, salivary glands, pharynx, and larynx. Environmen
tal factOrs and personal habits (e.g., tObacco use) are often closely
associated with the development of cancer in this region. 29
Physical therapy intervention may be indicated after the treatment
of head, neck, and facial tumors. Surgical procedures include radical
neck dissection, laryngectomy, and reconstructive surgery. Radical
ONCOLOGY
355
Clinical Tip
356
Neurologic Cal/eers
Tumors of the nervous system can invade the brain, spinal cord, and
peripheral nerves. Brain tumors can occur in astrocytes (astrocy
toma), meninges (meningeal sarcoma), and nerve cells (neuroblas
toma), or they can be the result of cancer that has metastasized to the
brain. 9 Symptoms related to cancers of the nervous system depend on
the size of the tumor and the area of the nervous system involved.
Neurologic symptoms can persist after tumor excision, owing to
destruction of neurologic tissues. Changes in neurologic status due to
compression of tissues within the nervous system can indicate further
spread of the tumor or may be related to edema of brain tissue.
Sequelae include cognitive deficits, skin changes, bowel and bladder
control problems, sexual dysfunction, and the need for assistive
devices and positioning devices. After resection of a brain tumor,
patients may demonstrate many other neurologic sequelae, including
hemiplegia and ataxia. Radiation therapy to structures of the nervous
system may also cause transient neurologic symptoms.
Clinical Tip
The therapist should assess the patient'S need for skin care,
splinting, positioning, assistance in activities of daily liv
ing, cognitive training, gait training, balance, assistive
devices, and special equipment. See Chapter 4 for further
treatment considerations.
Skin Cancer
ONCOLOGY
357
the sun, light eyes, and fair skin. Diagnosis is made with a biopsy or a
tissue sample. The following are five warning signs of basal cell carci
noma the physical therapist should look for when working with
patients31:
Open sore that bleeds, oozes, or crusts and remains open for 3
or morc weeks
Asymmetry
Irregular border
Varied color
Clinical Tip
358
FOR
I'HYSICAL lHERAPISTS
Knowing the stage and grade of cancer can help the physical
therapist modify a patient's treatment parameters and establish
realistic goals and intervention.
ONCOLOGY
359
References
I. Cotran RS, Kumar V, Robbins S, Schoes FJ (eds). Robbins Pathologic
Basis of Disease. Philadelphia: Saunders, 1994.
2. Goodman ee, Boissonnault WG (eds). Pathology: Implications for the
Physical Therapist. Philadelphia: Saunders, 1998.
360
3. Tamparo CD, Lewis MA (eds). Diseases of the Human Body (3rd cd).
Philadelphia, FA Davis,2000.
4. Thomas CL (ed). Taber's Cyclopedic MedICal D,CtlOnMY (17th edl. Phil
adelphia, FA Davis, 1993.
5. Baird S (cd). A Cancer Source Book for Nurses (6th cd). Atlanta, Amer
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6. American Cancer Sociery. Cancer Manual (8th ed). Boston: American
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7 Tierney LM,McPhee SJ,PapadakIS MA (cds). Current Medical Diagno
sis and Treatment. New York: McGraw-llill,2000.
8. Moreau D (ed). Nursing '96 Drug Handbook. Springhouse, I'A, Spring
house, 1996;657,944.
9. Wells Nj, Boyle je, Snelling CF, et al. Lower Cxtrcmlf)' burns and Unna
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10. Poole GH, Mills SM. One hundred consecutive cases of flap lacerations
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11. Budny PG, Lavelle], Regan Pj, Roberts AIL Pretiblallnlunes 111 the
elderly: a prospective trial of early mobilisation versus bed rest follow
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l3. Lewis RJ. Caccavale Rj,Bocage JP, Widmann MD. Video-assisted tho
racic surgical non-rib spreadlllg il11ultancously stapled iobecromYi a
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14. Sanrambrogio R, Montorsi M, Bianchi P, et al. Intraoperative ultra
sound during thoracoscopIc procedures for solitary pulmonary nodules.
Ann Thorac Surg 1999;68( I ),218-222.
15. Matin TA, Goldberg M. Surgical staging of lung cancer. Ontolog)'.
1999;13(5),679-685.
J 6. Burrell LO (ed), Adult Nursing 111 Hospital and Community Settlllgs.
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17. Baird S (ed). A Cancer Source Book for Nurses (6th cdl. Adanta: Amer
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18. Hicks JE. Exercise for Cancer Patients. In JV BasmaJlan, SL Wolf (cds),
Therapeutic Exercise. Baltimore: Williams & \'Vilkins, 1990;351.
19. Badger eM,Peacock JL,Mortimer PS. A randomized,controlled,paral
lel-groups clinical trial comparing multilayer bandagll1g followed b),
hosiery versus hosiery alone in the treatment of patients with lymph
edema of the limb. Cancer 2000;88(12):2832-28.l7.
20. Berlin E, Giorcs JE, Ivarsson C. er al. Postmasrcctomy lymphoedema.
Treatment and a five-year follow-up study. Int Anglol 1999;18(4P94298.
2 t. Johansson K, Alberrsson M,Ingvar C, Ekdahl C. Effects of compression
bandaging with or without manual lymph drainage treatment 10
patients with postoperative arm lymphedema. L)'mphology 1999;32(3):
103-110.
ONCOLOGY
361
22. Martiasson A. Discussion: bl:Jddcr and pelvic floor muscle tmining for
overactive bladder. Urology 2000;55(SuppI 5A):12-16.
23. Lewey J, Ltlas L. Electrical stimularion of the overactive bladder. Prof
Nurse 1999;15(3):211-214.
24. Cammu H, Van Nylen M, Am)' JJ. A 10-year follow-up after Kegel pel
vic floor muscle exercises for genuine stress incontinence. BJU Int
2000;85(6):655-658.
25. Gibbons G. Skin care and incontinence. Community Nurse 1996;
2(7):37.
26. Mure MM, Sacr MG, Oishi AJ. Pancreatic cancer. CA Cancer J Clin
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27. Brunner TB, Grabenbauer GG, Baum U. et al. Adjuvant and neoadju
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sccrahle pcnampullary cancer: analysis on the basis of controlled trials.
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29. Reese JL. Head and Neck Cancers. In R McCorkle, M Gram, M Frank
Stromberg, S Baird (cds), Cancer Nursing: A Comprehensive Textbook
(2nd cd). Philadelphia: Saunders, 1996;567.
30. Haskell CM (cd). Cancer Treatment (4th cd). Philadelphia: Saunders,
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31. Rohllls P, Kopf A. Squamous Cell Carcinoma Ipamphlet]. New York:
Skill Cancer oundanon, 1990;1.
6
Vascular System and Hematology
Michele P. West and Jaime C. Paz
Introduction
Alterations in the integrity of the vascular and hematologic systems
can alter a patient's activity tolerance. The physical therapist must
be aware of the potential impact that a change in blood composition
or blood flow has on a multitude of body functions, including car
diac Output, hemostasis, energy level, and healing. The objectives of
this chapter are to provide the following:
1.
A review of the structure and function of blood and
blood vessels
2.
A review of vascular and hematologic evaluation, including physical examination and diagnostic and laboratory tests
3.
A description of vascular and hematologic diseases and
disorders, including clinical findings, medical and surgical manage
ment, and physical therapy inrervenrion
363
364
Structure
The network of arteries, veins, and capillaries comprises the vascu
lar system. Living blood cells and plasma within the blood vessels
are the structures that comprise the hemarologic system. The lym
phatic system assists the vascular system by draining unabsorbed
plasma from tissue spaces and returning this fluid (lymph) ro the
heart via the thoracic duct, which empties into the left jugular
vein. The flow of lymph is regulated by intrinsic contractions of
the lymph vessels, muscular contractions, respiratory movements,
and gravity.'
Description
Function
Tunica intima
Innermost layer
Endothelial layer over a
basement membrane
Middle layer
Smooch muscle cells and
elastic connective tis
sue with sympathetic
innervation
Outermost layer
Composed of collagen
fibers, lymph vessels,
and (he blood vessels
that supply nutrients
to the blood vessel
Tunica media
Tunica adventitia
Source: Dam from The Cardiovascular System: Blood Vessels. In EN Marich, Human
Anatomy and Physiology (3rd cd). Redwood City, CA: Benjamin-Cummings, 1995.
365
Description
Artery
Vein
Capillary nerwork
Source: D:lt:1 from The C1rdiovascular Syslem: Blood. In EN Maricb, Human Anatomy
and Physiology (3rd cd). Redwood Cicy, CA: BenjaminCummings, 1995.
Function
The function of the blood vessels is to carry blood throughout the
body to and from the heart. Normal alterations in the vessel diameter
will occur depending on circulating blood volume and the metabolic
needs of the tissues.
The following are the seven major functions of blood2:
I.
The transport of oxygen and nutrients to body cells from
the lungs and gastroinrestinal organs, respectively
366
Description
Erythrocyte (red
blood cell) (RBC)
Leukocyte (whire
blood cell) (WBC)
Thrombocyte
(platelet)
Source: Data from The Cardiovascular System: Blood. In EN Maricb, Human AnalOmy
and Physiology (3rd cd). Redwood City, CA: BcnjammCummings, 1995.
2.
The transport of carbon dioxide and merabolic waste
products to the lungs and kidneys, respectively
3.
The rransport of hormones from endocrine glands to target organs
4.
The maintenance of body temperature via conduction and
dispersal of heat
5.
The maintenance of pH with buffers freely circulating in
the blood
6.
7.
The prevention of infection with white blood cells
(WBCs), antibodies, and complement
The vascular and hematologic systems are intimately linked, and
the examination of these systems is often similar. For the purpose of
this chapter, however, the evaluation of the vascular and hematologic
systems is discussed separately.
367
Physical Examination
Vascular Evalt/atio"
History
In addition to the general chart review (see Appendix I-A), the follow
ing information is important to gather during the examination of the
patiem with a suspected vascular disorder]:
Clinical Tip
Intermittent claudication is often abbreviated in the clini
cal setting as Ie.
Inspection
Observation of the following features can help delineate the location
and severity of vascular disease and help determine whether these
manifestations are arterial or venous in origin i.]:
Skin color. (Note the presence of any discoloration of the distal
extremities, which is indicative of decreased blood flow---e.g.,
mottled skin.)
Hair distribution. (Patchy hair loss on the lower leg may indi
cate arterial insufficiency.)
368
Presence of cellulitis.
Gait abnormalities.
Palpation
During the palpation portion of the examination, the physical
therapist can assess the presence of pain and tenderness, strength
and tate of peripheral pulses, respiratory rate, blood pressure, skin
temperature, and limb girth (if edematous). Changes in heart rate,
blood pressure, and respiratory rate may correspond to changes in
the fluid volume status of the patient. For example, a decrease in
fluid volume may result in a decreased blood pressure that results
in a compensatory increase in heart and respiratory rates. The
decreased fluid volume and resultant increased heart rate in this
situation may then result in a decreased strength of the peripheral
pulses on palpation. In patients with suspected or diagnosed
peripheral vascular disease, monitoring distal pulses is more
important than monitoring central pulses in the larger, more prox
imal vessels.3
The following are twO systems used to grade peripheral pulses:
1.
Absent
2.
369
Absent
Markedly diminished
Moderately diminished
Slightly diminished
Normal
Brachial
Ulnar
Radial
Femoral
Popliteal
Posterior tibial
Dorsalis pedis
Clinical Tip
Peripheral pulse grades are generally denoted in the
medical record by physicians in the following manner:
dorsalis pedis +1.
370
Auscultation
Systemic blood pressure and the presence of bruits (whooshing sound
indicative of turbulent blood flow from obstructions) are assessed
through auscultation.' Bruits are typically assessed by physicians and
nurses (see Chapter 1 for further details on blood pressure measurement).
Vascular Tests
Various tests that can be performed clinically to evaluate vascular flow
and integrity are described in Table 6-4. These tests can be performed
easily at the patient's bedside without the use of diagnostic equipment.
Diagnostic Studies
Noninvasive Laboratory SlIIdies
Indication
Description
Capillary refill
time
To assess vacular
perfusion and
indirectly assess
cardiac ourpO[
To assess anerial
perfusion
Elevation pallor
Trendelenburg's
test
To determine if
superficial or deep
veins are involved
in causing varicos
ities
Grading of palloro
o
no pallor in 60 sees
1
pallor in 60 sees
2 pallor in 30-60 sees
3 pallor in less than 30 sees
4 pallor with limb flat (not elevated or
dependent)
Greater saphenous veins are involved if
the varicosities fill slowly with the
tourniquet on and then suddenly dilate
when the tourniquet is removed.
Deep and communicating veins are
involved if the varicosities fill immedi
ately with the tourniquet still on.
=
<;:
'"
""
>
@
g
""
w
"
'"
"
N
Test
Indication
Description
Allen's test
Homans' signII-
"
g
'"
o
A 50% falseposirive rare occurs with this test. Vascular laboratOry studies are more sensitive.
Sources: Data from JM Black, E Matassarin-Jacobs (eds). Luckmann and Sorensen's Medical-Surgical Nursing: A Psycnophysiologic Approach
(4th ed). Philadelphia: Saunders, 1993; P Lanzer, J Rosch (eds). Vascular Diagnostics: Noninvasive and Invasive Techniques, Perilnterven
tional Evaluations. Berlin: Springer-Verlag, 1994; and JW Hallet, DC Brewster, RC Darling (cds). Handbook of Patient Care in Vascular Sur
gery (3rd ed). Boston: Little, Brown, 1995.
'"
:t
-<
,...
J!
'"
Description
Doppler ultrasound
High-frequency and low-intensiry (1-] 0 MHz) sound waves are applied to the
skin with a Doppler probe (and acoustic gel) CO detect the presence or
absence of blood flow, direction of flow, and flow character over 3neries and
veins with an audible signal. Low-frequency waves generally indicate low
velocity blood flow,
Velociry patterns of blood flow along witb visual images of vessel and plaque anat
omy can be obtained by combing ultrasound with a pulsed Doppler derector. Dis
tinctive color changes indicate blood flow through a stenotic area.
Plethysmography is the measurement of volume change in an organ or body region
(volume change in this context refers CO blood volume changes that represent
blood flow),
PVR and OPG are used CO evaluate arterial flow, whereas WG, PRG, and PPG are used
to evaluate venous flow.
Color duplex
scanning or imaging
Plethysmography
(5 types)
Pulse volume recorder (PVR)
Ocular pneumoplerhysmography
(OPG)
Impedance plethysmography (IPG)
Phlebotheography (PRG)
Phoroplerhysmography (PPG)
'"
-<
:>
;g
-<
'"
"
'"
:;!
Test
Description
Systolic blood pressures are taken in both upper extremities at the brachial arter
ies and both lower extremities above the ankle, followed by Doppler evalua
:>
tion of dorsalis pedis or posterior tibialis pulses. The higher of the lower
extremity pressures is rhen divided by the higher of rhe upper-extremity pres
sures (e.g., an ankle pressure of
Computed tomography
(CT)
"
"
2l
"
J:
-<
i
!il
:>
MRI has multiple uses in evaluating the vascular system and is now morc com
monly used to visualize the arterial system than arteriograms. Specific uses for
MRI include detection of deep venous thrombosis and evaluation of cerebral
edema.
Serial MRls can also be used to help detemline me optimal operative time for patients
with cerebrovascular accidents by monitoring their progression.
Sources: Data from JM Black, E l\tatassarin-Jacobs (cds). Luckmann and Sorensen's Medical-Surgical Nursing: A PsychophYSiOlogic
Approach (4th cd). Philadelphia: Saunders, 1993; P Lanzer,J Rosch (cds). Vascular Diagnostics: Noninvasive and Invasive Techniques,
Peri-Interventional Evaluations. Berlin: Springer-Verlag, 1994; KL McCance,SE Huether (cds). Pathophysiology: The Biological Basis
for Disease in Adults and Children (2nd ed). St. Louis: Mosby, 1994; JL Kee (cd). Laboratory and Diagnostic Tests with Nursing Impli
cations (5th cd). Stamford: Appleton & Lange, 1999,606; VA Fahey (cd). Vascular Nursing (3rd ed). Philadelphia: Saunders, 1999j76,
86; and LM Malarkey, ME Morrow (cds). Nurses Manual of Laboratory Tests and Diagnostic Procedures (2nd ed). Philadelphia: Saun
den. 2000;359.
r;:
"
)-
J:
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g
-<
w
376
Thrombi formation
Hematoma formation
Hemorrhage
to
Chapter 9)
Hematologic Evaluation
The medical work-up of the patient with a suspected hematologic
abnormality emphasizes the patient history and laboratory studies, in
addition to the patient's clinical presentation.
History
In addition to the general charr review (see Appendix I-A), the follow
ing questions are especially relevant in the evaluation of the patient
with a suspected hematologic disorder7-':
to
377
Respiratory rate
Palpation
The examination performed by rhe physician includes palpation
of lymph nodes, liver, and spleen as parr of a general physical
examination. For specific complaints, the patient may receive
more in-deprh examinarion of a body system. Table 6-6 summa
rizes rhe abnormal hematologic findings by body system on physi
cal examinarion. The physical rherapist may specifically examine
the following :
378
Sign/Symptom
Associated Condition
Cardiac
Tachycardia
Palpitations
Murmur
Angina.
Dyspnea
Orthopnea
Back pain
Bone pain
Joint pain
Sternal tenderness
Headache
Anemia, hypovolemia
Anemia, hypovolemia.
Anemia, hypovolemia
Anemia, hypovolemia
Anemia, hypovolemia
Anemia, hypovolemia
Hemolysis
Leukemia
Hemophilia
Leukemia, sickle-cell disease
Severe anemia, polycythemia,
metastatic tumor
Severe anemia, polycythemia
Severe anemia
Vitamin BI1 anemia, malignancy
Severe anemia,
malignancy, infection
Anemia, polycythemia
Thrombocytopenia, anemia
Iron-deficiency anemia
Lymphoma, hemolysis, sickle-cell
disease
Hemolytic anemia
Respirarory
Musculoskeletal
Nervous
Syncope
Vertigo, tinnitus
Paresthesia
Confusion
Visual
Gastrointestinal,
urinary, and
reproductive
Visual disturbances
Blindness
Dysphagia
Abdominal pain
Spleno- or
hepatomegaly
Hematemesis, melena
Integumentary
Hematuria
Menorrhagia
Petechiae
Ecchymosis
Flushing
Jaundice
Pallor
379
The standard complete blood cell (CBC) count consists of a red blood
cell (RBC) count, WBC count, WBC differential, hematocrit (Hct)
measurement, hemoglobin (Hgb) measurement, and platelet (Pit)
count. Table 6-7 summarizes the CBC. Figure 6-'1 illustrates a com
mon method used by physicians to document portions of the CBC in
daily progress notes. If a value is abnormal, it is usually circled within
this "sawhorse" figure.
Clinical Tip
Erythrocyte Indices
RBC, Hct, and Hgb values are used to calculate three erythrocyte
indices: ( I ) mean corpuscular volume (MCV), (2) mean corpuscular
Hgb, and (3) mean corpuscular Hgb concentration. At mOst institu-
w
00
o
Test
Description
Value
Indication/Inrerpreration
coum
of blood
4.5-11.0xlOJ
(4,500-11,000)
WBC differential
Neucrophils 54-62 %
Lymphocytes 23-33%
Monocytes 3-7%
Eosinophils 1-3%
Basophils 0-0.75%
i::
J:
>
g
'"
o
'"
J:
-<
Hematocrit (Het)
Percentage of RBCs in
whole blood
Female: 35-40%
Male: 39-49%
hemodilution.
Hemoglobin (Hgb)
Amount of hemoglobin
in 100 ml of blood
Male: 13.5-17.5
gllOO 1111
suppression.
Increased: polycythemia, dehydration.
Decreased: anemia, recent hemorrhage, fluid
Platelets (Pit)
Number of platelets in
I of blood
150-450
10'
150,000-450,000 I
overload.
To assess thrombocytopenia.
Increased: polycythemia vera, splenectomy,
malignancy.
Decreased: anemia, hemolysis, DIC, ITP,
viral infections, AlDS, splenomegaly, with
radiation or chemotherapy.
Lab values vary among laboratories. RBC, hemoglobin, and platelet values vary with age and gender.
AIDS acquired immunodeficiency syndrome; DIC disseminated intravascular coaguloparhy; ITP idioparhic thrombocytopenic purpura.
Sources: Adapted from RJ Etin. Laboratory Reference Inrervals and Values. In L Goldman, JC Bennett (cds), Cecil Textbook of Medi
cine, Vol. 2 (21 Sf cd). Philadelphia: Saunders, 2000;2305; and E Marassarin-Jacobs. Assessment of Clienrs with Hemarologic Disorders.
In JM Black, E Matassarin-Jacobs, M,edical-Surgical Nursing Clinical Management for Continuity of Care (5rh ed). Philadelphia: Saun
ders, 1997;1465.
=
;;
8
5:
"
o
J:
C)
-<
w
00
-
382
WBC
Count
Hgb
Hct
Pit
Count
Figure 6-1. Illustration of portions of the complete blood cell count in short
hemoglobin; Pit
platelet; \lIBe
tions, these indices are included in the CSc. Table 6-8 summari1.es
these indices.
Coagulation Profile
Coagulation tests assess the blood's ability to clot. The tests used to
determine c10rting are prothrombin time (PT) and partial thrombo
plastin time (PTT). An adjunct to the measurement of PT is the Inter
national Normalized Ratio (INR). The INR was created to ensure
reliable and consistent measurement of coagulation levels among all
Description
Value
Interpretation
80-100 pgJ
26-34 pglcell
Proportion of eaeh
RBC occupied by
Hgb
3 1-37 gldl
<
n
c
!;:
'"
>
Z
o
5
Q
w
00
w
384
ACUTE
CARE
Clinical Tip
When confirming an order for physical therapy in the phy
sician's orders, the therapist must be sure to differentiate
between the order for physical therapy and the blood tesr
(i.e., rhe abbreviarions for both physical therapy and pro
thrombin time are PT).
Pathophysiology
This section is divided into a discussion of vascular and hematologic
disorders.
Vasclilar Disorders
Vascular disorders are classified as arterial, venous, or combined arte
rial and venous disorders. Clinical findings differ berween anerial and
venous disorders, as described in Table 6-10.
Arterial Disorders
Atherosclerosis
Description
Value" (sees)
J ndicationlInterpretation
PrOthrombin rime!
PT 11-15
international
normalized ratio
bleeding disorders
(PT/INR)
VII, and X
Partial thromboplastin
rime (PIT) (acri
a rapid version of
VIII, IX, X, XI
PIT
60-70
APIT
30--40
PIT)
i:
"
-<
>
Values for prothrombin rime (PT) and PlT vary between laborarories.
:t
m
Source: Dara from KD Pagana, TJ Pagana. Blood Srudies. Mosby's Manual of Diagnostic and Laborarory Tests. St. Louis: Mosby, 1998.
"
-<
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00
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386
Arterial Disorders
Edema
Venous Disorders
Present
Worse at the end of the day
Improve with elevation
Muscle mass
Reduced
Unaffected
Pain
Intermittent claudication
Aching pain
Cramping
Pulses
Decreased to absent
Possible systolic bruit
Skin
Absence of hair
Small, painful ulcers on
pressure points, espe
cially lateral malleolus
Color
Brown discoloration
Dependent cyanosis
Dependent cyanosis
Temperature
Cool
Sensation
Pruritus
thrombophlebitis
Occasional itching, ting
ling, and numbness
Source: Data from JM Black, E Matassarin-Jacobs (eds). Luckmann and Sorensen's
Smoking
Diabetes mellitus
H ypenension
HHiATOLOGY
387
terol of more than 260 mgldl or triglyceride of more than 150 mgldl)
Gender (Men are at greater risk than women until women reach
menopause; then the risk is equal in both genders.)
Inactivity
Family history
388
Clinical Tip
Progression of ambulation d istance in the patient with
intermittent claudication can be optimized if ambulation is
performed in short, frequent intervals (i.e., before the
onset of claudicating pain).
Symptoms similar to intermittent claudication may have a neu
rologic origin from lumbar canal stenosis or disk d isease. These
symptoms are referred to as pseudoclaudication or neurologic
claudication. Table 6-11 outlines the differences between true clau
d ication and pseudoclaudication.18 Medications that have been suc
cessful in managing intermittent claudication include pentoxifylline
and cilostazol,'9
Treatment of atherosclerotic d isease is based on clinical presention
and can range from risk-factor modifications (e.g., low-fat diet,
increased exercise, and smoking cessation) to pharmacologic therapy
(e.g., anticoagulation and thrombolytics) to surgical resection and
grafting. Modification of risk factors has been shown to be the most
effective method to lower the risk of morbidity (heart attack or
stroke) from artherosclerosis.1 52o
Aneurysm
An aneurysm is a localized di latation or Outpouching of the vessel
wall that results from d egeneration and weakening of the support
ive network of protein fibers with a concomitant loss of medial
smooth muscle cells. Aneurysms most commonly occur in the
abdominal aorta or iliac arteries, followed by the popliteal, femo
ral, and carotid vessels. 6.1 5.21 , 22 The exact mechanism of aneurysm
formation is not fully understood but includes a combination of
the following:
389
Incerminem
Claudication
Acrivity-induced
Location
Yes
Unilateral buttock,
hip, thigh, calf and
foar
Cramping
lightness
Tircdness
Narure
Relieved by
No
Occurs at the same
distance each time
with walking on
level surface
Unchanged or
decreased distance
walking uphill
Unchanged or
increased distance
walking downhill
Stopping activity
Pseudoclaudication
Yes or no
Back pain and bilat
eral leg pain
Same as with intermit
tent claudication or
presence of tin
gling, weakness,
and clumsiness
Yes
Occurs at variable dis
tance each time
with walking on
level surfaces
Increased distance
when walking uphill
Decreased distance
walking downhill
Sitting
Sources: Data from JR Young, RA Graor, j\'V Olin, JR Bartholomew (eds). Peripheral
Vascular Diseases. St. Louis: Mosby, 1991; 183; and JM Fritz. Spinal Stenosis. In JD
390
Clinical Tip
Abdominal aortic aneurysms are frequently referred to as
AAA or Triple A in the clinical setting.
The following are additional clinical manifestations of aneurysms:
Ischemic manifestations, described earlier, in Atherosclerosis, if
the aneurysm impedes blood flow.
Low back pain (aortic aneurysms can refer pain to the low
back).
_.
391
_.J. ?, RenaJarteries
Abdominal
aorta
Iliac
arteries
tion from the ascending aorta across the arch of the aorta. C. Saccular
aneurysm of the descendmg aorta. (With permission from BL Bullock led).
Pathophysiology: Adaptations and Alterations in Function {4th ed}. Phila
delphia, Lippillcott-Ravell, 1996;532.)
392
Arterial Thrombosis
Arterial thrombosis occurs in areas of low or stagnant blood flow,
such as atherosclerotic or aneurysmal areas. The reduced or turbulent
blood flow in these areas leads to platelet adhesion and aggregation,
which then activates the coagulation cycle to form a mature thrombus
(clot). Blood flow may then be impeded, potentially leading to tissue
ischemia with subsquent clinical manifestations,21 ,23
Arterial Emboli
Arterial emboli arise from areas of stagnant or disturbed blood flow
in the heart or aorta. Conditions that predispose a person to emboli
formation are (1) atrial fibrillation, (2) myocardial infarction, (3) infec
tive endocarditis, (4) cardiac valve replacement (if not properly anti
coagulated), (5) chronic congestive heart failute, and (6) aortic
atherosclerosis. Areas in which arterial emboli tend to lodge and
interrupt blood flow are arterial bifurcations and areas narrowed by
atherosclerosis (especially in the cerebral, mesenteric, renal, and coro
nary arteries). Signs and symptoms of thrombi, emboli, or both
depend on the size of the occlusion, the organ d istal to the clor, and
the collateral circulation available."
Treatment of thrombi, emboli, or both includes anticoagulation
with or withom surgical resection of the atherosclerotic area that is
predisposing rhe formarion of rhrombi, emboli, or both. Medical
management of arterial thrombosis can also include antithrombotic
drugs (e.g., tissue factor or factor X a inhibitors) or combined anti
thrombotic therapy with aspirin, and thienopyridine and warfarin, or
both."
Hypertension
Hypertension is an elevated arterial blood pressure, both systolic and
diastolic, that is abnormally sustained at rest. Table 6- J 2 outlines
normal and hypertensive blood pressures for a given age group. Signs
and symptoms that can result from hypertension and its effects on
target organs are described in Table 6-13. Two general forms of
hypertension exist: essential and secondary.
Essential, or idiopathic, hypertension is an elevation in blood pres
sure that results without a specific medical cause bllf is related to the
following risk factors" 2 5 :
Genetic predisposition
Smoking
393
Age
(SystolicIDiastolic)
Infanrs
Children
Teenagers (age 1217 yrs)
Adults
25 yrs
45-60 yrs
Older than 65 yrs
80/40
90/60
100/60
120/80
115/70
130180
120-125/75-80
135/90
135-145185
140-160190-95
150/85
160/90
Sedentary lifestyle
Type A personality
Obesity
Diabetes mellitus
Atherosclerosis
Imbalance of vasomediator production, nitric oxide (vasodila
ror), and endothelin (parent vasoconstricror)
Secondary hypertension results fr0111 a known med ical cause,
such as renal disease and others listed in Table 6-14. If the causative
factors are treared sufficiently, systolic blood pressure may return to
normal limits.21
Management of hypertension consists of behavioral (e.g., d iet,
smoking cessation, activity modification) and pharmacologic inter
vention to maintain blood pressure within acceptable parameters.
The primary medications used are diuretics and angiotensin-con
verting enzyme inhibirors along with beta blockers, calcium channel
blockers, and vasodilarors. 2 1,26- 28 A summary of these medications,
their actions, and their side effecrs can be found in Appendix Tables
IV-I?, IV-2, IV-12, IV-14, and IV-3D, respectively.
394
Hypertensive Effect
Clinical Manifesrations
Brain
Cerebrovascular
accident
Encephalopathy
Eyes
Blurred or impaired
vision
Encephalopathy
Heart
Myocardial infarction
Congestive heart failure
Myocardial hypertrophy
Kidneys
Dysrhythmi,.
Renal insufficiency
Renal failure
C linical Tip
Knowledge of medication schedule may facilitate activ
ity tolerance by having optimal blood pressures at rest and
with activity.
395
Descri ption
Pheochromocytoma
Primary aldosteronism
Renin-secreting tumors
Renovascular disease
396
397
small and medillmsized arteries in the distal lower and upper extremi
ties. The thrombotic occlusions consist of microabscesses that are
inAammarory in nature, suggesting a collagen or autoimmune origin,
although the exact etiology is still unknown.I32 1 Rest pain is common,
along with intermittent claudication that occurs more in the feet than in
the calf regionJ
Treatment of Buerger's disease can include smoking cessation, cor
ticosteroids, prostaglandin EI infusion, vasodilators, hemorheologic
agents, antiplatelet agents, and anticoagulants. IJ,21
Giant Cell Arteritis Giant cell arteritis (GCA) is another granuloma
tous inflammatory disorder of an unknown etiology. It predominantly
affects the large arteries and is characterized by destruction of the
internal elastic lamina. Two clinical presentations of GCA have been
recognized: temporal arteritis and Takayasu's arteritis.21
Temporal arteritis is a more common and mild presentation of GCA
that occurs after 50 years of age. The primary signs and symptoms are
persistent headache (temporal and occipital areas), transient visual dis
turbances (amaurosis fugax and graying or blurring of vision), and iaw
and tongue pain. Polymyalgia rheumatica, a clinical syndrome charac
terized by pain on active motion and acute onset of proximal muscular
stiffness, is frequently associated with temporal arteritis. The primary
treatment for temporal arteritis is prednisone. 1 8,2 9
Takayasu's arteritis generally affects young Asian women but has
been known to occur in both genders of blacks and Hispanics as
well. It is a form of generalized GCA that primarily involves the
upper extremities and the aOrta and its major branches. Lower
extremity involvement is less common. Management of Takayasu's
arteritis may consist of prednisone and cyclophosphamide, along
with surgical intervention if the disease progresses to aneurysm,
gangrene, or both.18
RaYllaud's Disease
Raynaud's disease is a form of intermittent arteriolar vasoconstriction
that occurs in patients who have concurrent immunologic disease. The
exact etiology is unknown but may be linked to defects in the sympa
thetic nervous system. Evidence exists for and against the theory of sym
pathetic overactiviry, which is said to lead to Raynaud's disease. Women
16-40 years of age are mOSt commonly affected, especially in cold cli
mates or during the wimer season. Other than cold hypersensitivity,
emotional factors can also trigger the sudden vasoconstriction. Areas
generally affected are the fingertips, roes, and the tip of the nose.3,18,26
398
399
Compartment Syndrome
Compartment syndrome is the swelling in the muscle compartments
(myotendon, neural, and vascular structures contained withjn a fascial
compartmenr of an extremiry) that can occur after traumatic injury to
the arteries. These injuries include fractures, crush injuries, hematomas,
penetrating injuries, circumferential burn injury, electrical injuries, and
status post revascularization procedures. External factors, such as casts
and circular dressings that are too constrictive, may also lead to com
partment syndrome.6.'8.J6 Compartment syndrome can also occur as a
chronic condition that develops from overuse associated with Strenous
exercise. Diagnosis of comparrment syndrome is established by measur
ing compartment pressures. Comparrment pressures of 25-30 mm Hg
can cause compression of capillaries.J 6
Clinical Tip
Patient, staff, and family eduction on proper position
ing techniques can reduce the risk of swelling and subse
quent compartment syndrome .
The physical therapist should delineate any range-of
motion precautions that may be present after fasciotomies
that cross a joint line.
Venous Disorders
Varicose Veins
Varicose veins arc chronic d ilations of the veins that first result from a
weakening in the venous walls, which then leads to improper closure
of the valve cusps. Incompetence of the valves further exacerbates the
400
Venous thrombosis can occur in the superficial or deep veins (deep venous
thrombosis [DVT1) and can result from a combination of venous stasis,
injury to the endothelial layer of the vein, and hypercoagulability. The pri
mary complication of venous thrombosis is pulmonary embolism (PE).6
The following arc risk factors associated with venous thrombosis
formation 18,38:
Surgery and nonsurgical trauma, such as lower-extremity fracture
Immobilization
Limb paresis or paralysis
Heart failure or myocardial infarction
Previous DVT
Increasing age
Malignancy
Obesity
Pregnancy
Use of oral contraceptives
Signs and symptoms of venous thrombosis can include the
following18,,,:
Pain and swelling distal to the site of thrombus
401
Dilated veins
Low-grade fever
A dull ache or tightness in the region of DVT
Clinical Tip
Homans' sign (pain in upper calf with forced ankle dor
siflexion) has been lIsed as a screening tool for venous
thrombosis, but it is an insensitive and nonspecific test that
has a very high false-positive rate.1 .3....o
402
Clinical Tip
Physical therapy intervention should be discontinued imme
diately if the signs and symptoms of a PE arise during an
examination or treatment session.
Chronic Venolls Insufficiency and Postphlebilic Syndrome
Chronic venous insufficiency and postphlebitic syndrome are similat
disorders that result from venous outflow obstruction, valvular dys
function from thrombotic destruction of veins, or both. Valvular dys
function is generally the most significant cause of either disorder.
Within 5 years of sustaining a DVT, approximately 50% of patients
develop signs of these disorders. The hallmark characteristics of both
are the followingl6.42:
VASCULAR SYSTEM
AND
HE.MATOLOGY
403
Clinical Tip
Caution should be taken in providing compressive dress
ings and elevating the lower extremities of patients who
have arterial insufficiency, diabetes mellitus, and conges
tive heart failure.
Combined Arterial and Venous Disorders
Arteriovenous Malformations
Arteriovenous malformations (AVMs) involve shunting of blood
directly from the artery to the vein, bypassing the capillary bed. The
presence of an arteriovenous fistula in the AVM is usually the cause of
the shunt. The majority of AVMs occurs in the trunk and extremities,
with a certain number of cases also presenting in the cerebrovascular
region.1 3
Signs of AVMs may include the following13:
Venous varices
Edema
Limb deformity
Skin ulceration
Pulse deficit
Bleeding
404
Hematologic Disorders
Erythrocytic Disorders
Disorders of RBCs are generally categorized as a decrease or an
increase in the number of RBCs in the circulating blood.
Anemia
Anemia is a decrease in the number of RBCs. Anemia can be described
according to etiology as (1) a decrease in RBC production, (2) abnor
mal RBC maturation, or (3) an increase in RBC destruction? Anemia
can also be described according to morphology based on RBC size or
color.43 RBCs that are of normal size are normocytic; RBCs that are
smaller than normal are microcytic; and RBCs that are larger than nor
mal are macrocytic. RBCs of normal color are normochromic; RBCs of
decreased color are microchromic. Some of the most common anemias
are described in this section.
405
Dizziness
Headache
Irritability
Oral ulceration
406
Clinical Tip
Patients who receive monthly vitamin BI2 injections may
have improvements in their alertness and activity tolerance
for a few days after the injection. Therefore, physical ther
apy intervention and goal setting should accommodate
these changes.
Folic Acid Anemia Decreased folic acid (folate) causes the produc
tion of macrocytic, normochromic RBCs. Folic acid deficiency is asso
ciated with a diet low in folic acid, impaired intestinal absorption of
folic acid, pregnancy, or alcoholism. The presentation of folic acid
anemia is similar to vitamin 8 deficiency anemia, except there are no
12
neurologic sequelae. Folic acid anemia is diagnosed by clinical presen
tation, a low serum folate level, and elevated lactate dehydrogenase
and MCV values.'9 Management of folic acid anemia consists of folic
acid supplementation."
Aplastic Anemia Aplastic anemia is characterized by a decreased
RBC production secondary to bone marrow damage. The bone mar
row damage either causes irreversible changes to the stem cell popula
tion, rendering these cells unable to produce RBCs, or alters the stem
cell environment, which inhibits RBC production. The exact mecha
nism of stem cell damage is unknown; however, present theories
include exposure to radiation and chemotherapy or pharmacologic
agents, the presence of infection or malignancy, or as an autoimmune
407
Fever or infection
Sore throat
Jaundice
408
Retinopathy or blindness
Paresthesias
409
Clinical Tip
The use of oximetry can help the physical therapist and patient
monitor RBe oxygenation and gauge exercise imensiry.
Polycythemia
The three types of polycythemia are primary polycythemia (poly
cythemia vera), secondary polycythemia, and relative polycythemia.
They involve the abnormal increase in the number of RBCs and result
in increased blood viscosity.
1.
Primary polycythemia, or polycythemia vera, is an increase in the
number of RBCs, WBCs, and Plts.54 The origin of this disease is
unknown; however, there is an autonomous overproduction of erythroid
stem cells from bone marrow leading to increased blood viscosity and
expanded blood volume. Thus, there is a risk for thrombus formation and
bleeding " Primary polycythemia may convert to chronic myelogenous
leukemia or myelofibrosis.
2.
Secondary polycythemia is the overproduction of RBCs
owing to a high level of erythropoietin. The increased erythropoietin
level is a result of either altered stem cells (which automatically pro
duce erythropoietin or erythropoietin-secreting rumors, such as
hepatoma or cerebellar hemangioblastoma)" or chronic low oxy
genation of tissues, in which the body arrempts to compensate for
hypoxia. The latter is common in individ uals with chronic obstruc
tive pulmonary disease, cardiopulmonary disease, or exposure to
high altitudes.
3.
Relative polycythemia is the remporary increase in RBCs secondary to decreased Auid volume (dehydration), as with excessive
vomiting, diarrhea, or excessive diuretic use, or after a burn injury.
Signs and symptoms of polycythemia may include the following:
Fatigue
Headache
Dizziness
Blurred vision
410
Weakness
411
1.
Hemophilia A is characterized by the lack of factor VIll
and is inherited as an X-linked recessive trait.
2.
Hemophilia B (Christmas disease) is characterized by the
lack of factor IX and is inherited as an X -linked recessive trait.
3.
Hemophilia C is characterized by the lack of factor X I and
is inherited as an autosomal recessive trait.
4.
von Willebrand's disease is characterized by the lack of
factor VHf and is inherited as an autosomal dominant trait.
Patients with mild hemophilia experience bleeding only with
trauma or after surgical procedures, whereas patients with severe
hemophilia may bleed with minor trauma or spontaneously.47
Symptoms and physical findings of bleeding episode from hemo
philia may include the following:
Hematoma
Disorientation
Convulsions
4 t2
Clinical Tip
Watch for signs of joint effusion (warmth and edema) in
patients with hemophilia who are prone to hemarthrosis,
especially during weight-bearing activites.
Thalassemia
Thalassemia is an autosomal-recessive d isease characterized by
abnormal formation of Hgb chains in RBCs, resulting in RBC mem
brane d amage and abnormal erythropoiesis and hemolysis.
Hgb is composed of two alpha and two beta chains. a-Thalas
semia is a defect in alpha-chain synthesis in which one (alpha trait),
two (a-thalassemia minor), or three (Hgb H d isease) genes are
altered. Each type of a-thalassemia varies in presentation from a
lack of symptoms (alpha trait and minor) to chronic severe
hemolytic anemia (Hgb H) which requires regular blood transfu
sions.4 p-Thalassemia minor is a defect in beta-chain synthesis in
one of two beta chains and is usually asymptomatic. p-Thalassemia
major is a severe reduction or absence in beta-chain production
that results in severe anemia, growth failure, bony deformities,
hepatosplenomegaly, and j aundice with a life expectancy of 20-30
years from complications of heart failure, cirrhosis, and endocrin
opathy.47 Management of the thalassemia may include folate sup
plementation, blood transfusion, iron-chelating agents, and sple
nectomy.47
Thrombocytopellia
Thrombocytopenia is an acute or chronic d ecrease in the number
of Pits (less than 1 50,000/ 1 ) in the circulation. It can result from
decreased Pit production (caused by infection, drug or immune
responses, or blood vessel d amage), increased Pit destruction
(caused by malignancy, antiplatelet antibodies, or the use of
myelosuppressive drugs), or altered Pit d istribution (caused by car
diac surgery-induced hypothermia, portal hypertension, or sple
nomegaly).57
VASCULAR SYSTEM
AND
HEMATOLOGY
413
urine, or stool
present
Renal failure
Splenomegaly
Pulmonary embolism
414
TIIERAPISTS
Fever
Abdominal pain
Management
The management of vascular disorders includes pharmacologic ther
apy and vascular surgical procedures. Hematologic disorders may be
managed with pharmacologic therapy, as well as with nutritional
therapy and blood product transfusion.
415
Allticoagulatioll Therapy
The standard INR goal for anticoagulation therapy with warfarin
(Coumadin) is 1.5-2.5 times a control value and is categorized by
condition or clinical state according to the following":
INR 2.0-3.0
o DVT
Atrial fibrillation
INR 2.5-3.5
The physician will determine the PTflNR and PTT goal for each
K or fresh-frozen plasma.
416
N"tritiollai Therapy
Nutritional therapy is the treatment of choice for anemia caused
by vitamin and mineral deficiency. Appendix Table I V-2S describes
the indications and general side effects of the agents used to man
age iron deficiency, vitamin B1 , and folic acid anemias.
2
6-16 lists the signs and symptoms of various types of acute adverse
transfusion reactions. In addition to these reactions, complications
of blood transfusion include air embolism (if the blood is pumped
into the patient) or circulatory overload (from a rapid increase in
volume). Circulatory overload occurs when the rate of blood
(fluid) transfusion occurs faster than the circulation can accommo
date. Signs and symptoms include tachycardia, cough, dyspnea,
crackles, headache, hypertension, and distended neck veins. To
prevent circulatory overload during a transfusion, intravenous flu
ids may be stopped, or a diuretic (e.g., furosemide ILasixJ) may be
given. Delayed adverse transfusion reactions include iron over
load, graft-versus-host disease, hepatitis, human immunodeficiency
virus-l infection, or delayed hemolytic reaction (approximately 714 days post transfusion)."
Table 6-15. Common Blood Products and Their Clinical Indications and Omcomes
Product
Content
Clinicallndications
Outcome
Whole blood
plasma
3% in a nonbleeding
RBCs only
(RBCs)
i:
expansion.
Plaeelets (Pits)
<
Resolution of thrombocytopenia.
Prevention or resolution of bleeding.
Pit should increase 5,000 in a lO-kg adult
(per unie).
"
,.
z
"
:r
-<
...
"
...
00
Product
Content
Clinical Indications
Outcome
Fresh-frozen
All plasma
plasma (FFP)
components,
namely blood
factors and protein
levels.
proteins
fraction
globulins, and
(PPF)
plasma proreins
"
'"
J:
-<
R>r
Burn injury.
Albumin,
'"
'"
"
n
>
0
0
J:
>z
"
=
lopathy.
Factor Xl deficiency.
Albumin
>n
""
J:
m
'"
>
"i
Cryoprecipitate
hemoglobin.
Sources: Data from National Blood Resource Education Programs Transfusion Therapy Guidelines for Nurses. US Depanmem of Health and
Human Services, National Institutes of Health, September 1990; and adapted from WH Churchill. Transfusion Therapy. New York: Sciemific
American Medicine, 2001 ;4.
;;
<;
'"
-<
>
Z
"
-<
..
'"
...
'"
o
Cause
Febrile reaction
Allergic reaction
[0
Septic reaction
>
i::
13
11
o
'"
:r
Q
r
:i!
!il
>
Anaphylacric reaction
Hives (mild)
Wheezing or bronchospasm, an.xiery,
cyanosis, nausea, emesis, bloody
diarrhea, abdominal cramps, shock,
cardiac arrest (severe)
Onset: within a few seconds after expo
sure
Ig
immunoglobulin.
Sources: Adapted from B Kozier, G Erb, K Blais, JM Wilkinson (cds). Fundamentals of Nursing: Concepts, Process and Practice (5rh cd).
Redwood Cit)', CA. Benjamin-Cummings, 1995;110; and data from PJ Larison, LO Cook. Adverse Effects of Blood Transfusion. In OM
Harmening (cd), Modern Blood Banking and Transfusion Practices. Philadelphia: FA DavIs, 1999; and Narional Blood Resource Educa
tion Programs Transfusion Therapy Guidelines for Nurses. US Department of J-Iealrh and Human Services, Nadonal lnsritures of Health.
Seprember 1990.
<
'"
o
:l!
,.
Z
"
5
CJ
-<
...
N
422
Clinical Tip
423
Thrombosis
424
Supercial-4_.
femoral
ortery
-t
..
Popliteal-artery
ortery
Popliteal
artery
Anterior
tibial artery
Peroneal
artery
/fjHl'-- Posterior
tibial artery
Figure 6-3.
425
Infection
Renal failure
Sexual dysfunction
Colon ischemia
Endarterectomy
Endarterectomy is a process in which the stenotic area of an artery
wall is excised and the noninvolved ends of the artery are reanas
tomosed. It can be used to correct localized occlusive vascular dis
ease, commonly in the carotid arteries, eliminating the need for
bypassing the areaB
426
Clinical Tip
The abbreviation CEA is often used to refer
to
a carotid
endarterectomy procedure.
to
the hemodynamic
Clinical Tip
428
429
430
disorders does not occur at the same rate as in patients with nor
mal blood composition; therefore, the time frame for goal achieve
ment rnay need to be lengthened.
References
1. Black JM, Matassarin-Jacobs E (cds). Luckmann and Sorensen's Medi
cal-Surgical Nursing: A Psychophysiologic Approach (4th cd). Philadel
phia: Saunders, 1993;1286.
2. Marieb EN. Blood. In EN Marieb (cd), Human Anatomy and Physiol
ogy (3rd cd). Redwood City, CA: Benjamin-Cummings, 1995;584-611.
3. Knight CA. Peripheral Vascular Disease and Wound Care. In SB O'Sulli
van, TJ Schmirz (cds), Physical Rehabilitation: Assessmenr and Trear
ment (4th cd). Philadelphia: FA Davis, 2001;583-608.
4. Lanzer P, Rosch J (cds). Vascular Diagnosrics: Noninvasive and Inva
sive Techniques, Peri-Intervenrional Evaluarions. Berlin: Springer
Verlag, 1994.
5. Fahey VA (cd). Vascular Nursing (3rd cd). Philadelphia: Saunders, 1999.
6. Hallet JW, Brewster DC, Darling RC (cds). Handbook of Patient Care in
Vascular Surgery (3rd cd). Bosran: Litrle, Brown, 1995.
7. Hillman RS, Aulr KA (cds). Hemarology in Clinical Practice: A Guide co
Diagnosis and Management. New York: McGraw-Hili, J 995; 17.
8. Goodman ec, Snyder TK. Overview of Hemarology: Signs and Symp
roms. In ec Goodman, TK Snyder (cds), Differential Diagnosis in Phys
ical Therapy: Musculoskeletal and Sysremic Conditions. Philadelphia:
Saunders, 1990;114.
431
432
33.
34.
35.
36.
37.
38.
39.
40. Church, V. Sraying on guard for DVT & PE. Nursing 2000;30(2):34-42.
41. Saunders CS. Improving survival in pulmonary embolism. Patient Care
2000;34( 16):50.
42. Coats U. Management of venous ulcers. Crir Care Nurse Q 1998;21 (2):
14-23.
43. Purrillo DT, Purrillo RP (eds). A Survey of Human Diseases (2nd ed).
Boston: Little, Brown, 1989;287.
44. Lee GR. Acute Posthemorrhagic Anemia. In GR Lee, J Foerster, J
Lukens, et al. (eds), Wincrobe's Clinical Hematology, Vol. 2 (10th cd).
Balrimore: Williams & Wilkins, 1999;1485-1488.
45. Erythrocyte Disease. In AE Belcher (ed), Blood Disorders. St. Louis:
Mosby-Year Book, 1993;51.
46. The Hematopoietic and Lymphoid Systems. In Kumar V, Corran R,
Robbins SL (eds), Basic Parhology (6rh cd). Philadelphia: Saunders,
1997;34(}"'392.
47. Linker CA. Blood. In LM Tierney, S] McPhee, MA Papadakis (eds),
Current Medical Diagnosis and Treatment 200]. Stamford, Cf: Apple
ron & Lange, 2001 ;505-558.
48. Lehne RA. Drugs for Deficiency Anemias. In RA Lehne (cd), Pharmacol
ogy for Nursing Care (4rh ed). Philadelphia: Saunders, 2001;589-602.
49. Roper D, Stein S, Payne M, Coleman M. Anemias Caused by Impaired
Production of Erythrocytes. In BF Rodak (cd), Diagnostic Hematology.
Philadelphia: Saunders, 1995; 181.
433
br CoagulaTIon.
57.
58.
S9.
60.
61.
62.
63.
64.
65.
7
Burns and Wounds
Michele P. West, Kimberly Knowlton,
and Marie Jarrell-Gracious
Introduction
Treating a patient with a major burn injury or other skin wound is
often a specialized area of physical therapy.' Physical therapists
should, however, have a basic understanding of normal and abnormal
skin integrity, including the etiology of skin breakdown and the fac
tors that influence wound healing. The main objectives of this chapter
are therefore to provide a fundamental review of the following:
1.
2.
The evaluation and physiologic sequelae of burn injury,
including medical-surgical management and physical therapy
intervention
435
436
3.
The etiology of different types of wounds and the process
of wound healing
4.
The evaluation and management of wounds, including
physical therapy intervention
Structure and function: Normal Integument
Stnlcture
The integumentary system consists of the skin and its appendages
(hair and hair shafts, nails, and sebaceous and sweat glands),
which are located throughout the skin, as pictured in Figure 7-1.
Fr" nervI
endln91
TactlM! corpuscle
----t"'"'-fll
ir.\:It-''''m.' pipill.
DERMIS
S41bIceoullIl.nd
Blood_I
SubcutlllKlln
++......l
___
pepilll
Sw.t ,land
m""'.
H.ir follicle
----t
H.ir pipill.
SUBCUTANEOUS
CONNECTiVe
TISSUE
p.cini.n corpuscle
Nerve bundle
437
438
Composition
Function
Dead
Epidermis
Strarum
corneum
keratinocytes
Pigment layer
Melallocytes
Stratum
Mature
ultraviolet absorption
granulosum
Stratum
keratinocytes
waterproof
Langerhans' cells
Keratinocytes
spinosum
Stratum basale
ew keratinocytes
Merkel's cells
Detects touch
Areolar
Dermis
Papillary layer
connective
rogether
tissue
Meissner's
corpuscles
Blood and lymph
vessels
Reticular layer
Collagen, elastin,
and reticular
fibers
Hypodermis
Subcutaneous fat
Pacinian cells
Detects pressure
Detects cold
absorption
Source: Data from GA Thibodeau, KT Panon (cds), Structure and Function of the Iy
(11th ed). St Louis: Mosby, 2000.
439
Pathophysiology of Burns
Skin and body tissue destrucrion occurs from rhe absorprion of heat
energy and results in tissue coagulation. This coagulation is depicted
in zones (Figure 7-2). The ZOl1e of coagu/ali01l, locared in the cemer of
the burn, is the area of greatest damage and contains nonviable tissue
referred to as eschar. Alrhough eschar covers rhe surface and may
appear to take rhe place of skin, ir does nor have any of rhe characrer
istics or functions of normal skin. Instead, eschar is constrictive,
attracts micro-organisms, and houses burn toxins that may circulate
throughout rhe body.' The Z01le of stasis, which surrounds rhe zone of
coagularion, comains marginally viable rissue. The Z01le of hyper
emia, rhe ourermosr area, is the least damaged and heals rapidly.
c
Epidermis
Dermis
Subcutaneous
tissue
440
Bum Injury
Rot.... of Y1ISOaC1MIsubstancea
Edema IormatIon
RIsk 01 compartment
syndrome
Increased body weight
Low protein confllnt
EIectroly1e changes
Decreased IeYefs of K+
Hematologic changes
Increased Hct
(plasma volume loss)
DecnIased """"'"" of
RBCs (hemolyzed cotls)
Increased numbers 0'
wacs (hemoconcentration)
DecnIased numbers of
thrombocytes (platelet
destruction)
_ blood viscosity
441
Complications
Respiratory
Cardiovascular
GastroinrestinaV
genitourinary
Renal
Types of 8ums
Thermal Burns
Thermal burns can be the result of conduction or convection, as in
contact with a hot object, hot liquid, chemicals, flame, or steam. In
order of frequency, the most common 'Ypes of thermal burns are
scalds, flame burns, flash burns, and cOntact burns (Table 7-3)4 The
severity of burn depends on the location of the burn, the temperature
of the burn source, and the duration of contact.s
Electrical Burns
An electrical burn is caused by exposure to a low- or high-voltage
current and results in superficial burns, as well as less-visible but
massive damage of muscle, nerves, and bone. Tissue necrosis of
these deeper structures occurs from the high heat intensity of the
current and the electrical disruption of cell membranes.' Tissue
damage occurs along the path of the current, with smaller distal
areas of the body damaged most severely. This pattern of tissue
442
Description
Characterisrics
Scald burn
Spill of or immer
sion in a hot
liquid, such as
boiling water,
grease, or tar
thickness burns.
Exposure ro thicker liquids or
immersion causes a deeper burn
from increased contact time.
Immersion burns commonly cover a
larger total body surface area than
do spills.
Flame burn
Flame exposure
from fire or
flammable
liquids, or
ignition of
ciorhing
Flash burn
Explosion of
flammable
liquid, such as
gasoline or
propane
Contact burn
Exposure to hot
objects, such as
glass, plastic,
mecal, or coal
443
Lightning
Lightning, considered a form of very high electrical current, causes
injury via four mechanisms9:
1.
444
4.
Shock wave, in which lightning travels outside the person
and static electricity vaporizes moisture in the skin
Chemical Burns
Chemical burns can be the result of reduction, oxidation, corrosion, or
desecration of body tissue with or without an associated thermal injury.lo
The severity of burn depends on the type of chemical and its concentra
tion, duration of contact, and mechanism of action. Unlike thermal
burns, chemical burns significantly alter systemic tissue pH and metabo
lism. These changes can cause serious pulmonary complications (e. g. , air
way obstruction from bronchospasm, edema, or epithelial sloughing)
and metabolic complications (e. g., liver necrosis or renal dysfunction
from prolonged chemical exposure).
Ultraviolet and Ionizing Radiation Burns
A sunbun1 is a superficial partial-thickness burn from the overexposure
of the skin to UV radjation. Ionizing radiation burns with or without
thermal burn occur when electromagnetic or particulate radiation energy
is transferred [Q body tissues, resulting in the formation of chemical free
radicals. I I Ionizing radiation burns usually occur in laboratory or indus
trial settings. The severity of the ionizing radiation burn depends on the
dose, dose ra te, and the tissue sensitivity of exposed cells. Often referred
to as acute radiation syndrome, complications of ionizing radiation
burns include the following I L
Gastrointestinal: Cramps, nausea, vomiting, diarrhea, and bowel
i chemia
Classificatioll of a Bllm
The extent and depth of the burn determine its severity and dictate
acute care treatment.
445
Rille o( Nilles
The rule of nines divides the body into sections, seven of which are
assigned 9% of TBSA. The anterior and posterior trunk are each
assigned 18%, and the genitalia is assigned 1% (Figure 7-4). This
Front 18% !
\ Back 18% :
18%
18%
Figure 7-4.
446
formula is quick and easy to use, especially when a rapid initial esti
mation of TBSA is needed in the field or the emergency room. To use
the rule of nines, the area of burn is filled in on the diagram, and the
percentages are added for a TBSA. Modifications can be made if an
entire body section is not burned. For example, if only the posterior
left arm is burned, the TBSA is 4.5%.
447
Table 7-4. Lund and Browder Method of Assessing the Extenr of Burns'"
'1-4
5-9
10-14
15
Birth
yrs
yrs
yrs
yrs
Head
19
17
13
1I
Neck
Anrerior trunk
13
13
13
13
'13
13
Posterior trunk
13
13
13
13
13
13
Adult
Left butrock
2.5
2.5
2.5
2.5
2.5
2.5
Right burrock
2.5
2.5
2.5
2.5
2.5
2.5
Left forearm
Right forearm
Lef, hand
2.5
2.5
2.5
2.5
2.5
2.5
Righ' hand
2.5
2.5
2.5
2.5
2.5
2.5
Left thigh
5.5
6.5
8.5
9.5
Right thigh
5.5
6.5
8.5
9.5
5.5
6.5
5.5
6.5
Lef, foo,
3.5
3.5
3.5
3.5
3.5
3.5
Right foot
3.5
3.5
3.5
3.5
3.5
3.5
Genitalia
Upper extremity
Lower extremity
Partial
/'
Hair shaft
Epldennl.-{ qL,.,.....;r..,...
Denn-{
tissue
Muscle
r ' ;
\.l"o'!.uO&OOOq,
Sweat
gland
dODo
Bone
(a) Superflcial bum
Deep
partiel{
thickness
bum
(e)
()
C;
;;:
()
>
"
m
;:
Z
0
0
0
r.
"
J:
-<
i!
m
Full
thickness
bum
fA) superficial to (D) (ull thick"ess. (With permissio" (rom M Walsh [edt. Nurse
Practitioners: Clmical Skills and Pro(essional Issues. Oxford, UK: Butterworth-Heinemann, 1999;28.)
'"
>
n;
::Ik:$e
A
A
Appearance
Healing
Pain
Pink to red
Tenderness to
ialization
tOuch or
painful
5 days to 3 wks by
Very painful
Blanches
Sensation intact
Skin intact when rubbed
Moderate partial-thickness (second
degree)-superficial dermis injured
epithelialization
Pigmentation changes
are likely
3 wks to mas by
granulation tissue
formation and
intact
epithelialization
fourth degree)
Dry appearance without blanching
May be blistered
Insensate to pinprick
Depressed wound
Source: Data from P Wiebelhaus, SL Hansen, Burns: handle with care. RN 1999;62:52-75.
Very painful
No pain, perhaps
an ache
>
"
...
...
'<>
450
care is optimal for the patient. The American Burn Association rec
ommends medical care at a burn center if the patient has any of the
following":
Second- and third-degree burns that are greater than or equal to
10% of TBSA in patients younger than I 0 years of age or older
than 50 years of age
Burns of any type that are greater than 20% of TBSA in patients
between 10 and 50 years of age
Resuscitative Phase
The objectives of emergency room management of the patient who has
a major burn injury include simultaneous general systemic stabiliza
tion and burn care. The prioritization of care and precautions during
this initial time period have a great impact on survival and illustrate
some key concepts of burn care. General systemic stabilizacion involves
( 1) the assessment of inhalation injury and carbon monoxide (CO)
poisoning and the maintenance of the airway and vemilation with sup
plemental oxygen (see Appendix III-A) or mechanical ventilation (see
Appendix lII-B), (2) Auid resuscitation, (3) the use of analgesia (see
Appendix VI), and (4) the treatment of secondary injuries.16
451
has one or more of the following: ( I ) altered mental status; (2) burns
on the face, neck, or upper chest; (3) singed eyebrows or nose hairs;
(4) laryngeal edema; (5) arterial blood gas levels consistent with
hypoxia; (6) abnormal breath sounds; (7) the presence of soot in spu
tum; or (8) positive blood test results for chemicals.
The oropharynx and tracheobronchial tree are usually damaged by
thermal injury, whereas the lung parenchyma is damaged by the
chemical effects of the inhalant. Thermal airway injury is character
ized by immediate upper-airway mucosal edema, erythema, hemor
rhage, and ulceration.' Elective endotracheal intubation is indicated
with this type of injury, as progressive edema can readily lead to air
way obstruction. The patient remains intubated until airway edema is
decreased, usually 2-4 days post injury.17
The pathophysiology of inhalation injury generally occurs in
three stages: ( 1) inhalation injury (0-36 hours afrer injury), (2) pul
monary edema (6-72 hours after injury), and (3) bronchopneu
monia (3-10 days after injury). Pulmonary edema occurs from
increased lung capillary permeability, increased bronchial blood
flow, and impaired lymph function." There are de-epithelialization
and exudate formation throughout the airways, as well as
decreased alveolar surfactant' Decreased lung compliance (func
tional residual capacity and vital capacity) and hypoxia are the pri
mary effects of inhalation injury, each of which is dependent on the
location and severity of the injury. Supplemental oxygen, elective
intubation, bronchodilators, and fluid resuscitation are initiated to
maximize gas exchange and reverse hypoxia.19-21
The inhalation of CO, which is a colorless, odorless, tasteless,
combustible, nonirritating gas produced by the incomplete combus
tion of organic material, results in asphyxia. CO molecules displace
oxygen molecules from hemoglobin to form carboxyhemoglobin and
shift the oxyhemoglobin curve to the left, thereby decreasing the
release of oxygen. Additionally, CO molecules increase pulmonary
secretions and decrease the effectiveness of the mucociliary elevator.22
Elevated carboxyhemoglobin levels cause headache, disorientation,
nausea, visual changes, or coma, depending on the percentage. CO
poisoning is usually reversible with the use of 100% oxygen if the
patient has not lost consciousness.4
452
Tetanus prophylaxis
453
Clinical Tip
To minimize the risk of infection, the physical therapist
must use sterile techniques according to the burn unit pro
cedures when entering a patient'S room or approaching the
patient'S bedside. The physical therapist should be familiar
with the institution's policies regarding the use and dis
posal of protective barriers, such as gloves, gowns, caps,
and masks.
Body Temperature Maintenance
The patient with a major burn injury is at risk for hypothermia from
skin loss and the inability to thermoregulate. Body heat is lost
through conduction to the surrounding atmosphere and to the surface
of the bed. Initially, dry dressings may be placed on the patient to
minimize heat loss. The patient should be placed in a warm atmo
sphere to maintain body temperature. The patient'S room, burn unit,
or both may have overhead radiant heat panels and may be humidi
fied in an effort to preserve the patient's body heat.
Pain Management
A parienr with a burn injury can experience pain as a result of any of
the following:
Edema
Exudate accumulation
Mobiliry
Patients may also experience fear from the injury and burn treatment,
which can exacerbate pain. Analgesia, given intravenously, is there
fore started as soon as possible (see Appendix VI).
Initial Burn Care
To neutralize the burn source, the patient'S clothing and jewelry are
removed, and the burn is rinsed or lavaged (for a chemical burn). Ini-
454
455
Surgical Procedures
The cornetstone of present surgical burn management is
excision and grafting.
Excision
early
burn
Grafting
and joint surfaces grafted before other areas of the body." Permanent
grafting is ideal; however, grafting may be temporary. Temporary
grafting is indica red for small wounds expected to heal secondarily
and for large wounds for which an autograft would not last or if per
manent coverage is not available.29
Grafts, which typically adhere in 2-7 days, may not adhere or
Clinical Tip
456
Description
Tangential
excision
Full-thickness excision
Autograft
Split-thickness skin
graft (STSG)
Full-thickness skin
graft (FTSG)
Mesh graft
Sheet graft
Cultured epidermal
autOgraft (CEA)
Composite skin graft
Allogenic graft
Homograft
Heterograft
(xcnograft)
Amnion graft
Source: Data from SF Miller, MJ Staley, RL Richard. Surgical Management of [he Burn
Patient. In RL Richard, MJ Staley (cds), Burn Care and Rehabilitation: Principles and
Practice. Philadelphia: FA Davis, 1994.
Table 7-7. Temporary and Permanent Skin Substitutes for the Treatment of Burns
Product
Description
Use
Dermagrafr TC (Advanced
Tissue Sciences, La Jolla.
CAl
c
"
Z
>
z
o
...
'"
"
..,
'"
00
Product
Description
Use
Sources: Dala from SL Hansen, DW Voigt, P Wiebelhaus. eN Paul. Using skin replacement produces to treat burns and wounds. Adv Skin
Wound Care 2001;14:374; and P Dziewu!ski, JP BarreL Assessmenr, Operative Planning, and Surgery for Burn Wound Closure. In Sf Wolf,
DN Herndon (ed,,), Burn Care. Ausrin, TX: Landes Bioscience, 1999.
r;!
'"
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o
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459
mine whether the graft crosses a joint and how close the
graft borders the joint.
Nonsurgical Procedures
Burn cleansing and debridement may be performed many times a day
to minimize infection and promote tissue healing. These procedures,
as described in Wound Cleansing and Debridement, may be per
formed by a physician, nurse, or physical therapist depending on the
hospital's or burn unit's protocol. Table 7-8 lists the topical agents
used specifically for the treatment of burns.
IS
History
In addition to the general chart review (see Appendix I-A), the follow
ing information is especially relevant in the evaluarion, treatment
planning, and understanding of the physiological status of a patient
with a burn.
Did the patient get thrown (as in an explosion) or fall during the
burn incident?
Table 7-8. Topical Agents Commonly Used for the Treatment of Burns
...
:;
Agent
Description
Silver sulfadiazine
(Silvadene)
A
D
Mafenide acetate
(Sulfamylon)
Actico3r (Wcstaim
Biomedical, Exeter,
NH) silver dressing
Silver nitrate
Pseudomonas
&?
'"
m
:t
>
Z
c
"
o
'"
:t
J!
;::
>
A
D
Bacitracin
Nystatin
Collagenase
Sources: Data from ET Kaye, KM Kaye. Topical antibacterial agents. Infect Dis Clin North Am 1995;9:547-559; JO Kucan, EC Smoot. Five
percent mafenide acetate solution in the treatmem of thermal injuries. J Burn Care Rehabil 1993;14: 158-163; RS Ward, JR Saffle. Topical
agents in burn and wound care. Phys Ther 1995j75:526-538; and HS Soroff, DH Sasvary. Collagenase oinonent and polymyxin B sulfare!bac
itracin versus silver sulfadiazine cream in partial thickness burns: a pilot srudy. J Burn Care Rehabil 1994;15:13-17.
0;:
,.
"
o
...
'"
....
462
healing?
or suicide?
Level of consciousness
Posture
Heart rate and blood pressure, respiratory rate and partern, and
oxygen sarurarion
Clinical Tip
463
Pain Assessment
Good pain control increases patient participation and activity tol
erance; therefore, pain assessment occurs daily. For the conscious
patient, the physical therapist should nOte the presence, quality,
and grade of (I) resting pain; (2) pain with passive, active
assisted, or active ROM; (3) pain at the burn site versus the
donor site; and
(4)
apy intervention.
Clinical Tip
Rfl1lge of Motio1l
ROM of the involved joints typically requires goniometric measure
ments. Exact goniometric values can be difficult to measure when the
patient has bulky dressings; therefore, some estimation of ROM may
be necessary. The uninvolved joints or extremities can be grossly
addressed actively or passively, depending on the patient's level of
alertness or level of participation.
Clinical Tip
464
Strength
Strength on an uninvolved extremity is usually assessed grossly by
function. More formal strength testing, such as resisted isometrics or
manual muscle testing, is indicated on either the involved or unin
volved side if there is severe edema, electrical injury, or secondary
injury.30
Ftmctional Mobility
Functional mobility may be limited depending on state of illness,
medication, need for warm or sterile environment, and pain. The
physical therapist should evaluate functional mobility, as much as
possible, according to medical stability and precautions.
Clinical Tip
The skin at grafted areas, as well as at donor site areas, is
more fragile than normal skin. These areas should be ace
wrapped figure-of-eight style to provide support against
venous pooling when the patient is being mobilized Ollt of
bed. Without this extra support, the skin is more prone to
shearing at graft sites and subcutaneous bleeding.
465
sure, heart rate, and respiratory pattern and rate, as well as level of
alertness. MonitOring these variables will help the therapist gauge
pain level and determine how aggressively to intervene during the
therapy session.
4-7
days after
Time frames for physical therapy goals vary widely and are
based heavily on TBSA, the location of the burn, age, and pre
existing functional starus.
466
Considerations
Decreased ROM
and alrered limb
position
Decreased
strength
Decreased
endurance and
funcrional
mobiliry
Patienrlfamily
knowledge
deficit related to
burns and
physical therapy
ROlvl
range of mOlion.
467
with burns. For example, burns of the face, neck, and trunk
require intervention specifically directed to these areas.
The therapist should attend bedside rounds with the burn team
I)osition
Neck
Shoulder
ExtenSion, no rotation
Abduction (90 degrees)
External rotation
Horizontal flexion ( 10 degrees)
Extension With supll13tion
Neutral or slight extension
Functional position (dorsal burn)
Finger and thumb extension (palmar burn)
Straight postural alignment
Neutral extension/flexion
Neutral rotation
Slight abduction
Extension
Neutral or slight dorsiflexion
No IIlversion
Neutral roe extcnsion/flexion
Knee
Ankle
Sourcc: With permission from RS Ward. Splinting. Orthotics. :lOd Prosthetics In the
Management of Burns. In Ml Lusardi, CC Nielson (eds), Orthotics and Prosthetics in
Rehahllitatlon. Boston: BUiterworth-Heinemann. 2000;315.
468
Pathophysiology of Wounds
The different types of wounds, their etiologies, and the facrors that
contribute ro or delay wound healing are discussed in the following
sections.
Types of Wounds
Trauma Wounds
A trauma
wound
469
Clinical Indicators
Arterial insuffi
ciency
Intermirtent claudication
Extreme pain, decreased with rest and increased with
clevmion
Decreased or absent pedal pulses
Decreased temperaturc of the distal limb
Distinct, well-defined wound edges
Deep wound bed
Cyanosis
Localized limb pain, decreased with elevation and
increased with srandmg
Pam with deep pressure or palpation
Pedal pulses present
Increased temperature around the wound
Indistinct, Irregular edges
Edema Mound the wound
Shallow wound bed
Suhsranrial drainage
Painless ulcer; however, general lower-limb pain is
present
Absent pedal pulses
Decreased temperature in the distal limb
Deep wound bed frequently located at pressure points
(e.g., metatarsal heads)
Shin}- skill on dlsral limb
Venous
Insufficiency
Diabetic ulcer
Sources: D.t
l .1
Kloth. KH M111er (cds), Wound Ilc:lhnlt: Alternatives in Management. Ph1ladelphia: FA
Da\is, 1995; RG Sihbald. An approach to leg and foot ulcers:
Wound MJnage 1998;44:29; RG Ibbald. Venou!t leg ulcers. Osromy Wound Manage
1998;44:53; P Lamg. DI;Ibcrif.: foot ukcrs. AmJ Surg 1994;167(IA):31; and ML Levin,
LW O'Ncill, JII Bowker (cd). Thc D1abetlc Foot (5th cd). St. loUIS: Mosby, 1993.
470
471
472
473
Age
Skin, just like other tissues and organs, changes with age. Decreased
cellular activity during the aging process leads to decreased collagen
production thar results in less collagen organization in older individu
als. Reduced collagen organization resulrs in decreased tensile
strength of the skin that could result in greater damage after trauma
in the older individual. Other examples of skin changes with age
include delayed wound contraction, decreased epithelialization, and
delayed cellular migration and proliferation.56 Other comorbidities
that delay wound healing, such as diabetes, peripheral neuropathies,
and related vascular problems, occur with greater frequency in older
individuals.
474
Lifestyle
A patient's lifestyle can have a great impact on the prognosis for
healing, decision-making regarding wound management, and pre
ventive care. For example, occupations and hobbies that require
prolonged standing may predispose some individuals to varicosities
and other venous problems. Individuals exposed to traumatic situa
tions, such as construction workers, are also more likely to reinjure
healing wounds. Behaviors such as cigarette smoking can impede
wound healing significantly because of the vasoconstriction that nic
otine creates.
Nutrition
Good nutrition is necessary for the growth and maintenance of all
body tissues. Macronutrients, such as carbohydrates, fats, and pro
teins, and micronutrients, such as vitamins, are necessary for cell
metabolism, division, and growth. Therefore, nutrition is closely
linked with all phases of healing.57 Generally, poor nutrition
decreases the body's ability to heal. Additionally, patients with burns,
wounds, or infection who are adequately nourished at the time of
their injury or the development of their wound may also develop pro
tein-calorie malnutrition.
There are major metabolic abnormalities associated with injury
that can deplete nutritional stOres, including increased output of
catabolic hormones, decreased Output of anabolic hormones, a
marked increase in metabolic rate, a sustained increase in body tem
perature, marked increase in glucose demands, rapid skeletal muscle
breakdown with amino acids used as an energy source, lack of ketO
sis, and unresponsiveness to catabolism to nutrient intake.-8 Pro
tein-calorie malnutrition can delay wound healing and cause seriou
health consequences in patients with wounds, especially if infection
exists. Poor nutritional status, whether due to decreased intake or
the stress response, can set off a series of metabolic events leading to
weight loss, deterioration of lean tissues, increased risk of infection,
edema, and breathing difficulty.58
These events can lead to severe debilitation and even death. Inade
quate diet control in patients with diabetes exacerbates all symptOms
of diabetes, including impaired circulation, sensation, altered meta
bolic processes, and delayed healing. A nutritional assessment by a
475
Vascular Statlls
Any compromised vascular status may contribute to the development
of delayed wound healing owing to a lack of oxygenation and nutri
tion to the tissues.
Medical Status
Generally, compromised health causes a decrease in the body's ability
to progress through the healing process. Pre-existing infection or a
history of cancer, chemotherapy, radiation, acquired immunodefi
ciency syndrome, or other immunodeficiency disorders can decrease
the patient's ability to heal. Congestive heart failure, hypertension,
and renal dysfunction can also slow wound healing.
476
Medications
Steroids, antihistamines, nonsteroidal anti-inflammatory drugs, and
oral contraceptives may delay wound healing, as can chemotherapy
and radiation. These medications can decrease the tensile strength of
connective tissue, reduce blood supply, inhibit collagen synthesis, and
increase the susceptibility to infection.59 Amicoagulants thin the
blood and decrease its ability to clot; therefore, the healthcare pro
vider needs to diligently monitor bleeding during dressing removal
and consider debridement methods that will not cause bleeding.
Chronic Wounds
In healthy individuals without comorbidities, an acute wound should
heal within 3 to 6 weeks, with remodeling occurring over the next
year. If a wound remains in one of the stages of healing without pro
gression, it becomes a chronic wound.6o Chronic wounds are defined
as wounds that have "failed to proceed through an orderly and timely
process to produce anaromic and functional integrity, or proceeded
through the repair process without establishing a sustained anatomic
and functional result. "61 The acute care therapist should be inclined
to search for underlying causes of delayed wound healing, especially
when treating a wound thar has not healed in more than 6 weeks.
History
In addition to the general chart and medical history review (see
Appendix I-A), the following information is especially relevant for
determining wound etiology and risk facrors, an intervention plan,
and potential outcomes:
477
Wound History
Risk Factors
Where and for how long is the patient weight bearing on areas
involving the wound site?
Psychosocial Factors
478
Physical Exami1!atio1!
Sensation
Sensation to light touch, pressure, pinprick, temperature, and kines
thesia or proprioception, or both, should be examined. Impaired or
absent sensation should be addressed through instruction in the
appropriate prevention techniques, as well as modifications to shoes,
weight bearing, and water temperatures in bathing.
Pain
The evaluation of pain in the patient with a wound is not unlike the
evaluation of pain in any other type of patient. The therapist should
evaluate the nature of the pain, including the location, onset, severity
(using a pain-rating scale), duration, aggravating and alleviating fac
rors, and the impact on activities of daily living. Understanding the
nature of the pain will ultimately allow the physical therapist to pro
vide or recommend the appropriate intervention.
The pain experience associated with wounds has been described as
having one of three components: a noncyclic acute component, a
cyclic acute component, or a chronic wound pain component.
Noncyclic acute Waf/lid paill is a single episode of acute pain that is
likely ro occur with treatment (e.g., the pain felt during sharp debride
ment). Cyclic acute pain is wound pain that recurs throughout the
day because of repeated treatments. For example, a patient may expe
rience pain after several days of dressing changes, which creates repet
itive trauma to the wound. Chronic wound pain is persistent wound
pain that occurs intrinsically, nOt as a result of external intervention
(e.g., a patient with a neuropathic ulcer who has a constant, dull ache
in the foot).62
Range of Motion
Specific measurement of ROM may not be necessary in a patient with
a wound. However, specific goniometric measurements are necessary
if a wound crosses a joint line, if edema is present at a joint, or if
decreased ROM inhibits mobility. Decreased ROM that inhibits
mobility or increases weight bearing, pressure, or both may conrrib-
479
480
Clinical Tip
481
482
Wound Culture
A wound culture is a sampling of micro-organisms from the wound
bed that is subsequently grown in a nurrient medium for the purpose
of identifying the type and number of organisms present. A wound
culture is indicated if there are clinical signs of infection, such as
purulent drainage, large amounts of drainage, increased local or sys
temic temperature, inflammation, abnormal granulation tissue, local
erythema, edema, cellulitis, increased pain, foul odor, and delayed
healing.o, Results of aerobic and nonaerobic cultures can determine
whether antibiotic therapy is indicatedo,
Methods of culturing
Clinical Tip
Unless specifically prescribed otherwise, cultures should be
taken after debridement of thick eschar and necrotic mate
rial and wound cleansing; otherwise, the culture will
reAect the growth of the micro-organisms of the external
wound environment rather than the internal environment.
Surrounding Areas
The area surrounding the wound should also be evaluated and compared
to noninvolved areas. Skin color, the absence of hair, shiny or Aaky skin,
the presence of reddened or darkened areas, edema, or changes in the
nailbeds should all be examined and documented accordingly.
483
Clinical Tip
Increased localized temperature can indicate local infec
tion; decreased temperature can indicate decreased blood
supply.
Table
Stage
7-12.
Description
Reddened area on the skin with an intact epidermis
((
JIJ
Wound that exposes subcutaneous tissue down to, bur nor through,
IV
exposed
underlying fascia
such as tendon or joint capsule
Source: Dam from The National Pressure Ulcer Advisory Panel's Summary of [he
AHCPR Clinical Practice Guideline. Prcssure Ulcers in Adults: Prediction and Preven
[ion. (AHCPR Publication No. 92-0047). Rockville, MD. May 1992.
484
Clinical Tip
quart of boiling
485
used, does not cleanse the wound. The use of whirlpool jets
is actually mechanical debridement and therefore should be
used only if mechanical debridement is indicated.
486
Selective Debridemelll
Sharp Debridement
Sharp debridement involves the use of scalpels, scissors, and forceps
ro remove necrotic tissue. It is a highly skilled technique best per
formed by or under the direct supervision of an experienced clinician.
(Note: Nor all states and facilities allow physical therapists to per
form sharp debridement. ) Because rhe true selectiviry of sharp debride
ment depends on the skill of the clinician, sharp debridement can also
result in damage to healthy tissues that can cause bleeding and a risk
of infecrion. Sharp debridement is especially expedient in the removal
of large amounts of thick, leathery eschar. Removal of eschar is
important in the patient who is immunocompromised, because rhe
underside of eschar can provide a medium for bacterial growth. Sharp
debridement has been shown to increase the degree of wound healing
when combined with the usc of a topical growth factor."
Sharp debridement can be painful; it is therefore recommended
that pain medications or topical analgesics be administered before
treatment. When debriding, the clinician should spare as much tissue
as possible and be careful to have the technique remain selective by
not removing viable tissue. Because of the potential for excessive
bleeding, extra care should be taken with patients who are taking
anticoagulants.
Autolytic Debridement
Alltolytic debridemellt is the natural and most selective form of debride
ment. The body uses its own enzymes to lyse necrotic tissue and this is a
normal process that occurs in any wound. It is painless and does not
harm healthy tissues. Moist dressings facilitate autolytic debridement,
as do films, hydrocolloids, and calcium alginates, which keep the
wounds moist with the exudate from the wound.7274 When using
aurolytic debridement, it is important to cleanse the wound to remove
partially degraded tissue.74 Because it takes time for autolytic debride
ment to occur, sharp debridement of eschar is recommended before
autolytic debridement to expedite the removal of the necrotic tissue.
Owing to the risk of infection, autolytic debridement is contraindicated
as the primary method of debridement in patients who are immunosup
pressed or otherwise require quick elimination of necrotic material.
NOllselective Debridemellt
Mechanical Debridement
Mechal1ical debridement removes dead tissue by agitating the necrotic
tissue of the wound or adhering it to a dressing and removing it. Dry
487
488
by
Clinical Tip
When applying an enzymatic debriding agent to eschar
and it cannot be debrided, crosshatch the eschar and pull
in the edges to allow the enzymes to penetrate the eschar.
(4)
(2)
the
the surrounding
skin. Other significant factors include the patient's cognitive and physi
cal abiliry to apply the dressing and the accessibility of physical therapy
or nursing services to the patient. Cost is also a consideration.
A large number of wound care products are available, and it is vir
tually impossible to be aware of the purpose and application instruc-
489
2-3 days or changed daily for infected wounds. Indications for this
therapy include diabetic ulcers, pressure ulcers, traumatic wounds,
meshed grafts, and flaps. Contraindications include fistulas, necrotic
tissue or eschar, untreated osteomyelitis, malignancy in wound, and
exposed arteries or veins.81.82
Cadexomer-iodine is an iodine-based wound filler (e.g., lodoflex,
iodoform) and is indicated in highly exudating wounds. It is highly
absorbent, provides a moist healing environment, and lowers the pH
of the wound. The iodine is slowly released, so it is not cytotoxic to
good tissue, but the bacteriostatic and bactericidal effects of iodine
remain.
Skin Substitutes and Biologicals
Although these will not be a first line of defense, therapists in the
acute care setting should be aware of other agents that may be used to
..
'"
0
Type of Dressing
Indication
Description
Advantages
Disadvantages
Gauze
Highly porous.
Applied dry, wet-todry (i.e., the
dressing is put on
wet but will dry
before removal), or
wet-to-wet (i.e., the
dressing is pur on
wet and removed
when wet).
Nonimpregnated or
impregnated
(nonadherent
substance
integrated into
dressing) dressings
comprised of inert
materials that
conform to the
wound surface.
Readily available
Inexpensive
Nonadherenr
dressings
,.
()
'i
'"
()
:t
0
0
"
'"
Generally
nonirritating and
nonroxic
Less likely to adhere
to wound, causing
less tissue
disruption
Relatively inexpensive
:t
-<
!:?
5!
'"
'"
,.
Hydrocolloids
Semipermeable films
Hydrogels
Partial-thickness
wounds with
minimal drainage,
or as a secondary
dressing on a fullthickness wound
Prevent secondary
wound infection
Impermeable to water,
oxygen, and
bacteria
Available in many
forms (pastes,
powders, and
sheers)
Changed infrequently
Conforms well
Allow for visual
wound monitoring
..
c
Highly conformable
Safe for fragile skin
Available in many
forms
'"
Z
,.
Z
c
"
0
c
Z
c
...
'"
....
Table
7-13. Continued
...
'"
N
Type of Oressing
Indication
Description
Advantages
Disadvantages
Foams
Partial- or full-thick
ness wounds with
minimal-ro-moder
ate drainage
Polyurethane foam
with twO surfaces: a
hydrophilic inner
surface and a
hydrophobic outef
surface.
Nonadherenr to skin
surface
Highly absorbable
and conformable
Permeable to oxygen
(reduce risk of
anaerobic infection)
Highly conformable
Expensive
Calcium alginates
>
"
m
J:
1)
"
Require a secondary
dressing to keep
from drying out
Sources: With permission from J Cuzell, D Krasner. Wound Dressings. In PP Gogia (ed). Clinical Wound Management. Thorofare, NJ: Slack,
1995;)5 Feedar. Clinical Managemenr of Chronic Wounds. In LC Kloth, KH Miller (eds). Wound Healing: Alrernatives in Managemenr. Phila
delphia: FA Davis. 1995; ML Levin, LW O'Neal, JH Bower (cds), The Diabetic Foot (4th ed). St. Louis: Mosby. 1993; JC Lawrence. Dressings
and wound infection. Am J Surg 1994; 167( I A):21 j and CT Hess. When to usc hydrocolloid dressings. Adv Skin Wound Care 2000;13:63.
o
"
J:
-<
r
:;!
s:
493
The following are the primary goals of p hy sica l therapy for wound
treatment in the acute care scrring:
494
Table
7-14.
Physical Therapy
lnrervention
Pain manage
ment
Range of morion,
strength, and
functional
mobility
Edema
managemenr
Prevention
Consideration
Coordinate physical therapy session with pain premedi
cation to reduce acute cyclic and noncyclic pain.
Consider the use of positioning, relaxation techniques,
deep breathing, exercise, or modalities to relieve pain.
Modify wound treatmenr techniques as able to eliminate
the source of pain.
Adequate range of motion is necessary for proper
positioning and minimizing the risk of pressure ulcer
formation.
Care should be taken with manual contacts with fragile
skin, and care should be taken not to disturb dressings
during exercise.
Adequate strength is necessary for weight shifting and
functional mobility with the maintenance of weight
bearing precautions.
Depending on the etiology, exercise, compression
therapy, lymphatic drainage. limb elevation (used with
caution in the patient with cardiac dysfunction), or a
combination of these can be used to manage edema.
Education (e.g. , dressing application. infection control,
wound inspection, the etiology of wounds)
Positioning (e.g., splines, turning schedule)
Skin care and hygiene (e.g., dressing removal)
Pressure reduction surfaces (e.g., air mattress, wheelchair
cushion)
Footwear adaptations (e.g., orthotics, inserts, extra
depth shoes)
To minimize pain
495
References
1. Williams WG, Phillips LG. Pathophysiology of the Burn Wound. In DN
Herndon (ed), Total Burn Care. London: Saunders, 1996;63.
2. Falke! jE. Anatomy and Physiology of the Skin. [n RI Richard, Mj Sta
ley (eds), Burn Care Rehabilitation Principles and Practice. Philadelphia:
FA Davis, 1994; I O.
3. Totora Gj, Grabowski SR (eds). Principles of Anatomy and Physiology
(7th ed). New York: Harper-Collins College, 1989;126.
4. \Varden GD, Heimback DM. Burns. In 51 Schwartz (cd), Principles of
Surgery, Vol. I (7th cd). New York: McGraw-Hili, 1999;223-262.
5. johnson C. Pathologic Manifestations of Burn Injury. In RI Richard, Mj
Staley (eds), Burn Care and Rehabilitation Principles and Practice. Phila
delphia: FA Davis, 1994;29.
6. Rai J. Jeschke MG, Barrow RE, Herndon DN. Electrical injuries: a 30year review. j Trauma 1999;46(5):933-936.
7. High-Tension Electrical Burns. In RH Oemling, C laLonde (cds), Burn
Trauma. New York: Thieme, J989j223.
8. Winfree J, Barillo OJ. Burn management. Nomhermal injuries. Nurs
Clin North Am [997;32(2):275-296.
9. Lightning. In RH Oemling, C LaLonde (eds), Burn Trauma. New York:
Thieme, 1989;242.
10. Milner SM, Rylah LTA, Nguyen IT, et.1. Chemical Injury. In DN Hern
don (cd), Total Burn Care. London: Saunders, ] 996;424.
496
11. Milner SM, Nguyen IT, Herndon ON, Rylah LTA. Radiation injuries
and Mass Casualties. in ON Herndon (ed). Total Burn Care. London:
Saunders, 1996;425.
12. McManus WF, Pruin BA. Thermal Injuries. in OV F eliciano, EE Moore,
KL Martox (eds), Trauma. Stamford, CE Appleton & Lange, 1996;937.
13. Marvin J. Thermal Injuries. in VO Cardona, PO Hum, PJ Bastnagel
Mason, et al. (cds), Trauma Nursing: from Resuscitation through Reha
biliration (2nd ed). Philadelphia: Saunders, 1994;736.
14. Richard R. Assessment and diagnosis of burn wounds. Adv \Vound Care
1999;12(9):468-4 71.
15. American Burn Association. Hospital and prehospital resources for opti
mal care of patients with burn injury: guidelines for development and
operarion of burn centers. J Burn Care Rehabil 1990;11(2):98-104.
16. Gordon M, Goodwin CWo Burn management. initial assessment, man
agement, and srabilization. Nurs Clin North Am 1997;32(2):237-249.
17. Kao CC, Garner WL. Acure burns. Plasr Reconsrr Surg 2000;101(7):
2482-2493.
18. Schiller WR. Burn Care and Inhalarion Injury. In A Grenvik (cd), Texr
book of Critical Care (4rh ed). Philadelphia: Saunders, 2000;365-377.
19. Desai MH, Herndon ON. Bums. In DO Trunkey, FR Lewis, BC Decker
(cds), Current Therapy of Trauma (3rd ed). Philadelphia: Mosby, 1991;315.
20. Abraham E. Toxic Gas and inhalation Injury. In BE Brenner (cd). Com
prehensive Management of Respiratory Emergencies. Rockville, MO:
Aspen Publications, 1995;241.
21. Traber DL, Herndon ON. Parhophysiology of Smoke Inhalarion. In EF
Haponik, AM Munster (cds), Respiratory Injury: Smoke Inhalation and
Burns. New York: McGraw-Hili, 1990;61.
22. Crapo RO. Causes of Respiratory Injury. In EF Haponik, AM Munster
(cds), Respiratory Injury: Smoke Inhalation and Burns. New York:
McGraw-Hili, 1990;47.
23. Ahrns KS, Harkins DR. Initial resuscitation after burn injury: therapies,
strategies, and controversies. MCN Clin Issues 1999;10:46-60.
24. Edlich RF, Moghrader JC. Thermal Burns. In P Rosen (ed), Emergency
Medicine Concepts and Clinical Practice, Vol. 1 (4th ed). St. Louis:
Mosby, 1998;941-953.
25. Jordan BS, Harrington DT. Management of the burn wound. Nurs Clin
North Am 1997;32(2):251-271.
26. Linares HA. Pathophysiology of Burn Scar. In ON Herndon (ed), Toral
Burn Care. London: Saunders. 1996;383.
27. Wild B, Kemp H. Skin cultures in burns care nursing. Nurs Times
1999;95(36):46-49.
28. Miller SF, Sraley MJ, Richard RL. Surgical Management of rhe Burn
Parient. In RL Richard, MJ Sraley (eds), Burn Care and Rehabilirarion
Principles and Practice. Philadelphia: F A Davis, 1994;177.
29. Kagan RJ. Skin substitutes: implications for burns and chronic wounds.
Adv Wound Care 1999;12(2):94-95.
30. Richard RL, Staley MJ. Burn Patient Evaluation and Treatmcnc Plan
ning. In RL Richard, MJ Staley (cds), Burn Care and Rehabilitation
Principles and Practice. Philadelphia: F A Davis, 1994;20 1.
497
498
499
Source Book for Healthcare Professionals (2nd cd). Wayne, PA: Health
Managemcnr Publications, 1997;97-106.
70. Sussman G. Management of the \Vound Environment. In C Sussman, B
Bates-Jensen (cds), \'Vound Care: A Collaborative Practice Manual for
Physical Therapists and Nurses. Gaithersburg, MD: Aspen Publishers,
1998;212.
71.
72.
73.
74.
75.
76.
1998;389-403.
77. Sussman C. Whirlpool. In C Sussman, B Bates-Jensen (cds), \'Vound
78.
79.
80.
81.
82.
83.
84.
8
Gastrointestinal System
Jaime C. Paz
lntroduction
Disorders of the gastrointestinal (GI) system can have numerous
effects on the body, such as decreased ourridon, anemia, and fluid
imbalances. These consequences may, in turn, affect the activity toler
ance of a patient, which will ultimately influence many physical ther
apy interventions. In addition, physical therapists must be aware of
pain referral patterns from the GI system that may mimic musculo
skeletal symptoms (Table 8-1). The objectives of this chapter are to
provide the following:
I.
A basic understanding of the structure and function of the
G1 system
501
502
Structure
Segmenral
Innervation
Esophagus
T'Hi
Substernal region
Sromach
T6-IO
Small inrestine
T7-IO
Pancreas
T6-IO
Upper abdomen
Gallbladder
T7-9
Upper abdomen
Upper abdomen
Middle and lower thoracic spine
T7-9
T6-10
Upper abdomen
Large intestine
T1 1 -L1
Sigmoid colon
TII-12
and neck pain: part I. Pelvic and abdominal visceral disorders. J On hop Sports Phys
Thcr 1990;12,194.
4.
Information on the management of GI disorders, including
pharmacologic therapy and surgical procedures
5. Guidelines for physical therapy intervention
with GI diseases and disorders
In
patients
GASTROINffiSTINAL
Figure
SYSTEM
503
artwork by Peter
Clinical Evaluation
Evaluation of the GI system involves combining information gathered
through physical examination and diagnostic studies.
Physical Examillatioll
Physical examination of the abdomen consists of inspection, allsculta
tion, percussion, and palpation. Physicians and nurses usually per
form this examination on a daily basis in the acute care setting;
however, physical therapists can also petform this examination to
help delineate between systemic and musculoskeletal pain.
504
Function
Oral cavity
Pharynx
Esophagus
Stomach (cardia,
fundus, body, pylorus)
electrolytes
Ileum: absorbs bile acids and intrinsic factors to
Sources: Data from JC Scanlon, T Sanders (eds). Essentials of AnafOl11Y and Physiulogy
(2nd ed). Philadelphia: FA Davis. 1993;362; :ll1d AC Guyron, JE Hall (eds). Textbook
of Medicall)hysiology (9th ed). Philadelphia: Saunders, 1996;803-844.
GASTROINTESTINAl SYSTEM
Table
505
Srructure
Function
Teeth
Tongue
{Q
S.lhvary glands
Llvcr
Stores and releases bile IIltO the duodenum via the hepatic
Pancreas
Thc '>pleen
.\
not part 01 rhe gatrolllre!lrmal system bur l!i localed ncar orher gas
rrolllrerinal component!.
111
Source: Data from JC Scanlon, T Sanders. Essentials of Anatomy and Physiology (2nd
ed). PhLl.1delphta: rA DaVIS, 1993; and AC Guyron, JE Ilall. Texrbook of Medical Phys
Iology (9th cd). Philadelphia: S"unders, 1996;803-844.
History
Before performing the physical examination, the presence or absence
of Items related to GI pathology is ascertained through patient inter
view, questionnaire completion, or chart review. For a list of these
items, see Table 8-4. Appendix I-A also describes the general medical
record review.
Inspection
Figure 8-2 demonstrates the abdominal regions associated with
organ location. DUring inspection, the physical therapist should
notc asymmetries in size and shape in each quadrant, umbilicus
506
Table
Characteristics
Associated Disorders
History of hernia
Hemoptysis
History of hepatitis
Constipation
Hematochezia (bright
Diarrhea
Jaundice
Heartburn
abuse
Fatty food inrolerance
stools)
Abdominal pain
Sources: Data from MB Koopmeiners. Screening for Gastrointestinal System Disease.
In WG Boisonnauh (cd), Exammation In PhYSical Therapy Practice. New York:
Churchill LivingstOne, 1991; 1 13; and CC Goodman. The Gastrointestinal System. In
Righi upper
leflr
"""
GaI_
s_
"""'"'
Colon (hegebc llexure and lransverse) Pancntes
KlOOey and adrenal gland
Kd1ey and adrenal gland
DuOCl8nt.m with head of pancreas
Colon (spleric t\eJcUfe and IransvetSeJ
Smallnlestlne
SmaI in186lnt (jejl.R.lm)
Right lower
t..fllower
Smallnleslne
Figure
8-2. The four abdominal quadrants. shOlv'''g the vIscera found III
1989;783.)
GASTROINTESTINAL SYSTEM
507
Clinical Tip
Changes in abdominal girth, especially enlargement,
should be documented by the physical therapist. In addi
tion, the nurses and physicians should be notified. Abdom
inal enlargement may hinder the patient's respiratory and
mobility status.
Auscultation
The abdomen is auscultated for the presence or absence of bowel
sounds and bruits (murmurs) to help evaluate gastric motility and
vascular flow, respectively. Bowel sounds can be altered postopera
tively, as well as in cases of diarrhea, intestinal obstruction, paralytic
ileus, and peritonitis. The presence of bruits may be indicative of
renal artery stenosis. I
Percussion
Mediate percussion is used to evaluate liver and spleen size and bor
ders, as well as ro identify ascitic fluid, solid- or fluid-filled masses,
and air in the stomach and boweL' The technique for mediate percus
sion is described in the physical examination section of Chapter 2.
Palpation
Light palpation and deep palpation are used to identify abdominal
tenderness, muscular resistance, and superficial organs and masses.
The presence of rebound tenderness (i.e., abdominal pain worsened
by a quick release of palpatory pressure) is an indication of peritoneal
irritation from possible abdominal hemorrhage and requires immedi
ate medical attention. Muscle guarding during palpation may also
indicate a protective mechanism for underlying visceral pathology.'
Diagnostic Stlldies
Discussion of the diagnostic evaluation for the GI system will be
divided into ( I ) the examination of the GI tract and (2) the examina
tion of the hepatic, biliary, pancreatic, and splenic systems. Examina
tion of the GI tract includes the esophagus, sromach, and the
intestines (small and large). Table 8-5 summarizes the laboratory tests
'"
o
'"
Test
Descripcion
>
\:
"
'"
:t
>
Z
o
1)
\l
23
"
;;;
i
'"
Gastrin
Reference value: 25-90 pg/ml
Serologic test
Reference value: immunoglobulin G negative
Urea breath test
>
r
'"
o
'"
""
Test
Description
Serotonin (5-hyclroxytryptamine)
Reference value, 50-200 ng/ml
"
g
'"
:t
g"
o
"
::!
r.;
'"
"
'"
GASTROINTFSflNAL SYSTEM
511
Clinical Tip
Laboratory tests used to examine the liver are frequently
referred to as liver (llllction tests or LFTs.
Description
Purpose: To perform routine screening of the colon for the presence of polyps
or rumors and to investigate the cause of chronic diarrhea or other
undiagnosed Gl complaints.
Patients are sedated, and an endoscope is inserted inro the rectum and passed
through the various parts of the colon. Tissue biopsy may be performed
during this procedure.
Purpose: Used to detect intra-abdominal abscesses, rumors, infarctions,
perforation, obstruction, inflammation, and diverticulitis. Metastases ro
the abdominal cavity can also be detected. lntravenous or oral contrast
may be used during the procedure.
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Z
o
is
o
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-<
j1
m
'"
>
Esophageal manometry
Reference value: Lower esophageal sphinc
ter (LES) pressure: 12-25 mm Hg.
C)
,.
r
'"
'"
'"
....
Description
GI cytologic studies
Reference value: No evidence of abnormal
cells or infecrious organisms.
>
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o
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:;:
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Text or abbreviations
Source: Data from LM Malarkey, .ME McMorrow (eds). Nurse's Manual of Laboratory Tests and Diagnosric Procedures. Philadelphia: Saun
ders, 2000;432-468.
z
>
r
;,:
'"
....
'"
'"
Table 8-7. Laboratory Tests for the Hepatic, Biliary. and Pancreatic Systems'"
....
'"
Test
Involved Systems
Purpose
Hepatic
Hepatic, biliary
Hepatic, biliary
Heparic, biliary
Ammonia (NH J)
Reference value: 15-45 g1dl
Hepatic
Amylase, serum
Reference value: 27-131 U/liter
Pancreatic
f,?
"
m
;:;
o
'"
<5
"
i
-<
'"
f,?
:i
m
"
,.
'"
Amylase, urine
Reference values:
2-19 Ulh, (l-h, ,est)
4-37 Ul2 hrs (2h, ,est)
170-2,000 U/24 hrs (24-h, ,csr)
Pancreatic
Hepatic
Bilirubin
Reference values:
Total, 0.3-1.2 mg/dl
Direc, (conjuga,ed), 0-0.2 mg/dl
Indirect (unconjugated), <1.1 mg/dJ
Hepatic, biliary
Hepatic, pancreatic
52
z
>
r
v.
"
'"
00
Involved Systems
Pu.rpose
Ceruloplasmin
Reference value: 18-45 mgldl
Hepatic
Hepatic, biliary
Gamma-gluramyltransferase (y-glutamyl
transferase fGT], y-glutarnyl
transpepcidase IGGT, GGTP, G T P Il
Reference values:
Male, 22.1 Ullirer
Female, 15.4 Ulliter
Hepatic
Hepatic
g
'"
(3
'"
J:
-<
j!
>
Lipase
Reference value: <200 Ulliter
Biliary, pancreatic
Protein electrophoresis
Reference value: albumin, 3.S-S.0 gldl
Hepatic
Hepatic
Hepatic
Pancreatic
z
>
'"
\0
'"
'"
o
Involved Systems
Purpose
Pancreatic
Urobilinogen, fecal
Reference value, 40-280 mg/day
Hepatic, biliary
Urobilinogen, urine
Reference value:
Male, 0.3-2.1 mg/2 hrs
Female, 0.1-1.1 mg/2 hrs
Hepatic, biliary
'"
:t
>
Z
"
'"'
(;
'"
:t
-<
gr
:;i
(0
Source: Data from LM Malarkey, ME McMorrow (eds). Nurse's Manual of Laboratory Tests and Diagnostic Procedures. Philadelphia: Saun
ders, 2000:469-524.
>
m
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>
(.ASTROINTESnNAL SYSTI'J\.1
521
Purpose
Cholangiography, percu
taneous rranshepatic
Cholangiography, T
rube, and intravenous
Chol<C)',rography, oral
Computed lomography
522
Purpose
to identify gallstones.
Laparoscopy
Laparoscopy is the insertion of a laparoscope (a fiberoptic tube) into
the abdominal cavity through a small incision to the left of and above
the umbilicus. To perform this procedure, a local anesthetic is given,
and gas (i.e., nitric oxide or carbon dioxide) is infused into the
abdominal cavity to allow better visualization and manipulation of
the scope. Table 8-9 describes the diagnostic and therapeutic interven
tions that may be performed with a laparoscope.5
GASTROINTESTINAL SYSTEM
523
Boston: Lirde Browll, 1994;27; and Lvt Malarkey, tv1E McMorrow (eds), Nurse's Manu31
Pathophysiology
GI disorders can be classified regionally by the structure involved and
may consist of the following:
Motility disorders
Inflammation or hemorrhage
Enzymatic dysfunction
Neoplasms
524
Common Etiologies
Obstructive
Inflammatory
or infectious
Congenital
trouble swallowing. Consuitanr I 997;37( 1):75; TP Gage. Esophageal Rings, Webs, and
Diverticula. In MM van Ness, SJ Chobanian (eds), Manual of Clinical Problems in Gas
troenterology. 805mn: Little, Brown, 1994;32; and SS Shay, MM van Ness. Infectious
Esophagitis. In MM van Ness, SJ Chobanian (eds), Manual of Clinical Problems in
Gastroenterology. Boston: Little, Brown, 1994;35.
Esophageal Disorders
Dysphagia
Dysphagia, or difficulty swallowing, can occur from various etiologies
and is generally classified by the causative facrors (Table 8-10). Dys
phagia can also be classified by irs locarion as (1) proximal (cervical) or
oropharyngeal dysphagia or (2) distal or esophageal dysphagia.
Proximal dysphagia is difficulty swallowing in the upper, or proxi
mal, region of the esophagus and generally resultS from neurologic or
neuromuscular etiologies, such as stroke, myasthenia gravis, or poly
myositis. I 1-13
Distal dysphagia is difficulty swallowing in rhe lower, or distal,
portion of the esophagus and is usually rhe result of mechanical
obstruction to flow from peptic strictures, mucosal rings, or malig-
GASTROII'ITESTiNAL SYSTEM
525
526
Clinical Tip
Physical therapists should be aware of any positioning pre
cautions for parients wirh esophageal disorders that may
exacerbare their dysphagia or GERD.
GASTROIt-m:SrINAL SYSTE.M
527
Stomach Disorders
Gastrointestinal Hemorrhage
Bleeding in the GI system can occur in either the upper GI system
(upper gastrointestinal bleed [UGIBj) or in the lower GI system (lower
gastrointestinal bleed ILGIB]). A UGIB can result from one or more
of the following: ( I) duodenal u\cers, (2) gastric erosion, (3) gastric
u\cers, (4) esophageal varices, and (5) use of nonsteroidal anti-inflam
matory drug medications (NSAlDs). An LGIB can resulr from one or
more of the following: (I) inflammatory bowel disease, (2) neo
plasms, and (3) anal and rectal lesions (e.g., hemorrhoids). 24-26
Gl bleeds can be small and require minimal to no intervention or
very severe and constitute medical emergencies because of hemody
namic instability that can lead to shock. Hemalemesis or dark brown
("coffee-ground") emesis (vomitus), hematochezia (passage of blood
from the rectum), and melella (black, tatry stools) from acid degrada
tion of hemoglobin are the primary clinical manifestations of GI bleeds.
Patients are generally stabilized hemodynamically with intravenous
(i.v.) fluids, blood rransfusions, or both before the cause of bleeding can
be fully delineated. Nasogasrric tubes (see Appendix Table lll-A.6) are
typically used in the stabilization and management of UGIB. Manage
ment is targeted at the causative factors that resulred in either UGLB Ot
LGIB. Endoscopy, colonoscopy, or sigmoidoscopy can be perfotmed to
help evaluate or treat the source of upper or lower GI hemorrhage.",25,27
Gastritis
Gastritis is the general term used to describe diffuse inflammatory
lesions in the mucosal layer of the stomach. Gasrriris can be classified
as acute, chronic nonerosive, or chronic erosive.
Etiology of aClIte gastritis includes associations with smoking, alco
hol abuse, aspirin, NSAlDs, and corticosteroid use, as well as physio
logic stress and inrcnse emotional reactions. Clinical manifestations of
acute gastritis include nondescript complaints of burning or discomfort
in the stomach. Management of acute gastritis involves removing the
causative risk factors and relieving the mucosal inflammation.IS.28,29
The etiology of chrollic Ilollerosive gastritis has been definitively
linked to Helicobacter pylori bacterial infection, which is thought to
be transmirred by human-to-human contact.IS .28,JO.JI Patients with H.
pylori gasrritis may be asymptomatic until the gastritis leads to gastric
u\ceration, in which case there will be complaints of dull, gnawing
abdominal pain that rypically occurs when the stomach is empty.2S
Management of H. pylori gastritis includes rriple or quadruple antibi-
528
GASTROINTFSrINAL SYSTEM
529
n.1 ulcers arc linked with gastric acid hypersecretion and genetic predis
position.JI Other risk factors for developing duodenal ulcers include
tobacco lise, chronic renal failure, alcoholic cirrhosis, renal transplanra
tion, hyperparathyroidism, and chronic obstructive pulmonary disease.
Clinical manifestations of duodenal ulcer disease may include
sharp, burning, or gnawing epigastric pain that may be relieved with
food or antacids. Abdominal pain can also occur at night. Manage
menr of duodenal ulcers is similar to that of gastric ulcers.32,JJ
Zollinger-Ellison Syndrome
Zollinger-Ellison syndrome is a clinical triad that includes gastric acid
hypersecretion, recurrent peptic ulcerations, and a non-beta islet cell
tumor (gastrinoma) in the pancreas. Symptoms mimic peptic ulcer
disease, but consequences are more severe if left untreated. Patients
with Zollinger-Ellison syndrome may also present with diarrhea.
Management is primarily directed at surgical resection of the gasrri
noma, along with decreasing gastric acid hypersecretion.J236,37
Gastric Emptying Disorders
Abnormal gastric elprying is described as either decreased or increased
emptying. Decreased gastric emprying is also referred to as gastric
retelltioll and may result from or be associated with (1) pyloric stenosis
as a consequence of duodenal ulcers, (2) hyperglycemia, (3) diabetic
ketoacidosis, (4) electrolyte imbalance, (5) autonomic neuropathy,
(6) postoperative stasis, and (7) pernicious anemia. Pharmacologic
inrervenrion to promote gastric motility is indicated for patients with
decreased gastric emprying disorders.
Enhanced gastric emptying is associated with an interruption of
normal digestive sequencing that results from vagoromy, gastrectomy,
or gastric or duodenal ulcers. Gastric peristalsis, mixing, and grinding
are disturbed, resulting in rapid emprying of liquids, slow or
increased emptying of solids, and prolonged retention of indigestible
solids. With enhanced gastric emptying, blood glucose levels are sub
sequendy low and can result in signs and symptoms of anxiety, sweat
ing, inrense hunger, dizziness, weakness, and palpitations. Nutritional
and pharmacologic management are the usual treatment choices,J8
Gastric Cancer
The most common malignanr neoplasms found in the stomach are
adenocarcinomas, which arise from norma) or mucosal cells. Benign
tumors are rarely found but include leiomyomas and polyps. For a
more detailed discussion of gastric oncology, see Cancers in the Body
Systems in Chapter 5.
530
Intestinal Disorders
Appendicitis
Inflammation of the appendix of the large intestine can be classified as
simple, gangrenous, or perforated. Simple appendicitis involves an
inflamed but intact appendix. Gangrenous appendiciti is the presence
of focal or extensive necrosis accompanied by micro copic perfora
tions. Perforated appendicitis is a gross disruprion of the appendix
wall and can lead to serious complications if it is not managed
promptly]' The etiology of appendicitis includes a combination of
obstruction in the appendix lumen coupled with infection 'S
Signs and symptoms of appendicitis may include the following.l'4o:
Right lower quadrant, epigastric, or periumbilical abdominal
pain that fluctuates in intensity
Urinary frequency
GASTROINTESllNAL SYSTEM
531
Management of
followingJo J. :
diverticular
disease
includes
any
of
the
i.v. fluids
Pain medications
Ami-infective agents
Hernia
Abdomillal Hernia
532
Hiatal Hernia
A hiatal hernia is an abnormal protrusion of the stomach upward
through the esophageal hiatus of the diaphragm. Causative risk fac
tors for a hiatal hernia are similar to those for abdominal hernia.
Clinical manifestations include heartburn-like epigastric pain that
usually occurs after eating and with recumbent positioning.
Management of hiatal hernia can include behavior modifications,
such as avoiding reclining after meals, eating spicy or acidic foods,
drinking alcohol, and smoking tobacco. Eating small, frequent, bland
meals containing high fiber content may also be beneficial. Pharmaco
logic intervention typically includes acid-reducing medications.45 In
certain cases, when these measures have proven ineffective, surgical
management of the hiatal hernia can be performed laparoscopically.46
Clinical Tip
Positions associated with bronchopulmonary hygiene or
functional mobility may exacerbate pain in patients who
have a hernia, particularly a hiatal hernia. Therefore, care
ful modification of these interventions will be necessary
for successful completion of these activities.
lntestinal Obstructions
Failure of intestinal contents to propel forward can occur by mechan
ical or functional obstructions. Blockage of the bowel by adhesion,
herniation, volvulus (twisting of bowel on itself), tumor, inflamma
tion, impacted feces, or invagination of an adjacent bowel segment
constitutes mechanical obstructions. Loss of the propulsive activity of
the intestines leads to functional obstructions (paralytic ilells).
Obstructions may result from abdominal surgery, intestinal disten-
GASTROINTESTINAL SYSTEM
533
Abdominal distension
Vomiting
Obstipation (inability
Localized tenderness
to
Bloody stools
Intestinal Ischemia
Ischemia within the intestinal tract, also called ischemic colitis, can be
acute or chronic and result from many factors, such as thrombosis or
emboli to the superior mesenteric artery, intestinal strangulation,
chronic vascular insufficiency, hypotension, oral contraceptives,
SAIDs, and vasoconstrictors, such as vasopressin and dihydroergot
amine. Methamphetamine and cocaine have vasoconstrictive proper
ties that can also lead to intestinal ischemia. Significant ischemia that
534
Management
following"47;
of
intestinal
of
the
Anti-infective agents
Anticoagulation therapy
Analgesic agents
GASTROINTESTINAL SYSTEM
535
IBS may have bacterial overgrowth in their small intestines and are
being successfully managed with antibiotic therapy.'s
Signs and symptoms of IBS include the following'9.4o:
Constipation or diarrhea
No weight loss
Antispasmodic agents
Counseling or psychotherapy
Antibiotic therapy
Malabsorption Syndromes
Malabsorptioll sYlldrome is a general term for disorders that are char
acterized by the small or large intestine's failure to absorb or digest
carbohydrates, proteins, fats, vitamins, and electrolytes. This syn
drome is commonly associated with patients who have manifestations
of acquired immunodeficiency disease. The nutritional deficits that
result from malabsorption can lead to other chronic disorders, such as
anemia or osteoporosis. Malabsorption syndromes can result from
any of the foliowingJ9so.sL
Chronic pancreatitis
Pancreatic carcinoma
536
Lactase deficiency
Abdominal bloating
Bone pain
Antibiotic therapy
Peritonitis
Peritonitis is general or localized inflammation in the peritoneal cav
ity as a result of bacterial or chemical contamination. Etiologies can
include bacterial infection, ascites, perforation of the Gl tract, gan
grene of the bowel, trauma, and surgical irritants.39,40,52
Signs and symptoms of peritonitis include the following:
Fever
Abdominal distention
GASTROINTESTINAL SVSfEM
537
Tachycardia, hypotension
Antibiotic therapy
Pain management
Nasogastric suctioning
Crohn's Disease
Crohn's disea e is a chronic, idiopathic, inflammatory disorder
occurring in any part of the GI system. The small intestine, partic
ularly the ileum and the proximal portion of the colon, is most
commonly involved, whereas the esophagus and stomach are
rarely affected. Suspected causes of Crohn's disease include genetic
predetermination, exaggerated immunologic mechanisms, infec
tious agents, psychological factors, dietary factors, and environ
mental factors.39.54.55
Signs and symptoms of Crohn's disease include the following:
Constant crampy abdominal pain, often in right lower quad
rant, not relieved by bowel movement
Diarrhea
Low-grade fever
Fistula formation
538
Anribiorics
Nasogastric suctioning
Colon cancer
Gallstones
Obstructive hydronephrosis
Ulcerative Colitis
Ulcerative colitis is a chronic inflammation of the intestine limited to
the mucosal layer of the colon and rectum. The definitive etiology of
ulcerative colitis is unknown, but suspected causes are similar to
those of Crohn's disease. Inflammation can be mild, moderate, or
severe.39,54.55
Signs and symptoms of ulcerative colitis include the followingl9K
Crampy lower abdominal pain that is relieved by a bowel
movement
Rectal bleeding
Fever
GASTROINTESTINAL SYSTEM
Dehydration
Tachycardia
539
Activity limitations
Antidiarrheal agents
Colon cancer
Polyps
GI polyps are usually adenomas that arise from the epithelium above the
mucosal surface of the colon and rectum. Polyps are generally benign but
have the potential to proliferate intO carcinoma of the colon.J9,58
Signs and symptOms of polyps include the followingJ9,,,:
Constipation or diarrhea
540
Intestinal Tumors
Benign or metastatic neoplasms of the intestine include colonic ade
nomas (polyps), villous or papillary adenomas, lipomas, leiomyomas,
and lymphoid hyperplasia. Tumors affect motility and absorption
functions in the intestine (see Cancers in the Body Systems in Chapter
5 for further details).
A'lOrectal Disorders
Disorders of the anus and rectum generally involve inflammation,
obstruction, discontinuity from colon, perforations, or tumors. The
most common disorders are (1) hemorrhoids, (2) anorectal fistula,
(3) anal fissure, (4) imperforate anus, and (5) rectal prolapse. Signs
and symptoms include pain with defecation and bloody stOols. Man
agement is supportive according to the disorder, and surgical correc
tion is performed as necessary.
GASTROINTFSflNAL SYSTEM
541
Fever
Anorexia
Headache
Jaundice
Dark-colored urine
Anti-inflammatory agents
Antiviral agents
Clinical Tip
542
Viral hepatitis B, C, or D
Hemochromatosis
Wilson's disease
Alpha,-antirrypsin deficiency
Biliary obstruction
Cardiac failure
Malnutrition
Cystic fibrosis
Congenital syphilis
GASTROINTESTINAL SYSTEM
543
Fatigability
Jaundice
Lower-extremity edema
Fever
Paracentesis
Supplemental oxygen
544
Supplemental oxygen
Ammonia detoxicants
Anti-infective agents
Clinical Tip
Hepatic encephalopathy may also be referred to as portal
systemic encephalopathy (PSE) because of the association
GASTROII'ITF..5TINAl SYSTEM
545
Jaundice
Anorexia
Anti-infective agents
Pain management
i.v. fluids
Pallereatic Disorders
Pancreatitis
Inflammation of the pancreas can be acute or chronic. The incidence
of acute pancreatitis is rising, and the clinical sequelae are poten
tially fatal, including adult respiratory distress syndrome (ARDS)
and shock. This section therefore focuses on acute pancreatitis.
Acute pancreatitis can be categorized as necrotizing or interstitial.
Pancreatitis involves an exaggerated release and activity of pancre
atic enzymes into the peritoneal cavity, along with autodigestion of
pancreatic parenchyma. The exact trigger to this process is
546
Trauma
Metabolic disorders
Vasculitis
Pancreatic obstruction
Genetic predisposition
Renal failure
Hepatitis
Medications
Jaundice
Weight loss
GASTROINTfSTJNAL SYSTEM
547
Antacids
Nasogastric slIctioning
Management
General management of GI disorders may consist of any of the fol
lowing: pharmacologic therapy, nutritional support, dietary modifica
tions, and surgical procedures. Nutritional suppOrt and dietary
modifications are beyond the scope of this book. This section focuses
on pharmacologic therapy and surgical procedures. A discussion of
physical therapy intervention is also included.
piJamracologic Therapy
Medications used to treat GI disorders can be broadly categorized as
(I) those that control gastric acid secretion and (2) those that normal
ize gastric motility. Refer to Appendix IV (Tables 1Y.19 A-B and IV.20
A-B) for an overview of these medications. Other medications that do
not fall into these categories are mentioned in specific sections under
Parhophysiology, earlier in the chapter.
Surgical Procedures
Surgical intervention is indicated in GI disorders when medical inter
vention is insufficient. The location and extent of incisions depend on
548
Cholecystectomy
Colectomy
Colostomy
End colostomy
Doublebarrel
colostomy
GASTRQINfESTINAL SYSTEM
Loop colostomy
Gastrectomy
Billroth I
Billroth /I
549
Ileostomy
Resection and
reanastomosis
Whipple procedllre
(pallcreaticoduo
denectomy)
New
GI
slIrgical
procedures
550
Clinical Tip
GASTROINTFSllNAl SYSTEM
551
552
a)
Because NSAlDs are a causative risk factOr for many
inflammatOry and hemorrhagic conditions of the GI system,
these medications will typically be withheld from the patient
with any exacerbation of these conditions.
b)
Therefore, patients who were reliant on NSAlDs for
pain management before admission for their rheumatologic con
ditions may have limitations in functional mobility as a result of
altered pain management.
4.
Patients with ascites or large abdominal incisions are at
risk for pulmonary complications. Ascites and surgical incisions
create ventilatory restrictions for the patient.
a)
Additionally, these conditions can hinder cOllgh effectiveness and functional mobility, both of which can further con
tribute to pulmonary infection.
b)
Effective pain management before physical therapy
intervention, along with diligent position changes, instruction
on incisional splinting during deep breathing and coughing, and
early mobilization with or without assistive devices, will help
prevent the development of pulmonary complications and
deconditioning.
References
1. Koopmeiners MB. Screening for Gastrointestinal System Disease. In W'G
Boissonnault (ed), Examination in Physical Therapy Practice. New
York: Churchill Livingstone, 1991;105.
2. Malarkey LM, McMorrow ME (eds). Nurse's Manual of Laborarory
Tests and Diagnostic Procedures. Philadelphia: Saunders, 2000;412431.
3. Malarkey LM, McMorrow ME (eds). Nurse's Manual of Laboratory
Tests and Diagnostic Procedures. Philadelphia: Saunders, 2000;469.
4. Kapelman B. Approach to the Patient with Liver Disease. In DB Sachar,
JD Waye, BS Lewis (cds), Pocket Guide to Gastroenterology. Baltimore:
Williams & Wilkins, 1991;90.
5. Laparoscopy and Laparoscopic Surgery. In GL Eastwood, C Avunduk
(cds), Manual of Gastroenterology (2nd ed). Boston: Little, Brown,
1994;27.
6. Corbett Jv. Laboratory Tests and Diagnostic Procedures with Nursing
Diagnoses (5th cd). Upper Saddle River, NJ: Prentice Hall Healrh,
2000;698.
GASTROINTESTINAL SYSTEM
553
554
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
40.
41.
42.
43.
44.
45.
GASrROINTISTINAl SYSTEM
555
556
67. McMahon AJ, Fischbacher CM, Frame SH, MacLeod MCM. Impacr of
laparoscopic cholecystectomy; a popularion-based study. Lancet 2000;
356(9242):1632.
68. Margolin DA. Beck DE. Surgical therapy for ulcerative colitis. Ostomy
Q I 997;34( I ):36.
69. Wrighr KD. ColosrolllY. In K Boyden, D Olendorf (eds), Gale Encyclo
pedia of Medicine. Farmingron Hills, MI: Gale Group, 1999;760.
70. Madick SS. Sromach rumors and gamic surgery. AORN J 1999;69(4):
824.
71. Mergener K, Baillie J. Chronic pancreariris. Lancer 1997;350(9088):
1379-1385.
72. Dean E. Oxygen transport deficits in systemic disease and implications
for physical rherapy. Phys Ther 1997;77(2):187-202.
9
Genitourinary System
Jaime C. Paz
lntroduction
3.
A basic understanding of the various diseases and disorders of the genitourinary system
557
558
Table 9-1. Segmental lnnervarion and Pain Referral Areas of the Urinary System
Segmental
Structure
Innervation
Kidney
Tl0-L l
Ureter
T I 1-L2, 52-54
Upper abdomen
Groin
Upper and lower abdomen
Suprapubic region
Scrotum
Medial and proximal thigh
Thoracolumbar region
Urinary bladder
TII-L2,52-54
5ac,,1 apex
Suprapubic region
Thoracolumbar region
Source: Wirh permission from we Boisson:Hlir, C B..1SS. Parhological origins of trunk and
neck pain: part I. Pelvic and abdominal visceral disorders. J Orthop Phys Ther 1990; 12: 194.
4.
Information about the management of genitourinary disorders, including dialysis therapy and surgical procedures
5.
Guidelines for physical therapy intervention in patients
with genitourinary diseases and disorders
GENrrOURINARY SYSTF..M
Adrenal
Gland
559
-"tt-+-
Ouadratus
Lumborum
Vena
cava
Psoas
Major
and
Minor
Aorta
i;<Httr-_ lIiacus
,.,.:',
560
Papilla
bp_ Minor
calyces
_
_
M ajOr
Calyx
Renal
Petvis
-- Ureter
GENITOURINARY SYSTEM
561
Clinical Evaluation
Physical Examillatioll
History
Patients with suspected genitourinary pathology often present with
characteristic complaints or subjective reports. Therefore, a detailed
history, thorough patient interview, review of the patient's medical
record, or a combination of these provides a good beginning to the
diagnostic process for possible genitourinary system pathology. Renal
and urinary pains can vary according to their structural origins; how
ever, they are generally described as pain that is colicky, wave-like, or
burning, or occurring as dull aches in the abdomen, back, or buttocks]
Changes in voiding habits or a description of micturition patterns
are also noted and are listed below2-4:
Decreased force of urinary flow (can indicate obstruction in the
urethra or prostate enlargement)
Increase in urinary frequency (can indicate obstruction from
prostate enlargement or an acutely inflamed bladder)
Nocturia (urinary frequency at night, can indicate congestive
heart failure or diabetes mellitus)
Polyuria (large volume of urine at one time, can indicate diabe
tes mellitus, chronic renal failure I CRFJ, or excessive fluid intake)
Oliguria (usually less than 400 ml of urine in a 24-hour period,
can indicate acute renal failure [ARF] or end-stage renal disease
lESRD])
AliI/ria (less than J 00 ml of urine in a 24-hour period, can indi
care severe dehydration, shock, transfusion reaction, kidney dis
ease, or ESRD)
562
Clinical Tip
If the patient has a history of urinary incontinence, a
condom catheter (for men) or adult diapers (for men and
women) can be applied before mobility treatment to aid in
completion of the session.
Observation
The presence of abdominal or pelvic distention, peripheral edema,
incisions, scars, tubes, drains, and catheters should be noted when
performing patient inspection, because these may reflect current
pathology and recent interventions. Patients with genitourinary disor
ders may also present with skin changes, such a pallor or rough, dry
skin' The physical therapist must handle external tubes and drains
carefully during positioning or functional mobility treatments.
Clinjcal Tip
GENITOURINARY SYSTEM
563
Palpation
The kidneys and a distended bladder are the only palpable structures
of the genitourinary system. Distention or inflammation of the kid
neys results in sharp or dull pain (depending on severity) with palpa
tion. Kidney enlargement may be indicative of renal carcinoma.2,"1
Percussion
Pain and tenderness that are present with fist percussion of the kid
neys can be indicative of kidney infection or polycystic kidney disease.
Fist percussion is performed by the examiner's striking the fist of one
hand against the dorsal surface of the other hand, which is placed
along the costovertebral angle of the patient.
Auscultation
Auscultation is performed to examine the blood flow to the kidneys
from the abdominal aorta and the renal arteries. The presence of
bruits ( mllrlllllrs) can indicate impaired perfusion to the kidneys,
which can lead to renal dysfunction. Placement of the stethoscope is
generally in the area of the costovertebral angles and the upper
abdominal quadrants. Refer to Figure 8-2 for a diagram of the
abdominal quadrants.
Diagllostic Tests'
Urinalysis
Urinalysis is a very common diagnostic tool used not only to examine
the genitourinary system, but also to help evaluate for the presence of
The reference range of various laboratory values can vary among different
facilities. Be sure [Q verify the reference values located in the laboratory test
section of the medical record.
564
pH (4.5-8.0)
Clinical Tip
If the patient is having his or her urine collected (to
Creatinine Tests
Two measurements of Cr (end product of muscle metabolism) are
performed: measurements of plasma Cr and Cr clearance. Plasma Cr
is measured by drawing a sample of venous blood. Increased levels
are indicative of decreased renal function. The reference range of
plasma Cr is 0.5-1.5 mg/dJ.
(.fNITOLlRII'ARY SYSTEM
565
Etlolog),
Glycosuria (presence of
glucoc;e)
Proteinuria (presence of
proreins)
cells)
Bacteriuria (presence of
bacreria)
Ketonuria (presence of
ketones)
Bilirubmuria (presence of
bilirubin)
CrYMais (end producr" of
food metabolism)
"Ketones arc formed from protcm and fat membolism, and tracc amounts
III
(h e urine
41re norm,\1.
Soun::e'i: D.na from VC Scanlon, T Sander.. (cds). Essentials of Anawmy and Physiology
(2nd cd). Philadelphl.l: I;A Davis. 1995;416; P Bates. Nursing Assessment: Urinary Sys
tem. In SM Lewl\, 1\11\1 Ileltkempcr. SR Dirksen (cds), :-'Iedical-Surgical Nursing:
Asscssmenl and Managemelll of Climcal Problcms (5th cd). St. Louis: Mosby,
566
Clinical Tip
Noting BUN and Cr levels on a daily basis for any changes
may help explain changes in the patient'S mental status,
participation in physical therapy sessions, or both.
Radiographic Examination
Clinical Tip
This x-ray procedure is often abbreviated KUB.
Pyelography
Radiopaque dyes are used to radiographically examine the urinary
system. Two types of tests are performed: excretory urography (intra
venous pyelography) and retrograde urography. Excretory urography
is performed more commonly than retrograde urography.
Excretory IIrography consists of ( J ) taking a baseline radiograph
of the genitourinary system, (2) intravenous injection of contrast dye,
and (3) sequential radiographs to evaluate the size, shape, and loca
tion of urinary tract structures and to evaluate renal excretory func-
GENITOURINARY SYSTEM
567
Clinical Tip
Patients who are scheduled for procedures involving con
trast dye are generally restricted from eating or drinking 8
hours before the procedure. A patient who is scheduled for
an afternoon procedure may therefore be fatigued earlier
in rhe day and may want to defer a scheduled therapy ses
sion. Modifying the intended therapy session and respect
ing the person's wishes at this time are both suitable
alternatives.
568
that is used to view the prostatitic urethra (in men), external urinary
sphincters, and anterior urethra. 5-7
Clinical Tip
Patients may experience urinary frequency or dysuria
after cyStoscopic procedures; therefore, the therapist
should be prepared for sudden interruptions during a
therapy session that is conducted the same day after this
diagnostic procedure.
Urodynamic Studies
Uro(lowmetry
In IIro(lowmetry, voiding is analyzed graphically to determine the
rate, time, and volume of urinary Aow so that ureteral, urethral, and
bladder function can be examined and described. Increased flow rates
could be indicative of incontinence, whereas decreased flow rates may
indicate urethral or bladder neck obstruction.57
Cystometrogram
Cystometrogram is used to evaluate bladder tone, sensations of fill
ing, and bladder stabiliry. The procedure consists of inserting a cathe
ter into the bladder, followed by saline instillation and pressure
measurements of the bladder wall'
Radioisotope Studies
Renography
Renography consists of injecting a radioisotope intravenously and
allowing it to circulate through the urinary system to be excreted in
the urine. A renogram (graphic record) is taken to assess renal blood
flow, glomerular filtration, and tubular secretion.'
Renal Scali
A renal scan consists of using an external scanning device, such as a
scintillator, to outline the kidneys and ureters after intravenous radio
isotope injection. Blood flow, glomerular filtration, tubular function,
and excretion can be examined during this procedure. Decreased
areas of kidney function, as with abscesses, cysts, or tumors, do not
appear on the scan.4-6
GENITOURINARY SYSfEM
569
Rellal Biopsy
A renal biopsy consists of examining a small portion of renal tissue
that is obtained percutaneously with a needle to determine the patho
logic state and diagnosis of a renal disorder, monitor kidney disease
progression, evaluate response to medical treatment, and assess for
rejection of a renal transplant. A local aneSthetic is provided during
the procedure4 .5
570
Pathophysiology
2.
O/iguric or antlric (110 urine) phase occurs when urine output is less than 400 ml in 24 hours, which can last 8-15 days, with
prognosis worsening as rhe duration increases.
GENITOURINARY SYSTEM
571
4.
The late or recovery period is the time between falling to
stabilizing (i.e., within normal range) BUN levels.
5.
The convalescent phase occurs when urine output and
BUN levels are stable within normal ranges. This phase may last
several months and may ultimately progress to CRE
Clinical manifestations of ARF include the following8-' L
Acid-base imbalance
Hyperkalemia or hypokalemia
Infection
Hyperphosphatemia
Anemia
Diuretics
Nutritional support
572
CRF can resulr from primary renal disease or orher sysremic dis
eases. Primary renal diseases rhar cause CRF are polycysric kidney
disease, chronic glomerulonephriris, chronic pyelonephriris, and
chronic urinary obstruction. The two primary systemic diseases that
cause CRF are rype 2 diaberes and hypcrtension.1J Orher sysremic dis
eases rhar can resulr in CRF include gour, sysremic lupus erythemaro
sus, amyloidosis, and nephrocalcinosis. Complicarions of CRF are
similar ro rhose of ARF bur can also include decreased bone densiry as
a result of decreased activation of vitamin D, which impairs inrescinal
absorption of calcium, resulting in low serum calcium levels. Patients
wirh CRF can also experience episodes of ARF in siruarions when
they are noncompliant with their management, when their manage
ment proves insufficient, or both.8.9,12.14 .15
Management of CRF may consist of conservative management or
renal replacemenr rherapy.l.
Conservative management includes the following8.9.'2.16:
Pyelonephritis
Pyelonephritis is an acute or chronic inflammarory response in the
kidney, particularly the renal pelvis, from bacrerial, fungal, or viral
infection. It can be classified as acute or chronic.
ACt/te Pyelonephritis
Acute pyelonephritis is frequently associated with concurrent cystitis
(bladder infection). The common causative agents are bacterial,
including Escherichia c oli, Protells, Klebsiella, Enterobacter, and
Pseudomonas. Predisposing factors for acute pyelonephritis include
urine reAux from rhe urerer to rhe kidney (vesicollreteral reflllx), kid
ney srones, pregnancy, neurogenic bladder, carherer or endoscope
GENITOURINARY SYSTE.M
573
insertion, and female sexual trauma. Women are more prone to acute
pyelonephritis than men,',I6,17 Spontaneous resolution of acute pyelo
nephritis may occur in some cases without intervention.
Signs and symptoms of acute pyelonephritis may include the
following,,16-18:
Urinary frequency
Chrollic Pyelollephritis
Chronic pyelonephritis is recurrem or persistent inflammation and
scarring of one or both kidneys as a result of autoimmune infection.
Chronic pyelonephritis can also result from kidney stones or acute
pyelonephritis and may lead to CRE Specific eriologies are difficult to
diagnose. 9,16-18,2 1
Signs and symptoms of chronic pyelonephritis include the
following,,17,18:
Hypertension
574
Glomerulonephritis
Glomerulonephritis is an inflammation of the glomerular portion of
the kidney that can result from immunologic abnormalities, drug Ot
toxin effects, vascular disorders, or systemic disorders. Definitive eti
ology may be difficult to ascertain in some cases. Glomerulonephritis
can be classified according to cause, pathologic lesions, disease pro
gression, or clinical presentation. This section discusses the common
types of glomerulonephritis.9
Hematuria
Proteinuria
Oliguria
GENITOURINARY $Y$TE.."l.
575
Cytotoxic agents
Postinfectious ClomeTIIIOllephritis
As the name states, postin(ectiolls glomerulonephritis is acute inflam
mation in the renal system that occurs after infection. Group (X.- and
-hemolytic streprococci are the common causative pathogens that
lead ro the damage of surface proteins in the glomeruli.9,ls,',.25 Other
organisms that have been associated with this form of acute glomeru
lonephritis include hepatitis B virus, hepatitis C virus, and human
immunodeficiency virllS; spirochetes, slich as Treponema pallidum;
protozoa, such as Plasmodium Inalariae; and fungi, such as Candida
albicalls." Prognosis is generally good once the causative agent is
identified and appropriate anti-infective and supportive therapies are
provided. 2'. ,s
Signs and symptoms of poststreprococcal glomerulonephritis
include the foliowing'18.25;
Acute onset of fluid retemion, hypertension, and peripheral
edema
Oliguria
Hematuria
Anemia
Antibiotics
Antihypertensive agents
Diuretics
576
Severe oliguria
Plasma pheresis
Anticoagulation treatment
Hemodialysis
Renal transplantation
Chrollic G/omemlollephritis
Chronic glomerulonephritis is the culmination of diseases that can
affect the glomeruli leading to progressive renal failure in 10-20
years. These diseases include those mentioned in the previous section,
along with diabetes, hepatitis, and systemic lupus erythematosus.2'
Chronic glomerulonephritis involves scarring and obliteration of the
glomeruli, along with vascular sclerosis of arteries and arterioles.9,ls
Signs and symptoms of chronic glomerulonephritis include the
following',18:
GENnOURJNARY SYSTEM
Uremia
Proteinuria
Hypertension
Azotemia
577
Dialysis
Renal transplantation
Diabetes mellitus
Amyloidosis
Circulatory diseases
578
Pregnancy (pre-eclampsia)
Hypoalbuminemia
Generalized edema
Hyperlipidemia
Vitamin 0 deficiency
Management of
following8.9.28.29:
nephrotic
syndrome
includes
any
of
the
Albumin replacement
Diuretics
Anticoagulation therapy
Interstitial Nephritis
Infection, urinary tract obstruction, and reactions to medications,
particularly nonsteroidal ami-inflammatory agents, can result in
inflammatory, intcrstirial tissue damage, which is referrcd to as inter
stitial nephritis.8.l0.ll Scarring from the inflammatory process leads to
reduced kidney function that can progress to CRE Early detection is
helpful in treating the inflammatory response.'
Physical findings of interstitial nephritis include the following':
o
Polyuria
Nocturia
GENITOURINARY SYSTEM
Pyuria
Mild hematuria
Mild proteinuria
579
Renal transplantation
Nephrolithiasis
Nephrolithiasis is a condition that occurs more commonly in men
and is characrerized by renal calculi (kidney stones) thar form in rhe
renal pelvis. There are three primary types of kidney stOnes, which
are categorized according to the stone-forming substances: calcium
oxalate, struvite (composed of magnesium, ammonium, and phos
phate), and uric acid. Many factors contribute to stone formation
and include the foliowing8. 9J3J4:
Metabolic abnormalities
580
Hematuria
Fever
Variable urine pH
Analgesics
Anti-infective agents
Diabetic Nephropathy
Approximately 20-30% of people with type 'lor type 2 diabetes will
develop diabetic nephropathy," which is characterized by systemic
vascular changes in the kidneys that result in scarring (nephrosclero
sis) of the glomeruli and, ultimately, in reduced kidney function.
Pyelonephritis and necrosis of the renal papillae arc also associated
with diabetic nephropathy. Patients who demonstrate poor glycemic
control with resultant vascular disease and hypertension are more
likely to develop diabetic nephropathy. Hypertension can lead to or
result from diabetic nephropathy.8. 36,37
Signs and symptoms of diabetic nephropathy include the
following,,36.37:
Microalbuminuria, oliguria, anuria. Microalbuminuria is a criti
cal screening tool for early detection of nephropathy.
Peripheral edema.
GENITOURINARY SYSTEM
581
Hydration
Diuretics
Nutritional support
Dialysis
II yperrension
Microscopic hematuria
Peripheral edema
582
Anticoagulation agents
Analgesics
Dialysis
Flank pain
Gross hematuria
Proteinuria
Oliguria
GENITOURINARY SYSTEM
583
Dysuria
Nocruria
Urinary Calculi
Urinary calculi are stones (llrolithiasis) that can form anywhere in the
urinary tract outside of the kidneys. Formation of stones, symptoms,
and management are similar to that of kidney stones (see Nephroli
thiasis for further details on the formation and clinical presentation of
584
Prostate Disorders
Benign Prostatic Hypertrophy
Bellign prostatic hypertrophy (BPH) is a benign, progressive enlarge
ment of the prostate gland and is the mOSt common benign tumor in
men.s Almost all men older than age 60 develop BPH, which is asso
ciated with the normal aging process. Concern arises when enlarge
ment interferes with normal voiding patterns. Acute urinary retention
and urinary tract infection are the primary complications of BPH.46
Signs and symptoms of BPH include the following4 s46;
Straining to void
Postvoid dribble
GENITOURINARY SY$TIM
585
Description
Common Causes
Stress
Urge
Overflow
Functional
586
Intermittent self-catheterization.
Prostatitis
Prostatitis is an inflammation of the prostate gland. It can be divided
into four categories: (I) acute bacterial, (2) chronic bacterial, (3) non
bacterial, and (4) prostatodynia (presence of prostatitis symptoms
without physical findings). Nonbacterial prostatitis and prostato
dynia occur more commonly than do acute and chronic bacterial
prostatitis. Causative pathogens for acute and chronic bacterial pros
tatitis can include E. coli, Pseudomonas aeruginosa, Neisseria gonor
rhoeae, and Mycobacterium tuberculosis.45
Signs and symptoms of prostatitis include the following42 .,:
Fever with rectal, perineal, or low back pain (acute bacterial
prostatitis)
Bladder irritability
Nocturia
Sexual dysfunction
GENITOURINARY SYSTEM
587
Antipyretics
Managemenl
The specific managemenr of various genitourinary disorders is dis
cussed earlier in the respective pathophysiology sections. This section
expands on renal replacemenr rherapy and surgical procedures.
Guidelines for physical therapy intervention for patients who have
genitourinary dysfunction are also discussed.
Renal Replacelllent Therapy
588
Shock
Peritonitis
Abdominal adhesions
Hernias
GENITOURINARY SYSTEM
589
B
Figure 9-3. Schematic illustratio" of coutinuous ambulatory peritoueal dialy
sis. A. l"stillatioN of dialysate fluid. B. Drainage of excess fluid and solutes.
(Artwork by Peter IV".)
Intermittent Hemodialysis
Kidney functions that are controlled by intermittent hemodialysis
include ( I) fluid volume, (2) electrolyte balance, (3) acid-base balance,
and (4) filtration of nitrogenous waStes. The patient's arterial blood is
mechanically circulated through semipermeable tubing that is sur
rounded by a dialysate solution in the dialyzer (artificial kidney). The
dialysate fluid contains electrolytes similar to those in normal blood
plasma ro permit diffusion of electrolytes into Ot out of the patient'S
blood.6s As the patient'S arterial blood is being filtered through the
dialyzer, "clean" blood is returned to the patient'S venous circulation.
Figure 9-4 illustrates this process.
590
Blood
Infusion pump
Blood retvm
591
Vein
Fistvlo
(Anastomosis of ortery and vein
shunting orteriol blood into vein)
Rodiol ortery
Antecubital vein
II
Brochiol ortery
Looped groft
TeRon connector
Rad10I artery
nV\""J'\.--"::-";::;" \
jE
-
-=
Silastic tubing
lexternol segment)
Basilic vein
592
Acute poisoning
Hepatic coma
Metabolic acidosis
Transfusion reactions
No vascular access
Hemorrhagic diathesis
Extremes in age
GENITOURINARY SYSTEM
593
CAVH uses the femoral artery and vein as common sites for vascu
lar access. Pressure gradients between the arterial and venous system
along with oncotic pressures help drive the hemofiltration process,
which mimics the urine formation process in the renal glomerulus.
Heparin i infused to help prevent clotting in the hemofilter and tub
ing. Medications and nutrition can also be administered through the
cireuit',lo. " Figure 9-6 illustrates CAVH.
CWH is similar to CAVH, except that CW H only uses the
venous system as access sites for blood exchange, and without the
arterial system to drive blood flow, CW H requires a mechanical
pump to circulate the blood. CW H is sometimes preferable to
CAVH, as it is difficult to obtain and maintain arterial access for pro
longed time periods."
Indications for CRRT include the following:
Cardiovascular instability
Parenteral nutrition
Uncomplicated ARF
Hypereatabolic state
Hyperkalemia
Poisoning
Shock
Severe arthrosclerosis
v.
'l
., I
;0
m
J:
>
Z
o
Venous
H III
Infusion of substitution
fluid, drugs, nutrients
Hemofilter
/'
'"
>
r
---
'"
-;
'"
Heparin infusion
pump
Closed graduated
filtrate coUecoon
.
Arterial line
Figure
'"
>
GENITOURINARY SYSTEM
595
Clinical Tip
Pulmonary hygiene treatments can be performed during
dialysis; however, this depends on the hemodynamic sta
bility of the patient and is at the discretion of the nurse or
physician. Extreme caution should be taken with the
access site to prevent accidental disruption.
The dialysis nurse is generally nearby to monitor the
procedure and is a valuable source of information regard
ing the patient's hemodynamic stability.
Activity tolerance can be altered when fluid and electrolyte
levels are unbalanced. Patients will demonstrate variable levels
of fatigue; some are more fatigued before a dialysis session,
whereas others are more fatigued after a dialysis session.
Fluid and electrolyte imbalance can also alter the hemo
dynamic responses to activity; therefore, careful vital sign
and symptom monitoring should always be performed.
Surgical Interventions
Surgical interventions for genitourinary system disorders can be cate
gorized broadly as procedures that remove diseased portions of the
genitourinary tract or procedures that restore urinary flow. These
interventions are briefly discussed in the following sections. Refer to
Appendix V for general postoperative considerations.
Nephrectomy
There are three types of nephrectomy. The primary indications for
removing a part or all of the kidney include renal tumor, polycystic kid
ney disease, severe traumatic injury to the kidney, and organ donation, as
well as removing a failing transplanted organ.4748 Nephrectomy can be
performed as an open or laparoscopic procedure. Open nephrectomy is
the conventional method that requires an incision of approximately 7 in.
Laparoscopic nephrectomy involves five access sites, ranging from less
than 0.5 in. to 3 in. Laparoscopic nephrectomy is gaining acceptance as a
viable alternative to open nephrectomy, as there have been fewer postop
erative complications associated with the procedure.47-s o The types of
nephrectomy and their definitions follow:
596
Open Prostatectomy
Open prostatectomy is the surgical removal of a prostate gland
with or without irs capsule and is primarily indicated for parienrs
with prostare cancer. Five types of surgical approaches can be used:
( 1) transcoccygeal, (2) perineal, (3) retropubic, (4) transvesical, and
(5) suprapubic. This procedure is contraindicated if the prostate is
small and fibrou . The suprapubic and retropubic approaches of this
procedure are contraindicated in the presence of cancer.42
Transurethral Resection
Transurethral resectioll refers to the surgica I approach performed
when managing bladder tumors, bladder neck fibrosis, and pros
tatic hyperplasia. The most common type of transurethral resec
tion is a TURP, which this section focuses on. TURP is indicated
for obstructive BPH. Involved tissues arc resected with a resecto
scope that is inserted through the urethra. Excision and coagulation
of tissue are accompanied by continuous irrigation. Conrra-indica
tions for TURP include the presence of urinary tract infection and
a prostate gland weighing more than 40 g. TURP is also contrain
dicated with conditions that interfere with operative positioning
for the procedure, such as irreversible scrotal hernia or ankylosis
of the hip."
GENrrQURINARY SYSTEM
597
kidney)
598
Protruding abdominal
IT
Ileal segment
anastomosed to
sigmoid colon
Left ureter
anostomosed
to right ureter
/11
Cutaneous
ureterostomy
on abdomen
ti
Cutaneous
ureterostomy
on abdomen
tubing
Posterior view
Bilateral nephrostomy tubes
inserted into renal pelvis;
catheters exit through an
incision on each Rank, or
there may be just one
kidney
GENITOURINARY SYSTEM
599
ances and allow more control for the patient. The internal reservoir is
connected to an abdominal stoma, which does nOt continually drain
urine, and patients perform intermittent self-catheterizations through
the Stoma (see Figure 9_7).42.47
Orthotopic Bladder Substitution
Orthotopic bladder substitution involves reshaping a portion of the dis
tal ileum into a neobladder and connecting the ureters and the urethra to
it. Connecting the urethra to the neobladder allows for natural micturi
tion. However, incontinence still may occur occasionaiJy with this proce
dure, and the patient may also require intermittent catheterization.47
600
3.
Blood pressure regulation can be altered by the inability to
excrete body fluids and activate the renin-angiotensin system.53
4.
Activity rolerance can be reduced by the factors mentioned
in this list, as well as anemia that can result from decreased eryth
ropoietin secretion from kidneys, which is necessary for stimulat
ing red blood cell production. 53
5.
Patients with CRF may present with concurrent clinical
manifestations of diabetes mellitus, as diabetes mellitus is a strong
contributing factor to this disorder. Refer to Chapter I I for more
information on diabetes mellitus.
6.
As stated in the introduction ro this chapter, patients with
genirourinary dysfunction may have referred pain (see Table 9-1).
Physical therapists can play a role in differentiating the source of a
patient's back pain as well as providing symptomatic management
of this referred pain.
7.
Patients who are status post surgical procedures with
abdominal incisions are less likely to perform deep breathing and
coughing because of incisional pain. Diligent position changes,
instruction on incisional splinting during deep breathing, and
coughing, along with early mobilization, help prevent the develop
ment of pulmonary complications.
S.
For patients who are ambularory and present with urinary
urgency, possibly from diuretic therapy, the use of a bedside com
mode may be a beneficial recommendation to minimize the inci
dences of incontinence.
9.
Patients who are incontinent may benefit from a home exercise program, referral ro a physical therapist who specializes in pel
vic floor strengthening, or both on discharge from the hospital.
GENITOURINARY SYSTEM
601
References
1. Scanlon VC, Sanders T. Essentials of Anatomy and Physiology (2nd cd).
Pholadelph.a: FA Davis, 1995;416.
2. Bullock BL. Normal Renal and Urinary Excretory Function. In BL Bul
lock (ed). Pathophysiology: Adaptations and Alterations in Function
(4th cd). Pholadelphia: Lippincorr, 1996;616.
3. McLinn DM, Boissonnault WG. Screening for Male Urogenital System
Disease. In WG Boissonnault (ed), Examination in Physical Therapy
Practice: Screening for Medical Disease. New York: Churchill Living
rone, 1991;121.
4. Bates P. Nursing Assessment: Urinary System. In SM Lewis, MM Heit
kemper, SR Dirksen (eds), MedicalSurgical Nursing: Assessment and
Management of CI111icai Problems (5th ed). St. Louis: Mosby, 2000;
1241-1255.
S. Malarkey LM, McMorrow ME. Nurse's Manual of Laboratory Tests
and D.agnostic Procedures (2nd cd). Philadelphia: Saunders, 2000;3848, 629-670.
6. R.chard Cj. Urinary Function. In GA Harkness, JR Dincher (eds), Med
ical-Surgical Nursing: Total Patient Care (9th cd). St. Louis: Mosby,
1996;760.
7. Thompson FD, Woodhouse CRJ. Disorders of the Kidney and Urinary
Tract. London: Edward Arnold, 1987.
8. Renal System. In JM Thompson, GK McFarland, JE Hirsch, et al. (eds),
Mosby's Manual of Clinical Nursing Practice (2nd cd). St. Louis:
Mosby, 1989;1021.
9. Huether SE. Alterations of Renal and Urinary Tract Function. In KL
McCance, SF Huether (cds), Pathophysiology: The Biologic Basis for
Disease .n Adults and Chlldren (2nd cd). St. Louis: Mosby, 1994;1212.
10. Dirkes SM. Continuous rena) replacement therapy: dialytic therapy for
acute renal failure in intensive care. Nephrol Nurs J 2000;27(6):581.
II. Ford-Martin PA. Acute Kidney Failure. In K Boyden, D Olendorf (eds),
Gale Encyclopedia of Medicine. Farmington Hills, MI: Gale Group,
1999;33.
12. Ford-Martin PA. Chronic Kidney Failure. In K Boyden, D Olendorf
(edsl, Gale Encyclopedia of Med.clOe. Farmingron Hills, MI: Gale
Group, 1999;716.
13. Boone CA. End-stage renal disease in African-Americans. Nephrol Nurs
J 2000;27(6):.197.
14. Scon MS. Canng for rhe orthopaedic patient receiving cominuous
ambularory pemoneal dialysis. Orrhop Nurs 1999;18(4):59.
15. Brunier B, BaTtucci M. Acute and Chronic Renal Failure. In SM Lewis,
MM Heltkernper, SR Dirksen (cds), Medical-Surgical Nursing: Assess
ment and Management of Clinical Problems (5th ed). St. Louis: Mosby,
2000;1310-1330.
16. BoissOll3Uh WG. Urinary Tract Disorders. In CC Goodman, we Bois
sonnaulr (cds) Pathology: Implications for the Physical Therapist. Phila
delph..: Saunders, 1998;532-546.
17. Wright KD. Pyelonephritis. In K Boyden, D Olendorf (eds), Gale
Encyclopedia of Medicine. Farmington Hills, MI: Gale Group,
1999;2422.
602
GENITOURINARY SYSTEM
603
10
Infectious Diseases
Jaime C. Paz and V. Nicole Lombard
lntroduction
605
606
2.
Various infectious disease processes, including etiology,
pathogenesis, clinical presentation, and management
3.
Commonly encountered altered immune disorders, including etiology, clinical presentation, and management
4.
Precautions and guidelines that a physical therapist should
implement when treating a patient with an infectious process or
altered immunity
Definition of Terms
Evaluation
History
INFEcnous
DISEASES
607
Antigen (immunogen)
Carrier
olonization
Communicable
Disseminated
Host
Immunocompromised
Nosocomial infection
Opportunistic
response
Subclinical infection
Physical Examillatioll
Observation
Clinical presentation of infectious diseases is highly variable accord
ing to the specific system that is involved. However, common physical
findings that occur with infection include sweating and inflammation,
both of which are related to the metabolic response of the body to the
antigen. The classic signs of inflammation (redness and edema) in cer-
608
Components
Descri ption
First (ine of
Skin, conjunctivae,
Physical barriers
defense
Second line of
to
pathogens.
mucous membranes
Inflammamry response
defense
lmmune response
Humoral immunity
pathogens.
defense
(B cells)'
Cellular immunity
(T cells)'
T cells:
tain areas of the body can help delineate the source, location(s), or
both of infection. Delineating the source of infection is crucial to the
diagnostic process.
Palpation
The presence of warmth and possible pain or renderoess is another
typical sign of inflammation that may be consistent with active infec
tion. Lymphoid organs (lymph nodes and spleen) can also be swollen
and tender with infection, as lymphocytes (processed in these organs)
are multiplying in response to rhe antigen. lnAammarion and tender
ness .in these or other areas of the body can further help to delineate
the infectious process.
INFECllOUS DISEASES
609
Vital Signs
Heart Rate, Blood Pressure, and Respiratory Rate
610
Laboratory Shldies
INFEcnOUS DISEASES
611
4.
Safranin 0 or carbolfuchsin applied ro stain gram-negative
organisms pink to red
5.
Alcohol or acerone applied to decolor gram-negative
organisms
6.
612
tent) needed for the organism to reproduce into colonies. Once this
has taken place, the resultant infectious agent is observed for size,
shape, elevation, texture, marginal appearance, and color to assist
with identification. 9
Sensitivity and Resistance
fluid from a joint capsule. The fluid is then analyzed and used to assist
INFECfIOUS DISEASES
613
Other Studies
Imaging with plain x-rays, computed tomography scans, and mag
netic resonance imaging scans can also help identify areas with infec
tious lesions. In addition, the following diagnostic studies can also be
performed to help with the differential diagnosis of the infectious pro
cess. For a description of these studies, refer to the sections and chap
ters indicated below:
Infectious Diseases
614
Nosocomial Infections
Nosocomial infection is a general term that refers to an infection that
is acquired in the hospital setting. Many pathogens can cause a noso
comial infection, but the most commonly reported in the past years
have been Escherichia coli, Staphylococcus allreus, Enterococcus
faecalis, Pseudomonas aeruginosa, and coagulase-negative staphyloc
COci.16 Patients who are at risk for developing nosocomial infections
are those who present with the following:
1.
2.
Immunodeficiency; chronic diseases (cancer, chronic renal
disease, chronic obstructive pulmonary disease, diabetes, or
acquired immunodeficiency syndrome [AJDSJ)
6.
7.
to
pathogens
8.
Length of hospitalization-increases the exposure to
pathogens and medical intervention
The mode of transmission for pathogens that cause nosocomial
infections can vary from contact to airborne. Pathogens can also
become opportunistic in patients who are immunocompromised or
immunosuppressed. Common sites for nosocomial infections are in
the urinary tract, surgical wounds, and the lower respiratory tract
(e.g., pneumonia). Clinical manifestations and management of noso
comial infections vary according to the type of pathogen and the
organ system involved. However., the primary management strategy
for nosocomial infections is prevention by following standard and
specific precautions outlined in Table 10-4.'16,17
INFF.CfIOUS DISEASES
615
Description
Standard
Airborne'"
3 ft or less) is likely.
WJ Phipps, JK
5ands. JF Marek (ed). Medical-Surgical Nursmg. Concepts and Clinical Practice (6th
ed). St. LOUIS: Mosby. 1999:237-245: and KN Anderson (ed), Mosby's Medlc:lI, Nurs
mg, and Allied Health Dictionary (Sth ed). St. LOUIS; Mosby, 1998;2BA5.
Antibiotic-Resistant lnfections
Methicillill-Resistat,t Sraphylococcus aureus [nfectiOl'
616
617
Clinical Tip
Equipment that is used during physical therapy treatments
for patients with MRSA or VRE, such as assistive devices,
Cliff weights, or goniometers, should be left in the patient'S
room and not be taken out until the infection is resolved.
If there is an equipment shortage, thorough cleaning of the
618
Rhinitis
Rhinitis is the inflammation of the nasa) mucous membranes and can
result from an allergic reaction or viral infection. Allergic rhinitis is
commonly a seasonal reaction from allergens, such as pollen, or a
perennial reaction from environmental triggers, such as pet dander or
smoke. Viral rhinitis, sometimes referred to as the common cold, is
caused by a wide variery of viruses that can be transmitted by air
borne particles or by contacr.
Clinical manifestations of allergic and viral rhinitis include nasal
congestion, sneezing, watery, itchy eyes and nose, altered sense of
smell, and thin, watery nasal discharge. In addition to these, clinical
manifestations of viral rhinitis include fever, malaise, headache, and
thicker nasal discharge.
Management of allergic rhinitis includes antihistamines, deconges
tants, and nasal corticosteroid sprays. Management of viral rhinitis
includes rest, fluids, antipyretics, and analgesics.22 .B
Sinusitis
Sinusitis is the inAammation or hypertrophy of the mucosal lining of any
or all of the facial sinuses (frontal, ethmoid, sphenoid, and maxillary).
This inflammation can result from bacterial, viral, or fungal infection.
Clinical manifestations of sinusitis include pain over the affected
sinus, purulent nasal drainage, nasal obstruction, congestion, fever,
and malaise.
INFECTIOUS DISEASES
619
Clinical Tip
Despite the benign nature of rhinitis and sinusitis, the
manifestations (especially nasal drainage and sinus pain)
of these infections can be very disturbing to the patient
and therapist during the therapy session and may even
lower the tolerance of the patient for a given activity. The
therapist should be sympathetic to the patient's symptoms
and adjust the activity accordingly.
Influenza
Influenza (the flu) is caused by any of the influenza viruses (A, S, or C
and their mutagenic strains) that are transmitted by aerosolized
mucous droplets. These viruses have the ability to change over time
and are the reason why a great number of patients are at risk for
developing this infection. Influenza B is the mOst likely virus to cause
an outbreak within a community.
Clinical manifestations o f influenza include (I) a severe cough,
(2) abrupt onset of fever and chills, (3) headache, (4) backache, (5) myal
gia, (6) prostration (exhaustion), (7) coryza (nasal inflammation
with profuse discharge), and (8) mild sore throat. Gastrointestinal
signs and symptoms of nausea, vomiting, abdominal pain, and diar
rhea can also present in certain cases. The disease is usually self
limiting in uncomplicated cases, with symptoms resolving in 7-10
days. A complication of influenza infection is pneumonia, especially
in the elderly and chronically diseased individuals.I.'.I2.23
If management of influenza is necessary, it may consist of the
following 1.2. 12. 23 :
Anti-infective agents
Antipyretic agents
Adrenergic agents
Antitussive agents
620
I.V.
Clinical Tip
Health care workers should be vaccinated against the
influenza virus to decrease the risk of transmission.
Pertussis
Pertussis, or whooping cough, is an acute bacterial infection of the
Tuberculosis
TB is a chronic pulmonary and extrapulmonary infectious disease
caused by the tubercle bacillus. It is transmitted through airborne
Mycobacterium tuberculosis particles, which are expelled into the air
when an individual with pulmonary or laryngeal TB coughs or
sneezes." When M. tuberculosis reaches the alveolar surface of a new
host, it is attacked by macro phages, and one of two outcomes can
result: Macrophages kill the particles, terminating the infection, or
INFECTIOUS DISEASES
621
2.
3.
4.
5.
6.
*A person who has been exposed to the tubercle bacillus will demonstrate a
raised and reddened area 2 - 3 days after being injected with the protein derivative of the bacilli.
622
Anti-infective agents
Corticosteroids
INFEcnOUS DISEASES
623
Clinical Tip
Histoplasmosis
Histoplasmosis is a pulmonary and systemic infection that is caused
624
Anti-infective agents
Corticosteroids
Antihistamines
Legionellosis
Legionellosis is commonly referred to as Legionnaire's disease and is
an acute bacterial infection primarily resulting in patchy pulmonary
infiltrate(s) and lung consolidation. However, other organs may also
become involved, especially in the immunocompromised patient.
Legionellosis is transmitted by inhalation of aerosolized organisms
from infected water sources.
Primary clinical manifestations include high fever, malaise, myal
gia, headache, and nonproductive cough. Other manifestations can
also include diarrhea and other gastrointestinal symptoms. The dis
ease is rapidly progressive during the first 4-6 days of illness, with
complications that may include renal failure, bacteremic shock, and
respiratory failure. I,12,J2
Management of legionellosis may consist of the following' 1 2J2 :
Anti-infective agents
Cardiac Infections
Infections of the cardiac system can involve any layer of the heart
(endocardium, myocardium, and pericardium) and generally result in
acute or chronic depression of the patient'S cardiac output. Those
infections that result in chronic cardiomyopathy most likely require
cardiac transplantation. Refer to Chapters 1 and 12 for a discussion
o f cardiomyopathy and cardiac transplantation, respectively. This sec
tion focuses on rheumatic fever and resultant rheumatic heart disease.
INFE.cnOUS DISEASES
625
Anti-infective agents
Antipyretic agents
Corticosteroids
Bed rest
Neurologic Infections
Poliomyelitis
Poliomyelitis is an acute systemic viral disease that affects the cen
tral nervous system. Polioviruses are a type of enterovirus that
mulriply in rhe oropharynx and inrestinal rracr. There are rhree
serotypes of poliovirus, types 1, 2, and 3 respectively, with type 1
being the mOSt common cause of polio epidemics in certain areas
5
626
Bronchopulmonary hygiene
Postpoliomyelitis SY1ldrome
Postpoliomyelitis syndrome occurs 30-40 years after an episode of
childhood paralytic poliomyelitis. It results in muscle fatigue, pain,
and decreased endurance. Muscle atrophy and fasciculations may also
be present. Patients who are older or critically ill, who have had a pre
vious diagnosis of paralytic poliomyelitis, and who are female are at
greater risk for development of this syndrome.Js.J
Meningitis
Meningitis is an inflammation of the meninges, which cover the brain
and spinal cord, that results from acute infection by bacteria, viruses,
fungi, or parasitic worms, or by chemical irritation. The route of
transmission is primarily inhalation of infected airborne mucous
INFECfJOUS DISEASES
627
(2) Hae
Analgesics
I.
(e.g., dopamine)
E",;ephalitis
Ellcephalitis is an inflammation of the tissues of the brain and spinal
cord, commonly resulting from viral or amebic infection. Types of
encephalitis include infectious viral encephalitis, mosquito-borne viral
encephalitis, and amebic meningoencephalitis.
Infectious viral encephalitis is transmitted by direct contact of
droplets from respiratOry passages or other infected excretions and is
most commonly associated with the herpes simplex type 1 virus. Viral
encephalitis can also occur as a complication of systemic viral infec
tions, such as poliomyelitis, rabies, mononucleosis, measles, mumps,
rubella, and chickenpox. Manifestations of viral encephalitis can be
628
mild to severe, with herpes simplex virus encephalitis having the high
est mortality rate among all types of encephalitides.12.37. J8
Mosquito-bome viral encephalitis is transmitted by infectious mos
quito bites and cannOt be transmirred from person to person. The
incidence of this type of encephalitis can be epidemic in nature and
typically varies according to geographic regions and seasons.12.37.38
Amebic meningoencephalitis is transmirred in water and can enter
a person's nasal passages while he or she is swimming. Amebic menin
goencephalitis cannOt be rransmitted from person to person.
General clinical presentation of encephalitis may include any of the
following12.37.38,
Fever
Apha ia
Weakness
Hyperthermia
Anti-infective agents
indicated)
Sedation
INFEcnOUS DISEASES
629
Musculoskclctal lnfcctions
Osteomyelitis is an acute infection of the bone that can occur from
630
adjunct to the antibiotic therapy. If the infection has spread to the sur
rounding soft tissue and skin regions, then grafting, after debride
ment, may be necessary. Good results have also been shown with
Clinical Tip
Clarify weight-bearing orders with the physician when
performing gait training with patients who have any form
of osteomyelitis. Both upper and lower extremities can be
involved; therefore, choosing the appropriate assistive
device is essential to preventing pathologic fracture.
Skin Infections
Cellulitis, or erysipelas, is an infection of the dermis and the subcuta
neous tissue that can remain localized or be disseminared into the
bloodstream, resulting in bacteremia (rare). Cellulitis occurs most
commonly on the face, neck, and legs.
Groups A and G Streptococcus and S. aureus are the usual causative
agents for cellulitis and generally gain entry into the skin layers when
there are open wounds (surgical or ulcers). Patients who are at most
risk for developing cellulitis include those who are postsurgical and
immunocompromised from chronic diseases or medical treatment.
The primary manifestations of cellulitis are fever with an abrupt
onset of hot, stinging, and itchy skin and painful, red, thickened lesions
that have firm, raised palpable borders in the affected areas. Identifying
the causative agent is often difficult through blood cultures; therefore,
localized cultures, if possible in open wounds, may be more sensitive in
helping to delineate the appropriate antibiotic treatment.41-4 J
Gastrointestinal Infections
Gastroenteritis is a global term used for the inflammation of the
digestive tract that is typically a result of infection. The primary cause
of gastroenteritis is viral infection from rotavirus, adenovirus, astrovi
rus, calicivirus, and small round-structured viruses. Gastroenteritis
can also occur from bacterial infection from E. coli, Shigella (which
causes bacterial dysentery), Clostridium difficile, and Salmollella.
INFEcnOU5 DISEASES
631
foliowing'2.JL
of acute
gastroenteritis
may
consist
Anti-infective agents
of
the
Clinical Tip
Strict cOntact and enteric precautions should be observed
with patients who have a diagnosis of C.
dif{icile infection.
632
On entering the cell, the viral and cellular DNA combine, making
the virus a part of the cell. The exact pathogenesis of cellular destruc
tion caused by HIV is not completely understood, and several meth
ods of destruction may be entailed. It is known that immediately after
initial infection, HIV enters a latent period, or asymptomatic stage, in
which viral replication is minimal, but CD4' T cell counts begin to
decline.45 Continued reduction results in decreasing immunity, even
tually leading to symptomatic HN, in which diseases associated with
the virus begin to appear.4S This eventually leads to the onset of AIDS,
which the CDC defines as occurring when the CD4' T-Iymphocyte
COunt falls below 200 cells/Ill (normal, 650-1,200 cellS/ill) or below
14%, when 1 of 26 specific AIDS defining disorders is contracted, or
a combination of these factors.46
Five laboratory tests are available to detect HIV infection4748:
1.
Enzyme-linked immunosorbent assay or enzyme immunoassay test. This procedure tests for the presence of antibodies [0 HN
proteins in the patient's serum. A sample of the patient's blood is
exposed to H1V antigens in the test reagent. If HIV antibodies are
identified, it is inferred that the virus is present within the patient.
2.
Western blot test. This test detects the presence of antibodies in the blood to twO types of HIV viral proteins and is, therefore,
a more specific HIV test. It is an expensive test to perform and is
used as a confirmatory tool for a positive enzyme-linked immu
nosorbent assay test.
3.
Immunofluorescence assay. In this test, the patient's blood
is diluted and placed on a slide containing HIV antigens. The slide
is then treated with anti-human globulin mixed with a fluorescent
dye that will bind to antigen-antibody complexes. If a fluorescence
is seen when the specimen is placed under a microscope, then HIV
antibodies are present in the patient'S blood.
4.
p24 Antigen assay. This test analyzes blood cells for the
presence of the p24 antigen located on HN virions. It can be used
to diagnose acute infection, to screen blood for HIV antigens, to
determine HIV infection in difficult diagnostic cases, or to evaluate
the treatment effects of antiviral agents.
5.
Polymerase chain reaction for HIV nucleic acid. This highly
specific and extremely sensitive test detects the viral DNA molecule
INFECfIOUS DISEASES
633
634
that result directly from the virus, often result in multiple diagnoses
and medically complex patients. These manifestations of HIV can
affect every system of the body and present with a wide array of signs
and symptoms, many of which are appropriate for physical therapy
intervention. Table 10-5 lists common manifestations and com plica
rions of HIV and AIDS and the medications generally used in their
management.
Disorders affecting rhe nervous sysrem include HIV-associared
dementia complex, progressive multifocal leukoencephalopathy, pri
mary central nervous system lymphoma, toxoplasmosis, and neu
ropathies. These manifestations may cause paresis, decreased
sensation, ataxia, aphagia, spasticity, altered mental status, and
visual deficits 50 In the pulmonary system, TB, cytomegalovirus
(CMV), and pneumonia can result in cough, dyspnea, sputum pro
duction, and wheezing.51 In the cardiac system, cardiomyopathy,
arrhythmias, and congestive heart failure can cause chest pain,
dyspnea, tachycardia, tachypnea, hypotension, fatigue, peripheral
edema, syncope, dizziness, and palpitations.52
Physical therapy intervention can assist in minimizing the effect of
these deficits on functional ability, therefore helping to maximize the
independence and quality of life of the individual. However, the course
of rehabilitation in HIV-affected individuals can often be difficult
owing to coinciding opportunistic infections, an often-rapid downhill
disease course, low energy states, and frequent hospitalizations.
Mononucleosis
Mononucleosis is an acute viral disease that has been primarily linked
to the Epstein-Barr virus and less commonly to CMV. Mononucleosis
is transmitted generally through saliva from symptomatic or asymp
tomatic carriers (the Epstein-Barr virus can remain infective for 18
months in the saliva).12,5 3
The disease is characterized by fever, lymphadenopathy (lymph
node hyperplasia), and exudative pharyngitis. Splenomegaly, hepati
tis, pneumonitis, and central nervous system involvement may occur
as rare complications from mononucleosis. The infection is generally
self-limiting in healthy individuals, with resolution occurring in
approximately 3 weeks without any specific rreatment.12.53
INFFcrlOUS DISEASES
635
Medication
Cardiomyop.lthy
Cerebral toxoplasmosis
Trimcthoprim-sulfamethoxazole
Coccidioidomycosis
Cryptococcral meningitis
Amphotericin B or fluconazole
Cytomegalovirus
neuropathy
Herpes simplex
HIV-associared demen-
tia complex
Histoplrasl11oslS
Amphotencln B or irraconazole
KJpmi's arcoma
Lymphomas
Mycob,ulermlU aumm
complex
P,zeumocystls ca",,,,
pneumomll
Progressive multifocal
leukoencephalopathy
Pulmonary hypertension
636
Table
10-5. COllt"med
Complication
Medication
by certain medications
Tuberculosis
ton, D Talona, K Zwolskl (cds). llandbook of 11IV/AIDS Nur\lI1g. \1. LoUIs: .\losby.
2001;262,266.270; K Zwolskl. Paramic Infccllons.ln CA KIrton. DT'llona. K
Cytomegalovints IIt(echolt
CMV is a member of the herpesvirus group [hat can be found in all
body secretions, including saliva, blood, urine, feces, semen, cervical
secretions, and breast milk. CMV infection is a common viral II1fec
tion that is asymptomatic or symptomatic. ClV infection can remain
latent after the initial introduction into the body and can become
opportunistic at a later point in time.
INFEcrJOUS DISEASES
637
Antiviral agents
Corticosteroids
Immune globulins
Antipyretics
Toxoplasmosis
Toxoplasmosis is a systemic protozoan infection caused by the para
site Toxoplasma gOlldii, which is primarily found in cat feces. Trans
Sepsis
Sepsis is
shock).!!
638
Anti-infective agents
i. v. fluids
Blood transfusions
Cardiac glycosides
Anticoagulation
Management
Medical/llteroelltion
INFECfIQUS DISEASES
639
640
References
1. Smeltzer SC, Bare BG. Brunner and Suddanh's Textbook of Medical
Surgical Nursing (7th cd). Philadelphia, Lippincott, 1992.
2. Thomas CL (ed). Taber's Cyclopedic Medical Dicrionary (17rh cd). Phil
adelphia, Davis, 1993.
3. Goodman CC, Snyder TEK. Differential Diagnosis in Physical Therapy,
Musculoskeletal and Systemic Conditions. Phihldelphia: Saunders,
1995.
4. Kent TH, Hart MN (eds). Introducdon to Human Disease (4th cd).
Sramford CT, Appleron & Lange, 1998;21-30.
5. Gorbach SL, Barrlett jG, Blacklow NR (cds). Infecrious Diseases. Phila
delphi., Saunders, 1992.
6. Delost MD. Introduction to Diagnostic Microbiology: A Text and
Workbook. Sr. Loui" Mosby, 1997;1-9.
7. Malarkey LM, McMorrow ME (cds). Nurse's Manual of Laboratory
Tests and Diagnostic Procedures (2nd cd). Philadelphia: Saunders,
2000;49-81.
8. Linne J], Ringsurd KM (eds). Clinical Laboratory Science: The Basics
and Rourine Techniques. Sr. Loui" Mosby, 1999;669-699.
9. Linne jj, Ringsurd KM (eds). Clinical Laborarory Scienc", The Basics
and Rourine Techniques. Sr. Louis, Mosby, 1999;597-667.
10. Isenburg HD. Clinical Microbiology. In SL Borback, jG Barrlett, NR
Blacklow (eds), Infecrious Diseases. Philadelphi., Saunders, 1998;\23145.
11. Anderson KN (ed). Mosby's Medical, Nursing, and Allied Healrh Dic
rionary (4rh ed). Sr. Loui" Mosby, 1994.
12. Thompson jM, McFarland GK, Hirsch jE, er al (cds). Mosby's Manual
of Clinical Nursing (2nd cd). Sr. Loui" Mosby, 1989.
13. Malarkey LM, McMorrow ME (eds). Nurse's Manual of LaboratOry
Tests and Diagnostic Procedures (2nd cd). Philadelphia: Saunders,
2000;337-339.
lNfFcnOUS DISEASES
641
642
30.
3'1.
32.
33.
34.
35.
36.
37.
38.
INFEcnOUS DISEASES
643
Appendix 1 0-A:
Disorders of Altered Immunity
646
Raynaud's phenomenon
Sarcoidosis
Sarcoidosis is a systemic disorder that primarily affects women and
nonwhite adults in the third decade of their life. The definitive etiol
ogy is unknown, although an autoimmune process that is environ
memally triggered is the generally agreed on hypothesis. Sarcoidosis
may have periods of progression and remission. [,5-7
The lungs are the primary organs affected by sarcoidosis, with dysp
nea, dry cough, and chest pain being common symptoms. Pulmonary
involvement can be staged according to radiographic evidence"" :
Stage O-no radiographic abnormalities
Stage I-bilateral hilar lymphadenopathy
Stage II-bilateral hilar adenopathy and parenchymal infiltration
Stage Ill-parenchymal infiltration without hilar adenopathy
Stage IV-advanced fibrosis with evidence of honey-combing, hilar
retraction, bullae, cysts, and emphysema
Orher systems of the body can be affected as well, including the
following:
Hepatosplenomegaly
Arthralgia, arthritis
647
Amyloidosis
Tongue
Heart
Gastrointestinal tract
Liver
Spleen
Kidney
Peripheral nerves
Pancreas
Cerebral vessels
Skin
648
References
1. Bullock BL. Pathophysiology: Adaprarions and Alrerarions in Funcrion
(4th cd). Philadelphia: Lippincott, 1996.
2. Kimberly RP. Research advances in systemic lupus erythemarosus.
JAMA 2001;285(5):650.
3. McConnell EA. Abour sysremic lupus erythemarosus. Nursing 1999;
29(9):26.
4. Wallace OJ. Updare on managing lupus erythemarosus. J Musculoskele
tal Med 1999;16(9):531.
5. Chandrasoma P, Taylor CR. Concise Pathology (2nd ed). East Norwalk,
CT: Appleton & Lange, '995.
6. Morey 55. American Thoracic Society issues consensus statement on
sarcoidosis. Am Fam Physician 2000;61(2):553.
7. Johns CJ, Michele TM. The clinical management of sarcoidosis a 50year experience ar the Johns Hopkins Hospiral. Medicine 1999;
78(2):65.
8. Goodman ec, Snyder TEK. Differential Diagnosis in Physical Therapy:
Musculoskeleral and Systemic Conditions. Philadelphia: Saunders,
1 995.
11
Endocrine System
Jaime C. Paz
lntroduction
649
650
Hypothalamic
Nudei
PItuitary Gland
Adrenal
.....ll
.. --7'-' (Iuprarenal)
Glandl
0,,,..,
-+---f,I'M-I
ENDOCRINE SYSTEM
65]
Piruitary
a. Are menses regular? (If they are irregular, hypopituitarism
may be suspected.)
b. Has rhere been a change in vision? (Large piruitary tumors
can result in vision loss.)
2.
Adrenal
a. Is rhere skin darkening? (Chronic primary adrenal insuffi
ciency results in hyperpigmentation.)
b. Is there weight loss, nausea, vomiting, or syncope? (These
are suggestive of adrenal insufficiency.)
c. Have there been episodes of tachycardia, headaches, and
sweating? (These are suggestive of pheochromocytoma.)
3.
Thyroid
a. Is there a change in the patient'S neck size? (This can indi
cate the presence of goiter or hyperthyroidism.)
b. What is the room-remperature preference of the patient?
(60F suggests hyperthyroidism, whereas 80F suggests
hypothyroidism.)
4.
Parathyroid
a. Is there a history of thyroid surgery? (This is the usual
cause of hypoparathyroidism.)
b. Are kidney stones, polyuria, and constipation present?
(This could indicate hypercalcemia from hypoparathyroidism.)
652
5.
Pancreas
a. Is there nocturia or nocridipsia (urination or drinking at
night, respectively)? (Soth of these can suggest diabetes mellitus.)
b. Has there been a weight loss or gain and increased appe
tite? (These also suggest diabetes.)
Clinical Tip
An imbalance of hormone levels may affect the patient's
tolerance to activity. Familiarity with the endocrine tests
and values can help the clinician gauge the intended treat
ment parameters (i.e., type, duration, and intensity) for the
next session(s).
ENDOCRINE SY5fEM
653
Thyroid Gland
Function
Thyroid Tests
Thyroid hormones T4 and T3 circulate throughout the bloodstream
bound to proteins (approximately 99%) or unbound, in which case
Target Site(s)
Actions
Thyroxine (T4)
Systemic
and triiodothy
ronine (T3)
Thyrocaicicollin
Bone
Sources: Data from SF Fuller. Anatomy and Physiology of the Endocrine System. In
eM Hudak, 8M Gallo (eds), Critical Care NurSing: A Holistic Approach (6th ed). Phil
adelphia: Lippincott,1994;75; M Harrog (cd). Endocrinology. Oxford. UK: Blackwell
Scientific, 1987;23; and JV Corbect. Laboratory Tests and Diagnostic Procedures with
Nurslllg Diagnoses (5th cd). Upper Saddle River, NJ; Prentice Hall Health, 2000;409.
654
Test Description
Normal Value
Serum thyroxine
Radioimmunoassay
4-12 gldl
(RIA) measuremelll.
Serum triiodo
RIA measuremcnt.
40-204 ngldl
thyronine
Free thyroxine indcx
ment or indirect
calculated measure
memo
Thyroid-stimulating
Radioisotope and
0.4-8.9 pU/ml
chemical bhelmg
hormone (TSH)
measurcment.
Thyrotropin-releasing
hormone (TRH)
TRH augments the
function of TSII
Intravenous admll1is
tration of TRH to
patients.
The expected
in patients with
response is a rise in
hypothyroidism.
TSH levels.
Only performed
111
difficult diagnos
ric cases.
IS
2 U/
Hypothyroidism is mdi
cated by Increased
response to TRH.
Hypcrrhyroidism is indi
cated hy no response to
TRH.
Sources: Data frolll WM Burch (cd). Endocrinology for Ihe House Officer (2nd cd).
Baltimore: Williams & Wilkins, 1988; 1: JV Corbett (cd). LaboratOry Te:.t!. and Dla{t
nosric Procedures with Nursing Diagnoses (5th cd). Upper Saddle River. NJ: Prentice
ENDOCRINE. SYSTEM
655
Description
Triiodothyronine
resin uptake
(RT3U)
Thyroidal 24hr
radioactive
iodine uptake
Thyroid imaging
or scan
Ultrasound
Needle biopsy
Sources: Data from WM Burch (ed). Endocrinology for the House Officer (2nd ed).
Baltimore: Williams & Wilkins, 1988;1; M Harrog ted). Endocrinology. Oxford, UK:
man's Clinic<ll lmcrprctarion of L3borarory Tests (1, Ith ed). Philadelphia: FA Davis.
2000;786-793.
Clinical Tip
Low levels of thyroid hormones T3 or T4 may result in
weakness, muscle aching, and stiffness. Based on this
information, the physical therapist may decide to alter
treatment parameters by decreasing the treatment intensity
to optimize activity tolerance, minimize patient discom
fort, or both.
656
Thyroid Disorders
Disorders of the thyroid gland result from a variety of causes and can
be classified as hyper- or hypothyroidism.
Hyperthyroidism
Hyperthyroidism, or thyrotoxicosis, is characterized by excessive
sympathomimetic and catabolic activity resulting from overexposure
of tissues ro thyroid hormones. The most common causes of hyper
thyroidism are outlined in Table 11-4.
General signs and symptOms of hyperthyroidism include rhe
foIlO\vingl ,6:
Heat lmolerance
Diarrhea
Menstrual dysfunction
Presence of goiter
Tremor
Thyroid bruit
ENOOCRINE SYSTEM
657
Description
Graves' disease
Thyroiditis
Thyroid carci
noma
Exogenous hyper
thyroidism
Ecropic thyroid
hormone pro
duction
occurrence).
Sources! Data from WM Burch (cd). Endocrinology for the House Officer (2nd cd).
Bahimore: Williams & Wilkins, 1988;126; and N Woolf (cd). Pathology, Basic and Sys
temic. London: Saunders, 1998;863-873.
658
AClJTE
Radioiodine-131
Hypothyroidism
Hypothyroidism is the insufficient exposure of peripheral tissues to
thyroid hormones. It affects growth and development, as well as
many cellular processes. In the majority of cases, hypothyroidism
is caused by decreased thyroid hormone production rather than
the failure of tissues to respond to thyroid hormones. Primary
hypothyroidism refers to thyroid gland dysfunction, whereas sec
olldary hypothyroidism refers to pituitary disease resulting in
reduced TSH levels.
The following are the causes of primary and secondary hypo
thyroid ism 7IO:
ENDOCRINE SYSTEM
659
Paresthesia
Cardiac failure
Pericardial effusion
660
Clinical Tip
Properly managed hyper- or hypothyroidism should not
affect physical therapy intervention or activity tolerance. If
the signs or symptoms mentioned above are present during
physical therapy evaluation, treatment, or both, consulta
tion with the medical team is indicated to help differenti
ate the etiology of the physical findings. See Screening for
Metabolic and Endocrine Dysfunction for more informa
tion on screening.
Pituitary Gland
Function
Pituitary Tests
ENDOCRINE SYSTF.
661
Acrion(s)
Systemic
Liver
Formation of somatomedin
ThyrorroplIl
Th),roid
Adrenocorricorropln
Adrenal correx
Foiliclestimulating
Ovaries
Testes
Development of seminifer
Hormone(s)
Anterior lobe
Growth hormone
hormone
Ovaries
lating hormone
of progesterone
Prolacrll1 or lacroge
nic hormone
l\Iclanocyte-srimu
Testes
Secretion of tesrosterone
Mammary
Secretion of milk
glands
Skin
Pigmentation
Kidney
Reabsorption of water
lating hormone
Postcrior lobe
Amidlllretic hor
l,asopressin)
Oxytocin'"
Artenoles
Uterus
Contraction
Breast
Expression of milk
III
Sources; Dala from BF Fuller. Anatomy Jnd PhYSiology of the Endocrine System. In
eM Hudak. IM Gallo (eds). Critical Care Nursing: A HolistIC Approach (6th ed). Phil
662
Test Description
Growth hor
mone (GH)
normal values for men are 0-5 nglml; for women, 0-\0
nglml.
Growth hormone stimttlat;on test (arginine tcst or insulin
tolerance test). Indicated for children with retarded
growth and if pituitary tumor is suspected. A baseline
level of GH is established, then arginine or insulin is
administered to the patient, and serial blood draws are
performed to measure GH levels. GH should normally
rise. Decreased GH values, despite stimulation, could
indicate pituitary dwarfism or tumors.
Growth hormone suppression test (glucose load test).
Indicated to confirm diagnoses of gigantism in children
and acromegaly in adults. A baseline level of GH is
established, followed by patient ingestion of a glucose
solution. After 1-2 hrs, levels of GH are remeasured.
Normally, glucose inhibits the secretion of GH. If GH
levels remain high despite the glucose load, then gigan
tism or acromegaly can be confirmed.
Adrenocortico
tropic hor
mone
(ACTH)
Antidiuretic
hormone
(ADH or
vasopressin)
(01).
E.NDOCRINE. SYSTEM
Hormone(s)
663
Test Description
with 01, the osmolality remains unchanged. While
the patient is being deprived of water, vasopressin
may be administered to help delineate whether the
DI is caused by piruitary or renal dysfunction.
Water loading test. Indicated for diagnosing syndrome
of inappropriate anridiureric hormone (SIADH).
During the tesr, the patienr ingests 20-25 mUkg of
fluid, with hourly serum and urine osmolaliry levels
being measured for 4 hrs. Normally, with water
ingesrion, the plasma and urine osmolality should
decrease, and urine output should increase. With
SIADH, there is little or no change in these values.
Pih,itary Disorders
Dysfunction of the pituitary-hypothalamic system generally results
from hyper- or hyposecretion of tropic hormones. Hypersecretion of
pituitary hormones (hyperpituitarism) is most commonly due to benign
anterior pituitary tumors. Hyposecretion of pituitary hormones (pitu
itary insufficiency) can result from pituitary disease, diseases affecting
the hypothalamus or surrounding structures, or disturbance of blood
Aow around the hypothalamus and pituitary.'2,13
Hyperpituitarism
The overproduction of the pituirary hormones GH, ACTH, and
antidiuretic hormone (ADH) is discussed below.
Growth Hormone Ouerproductioll
The most common presentation of excessive GH secretion is acro
megaly in adults or gigantism in children. Excessive GH secretion has
been linked primarily to anterior pituitary adenomas and not neces
sarily from excessive hypothalamic stimulation of the pituitary.13
Signs and symptoms of acromegaly include the following113:
Enlargement of hands and feet, coarse facial features with fur
rowed brows
664
Sweating
Headaches
lmpotence in men
Diabetes mellitus
Hypertension
Clinical Tip
Given the multisystem effects in patients with acro
megaly, activity progression should proceed cautiously,
with a focus on energy conservation and joint protec
tion techniques.
Adrenocorticotropic Hormone Overproduction
An increase in ACTH production by the pituitary gland results in
increased levels of serum cortisol, which is a glucocorticoid secreted
by the adrenal glands. Glucocorticoids are involved with carbohy
drate, protein, and fat metabolism; therefore, excess cortisol levels
affect these cellular processes. Any clinical syndrome that results in
glucocorticoid excess is called Cushing's syndrome. Cushillg's disease,
however, is specific to pituitary lesions that cause bilateral adrenal
hyperplasia and is not discussed in this chapter.' Pituitary hypersecre
tion of ACTH occurs in approximately 70% of the patients with
Cushing's syndrome. The hypersecretion of ACTH is mainly from
pituitary adenomas or microadenomas.6
Signs and symptoms of Cushing's syndrome include the following"., '.13:
ENDOCRINE SYSTEM
665
Hypertension
Backache
Glucose intolerance
Clinical Tip
Management of weakness, myopathy, pain, edema, and
osteoporosis should be the focus of physical therapy inter
vention and be complementary to the medical manage
ment of the patient. Blood pressure changes during activity
should be monitored, given the possibility of hypertension.
Caution should also be taken to avoid bruising during
mobility. Refer to Diabetes Mellitus for further activity
considerations.
Antidiuretic Hormone Overproduction
The syndrome of inappropriate secretion of ADH (SIADH) is a condi
tion of fluid and electrolyte imbalance resulting in hyponatremia
(reduced sodium levels) from excessive water reabsorption. In this
condition, ADH is secreted from the posterior pituitary when it
should be inhibited.
Numerous etiologies of SIADH exist, with the most frequent cause
being small cell or oat cell carcinomas of the lung. Other etiologies
include the following'15:
666
Clinical Tip
The physical therapist should be aware of fluid restriction
guidelines for patients with SIADH, especially because
activity during physical therapy may increase the patient's
thirst. These guidelines are often posted at the patient's
bedside.
Hypopituitarism
There are numerous causes for primary (pituitary directly affected) or
secondary (hypothalamus or pituitary stalk affected) hypopituitarism.
The most common causes of primary hypopituiatarism are piruitary
neoplasms, such as pituitary adenomas and craniopharyngioma, and
ischemic necrosis occurring during the late stages of pregnancy (Shee
han's syndrome). Common causes of secondary hypopituitarism
include hypothalamic tumors, cranial trauma, sarcoidosis, surgical
destruction of the pituitary stalk, or a combination of these.6lJ, 1 6.17
ENDDCR[NE SYSTEM
667
Hypogonadism
Dilutional hyponatremia
Hypothyroidism
Glucocorticoid deficiency
Diabetes Insipidus
01 involves the excretion of a large volume (i.e., greater than 30
ml/kg per day) of dilute urine (hyporonic polyuria). 01 may result
from hypothalamic, pituitary, renal, or psychogenic disorders;
however, most incidences of DI are described as idiopathic,6.ls
Piwirary DI involves the failure to synthesize or release vaso
pressin (AOH). Renal, or nephrogenic, OJ is a deficiency of vaso
pressin receptors in the renal collecting ducts. Psychogenic or
dipsogenic OJ involves a large intake of fluid that may suppress
ADH secrcrion.781I,18
Signs and symproms of OJ may be transient or permanent and
include the following7,8,[6. [8:
Polyuria, nocruria
668
Dehydrarion
Weighr loss
Adrenal Gland
Function
The adrenal gland has two distinct areas, the outer correx and the
inner medulla, that differ in their function and embryologic ori
gin.- Table 11-7 summarizes the target sites and actions of the
adrenal gland.
Adrenal Tests
Evaluation of the adrenal cortical (glucocorricoids, androgens, and
mineralocorticoids) and medullary (epinephrine and norepinephrine)
hormones is described below. Anatomic investigation of the adrenal
glands may also be performed to diagnose possible adrenal dysfunc
tion. Common methods to accomplish this are computed tomography
scan (to identify adrenal tumors), radioisotope scan using seleno-cho
lesterol, ultrasound, arteriogram, adrenal venogram (allows measure
ments of hormone levels), and intravenous pyelogram (see Diagnostic
Tests in Chapter 9).",20
ENDOCRINE SYSTE..\1
669
Target site(s)
Action(s)
Kidney
Cortex
Mineralocorticoids
water
(aldosterone)
Elimination of potassium
Glucocorticoids
Systemic
Metabolism of carbohydrate,
protein, and fat
(cortisol)
Response to stress
Suppresses immune responses
Anti-inflammarion
Sex hormones
Systemic
(androgens.
progesterone,
acteristics
and estrogen)
Medulla
Epinephrine
Cardiac and
smooth muscle,
glands
Norepinephrine
Organs innervated
by sympathetic
nervous system
Emergency functions
Stimulates the action of the
sympathetic system
Chemical transmitter sub
stance
Increases peripheral resistance
Sources: Data (rom BF Fulle r. Anatomy and Physiology of the Endocrine System. In CM
Hudak, BM Gallo (cds), Critical Cllfe Nursing: A Holistic Approach (6th ed). Philadelphia:
Uppincort, 1994;875; and JV Corbcn (ed). L'lboratory Tests and Diagnostic Procedures
with Nursing Diagnoses (5th cd). Upper Saddle River, NJ: Prentice I-Iall l-le.'l lt h , 2000;391.
Clucocorlicoids
Glucocorticoids can be evaluated by testing serum and urine cortisol
levels, 24-hour urinary corticosteroids, or ACTH. Altered glucocorti
coid levels can affect protein and carbohydrate metabolism.
670
ACTH levels are usually examined concomitantly with cortisol levels, as ACTH secretion from the pituitary gland is necessary for
cortisol secretion from the adrenal glands. Refer to Table 1 1-6 for
details on ACTH measurement.
Androgens
Individual androgen levels can be measured by RIA in the serum or by
metabolic products (17-ketosteroids) in the urine. I High concentra
tions of androgens may result in the following changes in women:
Hirsutism, which is excessive hair growth in skin zones consid
ered male in distribution (i.e., upper lip, side burns, chin, neck,
chest, and lower abdomen)
Amenorrhea, which is the absence of menstruation in women
older than 16 years of age or the absence of menses for longer than
6 months in women of childbearing age who previously had been
menstruating
Voice change
Milleralocorticoids
Mineralocorticoids can be evaluated by testing serum electrolyte lev
els or plasma renin activity and aldosterone levels.11 Abnormalities of
serum electrolyte levels, such as an increased potassium level, provide
a valuable screening tool for mineralocorticoid secretion disorders.
Aldosterone is the primary mineralocorticoid and is controlled by the
renin-angiotensin system. A rise in serum potassium and angiotensin
II results in aldosterone sectetion, which helps to balance Auid and
electrolyte levels. Blood samples of aldosterone are usually taken first
in the early morning, while the patient is still recumbent, and then
again after 4 hours of being awake and active. Normal serum levels of
ENDOCRINE SYSTEM
671
Metabolic Tests
Metabolic tests are described in this section, as glucocorticoids (corti
sol) affect carbohydrate, protein, and fat metabolism.
Glucose Toleral/ce Test
A glucose tolerance test was primarily used to diagnose diabetes mel
litus; however, because of many confounding variables, it is currently
not relied on to establish diabetes mellitus, but rather to help confirm
the diagnosis in certain cases. However, the glucose tolerance test is
the primary method of establishing the diagnosis of gestational diabe
tes mellirus.4.6
To perform the test, a 75- or 1 00-g glucose load is given to the
subject in the morning after a l O-hour fast. Blood glucose levels are
then measured at variable time periods, ranging from every half
hour to every hour for the next 2 to 5 hours after the glucose admin
istration. The subject must remain inactive and refrain from smok
ing throughout the duration of the test. Normally, the blood glucose
levels should fall back to baseline values after a 2-hour period. Nor
mal glucose value for a fasting blood sugar (BS) is approximately
70-1 1 0 mgldl.'4 .6
672
Adrenal Disorders
Adrenal Insufficiency
Autoimmune dysfunction can lead to destruction of the adrenal cor
tex (i.e., primary adrenal insuf(iciellcy Ot Addisoll's disease). Addi
tionally, ACTH deficiency from the pituitaty gland can lead to
atrophy of the adrenal cortex (secondary adrellal il1sllf(iciellcy). The
net result is an impaired adrenal system with decreased levels of glu
cocorticoids (cortisols), mineralocorticoids (aldosterone), and andro
gens. Given the systemic functions of these hormones, Addison's
disease can have severe consequences if left untreated. Fortunately,
the incidence is rare.
Cortisol deficiency results in decreased gluconeogenesis (glucose
production), which in turn alters cellular metabolism. Decreased glu
coneogenesis also results in hypoglycemia and decreased ability ro
respond to stress. A ldosterone deficiency causes fluid and electrolyte
imbalance, primarily as a result of increased water excretion that
leads ro dehydration B."
The following are symproms and physical findings common ro
adrenal insufficiency l .6.25 :
Weakness, fatigue
Hyperpigmentation
Hypotension
ENDOCRINE SYSTEM
673
rinc. The occurrence is equal between men and women during their
twenties and thirties. Given the rare occurrence of this tumor, it often
goes undiagnosed. However, proper diagnosis is essential, as the sus
tained release of catecholamines can be life threatening. Early diagno
sis generally has favorable results. 6,25,27
Signs and symptoms of pheochromocytoma may include the
following 1.23.25.27:
Hypertension (sustained or paroxysmal), palpitations, tachycar
dia, and orthostatic hypotension
Excessive perspiration
Pancreatic Disorders
Diabetes Mellitus
Diabetes mellitus is a syndrome with metabolic, vascular, and neural
674
to
200 mgt
Meal planning.
ENDOCRINE SYSTEM
675
Description
Self-monitoring
Blood glucose fin
ger stick samples
Reference, 60-110
mgldl
Medical monitoring
Hyperglycemia results in saturation of hemoglobin
Glycosyl.ted
hemoglobin
(GHB)
Reference, 7.5-
11.4% of toral
hemoglobin for
a patient with
controlled
diabetes
Fructosamine or
glycated protein
Reference, 300
mmolliiter
excellent dia
betic control
Sources: Data from JV eorbert (ed). Laboratory Tests and Diagnostic Procedures with
Nursing Diagnoses (5th cd). Upper Saddle River, NJ: Prentice Hall Heahh, 2000; 192197; LM Malarkey, ME McMorrow (eds), Nurse's Manual of Laboratory Tesrs and
Diagnostic Procedures. Philadelphia: Saunders, 2000;577-580; and RA Sacher, RA
McPherson, JM Campos (eds). Widman's Clinical Interpretation of Laborarory Tests
(II ,h cd). Phil,delphiao D,vis, 2000;817-818.
676
Patient
candidacy
Pump desctiption
to
Pump
complications
[0
lin infusion. Clin Diaberes 1999; 17(3): I 13; Conrinuous subcmancolls insulin. Diabetes
Carc 2001;24( 1 ):598; and FR Kaufman, M Halvorson, C Kim, P Pitukcheew:mollt. Use
of insulin pump therapy at nighttimc only for children 7-10 years of age with rype 1
diabetes. Diabetes Care 2000;123(5):579.
ENDOCRINE SYSTEM
677
Clinical Tip
Type 2 Diabetes
Type 2 diabetes is more common in the United States than type 1
betes and generally occurs afrer 40 years of age. Type 2 diabetes is sig
nificantly linked to obesity, a sedentary lifestyle, and aging. Genetic
predisposition has also been established.3o.JI. 3J
678
Genital pruritus
Visual changes
Paresthesias
ENDOCRINE SYSTEM
679
Clinical Tip
680
Myalgia, hypotonia
Headache
Anorexia
Hypothermia
Uncoordinated movements
Hyporeflexia
ENDOCRINE SYSTEM
681
682
Do
Smoke.
Walk barefoot.
stockings.
\'(Iear sandals with thongs between
the roes.
Wear socks or stocking with raised
seams.
Place hands in shoes for inspection,
ENDOCRINE SYSTEM
683
SymptOms
Signs
Peripheral sensory
Paresrhcslas, numbness,
polrneuroparh),
Symmetric poly
neuropathies
Impairmem of vibration
sense in feet
Foar ulcers (often over
metatarsal heads)
worse at night
rcriphcTal motor
\Veakness
neuropathy
Bilateral imerosseous
muscle atrophy, claw
or hammer roes,
decreased grip
strength, decreased
manual muscle test
grades
Autonomic neu
roparhy
Constipation or diarrhea,
nausea or vomiting,
Incontinence, ortho
static hypotension,
tremulousness, Impo
tachycardia, periph
tence, dysphagia
684
Symproms
Signs
Palpebral prosis
Inward deviation of
one eye
Peripheral nervc-specific
or lancinating pain
motor loss
in trunk or abdomen
Cutaneous hyperesthesia
of the trunk
Proximal moror
Asymmetric proximal
neuropathy or
diabetic amyo
trophy
depression
Absent or diminished
weakness
knee jerk
Sources: Data fromJS Boissonault, D Madlon-Kay. Screening for Endocrine Syslem DIS
ease. In we Boissonauh (ed), Examination 111 Physical Therapy: Screening for Medical
Disease. New York: Churchill LivingstOne, 1991; 159; PA Melvin-Sater" Diabetic neurop"
:lthy. Physician Assistant 2000j24(7):63; and
CO Saudek.
DB Hellmann, PW L1.denson, Ct al. (cds), The PrinCiples and Practice of Medicine (23rd
cd). Stamford Cf: Appleton & L1.nge, 1996; 330.
Immunotherapy
Pancreatic transplant
Stroke
See Cerebrovascular Accident in Chapter 4 for a discussion of stroke.
Peripheral Vascular Disease
See Atherosclerosis in Chapter 6 for a discussion of peripheral vascu
lar disease.
ENDOCRINE SYSTEM
685
Nephropathy
See Chapter 9 for a discussion of nephropathy.
Hypoglycemia (Hyperinsulinism)
Hypoglycemia is a state of decreased BS levels. Excess serum insulin
results in decreased BS levels, which leads to symptoms of hypoglyce
mia. Causes for this imbalance of insulin and sugar levels can be
grouped as (1) fasting, (2) postprandial, or (3) induced.
Fastillg hypoglycemia occurs before eating and can be caused by an
insulin-producing islet cell tumor, liver failure, chronic alcohol inges
rion, GH deficiency, exrrapancrearic neoplasm, or leucine. Ir can also
occur in infants with morhers who have diabetes.
Postprandial hypoglycemia occurs after eating and can be caused
by reactive hypoglycemia (inapptopriate insulin release afrer a meal),
early diabetes mellitus, or rapid gastric emptying.
Hypoglycemia can also be induced by external causes, such as
exogenous insulin or oral hypoglycemic overdose.6,s
Signs and symptoms of hypoglycemia may include the following:
Hunger
Weight changes
Headache
Seizures
Dizziness
Visual disturbance
Loss of consciousness
686
Parathyroid Gland
FUlIctioll
Parathyroid hormone (PTH) is the primary hormone secreted from
the parathyroid gland. The target sites are the kidneys, small intestine,
and bone. The primary function of PTH is to raise blood calcium lev
els by mobilizing calcium that is stored in bone, increasing calcium
reabsorption from the kidneys, and increasing calcium absorption
from the small intestine.'45
Parathyroid Tests
Description
Serum calcium
Parathyroid hormone
Radioimmunoassays and urinalysis are lIsed to measure pararhyroid hormone levels. Reference value
is 10-60 pglml.
Sources: Data from WM Burch (ed). Endocrinology for rhe House Officer (2nd cd).
Balrimore: Williams & Wilkins, 1988; JV Corberr (cd). Laborarory Tesrs and Diag
nostic Procedures with Nursing Diagnoses (5th cd). Upper Saddle River, NJ: Pren
tice Hall Health, 2000;167-176; and RA Sacher, RA McPherson,JM Campos (eds).
Widman's Clinicallmerpretarion of Laboratory Tests (11 th cd). Philadelphia: FA
Davis,2000j803-804.
ENDOCRINE SYSTEM
687
Paratllyroid Disorders
Hyperparathyroidism
Hyperparathyroidism is a disorder caused by overactivity of one or
more of the parathyroid glands that leads to increased PTH levels,
resulting in increased blood calciulll level, decreased bone mineraliza
tion, and decreased kidney function. This disorder occurs more fre
quently in women than in men. Radiation therapy is also a risk factor
for developing this disorder46
Hyperparathyroidism can be classified as primary, secondary, or
tertiary. Primary hyperparathyroidism represents the most cases and
usually results from hyperplasia or an adenoma in the parathyroid
gland(s). Secondary hyperparathyroidism results from another organ
system disorder, such as renal failure, osteogenesis imperfecta, Paget's
disease, multiple myeiOlna, lymphoma, or bone metastases from pri
mary breast, lung, or kidney tumors. Tertiary hyperparathyroidism
occurs when PTH secretion is autonomous despite normal or low
serum calcium levels.6.23.47
The primary clinical manifestations of hyperparathyroidism
are hypercalcemia and hypercalciuria (calcium in urine). Hyper
calcemia may then result in the following cascade of signs and
symptoms23.4 6.47:
688
Fluid replacement
Hypoparathyroidism
Hypoparathyroidism is a disorder caused by underactivity of one or
more of the parathyroid glands that leads to decreased PTH levels.
Decreased levels of PTH occur most commonly as a result of damage
to the parathyroid glands during thyroid or parathyroid surgery. Less
common causes may include radiation-induced damage, infiltration
by metastatic cells, and autoimmune dysfunction.23,4 7
Signs and symptOms of hypoparathyroidism may include the
following23:
Hypocalcemia
Laryngospasm
Dysrhythmias
Convulsions
Cataracts
ENDOCRINE SYSTEM
689
690
Clinical Tip
ENDOCRINE SYSTEM
691
Osteomalacia
Osteomalacia, or rickets in children, is a disorder characterized by
decreased bone mineralization, reduced calcium absorption from the
gut, and compensatOry hyperparathyroidism. The etiology of osteo
malacia stems from any disorder that lowers serum levels of phos
phate, calcium, or vitamin 0.1147
Predisposition
Proximal myopathy
Waddling gait
to
thigh)
692
Administration of calcitonin
Promotion of mobility
Adequate hydration
Management
Clinical management of endocrine dysfunction is discussed earlier in
specific endocrine gland and metabolic disorders sections. This sec
tion focuses on goals and guidelines for physical therapy intervention.
The following arc general physical therapy goals and guidelines for
working with patients who have endocrine or metabolic dysfunction.
These guidelines should be adapted ro a patient's specific needs. Clini
cal tips are provided earlier ro address specific situations in which the
tips may be most helpful.
Coals
The primary physical therapy goals in this patient population are the
following: (1) ro optimize functional mobility, (2) ro maximize activ
ity tolerance and endurance, (3) to prevent skin breakdown in the
patient with altered sensation (e.g., diabetic neuropathy), (4) to
decrease pain (e.g., in patients with osteoporosis or hyperparathyroid
ism), and (5) to maximize safety for prevention of falls, especially in
patients with altered sensation or muscle function.
Cuide/i1les
Patients with diabetes or osteoporosis represent the primary patient
population with which the physical therapist intervenes. Physical
ENDOCRINE SYSTEM
693
2.
Consult with the clinical nutritionist to help determine the
appropriate activity level based on the patient's caloric intake,
because caloric intake and metabolic processes are affected by endo
crine and metabolic disorders.
References
I. Burch WM (cd). Endocrinology for the House Officer (2nd ed). Balti
694
ENDOCRINE SYSTEM
695
1 992;463.
33. Saudek CD. Diabetes Mellitus. In JD Srobo, DB Hellmann, PW Laden
34.
35.
36
37.
son, et al. (cds), The Principles and Practice of Medicine (23rd cd).
Stamford, CT: Appleron & Lange, 1996;32 1-3 3 1 .
Standards o f medical care for patients with diabetes mellitus. Diabetes
Care 2001;24(1 ):533.
Nutrition recommendarions and principles for people with diaberes mel
litus. Diabetes Care 200 I ;24( I ):544.
Zinran B, Ruderman N, Phil O, er al. Diabetes mellitus and exercise.
Diaberes Care 200 I ;24( 1 ):551
Saudek CD, Duckworth \'(fC, Giobbie-Hurdcr A, et al. Implamable
insulin pump vs multipledose insulin for noninsulin dependent diabe
tes mellitus: a randomized clinical trial. Deparrmem of Veterans
Affairs Implantable Insulin Pump Srudy Group. JAMA I 997;276( 1 6):
1 322-1 327.
38. Cefalu WT. Inhaled human insulin trearmeO[ in patiems with type 2 dia
betes mellitus (Abstract). JAM A 200 I ;285(12): 1559.
39. Skyler J , Cefalu WT, Kourides lA, et al. Efficacy of inhaled human
40.
41.
42.
43.
63.
44. Cooper PG. Insulinreacrion hypoglycemia. Clin Reference Syst Ann
2000:9 19.
45. Hudak CM, Gallo BM (eds). Critical Care Nursing: A Holistic Approach
(6th edl. Philadelphia: Lippincott, 1994;874.
46. Trorto NE, Cobin RH, Wiesen M. Hypothyroidism, hyperthyroidism,
hyperparathyroidism. Patient Care 1 999;33 ( 1 4): 186.
47. Levine MA. Disorders of Mineral and Bone Metabolism. In jD Stobo,
DB Hellmann, P\V Ladenson, et al. (cds), The Principles and Practice of
Medicine (23rd ed). Stamford, CT: Appleton & Lange, 1996;3 1 2-320.
48. Irvin GL 1Il, Carneiro DM. Management changes in primary hyperpar
athyroidism. JAMA 2000;284(8):934.
49. NIH Consensus Development Panel. Osteoporosis prevention, diagno
sis, and therapy. JAMA 200'1 ;285(6):785.
50. Altkorn D, Yoke T. Treatment of postmenopausal osteoporosis. JAMA
2001;285( 1 1 ): 14 1 5.
5 1 . Vieth R. Vitamin D supplementation, 25hydroxyvitamin D concentra
tions, and safety. Am J Clin Nun 1 999;69(5):842.
52. Hines SE. Paget's disease of bone: a new philosophy of treatmenr.
Patient Care 1 999;33(20):40.
12
Organ Transplantation
Jennifer Lee Hunt
Inrroduction
697
698
after
organ
transplantation,
including
4.
Guidelines for physical therapy intervention with the
transplant recipient
The kidney, liver, pancreas, heart, and lung are organs that are pro
cured for transplantation. The most frequent of those are the kidney,
liver, and heart.2 Double transplants, such as liver-kidney, kidney
pancreas, and heart-lung, are performed if the patient has multiorgan
failure. Although bone marrow is not an organ, bone marrow trans
plantation (BMT) is a common type of tissue transplant that will be
discussed.
ORGAN TRANSPLANTATION
699
or tissue
In addition ro these criteria, transplant candidates muSt demon
Strate emotional and psychological stability, have an adequate
support system, and be willing to comply with lifelong immuno
suppressive drug therapy. Other criteria, such as age limits and
absence of drug or alcohol abuse, are specific to rhe transplant
facility. To determine whether transplantation is the best treatment
option for the individual, all transplant candidates are evaluated
by a team of health care professionals consisting of a transplant
surgeon, transplant nurse coordinator, infectious disease physi
cian, psychiatrist, social worker, and nutritionist. The patient
undergoes many laboratory and diagnostic studies during the eval
uation process. Acceptable candidates for organ transplantation
are placed on a waiting list. Waiting times for an organ may range
between 1 and 4 years. 37
Transplant Donation
Cadaveric Oa./Ors
Cadaveric donors are brain-dead individuals who have had severe
neurologic trauma, such as from head or spinal cord injury, cerebral
hemorrhage, or anoxia.8 Death must occur at a location where car
diopulmonary support is immediately available to maintain the
potential organ donor on mechanical ventilation, cardiopulmonary
bypass, or both; preserve organ viability; and prevent ischemic dam
age ro viral organs." The cadaveric donor must have no evidence of
malignancy, sepsis, or communicable diseases, such as hepatitis B or
human immunodeficiency virlls. 6.9, I O
Living DOllors
Because there are nOt enough cadaveric organs donated to meet the
needs of all potential recipients, living donor transplantation offers an
alternative means of organ donation. Living donors are always used
700
for bone marrow transplants, often used for kidney transplants, and
sometimes used for liver, lung, and pancreas transplantation. They
may be genetically or emotionally related to the recipient-that is,
they are a blood relative (e.g., sister) or non-genetically related indi
vidual (e.g., spouse or close friend). Living donors also are evaluated
by the transplant team to determine medical suitability.
The age of a potential donor can r.nge from a term newborn to 65
years, depending on the organ considered for donation and the recipi
ent. Donors do not have a history of drug or alcohol abuse, chronic
disease, malignancy, syphilis, tuberculosis, hepatitis B, or human
immunodeficiency virus infection. Ideally, the donor's height and
weight approximate those of the recipient for the best "fit."
Donor Matching
Histocompatibility typing
Size
The donor and recipient muSt be ABO blood type identical or com
patible." The process of finding compatible donors and recipients is
called tisslle typing or histocompatibility typing. Histocompatibility
typing attempts to match the human leukocyte antigens (HLAs),
which are the antigens that cause graft rejection. It is performed sero
logically by adding a standard panel of typing antisera, complement,
and ttyphan blue stain to purified lymphocytes and then observing
the lymphocytotoxicity. 12 The better the histocompatibility match
and degree of genetic similarity between the donor and the recipient,
the less severe is the rejection response. In living related donors, an
identical match is ideal; however, a half match is acceptable. 9 Also, a
white cell crossmateh is performed in which the lymphocytes from the
donor are mixed with the serum from the recipient and then observed
for immune responses. A negative crossmatch indicates no antibody
reaction and that the recipient's antibodies are compatible with the
donor. A negative crossm.tch is required for successful kidney and
kidney-pancreas transplants.7
ORGAN TRANSPLANTATION
701
Allograft function
Rejection
702
Infection
Surgical
Medical
Rejection
Infection
Rejection
The major problem in organ transplantation is nOt the technical diffi
culties of surgery, but rather organ rejection, or the tendency of the
recipient's body to immediately reject anything that is "nonself. "
Graft rejection is actually a normal immune response to invasion of
foreign matter, the transplanted organ or tissue. Some degree of rejec
tion is normal; however, if the patient is not treated with immunosup
pressive drugs, the donor organ would be completely rejected and
cease to be viable in 10 days. IS Transplant recipients must receive
ORGAN TRAN5I'I.ANTAT10N
703
C!
...
immunosuppressive Drug
Action
>
Corticosteroids (methyl
prednisolone [Solu
Medral], prednisone)
immune responses
heart failure
immunity by blocking
transcription of early
activation genes
reverse, acme rejection
Prograf)
Azathioprine Omuran)
'"
r
>
g'"
"
"
:t
i2i
n
>
,...
'"
::l
>
Mycophenolare mofetil
(CelICepr)
o
,.
C)
,.
!;:
o
z
Cl
<n
706
Peripheral edema
Dyspnea
Electrolyte imbalances
ORGAN TRANWLANTATlOr-.;
707
cess, and ,t may take years before the organ fails, but eventually
rerransplantation is required.
Chronic rejection in patients with renal transplanrs presenrs as a
gradual 1I1crease in serum crearinine and BUN, electrolyte imbalance,
weight gain, new-onset hypertension, decrease in urine output, and
peripheral edema"
In patients with liver transplants, chronic rejection is seen as a
gradual rise in serum bilirubin and elevation of serum glutamic
oxaloacetic transaminasc.19 Progressive thickening of the hepatic
aneries and narrowing of the bile ducts occur and eventually lead to
progressive liver failure.
In patients with cardiac transplants, chronic rejection manifests
III the form of coronary allograft vasculopathy, in which there is
accelerated graft atherosclerosis or myocardial fibrosis and increas
ing blockage of the coronary arteries, which leads to myocardial
ischemia and infarction.b
Chronic rejection in patients with lung transplants is manifested as
hronchult.tis obliterans with symptoms of progressive dyspnea sec
ondary to increasing airflow obstruction and a progressive decline in
the forced expiratory volume in one second (FEV,)]"
I n patients with pancreas transplants, the pancreatic vessels
thicken, leading to fibrosis, and there is a decrease in insulin secretion
with resultant hyperglycemia.b
bl(eelioll
Supprc!o,sion of the Immune response prevents rejection of the trans
plantcd organj however, the recipient is more susceptible to infection.
Infection may occur in the lungs, liver, colon, and oral mucous mem
brane. In addition to a surgical wound infection, the recipient is at
risk for bacterial, fungal, and viral infections. Bacterial infections may
occur in the urinary tract, respiratory tree, and indwelling devices,
such as a central venous catheter. '" The highest risk for infection is
during the first 3 months after transplantation." If infection is noted,
fewer immunosuppressive drugs are given, and antibiotic treatment is
initiated. Antibacterial, antiviral, and antifungal medications are
often given prophylactically. Bacterial infections are treated using
antibiotics. The use of trimethoprimlsulfamethoxazole (Bactrim) in
prophylactic doses has been effective in preventing Plleul1Ioeyslis ear-
708
111t1
Fatigue
Shaking chills
Sweating
Dyspnea
Renal Transplantation
Glomerulonephritis
Chronic pyelonephritis
Diaberic nephropathy
ORGAN TRANSPLANTATION
709
Active vasculitis
Morbid obesity
710
ORGAN TRANSPLANTATION
711
using the same scale. When urine volumes are extremely high, intrave
nous fluids may be titrated. Other volume assessment parameters
include inspection of neck veins for distention, skin turgor and
mucous membranes for dehydration, and extremities for edema. Aus
cultation of the chest is performed to determine the presence of
adventitious breath sounds, such as crackles, which indicate the pres
ence of excess volume.'2
The most common signs of rejection specific to the kidney are an
increase in BUN and serum creatinine, decrease in urine Output,
increase in blood pressure, weight gain greater than 1 kg in a 24-hour
period, and ankle edema.7. 12.25 A percutaneous renal biopsy under
ultrasound guidance is the most definitive test for acute rejection.25
Sometimes, ATN occurs post transplantation. Twenty percent to 30%
of patients receiving cadaveric kidneys preserved for longer than 24
hours experience delayed graft function.25 This ischemic damage from
prolonged preservation results in ATN. The delayed kidney function
may last from a few days to 3 weeks. Therefore, dialysis is required
until the kidney starts to function7
Ureteral obstruction may occur owing to compression of the ureter
by a fluid collection or by blockage from a blood clot in the ureter. The
obstruction can cause hydronephrosis (dilation of the renal pelvis and
calyces with urine), which can be seen by ultrasound.25 The placement
of a nephrostomy tube or surgery may be required to repair the obstruc
tion and prevent irreversible damage to the allograftH
Urine leaks may occur at the level of the bladder, ureter, or renal
calyx. They usually occur within the first few days of transplantation. 25
Renal ultrasounds are performed to assess for fluid collections, and radi
onucleotide scans view the perfusion of the kidney. Other potential com
plications include post-transplant diabetes, renal artery thrombosis or
leakage at the anastomosis, hypertension, hyperkalemia, renal abscess
or decreased renal function, and pulmonary edema.6 .13.25 Thrombosis
most often occurs within the first 2 to 3 days after transplantation. 25
The most common cause of decreased urine output in the immediate
postoperative period is occlusion of the urinary catheter due to clot
retention, in which case aseptic irrigation is required. 12
Clinical Tip
Physical therapists should closely monitor blood pressure
with exercise. To ensure adequate perfusion of the newly
grafted kidney, the systolic blood pressure is maintained at
712
Liver Transplantation
Chronic hepatitis B or C
Sclerosing cholangitis
Wilson's disease
Budd-Chiari syndrome
Biliary atresia
Extrahepatic malignancy
ORGAN TRANSPLANTATION
713
Pretrallsplalttatiolt Care
2.
Livillg adult dOllar liver transplallt. A single lobe of the liver
from a living adult is transplanted into the recipient. The removal of
the lobe does not cause any decrease in liver function to the living
donor. 7 Because of the unique ability of the liver to regenerate, the
donor's and recipient's livers will grow back to normal size within
several months.7
3.
Split liver transplant. Split liver transplants are sometimes
used to expand the donor pool. Surgeons divide an adult cadaveric
liver in situ inro two functioning allografts. 29 Usual ly, the smaller
left lobe is donated to a child, and the larger right lobe is given to an
adultJO
4.
Domino liver transplant. Domino liver transplants are currently rare and are still experimental transplantations. They involve
patients with familial amyloidotic polyneuropathy (FAP). Patients
with FAP have a metabolic defect within the liver. The liver is StruC
turally and functionally normal, but it synthesizes an abnormal pro
tein, transthyretin, that forms amyloid fibrils and deposits them in the
peripheral and autonomic nerves, heart, kidney, and intestine. The
domino liver transplant involves three people: the donor, the patient
with FAP, and a patient listed on the liver transplant waiting list. The
patient with FAP receives the donated liver. The removed liver (from
the patient with FAP) is then transplanted into the other transplant
recipient, hence the term domino transplant. Liver transplantation for
patients with FAP leads to normal transthyretin protein production.
The recipient who received the FAP liver will likely never experience
any of the symptoms associated with FAP, because they take 40-60
years to manifest.?
714
Characteristics of
Liver Failure
Clinical Effects
Implications
t Bilirubin level
Jaundice.
None.
.J.. Albumin
Accumulation of ascites
synthesis
cavity causes
to respiratory and
abdominal swelling
and increased
abdominal girth.
May promote protein
nutritional difficulties.
Monitor for dyspnea
with activity.
Patient may have an
altered center of
nitrogen balance.
balance.
Increased prothrombin
thromboplastin time.
Impaired glucose
production
Porral
Presence of esophageal
varices.
hyperrension
Diminished
Spontaneous bacterial
phagocytic
peritonitis or
activity
cholangitis.
Failure to absorb
None.
vitamin 0
fractures.
elevated;
J..
decreased.
ORGAN TRANSPLANTATION
715
716
Clinical Tip
Postoperatively, many recipients still have ascites from
weeping of sodium- and albumin-rich fluid from the liver's
surface' Along with ascites and postsurgical fluid reten
tion, liver transplant recipients have an increased abdomi
nal girth and lower-extremity edema that lead to a shift in
the patient'S center of gravity and impaired balance. Often,
patients have an increase in lumbar lordosis and complain
of low back pain.
ORGAN TRANSI)LANTATION
717
Pancreas Transplantation
Major amputation
Complete bl indness
Morbid obesity
Active smoking
718
ORGAN TRANSIlLMITATION
719
720
Clinical Tip
Remind pancreas transplant recipients to drink enough n u
ids to rehydrate themselves during and after exercise.
Hydration is critical in patients with a bladder-drained pan
creas. Recipients must take in 3-4 liters of n uid per day."
Pancreas-Kidney Transplantation
Types of Pancreas-Kidney Transplaltts
1.
Simultalteous Paltcreas-Kidltey (SPK) traltSplOlltS. Typically,
SPK transplants are offered to patients who have type I diabetes mellitus
with diabetic nephropathy and renal insufficiency. SPK transplants are
more common than a non-life saving pancreas transplantation alone, as
physicians are reluctant to use potent immunosuppressive drugs in
patients with diabetes before they need a concomitant renal transplant.3
The benefits of a successful SPK transplant include normoglycemia, elim
ination of dialysis, and prevention of reoccurring diabetic nephropathy in
the kidney graft.3I ,3.
SPK transplants may be cadaveric or from living donors, in which
case a segmental pancreas transplant is performed. Using an abdomi
nal midline incision, the pancreatic graft is implanted first on the right
side, and then the kidney graft is implanted on the left side."
2.
Paltcreas after kidltey (PAK) traltsplaltts. A pancreas transplant is performed on a patient who has already received a cadaveric
or a living donor kidney transplant.
ORGAN TRANSPLANTATION
721
Cardiac Transplantation
C ard iomyopathy
Valvular d isease
to
Primary card iac tumo rs with no evid ence of spread to other systems
C ontraind ications
followi ng5 . 1 2.21.21 :
to
cardiac
transplantation
include the
722
ORGAN TRANSPLANTATION
723
724
ORGAN TRA:'\ISJ>U\NTATIO
725
Clinical Tip
The panenr is placed in a protccnve isolation room.
Posinve-pressure now rooms are recommended to limit the
transfer of airborne pathogens. The usc of a face mask and
strict hand washing are required.)"
In the initial postoperative period, mediastinal drainage
IS promoted by elevating the head of the bed to a 30degree angle and turning the patient every 1-2 hours.5
Phase I cardiac rehabilitation usually begins 2-3 days
postoperatively, once the patient is hemodynamically Sta
hle. r,ercise is progressive and based on the patient'S
activity tolerancc. Exercise is progrcssed from active
SUpll1C exercises without resistance to ambulation and sta
tionary biking. Vital signs are monitored before, during,
and immediately after exercise.
726
ORGAN TRANSPLANTAnON
727
Lung Transplantation
Emphysema
Bronchiectasis
Pulmonary fibrosis
728
Alpha,-antitrypsin deficiency
Scleroderma
ORGAN TRANSI'I.Af\.'TATION
729
3.
Livillg dOllar lobar trallsplalltatioll. Transplantation of lobes
involves bilateral implantation of lower lobes from two blood-group
compatible, living donors.' The donor's lungs are larger than the
recipients for the donor lobes to fill each hemithorax.' This procedure
is performed primarily for patients with cystic fibrosis. In addition,
patients with bronchopulmonary dysplasia, primary pulmonary
hyperrension, pulmonary fibrosis, and obliterative bronchiolitis may
benefit from a lobar transplantation.s.u
730
ORGAN TRANSI)LANTATION
731
Clinical Tip
If the recipient is intubated, sllctioning may be per
formed with a premeasured catheter ro prevent damage to
the anastomosis. Suctioning removes secretions and helps
maintain adequate oxygenation.
After lung transplantation, recipients should sleep in
reverse Trendelenburg position to aid in postural drainage,
as long as they are hemodynamically stable.
In the intensive care unit, during the first 24 hours after
surgery, patients with double-lung transplants should be
turned side to side. Turning is initiated gradually, begin
ning with 20- to 30-degree [Urns and assessing vital signs,
and then increasing gradually to 90 degrees each way,
every 1-2 hours. Prolonged periods in supine position are
avoided to minimize secretion retention. 12
Patients with single-lung transplants should lie on their
nonoperative side to reduce postsurgical edema, assist
with gravitational drainage of the airway, and promote
optimal inflation of the new lung.'2
Bronchopulmonary hygiene before exercise may enhance
the recipient's activity tolerance.
Schedule physical therapy visits after the patient
receives his or her nebulizer treatment and after the patient
is premedicated for pain control. Incisional pain can limit
activiry progression, deep breathing exercises, and cough
ing. Also, splinting the incision with the use of a pillow
can help reduce incisional pain while coughing.
Lung transplant recipients follow strict thoracotomy
precautions. They are nOt allowed to lift anything heavier
than 10 lb. They are restricred to partial weight bearing
of their upper extremities, which may limit the use of an
assistive device.
732
Heart-Lung Transplantation
COPD
Cystic fibrosis
Pulmonary fibrosis
Eisenmenger's syndrome
The heart and lung of the donor are removed en bloc and placed in
the recipient's chest. The anastomosis to join the donor organs is at
ORGAN TRANSI'LANTATION
733
2.
A syngeneic transplant is one in which bone marrow is
harvested from an identical twin.
3.
An alltologolls transplallf is one in which the donor and
recipient are the same. Bone marrow is harvested from the patient
when he or she is healrhy or in complete remission. The marrow is
then frozen and stOred for future reinfusion.
One type of autologous BMT is rhe peripheral blood srem cell
(PBSC) transplant. Stem cells are primirive cells found in bone mar
row or circulating blood that evolve into mature blood cells (whire
cells, red cells, and platelets). The parient's PBSCs are harvesred by
leukapheresis. During leukapheresis, the patient's blood is circulated
through a high-speed cell separator in which the peripheral srem
cells are frozen and srored, and the plasma cells and eryrhrocyres are
reinfused into the patient. The patient may require three to seven
harvests to achieve an adequate number of srem cells.' The PBSCs
are reinfused after rhe parient receives lethal doses of chemotherapy,
radiation, or borh. Allogenic PBSC transplant may be performed
from a donor or by using umbilical cord blood from a newborn
The hematologic recovery afrer PBSC rransplant is 10-12 days,
734
Non-Hodgkin's lymphoma
Multiple myeloma
NeuroblastOma
Testicular cancer
Breast cancer
Patient Preparati011
ORGAN TRANSPLANTATION
735
Clinical Tip
BMT recipients are very susceptible to infection. When
the patient'S neutrophil count is less than 1,OOO/mm3, the
patient is placed on reverse protective isolation or neutro
penic precautions. Patients are placed in reverse isolation
in a private, sterile, laminar airflow room. In the laminar
airflow rooms, an air filtration system preserves a sterile
environment, and all items entering the room must be ster
ile. Before entering the patient'S room, physical therapists
and other hospital staff must thoroughly wash their hands,
736
ORGAN TRANSPLANTATION
737
738
kidney, 3-7 days; liver, heart, and lung, 10-H days; pancreas, 5-12
days; kidney-pancreas, 10-16 days7.1 J.Il,J9 Given the short length of
stay for transplant recipients, physical therapists are consulted in the
early postoperative period to provide treatment and assist the trans
plant team with a safe discharge plan. If patients are medically stable
but need assistance for activities of daily living and ambulation, they
will require transfer to a rehabilitation facility for further physical
and occupational therapy before discharge home.
Goals
In the acute care setting, the primary physical therapy goals are simi
lar to those of postoperative abdominal or cardiothoracic surgical
patients. They include maximizing functional mobility and endur
ance; improving range of motion, strength, balance, and coordina
tion; and progressing the recipient to his or her maximum
independent functional level safely.
Many transplant recipients have experienced end-stage organ dis
ease for multiple years before receiving their transplant and may
present with other medical comorbidities. As a result, they are usually
physically deconditioned and present with a marked reduction in
exercise capacity and skeletal muscle strength owing to long-standing
pretransplant physical inactivity. For example, extreme fatigue and
weakness are exhibited in patients with chronic liver disease, reduced
muscle endurance is seen in patients with chronic heart failure, and
decreased oxygen uptake capacity is exhibited in heart and lung dis
ease.1 Generalized weakness results from the disease process, fluid
and electrolyte imbalance, and poor nutrition. After their transplant,
recipients generally require a longer time frame ro regain their
strength and endurance and to achieve their goals.
ORGAN TRANSPLAI'ITATION
739
740
Activity Progressioll
Activity is increased gradually, and treatment continues until the
parient is ambulating independently with sufficient endurance to
function safely ar home. At first, recipienrs will fatigue easily and
require frequent rest periods. Thus, shorrer and more frequent
treatment sessions are beneficial to patients.
Ambulation is progressed in terms of frequency, pace, and dura
tion. Stair climbing is progressed with the goal of achieving one to
two flights of reciprocal stair climbing.
Patient Education
Physical therapists assist in the education of transplant recipi
ents. Recipients must assume an active role in their health care post
transplantation. Patients are educated about what to expect after
transplantation. Initially, the recipient is very weak and may have
difficulty learning during the early post-transplant rehabilitation
phase. The physical therapist reinforces the activity protocol with
the patient. The transplant team usually provides the recipient with
a comprehensive guide that includes information on medications,
proper diet, exercise, and psychosocial changes. The patient must
adhere to the medication protocol post transplant and be able to
monitor for signs and symptOms of infection, rejection, and toxic
ity to the medications. Patients are instructed to monitor daily their
ORGAN TRANSPLANTATION
741
References
I . Kjaer M, Beyer
, Secher NH. Exercise and organ transplantation.
Scand J Med Sci Sports 1 999;9: 1 - 1 4.
2. Doenges ME, Moorhouse M I- Geissler AC (eds). Nursing Care Plans:
Guidelines for Individualizing Patient Care (4th ed). Philadelphia: FA
Davis, 1 997;774.
3. Arcasoy SE, Korloff RM. Lung rransplanration. N Engi J Med
1 999;340( 1 4): 1 0 8 1 - 1 09 1 .
4. Kesten S. Advances in lung transplantation. Dis Mon 1 999;45(3): 1 0 1 - 1 14.
5. Becker C, Petlin A . Heart transplantation: minimizing mortality with
proper management. Am J Nurs 1 999;(SuppJ 5):S- 1 4.
742
ORGAN TRANSPLANTATION
743
I-A
Medical Record Review
Michele P. West
745
746
Orders
The order section is a log of all instructions of the plan of care for the
patient, including medications, diagnostic or therapeutic tests and
procedures, vital sign parameters, activity level, diet, the need for con
suiration services, and resuscitation status. Orders may be written by
a physician, physician assistant, or nurse practitioner. A verbal or tele
phone order may be taken by a nurse or other health care provider,
including a physical therapist, according to departmental, facility, and
state policies. All orders should be dated, timed, and signed or
cosigned by the appropriate personnel.
History
The history portion of the record includes an admission note and
progress nOtes (a shortened version of the initial note, with emphasis on
the physical findings, assessment, and plan), a nursing admission assess
ment and problem list, consult service notes from physicians and allied
health professionals, and operative and procedural notes. Medication
sheets, now sheets, and clinical pathways are also included in this section.
Reports
A variety of reports are filed chronologically in individual sections in
the medical record (e.g., radiologic or laboratory reports). Each
report includes an interpretation or normal reference ranges, or both,
for various diagnostic or laboratory test results.
747
B.
C.
and allergies.
D.
F.
II.
to
A.
General information, including vital signs, laboratory findillgs, mental status, and appearance.
III.
B.
C.
Chest
D.
Heart (Cor)
E.
Abdomen
F.
Extremities
C.
Neurologic system
to
748
IV.
References
I. Wood DL. Documentation guidelines: evolution, future direction, and
I-B
Acute Care Setting
Michele P. West
Introduction
The physical therapist must have an appreCIation for the distinct
aspects of in-patient acute care. The purpose of this appendix is to
briefly present information about the acute care environment, includ
ing safety and the use of physical restraints, the effects of prolonged
bed rest, end-of-life issues, and some of the unique circumstances,
conditions, or patient responses encountered in the hospital setting.
The acute care or hospital setting is a unique environment with pro
tocols and standards of practice and safety that may not be applicable
to other areas of health care delivery, such as an outpatient clinic or
school system. Hospitals are designed to accommodate a wide variety
of routine, urgent, or emergent patient care needs. The staff and medi
cal-surgical equipment (see Appendices lII-A, -B, and -C) reAect these
needs. The nature of the hospital setting is to provide 24-hour care;
thus, the patient, family, and caregivers are faced with the physical,
psychological, and emotional sequelae of illness and hospitalization.
This can include the response(s) to a change in daily routine; a lack of
privacy and independence; or perhaps a response to a potential life
sryle change, medical crisis, critical illness, or long-term illness.
749
750
Leaving the bed or chair (e.g., stretcher chair) in the lowest posi
tion with wheels locked after physical therapy intervention is com
plete. Leave the top bed rails up for all patients.
Always leaving the patient with the call bell or other communi
cation devices within close reach. This includes eyeglasses and
hearing aids.
751
on the noor. Secure electrical cords (e.g., for the bed or intravenous
pumps) out of the way. Keep small-sized equipment used for physi
cal therapy intervention (e.g., cuff weights) in a drawer or closet.
Store assistive devices at the perimeter of the room when not in
use. Do not block the doorway or pathway to and from the
patient's bed.
Providing enough light for the patient to move about the room
or read educational materials.
Only using equipment (e.g., assistive devices, recliner chairs,
wheelchairs) that is in good working condition. If equipment is
unsafe, then label it as such and contact the appropriate personnel
to repair or discard it.
Disposing of linens, dressings, and garbage according to the pol
icies of the facility.
Latex Allergy
752
Use
of Restraints
The use of a restraint may be indicated for the patient who (I) is
unconscious, (2) has altered mental status at risk for wandering or
pulling out lines and tubes, (3) is unsafely mobile, (4) is physically
aggressive, or (5) is so active or agitated that essential medical-surgi
cal care cannor be complered.' The most common types of restraints
in the acute care setting are wrist or ankle restraints, mitt restraints,
or a vest restraint. An order from a physician, which must be
updated approximately every 24-48 hours, is required to place a
restraint on a patient.
General guidelines most applicable to the physical therapist for the
usc of restraints include
Usc a slipknot to secure a restraint rather than a square knot.
This ensures that the restraint can be rapidly untied in an emergency.
Ensure that the restraint is secure but not too tight. Place twO
fingers between the restraint and the patient ro be sure circulation
is not impaired.
Be sure the patient does nOt trip on the ties or "tails" of the
restraint during functional mobility training.
Consult with the health care team to determine wherher a
patient needs to have restrainrs.
753
Most patients on bed rest have been in the intensive care unit (ICU)
for many weeks with multisystem organ failure or hemodynamic
instability requiring sedation and mechanical ventilation. Other clini
cal situations classically associated with long-term bed rest include
severe burns and multi-trauma, including the need for skeletal trac
tion, spinal cord injury, or grade IV non-healing wounds of the lower
extremity or sacrum. It is beyond the scope of this text to discuss in
detail the effects of prolonged bed rest; however, Table I-B.'1 lists these
major changes.
Clinical Tip
MonitOr vital signs carefully, especially during mobili
zation out of bed for the first few times.
Progressively raise the head of the bed before or during a
physical therapy session to allow blood pressure to regulate.
A tilt table may be used if orthostatic hypotension persists
despite volume repletion, medication, or therapeutic exercise.
Time frames for physical therapy goals will likely be
longer for the parient who has been on prolonged bed rest.
Independent or family-assisted therapeutic exercise
should supplement formal physical therapy sessions for a
more timely recovery.
Be aware of the psychosocial aspects of prolonged bed
rest. Sensory deprivation, boredom, depression, and a
sense of loss of control can occur.' These feelings may
manifest as emotional lability or irritability, and caregivers
may incorrectly perceive the patient to be uncooperative.
As much as the patient wants to be off bed rest, the patient
will likely be fearful the first time out of bed, especially if the
patient has insight into his or her muscular weakness.
Leave the patient with necessities or commonly used
objects (e.g., the call bell, telephone, reading matetial, bev
erages, tissues) within reach to minimize the patient's feel
ings of being confined to bed.
End-of-Life Issues
End-of-life issues are often complex moral, ethical, or legal dilemmas,
or a combination of these, regarding a patient'S vital physiologic func-
754
Effects
Cardiac
exercise.
Hematologic
Respirarory
Gastrointestinal
Genirourinary
gastric secretion.
Musculoskeletal
compression neuropathy.
Neurovascular
Orthostatic hyporension.
Body composition
Vozmax
755
'-'
'"
'"
Table I-B.2. Comparison of Coma, Persistent Vegetative State (PVS), and Brain Death
Condition
Coma
Sleep-Wake
Cycle
Moror Control
Absent
Lacks
purposeful
movement
Present
PVS
Lacks
purposeful
Respiratory
Control
EEG Activity
Present, vari-
Present
able, usually
depressed
Present, normal
Absent
None or spinal
reflex move-
Absent
Metabolism
Prognosis
Reduced by
Usually recovers.
50% or more
Can progress to
PVS or death in
2-4 wks.
Present
movement
Brain death
Cerebral
Absent
Reduced by
50% or more
Absent
Variable recovery.
electroencephalogram.
No recovery.
Source: Adaprcd from LA Thclan. LD Urden, ME Lough, Kt"1 Stacy (eds). Neurological Disorders. In Critical Care Nursing: Diagnosis and
Management (3rd ed). St. Louis: Mosby, 1998;797.
'"
'"
'"
J:
"
Cl
ments only
EEG
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757
Com mOil Patiellt and Family Respo1tses to the /lIte1tsiue Care Ullit
Behavioral changes or disturbances can occur in the patient who
is critically ill as a result of distress caused by physically or psycho
logically invasive, communication-impairing, or movement-restrict
ing procedures.'o When combined with the environmental and
psychological reactions to the ICU, mental status and personality
can be altered. Environmental stresses can include crowding, bright
overhead lighting, strong odors, noise, and touch associated with
procedures or from those the patient cannot see.IO Psychological
stresses can include diminished dignity and self-esteem, powerless
ness, vulnerability, fear, an.xiety, isolation, and spiritual distress. 10
ICU psychosis is a state of delirium that occurs between the third
and seventh day in the ICU and is described as a "fluctuating state of
consciousness characterized by features such as fatigue, confusion,
distraction, anxiety, and hallucinations." II Delirium in the leU,
which is reversible, is thought to be caused by pain, the side effects
of drugs, and the ICU environment." Precipitants to delirium
758
CriricalIllness PolyneuropatlJY
Critical illness polyneuropathy is the acute or subacute onset of wide
spread symmetric weakness in the patient with critical illness, most
commonly with sepsis or multisyStem organ failure, or both.!' The
patient presents with distal extremity weakness, wasting, and sen ory
loss, as well as parasthesia and decreased or absent deep tendon
reflexes.15 The clinical features that distinguish it from other neuro
muscular disorders (e.g., Guillain-Barre syndrome) are a lack of oph
thalmoplegia, dysauronomia, and cranial nerve involvement and
normal cerebrospinal fluid analysis,'4.'5 Nerve conduction studies
show decreased motor and sensory action potentials.!S The specific
pathophysiology of critical illness polyneuropathy is unknown; how
ever, it is hypothesized to be related to drug, nutritional, metabolic,
759
and toxic factors, as well as prolonged leu stay, the number of inva
sive procedures, increased glucose level, decreased albumin level' and
the severity of multisystem organ failure. IS
eriticalllllless Myopathy
Critical illness myopathy, otherwise known as acule quadriplegic
myopathy or aClile steroid n1)'opathy, is the acute or subacute onset of
760
Confusion
Confusion may be acute or chronic (e.g., related to a neurodegenera
tive process). Acute confusion frequently occurs in the acute care set
ting, especially in the elderly. AClIle cotlf"siotl is defined as "the state
in which there is abrupt onset of a cluster of global, Auctuating distur
bances in consciousness, attention, perception, memory, orientation,
thinking, sleep-wake cycle, and psychomotor behavior. n18 Risk fac
tors for confusion related to medications include the use of analgesics,
polypharmacy, noncompliance, and inappropriate self-medicating."
Other risk factors include dehydration, electrolyte imbalance, hyp
oxia, infection, and poor nutrition. Acute or acute on chronic disease
states can result in confusion, especially if metabolic in nature.
Additionally, a change in environment can exacerbate medical risks
for confusion. This includes unfamiliar surroundings, noises, procedures,
and staff or a change in daily routine, activiry level, diet, and sleep.
761
Low-grade feve r
Hand tremor
References
I. Carpenito Lj. Latex Allergy Response. In Nursing Diagnosis: Applica
tion to Clinical Practice (8th cd). Philadelphia: Lippincott, 2000;553557.
2. Smith SF, Duell DJ, Martin BC (cds). Restraints. Clinical Nursing Skills:
Basic to Advanced Skills (5th ed). Upper Saddle River, NJ: Prentice Hall
Health, 2000;139-146.
3. Downey RJ, Weissman C. Physiological Changes Associated with Bed
Rest and Major Body Injury. In EG Gonzalez, SJ Myers, JE Edelstein, er
al. (cds), Downey and Darling's Physiological Basis of Rehabiliration
Medicine (3rd ed). Boston: Bunerworth-Heinemann, 2001;449.
4. Buschbacher RM, Porter CD. Decondirioning, Conditioning, and the
Benefits of Exercise. In RL Braddol11 (cd). Physical Medicine and Reha
bilitation (2nd ed). Philadelphia: Saunders, 2000;716.
5. American Association of Critical-Care Nurses. Position Statement on
Withholding and/or Withdrawing Life-Sustaining Treatment. In M R
Kinney, SB Dunbar, J Brooks-Brunn, et al. (eds), AACN's Clinical Refer
ence for Critical Care Nursing (4th ed). St. Louis: Mosby, I 998;12531254.
6. DeVita MA, Grenvik A. Forgoing Life-Sustaining Therapy in Intensive
Care. In A Grenvick (ed), Textbook of Critical Care (4th ed). Philadel
phia: Saunders, 2000;2110-2 I 13.
7. Schnell S5. Nursing Care of Comatose or Confused Clients. In JM
Black, E Matassarin-Jacobs (cds), Medical-Surgical Nursing: Clinical
762
8.
9.
10.
11.
"12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
II
Fluid and Electrolyte Imbalances
Susan Polich and Jaime C. Paz
Many causes and factors can alter a patient's fluid and electrolyte
balance. These imbalance
Kidney function
763
764
Fluid Imbalance
Fluid imbalance occurs when fluids are lost, either by loss of body water
or failure to intake, or gained, either by fluid shift from the vasculature to
the cell space or excessive intake without proper e1imination.I-3
Loss of bodily fluid (hypovolemia) can occur from loss of blood
(hemorrhage), loss of plasma (burns), or loss of body water (vom
iting, diarrhea). Any of these situations can result in dehydration,
hypovolemia, or shock in extreme cases. Clinical manifestations
include decreased blood pressure, increased heart rate, changes in
mental status, thirst, dizziness, hypernatremia, increased core
body temperature, weakness, poor skin turgor, altered respira
tions, and orthostatic hypotension.l-4 Clinical manifestations in
children also include poor capillary refill, absent tears, and dry
mucous membranes,s
Excessive bodily fluid (hypervolemia) can occur when there is a
shift of water from the vascular system to the intracellular space. This
can result from excessive pressure in the vasculature (venrricular fail
ure), loss of serum albumin (liver failure), or fluid overload (excessive
rehydration during surgery). Clinical manifestations of fluid over
load include weight gain, pulmonary edema, peripheral edema, and
bounding pulse. Clinical manifestations of this fluid shift may also
resemble those of dehydration, as there is a resultant decrease in the
intravascular fluid volume.I-3 Table II-I provides an overview of
hypovolemia and hypervolemia.
Clinical Tip
During casual conversation among physicians and nurses,
patients who are hypovolemic are often referred to as
being dry, whereas patients who are hypervolemic are
referred to as being wet.
Electrolyte 1mbalance
Fluid imbalances are often accompanied by changes in electrolytes.
Loss or gain of body water is usually accompanied by a loss or gain
of electrolytes. Similarly, a change in electrolyte balance often
Definition
Contributing Factors
Clinical Manifestations
Hypovolemia
Fluid volume
deficit
muscle cramps
Hypervolemia
Fluid volume
excess
Shorrness of breath,
Decreased hematocrit,
>
'"
transfusions, and
levels
"
prolonged corticosteroid
cough
Hypernatremia
Sodium deficit
(serum
disease, excessive
sodium level
sweating, hyperglycemia,
of <135
in severe states
mEqniter)
Sodium excess
x
..
therapy
Hyponatremia
r
c:
;:;
>z
"
'"
r
'"
r
(serum
hyperventilation, and
lethargy or restlessness;
sodium level
excessive corricosteroid,
sodium levels
01>145
sodium bicarbonate, or
weakness; irritability;
mEqniter)
sodium chloride
tachycardia; hyper- or
>
administration
hypotension; oliguria;
::j
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Vo
Table 0-1.
Continued
'"
Imbalance
Definition
Conrribudng Factors
Clinical Manifestations
>
Ilypokalemia
Potassium defi-
ST depression or pro
cit (serum
longed PR interval on
potassium
ECG
level of d.5
mEqniter)
digoxin therapy
Potassium
excess (serum
T waves; or absent P
potassium
sium-conserving diuretics,
followed by bradycardIa,
waves on ECG
level of >5
dysrhythmia, flaccid
mEqniter)
apy
paralysis, paresthesia,
irritability, and anxiety
BP
elearocardiogram; NPQ
m
J:
>
pressure
Hyperkalemia
'"
syndrome of mappropriate
8
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o
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...,
767
Clinical Tip
Electrolyte levels are generally represented schematically
in the medical record in a sawhorse figure, as shown in
Figure II-I.
Na
BUN
Cl
BS
K
Cr
blood sugar; CI
ate; K= potassium; Na
chloride; Cr
sodium.)
(8 UN
creatinine; HCOl
blood urea
=
bicarbon
768
Clinical Tip
arrhythmias.
References
I. Rose BD (ed). Clinical Physiology of Acid-Base and Elecrrolyre Disor
III-A
Medical-Surgical Equipment
in the Acute Care Setting
Eileen F. Lang
Introduction
The purpose of this appendix is to (1) describe the vatious types of medi
cal-surgical equipment commonly used in the acute care sening, inc1lld
ing oxygen (02) therapy and noninvasive and invasive monitoring and
management devices, and (2) provide a framework for the safe use of
such equipment during physical therapy intervention.
Some equipment is used in all areas of the hospital, whereas other
type of equipment are u ed only in specialty areas, such as the inten
sive care unit (leU). The ICU is defined as "a place for the monitor
ing and care of patient with potentially severe physiological
insrabiliry requiring technical andlor artificial life support." I The
presence of certain types of equipment in a patient's room can provide
the physical therapisr with a preliminary idea of the patient's general
medical condition and the appropriateness of therapeutic or prophy
lactic physical therapy intervention, or borh. The physical rherapist
may initially be intimidated by rhe abundance of medical-surgical
equipment (especially in the ICU); however, a proper orientation to
sllch equipment allows the physical therapist to appropriately inter
vene wirh safety and confidence.
769
770
Oxygen Therapy
The general indication for 0, therapy is hypoxemia. Hypoxemia is
considered to be present when the arterial oxyhemoglobin saturation
(Sao,) is less than 90%, corresponding to an arterial blood 0, partial
pressure (Pao,) of less than 60 mm Hg.' Refer to Table 2-4 for the rela
tion between 0, saturation as measured by pulse oximetry (Spo,) and
Pao, and to Figure 2-7 for the oxyhemoglobin dissociation curve. The
goal of 0, therapy is to treat and prevent hypoxemia, excessive work
of breathing, and excessive myocardial work by increasing the Pao,.3
0, moves across the alveolar-capillary membrane by diffus ioll,
the physiologic mechanism by which gas moves across a mem
brane from a region of higher to lower pressure and is driven by
the partial pressure gradient of 0, between alveolar air (Pao,) and
pulmonary capillary blood. To improve diffusion, a rise in I'ao,
can be attained by increasing the fraction of inspired 0, IFio,)
with supplemental 0,'
Supplemental 0, is delivered by variable performance ITable lIl
A.l) or fixed performance (Table IlI-A.2) systems. Each cannula or
mask is designed to provide a range of Fio,. A variable performance
system should not be used if a specific Fio, is required. Variable per
formance systems are nOt intended to meet the total inspiratory
requirements of the patient. The actual Fioz for a given flow rate in a
variable system is dependent on a patient's tidal volume and respira
tory rate, and the type, fit, and placement of the cannula or mask. If a
specific Fio, is required, then a fixed performance system is indicated.
Fixed performance systems deliver a specific Fio, despite the patient's
respiratory rate and pattern.4
0, delivery devices with masks or reservoirs allow 0, to collect
about the nose and mouth during exhalation, which increases the avail
ability of 0, during inhalation. As the storage capacity of the mask or
reservoir is increased, the Fioz for a given flow rate is also increased.s
The supplemental 02 requirements of a patient may fluctuate with
activity. Monitoring Sao, with pulse oximetry (identified as Spo,) and
subsequent titration (weaning) of 0, may be indicated during exer
cise. The physician may order parameters for resting and exercise
Spo, if a patient has a low activity tolerance or an abnormally low
Spo, at baseline.
A patient with chronic obstructive pulmonary disease who has
chronic carbon dioxide retention may become desensitized to the
respiratory stimulant effects of carbon dioxide. In these patients,
ventilation is driven by means of a reflex ventilatory response ro a
>
:g
DeviceIFio1
Description
Clinical Implications
Nasal cannula
RA::::: 21 % Fio1,
1 Ipm::::: 24% Fio2,
2 Ipm ::::: 28% Fio"
3 Ipm::::: 32% Fio;,
4 Ipm 36% Fio"
5 Ipm::::: 40% Fio2,
6 Ipm ::::: 44% Fiol
W.A.l).
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Device/Fio2
Description
Clinical Implications
Nasopharyngeal
catheter
Fio23S Nasal cal1nula, above
RA 21 % Fio21
1 Ipm ... 24% Fio2!
2 Jpm "" 28% Fio"
3 Ipm ... 32% Fio !
4 Ipm ... 36% Fio2,
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mouth.
i'i
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c
'"
Cl
(Figure 1Tl-A.3).
Purpose: used for longterm 02 therapy.
Fioz'
Fio1,
Fioz'
Fio1,
emphysema.
Fioz
device.
The use of this device for 0z delivery is delayed for 1
?-:
[3
catheter
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Transtracheal
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DevicefFio2
Description
Tracheostomy mask
or collar
Fio,
25-70%
Clinical Implications
rehreather mask
Fio2 = 35-95%
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necessary.
clearance.
Partial non
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m
Non-rebreather face
Fio2
"'"
mask
80-95%
n
::
"
.3
co
Fio2 fmcrion of inspired oxygen; Ipm liters per minure; O2 oxygenj RA room air.
Lisred from leasr to most oxygen support.
Sources: Data from RR Kirby, RW Taylor, JM Civerra (eds). Handbook of Critical Care (2nd ed). Philadelphia: Lippincon-Raven, 1 997; JM
Rothsrein (ed). The Rehabilitation Specialisr's Handbook (2nd cd). Philadelphia: FA Davis, 1 998; MR Kinney, S8 Dunbar, JM Virello-Cicciu, er
a1. (cds). AACN's Clinical Reference for Critic::d Care Nursing (4rh cd). St. Louis: Mosby, 1 998j JG Weg. Long-term oxygen therapy for CO PD.
Postgrad Mcd t 998;1 03: t 43-158; D Frownfelter, E Dean (eds). Principles and Practice of Cardiopulmonary Physical Therapy (3rd cd). St.
Louis: Mosby, 1 997; and EF Ryerson, AJ Block. Oxygen as a Drug: Clinical Properties, Benefits, Modes and Hazards of Adminisrration. In GG
Burton, JE Hodgkin (cds), Respiratory Care: A Guide to Clinical Practice (3rd cd). Philadelphia: lippincon, 1991.
=
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ri
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DevicefFio2
Description
Clinical lmplic3tions
...
24-50%
Fio,
2 1 -100%
need
patient.
;:
z
"
1)
o
"
"
:l:
-<
"
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>
Ir is held firmly m
50-80%
tration of supplemental 02 to an
ventilator.
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c:
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<'
i;!
,...
.0
!i
:;!
'"
,.
tion of 02 to be delivered.
BiPAP bilevel positive airway pressure; Fio2 fraction of inspired oxygen; Ipm liters per minute; 02 oxygen; RA room air.
Sources: Data from RR Kirby, RW Taylor, JM Civetta (eds). Handbook of CfltlCal Care (2nd ed). Philadelphia: Lippincott-Raven, 1997; JM
Rothstein (ed). The Rehabiluatlon SpecialiSt's Handbook (2nd cd). Philadelphia: FA DaVIS, 1998; and EF Ryerson, AJ Block. Oxygen as a Drug:
Chmcal Propenies, Benefits, Modes and Hazards of Adminisnatlon. In GG Burton, JE Hodgkin (eds), Respiratory Care: A Guide to Clmical
Practice (3rd ed). Philadelphia: Llppmcotr, 1991.
=
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,.
,.
:;
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778
779
Figure UI-A.2. Open (ace mask or tent. (Maersk Medical, Respiratory and
Anesthesia Product Catalog, McAllen, TX.J
The Fio, for a given system is dependent on its proper fit and
application. Ensure that all connections are intact, that the 02 is
780
Figure m-A.3. Closed face mask. (Maersk Medical, Respiratory and Anesthe
sia Product Catalog, McAllen, TX.)
781
782
Aerosol
Hood
280/0
Figure [I]-A.6. Air e"trainment mask or venturi mask. (Maersk Medical, Respt
02
used during
783
Hemodynamic Monitoring
Monitoring hemodynamic events provides information about the
adequacy of a patient's circulation, perfusion, and oxygenation of
the rissues and organ sysrems. The goal of hemodynamic moniroring
is to maintain rhe balance berween oxygen demand and oxygen
delivery.' Hemodynamic monitoring can be accomplished using
noninvasive (Table III-A.3) or invasive (Table III-A.4) merhods.
Noninvasive, or indirect, hemodynamic monitoring provides
physiologic information without the risks of invasive monitoring
and can be used in many serrings; however, the accuracy of the
dara obrained is affected by the applicarion of rhe device and the
comperence of rhe clinician gathering the data.s
Invasive, or direct, measurements are obtained by penetration
of the skin and insertion of a cannula or carheter into a blood ves
sel, chamber of rhe heart, or borh. The cannula or catheter is
attached to a monitoring system, which consists of a transducer,
amplifier, and oscilloscope for rhe display of rhe vascular wave
forms and pressure measurements.9 Direct monitoring can provide
continuous, accurate data; however, thrombosis, infections, air
embolisms, and trauma are potential complications.s
During invasive hemodynamic moniroring, the level of rhe righr
atrium is the standard zero reference point and is identified by the ph/e
bosratic ax is the intersection of rhe midaxillary line and the fourth
inrercosral space (see Figure In_A.7).'O The nurse will zero the system
using a level to align the patient's phlebostatic axis with the transducer.
Repositioning the patient may artificially alter waveforms by applying
pressure to the catheter, shifting the catheter or stopcock, or shifting the
phlebostatic axis relative ro the transducer. I I
-
ducer gives false high readings; lowering rhe phlebosratic axis gives
false low readings."
....
00
...
Description
Clinical Implications
>
BP cuff (sphygmomanometer)
'"
blood pressure.
CO
overestimates SP.
The cuff may be placed on the upper extremity
distal to the elbow with auscultation of the
radial artery.
Alternative sites for measurement in the lower
extremiry are proximal to the popliteal space
with auscultation of the popliteal artery or
proximal to the ankle with auscultation of the
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chest
percussion).
If an electrode(s) becomes dislodged, reconnect it.
ECC.
"
x
"
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c
"
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2)
tz
>
antennas.
Collaborate with the nurse to determine
whether patienrs who are "hard wired" to
monitors in their room may be temporarily
transferred to telemetry for ambulation
activities or whether the monitor may be
temporarily disconnected.
i
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Table flJ-A.3.
Continued
'"'
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Device
Description
Clinical lmplic3tions
Pulse oximeter
Normal Spo, (at sea level)
" 93-94%
AV arteriovenous; BP blood pressure; ECG electrocardiography; Sa02 arterial oxyhemoglobin saturation; Spo! measurement of Sa02
with pulse oximetry.
Sources: Data from RR Kirby, RW Taylor, JM Civetta (cds). Handbook of Crincal Care (2nd cd). Philadelphia: lippincott-Raven, 1997;jM
Rothstein (cd). The Rehabilitalion Specialist'S Handbook (2nd ed). Philadelphia: FA Davis, 1998; and MR Kinney, 58 Dunbar, JM Vitello
Cicciu, et al. (cds). AACN's Clinical Reference for Critical Care Nursing (4th ed). St. louis: Mosby, 1998.
=
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Description
Clinical Implicacions
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>-
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....
00
....
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oc
oc
Descri prion
Pacemaker (temporary)
Pulmonary artery
catheterization (PA line,
Swan-Ganz)
Normal values: PAP
(mean), 10-20 mm Hg;
PAWl' (mean), 6-12 mm
Hg; RAP, 0-8 mm Hg; core
temperature, 98.2100.zF (36.8-37.9C);
Clinicailmplic3rions
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>-
Aline arterial line; CI cardiac index; CO cardiac Output; CVP central venous pressure; LAP left atrial pressure; Jpm li ters per minute;
MAP mean arterial pressure; PAP pulmonary arrery pressure; PAWP pulmonary artery wedge pressure; RAP right atrial pressure.
Sources: Data from RR Kirby, RW Taylor, JM Civetta (cds). Handbook of Critical Care (2nd cd). Philadelphia: Lippincott-Raven, 1 997; MR Kin
ney, SB Dunbar, J M Virello-Cicciu, et al. (cds). AACN's Clinical Reference for Critical Care Nursing (4rh cd). Sr. Louis: Mosby, 1998; EK Daily,JP
Schroeder. Clinical Management Based on Hemodynamic Parameters. In FJ( Daily, JP Schroeder (eds), Techniques in Bedside Hemodynamic Mon
itoring (5th ed). Sf. Louis: Mosby, 1994; and EJ Bridges. Moniroring pulmonary artery pressures: JUSt the facts. Crit Care Nurse 2000;2 1 (16):67.
=
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790
PHLEBOSTATIC AX'S
4ICS
I
--
---
Mid-Point
A-P Chest Wall
Figure m-A.7. The phlebostatic axis at the intersection of the fourth intercos
tal space (lCS) and the midpoint of the anterior (A) and posterior (P) chest
wall. (Reprinted with permission from Edwards Lifesciences LLC.)
Aorta
Radial artery
Figure ID-A.8. Arteria/line tracing from different sites. (Repri"ted with per
mission from SM Yent;s, NP Hirsh, GB Smith leds/, Anaesthesia and Inten
sive Care A-Z. An Encyclopedia of Principles and Practice 12nd edJ. Oxford,
UK: Butterworth-Heinemann, 2000;45.)
fN THE AClITE
CARE SITTING
791
.....
'"
N
Device
Description
Clinical Implications
Epidural sensor
Subarachnoidl
subdural bol,
Intraventricular
catheter
(ventriculosromy)
()
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J:
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Z
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Fiberoptic transducer
tipped catheter
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Very reliable.
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7 94
Patients with elevated ICP are often positioned with the head
of the bed at 30 degrees, which maximizes venous blood flow
from the brain to help decrease ICP.'4 Therefore, be aware that
lowering the head of the bed may increase ICP. Other positions
that increase ICP are the Trendelenburg position, lateral neck
flexion, and extreme hip flexion.
Clinical Tip
>-
"l
Device
Description
Clinical Implications
AntithromboIytic
boots (pneumatic
compression stock
in a chair.
ings/Venodyne
boots)
Normal value,
CVP
0-8 mOl Hg
so
m
o
<;"
'"
Cl
.0
;r
involved extremity.
....
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f;:
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'"
'"
Device
Description
Clinical l mplications
Chest tube
breath, or mobility.
(0
a drainage
ment.
o
'"
(?
r
prevent tipping.
"
'"
:t
)
Z
g
'"
pneumothorax.
Prevent kinks in the line.
'"
facilitate drainage.
Ask the nurse or doctor whether the
chest rube may be temporarily
disconnected from suction during
mobiury activities. If the suction must
Esophagogastric
tamponade rube
(Blakemore tube,
Sengstaken
Blakemore tube,
Minnesota tube)
>
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c:
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c:
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Table
IU-A.6.
"
'"
00
COl/til/tied
Device
Description
Clinical Implications
Lumbar drainage
device (LDD)
L4-5 subarachnoid
Over-drainage or under-drainage
complications include tension
pneumocranium, central herniation
of the brain, compression of the brain
stem. and subdural hematoma .
g
."
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."
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Midline catheter
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ti
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Description
Cl inical I mplicatio ns
Nasogastric tube
(NGT)
Purpose: keeps the stomach empty after surgery and rests the
bowel by preventing gastric contents from passing through
the bowels. Some NGTs allow access to the stomach for
endoscopic
gastronomy!
jejunostomy tube
(pEG/PE]) tube
"
"
'"
J:
-<
r
Treatment time
s
i
usual1y 10-20
mms; however, the medications are
usually effective lor 3-6 hrs.
1.)
J:
,.
as nebs.
Percutaneous
Q
1::
,.
>
Percutaneous sheath
introducer (Cordis)
of pulmonary catheter.
Consists of: a Teflon sheath that often has a port for
I.V.
access.
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removed.
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Table
lli-A.6.
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o
N
Continued
Device
Description
Clinical Implications
Peripherally inserted
central venous
catheter
(Plcq
medications or fluid.
Rectal pouch/tube
dysfunction.
Consists of: a catheter pla.ced in the bladder through a
patient in bed.
g
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m
:t
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(3
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Surgical drain
Texas catheter
:;:
"
X
?:
"
oJ"
c
Ei
It is easily dislodged.
It may be held in place with a Velcro
strap.
The drainage bag should always be
below [he level of the bladder to
allow drainage by graviry.
Keep the collccrion bag off the Ooor.
Secure the collection bag or catheter
rubing to patient's leg, clothing, or
assistive device to prevent the patient
from tripping or becoming tangled in
the tubing during mobiliry activities.
.8
c
:;!
'"
i::
z
C)
00
o
'"
00
o
...
Description
Clinical Implications
Totally implantable
intravascular device
(Port-A-Cath,
MediPort)
Tunneled central
venous catheter
(Hickman, Broviac,
Groshong, Silasric,
and Quinton
catheters)
>
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'"
'"
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)
Z
"
1')
o
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o
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i
-<
Urinary catheter
(Foley carherer)
Yankauer suction
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>-
\:
'"
'"
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Description
Clinical Implications
Yankauer suctioning may stimulate a
cough and help clear secretions in
patients who are unable to dear
secretions independendy.
If a patient bites down on the
Yankauer, do not anempt to pull on
the device. Wait for the patiem to
relax, then gendy slide the Yankauer
from the patiem's mouth.
AV arteriovenous; CSF cerebrospinal fluid; CVP central venous pressure; TPN total parenteral nutrition.
Listed in alphabetical order.
Sources; Data from RR Kirby, RW Taylor, J M Civena (cds). Handbook of Critical Care (2nd cd). Philadelphia: Lippincorr-Raven, 1 997; F Hal
derman. Selecting a vascular access device. Nursing 2000; 1 1 :59-61; DF Colixxa. Actionstat: dislodged chest rube. Nursing 1 995;25-33; I-IJ
Thompson. Managing patients with lumbar drainage devices. Crit Care Nurse 2000;20:60-68; and Guidelines for intensive care unit admission,
discharge, and triage. Task Force of the American College of Critical Care Medicine, Society of Critical Care Medicine. Crit Care Med 1999;27:
633--638.
=
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J:
o
o
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o
;0
i:
i'i
>
...
:;Im
807
Figure [[I-A. I O. A chest drainage system has three mai" compartments from
left to right: ( 1) the suction control. (2) the water seal. (3) the collection
chamber. (Reprinted with permission from Genzyme Biosurgery.)
808
References
1 . Anonymous. Guidelines for intensive care unit admissions, discharge, and
triage. Task Force of the American College of Critical Care Medicine,
Society of Critical Care Medicine. Crit are Med 1 999;27(3),633--j)38.
2. Kirby RR, Taylor RW. Oxygen Therapy. In RR Kirby, RW Taylor, JM
Civetta (cds), Handbook of Critical Care (2nd cd). I'hiladelphi., Lippin
con-Raven, 1 997;254,260.
809
4.
5.
6.
7.
8.
9.
10.
II.
12.
13.
1 4.
Dimas (cds), The Essentials of Respiratory Care (3rd ed). St. Louis:
Mosh), 1 990;408.
Scanlan el, Heur A. Medical Gas Therapy. In DF Egan, CL Scanlan
(eds), Egan's Fundamentals of Respiratory Care (7th ed). St. Louis,
Mosby, 1 999;738,748.
Ryerson EF, Block AJ. Oxygen as a Drug' Clinical Properties, Benefits,
Modes and Hazards of Adminisrrarion. In GG Burron, JE Hodgkin
(cds), Respiratory Care, A Guide to Clinical Practice (3rd ed). Philadel
phi., Lippincott, 1 99 1 ;325-326.
Kacmarek RM. Neurologic Control of Ventilation. In RM Kacmarek,
CW Mack, S Dimas (eds), The Essentials of Respiratory Care (3rd ed).
St. LoUIS, Mosby, 1 990;80.
Dally FK, Schroeder JP. Clmical Management Based on Hemodynamic
Parameters. In FK Dady, JP Schroeder (cds), Techniques in Bedside
Hemodynamic Monironng (5rh cd). Sr. lOUIS: Mosby, 1994;235.
Whalen DA, Kelleher RM. Cardiovascular Parient Assessmenr. In MR
Kmney, SB Dunbar, JM Vitello-CiCClu, et al (eds), AACN's Clinical Ref
erence for Crincal Care Nursing (4rh ed). Sr. louis: Mosby, 1 998j303.
Smith RN. Conceprs of Monitoring and Surveillance. In MR Kinney, S8
Dunbar, JM Vircllo-Cicciu, er 31 (cds), AACN's Clinical Reference for
Cntlcal Care Nurs11lg (4th ed). St. Louis: Mosby, 1 998;1 9.
Bridges Ej. tvloniroring pulmonary ,urery pressures: jusr rhe facts. erir
Care Nurse 2000;20,67.
Daily EK, Schroeder JP. Principles and Hazards of MOnlroring Equip
ment. In EK Dally, JP Schroeder (cds), Techniques in Bedside Hemody
namic Moniroring (5th ed). St. louis: Mosby, 1 994;37.
Bridges El. \Voods SL. Pulmonary artery pressure measurement: state of
the art. Heart Lung 1 993;22,99.
Hickey jV. Theory and Management of Increased Intracranial Pressure.
In JV I hckey (cd), The Chnical Practice of Neurological and Neurosur
gical NUr<mg (4th cd). Philadelphi" Lippincott, 1997;3 1 6 .
Boss Bj. Nursing Management of Adults wirh Common Neurologic
I'rohlems. In PG Beare, JL Myers (eds), Adult Health Nursmg (3rd ed).
St. LouI" Mosby, 1 998;9 I 7-924.
III-B
Mechanical Ventilation
Sean M. Collins
811
812
2
The following are indications for mechanical ventilation ;
Partial pressure of arterial oxygen of less than 50 mm Hg with
supplemental oxygen
813
ostomy tube is inserted directly into the anterior trachea below the
vocal cords, generally performed in the operating room. Benefits of
tracheostomy include (I) reduced laryngeal injury, (2) improved oral
comfort, (3) decreased airflow resistance, (4) increased effectiveness
of airway care, and (5) feasibility of oral feeding and vocalization. If
the patient is able to be weaned from ventilatory support, humidified
oxygen can be delivered through a tracheostomy mask (Table IU-A.l).
814
Cuff
Approximately 0.5 in. from the end of an endotracheal or tracheal
tube is a cuff (balloon). The cuff is inflated to (1) ensure rhar all of rhe
supplemenral oxygen being delivered by rhe venrilator via the artifi
cial airway enters the lungs and (2) help hold the artificial airway in
place. Cuff inflation pressure should be adequate to ensure that no air
is leaking around the tube; however, cuff pressures should not exceed
20 mm Hg. High cuff pressures have been linked to tracheal damage
and scarring, which can cause tracheal stenosis.
Clinical Tip
815
may increase the pressure placed on the dependent lung tissue and
result in barotrauma. Conversely, in the same scenario, if a patient is
on a pressure-cycled ventilator, then pressure will be delivered to the
predetermined level, but because the patient's position may hinder
chest expansion, a resultant lower volume of inspired air may be
delivered, because the preset pressure limit was reached. Many newer
ventilators provide the clinician with more than one cycling option,
and certain modes of ventilation allow for more than one parameter
ro derermine the inspirarory phase (as discussed throughout this
appendix).
Clinical Tip
Modes of Ventilation
00
'"
,.
No Spontaneous
Breathing -
Some Spontnneous
Breathing: RR < 10
Dependence
effons:
Total Ventilator
Weak. inspiratory
VT<6mL1kg
Good Spontaneous
Spontaneous Breathing:
(RR < 10)
Brearbing: RR> 10
But inspiratory effort
still
weak:
ventilation and
Good EfTon:
able to
NIF> 20 em H:O
suppor t self
VT> 10 m.Vkg
Vt < 10 mllkg
lndependent with
physiologically
4
Synchronous
lntennittem
Mandatory
Ventilation
p"""",
Support
Ventilation
Continuous
Positive
[E,"d
Airway
p..,....
Figure ill-B.2. Schematic of mechanical ventilator modes: the ability of patients to participate in the process of ventilation and
oxygenation in part determines the mode of ventilation. Parameters used to determine the patient's ventilatory effort include the
presence of spontaneous breaths, the number of breaths per minute he or she initiates (respiratory rate [RR)). the volume of
those breaths per breath (tidal volume /VT}). and the negative inspiratory force (NIF) generated with those breaths. The values
indicated above are examples 0/ patient characteristics along the spectrum (rom complete ventilatory dependence to indepen
dence. The effectiveness of the patient's efforts needs to be assessed based not only 011 the above parameters. but on "outcon-te"
variables, such as oxygenation (Pao'}! oxygen saturation as measured by pulse oximetry). ventilation (Paco2), and overall status
(hemodynamic stability. symptonts).
9
i:;
s;
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817
Characteristics
CV
AV
A ssist!
control
ventilation
IMV
SIMV
Pressure
supponed
ventilation
818
Characteristics
Continuous
positive
airway
pressure
AV
assisted venrilation; CV
ventilation; PEEP
Intermittent mandatory
sensus Conference Isee comments). Chest 1993; 104: 1833; and SF !-lowman. Mechani
cal ve'nrilation: a review and update for clinicians. Hospital Physician 1999;December:
26-36.
Ventilatory Settings
819
Characteristics
Pressure control
ventilation
High-frequency
oscilla.rion
ventilation
Inverse rario
ventilation
Mandatory minute
ventilation
Noninvasive
positive pressure
ventilators
(NIPPV)
Negative pressure
ventilators
820
Characteristics
Airway pressure
release ventilation
(APRV)
High-frequency jct
ventilation
Partial liquid
ventilation
ACV
=
ratio; PEEP
SIMV
sensus Conference Isee commentsj. Chest 1993; I 04: 1833; and SF Howman. Mechani
cal ventilarion: a review and updare for clinicians. Hospital Physician I 999;Oecember:
26-36.
Setting
Characteristic
Oxygen
Fraction of
The percentage of inspired air that is oxygen; at normal respiratory rare (RR), tidal volume
ation
inspired oxy
gen
(FIO,)
(VT), and flow rates, an FlO! of 21% (ambient air) yields a normal oxygen partial pressure of
95-100 mm Hg; an increase in the percentage of oxygen delivered to the alveoli results in a
greater Paol and therefore a greater driving force for the diffusion of oxygen 1Oto the blood.
of 60% has been set as the threshold ....alue ro aVOid toxiclry with prolonged use.
Positive end
expiratory
pressure
(PEEP)
FIOZ
The pressure maintained by the mechanical ventilator in (he air""ays at (he end of expiration;
normal physiologic PEEP (maintained by sufficient sutfactant levels) is considered to be 5
em H 1 0.
Semngs are adjusted as needed to maintain functional residual capaclry above closing capacity
to avoid closure of alveoli.
Closure of alveoli can result in shunting of blood past the alveoli without gas exchange, which
results in decreased oxygenation.
Ventilation
RR
Set according to the amount of spontaneous ventilatory efforts by the patient; different
ventilatory modes, described in Table IlI-S.I, are prescribed according to the patient's needs;
patients who are unable to generate any spontaneous breaths are fully ventilated at
respiracory rates of
This rate is decreased accordingly for those who are able to generate spontaneous breaths.
The amount of volume delivered with each breath is adjusted with respiracory rate to control
partial pressure of arterial carbon dioxide (Pacoz)'
VT
Excessive volume leads to increased airway pressures, and therefore pressures are routinely
monitored to pre....ent barotrauma.
At times, hypercapnia is allowed to prevent high lung pressures due to the delivered volume
and noncompliance of lung tissue, termed permissive hypercapnia.
>
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Z
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X
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?:
l:
::;
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r
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00
tv
Table
ITI-B.3. Continued
Purpose
Serring
Characteristic
InspiratOry
flow rare
Set to march the parient's peak inspiracocy demands; if this match is not correct, it can
cause the patient discomfort while breathing with the ventilator.
High flow rates deliver greater volume in less time and therefore allow longer expirarory
rimes (prevents hyperinflation); however, this also leads to greater peak airway pressure
and the possibility of barotrauma.
If the rate is roo slow, the patient may attempt to continue to inhale against a closed circuit,
resulting in respiratory muscle fatigue.
The inspiratory to expiratory rario is set with the goal of allowing the ventilator to be as
synchronous as possible with the patient's respiratory ratio.
For patients who are not spontaneously breathing, this rario is set according to what is
required to maintain adequate ventilation and oxygenation.
Pressure change is required in the airway to trigger an ACV or PSV breath; typically -] to -3
em H,o.
If mechanical sensors respond poorly, then respiratory muscle fatigue can occur.
If [he sensors are too sensitive, then hyperventilation can develop.
Inspiratory to
expirarory
ratio
Sensitivity
ACV
00
....
....
>
pressuresupponed ventilarion.
Sources: Data from P Marino. The lCU Book (2nd ed). Philadelphia: Lea & Febiger, 1998; AS Slutsky. lech3nical ventilation. American Col
lege of Chest Physicians' Consensus Conference Is comments). Chest 1993; 1 04: 1833; and SF Howman. Mechanical ventilation: a review 3nd
update for clinicians. Hospital Physician 1999;December:26-36.
\?
Z
o
g
,.,
o
'"
-<
:i!
'"
'"
>
"
823
nary disease who are on ventilator modes that allow them ro initiate
ventilaror-assisted breaths (assisted ventilation, assist/control ventila
tion, synchronous intermittent mandatory ventilation [SLMV], pressure
supported ventilation [PSV]), the therapist should realize that activity
could increase the patient-generated respiratory rate. Some modes
will then, given the initiation of a breath, provide a set volume of air
(assisted ventilation, assistlcontrol ventilation, SIMV) that could
increase the likelihood of hyperinflation owing to autO PEEP. This can
also happen in modes that do nOt deliver a set volume of air (PSV),
because inspiration is assisted with positive pressure.
Barotrauma
Barotrauma refers to damage ro the lungs caused by excessive airway
824
not detected, gastric distention can occur with the initiation of pos
itive pressure.
Oxygen toxiciry: Oxygen levels rhar are roo high and maintained
for a prolonged rime can resulr in (1) subsrernal chesr pain rhar is
exacerbared by deep brearhing, (2) dry cough, (3) rracheal irrirarion,
(4) pleuriric pain wirh inspirarion, (5) dyspnea, (6) nasal sriffness
and congesrion, (7) sore rhroar, and (8) eye and ear discomfort.
Spontaneous breathing
API'F:NDIX
111-8:
MECHANICAL VENTILATION
825
Oxygenation
3.
Cardiovascular performance
4.
Psychological factors
5.
826
Bronchopulmonary Hygiene
During the weaning process, the physical therapist can play a vital role
on an interdisciplinary team responsible for coordinating the wean.
Physical therapists offer a combined understanding of the respiratory
difficulties faced by the patient, the biomechanics of ventilation, the
principles of exercise (weaning is a form of exercise), and the general
energy requirements of functional activities. Physical therapists can
work with the multidisciplinary team to optimize the conditions under
827
which the panent attempts each wean (time of day, activities before and
after the wean, position during the wean) and parameters to be manip
ulated during the wean (frequency, intensity, duration). Patients should
be placed in a position that facilitates the biomechanics of their ventila
tion.12 For many parients, rhis is seared and may also include the ability
ro sir forward with the arms supported.
Biofeedback to increase VT and relaxation has been shown to
improve rhe effecriveness of weaning and reduce time on the ventila
ror. n Inspirarory muscle resistive training has also been shown to
increase respiratory muscle strength and endurance ro facilitate the
weaning success. 14
References
I. Manno P. The ICU Book (2nd ed). Philadelphia: Lea & Febiger, 1998.
2. Slutsky AS. Mechanical ventilation. American College of Chest Physi
cians' Consensus Conference Isee commentsJ. Chest 1993;104:1833.
3. Howman SF. Mechanical vemilation: a review and update for clinicians.
Hosplt.1 Physician 1999;December:26-36.
4. Sadowsky liS. Thoracic Surgical Procedures, Monitoring, and Support
Equipment. In EA Hillegass, HS Sadowsky (eds), Essentials of Cardio
pulmonary PhYSIcal Therapy (2nd ed). Philadelphia: Saunders, 2001;
464-469.
5. Amuero A, Peters JI, Tob," MJ, et al. Effecrs of prolonged mechanical
ventilation on diaphragmatic function in healthy adult baboons. Crit
Care Med 1997;25:1187-1190.
6. Gerold KB. Physical therapists' guide to the principles of mechanical
ventilation. Cardlopul Phys Ther 1992;3:8.
7. Costello ML, Mathieu-Costello 0. West JB. Stress fracture of alveolar
epithelial cells studied by scanning electron microscopy. Am Rev Respir
DIS 1992;145:1446-1455.
8. Mathieu-Costello 0, West JB. Are pulmonary capillaries susceptible to
mechal1lcal stress? Chest 1994;105(Suppl):1025-107S.
9. Heimler R, Huffman RG, Starshak RJ. Chronic lung disease in prema
ture infams: A retrospective evaluation of underlying factors. Crit Care
Med 1988;16:1213-1217.
10. Yang KL, Tobin MJ. A prospective study of indexes predicting the out
come of trials of weaning from mechanical vencilation. N Engl J Med
1991;324:1446-1495.
11. Dries DJ. \Veaning from mechanical ventilation. J Trauma 1997;
43:372-384.
12. Shekleron ME. Respiratory muscle condition and the work of breaching
a critical balance in [he weaning patient. AACN Clin Issues Crit Care
1991;2:405-414.
828
13. Holliday JE, Hyers TM. The reduction of wean time frol11 mechanical
ventilation using tidal volume and relaxation biofeedback. Am Rev
Respir Dis 1990;141:1214-1220.
14. Aldrich TK, Karpel JP, Uhrlass RM, et 301. Weaning from mechanical
ventilation: adjunctive use of inspiratory muscle resistive training. Crit
Care Med 1989;17:143-147.
III-C
Circulatory Assist Devices
Jaime
C.
Paz
829
830
Balloon
inflated
Figure HI-C. I.
831
Balloon
deflated
Unstable angina
Cardiogenic shock
832
Clinical Tip
During IABP, the lower extremity in which femoral
access is obtained cannot be flexed at the hip, and the
patienr's head cannot be raised higher than 40 degrees in
bed.
833
Left Battery
omitted for clarity
External
Battery
Pack
XVE
LVAD
Skin
Line
Vent Adapter
& Vent Filter
XVE System
Controller
Figure IU-C.2. The HeartMate implantable left ventricular assist device
(LVAD). (XVE extended lead vented electric.) (Reprinted with permission
{rom Thoratec Corporation, Woburn, MA.}
=
834
right ventricle also needs assistance (right VAD). In more severe situa
tions, both ventricles need to be assisted (bivenrricular assist device) .
The various types and general characteristics of internal and external
VADs are described briefly in Table Illc.l. It is beyond the scope of
this appendix to describe in detail all the aspects of each type of VAD;
however, physical therapists working with patients on a VAD need to
be familiar wirh the type of machine that the patient is on, as well as
the safery features of the VAD.
Weaning from VAD involves a gradual decrease in flow rates,
which allows the patient's ventricle to contribute more to rotal sys
temic circulation. Complications of VAD include thrombosis, bleed
ing, and infection at or near the insertion sites of the access lines.
The combination of technological advancements and a lack of donor
organs has increased the use of VADs in patientS with cardiomyopathy.
Therefore, physical therapists are more likely to encounter rhis equip
ment in the hospital. Research has demonstrated that patients with a
VAD can be mobilized safely in the hospital and that their exercise tol
erance can be improved while awaiting transplantation.
835
Mechanism
Use
Pneumatic
Left ventricle
Internal VADs
HearrM:ne
or electric
Novacor
Electric
Left vencricle
SymbioniCardioWe"
Pneumatic
BOth ventricles
Bio-Medicus
Centrifugal
Thocatec
Pneumatic
Hemopump
Axial flow
Left ventricle
Pneumatic
5000
both
Sources: D;Ha from EF Bond, J Da:<. Nursing Man3gemem Crirical Care. In SM Lewis,
836
a.
b.
LVAD volumes dO ml
c.
d.
e.
f.
>
ECMO involves the use of a device external to the body for direct
oxygenation of blood, assistance with the removal of carbon dioxide,
or both. The primary indication for ECMO is cardiac or respiratory
failure that is not responding to maximal medical therapy. The pedi
atric population with respiratory failure seems to benefit from this
therapy the most; however, the successful use of ECMO in the adult
population is improvingJ-9
Patient situations that are likely to require ECMO include the fol
lowing:
Cardiac arrest
Cardiogenic shock
Arl'ENDIX
837
2.
Right atrium to the ECMO system back to the ascending aorta
3.
Femoral vein to the ECMO system back to the ascending aOrta
The system that lIses the venous drainage to venous rerum cannula
(V-V mode) is primarily used for patients who only have respiratory
failure. The V-V mode can be achieved in twO ways':
I.
Internal jugular vein to the ECMO system back to the
common femoral vein
2.
Common femoral vein drainage to the ECMO system
back to the concralateral common femoral vein
Patients who are on V-A mode ECMO are typically anticoagulated
with heparin and may require the use of IABP to further assist the
ventricle. Patients on the v-v mode may require sedation and or med
ical paralysis ro help improve oxygenation to organs and tissues by
minimizing the metabolic demands of an awake person.'
Complications of ECMO include lower limb ischemia, thrombocy
ropenia, thromboembolism, and failure of the oxygenaror device.9
838
to
References
1. Mahaffey KW, Kruse KR, Ohman EM. Intra-aortic Balloon Pump
Counterpulsation: Physiology, Parient Management, and Clinical Effi
cacy. In DL Brown (ed), Cardiac Intensive Care. Philadelphia: Saunders,
1998;647-653.
2. Bond EF, Dax J. Nursing Management; Critical Care. In SM Lewis, MM
Heitkemper, SR Dirksen (eds), In Medical Surgical Nursing: Assessment
and Management of Clinical Problems (5th edl. Sr. Louis: Mosby,
2000;1926-1927.
3. Smedira NG, Vargo RL, McCarthy PM. Mechanical Support Devices
for End-Stage Heart Failure. In DL Brown (cd), Cardiac Intensive Care.
Philadelphia: Saunders, 1998;697-703.
4. Humphrey R, Buck L, Cahalin L, Morrone T. Physical therapy assess
ment and intervention for patients with left ventricular assist devices.
Cardiopulmonary Phys Ther 1998;9(21:3-7.
5. Buck LA. Physical therapy management of three patients following left
ventricular assist device implantation: a case report. Cardiopulmonary
Phys Ther 1998;9(2):8-14.
6. Morrone TM, Buck LA, Catanese KA, ct al. Early progressive mobiliza
tion of patients with left ventricular assist devices is safe and optimizes
recovery before heart transplantation. J Heart Lung Transplant
1996;15:423-429.
IV
Pharmacologic Agents
Jaime C. Paz and Michele P. West
Pharmacologic Agents
The purpose of this appendix is to provide an overview of the pharmaco
logic agents that are commonly prescribed as an adjunct to the medical
surgical management of a wide variery of diseases and disorders. The
medications in this appendix are organized according to drug class in the
following index. A description of the indication(s), mechanism of action,
and common side effects is included for each rype of medication.
Nore rhat some pharmacologic agents are listed in another chapter
or appendix, as referenced below.
Drug Class
Location
Page
Number
Table IV-l
842
Angjorcnsin-converring enzyme
inhibirors
Table lV-2
842
Antiarrhythmic agents
Table IV-3
843
Anticoagulants
Table lV-4
844
839
840
Drug Class
Location
Page
Number
Anticonvulsant agents
Table IV-5
845
Antiemetic agents
Table IV-6
846
Antihistamines
Table IV-7
847
Antiinfectious agenrs
Table IV-8.A-F
848-850
Table IV-8.A
848
Cephalosporins
Table IV-8.B
848
Macrolides
Table IV-8.C
849
Penicillins
Table IV-8.D
849
Sulfonamides
Table IV-8.E
850
Tetracyclines
Table IV-8.F
850
Antiparkinsonian agents
Table IV-9
851
Antiplarelet agents
Table IV-IO
851
Antitussives
Table IV-I I
852
Aminoglycosides
Beta blockers
Table IV-12
853
Bronchodilators
Table IV-IJ
853
Table IV-14
854
Chemotherapy agents
Table IV-15.A-H
854-860
Alkylating agents
Table IV-15.A
854
Antibiotics
Table IV-15.B
855
Antimetabolite agents
Table IV-15.C
856
Hormones
Table IV-15.D
857
Plant alkaloids
Table IV-15.E
859
Interferons
Table IV-15.F
859
Table IV-15.G
860
Table IV-15.H
860
Corticosteroids (inhaled)
Table IV-16
861
Diuretics
Table IV-I 7
861
Endocrine medications
See endocrine
disorders in
Chapter I I
651-693
Expectorants
Table IV-18
862
Table IV-19.A-B
862
Antacids
Table IV-19.A
862
Antiulcer medications
Table IV-19.B
862
Table IV-20.A-B
863-864
Antidiarrhea medications
Table lV-20.A
863
Laxatives
Table IV-20.B
864
841
Page
Number
Drug Class
Location
Genitourinary medications
See genitourinary
disorders in
Chaprer 9
557
See Human
1mmunodeficiency
Virus Infection in
Chaprer 10 and
Table 10-5
614,635
Table 12-1
704
Intranasal sreroids
Table lV-21
864
Table lV-22
865
Mucolytics
Table lV-23
865
Nitrates
Table IV-24
866
Table IV-25
866
Osmoric diuretics
Table IV-26
867
Pain medications
See Appendix VI
879-884
Positive inotropes
Table IV-27.A-B
867
Cardiac glycosidcs
Table IV-27.A
867
Symparhomimetics
Table IV-27.B
867
Table TV-28
868
Table TV-29
868
460
Vasodilarors
Table IV-30
869
842
Sources: Data from Drug I:acts and ComparlSoJl!. 2000 (541h cd). \t. LOlll: Woller..
Kluwer, 2000; and Drug Facis and Compansons 2001 (.Ulh cd). \t. I.OUl'i: Wolrer ...
Kluwer, 200 I.
843
844
Danaparoid sodium
( Orgaran)
Heparin sodium
Lepirudin (Refludan)
845
monaryembolism.
Sources: Dam from Drug Facts and Comparisons 2000 (54th cd).
Kluwer,2000; and Anticoagulant, Amipiarclet, and Thrombolytic Drugs. Ln RA Lehne
(ed),
846
Family Name
Phenorhiazines
Generic Name
(Trade Name)
Side Effecrs
Chlorpromazine (Thora
zine)
Prochlorperazine
(Compazinc)
Promethazine
(Phenergan)
Haloperidol
(Haldol)
Droperidol
(Inapsine)
Cannabinoids
Tetrahydrocannabinol
(marijuana)
Antihistamines
Diphenhydramine
(Ben.dryl)
Dexamethasone
(Decadron,
Hexadrol,
Dexone)
Lorazepam
(Ativan)
Butyrophenones
Corticosteroids
Benzodiazepines
Family Name
Other
Generic Name
(Trade Name)
847
Side Effects
Mccociopra
mide (Reglan)
Trimethobenza
mide (Tigan)
848
APPENDIX
IV:
I'HARMACOLOGIC AGENTS
849
850
851
Ticlopidin e
hydrochloride
(lic\id)
Tirofiban
(Aggrasrar)
852
Abciximab
(ReoPro)
Anagreiide
hydrochloride
(Agrylin)
Dipyridamole
(Persancine)
Sources: Data from Drug Facts and Comparisons 2000 (54th cd). St. Louis: Wolters Klu
wer, 2000; and Anticoagulant, Antiplarelet, and Thrombolytic Drugs. In RA Lehne (ed),
Pharmacology for Nursing Care (4th ed). Philadelphia: Saunders, 200 1 .
853
854
Side Effects
Busulfan (Myleran)
Carboplatin (Paraplatin)
Carmustine (BiCNU)
Chlorambucil (leukeran)
Cisplatin (Platinol)
Cyclophosphamide
(Cyroxan)
Cardioroxicity, leukopenia,
thrombocyropenia, anemia, pulmonary
fibrosis
Dacarbazine (OTIC-Dome)
855
Side Effects
Ifosfamide (Ifex)
Lomustine (CeeNU)
Mechlorethamine
(Musrargen, Nitrogen
Mustard)
Melphalan (Alkeran)
Procarbazine
Streprozocin (Zanosar)
Thiotepa (ThiOtepa)
Uracil mustard
Dactinomycin
(Cosmegen)
Side Effects
Nausea, vomiting, fever, chills, anaphylaxis, alopecia,
sromaritis, erythema, pulmonary tOxicity (interstitial
pneumoniris), general weakness and malaise, head
ache, leukocytosis, pulmonary fibrosis, joint swelling
Nausea, vomiring, myelosuppression, tissue necrosis,
alopecia, mucositis
856
Side Effects
Daunorubicin
(Cerubidine)
Doxorubicin
(Adriamycin)
Mitomycin
(Mutamycin)
Mitoxantrone
(Novantrone)
Plicamycin
(Mithracin)
Sources: Dam from C Ciccone (cd). Cancer Chemotherapy. Philadelphia: FA Davis, 1 996;
and D Moreau (ed). Nursing '96 Drug Handbook. Springhouse, PA: Springhouse, 1996.
Side Effects
Cladribine (2-chlorode
oxyadenosine)
Cytarabine (Cyrosar-U)
Floxuridine (FUDR)
S -Fluorouracil (Adrucil)
Generic Name
(Trade Name)
857
Side Effects
Hydroxyurea (Hydrea)
Mercapropurine
(Purinethol)
Methorrexate (Folex,
Mexatc, Rheumatrcx)
Thioguanine (Lanvis)
Anriestrogens
Estrogens
Generic Name
(Trade Name)
Tamoxifcn (Nol
vadex)
Toremifene
Chlororrianisene
(TACE)
Diethylstilbesrrol
(DES)
Estradiol
(Oestradiol,
Valerate)
Medroxyproges
terone
858
Prednisolone
(Delra-Corref)
Androgens
Fluoxymesterone
(Android-F)
Anriandrogcns
Flutamide
(Eulexin)
Anasrra:z.ole
Aromarase
inhibitor
Aminoglurethimide
Gonadorropinreleasing
hormone
drugs
Leuprolide
(Lupron)
Adrenocorticosteroids
Anticachetics
Goserelin acetate
Goserelin
(Zoladex)
Megestrol
(Megace)
Megestrol
acetate
859
Eroposide (VePesid)
Teniposide (VM-26)
Interferon alfa-2a
Interferon alfa-2b
860
Side Effects
Filgrastim ( Neupogen)
Aminoglutethimide (Cytadren)
Aldesleukin (IL-2)
Hypoglycemia, anemia
Procarbazine (Matulane)
861
Table I V - I ? Diuretics
Indications: Heart failure, hypertension
Mechanism of action: Reduce preload and vascular volume
General side effects: Volume reduction, hypotension, arrhythmias, hyper- or
hypokalemia (Only potassium-sparing diuretics can lead to hyperkalemia,
all others generally lead to hypokalemia.)
Thiazides (generic name [ trade name!): Bendrofluazide (Aprinox, Cenryl),
bendroflumethiazide (Naturetin ) , benthiazide (Exna, Hydrex),
chlorothiazide (Diuril), chlorrhalidone (Hygroron ) , cyclorhiazide
(Anhydron ) , cyclopenthiazide (Navidrex), hydrochlorothiazide (Esidrex,
HydroDIURIL), hydroflumethiazide (Diucardin , Saluron ) , i n dapamide
(Lozol, Natri lix), methyclothiazide (Enduron, Aquatenscn), metolazone
(Mykrox, Diulo, Zaroxolyn ) , polythiazide (Renese), quinethazone
(Hydromox), trichlormcthiazide (Metahydrin, Naqua)
Loop (generic [trade name!): Bumetanide (Bumex), ethacrynic acid (Edecrin),
furosemide (Lasix, Furoside), frusemide (Frusetic, Frusid), pircranide (Arlix)
Potassium sparing (generic [ trade nameD: Amiloride (Midamor), potassium
canrenoate (Spiroctan-M), spironolactone (Aldactone) , triamrerene
(Dyrenium)
Carbonic anhydrase inhibitors (generic [ trade narnel): Acetazolamide
(Diarnox), dichlorphenamide (Daranide), methazolam ide (Neprazane)
Source: Data from K Grimes, M Cohen. Cardiac Medicafions. In EA Hillegass, HS Sad
owsky (cds), Esscnti"ls of Cardiopulmonary Physical Therapy (2nd cd). Philadelphia:
Saunders, 2001 ;537-585.
862
863
111
2001 D rug I landhook ( 2 1st ed) Springhouse, PA: Springhouse, 2001 ;653-672.
864
865
866
867
868
Anisrreplase (Eminase),
streptokinase
(Kabikinase, S treptase),
urokinase (Abbokinase)
CVA
cerebrovascular accidcm; MI
APPENDIX
IV:
PHARMACOLOGIC AGENTS
869
v
Effects of Anesthesia
Michele P. West
has stable viral signs for at least 1 hour, meers the criteria for dis
charge from the PACU.3 The criteria for discharge from the ambula
tOry recovery room are similar to that of the PACU and include
recovery from sedation or nerve block.3
The physical therapist should be aware of common postoperative
complications (and the protocols and procedures to address them) to
intervene as safely as possible, prioritize the physical therapy plan of
care, and modify treatment parameters.
871
872
I.
The major systemic effects of general anesthesia are the
following;
A.
B.
Respiratory effects,,6
1.
Arterial oxygenation
b.
c.
d.
Respiratory pattern
e.
Minute ventilation
f.
g.
Mucociliary function
h.
Surfactant
b.
c.
3.
873
c.
Smoking history
d.
Obesity
e.
Increased age
f.
g.
II.
for the proper function and return of all of the major body sys
tems. The most common postoperative complications include
the following2.):
A.
Neurologic complications
1.
sciousness
B.
C.
2.
3.
2.
Hypertension
3.
Dysrhythmia
4.
Myocardial infarction
5.
Hemorrhage
6.
7.
Pulmonary embolism
Respiratory complications
1.
Airway obstruction
2.
Hypoxemia
3.
Hypercapnia
4.
5.
Hypoventilation
6.
Pulmonary edema
874
AClITE
CARE
D.
E.
F.
G.
Renal complications
1.
2.
Urine retention
3.
Urinary infection
Gastrointestinal complications
1.
2.
Hiccups
3.
Abdominal distention
4.
Paralytic ileus
Integumentary complications
1.
Wound infection
2.
3.
Hematoma
Other complications
I.
Hypothermia
2.
Sepsis
3.
Hyperglycemia
4.
5.
Electrolyte imbalance
6.
Acid-base disorders
APPENDlX
V:
EFFECfS
Of
ANESTHESIA
875
References
l. Litwack K. Immediate Postoperative Care: A Problem-Oriented
Approach. In JS Vender, BD Spiess (eds), Posr-Anesrhesia Care. Philadel
phia: Saunders, 1992;1.
2. Litwack K. Posroperarive Patient. In SM Lewis, MM Heitkemper, SR
3.
4.
5.
6.
VI
Pain Management
Jaime
C.
Paz
Evaluation
The subjective complaint of pain is often difficult to objectify in the
clinical setting. However, an effective pain treatment plan depends on
an accurate evaluation of the pat.ient's pain,l.2 Each evaluation
requires a complere physical and diagnostic examination of the
patient's pain. The goal for evaluation should be toward individual
ization while maintaining consistency among patients. To assist with
this process, various pain rating rools have been developed. Table
VI-l describes some of the pain rating tools that are used in the acute
care setting, with the visual analogue and numeric raring scales being
the mOst commonly used.I3,4
877
878
Description
Faces scale
Pain diary
Clinical Tip
879
insight into the sympathetic tone of the patient, which can be indic
ative of their level of pain. This can be performed easily in the
intensive care setting, because the patient'S hemodynamic status is
being continuously monitored.
therapist should use the same pain rating tool as the medical-surgi
cal team to determine adequacy of pain management.
Management
Nonsteroidal anti-inflammatOry drugs (Table VI-2) and systemic opi
oids (Table Vl-3) are the most common pharmacologic agents pre
scribed for postOperative pain. Aspirin and acetaminophen (Tylenol)
are also common medications prescribed for pain relief and are cate
gorized as non-narcotic analgesic and antipyretic drugs.78 Alterna-
880
881
to
Mechanism of action:
Blocks tranmission of pain from the spinal cord to the cerebrum by
imeractmg with opioid receptors
Can he adminlsrered orally, IIlrravenously, IIlrramuscularly, subcutaneously,
and imrathecally
General side effecrs:
Decreased gastrointestinal morility, nausea, vomiting, and cramps
Mood changes and sedarion
Prurirus (itchmg)
Unnary retention
Respirarory and cough depression
Pupillary consmetlon
Medications: Generic name (trade name)
Allentanol hydrochloride (Allenta, Rapilen)
Buprenorphllle (Buprenex, Temgesic)
Butorphanol (Stadol)
Codeine (Paveral)
Dezocine (Dalg.n)
Fentanyl (Sublam,"e)
Fentanyl transdermal (Duragesic)
Ilydromorphone (D.I.udid, CD Palladone)
Levorphanol (Dromoran, Levorphan)
Meperidlllc (Demerol, CD Pamergan, CD Pethidine)
Methadone (Dolophinc, Merhadose, Physcprone)
Morphine (MS Contin, Roxanol, Anamorph, Astramorph, Morcap,
Duramorph, Epimorph, Infumorph, Oramorph, Rescudose, Starex)
N.lbuphone (Nubaon)
Naloxone (Narcan)
Oxycodonc (Roxicodone, Supeudol, Endodan, Tylox, Percocet, Percodan)
Oxymorphone (Nulllorphan)
Pentazocine (Fortral, Talwin)
882
883
Local anesthetics
Bupivacaine, ropivacaine (Naropin), or arricaine combined with
epinephrine
Nonsteroidal antiinflammatOry drugs
Acetaminophen, kerorolac (Toradol), or ibuprofen
Sources: Data from JC Ballantyne, D Borsook. Postoperarive Pain. In D Borsook,AA
LeBel, 8 McPeek (cds),The Massachusetts General Hospital Handbook of Pain Man
agement. 80ston: Little, Brown, 1996;252; C Pasero,M McCaffery. Providing epidural
analgesia. Nursing 1999;29(8):34; and WM Davis, MC Vinson. New drug approvals
of 2000,part 2. Omg Top;cs 2001; 145(5);89.
884
into the subcutaneous tissue in the lower right or leh abdominal quadrant.
A catheter, which is placed in the epidural or intrathecal space, is tunneled
subcutaneously along the flank and connected to the pump.
Pumps are programmable or nonprogrammable and require refilling every 212 wks.
Consideration:
Generally performed as all outpatient procedure, but patients may remain in
the hospital for several days for observation
General side effects:
Similar to systemic opioids (Table V I-3)
Medications: Generic (trade name)
Morphine or hydromorphone (Dilaudid)
Sources: Data from L Valentino, KY Pillay,J Walker, Managing chronic nonmalignant
pain with continuous intrathecal morphine. J Neurosci Nurs 1998;30(4):233; and M
York, JA Paice. Treatment of low back pain with intraspinal opioids delivered via
implanted pumps. Orrhop Nuts 1998; 17(3);61.
The physical therapist should instruct the parient nOt to hold his
or her breath during mobility, because doing so increases pain.
885
References
J. Kittclberger KP, LeBel AA, Borsook D. Assessment of Pain. In D 80r
sook, AA leBel, B McPeek (eds), The Massachusetts General Hospital
Handbook of Pain Managemcnt. Boston: Litrle, Brown, 1996;26.
2. Cristoph SD. Pain asscssment: the problem of pain in the critically ill
parient. Crir Care Nurs Clin N Am 1991;3(1):11-16.
3. Carey Sj, Turpin C, Smith j, ct al. Improving pain management in an
acute care setting; the Crawford Long Hospital of Emory University
experience. Orrhop Nurs 1997; 16(4):29.
4. Haggelil'. Pain management. J Neurosci Nurs 1999;31(4):251.
5. Turk DC, Okifuji A. Assessment of patients' reporting of pain: an inte
grared perspecrive. Lancer 1999;353(9166):'1784.
6. Acello B. Meeting jCAHO standards for pain control. Nursing
2000;30(3):52-54.
7. Nursing 2001 Drug Handbook (21st ed). Springhouse, PA: Springhouse
Corporarion, 200 I ;337-342.
8. Skidmore-Rorh L (ed). Mosby's Nursing Drug Reference. Sr. Louis:
Mosby, 200 I;70, 135.
VII
Amputation
Jason D. Rand and Jaime C. Paz
Introduction
This appendix describes the most common types of lower- and uppet
extremity amputations. The etiology of these amputations and the
physical therapy management that is pertinent to the acute care setting
are described. Although the incidence of upper-extremity (VE) amputa
tion is quite low compared to lower-extremity (LE) amputation, it is
important that the acute care physical therapist have an understanding
of all types of ampurarions ro properly plan for the evaluation and
treatment of the patient.
Lower-Extremity Amputation
Peripheral vascular disease accounts for approximately 85-90% of LE
amputations in the developed world, with 25-50% of this percentage
resulting from diabetes mellitus.' Refer to Chapter 11 for more informa
tion on the complications of diabetes mellitus. Trauma is the second
highesr cause of amputation in developed countries and is the primary
cause in developing parrs of the world.' Traumatic amputation often
results from environmental injury or land mines in various parts of the
887
888
Upper-Extremity Amputation
UE amputation is most often the result of trauma, such as automobile or
Discharge plans
889
Shoulder
disartlculatJon'
----
Above-elbow
amputation
8ekJw-elbow
amputation
A
Figure VII-t. Levels of amputation, A. Upper extremity. (Reprinted with per
mission from AB Maher. SW Salmo,Jd, TA Pel/ino /eds), Orthopaedic Nurs
illg (2 11d edt. Philadelphia, Sal/llders, 1998;724.)
890
Hemipelvectomy
---+
_
___
_
Hip
disarticulation
..
-- -
.... ..
.._
..
..
Above-knee
(translemoral)
amputation
Knee
disarticulation
-----l
Below-knee
(transtibial)
amputation
Syme's
It-..:!\---amputation
Transmetatarsal
amputation
Ray
amputatlon
hI\_1"':_\
____
Toe
amputation
---
891
Description
Ray
Transmeratars.11
S)'me's
amputacion
(ankle
disarticulation)
Below the knee
(rransribial)
Through-the-knee
(disarticulation)
Hip
disarticulation
(femoral head
from
acetabulum)
892
Description
Hemipelvectomy
(half of the
pelvis is
removed along
with the enrire
lower limb)
Unless otherwise stated, the etiology of these amputations is from peripheral vascular
disease.
Sources: Data from A Thompson, A Skinner, J Piercy (cds), Tidy's Physiotherapy (12th
cd). Oxford, UK: Butterworth-Heinemann, 1992;260; B Engstrom, C Van de Ven (cds).
Therapy for Amputees (3rd cd), Edinburgh, UK: Churchill Livingsrone, 1999;208, 187188, 149-150; B May (ed). Amputations and Prosthetics: A Case Study Approach. Phil
adelphia: FA Davis, 1 996;62-63; G Sanders (cd). Lower limb Amputations: A Guide to
Rehabilitarion. Philadelphia: FA Davis, 1986;101-102; M Lusardi, C Nielsen (cds),
Orthotics and Prosthetics in Rehabilitation. Bosron: Butterworth-Heinemann, 2000;
370-373; and JE Edelstein. Prosthetic Assessment and Management. In SB O'Sullivan,
TJ Schmin (eds), Physical Rehabilitation; Assessment and Treatment (4th ed). Philadel
phia: FA Davis, 2001;645-673.
Description
Transmetacarpal
Wrist disarticulation
Transradial
Elbow disarticulation
Type
Description
Transhumeral
893
Forequarter
IS
from trauma.
Sources: Data from B Engstrom. C Van de Ven (eds). Therapy for Amputees (3rd ed).
Edinburgh, UK: Churchill Livingstone, 1999;243-257; M Lusardi, C Nielsen (eds).
OrthOtiCS and Prosthetics in Rehabilitation. Boston: Butterworth-Heinemann,
2000;573; SN Baneqee (cd). Rehabilitation Management of Ampurees. Baltimore: Wil
hams & Wilkll1. 1982;30-33; and R Ham, L Cotton (eds). Limb AmpUiation: From
Aeuology to Rehahlln;nion. london: Chapman & Hall, 1991;136-143.
Tre::ltment Suggestions
Psychological
impact of
ampmatlon
Residual hmb
edema
[Q
the pacient's
894
Phantom limb
pain
Hypersensitivity
Skin condition
Treatment Suggestions
Safe residual limb wrapping involves the use of a figure
eight or angular pattern, anchoring turns around the
most proximal joint, increased distal pressure, and a
smomh or wrinkle-free application.
The physical therapist should elevate the residual limb in a
position that prevents joint contracture formation.
In patients with upper-extremity amputation, a sling may
be used to help manage edema.
Often described as a cramping, squeezing, shoming, or
burning pain felt in the part of the extremity that has
been removed. The physical therapist may use
desensitizing techniques (e.g., massaging the residual
limb), exercise, hot and cold therapy, electrical
stimulation, or other modalities when phantom limb
pain is determined as the cause of the patient's pain.
Patient should be encouraged to rub the residual limb with
increasing pressure as tolera[ed.
Ensure stability of new incision(s) before, during, and
after physical therapy intervention. Examine the inci
sion for any changes in [he appearance (size, shape,
open areas, color), temperature, and moisture level.
Instruct patient and nursing staff on importance of fre
quent position changes to prevent skin breakdown.
Implement out-of-bed activities as soon as possible.
Instruct patient in active movements and bed mobility
activities such as bridging, rolling, and moving up and
down in the bed.
Sources: 03ra from B Engslrom, C Van de Ven (eds). Thcrapy for Ampurees (3rd cd).
Edinburgh, UK: Churchill Livingsrone, 1999j27-37, 43-45; B May (cd). Amputations
and Prosrhcrics: A Case Study Approach. Phibdelphia: FA Davis, 1996;73,86-88; and
SN Banerjee (cd). Rehabilirarion Management of Ampurees. Balrimore: Williams &
W;lk;ns, 1982;30-33, 255-258.
895
Treatment Suggestions
Joint
conrracture
Upper extremiry
Physical therapy should consist of active movements of all
of the joints above the level of the amputation,
including movementS of the scapula. Patients who use
upper-extremity slings to fixate the arm in elbow
flexion and shoulder internal rotation should be
examined regularly for contractures.
Lower extremity
The physical therapist should provide the patient and
members of the nursing scaff with education on residual
limb positioning, proper pillow placement, and the use
of splint boards.
Patients with a below-the-knee amputation will be mOst
susceptible to knee flexion contraction. A pillow should
be placed under the tibia rather than under the knee to
promote extension.
Patients with above-the-knee amputations or disarticu
lations will be most susceptible to hip flexor and
abductor contractures.
The physical therapist should begin active range-of-motion
exercises and provide passive stretching as indicated.
Upper extremiry
During ambulation, patients tend to flex their tfunk
roward the side of the amputation and maintain a stiff
gait panern that lacks normal arm swing. Patients often
need gait, balance, posture retraining, or a combination
of these.
It is important to work on active movements, specifically
the movements that might be used for powering a pros
thesis, such as in [he following:
Transradial body powered prosthesis: elbow extension,
shoulder flexion, shoulder girdJe protraction. or a
combination of these
Transhumeral body powered prosthesis: elbow flexion,
shoulder extension, internal rotation, abduction and
shoulder girdle protraction and depression.
Decreased
functional
mobility
896
Table V U 4. Continued
-
Consideration
Treannenr Suggestions
Lower extremity
Techniques should range from bed mobiliry training to
transfer training to ambulation or wheelchair mobility.
Patients with bilateral above-knee amputacions will
need a custom wheelchair that places the rear axle in a
more posterior position to compensate for the
alteration in the patient's center of gravity when sitting.
References
I. Engsrrom
VIII
Postural Drainage
Michele P. West
avoided
Uncontrolled hypertension
897
898
...... Adult
BIIIknII
liighFowln'l position
po:"IIm.OI' segment
ApkalliCgmCnU
RIp' upper lobe
anlCl'ior1
,
LeR I.I(lptf lobe
..ft.
.
Ianll ltgllltnt
LR II['IIX'r Iobe
pos&mor sqpnenl
Righi middle
anterior segment
"
---.-----.-------.-
::
:,
TrcnddmbwJ's posiuon
Figure VUl-1. Positions (or postural drai"age. (With permission from PA Pot
ter, AG Perry. Ftmdamelllals of Nllrsing (5th ed{. Sr. LOllis: Mosby, 2001;
1165.)
Orthopnea
899
Hypotension
all
Acute hemoptysis
Bronchopleural fistula
Unstable pneumothorax
Pulmonary embolism
Physical therapy considerations and clinical tips for the use of pos
tural drainage include the following:
900
modi fying the time spent in each position, the angle of rhe bed, or
patient position.
bed that are needed to position rhe patient for postural drainage.
Each bed model, especially pressure relief or roraring beds, has dif
ferent comrols, locks, and alarms.
References
1. Starr jA. Chronic Pulmonary Dysfunction. In B O'Sullivan, TJ Schmitz
(cds), Physical Rehabilitation: Assessment and Treatment. Philadelphia:
FA Davis, 2001;46l.
2. Downs AM. Physiological Basis for Airway Clearance Techniques. In 0
Frownfelter, E Dean (eds), Principles and Practice of C::ardiopulmonary
Physical Therapy (3rd cd). Sr. Louis: Mosby, 1996;330-331.
3. Hess DR, Branson RD. Chest Physiotherapy, Incentive Spirometry,
inrerminenr Positive-Pressure Breathing, Secretion Clearance, and
Inspiratory Muscle Training. In RD Branson, DR Hess, RL Chatburn
(eds), Respiratory Care Equipment (2nd ed). Philadelphia: Lippincorr
Williams & Wilkins, 1999;340.
Equipment
Time
Reliability
Validity
Elderly
patients
who have
sustained
acute
cerebrovascular
accident
and/or are
in a rehabilitation
setting
Ruler
Stopwatch
Chair
Step stool
Flat surface
1 0 - 2 0 mins
required
to complete test
Concurrent
validity:
Tinetti, r =
0.91
Get up and
go,r =
-0.76
Predictive
validity: <45
score
predicts falls
x
Physical Therapy Considerations
for Patients Who Complain
of Chest Pain
Michele P. West
921
922
Possible Etiology
Pneumonia
Pulmonary embolism
Tuberculosis
Pleural
Pleuritis
Pneumothorax
Mediastinitis
Gastrointestinal
Hiatal hernia
Nausea, vomiting,
Esophagitis
burping, abdominal
Esophageal reflux
pain
Acute pancreatitis
Musculoskeletal
Muscle strain
Reproduction of pain
Repetitive coughing
Rib fracture(s)
Sources: Data from NH Holmes, M Foley, I'H Thompson (cds). Profcssional Guide to
Signs and Symproms (3rd cd). Springhouse, PA: Springhouse. 1997;1 53j and RL
Wilkins, SJ Kridcr, RL Sheldon (eds). Clinical Assessment in Respiratory Care (3rd ed).
St. Louis: Mosby, 1995;28.
Chest pain can present with signs and symptoms other than the
classic angina pectoris owing to myocardial ischemia. The mnemonic
OLD CARTcan be used as a rapid survey for the differential diagno
sis of chest pain during a physical therapy session '-3:
Onset-Sudden versus insidious, with exertion or stress versus rest?
(Cardiogenic chest pain is usually of sudden onset.)
Location-Substernal or on the left side of the chest? (Cardiogenic
chest pain typically occurs in this location, but can 21so present in
any area above the waisr.)
Duration-Lasts longer than 20 minutes? (Cardiogenic chest pain
typically lasts 2-20 minutes.)
923
Hypotension or hypertension
Bradycardia Ot tachycardia
Irregular pulse
924
Pathological
o wave
(a) Dead myocardium
Raised ST
segment
(b) Acutely damaged myocardium
Twave
(c) Myocardial ischemia
Note: There are a range of other
causes for Twave Inversion
References
1. Becker RC (ed). Chest Pain. Boston: Butterworrh-Heinemann, 2000;40.
2. McAvoy JA. Cardiac pain: discover the unexpected. Nursing 2000;
30:34.
3. Pathophysiology of Coronary Artery Disease. In FJ Brannon, MW Foley,
JA Starr, MG Black (eds), Cardiopulmonary Rehabilitation: Basic Theory
and Application (2nd ed). Philadelphia: FA Davis, 1993;82.
4. Chandra NC. Angina Pcccoris. In LR Barker, PD Burton, PD Ziere (eds),
Principles of Ambulatory Medicine (4th cd). Baltimore: Williams &
Wilkins, 1995;69 t.
Index
Abwdmab, 852r
Ahdomcn
indicate tables.
507
In genuourmary evaluation, 562-
563
palpation in, 507, 563
percussion Ill, 507, 563
Adenoma
560
Acid perfusion leSl, 5131
673
screenmg for, 651
925
926
Adrenal gland-continued
to latex, 751
rhinitis in, 6 1 8 , 864t
in transfusions, 4201
Alteplase, 868t
Alveoli
gas exchange In, 94-96
670
Amenorrhea, 670
Afterload, 7-9
Age. See also Elderly
491
Aminoglutethmude, 860t
Ammoma levels, 5 1 61
10
oxygen ther
Airways
auscultation of, in respiratOry evalua
tion, 99-105
in burns and inhalation injuries. 450451
obstruction of, air trapping in, 1 30
Albumin
electrophoresis of, 5 1 9r
serum levels of, S I9t
in liver failure, 7 1 4t
therapy with, 4 1 8t
Alcohol abuse, 760
withdrawal in, 760-761
Aldesleukin, 860t
Aldosterone, 670-67 1
Analgesia, 879-884
patient-controlled, 8831
Anaphylaxis
III
transfusion reactions,
42lt
Androgens, 668, 670
Alkalosis, 1 1 3, 1 14
common causes of, liSt
Alkylating agents in chemotherapy,
8541-8551
Allen's rest, 372t
Allergic reactions
antihistamines in, 847t
Anemia, 404--409
aplastic, 406-407
in blood loss, 404-405
in folic acid deficiency, 406, 4 1 6, 866t
hemolytic, 407-408
in iron deficiency, 405, 4 1 6, 866t
nutritional lherapy in, 4 1 6 , 866t
INDEX
epidural,882t, 8831
general, 871-874
Antibiotics, 848r-850t
of .or", 388,390,391f,427f
in chel11Olherapy, 855t-856r
cerebral,314, 390
61518
in ruberculosis, 623
Antibodies,607t
measurement in infections, 610-61 1
Anticoagulant therapy,415, 844r-845r
in pulmonar y embolism,143--144,402
thrombocytopenia in, 413-414
Anticonvulsant agents,845t
Prinzmetal's variant, 40
stable or exenional, 40
unstable, 40
Angiogenesis in transmyocardial revascu
lariznrion,52
Angiography, 38, 370, 376
of aorta, 38, 425f
cerebral, 302
complications in, 376
in chemotherapy, 342
coronary, 38
in radiation rherapy,341
digital-subtraction technique,302
Anrigen,607t
magnetic resonance
Antihistamines,847t
927
928
III
Arteries, 364
AOrfa
anatomy and function of, St
al50 Atherosclerosis
clinical findings in, 386t
Aortic valve
HypertenSIon
Raynaud's disease and phenome
non
Ill,
397, 398
398
Apnea, lOOt
rhrombosis, 392
Appendecromy, 548
Appendicitis, 530
in vasculitis, 395-397
Arteriosclerosis, 384. See also Athero
Appendix vermiform
fUllcrion of, 504r
infl:unmarion of, 530
surgical removal of, 548
sclerosis
Arteriovenous fistula, 403
in hemodialysis, 590, 591f, 795t
Arteriovenous malformations, 313-314,
403
Artemis
gaant cell, 397
Takayasu's, 397
ArthrocenteSIs, 612-613
56
drug therapy in, 60, 843r
Arthrography, 168
Arthroplasty, 190--209
of ankle, 206
111,
207
Ascites, 552
premature contractions
atrial, 75t
ventricular, 44, 77t, 8Sf
respirarory sinus, 12
INDEX
nosocomial, 6 1 4
Atriovemricular node, 9
Atrium
929
prevention of, 6 1 5 t
osteomyelitis in, 629
of skin, 630
82f-83f
diastole and systole of, 6
Aura in seizures, 3 1 8
Auscultation
in cardiac evaluation, 22-24, 24f, 68
in infections, 609
in gastroimesrinal evaluation, 507
in infections, 609
9 1 51, 9 1 61
Balloon pump, inrraaortic, 829-832,
830f-8 3 1 f
in infections, 609
landmarks for, 1 0 I, 1 0 J(
Baroreflexes, 10, IJ
823-824
Barren's esophagus, 526
Basal cell carcinoma, 356-357
AutOmaticity, cardiac, 3
aneurysm of, 3 1 4
Batista procedure, 58
Bed rest, prolonged, effects of, 752-753,
7541
Benzodiazepines in nausea and vomjring.
8461-8471
7041
Babinski sign, 297
Bacitracin in burns, 461 t
Bernstein test,S I 3r
Beta blockers, 853t
Bicarbonate blood levels, 1 1 2
in respiratory evaluation, 1 1 2, 1 14, 1 16
930
Biliary tract
Bleomycln. 8_S51
Blood
Bilirubmuria, 565t
to
Biopsy
to
.lSlr, .l8lf
III
mfecflons. 610
in cardiac cycle. 6
cerebral, J23
of liver, .52 1 t
of thyroid, 6Ht
gemtounnary sYStem
Blotherapy
10
III
regulatton of,
560. 600
m hypertension. 392-395. See also
Bladder
Ilypertension
caTheterization of
Foley carheters
111
Ill,
80St
suprapubiC, 802t
disorders o f
cystectomy
Ill,
597
hypotension, orrhostJtic
III
mfecllons, 639-640
III
III
cySUtlS, 582-583
arterial Ime
111
Ill,
787t, 790f
equipment
597-599, 598f
evaluation of, 56 1-570
111
7841
normal range
111.
Ill,
787r
and peripheral vascular reSistance, 12.
19
III
III
III
,es
III
INDEX
931
Brain, 260-274
and blood-brain barrier, 271-272
blood supply of, 272-274, 312-315.
rem
Bone
756r
herniation in imracranial pressure
cranial, 260
272
structure and function of, 260, 261f,
262t-268r
trauma of, 305-306, 307t-309t
tumors of, 356
Brain death, 755-757, 756r
Brain stem structure and function, 260,
266t-267r
Breast cancer, 346-348
Bronchi
in leukemia, 353
physical therapy in, 735, 736, 737
syngeneic, 733
Bronchodilators, 853t
Bronchophony, 104
Bronchopbsty, 151
Brachytherapy, 340
Bradykinin, IIr
Bradypnea, IDOt
932
Bronchopulmonary disorders-continued
posfllral drainage in, 897-900
Bronchoscopy, 119, 120t
in cancer diagnosis, 337t
Bronchospasm,130
activiryinduced,150
bronchodilawrs in, 853t
8461
Bypass surgery
CA 19-9,517t
Burns. 439--467
Calcium
serum levels
parathyroid disorders,
III
6861,687--{;88
III
electrical,441--443
gallstones,544-545
urmary,583-584
in kidneys, 566,579-580
percutaneous nephroscopic,
removal of,596
surgery In, 596-597
lightning, 443-444
447t
management of, 447-467
pain in, 453, 465
assessmem of, 463
846t
Capillaries, 364
characteristics of, 365t
refill rime, 371t
Carbon dioxide
464
physical therapy interventions in,
465-467
physiologic sequelae of,439--441,
440f
posirioning of patient in, 467,467t
from radiation,uluaviolet and ionizing,444
resuscitation in,450--45 2
Carboplarin, 854t
of lungs, 344
thermal,441,442t
of skin, 356-357
INOEX
Cardiac c yc le,6
Cardiac index, 6-7,788t
Cardiac output, 6-9
479-480
pulm onar y, 142
el ectroc ar diog raphy in, 74-79, 82-
933
88
embolism, 392,401-402
embolization therapy in, 326,422-
classification of,46 t
423
hyperlension, 392-395
sions, 755
Cardiovascular system,1-88
anatomy of
111
heart 111, 2, 3f
430
disorders of. 39-69. See also specific
dIsorders
aneurysms. 388-390,426-438
arrhythmias, 43-44
anerial, 384-399
in burns, 441t,443,444
bypass grafting in
coronary arrery. 52-53
perl pheral,423-425
c:lrdlomyo parhy,44,461
838
co mpa rt ment sy ndro me in,399
congenital vascular malformations,
403-404
drug therapy in, 59, 60-61,393,
8431
-adrenergjc blockers in, 853t
calcIUm channel blockers in,
8541
dig it aliS 10, 59, 60t,8671
dIUretics in, 861 t
nitrates in, 866t
470,479-480
syncope in, 318
thrombolytic th era py in,50, 423
thrombosis,392, 400-401
valvular,44, 45(,57-58
vasculitis. 395-397
vcnou',399-403,468-470
in Wegener's granulomatosis, 396
wound healmg in, 475
evaluation of, 13-39
angiography in, 38,370, 376. See
also Angiography
vasodibtOr, 869r
19-22,370
934
Cardiovascul3r system-continued
in cardiac disorders,13-39
diagnostic and laboratory measures
in, 25-39, 370-376
urinary
Foley catheters Ln, S05t
suprapubic, S02t
Texas catheters in,S03t
Cecum,504t
Celluliris, 630
370
in vascular disorders, 367-376
in wounds, 479-480
heart in. See Heart
structure and function of, 2-12, 364366
blood vessels in, 5t, 364, 364t,
365r
primary structures in, 4t-5t
Carmustine, 854t
Carotid arteries, 272, 273t
Doppler imaging of, 302
endarterectomy of, 425-426
219-220, 22 I f
Cast brace, 220
CastS,220-224
260, 267r-268r
Cerebral arteries, 273t
aneurysm of,314, 390
bivalve, 220
angiography of,302
spasm of,315
serial, 220
types of, 220, 222t-223t
Cerebrospinal fluid
circulation of, 269-271, 271
Catecholamines, 671
Catheterization, 794-808
in hydrocephalus, 315-316
cardiac, 36-38
precautionary period after, 38,52
central venous,795t
peripherally inserted, 802t
tunneled, 804t
epidural, in pain management, 882t883r
for hemodialysis, 590, 591f, 795t
intraventricular, in innacranial pres
sure monitoring, 792(, 793(
fiberoptic transducer in, 793t
midline, 799t
naso-pharyngeal,for oxygen delivery,
772r-773r
hemorrhage, 313
subarachnoid, 314-315
ischemia, 312, 313
transient attack,312
in vasospasm, 315
perfusion pressure in, 323
INDEX
Cerebrum
Cholecystectomy, 548
Cholecystitis, 544-545
Cholecystography, 5 2 1 t
Cholelithiasis,544-545
Cholest3sis,5 1 1
Cholesterol levels
in atherosclerosis,387
CerVical spine
III
respiratory function, 90
Cisplatin,854t
In gastrointestinal disorders,S25,
Cladribine, 856t
921 ,9221
esophageal,525
history of, 13-15, 922-923
III
935
Claudication
exercise testing in,374t
intermittent, 367
m atherosclerosis,387, 388
differentiated from pseudoclaudica
lion, 388, 389t
neurologic, 388, 389t
Clavicle fracrurcs, 1 8 5
Chest wall
palpation in respiration evaluation,
105-107, 1061
restrictive disorders of, 149-150
Cheyne-Stokes respiration, lOOt
Chlorambucil,854t
Clopidogrel, 85 II
Coagul3f1on
disorders of. 4 1 0-4 1 2
exerci guidelines in, 429-430
in hemophilia, 4 1 1 - 4 1 2
Cholangiography, 5 2 1 t
Cholnngiopancrearography. endoscopic
retrograde, 521 t
pancreatitIS after,546
in cardiac evaluation, 28
in liver failure,7 14t
936
Coagulation-COl1lil1lted
in liver transpi3ntation, 7 1 5
zones of, i n burns, 439, 439f
Coccidioidomycosis in HIV infection
52 1 1
i n genitourinary evaluanon. 569
in musculoskeletal eXamlOa(lon, 1 67-
168
in neurologic evaluation. 301
in vascular disorders, 374t
Concussion. cerebral. 3071
Conduction system of heart, S. 9f. 9- 1 0
clcctrophysiologic studies of, 38-39
Conducnol1 velocity studies, nerve, 304
Cold. common, 6 1 8
Confusion
Colectomy, 548
Colins
III
403-404
ischemic, 533-534
ulcerarive, 538-539
Collagenase in burns, 4 6 1 t
Colon
2841
in hepatic encephalopathy and coma,
543-544
in inrracralllal pressure increase, 323t
in syncope, 3 1 8-319
Constipation, laxatives in, 8641
III
III
spastic, 534-535
3951
Contractiliry, cardiac. 5
Conrractures
in amputation,8951
III
burns. 467
Contrast agents
in angiography, 370, 376
complications of, 376
in echocardiography, 32-33
Contllsion
cerebral, 3071
of lung, 140t, 144
in rib fractures, 144. 1 4 9
Coord Inalion lests. 299, 300t
Coronary arteries, 1 2
anatomy of, 3f
angiography of. 38
angioplasty of, 5 1
INDEX
anterior, 215-216,218t
posterior, 218t
Cryoprecipitate,419t
bypass graft,52-53
spasm of, myocardial ischemia in, 40
stem placement in,52
Corpectomy. 21 It
937
in wounds, 482
Cushing's disease and syndrome,664665
hypertension in, 395t
Cyclophosphamide,855t
Corticosteroid therapy,842t
704t
inhaled, 861t
Cystecromy,597
intranasal, 864t
Cystometrography, 568
Cysroscopy,567, 568
Cytarabine,856t
Cough
Cytology, 612
Dacarbazine,855t
Dactinomycin,855r
Daily living activities
in hip arthroplasty,192
in shoulder arthroplasty, 204
Dalteparin sodium, 844t
Danaparoid sodium,844t
Crackles,103-104
Daunorubicin, 856t
autolytic,486
enzymatic,488
Craniectomy,325, 326
mechanical,486-488
Cranioplasty,325
Craniotomy, 325
selective, 485,486,488
Cranium, 260
Creatine kinase levels in cardiac evalua
tion, 29-30, 30t
and physical therapy,31
Cre::ninine tests,564-565
after angiography, 370
Critical illness
myopathy in, 759
polyneuroPalhy in, 758-759
Crohn's disease. 537-538
sharp, 486
Decerebration,296
Decortication, 296
Decubitus ulcers, 162, 163,470-471
staging and classification of, 483,
483t
Defibrillator, automatic implantable car
diac, 56
Degenerative disorders of central ner
vous system, 319-321
938
Delirium, 282r
in intensive care unit, 757-758
tremens, in alcohol withdrawal, 760
Dementia, 282t
Dipyridamole, 852t
in thallium stress tcst, 36
Disc disorders, intervcrtebral, 210-213
artificial disc implantation in, 212-
213
indications for surgery in, 211t
Discecromy, 210, 211t
Discrimination, two-point, 298r
Dislocations
of hip, 176-177
in pelvic fractures, 175f
of shoulder, 185
Diuretics, 861t
osmotic, 867t
Diverticular disease, 530-531
Diverticulitis, 530
32, 33
Donors in transplantation procedures,
699-701
in bone marrow transplantation, 700,
733
cadaveric donors, 699
600
neuropathy in, 471-472, 681-684
signs and symproms of, 683t--684t
types of,683t-684t
physical therapy in, 677
skin disorders in, 681
ulceration in, 469t, 471-472
Doppler imaging
in neurologic evaluation, 301-302
in vascular evaluation, 373t
Doxorubicin, 856t
rype 1, 674-677
Drainage
Dialysis
active, 803t
Diasrole, 6
blood pressure in, 19, 19t, 393f, 784t,
787r
Diencephalon, 260, 265r-266t
Diffusion, 587
of oxygen, 770
Digitalis, 867t
toxicity of, 59, 60(, 867t
passive, 803t
postural, 897-900
conrraindicarions to, 897, 899
typcs of patient positions in, 897,
898f
from wounds, 481-482
Dressings, 488-489, 490r-492t
in burns, 460t, 46 It
INDf.X
debridement in,487
Drugs, 839-870
abuse of, 760-761
Egophony, 105
Duodenum
function 0(, 504t
peptic ulcer disease of,528-529
Dura mater,269
939
in olecranon fractures,186,188f
270r
111,
177
Echocardlography, 32-33
Edema,16, 19t
in amputation,893t-8941
in gemtounnary disorders,600
908-909
Tinetti mobility assessment in,911915,912t-915t,916t
Electrical burns,441-443
pitting,16, 19t
pulmonary, 139t, 142
spinal surgery,213
wounds,479-480, 494t
88
in :arial arrhythmias, 74t-75t,82(83f
in chest pam, 923,924f
electrode placement in, 785t
equipmcnt tn, 785t
heart ratc variability in, 26-27
in heart transplantarion,postopera
tive,727
Holter monitoring in, 25-26, 27
activity log in, 27
Indications for, 25
mterpretation of, 26t
10 burns, 466t
in Junctional arrhythmias,78t
III
knee arthroplasty,199,200
111
transplantation procedures,740741
Effusions
pericardial,47t
pleural, 145{, 148
tlon,43
in physical therapy,68-69
telemerric monitoring in, 27, 785t
cellular phone imcr(ercnce with,27
in ventricular arrhythmias,76r-77r,
83f-86f
940
Electroenceph31ography, 303-304
Electromyography, 304
Electrophoresis, protein, 5 1 9t
Embolism, 392
pulmonary, 400, 401-402
management of, 1 40t, 1 4 3 - 1 44,
cancer risk,
Enzymes
as biochemical markers in cardiac
4 0 1 -402
signs and symptoms in, 1 40r, 1 4 3
111
402
Epidermis
Emphysema, 1 33r, 1 3 6
subcutaneous, palp3tion of. 1 0 7
Empyema, 1 47t, 1 4 9
chest intubation i n , 796t
Encephalitis, 627--629
Encephalopathy in liver disease, 543544
Endoflife issues, 753-757
Endarterectomy, 425-426
Endocardium,4t
Eptifibatide, 852t
Equipment, 769-808
INDEX
cardiac evaluation, 28
transfusion of, 4 1 7t
941
algorithm on,65f
Esch." 439
angina in, 40
836,837-838
claudication in, 374t
Esophagogastroduodenoscopy,513t
Esophagus
echocardiography in, 32
Barren's, 526
disorders of, 524-526
cancer, 526
62
in physical therapy, 61-69
rate pressure product in,67
stability of response to,62-63,64f,
65f
in stress testing,32, 33-36
companment syndrome after, 399
deep-breathing, postoperative, 345
Estrogen
In breast tumor ceils, 343
target sites and actions of, 669t
therapy With, cancer related to, 334t
Ethical Issues m end-of-life care, 753757
Etoposide,859t
Evans and Russell-Taylor classification
of femoral fractures, 242t
Evoked potennals, 304
Excitability, cardiac, 3
ExerCise
after prolonged bed rest, 753
III
electrocardiography in,68-69
amputation, 888,893t-896t
musculoskeletal, 630
respiratory, 6 1 9
i n knee arthroplasty
in physical therapy,199-20 I , 209
in resection procedure, 209
weight bearing in, 199
in knee arthroscopy, 217t-2 1 S t
942
Excrcise-co1ttilltled
in ostcomyelitis, 630
in osteoporosis, 690
oxygcn supplementation in, 770. 779,
782-783
283, 284,
bronchospasm in, 1 5 0
non-rebreather, 775t, 78 1 f
parrial, 774t
open, 779f
Facial nerve, 290r
Factors, cloning, 385t
in disseminated intravascular coagula
i n thrombocytopenia, 429
in traction, 232
in transplantation procedures, 737-741
activiry progression in, 740
in bone m:lrrow fr:lI1splamation,
736, 737
education of patients on, 740-74 1
in heart transpl3ntation, 725-727
in kidney rransplanration, 7 1 1-7 1 2
tion, 4 1 0
in hemophilia, 4 1 1
Falx
cerebelli, 269t
cercbri, 269t
Fasciculus
cunearus, 276t
gracilis, 276t
FasciotOmy ill burns, 454
i n liver transplantation, 7 1 7
Fat, fecal, 5 1 8t
Feeding tubes
732
in gasrrostomy/jejunostomy, percura
neous endoscopic, SOOr-80 I t
nasocnrcric, 799t-SOOt
nasogaslric, 800t
Femoral artery
and aortofemoral graft, 425f
and popliteal bypass graft, 423. 424f
and posterior tibial bypass graft, 424f
Femoral nerve. 27St
injury in hip arthroplasty, 195
Femur
fractures of, t 77-179, 24 1 r-245t
INDEX
943
Fibrillation
carpal, 1 89
complications in, 172-174
In myocardial inbrcuon, 50
171
tr311SC3theler, 423
Flbropbsflc phase of wound healing,
472-473
01 fibula, 1 80-182
of foot, 182, 2 5 1 t
Fibula
In ankle anhroplasty, 206
Fllgrasnm. 860t
01 hand, 1 89-190
704t
Flail chest, 1 47r, 1 4 9
in osteomyelitis, 630
III
ostcoporosis, 690
Floxundillc. 856t
Fluids
o f shoulder, 1 85
Frank-Starling mechanism, 7
Fremitus, 106
Follicle-snmubting hormone, 6 6 1 t
Foot disorders
ampulanon in, 8 9 1 t
braces, splints, and onhoses
m,
226t-
2271
in diabetes mdlirus, 471 -472, 6 8 1 ,
6821
fractures of forefoot, 1 82, 2 5 1 t
ForaminOtomy. 2 1 0, 2 1 1 t
944
1I1, 797t
Gait
of esophagus, 524-526
gastroenteritis, 630-63 1
gastrostomy/jejunoslOmy tubes in,
9 1 7t
timed get up and go test in, 902,
percutaneous endoscopic,
BOOI-B021
90BI, 90B-909
lineni mobility assessment in,
9 1 1 -9 1 5, 9 121-9151, 9 1 61
in Parkinson's disease, 3 2 1
Gallbladder
cholccysteclOmy of, 548
of liver, 540-544
Gallstones, 544--545
in arterial blood
of pancreas, 545-547
in cardiac evaluation, 3 1
interpretacion of, 1 1 2- 1 1 6
peritonitis, 536-537
10
respiratory evaluation, 1 I 1 1 16
polyps, 539-540
positioning precautions
551
GastrectOmy. 549
of stomach, 527-529
surgery
Gastritis, 527-528
Gastroenteritis, 630-63 1
m,
547-550, 552
m,
postoperative, 874
10,
5 1 3t, 5 I 4t
cific disorders
anorectal, 540
appendicitis, 530
ascitcs in, 552
biliary, 544-545
in burns, 4 4 1 t, 444
Liver
INDEX
also Stomach
structure and function of, 502, 503f
accessory organs in, 505t
primary organs in, 504r
GastrostOmy, percutaneous endoscopic,
800,-802,
Gauze dressings, 490t
Gehrig, Lou, diseasc, 3 1 9
Genetic factors
945
908-909
Gianr cell arteritis, 397
Gigantism, 663
Gird lesrone procedure, 207, 208f, 209
Glasgow Coma Scale, 283-284, 284t
Glenohumeral joint
arthroplasry of, 202-204
dislocation and fracture of, 1 85
Glomerulonephritis, 574-577
chronic, 576-577
in cystic fibrosis, 1 3 6
in emphysema. 1 3 6
in hemophilia, 4 1 1
in sickle cell anemia. 408
in thabssemia, 4 1 2
Genitourinary system, 557-600
bladder
m.
See Bladder
574-575
postsrreptococcal, 575-576
rapidly progressive, 576
Glossoph:lfyngeal nerve, 2 9 1 t
Glucocorticoids, 668, 669-670
rarget sites and 3crions of, 669r
therapy with, 842t. See also Corticos
teroid therapy
Glucose
blood levels of, 67 1
in diabetes mellitus, 673-674,
percutaneous ncphroscopic
719
tolerance test, 67 1
urine levels of, 565r
in diabetes mellitus, 675t
Glut3mate pyruvate [ransamin3se, 5 1 I,
5 1 6r
Gluramic-oxalo3ceric trans3min3se, 5 1 1 ,
5 1 7t
y-Gluramylrransferasc levels, 5 1 8t
Gluteal nerves, 279t
Glycosuria, 565t
Goirer, 657r
of prostate, 584-587
59 1 f, 795,
skin
in rumors, 340
559f, 560f
946
Grafts-cotllinued
coronary artery,52-53
peripheral, 423-425
Gram's stain,6 1 1
Granulomatosis,Wegener's,396
Graphesthesia, 298t
Graves' disease,657t
in hematologic disorders,378t,379
Growth factor,platelet-derived,in
wound care,493
Growth hormone,662t
overproduction of,663-664
heterotopic. 722
Guillain-Barre syndrome,320
indications for. 72 1
with lung transplantation, 732-733
Hair
orrhotopic. 722
and hirsutism,670
in integumentary system,436,436f
Halo vest,226t
Hand
tions in,723-725
rejection in, 707, 724-725
casts for,223t
Heart failure
Head
Healing process,472-476
in fractures,172, 1 73t, 1 7 4
Hearing,cranial nerve functions in,2 9 1 t
Hean,1-69
cycle of,6
disorders of, 39-69
circulalOry assist devices in, 829838
electrocardiography in, 74-79, 8288
functional classification of, 48-49,
49<
m,
15
tion,724
signs and symptOms in,48,48t
rypes of. 48
ventricular assist device in, 832-836
Heart rate
autonomic mnervation of, 1 0
and cardiac output, 7
in infections, 609
in hypertension,394r
infections, 624-625
management of,50-69
palpation of, 1 6
INDEX
10 physical therapy,66
postoper:aive, In heart transplanta
rion, 723, 726
and rating of perceived exertion,34
m
stress testing, 34
Hemofiltration
aneriovenous, 592, 593, 594f
venovenOllS, 592, 593
Hemoglobin
in cardiac evaluation,27
glycosylated, in diabetes mellitus,
675r
10 physical therapy,68
Hellcobacter pylori Infections . 527528
382f
mean corpuscular, 379,383t
mean corpuscular concentration,379,
383r
diagnosis of,509t
Hemarthrosis in hemophilia,412
Hemaremesis,527
in thalassemia,412
Hemoglobin S5 in sickle cell anemia,
Hematochezia, 527
Ilematocrit
10 cardiac evaluation, 27
m
hematologic disorders,379,381t,
381, 429
burns, 444
408
Hemolysis in transfusion reactions,420t
Hemolytic anemia, 407-408
Hemophilia,411-412
Hemopneumothorax,149
Hemoptysis, 109
Hemorrhage
anemia in, 404-405
cerebrovascular accident in, 313
in disseminated inrravascul;u coagula
tion,410,411
cancer, 351-354
physical therap)' 10, 429-430
947
gastroinrestinal, 527
postoperative, 873
in esophageal varices,526,797t
10 infections, 610-611
hemothorax in,146t,149
subarachnoid, 314-315
I lematoma
epidural, 308t
in thrombocytopenia, 413
Hemothorax, 146t,149
IIllracerebral, 308t
subdural, 308t
Hemaruria. 562,565t
I-temianhroplasty,proximal humeral,
202. 203f
Hemipelvectomy,892r
Hemodoaly"" 589-592,590f, 591f
vascular access in, 590,591f
Hemodynamic monitoring,783
mvasive or direct methods,783, 787t789r
nOlllnvasive or indirect methods,783,
784r-786r
phlebostatic axis in, 783
physical therapy 10, 783
948
633
opportunistic infections in, 633-634
bilateral fOtal, 1 92 f
700-701
Humerus
fractures of, 185- J 86, 254t-256t
distal, 186, 187f
proximal, 1 85-186, 254t-255[
in shaft, 1 86, 255t-256t
in shoulder arthroplasty, 202-204
Hydroxyurea, 857t
65 1"";52
in gastrointestinal evaluation, 505,
50Gr
in genitOurinary evaluation, 56 1 -562
in hematologic evaluation, 376-377
in infections, 606
161
i n neurologic evaluation, 278-28 I
in respirarory evaluation, 97-98
in vascubr evaluation, 367
in wounds, 476-478
HIV infection and AIDS, 63 1-634
673-674
Hyperinflation of lung, 130
dynamic. ill positive end-expiratory
pressure, 8 1 8, 820, 823
Hyperkalemia, 766t
Hypernacremia, 765r
Hyperparathyroidism, 687-688
Hyperpituitarism, 663-666
tNDEX
Hyperplasia, 3n
949
Hyperpnea, lOOt
Hypersensitivity
reaction!>
sensory. after ampuratlon, 894t
Ifosfamide, 855t
lIeo!ltomy, 549
I lypertension, 392-395
Ileum
111
854t
dIUretics 111, 861,
portal. 542
Ill,
229
544
casts m, 220-224
pulmon,uy,
III
752-753, 754t
of knee, 227t
AIDS, 63lt
586, 196
702-707
Hypcrvcnlilanon, lOOt
H)pcrvolenua. 764, 76S(
I lypodcrmis, 4,8t
III
685
Ilypoglycenlic agent!!. oral.
III
575
diabetes
mellnu!>. 678
II ypokalem l a, 766t
Immunosuppression, 607,
111
Hyponatremia. 76.5t
Hypoparathyroldl!im, 688-689
HYPOpituitarism, 666-667
Hypotension. orthostatic
in heart transplantallOn, 726
Incontinence
Ilypothyroidlsm, 658-660
fecal,
Hypoventllalion, lOOt
Hypovolemia, 764, 765t
III
cancer, 349
950
Inconrinence--cotztitzlled
In cancer, 348, 349
respiratory. 6 1 8-624
Infarction
of skin, 630
cerebral, 3 1 3
subclinical, 607t
of
roxoplasmosls, 637
Infections, 605-640
in arthroplasty, 207
735-736
in lung transplantation, 730
in burns, 452-453
cardiac, 624-625
of wounds, 482
343
472-473
communicable, 607t
in diabetes mellitus, 6 8 1
disseminated, 607t
tion
InspirUion, 92-94
auscultation In, 1 0 1 , 103
flow rale
ratio
III
mechanical venrilation,
8221
to
UI1I1,
757-759
antibioticresistant, 6 1 5-6 1 8
opportunistic, 607t
in HIV infection and AIDS, 633634
Interferons, 8591
in antibiotic-resistant infections,
6 1 7 1 8
i n HIV infection, 634
in osteomyelitis, 630
in respiratory infections, 6 1 9
prevention of, 6 1 4, 615t, 639
INDEX
213
artificial disc implantation in, 2 1 2213
indications for surgery in, 21 1 t
intestines. See Gastroimesnnal system
Jejunum, 504t
Jewen brace, 226t
Joints
arthroplasty of, 190-209. See also
Arthroplasty
951
AJDS, 635t
Ketonuria, 565t
Kidneys
disorders of, 570-582
acure failure, 570-571
8 1 3f
600
cuff in, 8 1 4
glomerulonephritis, 574-577
and extubation, 8 1 2
Ischemia
of
postoperative, in transplantation,
710
radiographic examination in, 566
radionuclide scans in, 568
ultrasonography in, 569
952
Kidneys--couti" lled
Lamineclomy, 2 1 0, 2 1 1 t
Large imestine
funerion rests in 7 1 0
nl
referred paLn
Ill,
502r
in.7!()-7 1 1
L..
..
l.rynx
procedures Ulvolving, 1 5 1
struCture and function of, 9 1 t
51
Knee
amputation at level of, 891 r
diomyoplasry, 57
Lavage
Ill,
207, 209
gastric, 6 t 3
pulsed, in wound debridement, 487-
488
Laxatives, 864c
Legionellosis. 624
Leptrudin, 844t
2 1 9-220, l l l f
i n femoral fractures, distal, 179,
244r-245 r
immobilizer device for, 227t
in hip arthroplasty, 195
III
in cardiac evaluanon, 28
246,
380l, 38lf
III
infections, 6 1 0
III
trapping
III
venous insufficiency,
470
Leukoencephaloparhy, progressive mul
ufocal, in HIV infcCtlon and
AIDS, 635,
Leukoplakia. oral hairy, in I-IlV mfcction
and AIDS, 635r
in liver disorders, 5 1 J I 5 1 8t
Lipase lc"cls, 5 1 9r
INDEX
Lipids
953
fecal,5 1 8t
serum levels of
in atherosclerosis,28-29, 387
227t
casts for,222t
coordination tests of, 300t
fractures of,174-182,238t-251 t
serum levels of
165t
range of 1110tion in,166t
peripheral nerves of,274,278t
tendon reflexes of, 296t
traction applied to, 231 r
ulcerations of
in arterial insufficiency,468
in diabetes mellitus, 469f,471-472
neuropathic or neurOtropic,471-
472
in venous insufficiency, 468-470
Lumbar drainage device,798t
Lumbar puncture,303
Lumbar spine fractures, 182, 184f
postoperative, in transplantation,
715
failure of, 713, 714t
postoperative,111 transpl:lI1tarion,
716
function of, 505r
labor:uory tests on, 511,516t-520t
postoperative, In transplantation,
715
hepatitis of, 540-542
referred pain from. 502t
regeneration of,542
transplalllarion of,712-717
domino procedure, 713
donors in,700,713
funenoll tests in,715
indicanons for,712
orthotopic, 713
posroperative care and complica
tions in,7 J 5-716
rejection in. 707, 716
split liver procedure,713
veno-occlusive disease of, in bone
marrow transplantation, 736
Lomusrine,855t
Lower extremir)'
amputation in, 887-888
446, 447t
Lungs
air trapping in,130
auscultation of,99-105
landmarks for,10 I , 1 0 1f
barotrauma in mechanical ventilation,
823-824
in burns and inhalation injuries,451
cancer of, 344r. 344-345
diagnostic tests in, 337t
risk factors in,335t
conrusion of, 140t,144
in rib fractures,144,149
embolism in, 140t, 143-144. See also
Embolism,pulmonary
function rests of,121-124,122f-125f
capacity measurements in, 121,
122f, 126t-l27t
description and significance of,
126t-129t
flow-volume loops in, 1 2 1 , 125f,
129t
in obstructive disorders,121,123f,
125f
postoperative, in lung transplanta
tion, 729,730
954
Lungs-colltl1J11ed
III
125r
.1 5 1
MalformatIon!., vascular
hypermfbnon of, 1 3 0
congennJI, 403-404
Manometry, esophageal. 5 t 3r
MarshallMan.:hetil-Kranrl procedure.
197
scgmclltocromy of, 1 5 1
Masre((omy
94r
III
Mhanoreptof'j:. 1 1- 1 2
Mechlorethamine. 8.5.r
Mediasuno!.Cop)'. IS I
Mediastmum. 2
729, 730
with heart tr.msplamanon, 732-733
physical therapy
m,
729-730, 731-
732
postoperative care and complica
nons in. 729-731
Melena. $17
Ielphalan. 8551
tenmges
temnglus. 626-627
III
348
Lymphoma, .l33" 352" 352-353, 353,
Burkltts. 352
characteristics of, 352, 352,
U1
Mental tatu..
III
m.
286
m,
286
Mercapropunne. 8H(
tn musculoskeletal examUlatJon, 1 6 8
49, 62
INDEX
Metabolism
in burns, 439
disorders of
in resection procedure,208
screening for,651-652
Metacarpal fracrures,189-190
Metaplasia,332
Metastasis, 332
955
to bone,345-346
Mohs surgery,339
apy, 344
Mononucleosis, 634--6 36
Mosquito-borne viral encephalitis, 628
Motiliry disorders
of esophagus, 525
of intestines, 532, 534
of stomach, 529
Motor function
evaluation of, 294-297, 901-918
Berg balance [eS[ in, 902, 903f-
907, 9071
cranial nerve tests in,289t-292t
in Glasgow Coma Scale, 283, 284r
muscle tone in, 295-296
reach rest in, 909-9 1 1, 9 1 0t
Midbrain, 266t
Mineralocorticoids,668,670-671
target sites and actions of,669t
Minnesora rube,797t
Miromycin,856t
Mitoxantrone, 856t
908t, 908-909
Tinetti assessment in, 91 1 - 9 15,
Mitral valve
anatomy and function of, 4t
9121-9 1 5!,9161
lnd gastrointestinal motility disor
Mobility
323!
in amputation,895r-896t
in ankle arthroplasty,206
in burns, 464,466t
in claudication, intermirrent, 388
evaluation of
504!
Mucolytics,865t
Multiple sclerosis,320-321
j\1urmurs
cardiac,23t, 68
genitourinary, 563
956
electromyography of,304
respiratory, 92, 92t
strength testing of, 294-295
In burns, 464, 466[
in wounds, 479, 494t
structure and funcrion of, 1 60
636r
tuberculosis in,62 1 ,622, 636r
tuberculosis in. 6 1 3, 620-623, 636l
Mycophenolate mofetil in organ rrans
plantarion. 70Sr
Myelogcaphy, 1 68-1 69,304-305
prCC3utions after,305
Myocardium
Musculocutaneous nerve,277t
biochemical markers
111,
chest pain
Ill,
39-40, 92 1 , 923
cholestcrol levcls
casts in,220-224
cmical illness myopathy, 759
29-3 1 ,
301
111,
29
in electrical burns,443
230
fractures, 1 69-190, 237-258. See
also Fractures
854,
nitrates
Ill .
866t
lhrombolyti, 50
Infections,629--630
electrocardiography in, 43
mecabolic, 689-692
osteomyelitis,629-630
111
111.
50-52
oxygen demand
III
exercise,67
deliver)" 772r-773r
Nasotracheal tntubation in mechanical
ventilation,8 1 2
INDEX
957
anriparkinsonian, 321, 85 I t
diuretic, 867t
muscle relaxant, 868t
in chemotherapy, 34 1 , 342
in radiation therapy, 3 4 1
6361
Nebulizers, 800t
infections, 625-629
Neck
3 2 1 -324
2531
traction applied (0, 2 3 1 t
Nephrectomy, 595-596
in spine fractures, 1 82
syncope in, 3 1 9
traumatic, 305-310
ulceration in, 4 7 1-472
Nephrons, 558
ventricular, 3 1 5-3 1 6
Nephropathy
2921
observation
in,
281
cerebrovascular, 3 1 2-3 1 5
claudication in, 388
in compression from cast, 223
in critical illness polyneuropathy,
758-759
degenerative, 3 1 9-321
in diabetes mellitus, 47 1-472, 681684
signs and symptoms of, 683t6841
types of, 683r-684t
drug therapy in, 325
anticonvulsant, 845t
tem
and respiratory function, 90, 92t
structure and function of, 260-277
Neuropathy
in critical illness, 758-759
in diabetes mellinls, 471-472, 681-684
signs and symptoms of, 683t-684t
types of, 683t-684t
familial amyloidotic polyneuropathy,
liver transplantation in, 7 1 3
i n HlV infection and AIDS, 635t,
6361
ulceration in, 4 7 1-472
958
Neurosurgery, 325-326
in neurologic evaluation,281
in respiratOry evaluation,98-99
in extrapleural disorders, 1 45(147t
111
134t
obstructive disorders, t 3 1 t-
Norepmephrlne,668, 671
in ruberculosis therapy,623
in vascular evaluatIon,367-368
Nose,91t
Nosocomial infections, 607t,614
amibiotic-resistam,6 1 5-618
prevenuon of, 614, 615t, 639, 750
Nucleoside analogs in HIV infection and
AIDS, 633
5'-Nucleotidase levels,5 1 9t
OculomotOr nerve,289t
Odomoid process fracture,2521
Olecranon fractures, 186,188f,257t
Olfactory nerve,2881
Oliguria, 561
in acute renal failure,570
Oncology,331-359. See also Tumors
Nutrition
in anemia, 4 1 6, S66t
in chemotherapy, 342
in
in wounds,480-482
Obturator nerve, 278t
in gastrointestinal disorders,550551
OpportulllstlC infections,607r
in IfIV mfcct10n and AIDS, 633-634
Optic nerve,288t
Oral cavlry
535-536, 551
gastrostOmy/jejunostomy rubes in,
percutaneous endoscopic,
800t-801t
in hypoparathyroidism,689
nasoentcric feeding rubes in, 799t800t
nasogastric rubes in, SOOt
and wound healing, 474-475
Orders
on comfort measures,755
do not resuscitate/do not intubate,
755
medIcal records on,746
Orthopnea, l OOt
in hematologic evaluation,377
Osteoporosis. 689-690
in infections, 607-608
Osteosarcoma, 333t,3461
INDEX
Otorrhea, 316
959
Oxytocin, 661 t
111,
temporary, 788t
.l3Sr
surgery m, 3491
Pain, 877-884
OXlIlletry. 786t
III cardiac evaluation, 2S
111
111
III
III
III
in,210
Oxygen
cardiac evaluation, 31
III
burns, 463
arterial satur:ttion
879
scales used
In cardiac evaluation, 25
III
hypoxemia. 770
III
Ill,
878t
111
111
wounds, 478
esophageal, 525
III
physical therapy
10,
551-552
referral parrerns
10,
50 I , 502t
genitourinary disorders
hypoxia, 113. 1 3 0
III
III
7761-7771, 770
In mcchalllc:tl vemilanon, 821t
III
musculoskeletal, 161
In pancreatitis, 546. 547
III
therapy. 770-783
fixed performance system
Ill.
770,
III
10
wounds
c\lalu3tion of. 478
7761-7771
humidification
nephroluhlaSlS, 579
Ill.
Palpation
in burns, 462
]45
physIcal therapy
111,
778-782
Ill,
770, 7711-7751
Ir.lnspon of, 96-97
Oxygenation, exrral:orporeal membrane,
836-837
III
III
III
III
960
Palpation-continued
in obstructive disorders, 1 3 1 t-134t
physical therapy based on, 154r
in restrictive disorders, 1 3 8t-HOt
in vascular evaluation, 368-370
Pancreas, 545-547
disorders of
Ill,
32 1 , 85 1 t
Patella
fractures of, 179-1 80, 245t-246r
III
cancer, 350t, 35 1
Pelvis
pancreatitis, 545-547
posroperative, in transplantarion,
7 1 8- 7 1 9
gastrointeStinal functions of, 505t,
545-547
In resection and reanastomosis proce
dures, 549
transplanration of, 71 7-720
comparison of emeric and bladder
drainage in, 7 1 8
donors in, 700, 7 1 7-718
508,
Peptic ulcer disease, 528-529
drug therJPY
nl
posroperative care and complica
862t-863t
108f
indications for, 7 1 7
with kidney transplantation, 720-
Ill,
Percussion
Pancrearicoduodenecromy, 549
Pencardiocenresis, 6 1 2
Pancreaticojejunostomy, 549
))ericarditis, 47t
Pancreatitis, 545-547
))ericardium
Pancytopenia, 379
Papanicolaou smear, 337t
Papillary layer of dermis, 438t
Papillary muscle, anatomy and function
of, Sf
Paracentesis, 5 1 4[, 6 1 3
Pertussis, 620
pH
of arterial blood
in cardiaC evaluation, 3 1
INDEX
961
Plasma, 365
fresh frozen. 418t
protein fraction, 4 1 St
care, 493
Platelets, 366r
and antiplatelet agents, 8 5 1 t-852t
count of
in hematologic disorders, 379,
846,
Pheochromocytom:!, 672-673
hypertension in, 395t, 673
Phlebitis, and posrphlebitic syndrome,
402-403
Phleborheography, 373r
3 8 1 r, 3821, 429
in physical therapy guidelines, 429
in polycythemia vera, 409
in thrombocytopenia, 4 1 2-414
disorders of, 410-414
in disseminated intravascular coagula
tion, 4 1 0
cransfusion of, 4 1 7t
Photoplethysmography, 373r
Plethysmography, 373t
Pleura
Physical examination
disorders of
cancer, 344t
in burns, 462-464
pleurodesis in, 1 5 1
in infections, 607--609
thoracentesis in, 1 5 1 , 6 1 2
Pleural tap, 6 1 2
Pleurodesis, 1 5 1
Plicamycin, 856t
Pneumatic compression stockings, 79St
Pneumonc(omy, 1 5 1
hyperpituitarism, 663-666
Polycythemia, 409- 4 1 0
hypopituitarism, 666-667
Polyneuropathy
screening for, 65 1
663,
Plan( alkaloids in chemotherapy, 859t
962
Polyuria, 56 1
Pons, 267t
111,
336t
2 1 2-2 1 3
AIDS, 633
Proteins
electrophoresis of, 5 1 9t
plasma fraCtion, 4 1 St
serum levels of, 5 1 9t
in urine, 565t
decerebrate, 296
Proteinuria, 565t
decorticate, 296
in anticoagulant theupy, 4 1 5
i n cardiac evaluation, 2 8
and international normalized ratio,
382-384, 385',429
in liver disorders, 5 1 9t
Proton-pump inhibitors, 862t
Preload, 7
Psychological factors
Premature contractions
in amputation, 893t
atrial, 75t
585,
Psychosis in intensive care unit, 757-758
Pulmonary artery
Prodrome in seizures, 3 1 8
Progesterone, 669t
Prolactin, 66 1 t
Pronator drift rest, 299
Proprioception, evaluation of, 298r
cranial nerve tests in, 289t, 290t,
2 9 1 t , 292t
Prosratc, 584-587
benign hypertrophy of, 584-586
INDEX
Corrigan's, 17t
grading scale on, 368-369
569
in musculoskeletal examination, 1 68,
963
337t
thallium stress testing in, 36
of thyroid gland, 655t
of ventilation and perfusion, 1 20-
Pupils
121
increase, 323t
reaction to light, 289t, 293-294
shap< of, 293
size and equality of, 287, 293
Purpura, thrombotic thrombocytopenic,
4 14
257t-258r
in head or neck, 1 88f, 1 8 8-189, 257t
in shaft or distal, 189, 2S8t
Rales, 104
Raynaud's disease, 397, 398
Raynaud's phenomenon, 398
Pyelography, 566-567
Ieloluhotomy, 597
Pyelonephritis, 572-574
acute, 572-573
chronic, 566, 573-574
Pyramidal tracts, 276t
Quadricepsplasty, arthroscopic, 2 1 8t
Reflexes
cardiovascular, 10-12
corneal, 290t, 297
165t
in neurologic examination, 274, 296t,
296-297
deep tendon, 296t, 296-297, 297t
grades of response in, 296, 297,
2971
superficial, 274, 297
Reflux
gastroesophageal, 525-526
diagnostic procedures in, S 13t,
5 1 4r
drug therapy in, 862t
vesicoureteral, 572, 573
Rejection in organ transplantation, 702707
acute, 703-706
chronic, 706-707
in heart transplantation, 707, 724725
964
Rejection
111
organ transplantation
confirmed
hyperacute, 703
in kidncy transplantation, 707, 7 1 1
nl
al10n
836-837
10,
no
nl
physical thcrapy in, 739
4 4 l t . 4S0-451
chest pain in, 922t
in coronary artery bypass surgery,
Renal artery
angiography of. 567
postoperative, 53
drug therapy
10,
150
amihistamine, 847r
Renal vein
antitUSSIVe, 852r
bronchodIlator, 853t
corticosteroid, 8 6 1 t, 864t
Renin, 670
expcctor.1nr, 862t
mucolytic, 865t
sys[Cm
infections, 6 1 8-624
10
physical therapy
observation of, 99
111,
153
Ill,
1 2 1 . 123f. 12Sf
pathophysiology in, 125-150
physical therapy
Ill,
152-155
rate of, 99
in infections, 609
in mechanical venrilation, 8 2 1 r
i n ncurologic evaluation, 287
112- 1 5 3
goals of, 1 5 2
postoperative, 872-873
sighing, I O l t
401-402
restrictive, 125, 1 37- 1 5 0
INDEX
(racfures of
flail chesr in, t 49
149
physical therapy in, 153
pulmonary function rests in,
m,
1 2 1 . 1 24, 125f
thoracic procedures
965
1 5 1- 1 5 2
2 1 7, 2 19t
Rowe sling, 22St
Rubrospinal tract, 276t
Russell traction, 231 r
Kaposi's, 635r
Sargramostim, 860r
Rereplase, 868t
Reticular activating system, 272
Segmentectomy, pulmonary, 1 5 1
Seizures, 3 1 6-3 1 S
drug therapy
111,
845t
966
Skin
care measures
in radiation therapy,341
in wounds,483--495
cleansing and debridement in,
Sensory function
483-488
in amputation
dressings
III
111
i n diabetes mellitus,68 1
ulceration
111,
469t, 4 7 1 --472
Septicemia,638
Serotonin levels, SlOt
amputation, 894t
in burns, 453
in transfusion reactions,420t
487, 488--489,
disorders of
in wounds, 478
Sepsis,637"';; 3 8
Ill,
4901-492t
in hematologic disorders,378t
in 1I1fecrions,630
635t
in neuropathies, 471--472
postoperative, 468, 874
Shock
in burns, 452
111
traellon,23 1 ,232
septic,638
til
trauma wounds,468
111
Shoulder
amputation at level of,892t
arthroplasty of,202-204
indications for,202
physical therapy in,203-204
anhroscopy of,2 J 6-2 J7,2 1 9t
grafts of
in burns, 455-459, 456t, 464, 465
in tumors, 340
observation and irupecrion of
in musculoskelelal evaluatIOn,
1 62 - 1 6 3 , 1 6 9
in vascular disorders,367, 368,
386t
in wounds,480-482
palpation of,in musculoskeleral eval
uation, 1 63
111
burns, 457t-458t
Sigmoidoscopy,5 1 St
III
wound care,489,493
in Clncer diagnosis,337t
Sleep disorders
Sinoatrial node,9, 1 0
Small intestine
111
Sinusitis,6 I 8-6 I 9
INDEX
967
enteric drainage, 7 1 8
peptic ulcer disease of, 528-529
in, 184
thoracolumbar, 182, 253t-2541
hislory of, 98
arthroscopic, 2 1 5-217
Spirometry, 1 28t-129t
220, 221f
trauma of, equipment in management
of, 220-232
Spleen
evaluation of, 5 1 1 , 5 2 1 t-522t
function of, 505t
Splints, 225-229
Spasm
bronchial, 130
activity-induced, 150
bronchodilators in, 8531
hand, 218t
Spuwm analysis, 109, 1 1 9
in cancer diagnosis, 337t
of cerebral arteries, 3 1 5
in cough, 109
ischemia in, 40
of esophagus, diffuse, 525
Spasticity, 195
muscle relaxants in, 868r
Speech and language
methicillin-resistant, 6 1 5 -- 6 1 6 , 6 t 7
of skin, 630
Stasis zone in burns, 439
Sraws asthmaticus, 1 35
Smrus epilepticus, 3 1 8
Stem cells
in aplastic anemia, 406-407
transplantation of, 733-737
secondary, 309
Stereognosis, 298t
shock in, 3 1 0
Stereotaxis, 326
syndromes in, 3 1 1 t
Sterno-occipiromandibular immobilizer,
226,
Stomach
disorders of, 527-529
cancer, 348, 349t, 529
968
Sromach-coftt,,,,,ed
rISk facrors
hemorrhage
10,
336t
10,
10,
withdrawal
Ill ,
760--7 61
Sulfonamldcs, 8Ot
referred pam
.> 1 4-3 I .
10,
S02t
Sun exposure
burn In. 444
skin cancer in, .1)6-1)7
lavage procedure, 6 t 3
paroxysmal, 82f
Stool analysis
126 .\ 5 1
Sweat glands. I n IIltegume1Hary system.
416.417
Stratum
Sweat rest
111
basale, 438r
Syme's amputation. 8 9 1 t
corneum, 438t
granulosum. 438t
of heart. 1 0
spmosum, 438t
Syncope. 3 1 8-3 I 9
Strcngthenlng exercises
III
hip arthroplasty, 1 95
SympathomlmetlCs. 8671
Systole. 6
blood prl:ure In. 1 9, 19t. 391t. 7841,
7871
Streptococcal infections
glomerulonephrins
In,
57S-S76
T.1chycardm
Streptozocin, 855t
Junctional, 78t
supraventricular, 74t
757-758
Stress incontinence, 585t
Stress testing, 33-36. 374t
paroxysmal. 82C
ventricular, 76t. 83f
Tachypnea, 1 0 1 1
Tamponade
pericardia I, 47t
thallium in, 36
Stridor, 1 0 3
Stroke, 3 12-3 1 3
Stupor, 2S2r
Teeth. S05t
SCOpIC, 2 1 6, 2 1 7, 2 1 9t
Subarachnoid space, 270t
INDEX
Teletherapy, 340, 34 t
969
venous, 400-40 I
Temperature
In burns, 453
in infections, 609
of,437
in IIltracr:mial pressure IIlcrease man
400, 401-402
renal vein, 582
agement, 324t
testing of sensanon of, 298t
Temporal arteritis, 397
Temporal lobe, 26 ..[
Thyrocalcitonin, 653t
Thyroid gland, 6 5 1 , 653-660
disorders of, 656-660
Teniposide, 859t
hypothYTOidism, 658-660
Tetracyclines, 850t
screening for, 65 1
Thalassemia, 4 1 2
Thallium
III
stress resnng. 36
with dipyridamole, 36
Thioguanine, 857t
Thiotepa, 855t
Thoracentesis, 1 5 1 , 6 12
Thoracic nerve, long, 279t
2531-2541
Thoracolumbosacral orthosis, molded,
2261
Thoracoscopy, 1 5 2
Thromboangiitis obliterans, 396-397
Thrombocyres, 366t
Thrombocytopenia, 4 1 2-414
'Tibia
cardiaC evaluation, 28
Thrombosis
arterial, 392
in thromboangiitis obliterans, 396397
111
In thrombocytopenic purpura, 4 1 4
970
735-736
in lung transplantation, 730
of kidney, 708-7 1 2 . See also Kidneys,
transplantation of
Toxicity
transplantation of
of digitalis,59,60t, 867t
Toxoplasmosis,637
transplant:nion of
organ procurement and distribution
Trachea
creas, transplantation of
cancer of,344t
8 1 2-8 1 3, 8 I3f
735,736, 737
education of patients in, 740-741
goals of,738
delivery, 773t
Tracheostomy, 152, 812-8 1 3
731-732
in pancreas transplanration, 720
postoperative care in,701-702
rejection in, 702-707. See also Rejec
Traction, 230-232
complications of, 230-231 , 232
rypes of, 230, 231r
cry, 773r
Trauma
823-824
of b,,;n, 305-306, 307r-309r
Transplam:uion,697-741
INDEX
971
Tricuspid valve. 41
Triglyceride levels, 29
of pancreas, 350t, 3 5 1
Triiodothyronine, 653
resin uptake, 6! 5t
serum levels of, 654, 654t, 655
target sites and actions of, 653t
30-3 I
Tuberculosis, 620-623
of skin, 356-358
adventitia, 364t
intima, 364t
media, 364t
Tuttle test, 5 1 3t
353
of breast, 335[, 337r, 343, 346-348
chemotherapy in, 341-343, 854t860t. See also Chemotherapy
Ulceration
in arterial insufficiency, 468, 469t
in diabetes mellitus, 469t, 4 7 1 -472
540
diagnostic tests in, 337r
of esophagus, 526
risk factors in, 335t, 336t
of stomach, 348, 3491, 529
genitourinary, 335t, 337t, 348-349
hematologic, 35 1-354
Ultrafiltration, 587
Ultrasonography
phoma
metastasis of, 332
to bone, 345-346
physical therapy in, 358-359
972
poliovirus, 626
Vacuum Assisted Closure device, 489
Vagus nerve, 291 t
Valvular heart disease
pathophysiology in, 44
Vasodilators, 869t
Vasospasm
Urethra
biopsy of, 570
endoscopy of, 568
of cerebral artenes, 3 1 5
o f coronary artery, myocardial
ischemia in, 40
Veins, 364
Urine
skin dIsorders
Ill,
Uroflowmetry, 568
Vena cava, Sf
Urography
excretory, 566-567
retrograde, 567
Urokinase, 868t
Urolithiasis, 583-584
Ventilation, 92
470, 469t
alveolar. 127t
Vaccination
influenza, 620
controlled, 8 1 7t
definition of, 89
INDEX
973
Ventricles o f hean
anatomy of, 4t
intermittent mandatory, 8 1 7t
lation, 824
in, 56
inverse ratio, 8 1 9t
85
assist devices for, 832-836, 838
external, 833, 834, 835r
internal, 833, 833f, 835t
physical therapy in, 835-836
weaning from, 834
in Batista procedure, 58
diastole of, 6, 1 9 , 1 9 t
and end diastolic pressure, 6
ejection fraction of, 6
function of, 4t
factors affecting, 7, 8f
systole of, 6, 1 9, 19t
Venrriculectomy of heart, partiaJ Jeft, 58
Ventriculography, 38
cuff in, 8 14
extubation in, 8 1 2
Ventriculostomy
indications for, 8 1 2
i n intracranial pressure increase, 324t
intubation in, 8 1 2- 8 1 3 , 8 1 3f
complications of, 823-824
modes of, 8 1 5 , 8 1 6f
alternative, 8 1 9t-820t
conventional, 8 1 7t-81 8t
objectives of, 8 1 1 - 8 1 2
noninvasive, 8 1 9f
Vinblastine, 859r
pressure-cycled. 8 14, 8 1 5
Vincristine, 859c
time-cycled, 8 1 4
Viral infections
volume-cycled, 814-8 1 5
974
Viral infections-co1ltinued
rhinitis in, 6 1 8
Vision
cranial nerve functions in, 288t, 289t
chronic, 476
Vital signs
in chemotherapy, 343
in infections, 609
471
stagmg and classification of. 483,
483t
Vitamin 0, 437
in liver failure, 7 1 4 1
in osteomalacia, 6 9 1
III
neuroparhles, 471-472
483t
surgical, 468
Weaning
in trauma, 468
468-470, 469t
Wrist
Weight-bearing
in casts, 224
in hip arthroplasty, 192