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Emergency Medicine
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Dr. Donald Sefcik

Donald J. Sefcik is the Associate Dean at the Chicago College of Osteopathic Medicine (CCOM), Midwestern University (N[WU), in Downers Grove, IL. He is a tenured professor and board certified in both Emergency Medicine and Family Medicine. From June 1997 through May 2000, Dr. Sefcik served as Medical Director for the Physician Assistant Program, Coliege of Health Sciences (CHS), at MWU. Dr. Sefcik's lectures are based upon his experiences as a clinician and preceptor, tenure as a medical school faculty member, and his student assessrnent research.

Dr. Sefcik has practiced with physician assistants since 1988 and been involved in the clinical training of physician assistants since 1990. Prior to joining Midwestem University's faculty, Dr. Sefcik was a faculty member in the Pharmacology Department at Butler University and in the Nursing Department at Marian College, both in Indianapolis, Indiana. Dr. Sefcik has a Bachelor of Science in Pharmacy (1981), a Master of Science in Pharmacology (1994), both from Butler University, ffid an MBA (May 2004) from Purdue University.

CME Resources Certification & Recertification Exam Review

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Cerffication & RecertiJication Exam Review

CME Resources 2004
Emergency Medicine Topics Donald J. Sefoik, D.O., FACOEP

Learning Objectives
Upon completion of flris portion of the review course, the participant should be able to:

2. Describe colnmon toxidromes and their management. 3. Differentiate the three common causes of primary headaches. 4. Discuss cofirmon secondary headaches. 5. Describe the evaluation/management of common ophthahnologic fraumatic injuries. 6. Discuss hyperkalemia - its presentation and management. 7. Discuss cerebrovascular accidents and traumatic brain injuries. 8. List and describe corrmon abnormal findings in urine specimens. 9. List and describe common physical examination "signs" and findings.

1.

Discuss the basic principles of toxicolory.

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Overdose Sfafes
ldentifu the Druq
A, History
Who was there ? What did they find out ? Are there any bottles ? Abiliiy to 'quantity'the ingestion ? Pafient's medical history ?

'

Time since ingestion

B. Physical Data

1 Rate-----r ,Z-.1 gz SignsBiood Pressure / Toxidrome \ (-symptoms. Temperature / -1 \Heart Rate Respiratory * Level of consciousness, Pupil size, Breath..,.etc.

Toxidromes
Signs

VIChssic Toxidromes ,-+ AnTih"sIr rer,AGS q)9..d\.W \ LhS''- L Cholinergic Aqents nnticno[nerqic A
-.
S - Salivaiion

..Nff)

opiates

(-

L.

Lacrimaiion

U - Urination D - Defecation G - Gl Distress

E - Emesis

Hyperemia (Red as a Beet) Dry Skin (Dry as a Bone) Dilated Pupils (Blind as a Bat) Delirium (Mad as a Hatter) Tachycardia

IVliosis Bradycardia Hypotension

Iin;.t\ p.ry',r(

ftr'\.rxo^e-\

Hypoveniilation Reduced LOC

Flo'ir:;

sG'rr'r'u-u

?d^pt(

Nomoqrams
Acute, One-time lnqestions

*Acetarninophen - Rumack-Matthew
*

Aspirin -

Done

( b e".,e
ncr\v:.ig-^

Y1

\
)

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(G

eneralizations - Common F eatures)

CIIARACTERISTICS
Age of Onset

MIGRAINE
Childhood-< 3Oyo

TENSION
Eariy Adulthood

CLUSTER
20-40

LIt".u" Lln s)

F>M
Frequenelt

M>>F
Variable
30 min - weelcs Cyclic,

yo \ (,f .. t 1

l-4 /.month

(Muitipie/day) Duratiott
Description Site Time of Onsa Associated Featura

+-tzLrs
"Throbbiag"
Unilateral (65%) Variable (often AIv!

10-120 mi:r

"Vise-like'l
Biiateral
Later in day

t'Boring"
Peri-orbital Uniiateral
Bed time

AA{A/

(75o/o)

Anorexia
Muscle tendemess

Ipsilateral
AI,IS Dvsfxn

Anu&x"cr--f f\C^u\C4 t t'O''ASl

Aggravatkg Factors (Precipitdingfaaors)
Clinical Appestance
Tredtments

Phono/photophobia 70% Fam.IIx C/assic - aura Common - no aura

Lacrimation Rhinorrhea Ptosis/miosis Stess/Fatigue

Multiple
Withdrawal from activify
Prescription Rx

Aicohol
Pace

Mild disability
MildAaalgesics

Agitated

02
Many Rxs

Abortive
Prophylactic

hsgrp"d','.\ h nl
s*-:t<;;Ae

rale,

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elect S econdarv Ileadaches

SUBARACHNOI D HEMORRHAGE Sudden Onset & Severity

Usually innamanial areurysm (beny) rupture

50%(+; with Altered LOC Average age = 50yq,..: . "Sentinel" Headache Hx in 30% 75% Neck Stifiness V.f e e-,),,n5 15% New-onset Seizures CT Scan Misses 10-20% (False Negative) If CT Scan is negative and suspicion is high, DO A LUMBAR PLINCTTIRE

- ,f s,3

Hemo6hagrt fup (False Positive) a i;t-) a;t $Rr-'! ,\ isl'\i.tr '' ltuf b. Cerebral Aagiography is the "GOLD" standard for diagnosis/aneurysm location RE FENNAL TO NE UROS URGE ON
a,

ii$e-

BRAIN TUMOR HEADACHES

Dull, deep aching, nondescript, progressive
Often worse on awakening Usually worsened by valsalva maneuver or exerlion May have nausea/vomiting or focal furdings Vomiting that precedes headache- think posterior fossa fimor

crscans$S+t,

MEI-.llNGtTlS HEADACHE
Usualiy involves entire head Often associated with feverivomiting Often associated with Nuchal signs
Kcrnig's Sign Brudzinski's sign

Diagnosis requires high index of suspicion and a lumbar pulcture

q HYPERTENSIVE HEADACHE
Usually a throbbing, occipital headache Most often a morning headache Usually does not occur until the diqslolic biood pressure ir Often overdianosed cause of headaches Treafinent- Antihypertensives

o:gi-]{mmHg'

\4.

L TEMPORAL ARTERITIS

Pa1*-*^g.r,.

Rh"o*.";!z^ Lfncrc\

Infiln'ation of Temporal Artery with lymphocytes, plasma cells and multinucleate giant cells Disease of patients over 50yo/ESR> 50 t Women with 4:1 predorninance \i LUI<a { c:hcui'} Unilaterai, jabbing pain/worse at night Artery tender/pulseless- Biopsy=Diagnosis '*?t'* 'r', \e154\ sui''i'h to prevent biindness ?,0 High dose

rry

pt7

i*Y

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Ophthalmologic Trauma
ORBIT & LID

L Contusion ("Black Eye") a, RIO Other Injury

2, Orb it al Wall' Fr hittn'

a.

e' 1;'

bi o,w o ut Fr ac fiir e ")

Flydraulic forces tbroughout the globe; rupture of medial wall and floor, fapping faVmuscle and occasionally injuring nerve

b, Findings: - Diplopia on upward gaze - Enophthalmos

)r

' Infraorbital anesthesia - Subcutaneous emphysema ;'glsuding" of Maxillary Sinus

Consult

c. Treatrnent-

CORNEA A CONJUNCTWA
-1..

Chemical Init;a:ies Do NOT Delay Treannent

!!!

a.

Alkali Bums - Liquefaction Nemosis - Irrigate (sometimes 24 hrs+) Check pH with litnus paper -Refer/ConsultNOW !

b. Acid Burns

- Coagulation Necrosis - hrigate & Consult

3. Radiation

Butns (Iieratitis)($T Vrr,*

I' beqn sK'rq\ 1 s*'b'<th'n1 *A

a.IJV radiation causes comeal epithelial sweliing; pain & bluned vision, hours afterthe

exposure
a^reas

,s

ut4\})
Jce r,vr k RiSn
g(i\6b Lorrta {*TfD,.Ly. bdY
r

b.

Findings
Multiple Punctate
on fluorescein

staining

b,

Trearnent
- Mydriatic - Systemic Analgesic - Follow-up

agent

()- p*,{Jt \:2/

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4. Corneal Abrasions

a. b.

Complaint of foreign body "feeling"

Findings
- Foreign Body (+l) s Check Lid in eversion

c.

"Ice Rink Sign" with fluorescein

Treatnent
- Cycloplegic Agent
- Antibiotic topically - Follow-up in 24-48 hrs

. Sub conj

mctiv al Hemorchage

a. Bright Red blood overlying sciera b. Be sure no bleeding diathesis exists c. Blood Stops at limbus

d. Should NOT affect vision

e. No specific therapy

ANTERTOR CHAMBER & LENS

l.

Traumatic Hyphema
a. Blood in anterior charrber due to ciliary body or iris vessel disruption b. Best seen with patient sitting upright with slit lamp

c. Must R/O other iqiuries d. Findings - MaY be ary':nPtomatic - PainlPhotophobia.tslured Vision - May cause N & V e. Consult OphthaLnologist - Place a FOX Eye shield - Keep patient quiet @ 30-45 degree angle Risk of secondary glaucoma

2. Lens Dislocation a. Marked VA Decrease b. May be seen in Marfan's Syndrome

c. Consult your OphthaLnologist

3

. Tr^aumatic Mydriasis a.lmpairrrent of PSNS function b. Referffsualiy temporary

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^ ^ F{I?ERLATEMLA q R

t"rl

/o

L.,\rrnue\\u;\er

1. Definition

An elevated plasma potassium level (usually > 5.0 mEq/I-)

2. Pathophysiology

Hod\4/hy

does

it happen

Etiology L lncreased Potassium Load

a, Exogenous
t\,8

- Excess intake; Dietary; Suppiemental, .,

-Xedun'ibution t 'T uf)ll .r \r'so"o*htq\rb'^ Kt Y. 1, Hemolysis; lnsulin deirciency; Exercise . C'-t Acidosis: .KAJ 6r C G], \ 2. Decreased Excrerion b, Endogenous

Kr Lh.,ire kt" \

Renal Failure; Rx Effect: NSAIDs; ACE inhibitors; K-Sparing Diuretics

3. Factitious -

Hemolysis (of
Sims/Symptoms

sp

ecimen) ; Leuko cytosis ; Thromb

cyto sis ; Phiebotomy

Cardiac

Peaked T-waves

Fiat P-waves Widened QRS Y" V entricuiar fi brillation

^jU-*.-.-llh-t

Neuromusc-

Paresthesias

Weakness

Fiaccidity

^ni\**

/JWII.

3. Differential Diagnosis -

Hypocalcemia Neuromuscular disorder

EKG abnormalities from other cause

4. Treatment Plan a, Rx

Sodi'hpolystlrene

s{Y:}G\GXALATE)

orally or rectaiiy

More sevet'e cases (Cardiac arrhythnzias, etc) may require: Dextrose & Insulin fV - temporizing measure/shifts potassium intracellular S o dium B i carb onate - temp orizin g measure/shifts potas sium intraceilular Calcium Giuconate - cardioprotective/potassium antagonist c, Other

*\u_le"ut "{X s.

Hemodialysis

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Cerebrovascular Accidents (CVAs)

FACTS & FIGURES

A.

lncidence @ 730,000 per year

B. Risk Factors
Uncontrollable

a. b.

Advancing {ge - 2/3 occur in patients > 65 yo feach decade after 55 yo doubles the risk......] Gender:Verr t Women Diabetes mellitus:

c. Family History: CVA or TIA

d.
- 23 times the risk

Controllable

a.
b,

Hypertension:

- 4-

6 tirnes the risk

olo

A contributing factor in up to 70

of all CVAs

Atrial Fibrillaiion: - up to 6 iimes the risk A contribuiing factor in up to 15 % of all CVAs

lschemic Attack (TlA) Risk of a CVA is - 35 % wiihin 5 years

,c, Transient

d.

Cigarette smoking:

-2-3 times the risk

e.

Males:

Prior CVA

Females:

42 o/o risk of a second CVA within 5 years 24 % risk of a second CVA within S years

f,

Others: Myocardial lnfarction, Hypercholesterolemia, Sleep apnea

STROKE SYNDROMES

lschemic Attack (TlA) + - transient neurologic deficii, ihat by definition, lasts less than 24 hours rF 't - - 90 % last less than 60 minutes (many < 15 minutes) - Amaurosis fugax - transient, partial or complete monocular blindness - Rule of 1/3s r' 1/3 will have a CVA in \f l4l ,,r.,.1*",.trJ ./ 1/3 will have a second the future TIA ,/ 1/3 will have no sequelae \r rD^ lz.i fr. ir,l{ B, Lacunar lnfarct (Deep Subcortical/"Whiie Matter" Area Changes; - Contralateral PURE Motor Deficit (lnternal capsule) lj'T N) pt - Contralateral PURE Sensory Deficii (Thalamus) - Clumsy Hand - Dysarthria (Pons or lnternal capsule)

- Nofes

A. Transient

-LC

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Intracranial l{emorrhagic Events

Irrlr'acranial Hemorrhage
Snbarachnoitl llemorrhage

Cerebral Ischemic Evenl.s

l'hrombotic CYAs
Ernbolic CVAs

Onset/Progressiou

Ol-ten actiye at onset Rapid progression

May be active/nonactive Variable course

50% comatose at

Nonacl.ive at onset - 60 % during sleep Gradual progl'ession

Active at onset
Rapicl onset

presentation)

Etiology

Aneurysm (berry)

Itisk(s)

Ilypertension Bleeding Diathesis

Associated with polycystic

kidney disease aud aortic coarctation

fuleriosclerosis [Iypeftensiorr Diabetes Mellitus

I-Ieart (Valvular) Disease

furatomic Locatiott

Middle cerebralartery (comnon)

History

Severe Cephalgia

Severe Cephalgia

Stiff neck May be lristory of altered

level ofconsciousness

tlsually no Cephalgia Often history of TtAs

Usually no Cephalgia

Physical Exanr

Focal Neurological Signs

Nonfocal exam Nuchal rigidity

Focal Neurological Signs

Focal Neurological Signs

hrteural Carotid Bruit(s)

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Arteny'Site of Involvernent
lnternal Carotid Artery

Character-istic Feature(s) of CYA

Ipsilateml Monocular Blindness (Anaurosis Fugax) Contmlateral Herniparesis Contralateral l{emianesthesia/Hemianalgesia
Contralateral Lower Extremity paresis; aneslhesia,./analgesia Minirnal Contralateral Upper Extremity No Face Clnnges Contralateral Upper Extrcmities paresis; anesthesia/analgesia Contralateral Lower Face droop (Tongue cleviates to sicle opposite of lesion; no fasiculal.ions) Minimal/No Lower Extrernify Changes Aphasia (if dorninant hemisphere is involved) Contralateral l{omonymous Hemianopsia (rvith macu|ar sparing) Ipsilateral Cranial Nerve III Palsy Memory deficits (if hippocarnpus is involved)

Auterior Cerebral Artery

Middle Cerebral Artery

Posterior Cerebral Artery

Vertebrobasilar Artely

Diplopia (PPRF or CN ltr, fV, VD Watch for CN dysftrnction Ataxia / Vertigo (cerebellar signs) Bilateral Motor/Sensory Changes
Purc Motor (basilar pons or internal capsule) conlralateral to lesion Pure Sensory (thalalnus) contralateral to lesion Clurnsy I-Iand-Dysaltlu ia

Lacunar CVA

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Traumatic Brain Iniuries

FACTS & F/GURES

A. lncidence
a. - 2 million Americans with Head Trauma annually b, - 500,000 are admitted to the hospital c, - 100,000 deaths per year (- 60 % occur before arrivalto the ED) d, Aicohol consumpiion is involved in - 25 - 50 % of cases B. Classificaiions (arrival to ED) a. Mild Head lniury EYE Ooeninq 4
3 2
1

GLASGOW COIvIA SCALE

.ay
n

erra$1^*J ^. .. h{'-1 -( ' d9. n v-.<v"' b, Moderate Head lniurv ecs=9-13 d'n*>Z
oof' \
-ze%die
c. Severe head lniury

GCS=14-15
80 % of rniuries

Spontaneous To soeech To Pain No response

VERBAL Response
5

Alert & Oriented

Disoriented Nonsensical soeakino Moans/Unintelliqible sounds No response

-1o%oflnjuries

4
3

2
1

-40%die

- 10 % of lnjuries

GCS=Eorless

MOTOR Response
6

4
5

I
1

Follows commands Localizes pain Withdrawals from oain Decorticate posturinq Decerebrate posturinq No response

,R

C. Tvpes of Brain lniurv FO RCE(-1 00 ms)

Primary Injury
NeuralTissue ^/ lniuru
Contusion Laceration Difiuse Axonal lnjury

\.|
Cerebral
V ascul ar
I

niury

lntraparenchymal Hemorrhage Epidural Hematoma Subdural Hematoma Subarachnoid Hemorrhage

Secondary lnjury
Hypotension Hypoxemia Hypovolemia lncreased lntracranial Pressure

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SPECIFIC DIAGNOSTIC ENTITIES

cLosED "
{-Eng-aryAl

me''"5 r'rdrrrS Epidurai Hematota * SKr\ Rnr\.nc, I

i

rec Lesions

#hcrL,'.a'h

-l

,/ - 1 % of all traumatic brain injuries (- 12 % die) ./ - 80 - 90 % associated wiih a skull fracture (often tears a meningeal artery) \/ Only - 20 % have classic: lnjury - LOC - Lucid lnterval - Deterioration
Up to 60 % have no loss of consciousness Underlying brain injury is generally not severe 60 % occur in patients < 20 yo < 10 % occur in patients > 50 yo

'/ ./ r'
'v\.{a.

'/ '/ rrtsvln'r' -i*).,n *W"Y a' \

qJ-

Subdural Hematorna - 35 % of severe traumatic brain injuries Most occur in patients > 60 yo * Atrophic brains (elderly and alcoholics) are at greatest risk

l6$ff:l''}jr" l'F [6scAriem.,t

il

. t . ^. i,",*.r
'v

yd

vn,,X
-

'- J

i '/

mechanisms Underlying brain injury is generally more severe * Simple (no associated parenchymal injury - - 20 % die) * Complicated (associated brain injury - - 50 % die)

Hffiliil3.tffii$;,ti:1?H,ltiJlla...r.,"tion

Subarachnoid Bleed (Hemorrhage)

(:f1s(,^f/
b. lntra-axial Lesions - Cerebral Coniusions & Lacerations * Concussions

4t

Cn^

it:ru'cr{t,t\

cYc [c'-

- Diffuse Axonal lnjuries (Axonal Shearing)

lncreased lntracranial Pressure

- Herniation Syndromes

. Cushing Response (hyperiension; bradycardia; irregular respirations)

OPEN a. Penetrating lnjuries

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t,'

.-

f ro.'lrrt

INITIAL EVALUATION & TREATMENT

A, Salvage brain tissue not already irreversibly injured B. ldeniifyicorrect eniiiies that may cause secondary injury

tqtut ' t

/-'"'''

'

LFr"rl'+tt

lnjury

lmmobilize cervical spine (GCS < 6 = 14 % have C1 or C2 fracture)

GCS<9
lntubate (ETT) Hyperventilate lVs Monitors Resuscitate Sedation/Paralysis Secondary Survey (Life Threats....,)

GCS>9
lVs Monitors Frequent Serial Examinations (NEURO) Secondary Survey Monitor for ETTiHyperventilaiion need

,/ /
CT Scan

,/

4--""'
Neurosureeon

E lev ated Inttucranial Pressure Hyperventiiation Mannitol

Pentobarbiotai

----a

Operative Lesion
Epidural Hematoma Subdural hematoma lntracranial Hemorrhage with shift Depressed Skull Fracture

Non-Operative Lesion
Non-Depressed Skull Fracture Contusion Subarachnoid Hemorrhage

Causes

A. Causes

Motor Vehicle Accidents (MVA) - 45 o/o (cause - 60 % of deaths) Falls - 15 % (cause - 12 0/o of deaths) Assaulis - 14 o/o (Firearms - 14 o/o of deaths - approximately 75 o/o occur at the scene) OccupationalAccidents 10 % RecreationalAccidents 10 %

B.

Prevention

c. Firearm Legislation

a. Safety (Seat) Belts and Air Bags b. Helmets

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Considerations at Presentation:

a. Low-risk lniuries
- Not likely to deteriorate - Normal neurologic examination * Asymptomatic; Subjective complaints: Headache, Dizzy... .,. - Minor injury: * Scalp wound Hematoma, Abrasion, Laceration....
*"* Approximately 0,3

3 % will deteriorate

b. Moderate -risk lniuries

- Difficult group to ass.ign a prognosis - Neurologic Signs & Symptoms of unclear significance " Brief LOC; Vomiting; Post-traumatic amnesia.....
* Progressive headache; Child age < 2 yo..

- lnjury (?):
" Arduous Assessment to make (Work-up ???) *** Approximately 40 % will have an abnormal CT scan

** Approximately I

% will need a neurosurgical procedure

*n Approximately 10 % will deteriorate

c. Hiqh-risk lniuries
- Criteria-defined neurosurgical emergencies

- Neurolog ic Assessment dem onstrates si gnificant findings * Depressed LOC (not explained by drugs, EIOH...) * Focal Neurologic signs

" Decreasing LOC

* Skull Penetration or Depressed Fracture

- lnjury: Suspect Primdry or Secondary Brain lnjury

*** Approximately 25 % will need a neurosurgical procedure

References

Manual of Neurology; McGraw-Hill 2002 (0-07-137351-9) Handbook of Neurosurgery; Thieme New York; 2001 (0-865Z7-909-0) Emergency Medicine Reporls December 3, 2001: Head Trauma: Emergency Management and lmaging December 17,20Q1: Head Trauma: Severe, Moderate and Minor Head Trauma May 11, Traumatic Brain lnjury: State-of-the-Art Proiocols

1998: