Escolar Documentos
Profissional Documentos
Cultura Documentos
XAVIER UNIVERSITY
ATENEO DE CAGAYAN
Submitted to:
Ms. Geraldine Lacar, RN
Mr. George Gordon Lim, RN
Mrs. Leonora Sumaylo, RN
Fourth year Clinical Instructor
Submitted by:
Absin, Mary Grace
Abuzo, Ana Kris
Ardiente, Robbie Jay
Coraler, TC May
Cue, Marc Anthony
Dial, Mia Joy
Guzman, Van Ryan
Ilagan, Leah Elizabeth
Lawan, Gail
Manus, Gretta Carmel
Murillo, Joaquin II
Pasoquin, Joyce Dane
Taal, Mary Anneriza
Vega, Angela Paula
Yap, Lionel Bryan
TABLE OF CONTENTS
I. Introduction……………………………………………………………3
General objective…………………………………………………5
Specific objectives………………………………………………..5
Scope and limitations……………………………………………..6
II. Assessment
Patient demographic data…………………………………………7
Assessment tool…………………………………………………..8
Laboratory results………………………………………………..15
III. Anatomy and physiology……………………………………………16
IV. Pathophysiology
Narrative form……………………………………………………22
Schematic Diagram………………………………………………24
V. Medical management
General management…………………………………………….25
Drug study……………………………………………………….30
VI. Nursing management ………………………………………………61
VII. Discharge planning………………………………………………..72
VIII. Prognosis…………………………………………………………76
IX. Conclusion…………………………………………………………77
X. Recommendation……………………………………………………78
XI. Bibliography……………………………………………………….79
XII. Appendix………………………………………………………….81
3
INTRODUCTION
This is a case of patient RP, 34 years ols, male, admitted on august 10, 2007, with the
presenting diagnosis of Acute Respiratory Failure secondary to sepsis secondary to acute
necrotizing pancreatitis; Diabetes Mellitus type II secondary to acute necrotizing pancreatitis.
Under the care of the XUSN4 of block NC and NG during the I.C.U. rotation in Maria Reyna
Hospital.
Acute pancreatitis is defined as an acute inflammatory process of the pancreas with
variable involvement of other regional tissues or remote organ systems. In acute pancreatitis,
protease trypsinogen enzyme, produced by the exocrine pancreas, converts into active trypsin;
the enzyme most responsible for auto-digestion of the pancreas, causes primarily the pain and
complications of pancreatitis.
Acute pancreatitis is classified further into mild and severe forms. Mild acute pancreatitis
is associated with minimal organ dysfunction and uneventful recovery. Severe acute pancreatitis
is associated with pancreatic necrosis and may lead to organ failure or local complications.
The International Symposium on Acute Pancreatitis in 1992 defined pancreatic necrosis
as the presence of one or more diffuse or focal areas of nonviable pancreatic parenchyma, which
is often associated with peripancreatic fat necrosis. By definition, pancreatic necrosis represents
a severe form of acute pancreatitis.
Type 2 diabetes mellitus, previously known as adult-onset diabetes, maturity-onset
diabetes, or non-insulin-dependent diabetes mellitus (NIDDM)—is due to a combination of
defective insulin secretion and insulin resistance or reduced insulin sensitivity (defective
responsiveness of tissues to insulin), which almost certainly involves the insulin receptor in cell
membranes. In short, Type 2 diabetes occurs when your pancreas does not make enough insulin
or is unable to use the insulin effectively. When the body does not make enough insulin or has
trouble using insulin, the cells do not absorb enough sugar from the blood - leading to high blood
sugar levels and diabetes.
This disease condition occurred from pancreatic insulin producing beta cell damage. Beta
cells (beta-cells, β-cells) are a type of cell in the pancreas in areas called the islets of Langerhans.
They make up 65-80% of the cells in the islets. These cells are responsible in making and
releasing insulin, a hormone that controls the level of glucose in the blood.
4
Respiratory failure is a syndrome in which the respiratory system fails in one or both of
its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, respiratory
failure is defined as a PaO2 value of less than 60 mm Hg while breathing air, or a PaCO 2 of more
than 50 mm Hg. Furthermore, acute respiratory failure is characterized by life-threatening
derangements in arterial blood gases and acid-base status.
Acute renal failure (ARF) is the rapid breakdown of renal (kidney) function that occurs
when high levels of uremic toxins (waste products of the body's metabolism) accumulate in the
blood. This disease condition occurs when the kidneys are unable to excrete the daily load of
toxins in the urine.
The above mentioned disease conditions is a brief overview of the presenting diagnosis
of the patient. Thorough discussion of the presenting diagnosis shall be reflected in Anatomy &
Physiology and in Pathophysiology.
5
General objective
At the end of one hour of case presentation, we will be able to improve our knowledge in various
concepts related to our patient’s condition, and skills in careful assessment and rendering of
nursing interventions involved in the management of our client’s case; and develop positive
attitudes by cooperation and sense of teamwork as we accomplish our case study using concepts
that we have acquired from our NCM 104 classes and previous related subjects in the BSN and
AHSE curriculum.
Specific objectives
1. Perform a thorough assessment and careful gathering of data that are clinically significant
2. Further completion of data that will supplement our assessment, such as laboratory
4. Design individualized nursing care plans based on nursing diagnoses that are suitable and
5. Carry out nursing interventions that are effective, reality based, time-bounded, achievable
6. Come up with a medical management, a prognosis, and a discharge plan that are suitable
7. Develop a sense of teamwork in coming up with the case study by division of labor and
The study focuses on the assessment, anatomy, and pathophysiology and its diagram,
medical management-both ideal and actual, nursing care plans, ideal discharge plan, prognosis,
recommendation and conclusion revolving around the diagnosis of the patient which is Acute
Respiratory System and Urinary System were also taken into consideration to better understand
This study is limited only to the available records found on the patient’s chart and the
information being provided for by the family members present at the patient’s room during the
time of assessment. Other factors that will also be considered as limitations to this study would
Name of patient: RP
Sex: Male
Height: 5’11”
Nationality: Filipino
Occupation: unemployed
Income: None
Name of attending physician: Dr. Valmores, Dr. A. Sison, and Dra. Solas
8
College of Nursing
Xavier University
Ateneo de Cagayan
LEVEL IV
NURSING HISTORY & ASSESSMENT RECORD
ALLERGIES:
(/) None known ( ) Yes (Specify Allergen)
RP’s younger sister verbalized, “ Wala mana sya’y allergies sa pagkaon og tambal.”
NUTRITION/METABOLIC PATTERN
Meal pattern: Usually, RP eats three times a day. However, on our first assessment, RP is on
NPO status. He is getting nutrition through TPN.On our second assessment, RP is fed per NGT 6
times a day.
TEETH (/ ) Own
Comments: Yellowish white in color. RP’s younger sister verbalized that,”kumpleto pa man na
iyang ngipon, wala pud na sya gagamit og bisag unsa para ngipon.”
10
ELIMINATION PATTERN
BLADDER ( / ) Catheter
Comments: RP is on urinary catheter draining well to a yellow colored urine. RP’s latest intake
was 740 cc and his latest output was 860 cc. Polyuria was noted.
BOWEL ( / ) Diaper
Comments: RP’s younger sister verbalized that, “ makalibang na sya mga kausa sa usa ka adlaw,
ako may ga ilis sa iyang diaper.” His stool is yellowish brown in color, soft, and in moderate
amount.
ACTIVITY/EXERCISE
Activities of Daily Living (I= Independent, A=With Assistance, D=Dependent)
Eating: (D) Bathing: (D) Dressing: (D)
Grooming: (D) Toileting: (D) Ambulating: (D)
BEHAVIOR PATTERN
BEHAVIOR ( ) relaxed ( ) mildly anxious
(/ ) moderately anxious ( ) very anxious
Psychiatric History: Upon assessment patient is moderately anxious and irritable. According to
his sister RP had episodes of psychosis after he under went craniectomy because of a gunshot.
“Paghuman atong napusilan siya, naa na dayon times na makalina iyang storya, mura siyag
bata.” Og “naa gyud usahay mutukar na siya saputon lang kalit og di kaila.” As verbalized by
his sister.
SUBSTANCE ABUSE
Tobacco ( ) no ( / ) yes Cigarette/Cigar/Pipe 1 pack /day/wk
Drugs ( / ) no ( ) yes Type:____________
Alcohol ( ) no ( / ) yes Amount: 3 long neck/week
11
SEXUALITY/REPRODUCTIVE PATTERN
Comments/Nursing Problem Identified: As observed and verbalized by the significant other
patient has scrotal inflammation with minimal white discharges.
PHYSICAL ASSESSMENT
NEUROLOGICAL ASSESSMENT
On the first assessment, patient was conscious and able to respond by nodding. He
manifested weak lower extremities and because of this, pillows are placed under the legs to
prevent any further discomfort. He was oriented to the place but not the time. His speech and
4mm in size with the Right pupil sluggish and Left pupil briskly reactive to light
accommodation.
patient still had difficulty in vocalization with episodes of irritability and disorientation because
he could not identify some of his relatives. Both pupils briskly reactive to light accommodation
RESPIRATORY ASSESSMENT
On the first assessment, patient RP was hooked on mechanical ventilator but is not fully
dependent on it; the mode was set only to assist and control. Crackles noted on both lungs , there
On the second assessment, crackles still present and RP is coughing ineffectively due to
post-extubation and white secretions noted in RP’s oral cavity. Lips and mucous membranes are
CARDIOVASCULAR ASSESSMENT
RP has a heart rate of 119bpm and was noted with sinus tachycardia.
PERIPHERAL-VASCULAR ASSESSMENT
Partial range of motion noted in the lower extremities. Weak and thready pulse was noted
GENITOURINARY ASSESSMENT
RP was on a Foley Bag Catheter with urine clear and color yellow. Based on lab results,
presence of ketones was noted (40mg/dL). There was scrotal inflammation with minimal whitish
discharges.
Upon second assessment, there was an increase in urine output noted (O=870cc,
I=740cc). RP still on catheter and on diaper. Blister formation noted at the scrotal and sacral
area.
MUSKULOSKELETAL ASSESSMENT
There was full range of motion in RP’s upper extremities but with the lower, only partial.
SKIN ASSESSMENT
Oral mucosa was noted to be dry and lips were scaly and dry. Skin is intact except on the
right arm due to the presence of CVP catheter and on the three toes of his right leg due to
On the second assessment, blisters were still evident on the R toes but with additional
blister formation on the Right heel, scrotal and sacral area. Skin is dry.
CURRENT MEDICATIONS
Ranitidine 50 mg IV q12h
RP is fully dependent on the mother who resides in Germany due to the fact that he has
no work and has been unemployed for quite some time. He lives in Gran Europa with his 5
siblings and their families. They will also be the ones assisting RP when at home. Patient seems
to anticipate in returning home however, no order was made yet for any discharge due to further
evaluation and treatment. Patient RP is not in need of a social welfare service because the mother
EXAMINATION VALUES
ARTERIAL BLOOD GAS
> PaCO2 43.3 35 – 45 Normal
> HCO3 14.2 22 – 26 Low Metabolic Acidosis
> pH 7.2 7.35 – 7.45 Acidic
> PaO2 82.3 % 95% – 100% Low
CBC
> WBC 19.6 x 10^3/ uL 5 – 10 X10^3/uL High
> Platelet 80 x 10^6/ mm3 140 – 440 Low
x10^6/mm3
URINALYSIS
> BUN 58 mg/dL 8 – 20 mg/dL High
> Creatinine 3.2 mg/dL .8 – 1.5 mg/dL High
> Ketones 40 mg/dL Ketonuria
> Albumin Fraction 1.9 g/dL 3.5 – 5 g/dL Hypoalbuminemia
BLOOD CHEMISTRY
> Potassium 3.0 mmol/L 3.5 – 5.1 mmol/L Hypokalemia
HGT (Latest result) 151 mg/dL 60 – 110 mg/dL High
ANATOMY AND PHYSIOLOGY
The Pancreas
The pancreas is an endocrine and exocrine organ located retroperitoneally in the upper
abdomen overlying the spine. It is a glandular organ that secretes digestive enzymes and
hormones. In humans, the pancreas is a yellowish organ about 7 in. (17.8 cm) long and 1.5 in.
(3.8 cm) wide. It lies beneath the stomach and is connected to the small intestine at the
duodenum. The pancreas is supplied by the gastroduodenal arteries and by branches of the
splenic artery. The splenic vein and artery run superiorly and posteriorly; the mesenteric vein
lies in the angle between the head and body of the gland. At this point the superior mesenteric
vein and splenic vein join to form the portal vein.
16
Most of
the
The exocrine portion of the pancreas accounts for about 80% of the total glandular
volume. It consists of at least two functional units: acinar cells, which secrete primarily digestive
17
enzymes; and centroacinar or ductal cells, which secrete fluids and electrolytes. Pancreatic
secretion is regulated by several peptides that are released from the gastrointestinal tract. Some
of these peptides, such as secretin and cholecystokinin (CCK), stimulate pancreatic secretions,
whereas somatostatin and pancreatic polypeptide inhibit their release. The pancreas secretes
about 20 digestive enzymes and cofactors. Some enzymes are activated in the duodenum by
enterokinases and calcium. These enzymes account for most of the intraluminal digestion of
dietary proteins, triglycerides and carbohydrates. They are also important in the cleavage of
certain vitamins (such as A and B12) from carrier molecules, thereby allowing them to be
absorbed efficiently. Because pancreatic enzymes are secreted in great excess, maldigestion and
serious nutritional deficiencies occur only when over 90% of the gland has been destroyed.
The heart is the pump responsible for maintaining adequate circulation of oxygenated
blood around the vascular network of the body. It is a four-chamber pump, with the right side
receiving deoxygenated blood from the body at low pressure and pumping it to the lungs (the
pulmonary circulation) and the left side receiving oxygenated blood from the lungs and pumping
it at high pressure around the body (the systemic circulation).
1. These cells generate a rhythmical depolarization, which then spreads out over the atria to
the atrio-ventricular node.
2. The atria then contract, pushing blood into the ventricles.
3. The electrical conduction passes via the Atrio-ventricular node to the bundle of His,
which divides into right and left branches and then spreads out from the base of the
18
The 'squeeze' is called systole and normally lasts for about 250ms. The relaxation period,
when the atria and ventricles re-fill, is called diastole; the time given for diastole depends on the
heart rate.
lingula (a small remnant next to the apex of the heart), the right
lung is composed of the upper, the middle and the lower lobes.
Mechanics of Breathing
To take a breath in, the external intercostal muscles contract, moving the ribcage up and
out. The diaphragm moves down at the same time, creating negative pressure within the thorax.
The lungs are held to the thoracic wall by the pleural membranes, and so expand outwards as
well. This creates negative pressure within the lungs, and so air rushes in through the upper and
lower airways.
Expiration is mainly due to the natural elasticity of the lungs, which tend to collapse if
they are not held against the thoracic wall. This is the mechanism behind lung collapse if there is
air in the pleural space (pneumothorax).
Each branch of the bronchial tree eventually sub-divides to form very narrow terminal
bronchioles, which terminate in the alveoli. There are many millions of alveoli in each lung, and
these are the areas responsible for gaseous exchange, presenting a massive surface area for
exchange to occur over.
Control of Respiration
0ur respiratory rate changes. When active, for example, respiratory rate goes up; when
less active, or sleeping, the rate goes down. Also, even though the respiratory muscles are
voluntary, we can't consciously control them when we are sleeping.
20
Apneustic center (located in the pons) - stimulate I neurons (to promote inspiration) Pneumotaxic
center (also located in the pons) - inhibits apneustic center & inhibits inspiration
Factors involved in increasing respiratory rate:
Chemoreceptors - located in aorta & carotid arteries (peripheral chemoreceptors) & in the
medulla (central chemoreceptors)
Chemoreceptors (stimulated more by increased CO2 levels than by decreased O2 levels)
> stimulate Rhythmicity Area > Result = increased rate of respiration
21
NARRATIVE PATHOPHYSIOLOGY
parenchyma and focal enzymic necrosis of pancreatic fat and vessels. It is known to be
precipitated by chronic alcoholism. Other factors such as obesity and sedentary lifestyle are also
known to contribute to the development of the condition. It is common in people 30-40 years of
age and in those who take drugs such as Thiazide diuretics and steroids for drug therapy.
Given these factors, there will be partial obstruction of the sphincter of Oddi which leads
to obstruction to the outflow of pancreatic enzymes and leakage of these enzymes to pancreatic
tissues. Along with premature activation of these enzymes, autodigestion occurs, leading to acute
necrotizing pancreatitis.
22
Pancreatic enzymes may also leak into the blood stream and circulate into the lungs and
kidneys, prompting the release of proinflammatory mediators. These pancreatic enzymes and
mediators such as kinins increase vascular permeability and dilate blood vessels, further leading
to loss of plasma volume and increased permeability to protein. Increased permeability to protein
can lead to loss of albumin causing hypoalbuminemia. Loss of albumin stimulates lipoprotein
Increase in vascular permeability also causes loss of plasma volume which leads to
decrease in blood volume and decreased renal blood flow resulting to ischemia. Toxic oxygen-
free radicals are generated, promoting swelling, injury and necrosis of nephrons. Acute tubular
necrosis occurs leading to decrease in filtration pressure and decrease in GFR resulting to acute
renal failure.
On the other hand, pancreatic enzymes circulating in the blood goes to the lungs causing
injury to the capillary endothelium further leading into disruption of surfactant production by the
alveoli and increased capillary permeability. Increase in capillary permeability causes movement
of fluid and plasma protein from capillary to interstitial space (alveolar septum) and alveoli.
Decrease in blood volume (hypovolemia) and pleural effusion then occurs. Pleural effusion
results to pulmonary edema which impairs gas exchange. Blood oxygen level is then decreased
Another result of acute necrotizing pancreatitis is damage to the alpha and beta cells of
the islet of Langerhans. There is decrease in insulin production and increase in glucagon
production. Decrease in serum insulin level can cause significant increase in blood glucose level,
chronic elevation in blood glucose level. The increase in osmolarity will then lead to increased
23
capillary permeability leading to increased urine output and decreased body fluids. This will
trigger the thirst mechanism of the body resulting to polydipsia. Chronic elevations in glucose
level, on the other hand, will cause glycoprotein deposits in the cell wall leading to three possible
conditions namely: diabetic neuropathy, diabetic nephropathy and impaired immune function.
Production of excess glucagon results to production of glucose from protein and fat stores
(gluconeogenesis). There is wasting of lean body mass and serum ketones (byproduct of
MEDICAL MANAGEMENT
symptoms and treating its underlying causes. The following is a table presenting the ideal
management of the patient’s condition as well as the actual management given to the patient
DRUG STUDY
Classification: CNS STIMULANT Dosage/ Administration/ Route: 500 MG IVTT slow q12h
dependence
, including
alcoholism
and; with
hypertensio
n.
> Adjunct Increased Tanawa sa >Tachyarrhythmi Absorption: >Headach > Mydriasis > Monitor blood
to standard cardiac ang as Administered IV e >Hypotensi pressure, heart rate,
measure s to output, dosage >Pheochromocyt only, resulting in > Dyspnea on pulse pressure, ECG,
improve increased please oma complete >Palpitati > Angina pulmonary capillary
Blood blood >Hypersensitivit bioavailability ons weigh pressure
pressure, pressure y to bisulfites > Nausea (PCWP), cardiac
cardiac and Distribution: > output, CVP.
output, and improved Widely distributed Vomiting
urine blood but does not cross > Monitor urine
output. flow. the blood brain output frequently
barrier throughout
administration.
Metabolism and Report decreases in
Excretion: urine output
Metabolized in the promptly.
liver, kidneys, and
plasma. > If
hypotensionoccurs,
administration rate
should be increased.
If hypotension
continues more potent
vasoconstrictors
(nor-epinephrine may
be administered.
abdominal
distention,leg
cramps, and/or
cardiac
dysrhythmies.
Check serum
potassium levels.
Half-life:
42
Less than 2
hours.
result in nausea,
vomiting, unusual
tiredness or
weakness,
dizziness or
sweating.
glucose,
glucagon or
epinephrine.
Because
medication errors
involving insulin
have resulted in
serious patient
harm and death,
clarify all
ambiguous
orders.
intensified diabetes
control. Monitor
glucose level
closely in these
patients because
severe
hypoglycemia may
result before the
patient may develop
symptoms.
Generic Name: POTASSIUM CHLORIDE Brand name: (no brand name given)
Classification: MINERAL AND ELECTROLYTE REPLACEMENTS/SUPPLEMENTS Dosage/ Route: 60 mg IVTT
>Treatment/prevent >Replaceme > Maintain >Hyperkalemia Absorption: >Abdomin >Confusion > Assess for
ion of potassium nt acid-base > Severe renal Well absorbed al pain >Restlessne signs and
depletion balance, impairment following oral > Diarrhea ss symptoms of
>Prevention isotonicity and > Untreated administration > Nausea > Weakness hypokalemia
of electrophysiolo Addison’s >Vomiting >Arrhythmi and
deficiency gic balance of disease Distribution: as hyperkalemia
the cell > Severe tissue Enters > ECG Monitor
trauma extracellular changes pulse, blood
> Activator as >Hyperkalemic fluid; then >Ulecration pressure, and
many familial actively > Stenotic ECG changes
enzymatic periodic transported into lesions periodically
reactions; paralysis cells. > Irritation during IV
essential to > Potassium at Ivsite therapy.
transmission of acetate Metabolism and > Paralysis
nerve impulses; injection Excretion: >Paresthesi > Monitor
contraction of contains Excreted by the a serum
cardiac, aluminum, kidneys potassium
skeletal, and which may before and
smooth muscle, become toxic Half-life: periodically
gastric with prolonged Unknown. during
secretion; renal use to high risk therapy
function; tissue groups (renal
synthesis; and impairment, > Symptoms
carbohydrate premature of toxicity are
metabolism. neonates) those of
hyperkalemia
> If
hypokalemia
is seconfary
to diuretic
therapy,
consideration
55
should be
given to
decreasing
the dose of
diuretic,
unless there
is a history of
significant
arrhythmias
or concurrent
digitalis
glycoside
therapy.
>Maintenan
ce of > Healing Inhibits > Absorption: 50% >Confusi >Arrhythmias > Assess patient for
alkaline and the action Hyprsensitivi absorbed after PO on >Gynecomasti epigastric or
gastric pH prevention of of ty and IM >Dizzine a abdominal pain and
ulcers histamine > Cross administration ss >Agranulocyt frank or occult blood
at the H2 hypersensitiv >Drowsi osis in the stool, emesis, or
> Decreased receptor ity may occur Distribution: All ness > Aplastic gastric aspirate.
symptoms of site > Some oral agents enter breast >Halluci anemia
gastroephage located liquids milk and nations > Anemia > Instruct patient to
al reflux primarily contain cerebrospinal fluid >Headac >Neutropenia take medication as
in the alcohol and he >Thrombocyt directed for the full
> Decreased gastric should be Metabolism and > Nausea openia course of therapy, even
secretion of parietal avoided in Excretion: >Impoten >Hypersensiti if felling better. Take
gastric acid cells, patients with metabolized by the ce vity reactions missed doses as soon
resulting known liver, mostly on > Vaculitis as remembered but not
in intolerance. first pass, 30% if almost time for next
inhibition excreted unchanged dose. Do not double
of gastric by the kidneys after dose.
acid PO administration.
secretion > Advise patients
taking OTC
preparations as to take
the maximum dose
continuously for more
than two weeks
without consulting
health care
professional. Notify
health care provider if
difficulty swallowing
occurs if abdominal
pain persists.
57
Treatment of Bronchod Salbutamol Contraindicated in Peak: 2 hours Headache Tremor Monitor the
hypoxemia ilation binds to beta2- hypersensitivity to Metabolism Insomnia Hypokalemia patient’s response
caused by adrenergic drug and in and Dizziness Bronchospasm to the drug therapy
hospital receptors in patients peanut/ Distribution: Dry and Bronchitis to determine the
acquired airway smooth soy allergy. widely irritated Hypersensitivi effectiveness of the
pneumonia muscle, leading Cautious use in distributed nose and ty reactions dosage and to adjust
to activation of cardiac disease, and throat Tachycardia the dosage as
adenyl cyclase hypertension, metabolized Nasal Palpitation needed.
and increased hyperthyroidism, by the liver. congestion Muscle Provide comfort
level of cAMP diabetes, Enters the Nausea measures including
cramps
Ipratropium glaucoma, breastmilk. Vomiting rest periods, a quiet
Nervousness
inhibits geriatric patients, Excretion: Cough environment,
Hypertension
cholinergic pregnancy, excreted in dietary control of
Dyspnea CNS
receptors in lactation, children the urine. caffeine and
Wheezing Stimulation
bronchial below 2 y.o., headache therapy as
smooth muscles, patients with Altered needed, to help the
resulting in bladder neck taste patient cope with
decreased obstruction, Increased the drug therapy.
concentrations prostate appetite Watch out for side
of cGMP, hypertrophy and Malaise and adverse effects
causing during urinary of the drugs.
bronchodilation retention.
Generic Name: SODIUM BICARBONATE Brand name: (no brand name given)
Classification: ALKANIZING AGENTS Dosage/Administration/Route: 4 vials in 250 cc
D5NSS
>Manageme >Alkalinizatio > Acts as an > Metabolic or Absorption: >Flatulenc > Tetany > IV: Assess
nt of n alkalinizing respiratory Following oral e > Metabolic fluid balance
metabolic agent by alkalosis administration, > Gastric alkalosis
acidosis >Neutralizatio releasing > Hypocalcemia excess distention >hypernatremi > Report
n of gastric bicarbonate > Excessive bicarbonate is > Sodium a symptoms of
acid. ions. chloride loss absorbed and and water >hypocalcemi fluid overload
> As an antidote results in retention a
> Following following metabolic > Irritation >hypokalemia > Assess
oral ingestion of alkalosis and at IV site patient for
administratio strong mineral alkaline urine. signs of
n, releases acids acidosis,
bicarbonate, > Patients on Distribution: alkalosis,
which is sodium Widely paresthesia,
capable of restricted diets distributed into tetany, altered
neutralizing (oral use as an extracellular fluid. brerathing
gastric acid. antacid only) pattern,
> Renal failure Metabolism and hypernatremia,
(oral use as an Excretion: or
antacid only) Sodium and hypokalemia
> Severe bicarbonate are throughout the
abdominal pain excreted by the therapy.
of unknown kidneys
cause, as >Avoid
especially if Half-life: extravasation,
associated with Unknown. as tissue
fever (oral use irritation or
as an antacid cellulites may
only) occur. If
infiltration
occurs, confer
with physician
or other health
60
care
professional
regarding
warm
compresses
and infiltration
of site with
lidocaine or
hyaluronidase.
> Antacid:
Assess patient
for epigastric
or abdominal
pain and frank
or occult blood
in the stool,
emesis, or
gastric
aspirate.
PRECAUTIO DYNAMICS
NS
Prophylaxis Hemostasis Stop the Contraindicate Peak: 1 to 3 Dizziness Fertility Monitor clinical
for bleeding natural d in patients hours Tinnitus problems response and
tendencies / plasminogen with Headache Elevated clotting factor
hemorrhage clot- pronounced Onset: Rapid Weakness serum levels regularly,
dissolving thrombotic Nausea creatine in order to
mechanism tendency w/o Duration: Cramps phosphokin arrange to adjust
by blocking simultaneous Duration of ase (CPK) dosage, as
Diarrhea
its activation use of infusion needed.
Hypotensio
or by anticoagulant Offer support and
n
directly and in patients safety measures
inhibiting with defective Malaise
to prevent patient
plasmin. color vision. injury.
Use cautiously Monitor the
in renal patient for any
insufficiency signs of
and in massive thrombosis, in
bleeding o the order to arrange
upper urinary to use comfort
tract. and support
measures, as
needed.
NURSING MANAGEMENT
tungod sa mga secretions and will be able to: condition non- verbally by
plemas nya, unya impaired gag -demonstrate and association of
dili pa gyud nya reflex secondary maintain airway > elevate the head of the bed and > gravity decreases pressure on things like pillow
maluwa” as to presence of patency change position every 2 hrs the diaphragm and enhancing as smooth feeling/
verbalized by mechanical -demonstrate non- drainage of ventilation to relieved and
patient’s ventilator verbalize different lung segments comfort. Also
significant other. understanding of secretions were
causes and it’s >do suctioning of secretions using > helps in evacuation of improving
management suction machine secretions gradually
throughout
Long term: > reinforce techniques that would > for the client to understand improving with
Objective: At the end of 8 hrs, help client express his and express what he had wanted suctioning and
> attempts to the patient will be understanding on the information to verbalize or say since the expectorates/suctio
expectorate but able to: being given like: patient cant express verbally, ned secretions into
can’t do it - maintain clear association of words into action yellow to green
>crackles present airway and a. associate actions or things on or things may be a great help to colored at minimal
on both lungs demonstrate which the patient would like/ both the nurse and the patient. amount,. The
upon auscultation techniques that aids wanted to express patient was as well
>deep and in b.encourage by nodding, raising compliant to
labored breathing expectorant/suctioni eyebrows and raising thumb for procedures and
>use of accessory ng through approval and turning head side-to- interventions given
muscles secretion machine side for disapproval .
> weak and signs and symptoms respiratory alkalosis. private room
thready pulse of hyperglycemia during/ within our
>imcreased urine > monitor Intake and Output >Facilitates accurate measurement shift.
output Long term: every 4 hours. and effectiveness of volume
>> intake less At the end of 4 replacement and maintenance of
than output ( I- hours of nursing adequate circulation fluid volume.
740cc, O-860cc) interventions, the
patient will be able
to have vital signs > Assess patient’s mental status > Mental status changes occur
within normal range and observe for significant with exceedingly high or low
and have equal changes glucose levels, electrolyte
balance between imbalances and acidotic states.
intake and output.
>Instruct patient/family > Provides information and
members regarding signs and promotes more timely
symptoms of hyperglycemia. identification of complications.
Dependent:
> Administer Insulin glargine > Increases glucose transport
(Lantus) 30 “u” SQ before 8 across muscle and fat cell
am(long acting) feeding as membranes to reduce glucose
ordered. And insulin aspart 10 levels.
“u” SQ before each feeding
(short acting) as ordered.
“Nagniwang gyud Than Body mins. of nursing high nutrient and helps restore interventions, the
na siya sukad Requirements interventions, the liquids as bowel function. patient/SOs was
nahospital.” related to insulin patient/SOs will be soon as able to verbalized
deficiency able to determine patient is avoidance of diet
OBJECIVES: proper diet for the able to rich in fats, sodium ,
Fatigue patient, diet low in tolerate oral such as dried fish,
Weakness fats, sodium and intake with bagoong, fatty
Increased carbohydrates. progression meats, mayonnaise.
glucose to solid
level; Hgt: Long term: foods. At the end of 8 hrs.
151 mg/dL At the end of 8 hrs. Instruct - Complex of nursing
(NV: 60 – of nursing patient/SOs carbohydrates interventions, the
100 mg/dL) interventions, the in dietary decrease the amount patient was able to
(+) Weight patient will be able management of insulin needs, have intake of
loss: from to have intake of , with ideal reduce serum appropriate amounts
78kgs to appropriate amounts amount of cholesterol and help and types of calories
72.7kgs in and types of calories 60% CHO, to satiate patient. and have glucose
one week and have glucose 20% fats, Food should be levels within
Presence of levels within and 20% scheduled for peak acceptable range, as
appetite acceptable range. CHON to be effects of insulin as evidenced by Hgt of
changes divided in well as patient 90mg/dL.
Dry mucous designated preference.
membrane no. of meals - Diet high in fats,
and snacks Na and CHO
Scaly, dry
daily. increases blood
lips
sugar level.
Encourage
patient to
avoid diet
rich in fats
and sodium
and reduce - Increases glucose
67
Dependent:
Administer sedatives as -this is to make patient
ordered by the doctor. sleep comfortable.
71
DISCHARGE PLAN
PROGNOSIS
Early evaluation and risk stratification for patients with acute pancreatitis are
important to differentiate patients with mild versus severe disease because patients with
severe disease often need intensive care treatment. Several scoring systems can predict
the severity of pancreatitis, and recent work has attempted to compare their relative
predictive values.
In most cases, acute pancreatitis goes away on its own after a couple of days with
treatment.
continues. Over time, permanent damage may be done to the pancreas, and a chronic
Patients usually recover fully from acute pancreatitis and do not experience
is not the determined as the cause of the disease. Smoking, which stresses the body's
defenses against inflammation, should be stopped. If gallstones were the cause, then
removal of the gallbladder is required to prevent further attacks. For those patients in
whom a cause is not readily identified, there should be consideration of other diagnostic
CONCLUSION
Nursing care and management of the client with type 2 diabetes mellitus is both
complex and challenging. Especially that the disease is already severe and with
family considering that it needs be strict and lifelong. Having a thorough understanding
familiar with the standards of care, patient education in reference to the nature of the
disease, as well as educating the client’s significant others is essential for the better
understanding of the client’s condition. Hence, patient education in conjunction with the
nursing care could be a great factor in achieving positive outcomes. As student nurses, we
are responsible for developing an individualized plan of care that reflects the client’s
medications, diet and physical activity during the development and progression of
different phases of recovery. Not only would the health teachings be directed to the
The group would have had a complete and productive evaluation of patient RP’s
condition and his progress if we were able to conduct a home visit however, due to the
wrong information provided, i.e. address given by SO and as stated in the chart, the group
wasn’t able to do so. Some members of the group went to the specified location (Grand
Europa) but upon arrival to the area, the address particularly the block/street and lot was
not present or in existence. The group also tried calling up the patient or his SO through
the phone information but there were no record of the names of our patient and SO
(sister).
77
Recommendation
The proponents of this case analysis recommend that further study will be made
on the different diagnosis of the patient. In order for the health care providers including
nurses and student nurses will be equipped with knowledge, skills and attitude in
rendering care for patients having this type of diseases. Further study about these diseases
will help the family who have relative’s having this type of multiple disease, will have
better understanding about this condition, In order that they could better take care of their
family member.
This study is also recommended for nursing students who will conduct case
presentation that they will be able to have a flow on the proponents needed for a case
presentation. They will be equipped with knowledge, skills and attitude in conducting a
progress and compliance of the patient to the out-patient treatment regimen like being
able to conduct a home visit. Aside from this, the sources of data for this case
presentation is only limited to the assessments, laboratory results, patient’s chart and
personal interview with the patient, as well as on his significant others thus, other sources
of data, such as personal interview with the patient’s attending physician must also be
done for more information regarding the patient’s condition. Progression of the patient’s
recovery must also be monitored and documented regularly to determine the necessary
recommended to be used as a reference for future studies about type 2 diabetes mellitus.
78
BIBLIOGRAPHY:
- Nettina, Sandra M. RN, MSN, CS, ANP. The Lippincott Manual of Nursing
- Springhouse Nurse’s Drug Guide 2005. 6th ed. Lippincott Williams and Wilkins.
- http://www.infoplease.com/ce6/sci/A0812296.html
University Press.
- http://www.infoplease.com/ce6/sci/A0830631.html
- http://www.infoplease.com/ce6/sci/A0817329.html
- http://www.le.ac.uk/pathology/teach/va/anatomy/case2/frmst2.html
- http://www.niehs.nih.gov/oc/factsheets/ozone/ithurts.htm
- http://people.eku.edu/ritchisong/RITCHISO/301notes6.htm
80
Appendix
Nurses Notes
Date Notes
8-19-07
> received on bed awake conscious and coherent to
both verbal and tactile stimuli ; with pupils @ 5mm
sluggish, reactive light accommodation; normal
power on both upper and lower extremities; GCS q 4
score 15
> hooked to cardiac monitor on sinus rhythm (-)
arrythmias
Ineffective > initial v/s taken and recorded BP: 110/70 mmHg;
Airway O2 sat: 98%, HR: 88bpm
clearance
> with ET @ 22 cm Lip level to vent: TV: 400ml,
RR: 10cpm, F1O2 35% PS 10 cm H2O on SIMV
mode with minimal yellowish sticky oral secretions
with MOD yellow ETA. Secretions suctioned q hour
and PRN turned to sides q 2 – able to turn with NEB
q 6h; oral care BID
> with NGT for of 166 cc q 4 – tolerated FED with
NGT
aspiration precaution and due PO Meds; intake
Standard
measured and recorded; standard followed
8-20-07 (PM) > initial v/s taken and recorded with BP: 130/90
mmHg. HR: 87 bpm, RR: 12 cpm, and T: 35.6
> hooked to cardiac monitor on sinus rhythm (-)
PACs, (-) PVCs
IVF
> with blister @ R heel, toes, sacral and scrotum
Standard
area
Impaired > applied bactroban once on affected area
Skin > with Hgt monitoring q4h and relayed result to IM
Integrity ROD
> given aspart 10 u SQ pre-feeding
DM
> DM standard followed
Standard
> CXR film – for official recording
> decrease BUN and pressure support to 8 at 6am
Gen. Notes today
> for possible extubation @ 8 am today
> kept watched for any unusualities
> needs anticipated
> endorsed
Doctor’s Notes
8:25am
> for extubation – done
> suction excretion ET and Oral
> O2 inhalation at 5 L/ min via nasal canula
> possible trans-out tomorrow
9:00am
> start bladder training
11:00am
> may have sips of water/clear soup
> decrease O2 to 2 L/ min
>D/ IC IVF at left arm
86
> NNO
12:00nn
8-21-07
> include serum albumin on blood reaction
5:15 am
> remove FBC and refer if with out output for 4 hours
>D/C Prevoid once stock is consumed
> inform surg. Resident re = CVP line
> IVF TF with PLR @ 10 gtts/min
> CXR PA in Lab
> Resume NGT
9:30am
> Off O2
> incorporate 60mg KCl in present IVF
> shift ciprofloxacin IV to P.O 5mg BID
> D/C albumin
> may transfer to referred room of choice
> start diabetic diet at 1800 Kcal/ of single mg and more of
polysaccharide fat; CH 60%, CHO 30%, fat 20%
8-21-07
Trans-out Orders
breakfast
> Duavent + net q6hrs nebulization
> TPR; v/s q4hrs
> Hgt TID pre-breakfast, pre-lunch and pre-dinner – record in
separate sheet
> full diabetic diet at 1800 Kcal/ gw/ no more of single mgs and
more of polysaccharide fat with the ff: specifications:
HO 60% in 3 meals and 2 snacks
CHON 20%
Fat 20%
> strict aspiration precaution
> I and O qshift
> inform surgery resident
> effective accordingly
> inform APS
> for pt CXR PA in am
88
Progress Notes
8-15-07
8-17-07
Impression:
Acute Necrotizing Pancreatitis – resolving
Acute Respiratory Failure – resolving
Acute Renal Failure – resolving
Pulmonary Edema secondary to Hypoalbuminemia secondary to
Acute Illness