TINJAUAN

LAPORAN
PUSTAKA
KASUS

Acute Pancreatitis
Eva Roswati
Department of Internal Medicine, Faculty of Medicine, University of North Sumatera
Adam Malik Hospital, Medan, Indonesia

ABSTRACT
Essential diagnosis of acute pancreatitis are abrupt onset of deep epigastric pain (often with radiation to the back and history of previous
episodes, often related to alcohol intake), nausea, vomiting, sweating, weakness, abdominal tenderness and distention, fever, leukocytosis,
elevated serum amylase and elevated serum lipase. This article reports a case of acute pancreatitis with abrupt onset of epigastric abdominal
pain, nausea, weakness, abdominal tenderness, leucocytosis, elevated serum amylase and lipase, normal pancreas showed on USG and CT Scan.
The patient were kept strictly fasted for 3 days while intravenous fluid hydration were provided including antibiotic injection and lansoprazole
tablet. After 6 days of treatment, serum amylase and lipase were decreased, the clinical condition improved and the patient was permitted to
be discharged 3 days later.

Key words: acute pancreatitis, epigastric pain, amylase, lipase

ABSTRAK
Diagnosis pankreatitis akut terutama dibuat berdasarkan adanya gejala tiba-tiba berupa nyeri epigastrik mendadak (sering menjalar ke pung-
gung yang mungkin pernah dirasakan sebelumnya dan sering berhubungan dengan penggunaan alkohol), mual, muntah, berkeringat, rasa
lemah, nyeri tekan dan distensi abdomen, demam, leukositosis, serta peningkatan kadar amilase dan lipase serum. Artikel ini melaporkan
sebuah kasus pankreatitis akut. Pasien dipuasakan selama 3 bari, diberi carian intravena, antibiotik intravena, dan lansoprazol oral. Kadar amilase
dan lipase serum turun setelah 6 hari dan pasien boleh pulang 3 hari kemudian. Eva Roswati. Pankreatitis Akut.

Kata kunci: pankreatitis akut, nyeri epigastrik, amilase, lipase

INTRODUCTION
Acute pancreatitis is defined as an acute in-
flammatory process of the pancreas, it may
also involve peripancreatic tissues. Majority
of acute pancreatitis are mild and self-limiting
(80%) while 20% of cases are severe, often
complicated by necrosis and infection lead-
ing to complications SIRS (Systemic Inflam-
matory Response Syndrome).2,4 Pancreatic
inflammatory disease may be classified as (1)
acute pancreatitis or (2) chronic pancreatitis.
The pathologic spectrum of acute pancreati-
tis varies from interstitial pancreatitis, which
is usually a mild and self-limited disorder, to
necrotizing pancreatitis, in which the degree
of pancreatic necrosis correlates with severity
of the attack and its systemic manifestations.3,4
The incidence of pancreatitis varies in different
countries and depends on cause, e.g., alcohol,
gallstones, metabolic factors, and drugs. The
estimated incidence in England is 5.4/100,000
per year; in the United States 79.8/100,000
per year.1 In Indonesia, the incidence of acute
pancreatitis in adolescent is 16,1% and in
adult is 21.8%.2 Diagnosis of acute pancrea-
titis requires 2 of 3 features: (1) Characteristic
abdominal pain, (2). Serum amylase and/or
lipase 3 x upper normal limits, (3) Character-
istic findings of acute pancreatitis on Abdomi-
nal USG and/or CT scan.4
CASE REPORT
A 51-year old woman were admitted to the
emergency room with chief complaint of wors-
ening deep epigastric pain within 2 days. No
fever, vomiting or trauma. Her past history of ill-
ness including alcohol consumption were unre-
markable. On physical examination, the patient
was listless with blood pressure 140/80 mmHg,
pulse 72 x/minute, respiratory rate 28x/minute
and temperature 37C. There were palpable epi-
gastric pain and decreased of bowel sounds. No
Cullens sign and Turners sign. Greenish liquid
coming from open nasogastric tube.
Laboratory result showed leucocytosis, elevat-
ed serum amylase and elevated serum lipase
(Hb 13.1 g%, leucocyte 17,600/mm3, Ht 38%,
thrombocyte 213,000/mm3, glucose 181 mg/
dL, serum amylase 280 U/L, serum lipase 258
U/L, LDH 615 U/L). Liver associated enzyme
and renal function test were within normal
limit (total bilirubin 0.8 mg/dL, direct bilirubin
0.22 mg/dL, ALT 21 U/L, AST 13 U/L, phospa-
tase alkaline 46 U/L, ureum 17 mg/dL, creati-
nine 0.6 mg/dL). Electrolyte studies showed
hypokalemia and hypocalcemia (sodium 142
mmol/dL, kalium 2.9 mmol/dL, chloride 104
mmol/dL, calcium 6.3 mg/dL). Arterial blood
gases analysis showed pH 7.492, pCO2 32.3
mmHg, pO2 83.2 mmHg, HCO3 24.9 mmol/L,
BE 1.4 mmol/L, O2 saturation 97.1%. Lipid pro-
file showed no hypertriglyceridemia and no
hyperlipidemia (total cholesterol 121 mg/dL,
triglyceride 94 mg/dL, HDL-cholesterol 30 mg/
dL, LDL-cholesterol 72 mg/dL. ECG impression
was anteroseptal lateral ischemia.

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Patient were diagnosed as acute pancreati-

tis. Parenteral feeding were started with IVFD
D5%, NaCl 0.9%, Aminofusin to maintain he-
modynamic stability. No enteral feeding were
given for 3 days and then low fat and protein
liquid diet were instituted sequentially based
on patient appetite. Ceftriaxone 1 g/12 hour
IV given for 7 days, lansoprazole 2 x 30 mg tab-
let and kalium substitution (KCl). After 6 days
of treatment, the serum amylase and serum
lipase were decreased into normal (amylase
73 U/L, lipase 123 U/L). Patients condition im-
proved and discharged 3 days later.

DISCUSSION
There are many causes of acute pancreatitis
(Table 1), but the mechanisms have not been
identified. Gallstones continue to be the lead-
Figure 1 Minimal dilatation of the transverse colon. No free air

Figure 3 CT Scan showed: liver with normal size, regular surface and no hypodense lesion on parenchyma. Gall bladder
Figure 2 Abdominal USG showed pancreas with normal unexpanded. Gaster filled with contrast. Pancreas with normal size and no hypodense lesion. Spleen with normal size and
shape, size and echo. Pancreatitis could not be showed yet. no hypodense lesion. Both kidney were normal size and no stone. Conclusion : Liver, pancreas, spleen and both kidneys no
Liver, gall bladder, spleen and kidney were normal abnormalities

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Table 1 Causes of acute pancreatitis3
Common Causes
Gallstones (including microlithiasis)
Alcohol (acute and chronic alcoholism)
Hypertriglyceridemia
Endoscopic retrograde cholangiopancreatography (ERCP), especially after biliary manometry
Trauma (especially blunt abdominal trauma)
Postoperative (abdominal and nonabdominal operations)
Drugs (azathioprine, 6-mercaptopurine, sulfonamides, estrogens, tetracycline, valproic acid, anti-HIV
medications)
Sphincter of Oddi dysfunction
Uncommon Causes
Vascular causes and vasculitis (ischemic-hypoperfusion states after cardiac surgery)
Connective tissue disorders and thrombotic thrombocytopenic purpura (TTP)
Cancer of the pancreas
Hypercalcemia
Periampullary diverticulum
Pancreas divisum
Hereditary pancreatitis
Cystic fibrosis
Renal failure
Rare Causes
Infections (mumps, coxsackievirus, cytomegalovirus, echovirus, parasites)
Autoimmune (e.g., Sjgrens syndrome)
Causes to Consider in Patients with Recurrent Bouts of Acute Pancreatitis without an Obvious Etiology
Occult disease of the biliary tree or pancreatic ducts, especially microlithiasis, sludge
Drugs
Hypertriglyceridemia
Pancreas divisum
Pancreatic cancer
Sphincter of Oddi dysfunction
Cystic fibrosis
Idiopathic
ing cause in most series (3060%).3 In 10-30%
of cases, the cause is unknown; studies have
suggested that up to 70% of cases of idio-
pathic pancreatitis are secondary to biliary mi-
crolithiasis.5
Acute pancreatitis may occur when there is
imbalance of factors involved in maintaining
cellular homeostasis. The initiating event such
as alcohol use, gallstones, and certain drugs
may injure acinar cells and impair the secre-
tion of zymogen granules. The pathophysi-
ologic event that triggers the onset of acute
pancreatitis is still unclear. It is believed that
both extracellular factors (eg, neural response,
vascular response) and intracellular factors
(eg, intracellular digestive enzyme activation,
increased calcium signaling, heat shock pro-
tein activation) play a role. Acute pancreatitis
can also develop when ductal cell injury leads
to delayed or absent enzymatic secretion,
such as with the CFTR gene mutation.
Injury triggered chaotic cellular membrane
trafficking, with deleterious effects: (1) lyso-
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testinal hypomotility and chemical peritonitis
somal and zymogen granule compartments
fuse, enabling activation of trypsinogen to
trypsin; (2) intracellular trypsin triggers the en-
tire zymogen activation cascade; and (3) se-
cretory vesicles are extruded across the baso-
lateral membrane into the interstitium, where
molecular fragments act as chemoattractants
for inflammatory cells. Activated neutrophils
then exacerbate the problem by releasing su-
peroxide (the respiratory burst) or proteolytic
enzymes (cathepsins B, D, and G; collagenase;
and elastase). Finally, macrophages release cy-
tokines that further mediate local (and, in se-
vere cases, systemic) inflammatory responses.
The early mediators defined to date are tu-
mor necrosis factor-alpha, interleukin-6, and
interleukin-8. These mediators of inflamma-
tion cause an increased pancreatic vascular
permeability, leading to hemorrhage, edema,
and eventually pancreatic necrosis. As me-
diators are excreted into circulation, systemic
complications can arise, such as bacteremia
due to gut flora translocation, acute respirato-
ry distress syndrome, pleural effusions, gastro-
intestinal hemorrhage, and renal failure. The
LAPORAN KASUS
systemic inflammatory response syndrome
can also develop, leading to the development
of systemic shock. Eventually, the mediators of
inflammation can become so overwhelming
to the body that hemodynamic instability and
death ensue.5
Abdominal pain is the major symptom of
acute pancreatitis. Pain may vary from a mild
and tolerable discomfort to severe, constant,
and incapacitating distress. Characteristi-
cally, the pain, which is steady and boring in
character, is located in the epigastrium and
periumbilical region and often radiates to the
back as well as to the chest, flanks, and lower
abdomen. The pain is frequently more intense
when the patient is supine, and patients often
obtain relief by sitting with the trunk flexed
and knees drawn up. Nausea, vomiting, and
abdominal distention due to gastric and in-
are also frequent complaints.1,4
Physical examination frequently reveals a dis-
tressed and anxious patient. Low-grade fever,
abdominal tenderness and muscle rigidity are
present to a variable degree, but, compared
with the intense pain, these signs may be un-
impressive. Bowel sounds are usually dimin-
ished or absent. An enlarged pancreas with
organized necrosis or a pseudocyst may be pal-
pable in the upper abdomen. A faint blue dis-
coloration around the umbilicus (Cullens sign)
may occur as the result of hemoperitoneum,
and a blue-red-purple or green-brown discol-
oration of the flanks (Turners sign) reflects tis-
sue catabolism of hemoglobin. The latter two
findings, which are uncommon, indicate the
presence of a severe necrotizing pancreatitis.1,4
The diagnosis of acute pancreatitis is usually
established by the detection of an increased
level of serum amylase. Values threefold or
more above normal virtually clinch the di-
agnosis if overt salivary gland disease and
gut perforation or infarction are excluded.3
Elevations can occur in anyone with small
intestinal obstruction, mesenteric ischemia,
tubo-ovarian disease, renal insufficiency, or
macroamylasemia. Rarely, elevations may re-
flect parotitis.5 However, there appears to be
no definite correlation between the severity of
pancreatitis and the degree of serum amylase
elevation. Serum lipase activity increases in
parallel with amylase activity. Measurement of
both enzymes is important as serum amylase
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Table 2 Ranson criteria for assessing the severity of acute pancreatitis1
Three or more of the following predicts a severe course complicated by pancreatic necrosis with a
sensitivity of 6080%
Age over 55 years
White blood cell count > 16,000/mL
Blood glucose > 200 mg/dL
Serum lactic dehydrogenase > 350 units/L
Aspartate aminotransferase > 250 units/L
Development of the following in the first 48 hours indicates a worsening prognosis
Hematocrit drop of more than 10 percentage points
Blood urea nitrogen rise > 5 mg/dL
Arterial PO2 of < 60 mm Hg
Serum Ca < 8 mg/dL
Base deficit over 4 mEq/L
Estimated fluid sequestration of > 6 L
Mortality rates correlate with the number of criteria present1
Number of criteria
02
34
56
78
An APACHE II score >8 also correlates with mortality.
Table 3 Risk factors that adversely affect survival in acute pancreatitis
Severe acute pancreatitis
1. Associated with organ failure and/or local complications such as necrosis
2. Clinical manifestations
a. Obesity BMI > 30
b. Hemoconcentration (hematocrit > 44%)
c. Age > 70
3. Organ failure
a. Shock
b. Pulmonary insufficiency (PO2 < 60)
c. Renal failure (CR > 2.0 mg%)
d. GI bleeding
4. Ransom criteria (not fully utilizable until 48 h)
5. Apache II score > 8 (cumbersome)
a
Usually declares itself shortly after onset.
tends to be higher in gallstone pancreatitis
and serum lipase higher in alcohol-associated
pancreatitis. A threefold elevated serum lipase
value is usually diagnostic of acute pancrea-
titis. Leukocytosis (15,00020,000 leukocytes
per L) occurs frequently, may represent in-
flammation or infection.3,5 Patients with more
severe disease may show hemoconcentration
(Ht >44%) caused by loss of plasma into the
Mortality rate
1%
16%
40%
100%
retroperitoneal space and peritoneal cavity.
Hypocalcemia occurs in about 25% of pa-
tients, and its pathogenesis is incompletely
understood. Intraperitoneal saponification of
calcium by fatty acids in areas of fat necrosis
occurs occasionally, with large amounts (up to
6.0 g) dissolved or suspended in ascites fluid.
Such soap formation may also be significant
in patients with pancreatitis, mild hypocalce-
mia, and little or no obvious ascites Hypertrig-
lyceridemia occurs in 15 to 20% of patients,
however, be wary of the fact that baseline
serum triglyceride levels can be falsely low-
ered during an episode of acute pancreatitis.5
Finally, the electrocardiogram is occasionally
abnormal in acute pancreatitis with ST-seg-
ment and T-wave abnormalities simulating
myocardial ischemia.3
The differential diagnosis should include: (1)
perforated viscus, especially peptic ulcer; (2)
acute cholecystitis and biliary colic; (3) acute
intestinal obstruction; (4) mesenteric vascu-
lar occlusion; (5) renal colic; (6) myocardial
infarction; (7) dissecting aortic aneurysm; (8)
connective tissue disorders with vasculitis; (9)
pneumonia; and (10) diabetic ketoacidosis.3
It is important to identify patients with poor prog-
nosis. Scoring systems (Ranson, Imrie, Apache II)
are difficult to use, show poor predictive pow-
ers, and have not been uniformly embraced by
clinicians. The key indicators of a severe attack of
pancreatitis are listed in Table 3.
Currently, there is no specific medications for
acute pancreatitis. Therapy is primarily support-
ive and involves intravenous fluid hydration,
analgesics, antibiotics (in severe pancreatitis),
and treatment of metabolic complications
(e.g., hyperglycemia, hypocalcemia).5
CONCLUSION
We reported a case of acute pancreatitis based
on 2 out of 3 features\: characteristic abdomi-
nal pain and elevated serum amylase and/or
lipase 3 x upper normal limits. The patient
were treated with total fasting with intrave-
nous hydration for 3 days, antibiotic injection,
potassium substitution and lansoprazole tab-
let. Serum amylase and lipase were returned
to normal on day 6. The clinical condition
were improved after 9 days of treatment and
the patient was discharged.

REFERENCES
1. McPhee SJ, Papadakis MA. Acute pancreatitis. In: Current medical diagnosis and treatment. Ch. 39. Diseases of the Pancreas: Introduction. McGraw Hill-Lange; 2011.
2. Numan A. Pankreatitis akut. In: Buku ajar ilmu penyakit dalam. Jakarta: FKUI; 2007. p. 488-93.
3. Fauci, et al. Acute and chronic pancreatitis. In: Harrisons internal medicine. Ch. 307. 17th ed. The McGraw-Hill Co; 2008.
4. Rustam EY. Severe acute pancreatitis a serious illness: Clinical problems in adherence to managements. Paper presented at: Gastroentero-Hepatology Update; 2012 Oct 21-23; Medan,
Indonesia.
5. Gardner TB, Katz J. Acute pancreatitis. Medscape Drugs, Diseases, & Procedures [Internet]. 2011 Dec 2 [cited 2012 Jul 2]. Available from: http://emedicine.medscape.com/article/181364-
overview.
6. Karani J. Acute pancreatitis imaging. Medscape Drugs, Diseases, & Procedures [Internet]. 2011 May 25 [cited 2012 Jul 2]. Available from: http://emedicine.medscape/article/371613-
overview.

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