11 196Acute Pancreatitis

595CDK-196/ vol. 39 no. 8, th. 2012

TINJAUAN PUSTAKA

595

LAPORAN KASUS

CDK-196/ vol. 39 no. 8, th. 2012

INTRODUCTIONAcute pancreatitis is defi ned as an acute in-fl ammatory 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 Infl am-matory Response Syndrome).2,4 Pancreatic infl ammatory disease may be classifi ed 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 diff erent 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 fi ndings of acute pancreatitis on Abdomi-nal USG and/or CT scan.4

CASE REPORTA 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 37ºC. There were palpable epi-gastric pain and decreased of bowel sounds. No Cullen’s sign and Turner’s 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-fi le 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.

Acute PancreatitisEva Roswati

Department of Internal Medicine, Faculty of Medicine, University of North SumateraAdam Malik Hospital, Medan, Indonesia

ABSTRACTEssential 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 fl uid 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

ABSTRAKDiagnosis 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

CDK-196_vol39_no8_th2012 ok.indd 595CDK-196_vol39_no8_th2012 ok.indd 595 8/6/2012 3:14:58 PM8/6/2012 3:14:58 PM

596

LAPORAN KASUS

CDK-196/ vol. 39 no. 8, th. 2012

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). Patient’s condition im-proved and discharged 3 days later.

DISCUSSIONThere are many causes of acute pancreatitis (Table 1), but the mechanisms have not been identifi ed. Gallstones continue to be the lead-

Figure 2 Abdominal USG showed pancreas with normal

shape, size and echo. Pancreatitis could not be showed yet.

Liver, gall bladder, spleen and kidney were normal

Figure 3 CT Scan showed: liver with normal size, regular surface and no hypodense lesion on parenchyma. Gall bladder

unexpanded. Gaster fi lled with contrast. Pancreas with normal size and no hypodense lesion. Spleen with normal size and

no hypodense lesion. Both kidney were normal size and no stone. Conclusion : Liver, pancreas, spleen and both kidneys no

abnormalities

Figure 1 Minimal dilatation of the transverse colon. No free air


597

LAPORAN KASUS

CDK-196/ vol. 39 no. 8, th. 2012

ing cause in most series (30–60%).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 traffi cking, with deleterious eff ects: (1) lyso-

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 infl ammatory 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) infl ammatory responses. The early mediators defi ned to date are tu-mor necrosis factor-alpha, interleukin-6, and interleukin-8. These mediators of infl amma-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 fl ora translocation, acute respirato-ry distress syndrome, pleural eff usions, gastro-intestinal hemorrhage, and renal failure. The

systemic infl ammatory response syndrome can also develop, leading to the development of systemic shock. Eventually, the mediators of infl ammation 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, fl anks, and lower abdomen. The pain is frequently more intense when the patient is supine, and patients often obtain relief by sitting with the trunk fl exed and knees drawn up. Nausea, vomiting, and abdominal distention due to gastric and in-testinal hypomotility and chemical peritonitis 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 (Cullen’s sign) may occur as the result of hemoperitoneum, and a blue-red-purple or green-brown discol-oration of the fl anks (Turner’s sign) refl ects tis-sue catabolism of hemoglobin. The latter two fi ndings, 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 insuffi ciency, or macroamylasemia. Rarely, elevations may re-fl ect parotitis.5 However, there appears to be no defi nite 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

Common CausesGallstones (including microlithiasis)Alcohol (acute and chronic alcoholism)HypertriglyceridemiaEndoscopic retrograde cholangiopancreatography (ERCP), especially after biliary manometryTrauma (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 CausesVascular causes and vasculitis (ischemic-hypoperfusion states after cardiac surgery)Connective tissue disorders and thrombotic thrombocytopenic purpura (TTP)Cancer of the pancreasHypercalcemiaPeriampullary diverticulumPancreas divisumHereditary pancreatitis Cystic fi brosis Renal failure

Rare CausesInfections (mumps, coxsackievirus, cytomegalovirus, echovirus, parasites)Autoimmune (e.g., Sjögren’s 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, sludgeDrugsHypertriglyceridemiaPancreas divisumPancreatic cancerSphincter of Oddi dysfunctionCystic fi brosis Idiopathic

Table 1 Causes of acute pancreatitis3


598

LAPORAN KASUS

CDK-196/ vol. 39 no. 8, th. 2012

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 diff erential 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 diffi cult 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 specifi c medications for acute pancreatitis. Therapy is primarily support-ive and involves intravenous fl uid hydration, analgesics, antibiotics (in severe pancreatitis), and treatment of metabolic complications (e.g., hyperglycemia, hypocalcemia).5

CONCLUSIONWe 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.

Severe acute pancreatitis 1. Associated with organ failure and/or local complications such as necrosis2. Clinical manifestations

a. Obesity BMI > 30b. Hemoconcentration (hematocrit > 44%)c. Age > 70

3. Organ failure a. Shockb. Pulmonary insuffi ciency (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)

aUsually declares itself shortly after onset.

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: Harrison’s 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.

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 60–80% Age over 55 years White blood cell count > 16,000/mL Blood glucose > 200 mg/dL Serum lactic dehydrogenase > 350 units/LAspartate aminotransferase > 250 units/L

Development of the following in the fi rst 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 defi cit over 4 mEq/LEstimated fl uid sequestration of > 6 L

Mortality rates correlate with the number of criteria present1

Number of criteria Mortality rate

0–2 1%3–4 16%5–6 40%7–8 100%

An APACHE II score >8 also correlates with mortality.

Table 3 Risk factors that adversely aff ect survival in acute pancreatitis

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 (15,000–20,000 leukocytes per L) occurs frequently, may represent in-fl ammation or infection.3,5 Patients with more severe disease may show hemoconcentration (Ht >44%) caused by loss of plasma into the

retroperitoneal space and peritoneal cavity. Hypocalcemia occurs in about 25% of pa-tients, and its pathogenesis is incompletely understood. Intraperitoneal saponifi cation 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 fl uid. Such “soap formation” may also be signifi cant in patients with pancreatitis, mild hypocalce-


Documents

11 196Acute Pancreatitis