The incidence of acute pancreatitis ranges from 54 to 238 episodes per 1 million per year. Patients with mild pancreatitis respond well to conservative therapy, but those with severe pancreatitis may have a progressively downhill course to respiratory failure, sepsis, and death (less than 10%).
I. Etiology
A. Alcohol-induced pancreatitis. Consumption of
large quantities of alcohol may cause acute pan- creatitis.
B. Cholelithiasis. Common bile duct or pancreatic
duct obstruction by a stone may cause acute pancreatitis. (90% of all cases of pancreatitis occur secondary to alcohol consumption or cholelithiasis).
C. Idiopathic pancreatitis. The cause of pancreatitis
cannot be determined in 10 percent of patients.
D. Hypertriglyceridemia. Elevation of serum triglycer-
ides (>l,000mg/dL) has been linked with acute pancreatitis.
E. Pancreatic duct disruption. In younger patients,
a malformation of the pancreatic ducts (eg, pancre- atic divisum) with subsequent obstruction is often the cause of pancreatitis. In older patients without an apparent underlying etiology, cancerous lesions of the ampulla of Vater, pancreas or duodenum must be ruled out as possible causes of obstructive pancreatitis.
F. Iatrogenic pancreatitis. Radiocontrast studies of
the hepatobiliary system (eg, cholangiogram, ERCP) can cause acute pancreatitis in 2-3% of patients undergoing studies.
G. Trauma. Blunt or penetrating trauma of any kind to
the peri-pancreatic or peri-hepatic regions may induce acute pancreatitis. Extensive surgical manipulation can also induce pancreatitis during laparotomy.
Causes of Acute Pancreatitis
Alcoholism Cholelithiasis Drugs Hypertriglyceridemia Idiopathic causes Infections Microlithiasis Pancreas divisum Trauma
Medications Associated with Acute Pancreatitis
Asparaginase (Elspar) Azathioprine (Imuran) Didanosine (Videx) Estrogens
Ethacrynic acid (Edecrin) Furosemide (Lasix) Mercaptopurine (Purinethol) Pentamidine Sulfonamides Tetracyclines Thiazide diuretics Valproic acid (Depakote)
II. Pathophysiology. Acute pancreatitis results when an
initiating event causes the extrusion of zymogen granules, from pancreatic acinar cells, into the interstitium of the pancreas. Zymogen particles cause the activation of trypsinogen into trypsin. Trypsin causes auto-digestion of pancreatic tissues.
III. Clinical presentation
A. Signs and symptoms. Pancreatitis usually pres-
ents with mid-epigastric pain that radiates to the back, associated with nausea and vomiting. The pain is sudden in onset, progressively increases in intensity, and becomes constant. The severity of pain often causes the patient to move continuously in search of a more comfortable position.
B. Physical examination
1. Patients with acute pancreatitis often appear
very ill. Findings that suggest severe pancreati- tis include hypotension and tachypnea with decreased basilar breath sounds. Flank ecchymoses (Grey Tuner's Sign) or periumbilical ecchymoses (Cullen's sign) may be indicative of hemorrhagic pancreatitis.
2. Abdominal distension and tenderness in the
epigastrium are common. Fever and tachycar- dia are often present. Guarding, rebound ten-
derness, and hypoactive or absent bowel sounds indicate peritoneal irritation. Deep palpation of abdominal organs should be avoided in the setting of suspected pancreatitis.
IV. Laboratory testing
A. Leukocytosis. An elevated WBC with a left shift
a n d e l e va te d h e m a to c r i t ( i n dicating hemoconcentration) and hyperglycemia are com- mon. Pre-renal azotemia may result from dehydra- tion. Hypoalbuminemia, hypertriglyceridemia, hypocalcemia, hyperbilirubinemia, and mild eleva- tions of transaminases and alkaline phosphatase are common.
B. Elevated amylase. An elevated amylase level
often confirms the clinical diagnosis of pancreatitis.
C. Elevated lipase. Lipase measurements are more
specific for pancreatitis than amylase levels, but less sensitive. Hyperlipasemia may also occur in patients with renal failure, perforated ulcer dis- ease, bowel infarction and bowel obstruction.
D. Abdominal Radiographs may reveal non-specific
findings of pancreatitis, such as "sentinel loops" (dilated loops of small bowel in the vicinity of the pancreas), ileus and, pancreatic calcifications.
E. Ultrasonography demonstrates the entire pan-
creas in only 20 percent of patients with acute pancreatitis. Its greatest utility is in evaluation of patients with possible gallstone disease.
F. Helical high resolution computed tomography
is the imaging modality of choice in acute pancre- atitis. CT findings will be normal in 14-29% of patients with mild pancreatitis. Pancreatic necro- sis, pseudocysts and abscesses are readily de- tected by CT.
Selected Conditions Other Than Pancreatitis Associated with Amylase Elevation
Carcinoma of the pan- creas
Common bile duct ob- struction Post-ERCP Mesenteric infarction Pancreatic trauma Perforated viscus Renal failure Acute alcoholism Diabetic ketoacidosis Lung cancer Ovarian neoplasm Renal failure Ruptured ectopic preg- nancy
Salivary gland infection Macroamylasemia
V. Prognosis. Ranson's criteria is used to determine
prognosis in acute pancreatitis. Patients with two or fewer risk factors have a mortality rate of less than 1 percent, those with three or four risk-factors a mortal- ity rate of 16 percent, five or six risk factors, a mortal- ity rate of 40 percent, and seven or eight risk factors, a mortality rate approaching 100 percent.
Ranson's Criteria for Acute Pancreatitis At admission During initial 48 hours
1. Age >55 years 2. WBC >16,000/mm3 3. Blood glucose >200 mg/dL 4. Serum LDH >350 IU/L 5. AST >250 U/L 1. Hematocrit drop >10% 2. BUN rise >5 mg/dL 3. Arterial pO2 <60 mm Hg
4. Base deficit >4 mEq/L 5. Serum calcium <8.0 mg/dL 6. Estimated fluid sequestra- tion >6 L
VI. Treatment of pancreatitis
A. Expectant management. Most cases of acute
pancreatitis will improve within three to seven days. Management consists of prevention of complications of severe pancreatitis.
B. NPO and bowel rest. Patients should take noth-
ing by mouth. Total parenteral nutrition should be instituted for those patients fasting for more than five days. A nasogastric tube is warranted if vomiting or ileus.
C. IV fluid resuscitation. Vigorous intravenous
hydration is necessary. A decrease in urine output to less than 30 mL per hour is an indication of inadequate fluid replacement.
D. Pain control. Morphine is discouraged because
it may cause Oddi's sphincter spasm, which may exacerbate the pancreatitis. Meperidine (Demerol), 25-100 mg IV/IM q4-6h, is favored. Ketorolac (Toradol), 60 mg IM/IV, then 15-30 mg IM/IV q6h, is also used.
E. Antibiotics. Routine use of antibiotics is not
recommended in most cases of acute pancreatitis. In cases of infectious pancreatitis, treatment with cefoxitin (1-2 g IV q6h), cefotetan (1-2 g IV q12h), imipenem (1.0 gm IV q6h), or ampicillin/sulbactam (1.5-3.0 g IV q6h) may be appropriate.
F. Alcohol withdrawal prophylaxis. Alcoholics may
require alcohol withdrawal prophylaxis with lorazepam (Ativan) 1-2mg IM/IV q4-6h as needed
x 3 days, thiamine 100mg IM/IV qd x 3 days, folic acid 1 mg IM/IV qd x 3 days, multivitamin qd.
G. Octreotide. Somatostatin is also a potent inhibitor
of pancreatic exocrine secretion. Octreotide is a somatostatin analogue, which has been effective in reducing mortality from bile-induced pancreati- tis. Clinical trials, however, have failed to docu- ment a significant reduction in mortality
H. Blood sugar monitoring and insulin adminis- tration. Serum glucose levels should be moni-
tored.
VII.Complications A. Chronic pancreatitis
B. Severe hemorrhagic pancreatitis C. Pancreatic pseudocysts
D. Infectious pancreatitis with development of sepsis
(occurs in up to 5% of all patients with pancreati- tis)
E. Portal vein thrombosis
References, see page 282.