Anne Ryan is a 29-year-old woman who visits the emergency department with severe epigastric abdominal pain, nausea, and vomiting during the previous 2 to 3 days. She has a history of pancreatitis. She denies having fever, chills, or any other associated complaints. She denies the use of alcohol. Her medical history is significant for familial hypertriglyceridemia for which she is prescribed medication; she has a history of noncompliance. She has had no surgery. She is very thin and in moderate distress during physical examination. She has poor capillary refill; her blood pressure is 90/60 mm Hg; her heart rate, 120 beats per minute; her temperature, 38.3°C; her respiratory rate, 30 breaths per minute. The mid-epigastrium is quite tender, but there is no peritonitis or palpable mass.
What diagnosis is most likely?
Given Ms. Ryan’s history of pancreatitis and her epigastric pain associated with nausea and vomiting, acute pancreatitis is the likely culprit. The differential diagnosis includes gastritis, peptic ulcer disease, biliary disease, pneumonia, and myocardial infarction.
What are the symptoms and signs of pancreatitis?
The classic history is epigastric pain radiating to the back. The pain is described as a constant boring or knifelike pain often associated with anorexia, nausea, vomiting, and occasionally fever. The patient may give a history of pancreatitis. The abdominal findings may range from mild epigastric tenderness to diffuse peritonitis. A mass or ascites may be found with complicated pancreatitis (e.g., pseudocyst, abscess, pancreatic duct leak, severe acute pancreatitis). Any ecchymosis in the flank (Grey-Turner’s sign) or periumbilical area (Cullen’s sign) should be noted. Although very rare, they are both signs of retroperitoneal hemorrhage, which may accompany severe acute pancreatitis (1
What laboratory or radiologic tests support this diagnosis?
Elevated serum amylase, lipase, or urinary amylase is expected. However, many other conditions may result in hyperamylasemia. Abdominal film may show pancreatic calcification if the patient has chronic pancreatitis. The abdominal film often shows an ileus pattern of some dilated loops of small bowel with a few air-fluid levels. The ileus pattern may be diffuse or local, as with the sentinel loop, a single dilated jejunal loop in the upper abdomen, or colon cutoff sign. Here the colon is dilated to the mid-transverse colon, and little gas is seen distally. An upright chest film rules out pneumonia and free intraabdominal air. A left pleural effusion may be visible. Ultrasound may show an edematous pancreas and, more importantly, the presence or absence of gallstones or a dilated common bile duct (CBD). Abdominal computed tomography (CT) may show pancreatic edema, fluid collections, soft tissue stranding, necrosis, or associated complications of pancreatitis. However, CT generally is not recommended as a primary diagnostic tool in patients with simple acute pancreatitis.
What causes pancreatitis?
Pancreatitis is most frequently caused by gallstones or alcohol ingestion (Table 18.1
). Other causes include congenital abnormalities of the pancreas and its ductal system, hypertriglyceridemia, trauma, drugs (e.g., thiazides, azathioprine) (Table 18.2
), and iatrogenic causes (e.g., surgery, endoscopic retrograde cholangiopancreatography [ERCP]).
TABLE 18.1. Causes of Acute Pancreatitis and Hyperamylasemia
Biliary tract disease
Perforated peptic ulcer
TABLE 18.2. Drugs Implicated in the Initiation of Acute Pancreatitis
Reprinted from Townsend C, ed. Sabiston’s Textbook of Surgery. 15th ed. Philadelphia, Pa: WB Saunders; 1997, with permission.
What is the treatment for acute pancreatitis?
Because oral intake stimulates the pancreas, the patient is given nothing by mouth (NPO). If the patient is vomiting or has gastric distention, nasogastric decompression alleviates these symptoms and prevents aspiration. Intravenous (IV) fluids are given, and parenteral nutrition is considered if enteral nutrition will not be an option for a prolonged period. Histamine2
blockers may help suppress pancreatic secretion (2
The patient receives a fluid bolus of 1 L normal saline (NS), after which her vital signs stabilize. A Foley catheter is placed and laboratory tests performed, yielding the following results: calcium, 5.9 mg per dL; carbon dioxide, 18 mEq per L; creatinine, 1.4 mg per dL; glucose, 250 mg per dL; amylase, 1200 U per L; lipase, 9200 IU per L; triglycerides, 31,000 mg per dL; liver function tests, normal; hemoglobin, 10 g per dL; white blood cell count, 12,000 per mm3. She is given 2 g calcium IV and transferred to her room, where she is kept NPO and receives pain medication and maintenance IV fluids. She receives furosemide for oliguria. The next morning, she is in respiratory distress and has the following laboratory values: calcium, 4.2 mg per dL; creatinine, 4.9 g per dL; hemoglobin, 8 g per dL. She is transferred to the intensive care unit, intubated, and given more IV calcium and fluid boluses.
Why did Ms. Ryan deteriorate?
She was severely dehydrated and hypocalcemic. Although attempts were made to correct these deficiencies in the emergency department, she should have had more frequent monitoring of her vital signs and laboratory values to be sure that she was adequately resuscitated.
What are Ranson’s criteria?
) described a series of signs that help determine the severity of acute pancreatitis. They have recently been modified and are now known as the Glasgow criteria (4
). One group of signs are assessed at the time of admission and the others are assessed within 48 hours (Table 18.3
). At the time of Ranson’s study, patients with fewer than two criteria had 1% mortality; those with three or four signs, 15%; those with five or six signs, 40%; and those with more than six signs, 100%. With the advances in monitoring and treatment, the mortality for each subgroup has probably decreased, but the study has not been repeated recently.
TABLE 18.3. Ranson’s Criteria for Pancreatitis
During Initial 48 Hours
Age above 55 yr
Hematocrit falling >10%
WBC >16,000 cells/mm3
BUN falling >5 mg/100 mL
Blood glucose >200 mg/100 mL
Serum calcium <8 mg/100 mL
Serum lactate dehydrogenase >350 IU/L
Arterial PO2 <60 torr
AST >250 U/100 mL
Base deficit >4 mEq/L
Estimated fluid sequestration >6 L
AST, aspartate transaminase; BUN, blood urea nitrogen; WBC, white blood cell.
From Townsend C, ed. Sabiston’s Textbook of Surgery. 15th ed. Philadelphia, Pa: WB Saunders; 1997, with permission.
These criteria help identify severe pancreatitis and thus enable it to be treated aggressively. Because only five signs are assessed on admission, however, one should consider the possibility of severe pancreatitis if more than two or three signs are seen initially or if there are signs of hemodynamic instability or respiratory distress. Treatment should not wait until all criteria are met, which takes 48 hours.
Was this patient treated appropriately?
Ms. Ryan did not have all appropriate tests to determine how many Ranson’s or Glasgow signs she had. With her hemodynamic compromise, severe hypocalcemia, tachypnea, and oliguria, Ms. Ryan required more aggressive monitoring and resuscitation, even without accurate assessment of her pancreatitis.
During the next 48 hours in the intensive care unit, Ms. Ryan requires 15 L crystalloid, 6 units blood, 8 g calcium, and emergency plasmapheresis to manage her severe hypertriglyceridemia. With this treatment, her hemoglobin and calcium levels return to normal, and her creatinine decreases to 2.9 mg/dL after reaching a high of 9. As her pancreatitis improves, she requires less respiratory support as well. Antibacterial prophylaxis with imipenem is started.
A week later, although hemodynamically improved, Ms. Ryan continues to require ventilatory support and begins to spike fevers to 39.4°C. Her white blood cell count rises to 22,000 per mm3. She is now receiving total parenteral nutrition.
Is there a role for prophylactic antibiotics in patients with acute pancreatitis?
In a recent study, patients with severe acute pancreatitis who received prophylactic treatment with imipenem had fewer infectious complications (5
). Imipenem is the only drug that has been studied for this indication, although other broad-spectrum antibiotics may be as effective.
What are the infectious complications of pancreatitis?
Pancreatic abscess, infected pancreatic necrosis, infected pancreatic pseudocyst, line sepsis, pneumonia, infected pleural effusion, catheter-related urinary tract infection, and pancreatic or enteric fistulas may result from severe acute pancreatitis.
How is the cause of infection diagnosed?
All indwelling catheters, urinary or vascular, should be changed, and a thorough physical examination should be performed in search of findings such as cellulitis, abdominal mass, and increased abdominal tenderness. A chest radiograph helps assess for pneumonia and large pleural effusion. Often, the abdominal examination is difficult in a patient with pancreatitis either because of preexisting tenderness or because the patient is sedated or receiving pain medication. Therefore, when infection is suspected, abdominal CT is often required. If available, dynamic or spiral CT with contrast is best because it will demonstrate abscess, pseudocyst, or pancreatic necrosis.
What is the treatment for pancreatic abscess or infected pseudocyst?
If possible, radiology-guided percutaneous drainage is best, especially in already compromised patients (6
). If this cannot be done, surgical drainage is required.
What is the treatment for pancreatic necrosis?
Although it is controversial, most studies advocate nonoperative therapy for patients with only small areas of necrosis (less than 20% to 30%) or when no infection is suspected (7
). However, when infection is suspected—because of marked fever and leukocytosis, bacteremia, failure to improve clinically, or positive Gram stain on aspirated necrosis—surgical management is indicated. Intraoperative findings are thick necrotic tissue surrounding the pancreas, sometimes extending into the transverse mesocolon, small-bowel mesentery, or retroperitoneum. Extensive débridement is performed. Most often, this requires multiple visits to the operating room with the abdomen packed between visits. When no further débridement is necessary, drains are placed and the abdomen is closed. A sample of the necrotic tissue is sent to the laboratory for Gram stain and culture to guide antimicrobial therapy. It is prudent to place a feeding jejunostomy so that an elemental diet may be given when tolerated.
What is the treatment for gallstone pancreatitis?
If a patient with pancreatitis has gallstones, even if there are other possible causes of pancreatitis, the gallbladder should be removed after the pancreatitis has clinically resolved. This is usually done before the patient is discharged from the hospital to prevent another attack of pancreatitis, which may be more severe than the initial attack. Some literature supports early ERCP to remove the stone or a sphincterotomy if there is suspicion of a persistent, obstructing distal CBD stone in a patient whose pancreatitis fails to improve (8
). However, ERCP itself may worsen pancreatitis (10
). Some centers use magnetic resonance cholangiopancreatography (MRCP) as a diagnostic maneuver before ERCP because MRCP is noninvasive (11
). Although not a functional study, this technique has been shown to be very accurate in defining pancreatic and biliary structures and ductal anatomy, including the identification of choledocholithiasis, when performed by an experienced radiologist.
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