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Acute Pancreatitis
Welcome to our educational podcast! In this episode, we focus on acute pancreatitis, a potentially life-threatening condition that requires prompt recognition and management. We’ll discuss the common causes, including gallstones, alcohol consumption, and metabolic disorders, along with the pathophysiology behind acute inflammation of the pancreas.
Join us as we examine the clinical presentation, emphasizing key symptoms and complications that may arise. We’ll also review the diagnostic workup, including lab tests and imaging studies, to ensure accurate diagnosis and assessment. Furthermore, we’ll provide an overview of treatment, from supportive care and pain management to addressing underlying causes.
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Acute Pancreatitis
It can be classified into several causes. True idiopathic cases account for about 15 to 25 percent. Biliary tract disease is related to approximately 45 percent of cases. Heavy alcohol intake contributes to about 20 percent. Other causes include hypertriglyceridemia, hypercalcemia, abdominal trauma, certain medications, and congenital issues such as pancreatic divisum. Genetic factors, including CFTR gene abnormalities, may also play a role. Pancreatic neoplasms are a rare cause. Interestingly, celiac disease has been shown to increase the risk of both acute and chronic pancreatitis.
Patients typically present with abrupt-onset epigastric pain. The pain is steady and dull and may worsen with walking or lying flat while sitting and leaning forward, which can provide relief. This pain often radiates to the back and may also be felt on the left or right side.
Additional symptoms include nausea, vomiting, weakness, sweating, and anxiety. Patients may have a history of similar complaints or biliary pain and often report a heavy meal or alcohol intake before the onset of pain.
On examination, patients may exhibit fever, tachycardia, hypotension, pallor, and cool, clammy skin. Abdominal examination may reveal tenderness, with or without guarding, rebound tenderness, and rigidity. Mild jaundice may also be present.
Almost all patients require hospital admission.
Laboratory tests typically show elevated serum amylase and lipase levels, often three times the upper limit of normal. Lipase remains elevated longer and is more accurate. Leukocytosis may be present, with counts reaching as high as 30,000. Other lab findings may include hyperglycemia, elevated bilirubin levels, and serum creatinine. An ALT level greater than 150 units per liter suggests biliary pancreatitis in patients with clear evidence of pancreatitis. Hypocalcemia, often due to saponification, can occur, with levels below 7 mg per deciliter leading to tetany and a poor prognosis. In cases of pancreatitis due to hypertriglyceridemia, levels above 1000 mg per deciliter are notable. A CRP level greater than 150 mg per deciliter correlates with disease severity.
Plain Abdominal X-ray may reveal gallstones if they are calcified. Ultrasound is useful for identifying gallstones and assessing biliary tract disease.
A contrast-enhanced CT scan is considered the gold standard for diagnosing acute pancreatitis, however it is useful if differential diagnosis for acute abdomen are considered or clinical symptoms are not improved in the first 48 hours. It provides detailed images of the pancreas, allowing for the assessment of inflammation, necrosis, and complications such as abscesses or pseudocysts. MRI can be used when CT is contraindicated or further characterization of pancreatic lesions is needed. Endoscopic Ultrasound is highly sensitive for detecting biliary stones and pancreatic lesions.
The diagnosis of acute pancreatitis requires at least two of the following criteria: (1) acute-onset abdominal pain characteristic of pancreatitis, (2) elevated pancreatic enzymes at least three times the upper limit of normal, and (3) findings on cross-sectional imaging characteristic of acute pancreatitis.
Consider the following conditions in the differential diagnosis: acutely perforated duodenal ulcer, acute cholecystitis, acute intestinal obstruction, acute mesenteric ischemia, leaking abdominal aortic aneurysm, and renal colic.
Treatment:
For mild disease, non-severe pancreatitis often resolves spontaneously within several days. Treatment includes goal-directed therapy with moderate fluid resuscitation, beginning with a bolus of 10 milliliters per kilogram in patients showing signs of hypovolemia, followed by 1.5 milliliters per kilogram per hour. Lactated Ringer's solution is preferred over saline.
Avoid overly aggressive fluid resuscitation, as it can lead to fluid overload and increased abdominal pressure, which may necessitate diuretics. Pain management can include NSAIDs, acetaminophen, morphine, or meperidine, with doses adjusted according to renal or liver function. Oral intake of fluids and foods can be resumed when the patient is largely pain-free and has bowel sounds, even if amylase levels are still elevated. Start with clear liquids and gradually advance to a low-fat diet.
Following recovery from acute biliary pancreatitis, patients may undergo laparoscopic cholecystectomy, ideally during the same hospital visit. Stent placement may be indicated for pancreatic divisum and biliary or pancreatic sphincterotomy may be performed for Sphincter of Oddi dysfunction.
In cases of severe disease with necrotizing pancreatitis, large-volume fluid resuscitation with intravenous fluids is crucial, and Hemodynamic monitoring is essential in the ICU.
If hypocalcemia with tetany develops, calcium gluconate should be administered as needed. Infusions of fresh frozen plasma or serum albumin are indicated in the event of coagulopathy or hypoalbuminemia. If shock persists despite adequate volume replacement, vasopressors may be added, and central venous pressure and blood gases should be monitored regularly.
Enteral nutrition via nasojejunal or nasogastric tube is preferred, except in cases of ileus, where parenteral nutrition is the choice. Glutamine supplementation may help reduce the risk of infection and mortality. Routine use of antibiotics is generally not necessary; however, in cases of sterile necrotizing pancreatitis, treatment with cefuroxime, imipenem, or meropenem may be required. Indomethacin or diclofenac may be used for pain management.
The severity of acute pancreatitis can be evaluated using various scoring systems, including the Ranson criteria, APACHE II score, BISAP score, SOFA score, Modified Marshall Score, and the Pancreatic Activity Scoring System. According to the Revised Atlanta Classification, mild disease is characterized by the absence of organ failure, local complications, and systemic complications. Moderate disease includes transient organ failure lasting less than 48 hours, along with local and systemic complications. Severe disease is defined as persistent organ failure for more than 48 hours.
Complications of acute pancreatitis may include intravascular volume depletion due to fluid leakage into the pancreatic bed and ileus, leading to prerenal azotemia and acute tubular necrosis. Chronic fluid collection may result in pancreatic pseudocysts. Acute respiratory distress syndrome may occur, necessitating intubation, mechanical ventilation, and supplemental oxygen. A pancreatic abscess can present with rising fever, leukocytosis, localized tenderness, and an epigastric mass. Pseudocysts smaller than 6 centimeters often resolve spontaneously. A rare but serious complication is hemorrhage due to the erosion of blood vessels, leading to pseudoaneurysm formation. Other complications may include pancreatic ascites, abdominal compartment syndrome, intestinal ischemia, gastric outlet obstruction, and chronic pancreatitis.
That’s all for today’s episode. Thanks for listening to AudioBoards. Stay tuned for more educational content in our next episode!
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