Recognizing acute pancreatitis

Learn the most common causes of pancreatitis, how to differentiate it from other abdominal pathologies, and what to do when you suspect a secondary infection.

Olutayo A. Sogunro, DO FACS FACOS
Olutayo A. Sogunro, DO FACS FACOS
6th Oct 2021 • 6m read

In this video, you'll master the clinical and radiographic workup and CT scan findings in a patient with acute pancreatitis. You'll learn the most common causes of pancreatitis, how to differentiate it from other abdominal pathologies, and what to do when you suspect a secondary infection.

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Video transcript

In this Medmastery lesson, we will discuss acute pancreatitis. So what is pancreatitis? It is acute inflammation of the pancreas. In the United States, the annual incidence of acute pancreatitis ranges from 4.9 to 35 cases per 100,000 persons. Worldwide, the incidence is increasing due to increased rates of obesity and gallstones. Overall the mortality rate is approximately 5%.

Acute pancreatitis is sub divided based on severity into mild, moderately severe or severe. The cause of pancreatitis is based on the etiology. The three most common causes are gallstones, alcohol, and hyperlipidemia. Gallstones are the most common cause of acute pancreatitis and account for 40 to 70% of cases. However, only 3 to 7% of patients with gall stones actually develop pancreatitis.

When gallstones are the cause of pancreatitis, it is called gallstone pancreatitis. It is caused by either reflux of bile into the pancreatic duct, obstruction of the pancreatic duct or ampulla, or edema resulting from the passage of a stone. Alcohol is responsible for approximately 25 to 35% of cases of acute pancreatitis in the United States.

It is thought to act by increasing the synthesis and release of pancreatic digestive and lysosomal enzymes, which eventually damage the pancreatic tissue and leak out. Hyperlipidemia is found as the cause of pancreatitis in 1 to 14% of cases. It is usually caused by serum triglyceride concentrations above 1000 milligrams per deciliter or 11 millimoles per liter. Now let's look at the common signs and symptoms of pancreatitis.

Most patients with acute pancreatitis have acute onset of persistent severe epigastric abdominal pain. In patients with gallstone pancreatitis, the pain will begin in the epigastric region and can radiate to the right upper quadrant. The onset of the pain is rapid, reaching maximum intensity in 10 to 20 minutes. In patients with pancreatitis due to hereditary, metabolic or alcohol related causes, the pain may be poorly localized, and the onset of pain may be slower.

In approximately 50% of patients, the pain radiates to the back. Nausea and vomiting is present in about 90% of patients and can last for several hours. Patients with severe acute pancreatitis may have dyspnea, or shortness of breath due to inflammation of the diaphragm. There can also be alterations in vital signs, particularly hypotension, and even tachycardia. Now let's work up a patient with pancreatitis.

On observation the patient will take up pancreatitis will be ill appearing, the patient can also have scleral icterus, which is yellowing of the eyes secondary to obstructive jaundice from gallstones or edema of the pancreatic head. On abdominal palpation the patient will often have a mild or exquisite epigastric pain.

In more severe cases, the patient may present with diffuse abdominal pain and peritoneal signs, such as guarding, rebound tenderness, and abdominal rigidity. Please see the Medmastery course Abdominal Examination Essential for more details on peritoneal signs in the abdominal exam. In about 3% of patients with acute pancreatitis. bruising or discoloration may be observed in the periumbilical region called Cullen's sign, or along the flank, called Gray Turner's sign, which can indicate retroperitoneal bleeding.

Patients with severe acute pancreatitis may present with major alterations in their vital signs, particularly with fever, hypertension, tachypnea, and hypoxemia. So what might you expect to see in the lab results of a patient with pancreatitis? In acute pancreatitis there is a breakdown in the relationship between the synthesis of digestive enzymes and their secretion.

They continue to be synthesized while there is a blockade of secretion due to the inflammation, as a result the digestive enzymes leak out of the pancreatic acinar cells and eventually into the systemic circulation. The serum amylase is a lab tests that can be ordered to help confirm clinical suspicion for pancreatitis. Elevation of the amylase greater than three times the upper limit of normal is consistent with acute pancreatitis. It typically rises within 6 to 12 hours of the onset of pancreatitis.

The serum lipase can also be ordered. It typically rises within four to eight hours. Lipase elevations occur earlier and last longer than amylase and are more sensitive. Acute pancreatitis causes a release of several inflammatory mediators, including c reactive protein or CRP that can be ordered as a lab test. A CRP level above 150 milligrams per liter at 48 hours is associated with severe pancreatitis.

Patients with pancreatitis may have a leukocytosis and an elevated hematocrit due to hemo concentration from dehydration from fluid losses in to third spaces. Metabolic abnormalities including elevated or decreased blood glucose levels, or decreased calcium levels may also be seen. What about imaging? Contrast enhance abdominal computed tomography is the imaging modality of choice.

Findings positive for pancreatitis include edema, enlargement and inflammation of the pancreas, free fluid or acites may also be seen. This is an axial image of a CT scan of the abdomen and pelvis that happens to not be contrast enhanced, but still shows findings consistent with acute pancreatitis. You can see in the irregularly shaped pancreas with edema surrounding the pancreatic head, inflammation of the pancreas and free fluid in the upper abdomen.

Abdominal ultrasound can also be used to diagnose pancreatitis. In patients with acute pancreatitis the pancreas appears diffusely enlarged and hypoechoic on abdominal ultrasound. There may be Peripancreatic fluid seen from the third spacing. Gallstones may also be visualized in the gallbladder or the biliary ducts. Ultrasound however, has limitations to visualization of the pancreas, which can be obscured secondary to bowel gas or ileus, it also is operator dependent. So let's talk about the treatment for acute pancreatitis.

The initial treatment of a patient with acute pancreatitis is supportive care, with intravenous fluid resuscitation and pain control. Patients with acute pancreatitis should be monitored closely in the first 24 to 48 hours. Crystalloid solutions such as normal saline or laxated ringer solution, are first line in all patients except those with specific contraindications, such as severe cardiovascular or renal disease.

IV fluid hydration at a rate of 5 to 10 milliliters per kilogram per hour is recommended. In some patients with severe dehydration from pancreatitis more rapid repletion can be done with fluid boluses. Pain control for the predominant complaints of abdominal pain should be obtained with analgesics, such as hydromorphone, fentanyl, and meperidine.

Opioids are safe and effective at providing pain control in patients with acute pancreatitis. A non opioid alternative is ketorolac. Nutrition is very important in a patient with pancreatitis. As part of the initial treatment and resuscitation of pancreatitis the patient is kept NPO or nothing per mouth. This allows the inflammatory process to cool down and avoid further activation of pancreatic enzymes by food in the gastrointestinal system.

In mild to moderate cases oral nutrition can usually be restarted within 24 to 48 hours. In more severe cases where the patient cannot tolerate oral feeding, or has severe necrotizing pancreatitis or other major complications, nasal jejunal tube feed using an elemental or semi elemental formula is recommended.

Parenteral nutrition, which is an intravenous administration of nutrition containing proteins, carbohydrates, fat, minerals and electrolytes, as well as vitamins should only be initiated in patients who do not tolerate enteral feeding or if the target rate is not achieved by 72 hours, it is for the most severe of cases. Prophylactic antibiotics are not recommended in patients with acute pancreatitis regardless of the type.

Up to 20% of patients with acute pancreatitis develop an extra pancreatic infection, that is bloodstream infections, pneumonia, and urinary tract infections. These are associated with increased morbidity and mortality. When an extra pancreatic infection is suspected, antibiotics should be started while the source of the infection is being determined. If cultures are negative and no source of infections identified, antibiotics should be discontinued.