Pancreatitis: Clinical practice

Pancreatitis is inflammation of the pancreas.

In acute pancreatitis, the pancreas’ own digestive enzymes get suddenly get activated within the pancreas and cause autodigestion which results in inflammation and hemorrhaging.

In chronic pancreatitis, there are indolent causes of inflammation that damage the pancreas, leading to impairment of both endocrine and exocrine functions of the pancreas.

Now, first thing’s first. Acute pancreatitis is usually caused by gallstones and ethanol abuse, but there are other causes as well, and the full list can be remembered using the mnemonic “I GET SMASHED”: where ‘I’ refers to unknown, or Idiopathic, causes; ‘G’ is obstruction by Gallstones, ‘E’ is Ethanol abuse; ‘T’ is a pancreatic Trauma, which is more likely if the trauma is the result of a puncture injury, like a knife wound rather than a punch; ‘S’ is the use of Steroids; ‘M’ is infection with Mumps virus, ‘A’ is the result of Autoimmune diseases; the second ‘S’ is the result of a Scorpion sting—which is probably the most exciting item on this list and one of the more rare causes - so check your shoes!; ‘H’ is a cheat and stands for both Hypertriglyceridemia and for Hypercalcemia; ‘E’ is trauma from an Endoscopic retrograde cholangiopancreatography or ERCP which is a technique used to diagnose and treat various biliary and pancreatic diseases; and finally ‘D’ stands for Drugs, like sulfa drugs, reverse-transcriptase inhibitors, and protease inhibitors.

Individuals with acute pancreatitis usually have severe epigastric abdominal pain that radiates to the back, along with nausea and vomiting over several hours.

In mild cases, there may be tenderness in the epigastrium, and in severe cases, there might be hypovolemic shock which can cause tachypnea, hypoxemia, and hypotension or systemic inflammatory response syndrome or SIRS, which can cause those same symptoms as well as fever.

So for SIRS - three of the hallmarks - tachypnea, hypotension, and fever - are identified in the vital signs.

Sometimes, there’s a Cullen sign which is an ecchymotic discoloration in the periumbilical region or a Grey Turner sign where the ecchymotic discoloration is along the flank.

Both of these signs suggest retroperitoneal bleeding due to pancreatic necrosis.

Now, some clues also point to the etiology. With alcoholic pancreatitis, there may be hepatomegaly.

With hyperlipidemic pancreatitis there may be xanthomas - which are lipid deposits that can appear anywhere in the body.

And with mumps pancreatitis, the parotid gland may be swollen.

In acute pancreatitis, the first set of lab work is aimed at confirming the diagnosis.

In pancreatitis, the serum lipase- which is the most sensitive test for acute pancreatitis- rises within 8 hours from the onset of symptoms and returns to normal within 14 days- and serum amylase which rises within 12 hours from the onset of symptoms and returns to normal within 5 days. Usually, both rise to at least 3 times the upper limit of normal.

Next, to assess severity, a CBC may show leukocytosis or an elevated hematocrit due to dehydration or acute hemorrhaging.

The CRP and LDH are usually elevated due to inflammation.

The BUN and creatinine are done to assess for signs of dehydration.

Ionized calcium levels can be low, because if there’s fat necrosis, this consumes the calcium.

The individual may also have hypoglycemia or hyperglycemia depending on levels of insulin and glucagon.

In addition, electrolytes, ALT and AST, bilirubin, and albumin should be obtained to rule out other causes of abdominal pain like cholecystitis and finally triglyceride levels can be done to rule out or confirm hypertriglyceridemia as a cause of acute pancreatitis.

In individuals with symptoms suggestive of SIRS, an ABG might show a pO2 below 60 mm Hg - which defines hypoxemia.

Next, on an abdominal ultrasound the pancreas will be enlarged and hypoechoic.

And with gallstone pancreatitis, stones are usually present in the gallbladder.

If the diagnosis of acute pancreatitis is still unclear, then an abdominal CT with contrast can be done, and a scoring system called the Balthazar score can be used.

This scoring system assesses the severity of acute pancreatitis based on the degree of necrosis, inflammation, and fluid collection around the pancreas.

Abdominal and chest x-rays can also be done.

In severe cases, a sentinel loop may be seen on the abdominal x-ray due to ileus inflammation that’s caused by adjacent pancreatic inflammation.

And on a chest x-ray, a pleural effusion may be present.

Next, the severity of acute pancreatitis is assessed. A frequently used scoring system is the Atlanta classification, which has mild acute pancreatitis- where there’s no organ failure or complications, moderate acute pancreatitis- where there’s transient organ failure that resolves within 48 hours plus or minus complications and severe pancreatitis- in which organ failure persists for more than 48 hours.

There’s also the Ranson’s criteria which has a total of 11 parameters - 5 are assessed at admission and then 6 are assessed 48 hours after admission.

At admission, the measured parameters are age over 55 years, high white blood cell count, hyperglycemia, high LDH, and high AST, and at 48 hours, the criteria include low hematocrit, high BUN, low serum calcium, low partial pressure of oxygen, elevated base deficit, and fluid sequestration.

The presence of 1 to 3 of these criteria represents mild pancreatitis, and the presence of more than 3 criteria represents severe pancreatitis and a higher mortality risk.

Now, acute pancreatitis is usually mild, but with severe pancreatitis, there’s a systemic inflammatory response triggered by cytokines and activated pancreatic enzymes that are released in the blood. This leads to significant 3rd spacing - where fluid shifts into the tissues - causing multiple organ failure, especially acute respiratory failure and kidney failure.

Treatment of mild pancreatitis, starts with fluid resuscitation which is done using isotonic crystalloid solutions, like saline or lactated Ringer solution at a rate of 5 to 10 milliliters per kilogram per hour for the first 12 to 24 hours, and then adjusted based on hydration status.

Hydration is very important because if there’s persistent hypotension, it can lead to ischemia and necrosis of the pancreas.

With severe pancreatitis, fluid resuscitation is done more aggressively at a rate of 20 milliliters per kilogram per hour in the first 30 minutes followed by 3 milliliters per kilogram per hour for the next 12 hours.

If acute pancreatitis was caused by hypercalcemia, then lactated Ringer is contraindicated because it contains calcium, so saline is used instead.

Pain control is done with IV opioids, such as Hydromorphone or Fentanyl.

In mild pancreatitis, oral nutrition can usually be started within 24 hours, but in severe pancreatitis, enteral feeding is initiated- with a tube that extends from the nose to the jejunum.

Alternatively, parenteral nutrition can be done if the individual doesn’t tolerate enteral nutrition.