Pancreatitis
A man comes into the ED develops a fever. A FBC shows his serum lipase is 3 times its normal limit. He is vomiting extensively and has pain around his sternum that travels to his back. What is your likely diagnosis?
Pancreatitis is an inflammatory condition of the pancreas. To quickly revise our pancreatic functions, it comprises exocrine and endocrine components. In terms of its exocrine function, it houses digestive enzymes that are stored as pro-enzymes called zymogens, meaning they are not yet activated. This is to ensure these enzymes do not auto-digest the pancreas.
This leads us to the pathophysiology. Pancreatitis arises when there is an obstruction to the outflow of the pancreatic duct. This ductal outflow obstruction causes early activation of these lipolytic and proteolytic pancreatic pro-enzymes, destroying the pancreatic parenchyma through liquefying it. This process is known as liquefactive hemorrhagic necrosis. Destruction of the pancreatic parenchyma attracts neutrophils + macrophages. These cells release cytokines which ultimately cause pancreatitis.
An important thing to note is that distributive shock may arise. The mass cytokine release that has occurred can increase permeability and vasodilation of vessels, causing fluid to enter the interstitial space, resulting in hypotension and tachycardia, leading to distributive shock. This may show as increased hematocrit concentration on FBC.
The causes of pancreatitis are easy to remember through the simple mnemonic "I get smashed." This stands for idiopathic, gallstones, ethanol, trauma, steroids, mumps, autoimmune conditions, scorpion stings, hypercalcemia, hypertriglyceridemia, ERCP (endoscopic retrograde cholangiopancreatography), and drugs. The three most common causes of pancreatitis are ethanol, idiopathic, and gallstones.
The main symptoms of pancreatitis were all in the clinical case. These include epigastric pain radiating to the back, nausea/vomiting, and fever.
To diagnose acute pancreatitis, 2 of the 3 features are required: characteristic abdominal pain, increased serum pancreatic enzymes (lipase – more specific / amylase >3x upper limit of normal), and pancreatitis on imaging.
Now for imaging. Abdominal US (first-line imaging) shows a hypoechoic pancreas (edema) and potential cholelithiasis. Contrast CT pelvis + abdomen is done if there is diagnostic uncertainty or lack of improvement after 7 days. Features include enlargement of parenchyma with edema, indistinct margins with surrounding fat stranding (grey streaks surrounding the pancreas).
An important scoring system for pancreatitis is Ranson’s criteria. This can be done on admission or 48hrs after admission to determine the severity of pancreatitis.
In terms of treatment for pancreatitis, it can be self-limiting. If this is not the case, treatment is conservative initially, and then treatment is done to approach the underlying cause. This involves analgesia admission (NSAID or opioid IV), fluid resuscitation (crystalloid), nutrition support eating as required in mild cases, otherwise enteral nutrition (via NG tube) to prevent villous atrophy. Gut rest is associated with villous atrophy, bacterial overgrowth --> systemic inflammation and multiple organ dysfunction. Therefore, enteral > parenteral > no feeding. Treat underlying cause which may involve surgical intervention.