Izabella Godlewska

70039
group 2, 5th year of Medicine

ACUTE PANCREATITIS
Acute pancreatitis is an inflammation of the pancreas due to autodigestion by proteolytic
enzymes. The clinical picture ranges from mild and self-limiting to severe cases of sepsis or
multiorgan failure.
The most common etiology of acute pancreatitis is cholelithiasis or alcohol abuse, however
idiopathic inflammation is another common reason. Other causes are hyperlipidemia,
hypercalcemia, trauma, abdominal surgery/ERCP, pancreatic duct obstruction (tumour,
pancreatic divisum), vasculitis (and autoimmune pancreatitis), scorpion venom, viral
infections (mumps, CMV, coxsackie B), drugs and complications of end-stage kidney disease
or posterior perforation of peptic ulcer. Common drugs that increase the risk of acute
pancreatitis are metronidazole, methyldopa, cimetidine, steroids, estrogen, valproate,
isoniazid, pentamidine and sulfonamides.
Clinically, the mortality of acute pancreatitis is around 10%, but the specific mortality risk is
evaluated via the Ranson’s criteria scale. The criteria are based on age, blood glucose levels,
AST, LDH, WBC at admission and blood urea nitrogen, fluid deficit, calcium levels, drop in
hematocrit, base deficit, oxygen saturation within 48h. If the sum of risk factors is lower or
equal to 3, the mortality is around 1%, but if the sum of risk factors is above six, the
mortality is above 70%.
The patient usually presents with epigastric pain radiating to the back, which may be
improved with sitting forward or standing. Other symptoms are nausea, vomiting. A
complete history must be taken, focusing on the drugs taken as well as alcohol use, last
meal (fatty meal), trauma, other diseases (gallstones) and family history. On physical exam
the patient may have a slight fever, tachypnoea, tachycardia and abdominal tenderness.
Sings of shock or dehydration may be present. Cullen’s sign (blueish discoloration of
periumbilicus) or Grey-Turner’s sign (blueish discoloration of flank) may be present in
severe, hemorrhagic pancreatitis.
The differential diagnoses are acute cholecystitis, peptic ulcer disease, MI, ruptures
abdominal aortic aneurysm, mesenteric ischemia and pneumonia.
Serum amylase and lipase are the most common blood test for diagnosing acute
pancreatitis. Serum amylase has a high sensitivity, but low specificity and can be correlated
with most intra-abdominal problems, while serum lipase is more specific and sensitive for
the pancreas. A high increase in CRP within 48h is associated with poorer prognosis. A
simple chest x-ray may exclude pneumonia. An abdominal ultrasound can find or exclude
biliary tree diseases, abscess, phlegmons or pseudocysts. Computer tomography is the test
of choice to diagnose acute pancreatitis, as it shows pancreatic inflammation, oedema and
necrosis, as well as the complications of pancreatitis.
The treatment of acute pancreatitis begins with aggressive hydration with electrolyte
monitoring, since lack of fluid may lead to shock. Euvolemia and hemodynamic normalcy are
proven to improve the prognosis. Appropriate analgesia is recommended, morphine is
contraindicated due to a possible spasm of sphincter of Oddi. Meperidine or
hydromorphone are good alternatives. Proton pump inhibitors or H2 antagonists may be
given as stress ulcer prophylaxis. Patients with nausea and vomiting should be given
antiemetics, such as ondansetron parenterally. Furthermore, such patients should have a
nasogastric tube placed until nausea/vomiting stops and pancreatic enzymes have
normalized. Parenteral nutrition may be taken into consideration in severe cases. Antibiotics
are not recommended unless in the case of necrotizing pancreatitis, where an infection
must be proven by a fine needle aspiration and culture. In such a case, appropriate
antibiotic regimen (imipenem/ciprofloxacin with metronidazole for up to 7-10days) should
be given along with surgical debridement.
Surgery is indicated for complications of acute pancreatitis, such as infected necrosis,
pseudocysts, abscess or hemorrhage. Pancreatic parenchymal necrosis may be sterile or
infected. CT is an important aspect of diagnosing this complication. Infected necrosis must
be treated with appropriate antibiotics and surgical debridement; thus, a good diagnosis is
essential. Pseudocysts are collections of pancreatic secretions surrounded by fibrous tissue
and other organs; they are the consequence of ductal leaks. They develop in 10% of patients
with AP and most resolve spontaneously after 4-6 weeks. After 6 weeks, the resolution is
less likely and surgical intervention is needed, usually ending in cystogastrostomy or
cystojejunostomy. Pancreatic abscess are collections of pus, which are commonly microbial
(Candida species or enteric bacteria). Adequate drainage is vital, and it can be achieved by
either percutaneous drainage or surgical debridement. It is common to leave a sump drain
in the pancreatic abscess with closure of the abdomen. Hemorrhage may be caused by
splenic vein thrombosis or false aneurysms. Other complications, such as pancreatic fistulas
are not indications for surgical intervention.
ERCP with endoscopic sphincterotomy may be used acutely when pancreatitis is associated
with biliary tree diseases (common bile duct stones) or when the cause of pancreatitis is
unclear. Early ERCP is found to decrease morbidity and mortality, however there is a risk of
acute pancreatitis are a complication of ERCP. Early cholecystectomy is recommended for
biliary pancreatitis after acute inflammation has resolved.
Unfortunately, acute pancreatitis is a problem with a wide-spectrum of clinical
presentations often having a relatively high mortality, while treatment is largely supportive.

Sources:
1. Ganti Latha, Kaufman Matthew, Mishra Nitin, First aid for the Surgery Clerkship, Mc Graw Hill
Education, 2017
2. Zaslau Stanley, Vaughan Richard A., Step up to Surgery, Lippincott Williams & Wilkins, 2014
3. https://wum.lecturio.com/#/
4. https://www.medicalnewstoday.com/articles/321804
5. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2999082/