Introduction

Whilst being on the surgical ward, I was astounded at the number of patients who presented with pancreatitis. I was soon prompted by the intern about all the causes of pancreatitis and its management, to which I vaguely remembered the I GET SMASHED mnemonic. An easy way to remember the causes of pancreatitis is by using the mnemonic I GET SMASHED. Statistically, you should find the cause of the pancreatitis and help you manage your patient.

The three most common causes for acute pancreatitis are:

• Biliary pancreatitis represents 40% of the cases due to gallstones.

• Idiopathic represents about 25% of the cases.

• Alcohol-induced acute pancreatitis represents 20% of the cases.

Essentially, each of the causes in I GET SMASHED will trigger the pancreatic enzymes to be activated prematurely, causing an inflammatory response and a fluid shift from the increased vascular permeability (third spacing). After damaging its surroundings, the enzymes released from the pancreas will eventually join the systemic circulation and digest the fats and blood vessels. Hypocalcaemia soon follows as the necrosis cause free fatty acids to be released and saponifies with calcium making a chalky-white appearance. See The Different Types of Necrosis and Their Histological Identifications.

I GET SMASHED

Pancreatitis is an inflammatory condition of the pancreas, an organ that aid in the digestive and endocrine systems. Tucked in the retroperitoneal space and sitting comfortably posteriorly to the stomach, the pancreas spans about 25 cm with a head, uncinate process, neck, body and tail. It is innervated by the vagus nerve (CN X, parasympathetic) and the greater and lesser splanchnic nerves (sympathetic), supplied by the pancreaticoduodenal, splenic, gastroduodenal, and superior mesenteric arteries, and drains into the pancreaticosplenic and pyloric lymph nodes. The pancreas is a delicate organ that can easily become upset through various causes. Below is an easy way to find the causes of pancreatitis in your patient.

I – IDIOPATHIC

Starting off with not knowing why the patient has pancreatitis. An idiopathic cause almost accounts for 1 in 4 patients, and because the cause is unknown, the treatment can be more difficult and frustrating. Either way, you have to accept the unknown cause and start supportive management.

G – GALLSTONES

Gallstones originate from the bile. If the bile flow is slowed or stopped, the bile then precipitates and create stones (cholelithiasis). There are three main types of gallstones; cholesterol stones (accounts for 80%), black pigment stones (10%) and mixed stones (10%). In pancreatitis, the stones will go through the bile ducts and become stuck. The biliary flow is then stopped; if this occurs around the ampulla of Vater, the pancreatic flow is also blocked. It is not a good thing for pancreatic enzymes, which can break down fat, protein, starch and essentially your living tissues, to be in a static environment. These enzymes, lipase, protease, elastase, trypsin and amylase, becomes activated when the flow stops. Subsequently, the enzymes break down and digest the surrounding tissues. When a stone blocks an area, there is increased pressure to the surrounding tissue, which causes interstitial oedema -> impaired blood flow -> ischaemia -> acinar cell injury -> enzyme activation -> auto-digestion.

E – ETHANOL

Excess alcohol causes three mechanisms in damaging the pancreas.

1. Chronic alcohol causes a blockage -> interstitial oedema -> impaired blood flow -> ischaemia -> acinar cell injury -> enzyme activation -> auto-digestion.

2. Alcohol causes acinar cell injury by releasing intracellular proenzymes and lysosomal hydrolase -> activation of enzymes -> auto-digestion.

3. Alcohol causes defective intracellular transport and excess alcohol creates toxic substances like free radicals that can damage pancreas cells.

T – TRAUMA

As mentioned before, the pancreas is a delicate organ. Regarding trauma, the pancreas is more prone to trauma in children. Having force applied to the soft organ, such as in a car crash, can rupture its architecture and spill its content. As a result, some cells will die from the force, or blood vessels may rupture, causing ischaemia to the pancreas. Necrosis and inflammation then occur.

S – STEROIDS

Long term, recent or increased dose in steroids use such as corticosteroids may induce pancreatitis. However, it is rare, thus rule out other possibilities before arriving to this conclusion.

M – MUMPS

More common in unvaccinated children as a complication, about 1 in 25 cases of mumps lead to short-term inflammation of the pancreas. The mumps virus causes acinar cell injury (just like alcohol) by releasing intracellular proenzymes and lysosomal hydrolase -> activation of enzymes -> auto-digestion.

A – AUTOIMMUNE

With the immune system, every tissue in the body is at risk of mistakenly being attacked. The immune system attacks and breakdown the pancreas integrity, resulting in enzymes leaking to its surroundings and causing inflammation with possible necrosis. Other methods are fibrosis of the pancreas, causing organ dysfunction.

S – SCORPION STING

Amusingly the most remembered one. The venom being released irritates the pancreas causing inflammation and swelling. These scorpions are mainly found in Barbados, Brazil and Trinidad.

H – HYPERCALCEAMIA / HYPERTRIGLECYRIDES

A high amount of triglycerides and calcium in the blood damages the pancreas. Triglyceridemia of x > 885 mg/dL or around 10 mmol/L is associated with pancreatitis. The lipase enzyme breakdown the triglyceride and causes a toxic amount of fatty acids.

Hypercalcemia refers to high serum calcium levels (total Ca > 10.5 mg/dL or ionized Ca2+ > 5.25 mg/dL). This calcium range has been shown to cause pancreatitis.

In both hypercalcaemia and hypertriglyceridaemia, it is essential to find why these occur and treat the cause.

E – ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY (ERCP)

The pancreas is a delicate organ that does not like being messed around. The endoscopic retrograde cholangiopancreatography (ERCP) is an endoscopic technique that is complex and is relatively safe. It combines endoscopy and fluoroscopy to diagnose or treat specific problems within the biliary or pancreatic ductal system. About 3.7% of ERCP procedures end up with a pancreatitis complication, which is by far the most common.

D – DRUGS

Azathioprine, NSAIDs, or diuretics or found to cause pancreatitis. The risk is low but is amplified if multiple drugs are used at once.

Clinical signs

On history, patients will often present with sudden 8/10 (or more) epigastric pain that radiates to the back with nausea and vomiting. Upon physical examination, there may be tenderness around the epigastric region with or without guarding. Due to necrosis causing inflammation, patients may not be haemodynamically stable, especially with the addition of the “third spacing” phenomenon. Uncommonly there are Cullen’s and Turner’s signs to look for. In addition, look out for any hypocalcaemia signs such as Trousseau’s or Chvostek’s signs or cramping/tetany.

Management

Unfortunately, pancreatitis is a condition to “ride it out”. The management is mainly supportive measures and preventing any complications. Always be mindful of the cause; identify the cause and treat it to stop further advancement of pancreatitis.

• Intravenous fluids are necessary as patients can rapidly become haemodynamically unstable. Correct any types of shock before proceeding. Use the MET call and get help.

• Find the original cause and treat it once the patient is stabilised.

• A nasogastric tube may be used if patients cannot tolerate food or are vomiting. Use antiemetics if needed.

• Catheter to monitor urine output and fluid balance.

• Analgesia to alleviate pain.

• Broad-spectrum antibiotics may be used prophylactically in case of necrosis. However, confirm necrotic damage/tissue before starting antibiotics.

Published 15th October 2021. Last reviewed 10th February 2022.

Reference

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