In the distant days when I was still a med student (last year) a surgeon of extraordinary skills and questionable morals gave me a piece of advice after I told him about my taste for General Surgery as a specialty: “don't f*ck with the pancreas". After hours of reading I learned the reason; even minor traumas can induce the release of pancreatic enzymes and cause a pancreatitis that can endanger the patient’s life, which is why this organ is, along with the amenorrhea of the undergraduate intern who was invited to last week’s shift, a surgeon’s greatest fear.
But you, (presumably) young reader, will learn enough today as to not fear a small organ shaped like a deformed caterpillar. Let me make the most of those hours of study, and teach you about acute pacreatitis.
Dr. Mike's Guide to Acute Pancreatitis
Starting, as always when talking about something surgical, with the anatomy; the pancreas is a retroperitoneal organ located obliquely upward, from the C-loop of the duodenum to the splenic hilum, with an appearance that some literatures describe as a feather but I prefer to see it as a parasitic worm emerging from the intestine and caught in-between its upward path towards the diaphragm. It is composed of soft yellowish glandular tissue, has an average length of 15 to 20cm, a weight of 75 to 100 grams, and is divided into 4 regions: head, neck, body and tail. Its location deep in the abdomen explains the diffuse and difficult-to-pinpoint nature of pancreatic pain and its radiation to the back that can be mistaken for a renal colic or lower back pain. The pancreas fulfills a dual endocrine and exocrine role, and is the source of most digestive enzymes that, surprise, are responsible for the digestion of food.
Generally speaking, the pancreas has two pancreatic ducts through which it exerts its secretory function: almost the entire pancreas drains through the Wirsung duct or main pancreatic duct, merging with the bile duct and creating a common conduit of variable length. Normally, there is another minor duct called Santorini duct or accessory pancreatic duct, which drains directly into the duodenum, however, in 30% of individuals this duct is closed and does not lead to the duodenum, and in 10 % of people the Wirsung and Santorini ducts do not fuse, having the useless mutant power of draining most of its secretions through the Santorini duct while the lower portion of the head of the pancreas drains through the Wirsung duct. This variant is known as Pancreas Divisum and it’s a risk factor for the development of pancreatitis because the minor papilla, where the accessory duct ends in, is not prepared to handle a high flow, much like the average newborn baby's diaper.
As I said before the pancreas fulfills both endocrine and exocrine functions, working through a feedback system with the other systems of the body to secrete digestive enzymes and hormones. The exocrine pancreas secretes around 500 to 800ml of colorless, odorless and alkaline pancreatic juice daily, in addition, the acinar cells release amylase, proteases and lipases, the enzymes that are responsible for digesting the 3 types of food: carbohydrates, protein and
Now that we know enough about the affected organ, we can talk about the pathology that affects it: an acute pancreatitis is an inflammatory disease of the pancreas, being one of the most frequent causes of acute abdominal pain, and that, if not treated in time, can lead to serious complications such as sepsis or shock. It has an annual incidence of 13 to 45 cases per 100,000 inhabitants, with 300,000 cases and 4,000 deaths annually in the United States alone. It is triggered by a process of self-digestion due to the inadequate activation of pancreatic enzymes, showing evolution that perhaps it is not such a good idea for an organ to be able to be digested by the same enzymes that it secretes, and causing damage and inflammation in the pancreatic tissue.
The most common cause in 80-90% of cases is due to gallstones that obstruct the lumen of the pancreatic duct or the ampulla of Vater, the exact mechanism is still debated but it is believed that this causes a retrograde flow of bile or duodenal juice towards the pancreas. The second most common cause is alcoholism, again, the mechanism is not entirely clear, but research suggests that it is related to the fact that alcohol causes spasms in the sphincter of Oddi with subsequent retrograde flow into the pancreas, others studies show that its consumption can cause inappropriate activation of trypsin (come on, we all get confused when drunk), and it also temporarily decreases blood flow to the pancreas, which can cause ischemic lesions. Other causes are post-operative injuries or during ERCP (a procedure to remove gallstones from the bile ducts), tumors, trauma, infection, or inappropriate use of drugs.
Still, I prefer a stone in my pancreas than in my urethra.
Moving on to the signs and symptoms we have that pancreatitis can occur at any age, however it is rare in children and young adults (those who stay sober, at least), because of its etiology it usually occurs in middle-aged or elderly patients. The symptoms can vary remarkably; some have a mild form of the disease that remits on its own, while others have a more severe form that can be fatal.
The pain is of rapid onset, intense and constant, usually in the epigastrium or in the left hemicbelt with radiation to the back. The patient is usually sitting bent forward due to pain, and can easily be mistaken for a person who has just eaten at Wendy’s, but without diarrhea. Bowel sounds are usually absent or decreased, and vomiting is frequent, early, and profuse. Around 30% of patients have jaundice, there is usually a fever of up to 39.5ºC, the patient may be in shock, tachycardic, tachypneic, hypotensive, with generalized hypersensitivity in the abdomen and signs of muscular defense. There may be steatorrhea, or oily stools with high lipid content, and in severe cases pleural effusion or even ascites due to the transfer of exudative transdiaphragmatic fluid or the creation of a pancreatic-pleural fistula.
Some of the clinical signs that can be seen in pancreatitis are the Waring Griffiths sign, which is described as earthy yet cyanotic paleness of the cheeks, coldness of the nose, and sunken eyes, like a competitive Starcraft player after 42 hours of training without rest. The Gray-Turner sign, which is characterized by the appearance of bruises on both flanks, and Cullen's sign, a periumbilical hematoma, caused by the extravasation of bloody pancreatic juice in necrotizing pancreatitis.
The clinical diagnosis of pancreatitis is one of exclusion. Some conditions that can be confused with this pathology would be a perforated peptic ulcer, gangrenous obstruction of the small intestine and acute cholecystitis. During the anamnesis, it is necessary to inquire about when the pain began, it usually comes after a large meal, and another fact is that vomiting does not relieve the pain. On physical examination, the patient usually has tachycardia, tachypnea, hypotension, and hyperthermia, although in mild cases there is usually only a mild fever, bowel sounds will be absent or decreased, and the abdomen may be distended and with ascitic fluid. Also, as I said before, there may be the presence of the Gray-Turner or Cullen’s sign. There are also a variety of paraclinical and imaging studies that can help us.
An example of Cullen’s sign.
Some useful paraclinical tests are a complete hematology where there is usually leukocytosis and anemia in severe cases, serum electrolytes, since calcium may be decreased by the saponification of fats, a lipid profile, liver profile, kidney profile, and especially pancreatic enzymes, of these the most useful for diagnosis is amylase, which is usually very high in concentrations that can be up to 5 times the normal amount. Serum amylase rises in the acute phase but its concentration drops in 2 or 3 days, but urine amylase is high for a longer period and may be useful in cases with a longer evolution time. In addition to amylase, lipase can also be useful, since its serum elevation remains high for longer than amylase, making it more specific and sensitive.
Moving on to the imaging diagnoses, chest and abdominal X-rays are usually not very useful, but they can rule out other pathologies such as perforated duodenal ulcers or intestinal obstructions, in some cases the sentinel loop sign is observed, which is a single dilated individual loop of the proximal jejunum, and some types of gallstones may be visible on an X-ray. Abdominal ultrasound is the best way to confirm the presence of gallstones when biliary pancreatitis is suspected, in addition you can see the increase in size of the pancreas and any accumulation of fluid that may exist in the area, but it is true that in 20% of cases, intestinal gas can cover the pancreas and make it difficult to scan it. CT is indicated in mild forms or when it is difficult to diagnose and is very accurate, in addition to estimating the severity of the condition; in patients with suspected severe pancreatitis, a CT with IV contrast should always be performed. Magnetic resonance imaging has indications similar to CT, it is used when there is hypersensitivity to contrast, and it allows evaluating the Wirsung duct and the presence of liquid collections. Finally, ERCP (endoscopic retrograde cholangiopancreatography, and no, it is far from being the longest term in medicine) can be performed in cases of choledocholithiasis.
Finally, the treatment requires good intravenous fluid resuscitation due to fluid sequestration in the interstitial space causing hypovolemia. Aggressive administration of fluids in the first 24 hours reduces mortality, crystalloids such as 0.9% saline or lactated Ringers are often used. The most used painkillers in mild cases are NSAIDs such as diclofenac or ketoprofen, and in moderate or severe cases opiates such as Petidine are recommended. Diet is one of the key points in the treatment of pancreatitis, in mild cases without organ failure, a low-fat diet may be indicated, in severe cases or when there is intolerance to the oral route, total parenteral nutrition is indicated during first 3-5 days until symptoms and inflammatory markers improve, and then the patient is fed through a nasojejunal tube, which is better than nasogastric because it decreases pancreatic secretion. Antibiotics are rarely necessary since acute pancreatitis is usually a sterile inflammation, and it is important to note that in severe cases the use of heparin has been shown to decrease mortality.
An example of the Grey-Turner sign. Or a Fight Club member.
And although this disease’s treatment is mostly medical, surgical interventions can also be performed to improve the condition: in patients with mild biliary pancreatitis, an early cholecystectomy should be performed (first 48 hours after admission), as this shortens the hospital stay in compared to when performed after the resolution of pain and normalization of enzymes. In acute necrotic pancreatitis, it is delayed until inflammation and fluid collections stabilize or disappear, which can take up to 6 weeks.
It should be noted that there are a variety of scales and classifications for pancreatitis, which allow us to get an idea of the prognosis of the disease, but with this (I hope) useful guide summarized in one night under the influence of massive amounts of coffee and self-loathing you have enough for most times, or at least to diagnose and refer to someone more capable. But going back to the first paragraph of this article, I would like to recall the advice given by my friend the surgeon, and adjust it more to reality to make it more useful during medical practice: "If you are going to fuck with the pancreas, it should be with drugs". Not under their influence of course. You know what I mean.
References:
- S. I. Schwartz, et al. Schwartz's Principles of Surgery, 9ª Ed., 2.010.
- Harold Ellis, et al., General Surgery – Lecture Notes, 12ª Ed., 2011.