This chapter deals with the management of acute pancreatitis so severe that it requires ICU level care. It is not your average Sunday Morning Pancreatitis. The college loves this condition, and it is well represented among the past papers. Specifically, the following questions have required an indepth understanding of this condition:
Specific issues which have been asked about, and which the candidates need to be familiar with. These issues form the headings for the subsections of this chapter, to simplify revision. As far as pulished literature goes, the time-poor candidate may safely limit their reading to Maheshwari & Subramanian (2016) from Critical Care Clinics.
Question 23 from the first paper of 2009 offered the candidates an obese hypoxic woman in a state of shock, with a history of abdominal pain and vomiting. They also gave them a high lipase, making pancreatitis the most likely explanation. But what if they didn't? Differentials for an acute shocked abdomen include the following easily remembered list:
Infectious causes: sepsis from any origin, but more likely the gut,
Autoimmune causes eg. inflammatory bowel disease with perforation
Traumatic causes eg. Boerhaave's syndrome due to excessive vomiting
Endocrinological cause of abdo pain and SIRS, eg. pacreatitis due to any number of causes
All clever bullshit aside, 70% of the time its either gallstones or alcoholism.
However, the College expects us to be able to generate a torrential stream of differential aetiologies for pancreatitis, and this is not a complete waste of time, because one of these days one will encounter a pancreatitis caused by something very rare and weird.
LITFL offers a nice mnemonic for these aetiologies: I GET SMASHED
We have had these since 1974. I found a simple breakdown in the ANZ Journal of Surgery.
Age > 55 yrs
WCC > 16,000
LDH > 600 U/I
AST > 120 U/I
Glucose > 10 mmol/L
Within 48 hours
Haematocrit fall > 10%
Urea rise > 0.9 mmol/L
Calcium < 2 mmol/L
pO2 < 60mmHg
Base deficit > 4
Fluid sequestration > 6 L
You get one point for each criteria met. The mortality from pancreatitis by these criteria, according to the score generated, are as follows:
< 3 = 1%
3-4 = 15%
5-6 = 40%
> 6 = 100%
Thus, if you are an elderly person who has rocked up to ED hyperglycaemic, with a high WCC, high LDH, deranged LFTs, acidosis, hypoxia and hypocalcemia - you are not going to do well.
Of course, since Ranson's days, we have improved our management somewhat, and these days mortality from severe acute pancreatitis in the ICU is closer to 15%. From this, one may be tempted to reach the conclusion that the Ranson criteria are no longer worth very much as a predictor of survival.
Several trials have been analysied; there does not appear to be any benefit.
Aprotinin and gabexate mesilate were supposed to decrease pancreatic "autodigestion" by inhibiting the pancreatic proteases. Turns out, they dont work.
About 50% of these people will get their pancreatic pseudocyst infected with various organisms.
In the 1990s, people believed in prophylactic antibiotics because small-scale trials demonstrated a benefit. However, a recent review suggests that there does not appear to be any benefit, even on the basis of studies which were not adequately powered to detect a subtle benefit. This review, it must be added, excluded the cases of severe necrotising pancreatitis, so the hardcore proponents of antibiotic therapy still recommend prophylaxis.
If your pseudocyst is infected, or if you are a firm believer in hosing your patients with antibiotics, then it seems you need carbapenems, because their penetration into pancreatic tissue tends to be the best.
Like in all shock states of critical illness, there is perhaps a role here for "stress dose" steroids. In the absence of actual evidence, this is still a hypothesis with some merit.
The more severe your pancreatic necrosis, the more likely you are to get it colonised with a fungus. Thus, there may be a role for antifungal drugs here, at least in the opinion of some people, as a means of delaying surgery. Others may argue that the surgery should be delayed as long as possible anyway, and by that stage one does not wish to be colonised by a species which has been selected for resistance to routine antifungal drugs.
In short, TPN either does nothing to improve mortality, or is associated with increased mortality.
The 2009 Canadian Guidelines mention 3 meta-analysis studies, which all show a mortality benefit with early eneteral nutrition. This is thought to be the result of a decreased SIRS response, which in turn is due to diminished bacterial translocation from the healthier gut.
Oh's Manual quotes the International consensus guidelines for nutrition therapy in pancreatitis, which suggest a few simple rules. These have been modified slightly with the addition of whatever the college examiners wrote in their model answer to Question 16 from the second paper of 2017.
A part of Question 16 from the second paper of 2017 and the whole 10-mark lot of Question 1 from the first paper of 2016 asked the candidates to discuss this issue. The college answer to the latter question was quite good, and is used to create the summary below. In brief, there is no role for prophylactic antibiotics in severe acute pancreatitis, and one may briefly conclude this issue by saying that clinically significant extrapancreatic infections should still be treated with antibiotics (as you normally would), as well as any infected pancreatic material (which has been proven to be infected). However, in order for future generations to have a prefabricated answer in their pocket, the issue will be critically evaluated below.
Potential uses of antibiotics in pancreatitis
Coincidental treatment of extrapancreatic infection
Treatment of infected pancreatic necrosis
Arguments for the use of prophylactic antibiotics in severe pancreatitis
Counterarguments to the wanton abuse of antibiotics
Antibiotic choice (if you felt compelled to give them)
Guidelines and "own practice"
This came up as a minor 20% part of Question 16 from the second paper of 2017.
Oh's Intensive Care manual: Chapter 43 (pp. 495) Severe acute pancreatitis by Duncan LA Wyncoll
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