There is an outstanding review of pancreatitis in this week's New England Journal of Medicine. I thought I would add it here as a reference for any addiction or medical psychiatrists who come across this post and may not be regular readers of the NEJM. I recommend getting the entire article because it has an excellent table and infographic. The table is on the causes of acute pancreatitis. The top two - gallstones (40%) and alcohol (30%) have not changed since I was in medical school. Hypertriglyceridemia (defined as fasting triglycerides >1000 mg/dl) was the third most common cause at about 2-5% or the total. Some of the causes occur only in a very specific context like endoscopic retrograde cholangiopancreatography (ERCP) and patients undergoing cardiopulmonary bypass. In both cases, the authors estimated that 5 -10% of patients undergoing these procedures got pancreatitis. Although the ERCP was expected I was surprised that many cardiopulmonary bypass patients got pancreatitis. The remaining 5-8% are caused by medications, viral and parasitic infection, and blunt trauma. Psychiatrists should be aware of valproic acid/valproate correlation with pancreatitis, especially if they are treating patients with significant alcohol exposure. Some facilities use a valproate detox protocol and those patients need to be carefully assessed for alcoholic liver diseases and undiagnosed pancreatitis.
The diagnostic features of acute pancreatitis are reviewed and these are important for any acute care psychiatrist who is seeing patient with associated risk factors. At the clinical level abdominal pain and elevations of amylase and lipase 3 times the upper limit of normal are the initial features that require confirmation by MRI or CT imaging finding consistent with the disease. From a diagnostic perspective the availability of testing and practicing in a medical facility are limiting factors. Any abdominal pain with a suspicion of pancreatitis in a non-medical facility makes a trip to the emergency department for rapid assessment and diagnosis most reasonable.
The infographic was on the time course and management of acute pancreatitis. The time frame used was 6 weeks. 80% of patients with acute pancreatitis have self limited disease and are discharged from the hospital in a few days. The incidence of acute pancreatitis is rising with a 20% increase in admissions in the past decade. On the mortality dimension half of the deaths occurred in the first two weeks due to multiple organ system failure. The other other half of the death occur after two weeks and are due to pancreatic and extrapancreatic infections. On the pathophysiology dimension, 80-85% of the disease was the interstitial form and 10-15% the necrotizing form. There was also a therapy dimension outlining critical markers such as aggressive fluid resuscitation in the first 24 hours and enteral nutrition after day 5 if tolerated. The therapy dimension was linked to the text that reviewed state of the art details on the medical and surgical management of the disorder. These sections will not apply to psychiatrists, but the authors point out common mistakes in management including the unnecessary use of total parental nutrition and antibiotics for presumed pancreatic infection. The main lessons for psychiatrists at that stage is that patient management has exceeded the capabilities of psychiatric settings and that the patient must be transferred as soon as possible to an appropriate medical setting. Once that has occurred, the plan to take the patient back when stable also requires a clear plan with the attending who is discharging the patient.
The other highlights in this article from a psychiatrist's perspective was the estimated dose of alcohol necessary to cause pancreatitis. The authors give that as 4 - 5 drinks per day for 5 or more years. This is well below the dose of alcohol required for cirrhosis and probably explains why larger numbers of young patients are seen with pancreatitis. Apparently, in the 2-5% of heavy drinkers that develop pancreatitis it occurs as a chronic form initially with episodic acute exacerbations superimposed on this chronic form. That also explains why binge drinking does not precipitate acute pancreatitis. Diabetes, smoking, and obesity are seen as correlates of acute pancreatitis but not direct causes and these are all significant comorbidities in patients with psychiatric disorders. Once an episode of pancreatitis has occurred abstinence from alcohol is critical because it decreases the likelihood of recurrence. The authors reference a structured consistent intervention that they cite as being successful (2). I don't have access to the full text of this article, but it suggests that an infrequent intervention by a nurse in outpatient clinic is more effective than a single intervention during hospitalization in preventing relapses.
This was a great overview of acute pancreatitis by some of the top experts in the field. It is another problem that you never want to miss. It is a reason to resist simplifying biochemical screening of patients on admission or clinic intake. Since metabolic syndrome, obesity, and tobacco use is high and elevated triglycerides may be a factors in the pathophysiology of pancreatitis - it seems reasonable to do metabolic screening on patients without recent testing. If you are seeing patient with risk factors particularly alcohol use, tobacco use, obesity, and diabetes - discussion of lifestyle management, smoking cessation, and abstinence from alcohol is useful in addition to the discussion about their primary psychiatric problem. Addiction psychiatrists will probably see significant numbers of patients with chronic pancreatitis and a discussion with them on how to prevent recurrences and their understanding of the illness is important.
George Dawson, MD, DFAPA
References:
1. Forsmark CE, Vege SS, Wilcox CM. Acute Pancreatitis. N Engl J Med 2016; 375: 1972-1981.
2. Nordback I, Pelli H, Lappalainen-Lehto R, Järvinen S, Räty S, Sand J. The recurrence of acute alcohol-associated pancreatitis can be reduced: a randomized controlled trial. Gastroenterology. 2009 Mar;136(3):848-55. doi:10.1053/j.gastro.2008.11.044. PubMed PMID: 19162029.
