Ten Pearls of Wisdom From Acute Pancreatitis Experts

David A. Johnson, MD


December 13, 2016

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Hello. I am Dr David Johnson, professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, Virginia.

Acute pancreatitis is a real problem in the United States. It has a tremendous health economic impact, with approximately $2.5 billion in associated costs and over 275,000 admissions each year.[1] This has become additionally problematic given that the incidence of acute pancreatitis has increased at least 20% over the past 10 years.[2] In particular, we are seeing increasing patients among those in the pancreatic population who were perhaps not at risk before. In the adult population, it appears that this increased risk is occurring somewhat in parallel with the obesity epidemic and the increasing risk for gallstones.

Dr Chris Forsmark and two experts in pancreaticobiliary diseases recently wrote a brilliant article in the New England Journal of Medicine on acute pancreatitis.[2] I wanted to put into perspective some of the pearls of wisdom I took from this article in the form of my top 10 game changers (listed in no particular order) that I think we all need to be aware of as we start to apply the diagnosis of acute pancreatitis.

Risk Factors and Predictors of Severity

First, we must recognize that there are certain risk factors for acute pancreatitis. It is particularly evident that morbid obesity and type 2 diabetes are independent risk factors, with an increased odds ratio of nearly 2 to 3 times. There are a number of genetic risk factors, but it appears that alcohol and smoking in particular may be co-factors that actually trigger some of these genetic factors into precipitating acute pancreatitis. Those are important to recognize, but clearly the focus is on morbid obesity and type 2 diabetes. Although we think about diabetes as a subsequent consequence of pancreatitis, it may be an independent risk factor in the development of pancreatitis as well.

Second, the three experts behind this New England Journal of Medicine article suggested that vague symptoms and minimal amylase or lipase elevation (defined as < 3 times the upper limit of normal) should not be diagnosed as having acute pancreatitis. We need to recognize that renal failure will also cause elevation of the amylase and lipase due to delayed clearance, and put into perspective who we are saying has acute pancreatitis. Maybe some of these patients do not need to be admitted. We need to be looking elsewhere—beyond their symptoms.

My third point is regarding predictors of severity, which I think this article illustrated very well. When it comes to elevations to admit over the next 24 hours, we're often taught about hemoconcentrations. Hematocrit is in the range of 44% on admission, or has failed to diminish over the next 24-48 hours with hydration, which we'll talk about shortly. Elevations in blood urea nitrogen (BUN) > 20 mg/dL or creatinine > 1.8 mg/dL and systemic inflammatory response syndrome, with a temperature below 36° C or above 38° C; a pulse that is at or approaching tachycardic (> 90 [beats per minute]); a respiratory rate > 20 [breaths per minute]; or a corresponding arterial CO2 < 32 [mm Hg], reflecting a hyperventilation response; and a white cell count considered either extremely low (< 4000) or high (> 12,000)—these are the kinds of patients who, on admission, should be immediately directed to high-intensity nursing units. There are a number of scoring systems related to acute pancreatitis and risk factors; I cannot remember those things, so instead just think about very systemic things like hematocrit, BUN, and systemic inflammatory response syndrome—temperature, tachycardia, respiratory rate, and white cell count. These are patients who need to be at least considered for a higher-intensity nursing unit on admission.

New Recommendations Challenge Old Conceptions

The fourth point is about vigorous hydration. We are all taught in medical school, residency, or fellowship that vigorous hydration is very important. There are some recent data that Ringer's lactate solution may be superior, although the authors behind this present review paper suggest that it needs further study. The importance here is [vigorous hydration] in the first 12-24 hours—an estimated 200-500 mL per hour. We can think about this as retroperitoneal burn, where there is a huge immediate fluid replacement that is required to avoid the consequences of underperfusion. The math calls for 5-10 mL/kg, or more easily 2500-4000 mL, of my preference, which is Ringer's lactate. After 24 hours, it is of limited value, and in fact there is a trade-off over consequences like fluid resuscitation and fluid overload. Therefore, we should think about fluid aggressively and immediately, but with caution about using it for 24 hours or more.

The fifth point deals with mild pancreatitis. Many of us may practice according to the idea that we cannot feed a patient until there is resolution of pain and they are off pain medications. In fact, the data show that there is no need for complete resolution of pain before beginning oral solid or soft food. Low-fat feedings are associated with shorter hospital stays than with the clear liquid diets, which I think many of us have commonly used. This is a patient population that is typically slower to discharge anyway. There is no need for complete resolution of pain or normalization of their pancreatic enzymes to begin oral refeeding.

When it comes to the need for artificial refeeding, the key element here is that if you need to use feeding that is not oral, a nasogastric or nasoduodenal approach is equivalent to nasojejunal feeding. Many of us were taught that we needed to use postpyloric or postduodenal feeding to minimize pancreatic secretions. Although that is best at minimizing pancreatic secretion, randomized controlled trials and meta-analyses have shown that nasogastric or nasoduodenal feeding is equivalent. Simple tube feeding should be the replacement when moving toward total parenteral nutrition, which should really be reserved for rare cases where patients are not meeting nutritional goals, in particular after day 5. Recognize that when you do total parenteral nutrition, you get gut inanition, you get atrophic changes, and you have translocation risks for infection. Early initiation of nasoenteric feeding is important, but it is not that important that you have to get there within the first 2-3 days. In fact, it is not superior to a strategy of attempting oral feeding at 72 hours and maybe waiting until the patient's nausea and vomiting are better. If it is not better at that point, consider tube feeding as opposed to oral feeding, which can usually be initiated when the symptoms improve, typically within 3-5 days. So the sixth point is to be appropriately aggressive in your enteral feeding. You can start to assess that, and not be rushed into doing it, within the first 3 days.

Treatment, Intervention, and Prevention

The seventh point is about antibiotics. Many of us were taught that when severe patients present, maybe we should give them prophylactic antibiotics. The data are strongly against that approach. Infection occurs within the first 2-4 weeks. Prophylactic antibiotics are not beneficial for the prevention of infected necrosis. It is very rare within the first 2 weeks. The development of necrosis and infection is usually related to monomicrobial therapy or infection agents; gram-negative rods, Enterobacter species, or gram-positive organisms, like Staphylococcus, do start to drift in. Again, this is something that is not evident in the first 2 weeks. A pancreatic CT in patients defined as being of concern may show air bubbles in the necrotic pancreas, at which point you should begin initiation of broad-spectrum antibiotics. Aspiration and culture in the first 2-4 weeks are not required. We used to say that that was the way to diagnose infected necrosis. According to current practice standards, you should delay by at least 4 weeks all efforts to make any invasive intervention to allow walling off or maturation of the pancreatic wall and allow this necrotic collection to have demarcation borders. Again, if you have to intervene, it is best to do so percutaneously and not to do something endoscopically or surgically within the first 4 weeks. This is something that is really important. The setup should be to delay as best as we can. If percutaneous [intervention] is needed, then delay it several weeks before you have any concern or direction toward minimally invasive debridement, if this is required. It is clearly appropriate to consider this over what was previously thought as appropriate—necrosectomy and an open surgery procedure; again, this is a game changer.

The eighth point is the concept of what to do in regard to counseling patients. Reducing or abstaining from alcohol and smoking are probably the two biggest things that decrease risk. These patients may need to be counseled or placed in a rehab program. This may be something for which we need to act as stewards rather than just telling them. We may need to employ some risk-mitigation strategies to lead them that way.

The ninth point relates to drug-induced pancreatitis. We think about the classic drugs associated with pancreatitis, like mesalamine, valproate, or 6-MP [6-mercaptopurine]. ACE inhibitors are another one. The pancreatitis associated with these drugs is typically quite minimal. It is very difficult sometimes to attribute a lone cause because these patients sometimes are on a lot of these drugs, and removing all of them is not necessarily possible. Typically, drug-induced pancreatitis is pretty rare. It accounts for less than 5% of patients overall, and the course is typically mild.

The tenth and final point relates to primary prevention, particularly with endoscopic retrograde cholangiopancreatography (ERCP). I invite you to look at a viewpoint that I have just done on this as it relates to primary prevention for ERCP pancreatitis, including those on using lactated Ringer's in concert with rectal indomethacin, as well as reviews of two randomized trials on this topic. The bottom line is that the combination of both therapies, plus emphasis on hydration—in particular the Ringer's lactate—seems to be the preventable way that we can look at risk mitigation for ERCP-related pancreatitis.

A number of things have changed. These are hopefully bell-ringers for a lot of us, myself included. Many of the things that were taught traditionally are no longer the case. The pearls brought up by these experts, I think, are superb. Take a look at this article and read it several times. Look at the issues that I have identified as pearls, but also read the article in detail, because we all deal with acute pancreatitis and there is a significant need for improvement.

I am Dr David Johnson. Thanks again for listening.


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