Managing acute pancreatitis, for all its commonality and ironclad rules of resuscitation, is one of the most data-devoid topics in modern emergency medicine. Even the most cursory examination of societal guidelines dictating practice will reveal a paucity of high-quality research, with most recommendations based on expert consensus from retrospective data dredges and small prospective observational cohorts.
Medical school mantras warning against interfering with the mysterious organ seem to drive recommended practice more than any rigorous investigation. Such scholastic shortcomings are not unique to pancreatitis, of course, but they contrast sharply with the surety with which we have long approached this disease's management. Original investigations and skeptical consideration, however, have begun to hold our practices to account, and re-examination of what was once holy is slowly revolutionizing the diagnostic and therapeutic approach to acute pancreatitis.
Managing acute pancreatitis revolves around supportive care, adequate nutrition, and intravenous hydration. The rationale for hydration—the cornerstone of treatment—is based on the need to resolve the hypovolemia that occurs secondary to vomiting, reduced oral intake, and third-space extravasation. Early hydration also theoretically provides macrocirculatory and microcirculatory support to prevent the cascade of events leading to pancreatic necrosis. (World J Gastroenterol. 2014;20:18092; http://bit.ly/36x8SUi.)
Early fluid therapy is universally recommended, but there is debate about the type, rate, amount, and end-points of fluid replacement. Emerging literature has demonstrated that a less aggressive fluid resuscitation strategy does not lead to worse outcomes, and conversely that administering large volumes of fluid is associated with an increased rate of adverse events. Multiple investigations have shown that patients receiving four or more liters of resuscitative fluids had increased respiratory and infectious complications compared with those under more restrictive fluid strategies. (Curr Opin Crit Care. 2014;20:189.)
The weak data arguing for a conservative fluid approach stand alone in an otherwise barren landscape of literature supporting traditional methods. And temperance in fluid administration seems concordant with hard-won lessons about the harms of large-volume resuscitation learned from managing conditions such as sepsis, burns, and sickle cell disease.
The best fluid volume remains an exciting and evolving question in management, but the recommended type of fluid for administration does seem to have found firm, if not overly impressive, data-driven traction. Balanced crystalloid (lactated Ringer's, PlasmaLyte, etc.) almost certainly edges out the venerable normal saline in managing acute pancreatitis, with one study demonstrating consistent improvement in inflammatory markers. (Clin Gastroenterol Hepatol 2011;9:710.) A meta-analysis also found decreased odds of persistent SIRS criteria (J Dig Dis. 2018;19:335), one trial showed lower rates of post-ERCP pancreatitis (Endoscopy. 2018;50:378), and multiple smaller papers suggested improved mortality outcomes (though never met the hallowed p-value cutoff).
Taken in context with the bevy of literature comparing isotonic fluids in sepsis and other illnesses (SALT-ED, SMART, and nearly every systematic review ever published), there is little question that lactated Ringer's should be the only fluid administered for resuscitation of the pancreatitis patient.
It should come as no surprise that classic concepts in fluid resuscitation are being questioned, perhaps because the most fundamental edict of pancreatitis management—bowel rest and nil per os—has long been debunked and demonstrated as likely harmful in early management. Evidence clearly shows disruption of the gut mucosal barrier during acute pancreatitis, and though hampered by a lack of massive and unassailable top-level data, multiple trials have consistently demonstrated benefits of early enteral nutrition preventing progression to pancreatic necrosis, multi-organ failure, and death. Engaging the bowel in the process of digestion fights back against the microcirculatory consequences and endothelial disruption, promoting nutrition and restoring barriers to bacterial translocation. With little exception, early feeding should be the preferred management strategy in patients with acute pancreatitis. (BMJ. 2004;328:1407; http://bit.ly/38usmuV.)
It's not only a change in therapeutics but also a shifting paradigm in the diagnostic and prognostic approach to pancreatitis that we've witnessed. Diagnosing pancreatitis is straightforward—two of three positives: a serum lipase greater than three times the normal limit, characteristic abdominal pain, or imaging findings consistent with pancreatic inflammation—yet some still cling to the antiquated amylase or insist on advanced imaging even after the diagnosis has been made.
A major factor complicating the diagnosis, however, is the failure to discriminate its mild and severe forms in the initial stages. Such differentiation is critical in the ED where therapeutic momentum and disposition can drive outcomes. Classic scoring systems such as Ranson's criteria require days' worth of information for prognostication, and overall perform poorly in the emergency department. A newer algorithm, the Bedside Index of Severity in Acute Pancreatitis (BISAP) score, uses clinically relevant and easily obtainable input. It assesses five criteria: blood urea nitrogen (BUN) greater than 25 mg/dL, age over 60, impaired mental status, SIRS, and pleural effusion. A BISAP score of greater than 2 is associated with a 10-fold increase in mortality risk. Small trials showed that BISAP performs similarly to other (more complex) scoring systems. (Am J Gastroenterol. 2010;105:435.)
BISAP performed poorly in other trials, however, suggesting that scoring systems themselves perform differently depending on the population, setting, and causative etiology of pancreatitis and that the concept of a universal scoring system may be elusive. (Curr Opin Crit Care. 2014;20:189.) Many of us as residents or medical students may have faithfully put lab results into a clinical calculator to gauge prognosis, but it has become abundantly clear that the heterogenous nature of pancreatitis, its synergistic insult to comorbidities, and its fickle response to subtle differences in management create a conundrum inherently resistant to prediction, and novel models are needed to improve predictive accuracy and ensure the best disposition from the ED.
Pancreatitis is commonly encountered in the ED, but it is beset by profound variability and inconsistency in diagnosis, treatment, and prognosis, which are induced by striking shortcomings in data to guide practice and a silently shifting evidence base that has received little attention or focus despite the disease's frequency and potential severity. It is critical that emergency physicians recognize long-held misconceptions and parochial practices and embrace our slowly evolving understanding of best practices in managing acute pancreatitis.
Dr. Pescatoreis an emergency physician in New Jersey and the host with Ali Raja, MD, of the podcast EMN Live, which focuses on hot topics in emergency medicine:http://bit.ly/EMNLive. Follow him on Twitter@Rick_Pescatore, and read his past columns athttp://bit.ly/EMN-Pescatore.