Type of Intravenous Fluid to Administer
Recent randomized controlled trials have compared normal saline and lactated Ringer’s as an optimal fluid for resuscitation in AP [41,42]. These trials used surrogate markers of severity as end points and did not necessarily use more salient clinical outcomes such as mortality and organ failure. However, lactated Ringer’s solution appears to be more beneficial, resulting in fewer patients developing SIRS when compared with normal saline [42,43]. Although the data is still limited, current clinical guidelines (ACG, IAP/APA) recommend using Ringer’s lactate as the preferred intravenous fluid over normal saline [5,29,44]. The AGA technical review analyzed two studies using hydroxyethyl starch (HES) in AP and noted that multiorgan failure was significantly increased with administration of HES [28]. AGA clinical guidelines do not recommend using HES in AP [29].
Antibiotics
Routine administration of antibiotics in patients with AP is not currently recommended. In the past, prophylactic antibiotics were administered to decrease risk of infection in pancreatic necrosis. A few unblinded studies showed that imipenem was beneficial in preventing infection in pancreatic necrosis [45]. However, better‐conducted studies have shown that prophylactic antibiotics do not reduce risk of infection in necrotizing pancreatitis [46,47]. The AGA technical review observed that recent clinical trials showed no difference in risks of infected pancreatic and peripancreatic necrosis or mortality with prophylactic antibiotic usage [28]. Patients presenting with concomitant cholangitis or other coexisting infection should receive antibiotics in the emergency room. In all other patients, both mild and severe pancreatitis, routine antibiotic prophylaxis is not recommended [29].
In many instances, severe AP is indistinguishable from sepsis or concomitant cholangitis. In such scenarios when infection is suspected, antibiotics should be promptly administered after drawing blood sample for cultures. Once blood cultures are found to be negative, and no other source of infection is identified, antibiotics should be discontinued [5,29].
Pain Control
AP can result in severe abdominal pain, which should be treated in the emergency room. Abdominal pain is often reproduced early in the course with oral intake and patients should be kept nil by mouth for the initial few hours when the pain is severe [48]. Mild abdominal pain can be treated with intravenous acetaminophen or tramadol, although most patients require opioid analgesics for better pain control.
Nutrition
Bowel rest is no longer the standard of care in AP. In the past, it was believed that allowing patients to take anything by mouth had a theoretical risk of stimulating the pancreas and thereby worsening pancreatitis. However, several studies have now shown that patients initiated on oral feeding early in the course of AP have shorter hospital stay, reduced infectious complications, and decreased mortality [28,49–52]. The current recommendation to initiate early oral feeding relies on the fact that enteral nutrition likely serves to protect the mucosal barrier of the gut and diminish bacterial translocation, thereby reducing the risk of developing infections in the pancreatic necrosis [29]. When compared to parenteral nutrition, early enteral nutrition is associated with decreased rates of overall infection and lower risk of complications [28,49,53,54]. Patients who cannot tolerate immediate oral feeding may require nasogastric tube placement for nutritional support. There is no advantage in placing a nasojejunal tube (post‐pyloric) compared with gastric tube placement [54,55].
Summary
Clinicians in the emergency room play a crucial role in the management of AP. Prompt accurate diagnosis is usually made by physical examination, laboratory assessment (including lipase and liver function tests), and right upper quadrant ultrasound scan. Certain special scenarios may warrant CT or MRI in the emergency room. A quick risk stratification facilitates appropriate triage and suitable consultations. Initiating judicious early aggressive fluid resuscitation is the cornerstone of management of AP. After providing adequate pain control, early oral feeding should be encouraged. Pancreatitis, a potentially fatal disease, can be managed effectively in the first few hours of presentation and this can change the natural course of disease towards a better outcome.
References
1 1 Peery AF, Crockett SD, Murphy CC, et al. Burden and cost of gastrointestinal, liver, and pancreatic diseases in the United States: update 2018. Gastroenterology 2019; 156:254–72.e11.
2 2 Yadav D, Lowenfels AB. Trends in the epidemiology of the first attack of acute pancreatitis: a systematic review. Pancreas 2006; 33:323–330.
3 3 Fagenholz PJ, Castillo CF, Harris NS, et al. Increasing United States hospital admissions for acute pancreatitis, 1988–2003. Ann Epidemiol 2007; 17:491–497.
4 4 Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis – 2012: revision of the Atlanta classification and definitions by international consensus. Gut 2013; 62:102–111.
5 5 Tenner S, Baillie J, DeWitt J, Vege SS. American College of Gastroenterology guideline: management of acute pancreatitis. Am J Gastroenterol 2013; 108:1400–1415; 1416.
6 6 Singh VK, Wu BU, Bollen TL, et al. Early systemic inflammatory response syndrome is associated with severe acute pancreatitis. Clin Gastroenterol Hepatol 2009; 7:1247–1251.
7 7 Jacobs ML, Daggett WM, Civette JM, et al. Acute pancreatitis: analysis of factors influencing survival. Ann Surg 1977; 185:43–51.
8 8 Lankisch PG, Schirren CA, Kunze E. Undetected fatal acute pancreatitis: why is the disease so frequently overlooked? Am J Gastroenterol 1991; 86:322–326.
9 9 Kesavan CR, Pitchumoni CS, Marino WD. Acute painless pancreatitis as a rare complication in Legionnaires disease. Am J Gastroenterol 1993; 88:468–469.
10 10 Lankisch PG, Muller CH, Niederstadt H, Brand A. Painless acute pancreatitis subsequent to anticholinesterase insecticide (parathion) intoxication. Am J Gastroenterol 1990; 85:872–875.
11 11 Muniraj T, Dang S, Pitchumoni CS. Pancreatitis or not? Elevated lipase and amylase in ICU patients. J Crit Care 2015; 30:1370–1375.
12 12 Gumaste VV, Roditis N, Mehta D, Dave PB. Serum lipase levels in nonpancreatic abdominal pain versus acute pancreatitis. Am J Gastroenterol 1993; 88:2051–2055.
13 13 Stimac D, Miletic D, Radic M, et al. The role of nonenhanced magnetic resonance imaging in the early assessment of acute pancreatitis. Am J Gastroenterol 2007; 102:997–1004.
14 14 Gullo L, Migliori M, Olah A, et al. Acute pancreatitis in five European countries: etiology and mortality. Pancreas 2002; 24:223–227.
15 15 Moreau JA, Zinsmeister AR, Melton LJ III, DiMagno EP. Gallstone pancreatitis and the effect of cholecystectomy: a population‐based cohort study. Mayo Clin Proc 1988; 63:466–473.
16 16 Trna J, Vege SS, Pribramska V, et al. Lack of significant liver enzyme elevation and gallstones and/or sludge on ultrasound on day 1 of acute pancreatitis is associated with recurrence after cholecystectomy: a population‐based study. Surgery 2012; 151:199–205.
17 17 Lowenfels AB, Maisonneuve P, Sullivan T. The changing character of acute pancreatitis: epidemiology, etiology, and prognosis. Curr Gastroenterol Rep 2009; 11:97–103.
18 18