The diagnosis of AP may be often overlooked [8]. While most patients present with abdominal pain, a small proportion of patients may present without any pain [9,10]. Very sick patients presenting to the emergency room may be sedated, intubated, or unconscious from medical conditions and it is often not possible to elicit history regarding abdominal pain or perform a good abdominal examination. In rare patients the pain may be only in the right upper quadrant or even in the lower abdomen. Unless routine blood work reveals elevated levels of amylase and/or lipase, a true pancreatitis might go undiagnosed for many days, while the patient is being treated for other causes of SIRS [11]. Serum amylase level has several limitations: it can be elevated in nonpancreatic diseases, and it returns to normal rapidly. Therefore, serum lipase, either alone or in combination with amylase, is preferred for diagnosis of AP [12]. However, physicians should remember that both amylase and lipase could be elevated in some critically ill patients without pancreatitis [11]. On initial presentation, contrast‐enhanced computed tomography (CT) and/or magnetic resonance imaging (MRI) of the pancreas should be performed only in patients where the diagnosis is uncertain from clinical and laboratory evaluation alone or in those where initial evaluation suggests a severe AP, in order to look for local complications like necrosis [13].
Initial Work‐up for Etiology
When considering the diagnosis of AP, emergency room clinicians should order basic laboratory which including complete blood count, lipase, amylase, liver function tests, blood urea nitrogen, creatinine, LDH, and triglycerides.
Gallstones and alcohol are the two most common causes of AP. Gallstones are estimated as culprit in 40–70% of cases [14]. Therefore, a transabdominal ultrasound should be obtained in all patients presenting with AP to the emergency room [15]. However, if the patient has normal liver function tests at the time of diagnosis of AP and has gallstones, the gallstones may not be the cause of AP as evidenced by recurrence of AP in approximately 34% of cases after cholecystectomy [16]. Alcohol intake is the second most common cause, noted in 25–40% of patients [14,17]. For alcohol to cause AP, it is considered that the patient should have a history of chronic alcohol abuse, consuming more than 50 g of alcohol per day for more than five years. Binge drinking in such patients can cause AP after an interval from cessation of drinking [18,19]. However, it should be noted that only a small proportion of such heavy drinkers (<5%) will develop pancreatitis. The presence of an abnormality in the gene for claudin‐2 (CLDN2) may explain those who might suffer pancreatic disease [20]. A thorough alcohol history should be obtained in all patients presenting with AP.
In absence of gallstones or significant alcohol intake, other less common causes should be considered. Hypertriglyceridemia (triglyceride levels >1000 mg/dl) can cause AP [21]. Patients who have undergone recent ERCP could develop acute post‐ERCP pancreatitis as an adverse event from the procedure [22,23]. Many medications have been hypothesized to cause pancreatitis. Some of the well‐known culprits are 6‐mercaptopurine or azathioprine, L‐asparaginase, isoniazid, loop diuretics, and didanosine [24]. Rarely, pancreatic neoplasm or cysts (intraductal papillary mucinous neoplasm) can present as AP. If no obvious etiology is found after initial work‐up with blood tests and transabdominal ultrasound, further work should be done by seeking expert consultation.
Severity Assessment, Triage, and Disposition
There is very little data that can be used to assess which patients with AP can safely be discharged from the emergency room. Whitlock et al. [25] looked at scoring systems to predict readmission within 30 days and identified the following discharge characteristics as risk factors: inability to tolerate a solid diet, any gastrointestinal symptoms (nausea, vomiting, diarrhea), pain, pancreatic necrosis, and treatment with antibiotics. Although this is primarily for inpatient hospitalization, one could argue this could also be used in the emergency room.
It is crucial to promptly identify patients who need intensive care unit versus medical floor hospitalization and those who need subspecialist consultation. Although there are numerous scoring systems for assessing the severity of AP, most of these systems have been criticized as they require more than 48–72 hours before score parameters become evident and are therefore not very useful in the emergency room setting [26,27]. The most practical and useful evaluation includes assessment of SIRS criteria [6]. It is critical in the early phase of management to (i) determine patient‐related factors such as age and body mass index; (ii) perform a careful clinical examination; and (iii) utilize the available laboratory results to assess early fluid losses (e.g. rising blood urea nitrogen, creatinine, hematocrit), hypovolemic shock, and signs of organ dysfunction (Table 7.1).
Specialty Consultation
Prompt specialist consultation should be sought for patients with AP. A routine gastroenterologist or pancreatologist consultation should be obtained for all patients presenting with AP. When gallstone etiology is suspected, a surgical consultation for possible early cholecystectomy during the same admission is recommended by American Gastroenterological Association (AGA) guidelines [28,29]. Some of the patients with gallstone pancreatitis may have concomitant acute cholangitis and/or choledocholithiasis from gallstones obstructing the common bile duct. Cholangitis, as in those patients without AP, is an indication for urgent ERCP [29]. If liver dysfunction and/or dilated bile ducts are noted on the ultrasound, consultation with an interventional endoscopist for possible ERCP is recommended.
Table 7.1 Clinical findings associated with a severe course for initial risk assessment.a
Source: Tenner et al. [5]. Reproduced with permission of Wolters Kluwer Health, Inc.
| Patient characteristics Age >55 years Obesity (BMI >30 kg/m2) Altered mental status Comorbid disease Systemic inflammatory response syndrome (SIRS) Presence of more than two of the following criteria: Pulse >90 bpm Respirations >20/min or PaCO 2 >32 mmHg Temperature >38°C or <36°C WBC count >12 × 109/l or <4 × 109/l or >10% immature neutrophils (bands) Laboratory findings Blood urea nitrogen (BUN) >20 mg/dl Rising BUN Hematocrit (HCT) >44% Rising HCT Elevated creatinine Radiology findings Pleural effusions Pulmonary infiltrates Multiple or extensive extrapancreatic collections |
a The presence of organ failure and/or pancreatic necrosis defines severe acute pancreatitis.
BMI, body mass index; WBC, white blood cell.
Management
First‐line Medical Management: Fluid Resuscitation
Time is of the essence in managing AP. There is no pharmacological therapy for AP. Fluid resuscitation is the mainstay of therapy in AP, where patients often present in a volume‐depleted state due to vomiting, poor oral intake, and insensible losses. An acute surge in release of inflammatory mediators results in increased vascular permeability and third spacing of fluids [30]. Early administration of adequate fluid therapy to prevent hypovolemia and organ hypoperfusion is critical in the management of AP. Despite multiple guidelines and publications, a recent exhaustive technical review by the AGA observed that there is no clear evidence to recommend the volume, type, duration, or rate of fluid administration [28]. Current clinical guidelines recommend goal‐directed fluid therapy which focuses on administering intravenous fluids and monitoring heart rate, mean arterial pressure, central venous pressure, urine output, blood urea nitrogen concentration, and hematocrit [29]. Inadequate fluid resuscitation in the first 24 hours, as evidenced by hemoconcentration, has been associated with increased rate of pancreatic necrosis [31,32]. Aggressive intravenous fluid resuscitation during the initial few hours provides microcirculatory and macrocirculatory support to prevent development of pancreatic necrosis [33].