Predicting severity of AP should be simple and allow prediction early in the patient’s course. This is best accomplished by the Bedside Index for Severity in Acute Pancreatitis (BISAP) or SIRS, which can predict severity within the first 24 hours. The BISAP includes blood urea nitrogen (BUN) greater than 25 mg/dl, impaired mental status (Glasgow Coma Scale score <15), SIRS score 2 or above, age over 60 years, and pleural effusion. One point is given for each and a score of more than 3 indicates an increased risk of death [54]. A follow‐up evaluation by Singh et al. [55] on the BISAP score reported that a score of 3 or more was associated with an increased risk of developing organ failure, persistent organ failure, and pancreatic necrosis.
SIRS is defined by the presence of two or more of heart rate above 90 bpm, respiratory rate above 20 breaths per minute or PaCO 2 below 32 mmHg (4.3 kPa), body temperature below 36 or above 38°C, and leukocyte count less than 4 × 109/l or more than 12 × 109/l. Its presence during the first 24 hours of admission has high sensitivity for predicting severe disease (85%). However, persistent SIRS predicted the development of persistent organ failure in only a minority of patients [56].
On admission, hematocrit above 44% and rise in BUN at 24 hours may be optional predictive tools. Reducing BUN and hematocrit should be utilized to guide fluid resuscitation over the first 12–24 hours and are an accurate predictor of death [57]. We agree with Forsmark and Yadav [58] that monitoring serum BUN and hematocrit along with SIRS over the first 48 hours is simple and an effective scoring system for predicting severe AP.
Classification
The revised Atlanta Classification of Acute Pancreatitis classifies severity into mild, moderately severe and severe using both clinical and radiographic criteria (Table 1.4) [59]. In mild AP, patients usually improve rapidly with supportive care (fluid resuscitation) and mortality is rare, except in patients with severe comorbidity [60]. Patients with acute mild pancreatitis by definition do not have local complications such as peripancreatic collection, sterile pancreatic necrosis, and exacerbation of a comorbidity, and they do not have a modified Marshall score of 2 or more that defines the presence of organ failure (respiratory, renal, cardiovascular) [59].
Moderately severe AP is defined as the presence of transitory organ system failure (<48 hours) and/or local or systemic complications exacerbating comorbid disease without persistent organ failure [59]. Severe AP is characterized by single or multiple organ failure for longer than 48 hours, determined by analysis of the respiratory, renal and/or cardiovascular systems using the modified Marshall scoring system. Patients with persistent SIRS for longer than 48 hours, or with infected necrosis, are usually in this category, although infected necrosis can be present without organ failure. (Table 1.5).
Table 1.4 Classification of acute pancreatitis.
Source: adapted from Banks et al. [59].
| Mild | Moderate | Severe | |
|---|---|---|---|
| Organ failure | None | Transient (resolves within 48 hours) | Persistent organ failure (>48 hours) of one or more organs |
| Local complications | None | Yes, without persistent organ failure | |
| Systemic complications | None | Yes, without persistent organ failure |
Table 1.5 Predictors of severe acute pancreatitis.
Source: adapted from Forsmark et al. [52].
| Patient | Age, obesity (BMI >30), altered mental status, numerous and severe comorbidities including coronary artery disease, congestive heart failure, chronic obstructive pulmonary disease, diabetes mellitus, chronic liver disease, long history of alcohol abuse |
| SIRS | Present and persists >48 hours |
| Laboratory | Hematocrit >44% and no decrease with hydration Urea nitrogen >20 mg/dl (>7.1 mmol/l) rising and/or no decrease with hydration, and/or elevated creatinine >1.8 mg/dl (>159 mmol/l) |
| Imaging | Pleural effusion or infiltrates |
Treatment
The foundation for therapy of patients with AP is fluid restoration, as the major effect of pancreatic inflammation is fluid sequestration. The goals of fluid therapy are to replenish the lost circulatory fluids to maintain organ system perfusion and oxygenation including the pancreas. Unfortunately, our recommendations are not based on conclusive scientific information [61]. Sinha et al. [62] reported variables that independently predicted increased fluid sequestration within the first 48 hours after hospital admission; these included younger age (<40 years), alcohol etiology, hemoconcentration, and SIRS. Increasing volumes of fluid sequestration were associated with longer hospitalizations, persistent SIRS, and persistent organ system failure [63]. Buxbaum et al. [64] reported a randomized trial of patients with nonsevere AP to aggressive (20 ml/kg bolus followed by 3 ml/kg per hour vs. standard therapy with 10 ml/kg bolus followed by 1.5 ml/kg per hour) hydration with Ringer’s lactate solution. They found that a significantly higher proportion of patients treated with aggressive compared with standard hydration showed clinical improvement. In addition to higher volumes of fluid, early fluid resuscitation reduces morbidity among patients with AP. Warndorf et al. [65] reported that early resuscitation, defined as the administration of one‐third or more of the total 72‐hour fluid volume within 24 hours of presentation, was associated with decreased SIRS as well as reduced organ failure, lower rate of admissions to the intensive care unit (ICU), and reduced length of hospitalization; the fluid of choice is Ringer’s lactate [65]. The clinical goals of fluid replacement therapy are to achieve hemodynamic stability. Clinically, we follow the parameters of heart rate, urine output, and blood pressure; in addition, we follow the laboratory markers BUN and hematocrit. Thus, the volumes infused are based on the patient’s vital signs, incorporating blood pressure, pulse and respiratory rates, age, cardiac and renal disease, laboratory values (BUN, creatinine and hematocrit), and the presence of SIRS. This so‐called goal‐directed therapy for fluid management is defined as titration of intravenous fluids to specific clinical and biochemical targets of perfusion [66].
Table 1.6 Fluid therapy for patients with moderately severe or severe acute pancreatitis.
Source: adapted from DiMagno MJ. Clinical update on fluid therapy and nutritional support in acute pancreatitis. Pancreatology 2015;15(6):583–588.
| Bolus of Ringer’s lactate: administer 1 liter in the emergency roomInfusion of Ringer’s lactate at 5–10 ml/kg per hour until clinical hemodynamic stability and laboratory parameters are reachedChange intravenous fluid rate to 3 ml/kg per hour once parameters are reached |
Fluid therapy is most effective if given early in the course of AP. This was shown by an international multicenter