Recent national survey data indicate a rising incidence of acute pancreatitis in the United States, attributed primarily to a rise in biliary pancreatitis. At present, there are more than 300,000 admissions for acute pancreatitis on an annual basis at a direct cost exceeding $2 billion. Although acute pancreatitis is typically a self-limited illness, up to 15% of patients experience a severe life-threatening form of disease. Length of stay and direct costs vary considerably by severity of disease. In this age of cost containment, modern management of acute pancreatitis has evolved to emphasize effective interventions for prevention and management of complications, as well as appropriate resource utilization. This article addresses recent developments in the management of acute pancreatitis starting from initial hospital presentation extending through discharge and includes discussion of approaches secondary prevention.
Initial Assessment of Severity
Since the Ranson criteria were originally published in 1974, numerous clinical prognostic scoring systems have been developed, the most prominent of which is the APACHE II score. Although it is a widely validated instrument and clearly useful for research purposes, the APACHE II score has failed to gain widespread application in clinical practice as a result of its complexity. A simplified scoring system known as the Bedside Index of Severity in Acute Pancreatitis (BISAP) was developed based on data from 177 U.S hospitals and more than 17,000 cases of acute pancreatitis ( Table 1 ) . This five-factor scoring system contains elements that are routinely available at the time of hospital admission and its use during the initial 24 hours of hospitalization has now been validated in several prospective cohort studies. Two specific elements of the BISAP score warrant further discussion. First, blood urea nitrogen (BUN) has received renewed interest as an early prognostic marker in acute pancreatitis. Either an elevated BUN at admission or early rise in BUN was found to be a strong risk factor for mortality in several retrospective and prospective cohort studies of acute pancreatitis. Another component of the BISAP, the systemic inflammatory response syndrome (SIRS), has also been evaluated as a potential risk factor for severe acute pancreatitis ( Table 2 ). Several prospective cohort studies of acute pancreatitis have shown that persistent SIRS, lasting 48 hours or more, is associated with increased risk of necrosis, multiorgan failure, and death ( Fig. 1 ) .
Table 1
BISAP score and its associated mortality
Parameters
Value
If Present, Points Allocated
Serum BUN
>25
1
Mental status
Impaired
1
SIRS
Present
1
Age of the patient
>60 years
1
Pleural effusion
Present
1
Total Score
Mortality (%)
0
0.20
1
0.60
2
2
3
5–8
4
13–19
5
22–27
Table 2
SIRS criteria, defined by the presence of two or more
Parameters
Value
Temperature
<36°C or >38°C
Heart rate
>90 per minute
Respiratory rate
>20 per minute or Pa co 2 <32 mm H g
White blood cell count
<4000 cells/mm 3 or >12,000 cells/mm 3 or 10% bands
Fig. 1
Association of SIRS with Severe Acute Pancreatitis. Pers OF = persistant organ failure; Necrosis = pancreatic Necrosis; ICU = ICU admission; Mortality = Death.
Initial Assessment of Severity
Since the Ranson criteria were originally published in 1974, numerous clinical prognostic scoring systems have been developed, the most prominent of which is the APACHE II score. Although it is a widely validated instrument and clearly useful for research purposes, the APACHE II score has failed to gain widespread application in clinical practice as a result of its complexity. A simplified scoring system known as the Bedside Index of Severity in Acute Pancreatitis (BISAP) was developed based on data from 177 U.S hospitals and more than 17,000 cases of acute pancreatitis ( Table 1 ) . This five-factor scoring system contains elements that are routinely available at the time of hospital admission and its use during the initial 24 hours of hospitalization has now been validated in several prospective cohort studies. Two specific elements of the BISAP score warrant further discussion. First, blood urea nitrogen (BUN) has received renewed interest as an early prognostic marker in acute pancreatitis. Either an elevated BUN at admission or early rise in BUN was found to be a strong risk factor for mortality in several retrospective and prospective cohort studies of acute pancreatitis. Another component of the BISAP, the systemic inflammatory response syndrome (SIRS), has also been evaluated as a potential risk factor for severe acute pancreatitis ( Table 2 ). Several prospective cohort studies of acute pancreatitis have shown that persistent SIRS, lasting 48 hours or more, is associated with increased risk of necrosis, multiorgan failure, and death ( Fig. 1 ) .
Table 1
BISAP score and its associated mortality
Parameters
Value
If Present, Points Allocated
Serum BUN
>25
1
Mental status
Impaired
1
SIRS
Present
1
Age of the patient
>60 years
1
Pleural effusion
Present
1
Total Score
Mortality (%)
0
0.20
1
0.60
2
2
3
5–8
4
13–19
5
22–27
Table 2
SIRS criteria, defined by the presence of two or more
Parameters
Value
Temperature
<36°C or >38°C
Heart rate
>90 per minute
Respiratory rate
>20 per minute or Pa co 2 <32 mm H g
White blood cell count
<4000 cells/mm 3 or >12,000 cells/mm 3 or 10% bands
Fig. 1
Association of SIRS with Severe Acute Pancreatitis. Pers OF = persistant organ failure; Necrosis = pancreatic Necrosis; ICU = ICU admission; Mortality = Death.
Early Fluid Resuscitation
Vigorous fluid resuscitation is a cornerstone of therapy during the early management of acute pancreatitis. However, recommendations on fluid resuscitation have been based primarily on expert opinion and data from animal models. One retrospective study suggested that timing of fluid resuscitation may be more important than the total volume of fluid administered; in this study, patients receiving a greater proportion of their total fluid resuscitation during the initial 24 hours had reduced complications. However, there are potential hazards associated with vigorous fluid resuscitation, such as pulmonary sequestration, as suggested by a prospective cohort study from Spain. The data are difficult to interpret because fluid resuscitation parameters were driven by clinician judgment, and as such patients with more severe disease would most likely be those receiving the more aggressive fluid resuscitation. An additional randomized controlled trial (RCT) from China showed that patients who were randomized to rapid hemodilution (targeting hematocrit <35%) received on average more than 10 L of fluid on the first hospital day and experienced greater frequency of sepsis and higher mortality. Although these findings are difficult to generalize to Western populations because of variations in the underlying treatment of acute pancreatitis, these findings underscore the potential risks associated with very aggressive fluid resuscitation without hemodynamic monitoring. As a result of these potential concerns, a recent RCT evaluated the impact of a targeted approach to early fluid resuscitation in acute pancreatitis. Although the study was underpowered to assess the effect of a goal-directed resuscitation algorithm because of a significant crossover effect, the study investigators found a reduction in SIRS based on the type of fluid used for initial resuscitation. Specifically, use of the more pH-balanced lactated Ringer’s solution led to greater reduction in SIRS compared to the use of normal saline. In addition, there was no evidence of pulmonary sequestration among the 40 patients included in the trial.
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