Pancreatitis and Liver Failure
The conditions described in this chapter (i.e., necrotizing pancreatitis and liver failure) share the following features: (a) both are associated with injury in multiple organs, (b) both are plagued by infections from pathogens that reside in the bowel, (c) the management of both conditions is mostly supportive care, and (d) mortality rates remain high.
I. Acute Pancreatitis
A. Classification
Two types of acute pancreatitis are identified (1):
Edematous pancreatitis is the most common form of pancreatitis, and is characterized by inflammatory infiltration of the pancreas without involvement of other organs. The clinical presentation is usually a self-limited period of abdominal pain, nausea, and vomiting. The mortality rate is low (<2%) (2), and management rarely requires ICU-level care.
Necrotizing pancreatitis occurs in 10–15% of cases (1), and is characterized by areas of necrotic destruction in the pancreas, usually accompanied by progressive systemic inflammation and inflammatory injury in one or more extrapancreatic sites (e.g., lungs, kidneys, and circulatory system) (3). The mortality rate can be as high as 40% (2), and management requires ICU-level care.
B. Etiology and Diagnosis
The conditions that produce pancreatitis are shown in Table 31.1. About 90% of cases are the result of gallstones (40%), alcohol abuse (30%), or are idiopathic (20%) (2,4,5).
The diagnosis of acute pancreatitis requires the following (1):
An increase in the serum levels of pancreatic enzymes (amylase and lipase) to at least 3 times the upper limit of normal.
Evidence of pancreatitis on contrast-enhanced computed tomography.
Table 31.1 Etiology of Acute Pancreatitis | |||
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C. Pancreatic Enzymes
1. Amylase
Amylase is an enzyme that cleaves starch into smaller
polysaccharides. The principal sources of amylase are the pancreas, salivary glands, and fallopian tubes.
polysaccharides. The principal sources of amylase are the pancreas, salivary glands, and fallopian tubes.
Serum amylase levels begin to rise 6–12 hours after the onset of acute pancreatitis, and they return to normal in 3–5 days.
An increase in serum amylase levels to 3 times the upper limit of normal (the threshold for the diagnosis of acute pancreatitis) has a high sensitivity (>90%) but a low specificity (as low as 70%) for the diagnosis of acute pancreatitis (6).
The low specificity of serum amylase is a reflection of the numerous conditions that can elevate serum amylase levels, which are listed in Table 31.2 (7).
Note: The reference range for serum amylase is not mentioned because it often varies in different clinical laboratories.
2. Lipase
Lipase is an enzyme that hydrolyses triglycerides to form glycerol and free fatty acids. The principal sources of lipase are the tongue, pancreas, liver, intestine, and circulating lipoproteins.
Serum lipase levels begin to rise 4–8 hours after the onset of acute pancreatitis (earlier than the rise in serum amylase), and the serum levels remain elevated for 8–14 days (longer than the rise in serum amylase).
Like amylase, there are several conditions that can elevate serum lipase levels, as shown in Table 31.2. However, unlike amylase, nonpancreatic conditions rarely raise serum lipase levels high enough to overlap with the levels seen in acute pancreatitis (8).
An increase in serum lipase to three times the upper limit of normal has a sensitivity and specificity of 80–100% for acute pancreatitis (6). Therefore, serum
lipase is more specific than serum amylase for the diagnosis of acute pancreatitis.
RECOMMENDATION: The serum lipase can be used alone for the diagnostic evaluation of pancreatitis. Adding the serum amylase does not increase diagnostic accuracy (6).
Table 31.2 Sources of Elevated Serum Amylase and Lipase | ||||||
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D. Computed Tomography
Contrast-enhanced computed tomography (CT) is the most reliable diagnostic test for acute pancreatitis, and can identify the type of pancreatitis (edematous vs. necrotizing) and localized complications (e.g., infection).
A contrast-enhanced CT image of edematous pancreatitis is shown in Figure 31.1. The pancreas is thickened and enhances completely, and the border of the pancreas
is blurred, which is characteristic of pancreatic edema.
FIGURE 31.1 Contrast-enhanced CT image showing edematous pancreatitis. The pancreas (outlined by the dotted line) is enlarged and enhances completely. There is also blurring of the pancreatic border, which is characteristic of edema formation.
A contrast-enhanced CT image of necrotizing pancreatitis is shown in Figure 31.2. Note the large area that is not contrast-enhanced in the region of the neck and body of the pancreas. This represents pancreatic necrosis. The full extent of pancreatic necrosis may not be evident on CT imaging for the first week after the onset of symptoms (1).
Without IV contrast, CT imaging is less likely to distinguish between edematous and necrotizing pancreatitis.
E. Biliary Evaluation
Since gallstones are the leading cause of acute pancreatitis in the United States (4), an evaluation of the gall bladder and
biliary tree is advised in all cases of acute pancreatitis. Contrast-enhanced CT images may suffice for this evaluation; otherwise, ultrasonography is recommended.
biliary tree is advised in all cases of acute pancreatitis. Contrast-enhanced CT images may suffice for this evaluation; otherwise, ultrasonography is recommended.
 FIGURE 31.2 Contrast-enhanced CT image showing necrotizing pancreatitis, which is shown by the spotty enhancement of the pancreas. A large area of necrosis is indicated by the arrows. Image from Reference 1. |
II. Severe Pancreatitis
Severe pancreatitis is defined as acute (usually necrotizing) pancreatitis that is associated with persistent (>48 hrs) injury in at least one other organ system (1).
The extrapancreatic organ injury is inflammatory in origin, and typically involves the lungs (acute respiratory distress syndrome), kidneys (acute kidney
injury), and circulatory system (hypotension and circulatory shock).
The management of severe pancreatitis in the ICU includes: (a) circulatory support, (b) nutritional support, and (c) treating intraabdominal complications (e.g., infection).
A. Circulatory Support
Circulatory support includes volume resuscitation and vasopressor drugs, if necessary.
1. Volume Resuscitation
Severe pancreatitis is accompanied by loss of intravascular fluid through leaky systemic capillaries, and the resulting hypovolemia can produce additional pancreatic necrosis. As a result, aggressive volume resuscitation is advised early in the course of severe pancreatitis (9). The typical regimen for volume resuscitation is summarized as follows:
Using an isotonic crystalloid fluid, begin by infusing 20 mL/kg (about 1.5 liters) over 60 to 90 minutes.
Follow with an infusion rate up to 250 mL/hr for the next 24–48 hours, to maintain a mean arterial pressure ≥65 mm Hg, and a urine output ≥0.5 mL/kg/hr.
CAUTION: Aggressive volume infusion has not been shown to improve outcomes in severe pancreatitis (10), and this practice promotes edema formation, which can aggravate conditions like ARDS (see Chapter 17, Section III-A), and increases the risk of abdominal compartment syndrome (see Chapter 26, Section III-D-1). Therefore, after the initial 24–48 hours of aggressive volume infusion, the infusion rate of IV fluids should be reduced to match the urine output.
2. Vasopressor Therapy
There are no official recommendations regarding vasopressor therapy in severe pancreatitis, but norepinephrine (2–20 μg/min) is an appropriate choice. All vasoconstrictor drugs can reduce splanchnic blood flow (especially epinephrine), and could aggravate pancreatic necrosis, so careful titration of infusion rates (and avoiding epinephrine) is advised.
B. Nutrition Support
Nutrition support should be started early (within 48 hours after the onset of illness) using enteral tube feedings, if possible (11).
The preference for enteral nutrition is based on the ability of tube feedings to exert a trophic effect on the bowel mucosa (see Chapter 37). Enteral nutrition is associated with fewer infections, less multiorgan failure, and a lower mortality rate than total parenteral nutrition in patients with severe pancreatitis (12).
Tube feedings should be infused into the jejunum using long feeding tubes that can be placed with fluoroscopic or endoscopic guidance. Although intragastric feedings are not currently advised, one small study has shown no apparent harm from nasogastric feedings in severe pancreatitis (13).Related posts:
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