The Gastrointestinal System
BASIC PHYSIOLOGY
The reader is referred to gastrointestinal disease textbooks to review the basic physiology of the intestinal tract. This chapter will highlight gastrointestinal pathophysiology linked principally to surgical critical illness.
THE RESPONSE TO HYPOPERFUSION
Diminished cardiac output sufficient to stimulate “flow receptors” results in the activation of neuroendocrine mechanisms that increase peripheral resistance (see chap. 3). The gastrointestinal tract (GIT) is the principal location of this increase in resistance. Activation of the sympathetic nervous system and constriction of GIT afferent arterioles result in a proportional reduction in intestinal blood flow (i.e., if cardiac output is decreased by 25%, this process decreases intestinal blood flow by 25%). However, activation of angiotensin II and vasopressin release results in a disproportionate reduction in perfusion via further arterial constriction. Hypersensitivity of mesenteric arteries to angiotensin II appears to be the principal mechanism of this response (1).
THE RESPONSE TO INFLAMMATION
Since inflammation begets hypoperfusion, severe systemic inflammation may result primarily in a global or regional decrease in perfusion to the splanchnic organs, thereby producing hypoxic injury. However, following hypoperfusion the GIT is a potent site of reperfusion physiology (hypoperfusion begets inflammation). Toxic oxygen moities as well as activation of inflammatory mediators and cells can result in apoptosis of intesintal lymphatic and mucosal cells along with disturbances in GIT function that may or may not be associated with anatomical damage (Table 8.2) (3, 4, 5, 6, 7, 8).
Similar to the effect of severe hypoperfusion, severe inflammation can interfere with the mucosal barrier function of the GIT that prevents the migration of microorganisms and the breakdown products of microorganisms from gaining access to extraluminal sites (e.g., peritoneal cavity, lymph nodes draining the GIT, portal blood). Many insults that result in inflammation (e.g., ischemia/reperfusion, burns, endotoxin, infusion of live bacteria) increase the migration of intestinal organisms or inflammatory mediators across the lumen (9, 10, 11).
Despite evidence of decreased blood flow during inflammation, severe inflammation can affect the liver differently from severe hypoperfusion alone. Microscopic examination of liver tissue of patients suffering from severe inflammation can demonstrate intrahepatic cholestasis rather than the centrilobular necrosis that is characteristic of isolated hypoperfusion. Several experimental studies have documented altered hepatic metabolism and cholestasis following ischemia/reperfusion and severe inflammatory insults that develop despite well maintained or increased regional blood flow. Therefore, severe inflammation may result in hepatic insults that are not primarily hypoperfusion induced (12, 13, 14, 15).
SPECIFIC GASTROINTESTINAL DISEASE STATES (TABLE 8.3)
Esophageal Hemorrhage
Esophageal varix hemorrhage occurs most often in patients with severe liver disease and results in further deterioration of the metabolic, hemodynamic, hematologic, and renal alterations already present. The management of esophageal variceal bleeding usually follows the sequence of steps listed in Table 8.4, although balloon tamponade may be necessary before endoscopic procedures can be applied. The non-operative intervention of a transinternal
jugular portal-systemic shunt (TIPS) has the advantage of decompressing the portal venous system without the potential deleterious effects of major abdominal surgery. Surgical shunt procedures are rarely performed. Early TIPS appears to be advantageous, especially in patients with advanced liver disease (16, 17).
jugular portal-systemic shunt (TIPS) has the advantage of decompressing the portal venous system without the potential deleterious effects of major abdominal surgery. Surgical shunt procedures are rarely performed. Early TIPS appears to be advantageous, especially in patients with advanced liver disease (16, 17).
Table 8.1 Gastrointestinal Alterations Secondary to Hypoperfusion: Too Little Oxygen Delivery | |
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Table 8.2 Inflammation-Induced Gastrointestinal Tract Alterations | |
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Table 8.3 Common Gastrointestinal Problems in the Surgical Intensive Care Unit | |
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Table 8.4 Medical Management of Variceal Hemorrhage | |
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Mallory-Weiss tear hemorrhage is usually controlled with conservative measures, which may include vasopressin infusion.
Stomach and Duodenum
As stated above, following any etiology of hypoperfusion and severe inflammation, the entire intra-abdominal GIT supplied by the celiac axis and the superior and inferior mesenteric arteries suffers insults that may be disproportionally large, as compared to the heart, lungs, and brain. Since the GI mucosa is the most actively metabolic layer, the mucosa suffers the most from metabolic insults. The damaged mucosa becomes more susceptible to other insults such as acid, steroids, non-steroidal anti-inflammatory drugs, and, possibly, components of bile and/or pancreatic secretions (18).
In the stomach and duodenum, this mucosal damage can be clinically manifest as gastritis, duodenitis, gastric ulcers, and duodenal ulcers (19). These alterations can result in upper intestinal bleeding and are seen at the time of diagnostic upper endoscopy. However, stress damage is not necessarily limited to the mucosa. Full-thickness damage and perforation are also possible, but very rare.
The most convincing evidence that acid promotes the “stress” injury in the stomach and duodenum is that controlling gastric pH significantly reduces upper GI bleeding in critically ill surgical patients (20). Prior use of antacid has been replaced with the use of histamine-2 receptor antagonists (HRAs) or proton pump inhibitors (PPIs). At present, PPIs have not been shown to be more effective than HRAs and the application of any acid inhibition has been questioned for patients receiving enteral nutrition (21, 22).
The concept of direct mucosal protection with sucralfate without acid inhibition gained popularity in the 1990s, especially when infectious disease frequency (e.g., pneumonia) seemed reduced (23). Subsequent investigations in trauma patients have failed to support this distinction (24, 25). However, if all mechanically ventilated patients are included for study, regardless of the reason for ICU admission, then sucralfate may provide protection against pneumonia (26).
Liver and Biliary Tree
Jaundice
Jaundice is quite common during surgical critical illness and can be secondary to many factors (Table 8.5). The measurement of common liver tests usually provides an indication of jaundice that is associated with hepatocyte necrosis (marked aspartate aminotransferase and alanine transaminase elevations). Such hepatocellular damage is more consistent with severe
hypoperfusion (“shock” liver) and hepatitis. Acute, infectious hepatitis is not common in surgical critical care, but drugs, including alcohol, may cause direct hepatocellular insults.
hypoperfusion (“shock” liver) and hepatitis. Acute, infectious hepatitis is not common in surgical critical care, but drugs, including alcohol, may cause direct hepatocellular insults.
Table 8.5 Etiologies of Post-operative Jaundice | |
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Jaundice without significant aspartate aminotransferase/alanine transaminase elevation is quite common and may or may not be associated with increased alkaline phosphatase (AP) levels. An elevation primarily in unconjugated bilirubin without an elevation in AP would suggest hemolysis as a cause of jaundice. This can be further supported by measuring decreased haptoglobin levels and increased urine free hemoglobin. Jaundice with an elevated conjugated bilirubin and an equivalent increase in AP (i.e., bilirubin of 4 mg/dl associated with an AP of 400 units/L) suggests cholestasis of extrahepatic origin. When conjugated bilirubin increases rapidly without a comparable increase in AP or gamma glutamyltransferase, this is often a manifestation of intrahepatic cholestasis secondary to severe inflammation remote from the liver and biliary tree (i.e., pneumonia, necrotizing soft-tissue infection) (27).
Regardless of the pattern of bilirubin and/or AP elevation, evaluation of the biliary tree using a non-invasive approach like ultrasound is reasonable to assess the possibility of extrahepatic obstruction in any critically ill, jaundiced patient. However, except for the occurrence of acalculous acute cholecystitis, there is little reason to expect an extrahepatic biliary tree disease in most critically ill surgical patients who develop jaundice without a prior injury or surgical disease related to the liver or biliary tract.
Manifestations of Liver Failure (Table 8.6)
Liver test alterations may be the predominant manifestation of hypoperfusion/severe inflammation-induced organ malfunction. However, liver failure sufficient to result in life-threatening deficits is much more likely when severe hypoperfusion/inflammation impinge on a liver that is already diseased.
The magnitude of preexisting liver disease is frequently categorized using Child’s criteria and/or the model for end-stage liver disease (MELD) score (Table 8.7) (28). Mortality risk in surgical patients is directly linked to the severity indicated by these classifications (28, 29). Interestingly, for medical intensive care unit (ICU) patients, mortality risk is better linked to multi-organ failure analysis than liver failure, per se (30). In addition, severe liver disease is frequently associated with the hypoadrenalism of critical illness (see chap. 7). Providing physiologic hydrocortisone replacement may have a benefit in this population (31).
Coagulopathy unresponsive to vitamin K and coagulation factor administration, hypoglycemia, and persistent elevation of lactic acid all portend a poor prognosis.
Hepatorenal Syndrome
Hepatorenal syndrome (HRS) is diagnosed on the basis of a serum creatinine >1.5 mg/dl that does not decrease to <1.0 mg/dl following the administration of albumin and the discontinuation of diuretics. Type 1 HRS is designated as an increase in creatinine >2.5 mg/dl in less than two weeks. Type 2 HRS is indicated by a “stable” elevation or a gradually increasing creatinine up to 2.5 mg/dl over more than two weeks (32, 33). Type 1 is associated with acute illness and has a worse prognosis.
Renal hypoperfusion from systemic and intra-renal vasodilation is considered the primary mechanism that is treated with the vasopressin analogue terlipressin. Acute hypovolemic states such as gastrointestinal hemorrhage and/or progressive systemic inflammation can
demand augmentation of intravascular volume. Usually, albumin solutions are selected for patients with liver failure (33).
demand augmentation of intravascular volume. Usually, albumin solutions are selected for patients with liver failure (33).
Table 8.6 Manifestations of Severe Liver Disease/Failure | |
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Table 8.7 Child’s Criteria | |||||||||||||||||||||||||||||||
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The use of TIPS fir HRS is controversial, with some reports indicating that improved renal function can increase the success of liver transplantation (32).
Ascites
Alcohol-induced cirrhosis is characterized by and increase in both pre- and post-sinusoidal resistance to sinusoidal blood flow. An increase in pre-sinusoidal pressure will principally augment portal pressure with little effect on the hepatic lobule, per se. Such an increase in hydrostatic pressure will result in a transudate from the surface of the intestinal tract drained by the portal vein. Post-sinusoidal obstruction will also increase portal vein pressure, but, in addition, hepatic lymphatics become distended and lymph can spill from the liver into the peritoneal cavity, resulting in ascites that is more characteristic of an exudate. Therefore, examination of ascites can result in measurements that do not clearly distinguish a transudate from an exudate (34).
Abdominal procedures in patients with ascites, exclusive of liver transplanation and porto-caval shunts, pose additional risks related to fluid and protein losses, tension on the abdominal wall, healing of anastomoses, and recurrent intra-abdominal infection. Typically, critical surgical illness does not allow sufficient time for ascites management strategies like diuretic administration and/or repeated paracentesis to be effective.
Compared to paracentesis, TIPS has been shown to be more effective and associated with better short-term survival (35). Elective abdominal surgery in cirrhotics with ascites appears to be less complicated in patients who undergo a pre-operative TIPS (36, 37). Elective liver resection appears to be less complicated with the use of closed ascites drainage (38). No well-studied management plan for the critical surgical abdomen in patients with ascites is available. A choice between closed drainage and TIPS seems to be supported by the elective abdominal surgery literature.
Acute Acalculous Cholecystitis
Another manifestation of the “stress” injury to the GIT is acute acalculous cholecystitis (AAC). Decreased mucosal blood flow, increased inflammatory mediator production, and decreased gallbladder contractile function have all been associated with AAC (2, 5).
Most often seen in males who have been injured, AAC may become clinically evident several days after an insult, with a spectrum ranging from vague clinical manifestations, such as fever and jaundice, to frank right upper-quadrant peritonitis. Usually, the diagnosis requires a high index of suspicion in critically ill patients who are often sedated and/or paralyzed. This disease is primarily a condition that results from direct damage to the gallbladder wall rather than indirectly from pressure increasing in the gallbladder lumen. Therefore, the precise diagnosis typically requires direct inspection of the gallbladder wall rather than the use of less invasive techniques. As a consequence, ultrasound and cholecystographic scans are not as useful as in calculous acute cholecystitis. Both are subject to a high false-positive rate in surgical critical illness. A normal scintigraphy scan, however, makes the diagnosis extremely unlikely (2, 5, 39).
Since the diagnosis is best discerned based on the appearance of the gallbladder wall, a high index of suspicion may require direct inspection of the gallbladder. This can be accomplished with laparoscopy when a patient can tolerate general anesthesia and abdominal insufflations, or can be accomplished by a minilaparotomy under local anesthesia. With either technique, if the gallbladder looks normal, no intervention is needed. If the gallbladder wall looks viable but the gallbladder is markedly distended, a cholecystostomy tube can be placed. If the gallbladder is abnormal, the gallbladder should be removed (40).
Some authors advocate the percutaneous drainage of the distended gallbladder in the critical care setting, and claim it as a treatment for acalculous cholecystitis. Since the specific diagnosis of acalculous cholecystitis requires inspection of the gallbladder wall, it is difficult to interpret the sensitivity and specificity claims of such reports. If the gallbladder wall is severely diseased, simple decompression is inadequate therapy and cholecystectomy is required. Therefore, any patient subjected to percutaneous gallbladder drainage who does not improve as expected should have the gallbladder directly visualized to assess this diagnosis and the effects of the tube decompression (41).
Acute Pancreatitis
The common etiologies of acute pancreatitis along with potential etiologies encountered in the surgical ICU setting are listed in Table 8.8.
Hypoperfusion
Perhaps no other acute abdominal condition is as potent an example of the intimate linkage between hypoperfusion and inflammation as is acute pancreatitis (hypoperfusion begets inflammation, inflammation begets hypoperfusion). Pancreatitis can be caused by hypoperfusion and can result in hypoperfusion (42, 43, 44).
The principal mechanism of hypoperfusion from pancreatitis is plasma volume depletion from “third space” losses (see chap. 4 and 7) (42, 45, 46, 47). As with any systemic inflammatory process, myocardial depression is possible, but much less likely (48).
The severity of pancreatitis is the major determinant of associated physiologic disturbances and has been classically categorized by Ranson’s clinical criteria (Table 8.9). However, Ranson’s and other methods of severity designation often fail to provide early identification of severe acute pancreatitis (SAP), that is, a diagnostic designation when the patient is first seen. Certainly, parameters such as those listed in Table 8.10 would alert the clinician about the severity of the pancreatitis (45). But, none of these alterations might be present early and only emerge over the next hours to a few days. Therefore, the most practical and effective tactic is to assume that each case that is not already severe will become severe (42, 45).
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