Hepatobiliary and Gastrointestinal Disturbances and Anesthesia

Chapter 30


Hepatobiliary and Gastrointestinal Disturbances and Anesthesia



The hepatobiliary system plays an integral role in anesthetic management. An intimate familiarity with diseases of the hepatobiliary and gastrointestinal systems can help avoid negative anesthetic outcomes. The liver is the largest internal organ and is critical in maintaining the homeostasis of many other physiologic systems, the least of which is drug metabolism. As such, acute or chronic liver dysfunction can impair the intended response to anesthesia.1


The purpose of this chapter is to give an overview of pathophysiologic processes specific to the hepatobiliary and gastrointestinal system commonly encountered by the anesthetist. Fundamental relevant anesthetic considerations are described. More specifically, this chapter reviews the anatomy, physiology, and pathophysiology of the liver, to include evaluation of liver function, anesthesia effects on liver function, and perioperative management of patients with liver disease. The chapter continues with diseases of the biliary tract, esophagus, stomach, peritoneum, intestinal tract, and spleen and anesthetic management of patients with conditions affecting these systems. Special consideration is given to carcinoid tumors and transplantation.



Liver Disease



Anatomic, Physiologic, and Pathophysiologic Considerations


Located in the thoracic portion of the abdominal cavity, the liver is the largest organ in the body and generally extends from rib 7 to rib 11 along the right midaxillary line. The liver spans from the right hypochondrium to a portion of the left hypochondrium and is classically divided into four lobes, which may be subdivided into multiple segments as described, for example, by the Couinaud system.2 These subdivisions are based on the anatomic proximity of hepatic and portal veins, though multiple classifications are used that contain different terminology and no system is recognized as superior.


The functional unit of the liver is the hepatic lobule or acinus. The acinus forms around a portal canal consisting of a portal venule, hepatic arteriole, bile ductule, lymphatic vessel, and nerves. The acinus architecture radiates around a central vein that empties into the hepatic veins and then into the vena cava (Figure 30-1). Hepatic lobules number between 50,000 and 100,000 in the normal liver.



The filtering function of the liver has a prominent physiologic role. Blood from the gut contains large quantities of colonic bacilli; it is cleansed of more than 99% of the bacterial load by Kupffer cells (macrophages) that line the hepatic sinuses.3 Endothelial cells that line the hepatic sinuses permit diffusion of large plasma proteins and other substances into the extravascular spaces in the liver. This phenomenon results in a large quantity of lymph that is nearly equal in protein concentration to plasma.


The metabolic functions of the liver require a significant quantity of blood, which comes from arterial and venous sources. The portal vein and the hepatic artery provide the primary blood supply to the liver, delivering approximately 1.5 liters per minute of blood flow. The hepatic artery branches off of the abdominal aorta and delivers 400 to 500 mL/minute of oxygenated blood. According to the anatomic peculiarity of the double afferent blood supply of the liver, 75% to 80% of the blood entering the liver is partially deoxygenated venous blood supplied by the portal vein, which collects all the blood that leaves the spleen, stomach, small and large intestine, gallbladder, and pancreas. The blood entering the liver via the hepatic portal vein contains some oxygen and is high in nutrients that have been absorbed from the digestive tract into the mesenteric and portal veins. Hepatic venous blood supply is shown in Figure 30-2. It is responsible for 70% of blood flow to the normal liver (≈1 L/minute), but only 50% of the liver oxygen supply. The dual supply of blood allows the liver to be relatively resistant to hypoxemia. The combined blood from both sources joins in the hepatic sinusoidal channels lying between the layers of cells in the lobule. These channels serve as capillaries. Endothelial cells and Kupffer cells line the sinusoids. Bile canaliculi are located between hepatocytes; these canaliculi empty into terminal bile ducts. A coalescence of central veins from hepatic lobules forms the hepatic veins, which empty into the inferior vena cava. An extensive arcade of lymphatic vessels is also present within the layer of cells.4



The mean pressure in the hepatic artery is similar to that in the aorta, whereas portal vein pressure has been reported to range between 6 and 10 mmHg in humans. This relatively low pressure allows the liver to function as a circulatory reservoir. Hepatic blood volume may expand considerably in cardiac failure and, in turn, serves as an important blood reservoir in case of bleeding episodes, and compensates up to 25% of the hemorrhage by immediate expulsion of blood from the capacitance vessels.5 Both α- and β-receptors are present in the hepatic arterial circulation, but only α-receptors are noted in the portal circulation. There is disagreement as to whether the hepatic arterial vasculature exhibits autoregulation of blood flow. Portal blood flow is dependent on the combined venous outflow from the spleen and gastrointestinal tract. A decrease in either portal or arterial blood flow affects a compensatory increase in blood flow delivered by the other system.6


Potent inhaled anesthetics can affect hepatic blood flow, particularly portal blood flow, but present evidence suggests that flow is well maintained relative to oxygen demand. None of the present anesthetics adversely influence hepatic integrity by its effects on blood flow.7 Effects of volatile anesthetics on hepatic blood flow are described in Table 30-1.



Changes in hepatic artery or portal vein blood flow may not result in an overall change in total hepatic flow due to the hepatic artery buffer response (HABR). This response is a semireciprocal autoregulatory mechanism whereby changes in portal flow inversely affect hepatic arterial flow.8 The similarity in total hepatic flow between agents implies an intact HABR.


The liver has many physiologic functions, including synthesis and metabolism of various essential proteins, lipids, and hormones (Box 30-1). There are no artificial devices that can duplicate all of the functions of the liver.



BOX 30-1   Selected Essential Physiologic Functions of the Liver





Carbohydrate Metabolism


Because nutritional ingestion and energy demand may not be synchronous, the body relies upon a dynamic system of energy storage and utilization. Glucose is the primary fuel source for many cells of the body (e.g., kidney, red blood cells) and is the preferred energy source for other tissues (e.g., brain). To maintain a steady blood glucose level, the liver moderates gluconeogenesis and glycogenolysis.


Gluconeogenesis is the formation of glucose from noncarbohydrate molecules lactate and pyruvate and amino acids, all of which are products of anaerobic and catabolic metabolism. It is stimulated by reduction of glycogen stores. During periods of fasting, the liver maintains glucose levels at relatively normal levels through glycogenolysis. Initiated by epinephrine and glucagon, glycogenolysis is the process of liberating glucose from glycogen stores found in the liver (and skeletal muscle). Hypoglycemia may therefore be encountered in patients with severe liver disease caused by derangements in insulin clearance, a decrease in glycogen capacities, and impairment in gluconeogenesis. Because these processes deplete stored nutrients, the body’s energy needs can only be maintained for a limited time.



Protein Synthesis


Protein synthesis occurs primarily in the liver; this excludes immunoglobulins, which are produced by the humoral immune system. With significant liver disease, a reduction in circulating plasma protein will result in a decrease in plasma oncotic pressure. Additionally, drugs bound to proteins produced by the liver would have a greater unbound fraction if circulating proteins were reduced due to liver disease. In addition, overexpansion of the interstitial space and third-spacing secondary to derangements in plasma oncotic pressure result in a large increase in the volume of distribution of clinically used medications. Clinical concerns should therefore focus on the potential for an exaggerated effect with a given dose of drug, particularly a drug that is highly protein bound. The amount of nondepolarizing muscle relaxant may also need to be increased to achieve a given level of blockade. This is secondary to an increased volume of distribution of the drug (secondary to alterations in plasma protein binding and body fluid shifts). Plasma cholinesterase, which is produced in the liver, also may be deficient. This condition may prolong the effects of succinylcholine as well as enhance the potential toxicity of ester local anesthetics.





Bile Production


The liver aids intestinal digestion by forming bile and secreting it into the common bile duct (CBD). Hepatocytes in each lobule continuously secrete fluid that contains phospholipids, cholesterol, conjugated bilirubin (the end product of hemoglobin metabolism), bile salts, and other substances. Bile is stored and concentrated in the gallbladder. In response to the intestinal hormone cholecystokinin (CCK), bile is released by the gallbladder. The presence of fat and protein in the duodenum initiates contraction of the gallbladder and movement of bile via the common bile duct. This duct merges with the pancreatic duct at the ampulla of Vater, which empties into the duodenum via the sphincter of Oddi (major duodenal ampulla). Obstruction of either of these ducts may result in pathologic illness that may necessitate surgical correction.


Ductal patency may be confirmed by radiologic evaluation. Endoscopic retrograde cholangiopancreatography (ERCP) is performed by passing an endoscope into the lower gastrointestinal (GI) tract and locating the major duodenal ampulla. The ampulla is cannulated and examined using radiographic dye to determine whether the blockage is due to a common bile duct stone. If a stone is present, typically it can be retrieved endoscopically. Sphincterotomy also may be performed to facilitate removal of CBD stones. Correction of ductal stenosis also may require sphincterotomy or insertion of a stent.


Bile secretion assists in the absorption of fat and fat-soluble vitamins (vitamins A, D, E, K). The metabolic end products of many drugs are also removed via the bile. Liver disease may result in impaired bile production or flow, leading to steatorrhea, vitamin K deficiency, and delayed removal of active drug metabolites.


A deficiency in vitamin K results in coagulopathy due to impaired production of clotting factors II (prothrombin), VII, IX, and X.9 Except for factor VIII, which is produced in endothelial cells, the liver is responsible for producing all clotting factors. Hepatocellular disease therefore results in decreased clotting factor levels and abnormal bile production. Impaired bile production ultimately manifests as altered production of vitamin K–dependent clotting factors.


Intrahepatic obstruction of blood flow (due to disease pathology) ultimately causes portal hypertension. A consequence of the resultant transmission of backward pressure is congestive splenomegaly, leading to platelet sequestration and thrombocytopenia. Therefore, severe liver disease with portal hypertension induces coagulopathy not only as a result of impairment in hepatic coagulation factor production but also as a result of diminution in circulating functional platelets. In the presence of biliary deficiency, parenteral vitamin K administration helps correct coagulopathy. However, significant hepatocellular disease may dictate the need for fresh frozen plasma (FFP) for immediate correction of coagulation-factor deficits.


The use of subarachnoid and epidural blockade should be avoided in the presence of coagulopathy. Derangements in parameters such as prothrombin time (PT), activated partial thromboplastin time (PTT), and platelet count are a relative contraindication to these techniques; most procedures in which bleeding is a possibility are often postponed when international normalized ratio (INR [prothrombin time]) is greater than 1.5. Nasopharyngeal instrumentation and invasive procedures must be performed cautiously and carefully in the presence of increases in PT and activated PTT, a low platelet count, or other laboratory signs that arouse suspicion of coagulopathy.



Insulin Clearance


The liver is the main site for insulin clearance, removing 50% during the first portal passage, but this percentage varies widely under different conditions.10 During obesity, hyperinsulinemia, insulin-resistant state, dyslipidemia, and type II diabetes mellitus insulin clearance in the liver decreases. A reduction in hepatic insulin extraction would lead, in insulin-resistant states, to a substantial peripheral hyperinsulinemia (due to insulin hypersecretion and reduced hepatic extraction of insulin).11



Drug Metabolism/Transformation


The enzyme systems involved in the biotransformation of drugs are located primarily in the liver. Proper hepatic function is necessary to maintain the pharmacokinetic machinery detailed earlier in this textbook. Orally administered drugs may be metabolically inactivated in the liver before reaching the systemic circulation. This first-pass metabolism may limit the oral availability of highly metabolized drugs. Within the liver, phase I and phase II reactions are responsible for metabolism of many exogenous substances and most drugs. The subsequent products are then excreted via excretory transporters on either the canalicular or sinusoidal membranes12 (Box 30-2). The end products of these processes (except in the case of prodrugs or an active metabolite) are the result of deactivation and transformation of substances into benign by-products capable of being excreted in the bile or urine.



BOX 30-2   Drug Metabolism in the Liver




The cytochrome P450 (CYP) class of enzymes are primarily responsible for phase I reactions. More than 50 CYPs have been identified in humans, yet nearly 50% of drugs currently manufactured are metabolized by CYP 3A4/5.13 Differences in the rate of metabolism of a drug can be due to drug interactions. When two drugs are coadministered and subjected to metabolism by the same enzyme system, the rate of metabolism can be either decreased or increased. Enzyme induction hastens metabolism of certain coadministered medications (e.g., ethanol, barbiturates, ketamine, some benzodiazepines) and promotes tolerance to other medications metabolized by the same enzyme class. This relative tolerance can increase the clinical requirement for other drugs (e.g., sedatives, opioids, steroid muscle relaxants). Conversely, coadministration of drugs metabolized by a single CYP (e.g., cimetidine, chloramphenicol) will compete for binding to the enzyme’s active site. This can result in enzyme inhibition of metabolism of one or both of the drugs and lead to elevated plasma levels culminating in increased sensitivity or toxicity.


Tolerance to certain drugs results from overproduction of enzymes within hepatic enzyme systems, including the cytochrome P-450 system. Drugs capable of inducing this process include ethanol, benzodiazepines, ketamine, barbiturates, and phenytoin. The result is an increased clinical requirement for certain drugs like sedatives, opioids, and muscle relaxants, such as vecuronium and rocuronium.


Certain drugs, such as lidocaine, morphine, meperidine, and propranolol, are highly dependent on hepatic extraction from the circulation for sufficient metabolism. Decreased blood flow to the splanchnic circulation, which occurs during hypotensive states and even during uneventful laparotomy, may decrease metabolic clearance of these drugs.



Laboratory Evaluation of Liver Function


No single laboratory test reliably assesses liver function. As stated previously, the huge capacity and functional reserve of the liver allow for the presence of significant disease processes before evidence of liver failure is reflected in abnormal laboratory findings; abnormalities do, however, aid in differentiating parenchymal from obstructive disorders. Parenchymal disorders reflect dysfunction at the hepatocellular level, whereas obstructive disorders reflect disease processes caused by dysfunctional bile excretion.


Ammonia is cleared by the liver and may be used to evaluate hepatic encephalopathy, but ammonia levels do not correlate well with severity of the clinical presentation. As such, its usefulness is limited. Bilirubin levels also reflect hepatic clearance effectiveness, but it is elevated in most significant liver diseases and is not specific in diagnostic value. Albumin synthesis occurs in the liver, and hypoalbuminemia can indicate chronic liver disease once nonhepatic etiologies have been ruled out. Because albumin has a half-life of 14 to 21 days, quantitative laboratory analysis will be slow to decrease in relation to worsening liver function, making it an unreliable indicator of hepatic synthetic function in acute liver injury. The most common reason for a low albumin is chronic liver failure caused by cirrhosis. The serum albumin concentration is usually normal in chronic liver disease until cirrhosis and significant liver damage has occurred. In advanced liver disease, the serum albumin level may be less than 3.5 g/dL. Biochemical markers of liver function are identified in Table 30-2.



Serum transferases (transaminases) are most sensitive in identifying acute hepatic injury. Elevations in transferase levels are common in all forms of liver injury, but the degree of elevation combined with physical examination and patient symptoms can aid in the differential diagnosis of probable types of hepatic disease.


Patients who present soon after passing common bile duct stones can be misdiagnosed with acute hepatitis because aminotransferase levels often rise immediately, but alkaline phosphatase and γ-glutamyl transferase levels do not become elevated for several days. Asymptomatic patients with isolated, mild elevation of either the unconjugated bilirubin or the γ-glutamyl transferase value usually do not have liver disease and generally do not require extensive evaluation.14


Overall hepatic function can be assessed by applying the values for albumin, bilirubin, and prothrombin time in the Child-Pugh classification system, which is modified from the earlier Child-Turcotte grading system15 (Table 30-3).




Effects of Anesthesia on Liver Function


Patients with liver disease who require surgery are at greater risk for surgical- and anesthesia-related complications than those with a healthy liver.16 The degree of the risk is dependent on the anesthetic technique and associated sequelae, the surgery being performed, and specific type of liver disease and its severity.



Volatile Anesthetic Selection


Given the global nature of general and regional anesthesia, hepatic blood flow may be reduced in a dose-dependent manner. The reduction in mean arterial pressure and cardiac output frequently seen with the use of volatile anesthetics proportionately reduces hepatic blood flow. Another factor that impairs hepatic blood flow is the vasoconstrictive response of the splanchnic circulation; this response occurs as a sympathetic reflex to reduced mean arterial pressure. Isoflurane increases hepatic blood flow through direct vasodilatory properties. This effect is likely offset, however, by a reduction in portal blood flow. Hypotension secondary to regional anesthetic–induced sympathectomy (e.g., epidural or subarachnoid blockade) principally accounts for the reduced splanchnic blood flow associated with the use of these techniques.


All of the volatile anesthetics also have been shown to reduce hepatic blood flow. Halothane causes the greatest reduction, and the use of desflurane has been shown to have hepatic effects similar to those of isoflurane. A rise in serum glutathione-S-transferase (GST) level indicates a decrease in splanchnic circulation, which causes a transient reduction in the oxygenation of hepatocytes. Anesthesia with desflurane has demonstrated that liver function is well preserved.17 Sevoflurane undergoes hepatic biotransformation, producing organic and inorganic fluoride ion. In human subjects, levels of serum inorganic fluoride ion secondary to sevoflurane metabolism are generally below nephrotoxic levels. Prolonged use of higher concentrations, however, may lead to problematic levels. Anesthetic agents may reduce hepatic blood flow by 30% to 50% after induction. Animal data suggest, however, that isoflurane (along with desflurane and sevoflurane, which are believed to be similar) causes less perturbation in hepatic arterial blood flow than other inhaled anesthetic agents and therefore is preferred for patients with liver disease. Studies continue with sevoflurane to determine the influence of biotransformation on renal and hepatic function, but no significant clinical toxicity has yet been reported and they appear to be safe in clinical use.18,19


In developed countries, clinical use of halothane as a volatile anesthetic agent is being superseded by the newer low-solubility agents desflurane and sevoflurane. Halothane, however, is still in use in some countries and remains on the 2011 World Health Organization Model List of Essential Medicines, which is a list of minimum medical needs for a basic health care system. Continued awareness of the potentially deleterious effect of halothane on hepatic function is therefore justified.


Halothane administration is associated with two types of postoperative liver injury. Minor injury in 10% to 30% of patients may result in elevations in alanine aminotransferase (ALT) levels during postoperative days 1 through 10. Risk of hepatotoxicity is higher after repeat exposure to halothane. Major injury involves halothane-induced hepatotoxicity, which is a severe hepatic reaction with elements of autoimmune allergy. The phenomenon of halothane-induced liver damage has been termed halothane hepatitis due to a similar clinical presentation. Clinical features of halothane hepatitis are listed in Box 30-3. Hepatic necrosis may be seen histologically, and the case fatality rate ranged from 14% to 71% (before liver transplant was an option). Evidence for the role of hypersensitivity is found in the increased susceptibility and shortened latency after repeat exposure, the hallmark symptoms and signs of drug allergy. Risk factors for halothane hepatitis are listed in Box 30-4. An estimated 1 in 10,000 patients develops postoperative jaundice after halothane exposure. In this population, a viral source of infection is more likely to be the cause—for instance, as a complication of intraoperative blood transfusion.



BOX 30-3   Clinicopathologic Features of Halothane Hepatitis




• Estimated incidence



• Female-to-male ratio 2 : 1


• Latent period to first symptom



• Jaundice as presenting symptom in 25% (range of serum bilirubin: 3-50 mg/L)


• Fever in 75% (precedes jaundice in 75%); chills in 30%


• Rash in 10%


• Myalgias in 20%


• Ascites, renal failure, and/or gastrointestinal hemorrhage in 20%-30%


• Eosinophilia in 20%-60%


• Serum ALT and AST levels: 25-250 x ULN


• Serum alkaline phosphatase level: 1-3 x ULN


• Histologic features:



• Course and outcome:



• Adverse prognostic findings:



ALT, Alanine aminotransferase; AST, aspartate aminotransferase; ULN, upper limit of normal.


From Lewis JH. Liver disease caused by anesthetics, toxins, and herbal preparations. In: Feldman M, et al, eds. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. 9th ed. Philadelphia: Saunders; 2010:1448.



BOX 30-4   Risk Factors for Halothane Hepatitis




CYP2E1, Cytochrome P450 2E1.


From Lewis JH. Liver disease caused by anesthetics, toxins, and herbal preparations. In: Feldman M, et al, eds. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. 9th ed. Philadelphia: Saunders; 2010:1448.




Anesthesia-Related Activity: Mechanical Ventilation


The sequelae of mechanical ventilation have been implicated as a contributing factor in a reduction of hepatic blood flow. Positive pressure ventilation can result in airway pressures that adversely affect venous delivery to the right atrium. Increased airway pressures also result in reduced cardiac output,20 with a consequent reduction in hepatic blood flow. Positive end-expiratory pressure further exacerbates this condition. Impairment in hepatic blood flow under these conditions may result from increased hepatic venous pressure from increased intrathoracic pressure and from increased reflex sympathetic tone caused by reduced cardiac output. Hypercapnia and acidosis have vasodilatory effects on the hepatic circulation that result in increased blood flow, whereas hypocapnia and alkalosis exert vasoconstricting effects that result in decreased flow. The interplay of various intraoperative variables (e.g., surgical site, ventilatory mode, direct and indirect effects of anesthetics used, physiologic responses to intraoperative events) influences the degree of variation in hepatic blood flow.




Diseases of the Liver


Signs and symptoms indicating liver disease vary widely depending on the etiology of the underlying pathologic process. Decline in liver function may be acute, related to drug toxicity or infection, or it may follow a chronic subclinical course. The following discussion focuses on the more commonly encountered diseases of the liver and offers guided clinical anesthetic implications.




Viral Hepatitis


Hepatitis is a generic term that means liver inflammation. Hepatitis may be caused by several factors (e.g., toxins, alcohol, medications, viral or bacterial infections, autoimmune diseases), and viral hepatitis is the leading cause of liver cancer and the most common reason for transplantation.22


Although several types of hepatitis viruses are known to cause illness, typically only hepatitis A, B, and C (infections caused by the hepatitis A virus [HAV], hepatitis B virus [HBV], and hepatitis C virus [HCV], respectively) affect persons living in the United States.22 Hepatitis D requires co-infection with HBV; hepatitis E virus (HEV) diagnosis is made by exclusion after travel to an endemic area (e.g., South/Central America or Southeast Asia). Hepatitis A and E are transmitted by the oral-fecal route, and hepatitis B, C, and D are transmitted by contact with body fluids and physical contact with disrupted cutaneous barriers.


The common clinical course of viral hepatitis begins with a 1- to 2-week prodromal period, the signs and symptoms of which include fever, malaise, and nausea and vomiting. Progression to jaundice typically occurs, with resolution within 2 to 12 weeks. However, serum transaminase levels often remain increased for up to 4 months. If hepatitis B or C is the cause, the clinical course is often more prolonged and complicated. Cholestasis may manifest in certain cases. Fulminant hepatic necrosis in certain individuals is also possible. Table 30-5 lists the major characteristics of hepatitis types A, B, C, D, and E.




Drug-Induced Hepatitis


Drug-related injury to the liver results from an idiosyncratic reaction to a substance or an overdose resulting in toxicity. For idiosyncratic reactions, genetic predisposition is presumed to be the most critical determinant. Important risk factors include age, gender, exposure to other substances, a history or family history of previous drug reaction, other risk factors for liver disease, and concomitant medical conditions.23 Factors related to the risk of liver injury are summarized in Table 30-6.



Alcoholic hepatitis is probably the most common form of drug-induced hepatitis and results in fatty infiltration of the liver (causing hepatomegaly), with impairment in hepatic oxidation of fatty acids, lipoprotein synthesis and secretion, and fatty acid esterification.6



Chronic Hepatitis


Chronic hepatitis occurs in 1% to 10% of acute hepatitis B infections and in 10% to 40% of hepatitis C infections,6 but does not occur in hepatitis A infections.


Because chronic persistent hepatitis is limited to portal areas and is relatively benign, hepatic cellular integrity is preserved, and progression to cirrhosis is rare. Chronic lobular hepatitis involves recurrent exacerbations of acute inflammation; as in persistent hepatitis, progression to cirrhosis is rare.


Chronic active hepatitis is progressive and results in hepatocyte destruction, cirrhosis, and progressive deterioration of hepatic function. Hepatic failure and death from chronic hepatitis is marked by clinical manifestations such as multiorgan system failure (e.g., hepatorenal syndrome), encephalopathy, and hemorrhage from esophageal varices. Exposure to certain drugs (e.g., methyldopa, isoniazid, and nitrofurantoin) and autoimmune disorders (e.g., systemic lupus erythematosus) are potential causative factors implicated in hepatic failure, though hepatitis B or C are more typical.


Other symptoms present in chronic hepatitis include marked fatigue and jaundice; thrombocytopenia, glomerulonephritis, myocarditis, arthritis, and neuropathy also may be present. Plasma albumin levels are usually decreased related to synthetic dysfunction and PT is prolonged.



Anesthetic Management for Patients with Hepatitis


Evidence from studies indicates that mild chronic hepatitis confers no additional risk of surgical morbidity or mortality during laparoscopic cholecystectomy.24 Surgical outcomes in patients with acute hepatitis are less well studied, and recommendations suggest that elective surgery should be postponed until normalization of biochemical profiles. Existing studies are many decades old and the statistical risks associated may not reflect improvements in either surgical technique or anesthetic management. Anesthetic management recommendations are found in Box 30-5.



BOX 30-5   Anesthetic Management of the Patient with Acute Hepatitis


Preserve hepatic blood flow:


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May 31, 2016 | Posted by in ANESTHESIA | Comments Off on Hepatobiliary and Gastrointestinal Disturbances and Anesthesia

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