Cirrhosis is a serious and progressive disease that eventually results in hepatic failure, and the most common cause of cirrhosis in the United States is chronic alcohol abuse. Other causes include chronic active hepatitis (postnecrotic cirrhosis), chronic bili-ary inflammation or obstruction (primary biliary cirrhosis, sclerosing cholangitis), chronic right-sided congestive heart failure (cardiac cirrhosis), autoimmune hepatitis, hemochromatosis, Wilson’s disease, α1-antitrypsin deficiency, nonalcoholic ste-atohepatitis, and cryptogenic cirrhosis. Regardless of the cause, hepatocyte necrosis is followed by fibrosis and nodular regeneration. Distortion of the liver’s normal cellular and vascular architecture obstructs portal venous flow and leads to portal hypertension, whereas impairment of the liver’s nor-mal synthetic and other diverse metabolic functions results in multisystem disease. Clinically, signs and symptoms often do not correlate with disease sever-ity. Manifestations are typically absent initially, but jaundice and ascites eventually develop in most patients. Other signs include spider angiomas, pal-mar erythema, gynecomastia, and splenomegaly. Moreover, cirrhosis is generally associated with the development of three major complications: (1) vari-ceal hemorrhage from portal hypertension, intractable fluid retention in the form of ascites and the hepatorenal syndrome, and (3) hepaticencephalopathy or coma. Approximately 10% of patients with cirrhosis also develop at least one episode of spontaneous bacterial peritonitis, and some patients eventually develop hepatocellular carcinoma.
A few diseases can produce hepatic fibrosis without hepatocellular necrosis or nodular regener-ation, resulting in portal hypertension and its asso-ciated complications with hepatocellular function often preserved. These disorders include schistoso-miasis, idiopathic portal fibrosis (Banti’s syndrome), and congenital hepatic fibrosis. Obstruction of the hepatic veins or inferior vena cava (Budd–Chiari syndrome) can also cause portal hypertension. The latter may be the result of venous thrombosis (hypercoagulable state), a tumor thrombus (eg, renal carcinoma), or occlusive disease of the sublobular hepatic veins.
The detrimental effects of anesthesia and sur-gery on hepatic blood flow are discussed below. Patients with cirrhosis are at increased risk of deterioration of liver function because of their limited functional reserves. Successful anesthetic management of these patients is dependent on recognizing the multisystem nature of cirrhosis
(Table 33–3) and controlling or preventing its complications.
Portal hypertension leads to the development of extensive portosystemic venous collateral channels.
Four major collateral sites are generally recognized: gastroesophageal, hemorrhoidal, periumbilical, and retroperitoneal. Portal hypertension is often apparent preoperatively, as evidenced by dilated abdominalwall veins (caput medusae). Massive bleeding from gastroesophageal varices is a major causeof morbidity and mortality, and, in addition to the effects of acute blood loss, the absorbed nitrogen load from the breakdown of blood in the intestinal tract can precipitate hepatic encephalopathy.
The treatment of variceal bleeding is primarily supportive, but frequently involves endoscopic pro-cedures for identification of the bleeding site(s) and therapeutic maneuvers, such as injection sclerosis of varices, monopolar and bipolar electrocoagulation, or application of hemoclips or bands. In addition to the risks posed by a patient who is physiologi-cally fragile and acutely hypovolemic and hypo-tensive, anesthesia for such endoscopic procedures frequently involves the additional challenges of an encephalopathic and uncooperative patient and a stomach full of food and blood. Endoscopic uni-polar electrocautery may adversely affect implanted cardiac pacing and defibrillator devices.
Blood loss should be replaced with intra-venous fluids and blood products. Nonsurgical treatment includes vasopressin, somatostatin, propranolol, and balloon tamponade with a Sengstaken–Blakemore tube. Vasopressin, soma-tostatin, and propranolol reduce the rate of blood loss. High doses of vasopressin can result in con-gestive heart failure or myocardial ischemia; con-comitant infusion of intravenous nitroglycerin may reduce the likelihood of these complications and bleeding. Placement of a percutaneous transjugu-lar intrahepatic portosystemic shunt (TIPS) can reduce portal hypertension and subsequent bleed-ing, but may increase the incidence of encepha-lopathy. When the bleeding fails to stop or recurs, emergency surgery may be indicated. Surgical risk has been shown to correlate with the degree of hepatic impairment, based on clinical and labora-tory findings. Child’s classification for evaluating hepatic reserve is shown in Table 33–4. Shunting procedures are generally performed on low-risk patients, whereas ablative surgery, esophageal tran-section, and gastric devascularization are reserved for high-risk patients.
Anemia, thrombocytopenia, and, less commonly, leukopenia, may be present. The cause of the ane-mia is usually multifactorial and includes blood loss, increased red blood cell destruction, bone marrow suppression, and nutritional deficiencies. Congestive splenomegaly secondary to portal hypertension is largely responsible for the thrombocytopenia and leukopenia. Coagulation factor deficiencies arise as a result of decreased hepatic synthesis. Enhanced fibrinolysis secondary to decreased clearance of acti-vators of the fibrinolytic system may also contribute to the coagulopathy.
The need for preoperative blood transfusions should be balanced against the obligatory increase in nitrogen load. Protein breakdown from excessive blood transfusions can precipitate encephalopathy. However, coagulopathy should be corrected before surgery. Clotting factors should be replaced with appropriate blood products, such as fresh frozen plasma and cryoprecipitate. Platelet transfusions should be considered immediately prior to surgery for counts less than 75,000/µL.
End-stage liver disease, and, in particular, cirrhosis of the liver, may be associated with disorders of all major organ systems (Tables 33–3 and 33–5). The cardiovascular changes observed in the patient with hepatic cirrhosis are usually that of a hyperdynamic circulation, although clinically signif-icant cirrhotic cardiomyopathy is often present and not recognized (Table 33–6). There may be a reduced cardiac contractile response to stress, altered dia-stolic relaxation, downregulation of β-adrenergic receptors, and electrophysiological changes as a result of cirrhotic cardiomyopathy.
Echocardiographic examination of cardiac function may initially be interpreted as normal because of significant afterload reduction caused by low systemic vascular resistance. However, both
systolic and diastolic dysfunction are often found. Noninvasive stress imaging is frequently used to assess coronary artery disease in patients older than age 50 years and those with risk factors.
The effects of hepatic cirrhosis on the pulmo-nary vascular resistance (PVR) vessels mayresult in chronic hypoxemia. Hepatopulmonary syn-drome (Table 33–7) is found in approximately 30%of liver transplant candidates and is characterized
by pulmonary arteriolar endothelial dysfunction. The resultant intrapulmonary vascular dilata-tion causes intrapulmonary right-to-left shunting and an increase in the alveolar to arterial oxygen gradient.
Pulmonary vascular remodeling may occur in association with chronic liver disease, involving vascular smooth muscle proliferation, vasoconstric-tion, intimal proliferation, and eventual fibrosis, all presenting as an obstructive pathology that causes an increased resistance to flow. This may result in pulmonary hypertension; if associated with portal hypertension, it is termed portopulmonary hyperten-sion (POPH;Table 33–8).
The diagnostic criteria for POPH include a mean pulmonary artery pressure (mPAP) >25 mm Hg at rest, and a PVR > 240 dyn.s.cm−5. The transpulmo-nary gradient of >12 mm Hg (mPAP – pulmonary arteriolar occlusion pressure [PAOP]) reflects the obstruction to flow and distinguishes the contribu-tion of volume and resistance to the increase in mPAP.
POPH may be classified as mild (mPAP 25–35 mm Hg), moderate (mPAP 35 and 45 mm Hg), and severe (mPAP 45 mm Hg). Mild POPH is not associated with increased mortality at liver transplantation, although the immediate recovery period may be challenging if there is a significant increase in cardiac output after reperfusion of the new graft. Moderate and severe POPH are associ-ated with significant mortality at transplantation. However, the key factor is not mPAP, but rather right ventricular (RV) function.
The success of liver transplantation will depend on the right ventricle maintaining good function during and after the transplant procedure despite increases in cardiac output, volume, and PVR. If RV dysfunction or failure occurs, graft congestion with possible failure and serious morbidity, includ-ing mortality, may ensue. Assessment of the right ventricle using transesophageal echocardiography (TEE) is often helpful.
The role of liver transplantation in the manage-ment of POPH is not well defined. In some patients, pulmonary hypertension will reverse quickly after transplant; however, other patients may require months or years of ongoing vasodilator therapy. Other patients may continue to progress and even-tually develop RV failure. Some patients will develop pulmonary hypertension after liver transplantation. Liver transplantation offers the best outcome in patients with POPH that is responsive to vasodilator therapy.
Disturbances in pulmonary gas exchange and venti-latory mechanics are often present. Hyperventilation is common and results in a primary respiratory alka-losis. As noted above, hypoxemia is frequently pres-ent and is due to right-to-left shunting of up to 40% of cardiac output. Shunting is due to an increase in both pulmonary arteriovenous communications (absolute) and ventilation/perfusion mismatch-ing (relative). Elevation of the diaphragm from ascites decreases lung volume, particularly func-tional residual capacity, and predisposes to atelec-tasis. Moreover, large amounts of ascites produce a restrictive ventilatory defect that increases the work of breathing.
Review of the chest radiograph and arterial blood gas measurements is useful preoperatively because atelectasis and hypoxemia are usually not evident on clinical examination. Paracentesis should be considered in patients with massive ascites and pulmonary compromise, but should be performed with caution because excessive fluid removal can lead to circulatory collapse.
Derangements of fluid and electrolyte balance may manifest as ascites, edema, electrolyte disturbances , and hepatorenal syndrome. Important mechanisms responsible for ascites include (1) portal hyper-tension, which increases hydrostatic pressure and favors transudation of fluid across the intestine into the peritoneal cavity; (2) hypoalbuminemia, which decreases plasma oncotic pressure and favors fluid transudation; (3) seepage of protein-rich lymphatic fluid from the serosal surface of the liver secondary to distortion and obstruction of lymphatic channels in the liver; and (4) avid renal sodium and water retention.
Patients with cirrhosis and ascites have decreased renal perfusion, altered intrarenal hemo-dynamics, enhanced proximal and distal sodium reabsorption, and often an impairment of free water clearance. Hyponatremia and hypokalemia are com-mon. The former is dilutional, whereas the latter is due to excessive urinary potassium losses (from sec-ondary hyperaldosteronism or diuretics). The most severe expression of these abnormalities is seen with the development of hepatorenal syndrome. Patients with ascites have elevated levels of circulating cate-cholamines, probably due to enhanced sympathetic outflow. In addition to increased renin and angio-tensin II, these patients are insensitive to circulating atrial natriuretic peptide.
Hepatorenal syndrome is a functional renaldefect in patients with cirrhosis that usually follows gastrointestinal bleeding, aggressive diuresis, sepsis, or major surgery. It is characterized by pro-gressive oliguria with avid sodium retention, azo-temia, intractable ascites, and a very high mortality rate. Treatment is supportive and often unsuccessful unless liver transplantation is undertaken.
Judicious perioperative fluid management in patients with advanced liver disease is critical. The importance of preserving kidney function periop-eratively cannot be overemphasized. Overzealous preoperative diuresis should be avoided, and acute intravascular fluid deficits should be corrected with colloid infusions. Diuresis of ascites and edema fluid should be accomplished over several days. Loop diuretics are administered only after measures such as bed rest, sodium restriction (<2 g NaCl/d), and spironolactone are deemed ineffective. Daily body weight measurements are useful in prevent-ing intravascular volume depletion during diuresis.
In patients with both ascites and peripheral edema, no more than 1 kg/day should be lost during diuresis; in those with ascites alone, no more than 0.5 kg/day should be lost. Hyponatremia (serum [Na+] < 130 mEq/L) also requires water restric-tion (<1.5 L/d), and potassium deficits should be replaced preoperatively.
Hepatic encephalopathy is characterized by altera-tions in mental status with fluctuating neurological signs (asterixis, hyperreflexia, and/or inverted plan-tar reflex) and characteristic electroencephalo-graphic changes (symmetric high-voltage, slow-wave activity). Some patients also have elevated intracra-nial pressure. Metabolic encephalopathy seems to be related to both the amount of hepatocellular damage present and the degree of shunting of portal blood away from the liver and directly into the systemic circulation. The accumulation of substances origi-nating in the gastrointestinal tract (but normally metabolized by the liver) has been implicated
Factors known to precipitate hepatic encepha-lopathy include gastrointestinal bleeding,increased dietary protein intake, hypokalemic alka-losis from vomiting or diuresis, infections, and worsening liver function.
Hepatic encephalopathy should be aggressively treated preoperatively. Precipitating causes should be corrected. Oral lactulose 30–50 mL every 8 hr or neomycin 500 mg every 6 hr is useful in reduc-ing intestinal ammonia absorption. Lactulose acts as an osmotic laxative, and, like neomycin, likely inhibits ammonia production by intestinal bacteria. Sedatives should be avoided.
Patients with postnecrotic cirrhosis due to hepatitis B or hepatitis C who are carriers of the virus may be infectious. Universal precautions are always indi-cated in preventing contact with blood and body flu-ids from all patients.
The response to anesthetic agents is unpredictable in patients with cirrhosis. Changes in central nervous system sensitivity, volumes of distribution, protein binding, drug metabolism, and drug elimination are common. An increase in the volume of distribution for highly ionized drugs, such as neuromuscular blockers (NMBs), is due to the expanded extracel-lular fluid compartment; an apparent resistance may be observed, requiring larger than normal loading doses. However, smaller than normal maintenance doses of NMBs dependent on hepatic elimination (pancuronium, rocuronium, and vecuronium) are needed. The duration of action of succinylcho-line may be prolonged because of reduced levels of pseudocholinesterase, but this is rarely of clinical consequence.
The cirrhotic liver is very dependent on hepatic arterial perfusion because of reduced portal venous blood flow. Preservation of hepatic arterial blood flow and avoidance of agents with potentially adverse effects on hepatic function are critical. Regional anesthesia may be used in patients without throm-bocytopenia or coagulopathy, but hypotension must be avoided. A propofol induction followed by iso-flurane or sevoflurane in oxygen or an oxygen–air mixture is commonly employed for general anesthe-sia. Opioid supplementation reduces the dose of the volatile agent required, but the half-lives of opioids are often significantly prolonged, which may cause prolonged postoperative respiratory depression. Cisatracurium may be the NMB of choice because of its nonhepatic metabolism.
Preoperative nausea, vomiting, upper gastroin-testinal bleeding, and abdominal distention due to massive ascites require a well-planned anesthetic induction. Preoxygenation and a rapid-sequence induction with cricoid pressure are often performed. In unstable patients and those with active bleeding, either an awake intubation or a rapid-sequence induction using ketamine or etomidate and succi-nylcholine is suggested.
Pulse oximetry should be supplemented with arterial blood gas measurements to monitor acid–base sta-tus. Patients with large right-to-left intrapulmonary shunts may not tolerate the addition of nitrous oxide and may require positive end-expiratory pressure (PEEP) to treat ventilation/perfusion inequalities and subsequent hypoxemia. Patients receiving vaso-pressin infusions should be monitored for myocar-dial ischemia from coronary vasoconstriction.
Continuous intraarterial pressure monitoring is often used because hemodynamic instability fre-quently occurs as a result of excessive bleeding and surgical manipulations. Intravascular volume sta-tus is often difficult to optimize, and goal-directed hemodynamic and fluid therapy utilizing esopha-geal Doppler, arterial waveform analysis, or echocar-diography should be considered. Such approaches may be helpful in preventing the hepatorenal syn-drome. Urinary output must be followed closely; mannitol may be considered for persistently low urinary outputs despite adequate intravascular fluid replacement.
Most patients are sodium-restricted preoperatively, but preservation of intravascular volume and uri-nary output takes priority intraoperatively. The use of predominantly colloid intravenous fluids (albumin) may be preferable to avoid sodium over-load and to increase oncotic pressure. Intravenous fluid replacement should take into account the excessive bleeding and fluid shifts that often occur in these patients during abdominal procedures. Venous engorgement from portal hypertension, lysis of adhesions from previous surgery, and coag-ulopathy lead to excessive bleeding during surgical procedures, whereas evacuation of ascites and pro-longed surgical procedures result in large fluidshifts. Following the removal of large amounts of ascitic fluid, aggressive intravenous fluidreplacement is often necessary to prevent profound hypotension and kidney failure.
Most preoperative patients are anemic and coag-ulopathic, and perioperative red blood cell transfusion may lead to hypocalcemia (citrate toxicity) because of elevated plasma citrate levels resulting from impaired citrate metabolism in the cirrhotic liver. Citrate, the anticoagulant in stored red blood cell preparations, binds with plasma calcium, producing hypocalcemia. Intravenous calcium is often necessary to reverse the negative inotropic effects of decreased blood ionized calcium concentration .
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