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Perioperative Management and Nutritional Support in Patients With Liver and Biliary Tract Disease
Even the most straightforward surgical procedure can become exceptionally challenging when performed on a patient with an underlying hepatobiliary disorder. Hepatic dysfunction, as manifest by portal hypertension, synthetic impairment, and cholestasis may be present to varying degrees, and can have a profound influence on the physiology of other organ systems. Depending on the severity of the underlying dysfunction and the nature of the operation, even seemingly minor procedures can precipitate a cascade of events resulting in hemodynamic instability, bleeding, and hepatic decompensation. To avoid such complications, the surgeon must anticipate and appropriately assess in advance any patient who falls along the spectrum of hepatobiliary disease. This chapter focuses on the perioperative issues related to patients with varying degrees of dysfunction caused by primary liver disease and/or the consequences of biliary obstruction. A review of the pathophysiology of hepatobiliary disease first allows a context for understanding the importance of perioperative care in this patient population. A detailed examination of the preoperative, intraoperative, and postoperative considerations for surgical candidates with hepatobiliary dysfunction then follows.
Pathophysiology of Cirrhosis and Obstructive Jaundice
As evidenced by the suffering of Prometheus in classical Greek mythology, the unique regenerative capacity of the liver has long been appreciated. In the clinical setting, regeneration of a healthy liver usually restores normal hepatic function. However, repeated cycles of regeneration due to chronic inflammation lead to significant alterations to the normal parenchymal architecture. This results in fibrosis, and ultimately cirrhosis, with progressive liver dysfunction. The dual arterial and portal venous perfusion of the hepatic sinusoids also changes as fibrosis progresses. The resultant regenerative nodules have only hepatic arterial inflow, as portal venous flow cannot penetrate the fibrotic collagen deposits. Impairment in the first-pass metabolism of substances absorbed from the gastrointestinal tract then becomes one of the first clinically relevant aspects of managing such patients.
In addition to mechanical resistance, a decrease in the secretion of vasodilators and an increase in the secretion of vasoconstrictors in the sinusoids contribute to an increased resistance to portal venous flow within the liver. Outside the liver, there is a further release of vasodilators in the splanchnic circulation to compensate for the increased resistance to portal venous flow. Portal hypertension thus develops as a result of both resistance to blood flow through the liver and overall increased inflow in the splanchnic bed. The increased pressure gradient between the portal and systemic circulations gives rise to the shunting of blood to the spleen and the development of collateral pathways of portal venous flow around the liver. These portosystemic collaterals typically form gastroesophageal, retroperitoneal, periumbilical, and rectal varices, which can lead to gastrointestinal bleeding in the perioperative period and major hemorrhage intraoperatively. Splenomegaly, hypersplenism, and spontaneous splenorenal shunts are other direct consequences of portal hypertension that have clinical implications. Patients with cirrhosis and portal hypertension display multiple interacting physiologic changes that greatly complicate perioperative care ( Fig. 120.1 ).
Hemodynamic Considerations
Cirrhosis leads to profound hemodynamic changes that are part of a complex pathophysiology based primarily on vasodilation. Portal hypertension leads to a release of vasodilators, such as nitric oxide in the splanchnic vasculature to augment blood flow through the cirrhotic liver. These vasodilators are not metabolized normally by the dysfunctional liver and so accumulate, causing further splanchnic, and ultimately systemic, vasodilation. Vasodilation causes low systemic vascular resistance and decreased effective circulatory volume. This leads to activation of both neural and hormonal changes that move to restore effective circulatory volume through vasoconstriction and sodium and water retention. This compensatory vasoconstriction can cause renal ischemia, and the resultant sodium and water retention can contribute to worsening hyponatremia, ascites, and edema. Because of these changes, patients with cirrhosis usually display a baseline tachycardia, relative hypotension, and elevated cardiac output, all reflective of a significant hyperdynamic state.
A variety of interventions may improve overall hemodynamics in patients with cirrhosis. Judicious administration of intravenous colloid can help to temporarily restore intravascular volume. However, excess fluid administration can exacerbate ascites and peripheral edema and lead to volume overload. Splanchnic vasoconstrictor therapy may improve hemodynamics, particularly when renal dysfunction is present. In later stages of cirrhosis, patients may require vasopressors to support blood pressure. Pulmonary artery catheterization, or other assessments of central pressure, may be helpful in some cases to guide fluid resuscitation and vasopressor management. Hypotension despite adequate filling pressures indicates advanced hepatobiliary dysfunction and should give the surgeon pause to reassess the indications for the proposed surgical intervention.
Cardiopulmonary Issues
Cardiopulmonary disease often is present in patients with cirrhosis. The persistence of chronic volume overload and a high cardiac output state can lead to valvular dysfunction and progressive heart failure, with portal hypertension itself contributing to overall cardiac impairment. Patients with alcoholic liver disease or hemochromatosis are particularly predisposed to cardiomyopathy and arrhythmia. Many cirrhotic patients are also at risk for coronary artery disease from long-standing associations, such as those related to cigarette smoking or diabetes mellitus.
Liver disease can also significantly impact the lungs. Patients with cirrhosis and ascites are at risk for developing hepatic hydrothorax, hepatopulmonary syndrome, and portopulmonary hypertension. Hepatic hydrothorax (HH) is most commonly found in the right chest and is usually a transudative pleural effusion that results from passage of ascites across the diaphragm. This can often be appreciated on a preoperative physical exam or on a simple chest radiography. Patients with HH are at risk for spontaneous bacterial empyema. Consideration should be given to treating HH perioperatively depending on size and symptoms. When significant, it can impair mechanical ventilation during or after surgery. It can also cause pressure on the right hemidiaphragm sufficient to limit exposure and mobilization of the liver for the surgeon. Similar to ascites, HH is managed with dietary salt restriction, diuretics, thoracentesis, transjugular intrahepatic portosystemic shunt (TIPS), and ultimately liver transplantation.
Both the hepatopulmonary syndrome (HPS) and portopulmonary hypertension (PPH) result when various vasoactive substances bypass the diseased liver and accumulate in a manner that alters the pulmonary vasculature. HPS is defined by pulmonary vascular dilation causing ventilation-perfusion mismatch and chronic hypoxemia (Pa o 2 <60 mm Hg) in the setting of chronic liver disease. Transthoracic echocardiography with bubble contrast can identify intrapulmonary shunts to confirm the diagnosis. Supplemental oxygen and oral garlic supplementation can temporize HPS, but liver transplantation is the only definitive treatment. PPH is defined by pulmonary vascular constriction causing pulmonary hypertension (mean pulmonary artery pressure >25 mm Hg) in the setting of portal hypertension. Echocardiography can suggest the diagnosis when estimated pulmonary artery systolic pressures are 40 to 50 mm Hg, but pulmonary artery catheterization is necessary for confirmation. Temporizing treatment of PPH consists of pulmonary vasodilators such as prostaglandin analogues, phosphodiesterase inhibitors, nitric oxide, and endothelin receptor antagonists. Again, liver transplantation is the only definitive cure.
Finally, it should be appreciated that some underlying liver diseases, such a primary biliary cirrhosis or sarcoidosis also have associated intrinsic pulmonary disease.
Cholestasis
Cholestasis is defined as the impaired flow of bile from the liver into the gastrointestinal tract, and pathology at any point between the hepatocyte and the duodenum can be its cause. This can range from mechanical obstruction, for instance gallstones or a malignancy, to metabolic abnormalities such as sepsis or even genetic defects. Cholestasis per se can lead to hepatocellular injury that, in turn, can result in parenchymal changes and impaired liver function similar to that seen with early cirrhosis. Indeed, chronic biliary obstruction can lead to secondary biliary cirrhosis.
Cholestasis does not immediately reverse with correction of metabolic abnormalities or relief of biliary obstruction, and the systemic accumulation of those substances normally excreted in the bile can impact and injure biological membranes and cause cellular dysfunction throughout the body. Cholestasis can thus profoundly affect many organs, including the nervous, cardiovascular, gastrointestinal, renal, hematologic, and immune systems. Patients with jaundice often develop impaired cardiac function, nutritional deficiencies, acute renal failure, and infectious complications. One critically important consideration in the perioperative period is the association between cholestasis and coagulopathy (as further discussed in subsequent text).
In patients with obstructive jaundice, preoperative decompression of the biliary tree has been used theoretically to improve liver function and decrease morbidity. However, biliary decompression does not always expeditiously normalize the serum bilirubin level, particularly in the setting of long-standing obstruction and consequent hepatocellular dysfunction. Mounting evidence of greater rates of serious complications argues against routine use of preoperative biliary decompression in patients undergoing surgery for obstructive jaundice. Instrumentation of the biliary tree is also associated with increased infectious complications, and stent placement itself can delay or complicate the planned operation. Percutaneous or endoscopic decompression of the biliary tree is appropriate in patients unfit for surgery and in limited cases where preoperative decompression and nutritional supplementation may be beneficial.
Coagulopathy
Perioperative hemorrhage due to coagulopathy is of particular concern when contemplating any surgical intervention on a patient with liver disease. Most proteins involved in hemostasis and fibrinolysis are synthesized exclusively by the liver, including vitamin K-dependent factors II, VII, IX, X, protein C, and protein S; factors V and XIII; fibrinogen, antithrombin, α 2 -plasmin inhibitor, and plasminogen. Prolonged prothrombin time (PT) and international normalized ratio (INR) result from the liver's reduced synthesis of these coagulation factors. Whether from intrinsic hepatocyte dysfunction or extrahepatic biliary obstruction, cholestasis further contributes to coagulopathy by inhibiting the absorption of vitamin K and the function of all those requiring this cofactor. Thrombocytopenia results from the reduced synthesis of thrombopoietin and sequestration of platelets due to portal-hypertensive hypersplenism, further potentiating bleeding in the perioperative period.
Treatment of coagulopathy in patients with hepatobiliary disease is based on the underlying pathology. Parenteral administration of vitamin K can correct the coagulopathy related to chronic biliary obstruction or malnutrition, but is less effective for the coagulopathy related to severe hepatic parenchymal disease. Transfusion of fresh-frozen plasma (FFP) and platelets can correct coagulopathy and thrombocytopenia prior to invasive procedures or in patients with active bleeding. Hypofibrinogenemia may require transfusion of cryoprecipitate, and acute bleeding due to fibrinolysis may require aminocaproic or tranexamic acid infusion. The prophylactic uses of recombinant factor VIIa for severe coagulopathy or thrombopoietin for severe thrombocytopenia remain under investigation.
Ascites
Ascites can be a transudate (low protein, low lactate dehydrogenase [LDH], high pH, normal glucose, and few white blood cells) or exudate (high protein, high LDH, low pH, low glucose, and numerous white blood cells). In hepatobiliary disease, ascites most often is a transudate as a result of the portal hypertension and hypoalbuminemia of chronic liver disease, which cause increased capillary hydrostatic pressure and decreased capillary oncotic pressure in the splanchnic bed. Exudative ascites suggests malignancy and should prompt concern for metastatic peritoneal disease. The serum ascites albumin gradient (SAAG) is a useful calculation to differentiate transudate versus exudate, with a high SAAG greater than 1.1 g/dL suggesting transudative ascites caused by portal hypertension.
The perioperative control of ascites is essential, since ascites predisposes patients to bacterial peritonitis, impairs ventilation, and delays wound healing. Management of ascites includes a dietary salt restriction, diuretics, and paracentesis, with the goal of an ascites-free peritoneal cavity prior to abdominal operation. However, the use of both diuresis and paracentesis should be measured, as these can contribute to acute kidney injury (AKI) due to intravascular volume depletion. In those individuals who are intolerant of, or refractory to, diuretics, a TIPS device may effectively control ascites. Patients with ascites that cannot be controlled with diuretics or TIPS have increased perioperative morbidity and mortality and should not have any elective surgical procedure. If the surgeon must operate in the presence of ascites, an operative drain may be placed temporarily to divert ascites while the incision heals. In this hopefully avoidable circumstance, postoperative fluid and electrolyte management can be exceptionally challenging, requiring meticulous attention to serum electrolytes, the volume of ascites drained, and the volume and content of replacement fluids.
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