Cardiac Evaluation

Patients undergoing liver surgery are at significant risk of cardiovascular morbidity and mortality. Although the perioperative event rate has declined as a consequence of better anesthetic and surgical techniques, perioperative cardiac complications remain a significant problem. The first step in preoperative care is to identify patients at risk for perioperative cardiac events. The risk of perioperative cardiac complications is the summation of an individual patient’s risk and the cardiac stress related to the surgery. Clinical history, physical examination, and review of the electrocardiogram usually provide enough data to estimate cardiac risk. Active cardiac conditions may preclude all but emergent surgery.

For most stable patients, cardiac risk can be derived from the Revised Cardiac Risk Index (Lee et al, 1999b). This simple index identifies six independent risk factors: 1) high-risk type of surgery, 2) history of ischemic heart disease, 3) history of congestive heart failure, 4) history of cerebrovascular disease, 5) diabetes mellitus, and 6) renal insufficiency. The number of clinical risk factors, the risk level of the surgery, and the functional capacity of the patient will determine the need for further testing prior to surgery or pharmacologic intervention perioperatively (Poldermans et al, 2008). For those patients with clinical risk factors, the 2007 American College of Cardiology/American Heart Association guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery are an excellent framework for evaluating cardiac risk in the perioperative period for patients undergoing liver surgery (Fleischer et al, 2007).

Over the years, a shift in perioperative management has been seen, away from treating coronary obstruction with interventions such as surgery and stents and toward medical therapy aimed at stabilizing coronary plaque and preventing myocardial oxygen supply and demand mismatch. Today, preoperative cardiac testing, cardiac stenting, and coronary revascularization are performed for the same indications as those used in the nonoperative setting (Poldermans et al, 2008), but β-blockers, statins, and aspirin are now widely used in the perioperative setting. Compelling evidence supports perioperative β-blocker therapy, unless contraindicated, in patients with coronary artery disease. β-Blocker therapy has been shown to reduce the incidence of perioperative ischemic events and myocardial infarction (Goldman, 2001; Lee et al, 1999a). Recently the risk benefit of this therapy in patients without coronary artery disease has been challenged. The perioperative ischemic evaluation (POISE) study showed an increased incidence of ischemic stroke in combination with intraoperative bradycardia and hypotension (Devereaux et al, 2006). In a retrospective review of patients who underwent noncardiac surgery, perioperative β-blockers showed no benefit—and possible harm—in low-risk patients, but in high-risk patients, a benefit was seen (Lindenauer et al, 2005).

Communication among the patient’s cardiologist, surgeon, and anesthesiologist is essential for the management of hepatobiliary surgical patients who have coronary artery stents. Clinical judgment is of the utmost importance to balance the risk–benefit ratio of antiplatelet therapy interruption versus continuation. Aspirin should never be interrupted, unless the risk of bleeding far outweighs the risk of stent thrombosis (Newsome et al, 2008).

In hepatobiliary patients with a history of alcohol abuse, cardiac assessment should include the evaluation of myocontractile function. Cirrhotic cardiomyopathy classically occurs in men 30 to 55 years old who have been alcohol abusers for more than 10 years (Braunwald, 1997). Putative mechanisms of damage are direct toxic effects of 1) ethanol and its metabolite acetaldehyde; 2) nutritional deficiencies, particularly of thiamine (beriberi); and 3) additives in commercial products, such as cobalt in beer. Alcohol and acetaldehyde have been shown to decrease calcium binding and transport, myocardial lipid metabolism, myocardial synthesis, and myocardial adenosine triphosphatase (ATPase) activity. The two basic patterns of cardiac dysfunction are 1) left ventricular dilation with impaired systolic function and 2) left ventricular hypertrophy with diminished compliance and normal or increased contractile performance. Presenting manifestations range from insidious onset to catastrophic left-sided cardiac failure. Anginal chest pain does not occur, unless the patient has concomitant coronary artery disease or aortic stenosis.

Pulmonary Evaluation

Despite steady advances in care, patients with respiratory disease remain at increased risk for postoperative pulmonary complications (PPCs). Indeed postoperative pulmonary complications may rival cardiovascular complications in frequency and severity (Lawrence et al, 1995). Studies that examine risk factors for PPCs have limitations, but some consistent patterns are seen. The three most important risk factors for PPCs are 1) pulmonary disease, 2) cigarette smoking, and 3) the site of surgery, with abdominal surgery being one of the highest risk sites (Warner, 2000). Of note, pulmonary function testing per se is not useful in predicting risk (McAlister et al, 2003); thus routine pulmonary function testing is not justified unless it is part of an effort to optimize preoperative pulmonary status. The definition of “optimization” depends on the type of respiratory disease and the individual patient. Consultation with the surgeon and pulmonologist will help determine whether a course of systemic corticosteroids or antibiotics is warranted perioperatively. Despite the increased risk of PPCs in patients with preexisting pulmonary disease, no prohibitive level of pulmonary function has been established for which surgery is contraindicated (Nunn et al, 1988; Kroenke et al, 1993). A prospective study did not find an elevated Paco₂ level to be a risk factor among surgical candidates, hence clinicians should not use arterial blood gas analyses to identify patients for whom the risk of surgery is prohibitive (Kearney et al, 1994).

Obese patients are at risk of suffering from a number of respiratory derangements, including obstructive sleep apnea (OSA), obesity hypoventilation syndrome, and restrictive impairment. The increase in body mass also results in increased oxygen consumption and carbon dioxide production. With these isssues in mind, it is not surprising that acute PPCs are twice as likely in obese and OSA patients (Rose et al, 1994; Dindo et al, 2003). Many patients with OSA are undiagnosed, but a strong relationship exists between obesity and OSA (Strohl et al, 1996). The American Society of Anesthesiologists addressed this issue with practice guidelines to assess patients for possible OSA before surgery and to provide careful postoperative monitoring for those suspected to be at risk (Gross et al, 2006).

An association was also found between obesity and OSA and several medical conditions, such as increased risk of venous stasis, pulmonary embolism, hypertension, cerebral vascular acccidents, cardiomyopathy, arrythmias, and ischemic heart disease (Dominguez et al, 1993; Strohl et al, 1996; Gupta et al, 2001). With these issues in mind, the anesthesiologist should have an informed discussion with the patient about the increased risk of morbidity and mortality and should also work with other members of the patient care team to determine whether any interventions need to be initiated before surgery in an effort to minimize complication risk.

Polysomnography is the gold standard for diagnosis of OSA, but it is an expensive and limited resource. The most reasonable approach is to check room air pulse oximetry. If the patient has an oxygen saturation level less than 96%, further evaluation is warranted; a 2-week period of continuous positive airway pressure therapy has been shown to be effective in correcting abnormal ventilatory drive and improving cardiac function (Lin, 1994; Loadsman et al, 2001). In addition, deep venous thrombosis prophylaxis should be discussed with the surgeon.

Hepatic Evaluation

Risk factors and symptoms of liver disease are not as well defined as those in other organ systems. The diagnosis of liver disease requires a high degree of suspicion and careful probing of the clinical history to identify specific risk factors for liver disease, such as previous blood transfusions, jaundice, travel, tatoos, high-risk sexual behavior, illicit drug use, excessive alcohol intake, and chemotherapy (Suman & Carey, 2006).

In North America and Europe, most hepatic resections are performed for metastatic disease. The operative outcome for hepatobiliary surgery is linked to severity of hepatic parenchymal disease and the extent of postoperative functional reduction (see Chapter 2). In patients with mild or well-compensated chronic hepatic disease, operative outcome is likely to be indistinguishable from the outcome in the general population. Patients with hepatocellular carcinoma (HCC) have poorer outcome than those with metastatic disease given the propensity of HCC to develop in the cirrhotic liver (Fattowich, 2003).

The goal of preoperative screening is to determine the presence of preexisting liver disease without the need for extensive or invasive monitoring. Liver function tests can measure different aspects of hepatic function, but as a group of tests, they lack specificity and are often affected by nonhepatic function. These biochemical markers cannot quantify the hepatic disease. Another issue is finding abnormal hepatic function test results in asymptomatic patients. In general, for asymptomatic patients with mildly elevated alanine and aspartate aminotransferase levels and a normal bilirubin concentration, cancellation of surgery is rarely indicated. In patients with significant abnormalities, detailed investigation is warranted to evaluate for underlying cirrhosis, given the high perioperative risk observed in patients with cirrhosis. The need for further investigation in these patients is highlighted by studies that report an incidence of undiagnosed cirrhosis of 34% in asymptomatic patients with abnormal liver function results (Hay et al, 1989; Hultcrantz et al, 1986). It is important to identify patients with underlying hepatic impairment, because they may be at increased risk for further injury from alterations in splanchnic blood flow that occur during anesthesia and intraabdominal surgery.

Measurement of metabolic liver function would provide the necessary predictive information to assess this risk. Metabolic liver function tests (see Chapter 2), such as the aminopyrine breath test and indocyanine green clearance, may have predictive value in this regard but are not routinely performed. To date, risk assessment has been primarily performed in patients with known liver disease (Child-Turcotte-Pugh score), but the quantification of risk in asymptomatic patients should not be extrapolated from these studies. The risk of postoperative hepatic insufficiency is closely related to the volume and function of the remnant liver, and several methods for liver volume determination are available. Most use computerized tomography (CT) combined with three-dimensional CT volumetry (Denys et al, 2002). When the functional liver remnant volume is below a certain threshold, generally 25% to 30% for normal liver and 40% for diseased liver, the risk of postoperative hepatic failure is high, and portal vein embolization may be indicated prior to hepatic resection (Vauthey et al, 2000).

Bloodless Surgery

In the early years of hepatic resection, major intraoperative blood loss was common, transfusion of blood products was routine, and morbidity and mortality were unacceptably high (Foster & Berman, 1977). General improvements in hepatic resection techniques have reduced intraoperative blood loss and transfusion rates; nevertheless, perioperative transfusion remains a potent predictor of increased perioperative morbidity and mortality (Jarnagin et al, 2002). In recent years, liver resection without the need for blood transfusion has become increasingly possible (Belghiti et al, 2000; Cunningham et al, 1994; Fan et al, 1999; Jarnagin et al, 2002). Patient blood management is based on three pillars: 1) detecting and treating preoperative anemia, 2) reducing the loss of red blood cells perioperatively, and 3) optimizing the treatment of anemia (Spahn et al, 2008).

Thorough preoperative planning is essential to avoid perioperative allogeneic transfusion. Any history of bleeding disorders and management of anticoagulation must be evaluated, including discontinuation of drugs that adversely affect clotting (e.g., acetylsalicylic acid, nonsteroidal antiinflammatory drugs, and anticoagulants). In patients with anemia, recombinant human erythropoietin or iron therapy may optimize the starting operative hemoglobin (Monk, 1996). Preoperative autologous donation also has been used to reduce the need for allogeneic red blood products (Brecker & Goodnough, 2001). Preoperative autologous donation may not avoid allogeneic blood, however, because almost half of the patients who donate blood before surgery are anemic on the day of operation, and preoperative strategies to augment the red blood cell mass require more time than is generally reasonable for optimal efficacy. Patients with low hemoglobin levels at the start of surgery are at an increased risk of receiving allogeneic blood (Armas-Loughran et al, 2003). In addition, preoperative autologous donation is costly; it can be associated with clerical errors; and for every 2 units donated, usually only 1 unit gets transfused (Goldman et al, 2002). If the patient is optimized and surgery is bloodless, the autologous units are discarded. Other blood conservation strategies, such as intraoperative blood salvage (cell saver) and acute normovolemic hemodilution (ANH) have been used successfully for hepatobiliary surgery in Jehovah’s Witness patients (Jabbour et al, 2005). ANH has been shown in two prospective studies to reduce the amount of red blood cells transfused per patient in major liver resections (Matot et al, 2002a; Jarnagin et al, 2008).

Volatile Anesthetics

Intravenous Anesthetics and Muscle Relaxants

Inhaled anesthetics supply all the aspects needed for anesthesia in one package, but today most anesthesiologists choose multiple drugs to reach their goals: immobility, amnesia, suppression of autonomic reflexes, muscle relaxation, and analgesia. Over the past several decades, dramatic advances have been made in intravenous anesthesia with the result that total intravenous anesthesia is now a workable alternative to the traditional inhalation anesthetic. Anesthesiologists using multiple drugs take advantage of interactions among drugs that have different mechanisms of action but similar therapeutic effects. The therapeutic goal of the anesthetic can often be achieved with less toxicity and faster recovery than when individual drugs are used alone in higher doses. The safety of intravenous anesthetics and muscle relaxants in patients having hepatobiliary surgery is well documented (Gelman, 1992).

The main mechanisms that affect hepatic elimination of a drug are changes in hepatic blood flow and changes in the ability of the liver cells to biotransform and/or excrete a drug. These two mechanisms, hepatic blood flow and hepatocyte function, play an important role in the choice of anesthetics for patients undergoing hepatobiliary surgery. High-extraction drugs (ketamine, flumazenil, morphine, fentanyl, sufentanil, lidocaine) are directly related to liver blood flow and are essentially cleared as they pass through the liver. Protein binding, enzymatic induction, intrahepatic shunting, and the effect of anesthetics on liver blood flow may influence the elimination of drugs with a high extraction rate. Reduced metabolic clearance results in increased peak drug level with minimal change in the elimination half-life. Drugs with a low extraction rate (benzodiazepines) differ from high-extraction drugs in that concentration changes little after passage through the liver, and intrinsic clearance depends on hepatic metabolic function as determined by liver size and total enzyme capacity (Colli et al, 1988). In patients with impaired liver function, such drugs have a prolonged length of activity with no increase in peak levels.

Anesthesia for Hepatectomy

Fluid loading before resection is commonly practiced in preparation for hepatic resection. This fluid loading often results in a distended and tense vena cava and dilated hepatic veins, both of which contribute to increased blood loss during liver mobilization and parenchymal transection. A relationship exists between extent of intraoperative blood loss and morbidity; blood loss greater than 5 L in an adult is associated with prohibitive mortality (Yanaga et al, 1988). Inadvertently, fluid loading to provide hemodynamic stability during episodes of uncontrolled bleeding may cause technical difficulties and handicap repair of venous injuries.

Another approach, low central venous pressure (CVP) anesthesia, is designed to preclude vena caval distension to facilitate mobilization of the liver and dissection of retrohepatic vena cava and major hepatic veins (Cunningham et al, 1994; Melendez et al, 1998). This surgical anesthetic technique compares favorably with other techniques for major hepatic resection (Delva et al, 1989; Segawa et al, 1993; Yanaga et al, 1988). Low CVP anesthesia is performed in combination with surgical inflow and outflow vascular control before parenchymal transection. Such an approach requires close cooperation between the anesthesiologist and the surgeon. Low CVP anesthesia minimizes hepatic venous bleeding during parenchymal transection and facilitates control of inadvertent venous injury. The blood loss resulting from a vascular injury is directly proportional to the pressure gradient across the vessel wall and the fourth power of the radius of the injury. If the CVP is lowered from 15 mm Hg to 3 mm Hg, the blood loss through a vena caval injury consequently falls by a factor greater than 5. Lowering CVP lessens the pressure component of the equation and also minimizes the radial component of flow by reducing vessel distension (Fig. 22.1).

FIGURE 22.1 Vena caval injury profile under various central venous pressure (CVP) conditions. A, High CVP. B, Low CVP. Increased CVP leads to distension of the vena cava with ensuing enlargement in diameter of injury and increase in the bleeding driving pressure.

Fluid restriction is an important aspect of the low CVP anesthesia technique. Preoperative overnight fluid replacement, a maneuver commonly performed before or immediately after the induction of general anesthesia, is withheld. Strict fluid restriction is practiced until the liver resection is completed. Intermittently, small fluid boluses may be given to maintain hemodynamic stability. To guarantee the safety of patients, appropriate cannulation is carried out, and a high level of vigilance is maintained. Transfusion equipment, such as the Woods pump coupled to a level 1 system, is an important aid to emergency fluid resuscitation, although this is infrequently needed. Intravascular hypovolemia is counteracted with 15-degree head-down tilt. Steep head-down tilt preserves hemodynamic stability and renal function by improving venous return. In animals, head-down tilt increases glomerular filtration rate, sodium excretion, and urine output lasting 8 hours (McCombs et al, 1996). Prolonged head-down tilt improves venous return and yields a 70% increase in plasma atrial natriuretic protein (Hughson et al, 1995; Terai et al, 1995). Although some investigators report intraoperative oliguria during low CVP anesthesia, no increase in the incidence of postoperative renal failure has been observed (Melendez et al, 1998).

Anesthesia is maintained with a combination of isoflurane in oxygen and narcotics, because isoflurane provides vasodilation with minimal myocardial depression (Schwinn et al, 1990). Elimination of nitrogen from the anesthetic gas mixture is necessary to permit expiratory nitrogen monitoring for air emboli. Restriction of nitrous oxide in the gas mixture prevents the diffusion-mediated increase in the volume of circulating air. Consistent with its minimal effect on cardiac output and systemic pressure, fentanyl has no effect on liver blood flow and oxygen delivery. In combination with isoflurane, fentanyl has the least effect on hepatic hemodynamics of any opiate, making it the narcotic of choice for anesthetics. In most patients, fentanyl is the ideal narcotic to aid in the maintenance of anesthesia, providing analgesia with minimal hypotension (Rosow et al, 1982). In a small group of patients, the anesthetic is supplemented with morphine to achieve the desired CVP. Morphine reduces CVP by inducing venous vasodilation caused by histamine release and µ₃ receptor activation (Grossman et al, 1996; Rosow et al, 1982; Stefano et al, 1995). The combination of these anesthetics readily provides the favorable low CVP environment for hepatic resection. With this technique, intravenous nitroglycerin to lower CVP to less than 5 mm Hg is rarely necessary.

The risk of intraoperative air emboli is likely to increase under low CVP anesthesia. Transesophageal echocardiography can be used to monitor air emboli, but this technology is sensitive and overdiagnoses clinically insignificant events. With surgical vigilance and rapid occlusion of open venous channels (see Chapters 90A and 92), low CVP anesthesia results in a low incidence (0.4%) of clinically significant air emboli. More complex low CVP anesthesia management techniques have been described (Rees et al, 1996). They employ epidural blockade and intravenous nitroglycerin. These patients may require intraoperative dopamine for systemic pressure support, a technique this is cumbersome and adds an unnecessary level of complexity to an already challenging situation.

Bloodless Surgery

Red blood cell transfusions are indisputably associated with an increase in mortality, major adverse cardiac and noncardiac outcome, acute lung injury, nosocomial infection, tumor growth, duration of hospitalization, and cost (Murphy et al, 2007; Beattie et al, 2009; Kulier et al, 2007; Marik et al, 2008; Atzil et al, 2008; Shander et al, 2007). Therefore it is important not to confuse the momentary helpful effect of red blood cell transfusion on hypotension and hypovolemia with an outcome benefit. Intraoperative blood cell salvage, hemodilution, and tolerance of normovolemic anemia (Gozzetti et al, 1995) all may contribute to reduced allogeneic red blood cell transfusion in major liver surgery. Autologous blood cell salvage (intraoperative autotransfusion) involves recovery of the patient’s shed blood from a surgical wound. The blood is then washed or filtered and reinfused into the patient. Hepatectomies often are performed for cancer but previously, cell salvage had been excluded in oncologic surgery because of the concern for potential dissemination of cancer cells. This concern has been challenged because of the availability of leukocyte-depleting filters and irradiation of blood removed during cancer surgery (Hansen et al, 1999).

Another transfusion-sparing technique is acute normovolemic hemodilution (ANH), a recycling technique that can be performed intraoperatively by the anesthesiologist. Blood is removed from the patient after induction and is replaced with crystalloid or colloid fluid. By removing the patient’s blood and replacing it with acellular fluid, the blood loss is diluted. The previously removed blood is stored at room temperature in the operating room and is returned to the patient at the conclusion of the operation. Two randomized studies of ANH in major hepatic resection showed a significant reduction in the percentage of patients requiring allogeneic red blood cell transfusion (Matot et al, 2002a; Jarnagin et al, 2008).

Epidural Anesthesia and Analgesia

Epidural block is widely used to manage major abdominal surgery and postoperative analgesia, but its risks and benefits are uncertain. Studies do not support the routine use of epidural anesthesia (EDA), rather than parenteral analgesia, to prevent postoperative mortality (Fanzca et al, 2002; Park et al, 2001; Wijeysundera et al, 2008). There are, however, other reasons to prefer EDA, including better postoperative pain relief and reduced pulmonary complications (Fanzca et al, 2002). In contrast to EDA for other abdominal surgery, the use of an indwelling epidural catheter and the timing of its removal in patients undergoing liver resection remain controversial (Matot, et al, 2002b).

The hemostatic abnormalities associated with liver resection are not always predictable and/or reversible. Significant disturbances of prothrombin time (PT) can be seen in patients undergoing uncomplicated liver resection. In patients who undergo minor liver resections, the PT usually returns to control levels within 1 day. In patients having major liver resections, the disturbances in PT can be prolonged and, as a result, the epidural catheter cannot be removed without administering fresh frozen plasma to normalize the coagulation profile because of a theoretically increased risk of spinal hematoma (Siniscalchi et al, 2004). In addition, thoracic EDA is associated with a decrease in hepatic blood flow and, if combined with continuous infusion of norepinephrine to counteract the EDA-related decrease in systemic arterial blood pressure, hepatic blood flow is decreased further (Meierhenrich et al, 2009; Tanaka et al, 1997). Hepatic hypoperfusion is regarded as an important factor in the alteration of hepatic oxygen balance and metabolic activity and the pathophysiology of perioperative liver injury. Furthermore, it has been hypothesized that hypoperfusion of the liver may initiate or contribute to the development of a systemic inflammatory response syndrome that may lead to multiple organ failure (Maynard et al, 1997). The decision to insert an epidural catheter for either intraoperative anesthesia or postoperative analgesia in patients undergoing hepatic resection should be made with care.

Obstructive Jaundice

Bile duct obstruction affects hepatic hemodynamics. Acute biliary obstruction is associated with an increase in liver blood flow (see Chapter 4), but flow is decreased with chronic obstruction. Relief of long-term obstruction is not associated with a return to normal pressures and may be associated with hemodynamic embarrassment and shock. The exact cause of hemodynamic derangement in the face of biliary obstruction is unknown, but increased portal resistance is believed to play a role. Biliary sepsis may contribute to the exacerbation of the hemodynamic embarrassment. In these cases, aggressive hemodynamic monitoring may be lifesaving. Either by percutaneous or endoscopic approaches, preoperative biliary drainage does not necessarily improve the perioperative morbidity of patients who show no evidence of infection, and it is therefore not recommended as a routine (Lai et al, 1994; see Chapter 50A, Chapter 50B, Chapter 50C, Chapter 50D ). When there is clinical concern for the development of acute cholangitis, rapid biliary decompression and intravenous antibiotics should be administered preoperatively, and surgery should be delayed until the infection resolves (Lai et al, 1992).

Immediate Postoperative Concerns

Some of the problems that cause metabolic and functional changes after hepatobiliary surgery are common to all major intraabdominal procedures (Aronsen et al, 1969). Others are unique and require an in-depth understanding of liver physiology. Immediate postoperative concerns are bleeding, intravascular volume, renal function, and oxygenation. Important laboratory tests are hematocrit, electrolytes, serum creatinine, blood urea nitrogen, PT/partial thromboplastin time, liver enzymes, and chest radiograph.

At least three mechanisms contribute to impaired pulmonary function in the postoperative period: 1) respiratory muscles disrupted by surgical transection of the abdominal muscles will not function normally; 2) patients may limit motion of respiratory muscles to minimize postoperative pain; and 3) stimulation of the visceral afferent nerves markedly changes the activation of respiratory muscles. For example, removal of the gallbladder activates vagal efferents that produce a reflex inhibition of diaphragmatic activity. Of note, laparascopic surgery may ameliorate the first two mechanisms but not the third, and significant decrements in pulmonary function may still be observed after laparascopic surgery.

The nature and magnitude of the patient’s preexisting respiratory condition determine the effect of a standard anesthetic on respiratory function. Anesthesia results in a decrease in mucus transfer and reductions of the functional residual capacity/closing capacity ratio. Airway closure can occur with mild, active expiration in patients with emphysema, bronchitis, and asthma. In addition, inflammation and scarring can compromise bronchial structural integrity and increase further the risk of alveolar collapse. In patients with asthma or obstructive lung disease, high airway resistance favors deep, slow respiration; this may not be possible in patients with large abdominal incisions. Anticipated respiratory compromise after upper abdominal surgery may preclude early extubation, especially in combination with any baseline abnormality in gas exchange.

Unique postoperative concerns in patients after hepatobiliary surgery include phosphorus replacement, anesthetic elimination, drug metabolism, coagulation, and postoperative pain control. Data suggest that hepatocellular regeneration may be critically dependent on cellular ATPase stores (Campbell et al, 1990; Greene, 1981). Liver regeneration after partial hepatectomy involves rapid cell division 24 to 72 hours after liver resection. Standard therapy for posthepatic resection should include the supplementation of intravenous fluids with sodium or potassium phosphate. Particular attention must be paid to anesthetic elimination and residual drug effect—especially sedative, analgesic, and neuromuscular blockers—in patients who have altered drug pharmacodynamics and pharmacokinetics. Postoperative pain management must be adapted to this population. Patient-controlled analgesia, commonly employed for postoperative pain management, should be employed initially without a basal narcotic infusion rate. After hepatic resection, patients experience an unpredictable reduction in the metabolism of narcotics.

The half-life of coagulation factors is 6 hours, so coagulation factor deficiency is likely to evolve rapidly. Routine parenteral administration of vitamin K commonly corrects the coagulation abnormalities within 48 hours. More rapid correction may be accomplished by fresh frozen plasma but is rarely needed, unless the PT or international normalized ratio (INR) exceeds 2, or if there are concerns of ongoing postoperative blood loss (Martin et al, 2003).

Delayed Perioperative Complications

Identifying patients at high risk for complications is an important but difficult component of the overall management strategy. A study from Memorial Sloan-Kettering Cancer Center showed that when postoperative hepatobiliary patients required admission to the intensive care unit, mortality ranged from 37% to 79% regardless of admission diagnosis (Melendez et al, 1998). A systematic proactive approach that identifies early deviations from the norm would be preferable to having to treat organ failure (Sesto et al, 1987).