Liver injury which results from anesthesia and surgery is at least in part due to changes in hepatic hemodynamics. Increased hepatic venous resistance often coincides with decreased arterial perfusion pressure. Preoperative optimization requires assessment of the patient’s cardiovascular status, renal function, and pulmonary function. Cirrhosis is associated with cardiomyopathy which is manifest by conduction abnormalities and diastolic dysfunction [6, 7]. Preoperative assessment with transthoracic echocardiography can be complemented by intraoperative transesophageal monitoring. In particular, right ventricular function can be assessed as intravascular volume and vasopressors are manipulated. Stress echocardiography is often used as a screen for hemodynamically significant coronary artery disease.

Patients with cirrhosis are often volume-overloaded with ascites and edema. Renal dysfunction is often masked as low creatinine and urea nitrogen may reflect sarcopenia and impaired ureagenesis rather than normal glomerular filtration rate (GFR). However, in early hepatorenal syndrome, the sodium avidity of the kidney indicates hypoperfusion, and echo demonstration of underfilling of the left ventricle will confirm intravascular volume contraction. This is often associated with significant arterial vasodilation which correlates with the severity of cirrhosis. Preoperative optimization includes restoration of perfusion pressure by increasing arterial tone and intravascular volume while controlling ascites and decreasing edema. Arterial vasodilation may reflect hypocalcemia and severe anemia as well as concomitant adrenal insufficiency [8, 9]. Hypoalbuminemia may be addressed with hyperoncotic albumin and judicious diuresis undertaken. Persistent arterial vasodilation may require vasopressor support. Terlipressin is not available in the United States but would be the first-choice agent in much of the world. Our preference is norepinephrine. Large-volume paracentesis may also be considered in an effort to optimize renal function once arterial tone and intravascular volume are optimized. The need for significant vasopressor support in advance of induction of anesthesia heralds an even higher risk of perioperative morbidity and mortality.

Electrolyte imbalance is common in cirrhosis. Hyponatremia, hypokalemia, hypomagnesemia, hypophosphatemia, and hypozincemia can be addressed preoperatively. Care should be taken to avoid exacerbating metabolic acidosis by administering hyperchloremic solutions. Balanced electrolyte solutions are commercially available. In addition, the relatively high chloride content of blood products including albumin can be counterbalanced by creating a solution of 0.45% sodium chloride with 50–75 mEq/L which is readily available and inexpensive. Over-rapid correction of hyponatremia which is associated with central pontine myelinolysis also can be avoided with this approach. Although colloid administration is controversial, patients with cirrhosis appear to benefit from albumin particularly in the settings of infection and renal failure. However, other colloids such as hydroxyethyl starch (Hetastarch) are associated with renal failure and relatively contraindicated in the setting.

Hepatic encephalopathy develops with deteriorating liver function and worsening portosystemic shunting. It often heralds infectious complications or acute bleeding. Agitation, delirium, and altered nociception are typical. If the enteral route is available, we continue rifaximin and lactulose, and zinc if hypozincemia. We do not restrict protein but do occasionally use branched chain enriched formulae if encephalopathy is refractory to standard measures. We address environmental factors such as early mobilization of the patient out of bed, daylight during the daytime, and promote sleep hygiene with efforts to minimally disturb the patient at night. Local therapy such as repositioning, a heating pad, and/or lidocaine patch serve to minimize systemic narcotic requirements. Although we are hesitant to place epidural catheters in coagulopathic patients, regional anesthesia is often a very useful adjunct.

The metabolism of sedative hypnotics and narcotics is impaired in liver failure but unpredictably. We avoid benzodiazepines and minimize narcotics—treating as needed rather than with continuous infusions. Non-narcotic approaches are limited as nonsteroidal anti-inflammatory agents may increase the risk of GI bleeding. Acetaminophen is effective and can be administered parenterally if needed, but the total daily dose should be reduced in liver failure to 2 g. Ketamine is an excellent analgesic in small doses of 10–25 mg and does not cause respiratory depression or worsen hemodynamic instability. Gabapentin is an effective adjunct [10]. Even a single preoperative dose lowers narcotic requirements [11].

Hepatic encephalopathy seems to reduce the incidence of recall during anesthesia. Isoflurane and sevoflurane have minimal direct impact on hepatic function [12]. However, both may exacerbate arterial vasodilation and result in hypotension requiring vasopressors. Although the minimum alveolar concentration for volatile anesthetics is higher in chronic alcohol users, it is significantly lower in the setting of liver disease [13].

Respiratory function may be impaired in cirrhosis because of mechanical factors such as ascites and chest wall edema as well as altered respiratory drive related to hepatic encephalopathy. Gas exchange may also be affected by atelectasis, pulmonary edema, and pneumonia. In the absence of radiographic abnormalities, the diffusing capacity is often low and reflects intrapulmonary shunting due to hepatopulmonary syndrome, which can be demonstrated with echocardiography using microbubbles. In addition to optimizing the patient’s volume status preoperatively, discontinuation of tobacco smoking and management of obstructive airways with appropriate bronchodilation are imperative. Once intubated and mechanically ventilated, such patients are particularly prone to lung injury. Consequently, a lung-protective ventilating strategy should be undertaken with low tidal volumes (6 mL/kg IBW) and PEEP [14]. We use the ARDS-Net high PEEP protocol [15] to titrate PEEP and FiO₂ and start with the PEEP set at BMI/4. The duration of intubation and mechanical ventilation should be minimized. This requires minimizing sedation in the ICU changing intraoperative anesthetic management. We attempt extubation within 6 h, in the OR if possible. We use noninvasive ventilation with CPAP or BiPAP until the patient can mobilize out of bed and cough effectively. These patients often have impaired gastric motility. Aspiration of gastric contents is often a life-ending event, prompting us to routinely decompress the stomach with a gastric tube until the patient can protect the airway.

Malnutrition is common in liver failure [16], with muscle wasting and sarcopenia evident on exam and abdominal CT [17] even in obese patients with nonalcoholic fatty liver disease [18]. The MELD score fails to capture this comorbidity which correlates with weakness and risk of postoperative infection. Cirrhosis is a catabolic process which is difficult to reverse. However, if time permits, a trial of nutritional supplementation is indicated, with postpyloric placement of a small-bore feeding tube [19] if sufficient calories and protein cannot be reliably ingested per os. We aggressively treat hepatic encephalopathy rather than reduce protein. Vitamin deficiencies should be anticipated, particularly fat-soluble vitamins in cholestatic liver disease. Thiamine supplementation is indicated particularly in alcohol-induced liver disease.