Anesthesia for liver cirrhosis

CIRRHOSIS



Cirrhosis is a serious and progressive disease that eventually results in hepatic failure.

causes include

• chronic active hepatitis (postnecrotic cirrhosis),
• chronic biliary inflammation or obstruction (primary biliary cirrhosis, sclerosing cholangitis),
• chronic right-sided congestive heart failure (cardiac cirrhosis),
• autoimmune hepatitis,
• hemochromatosis,
• Wilson's disease,
• 1-antitrypsin deficiency,
• nonalcoholic steatohepatitis, and
• cryptogenic cirrhosis.

Preoperative Considerations


Patients with cirrhosis are at increased risk for 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 and controlling or preventing its complications

Gastrointestinal Manifestations

Portal hypertension (> 10 mm Hg) leads to the development of extensive portal-systemic venous collateral channels. Four major collateral sites are generally recognized: gastroesophageal, hemorrhoidal, periumbilical, and retroperitoneal.
In patients with cirrhosis, massive bleeding from gastroesophageal varices is a major cause of morbidity and mortality. In addition to the effects of acute blood loss, the increased nitrogen load (from the breakdown of blood in the intestinal tract) can precipitate hepatic encephalopathy.
The treatment of variceal bleeding is generally supportive (medical).
Blood loss should be replaced with intravenous fluids and blood products.
Nonsurgical treatment includes vasopressin (0.1–0.9 U/min intravenously), somatostatin (250 g followed by 250 g/h), propranolol, balloon tamponade (with a Sengstaken–Blakemore tube), and endoscopic sclerosis of the varices.
Percutaneous transjugular intrahepatic portosystemic shunts (TIPS) can reduce portal hypertension and subsequent bleeding (however, it may increase the incidence of encephalopathy).
When the bleeding fails to stop or it recurs, emergency surgery may be indicated. Surgical risk has been shown to correlate with the degree of hepatic impairment, based on clinical and laboratory findings. Shunting procedures are generally performed on low-risk patients, whereas ablative surgery, esophageal transection, and gastric devascularization are reserved for high-risk patients.

Child's Classification for Evaluating Hepatic Reserve.1
Risk Group                            A                                         B                                           C
Bilirubin (mg/dL)                 < 2.0                              2.0–3.0                                       > 3.0
Serum albumin (g/dL)           > 3.5                            3.0–3.5                                        < 3.0
Ascites                                None                           Controlled                               Poorly controlled
Encephalopathy                  Absent                          Minimal                                   Coma
Nutrition                             Excellent                        Good                                      Poor
Mortality rate (%)                 2–5                              10                                                    50


Hematological Manifestations

Anemia, thrombocytopenia, and, less commonly, leukopenia, may be present. The cause of the anemia is usually multifactorial and includes blood loss, increased red cell destruction, bone marrow suppression, and nutritional deficiencies.
Congestive splenomegaly (from 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 activators of the fibrinolytic system may also contribute to the coagulopathy.
coagulopathy should be corrected before surgery. Clotting factors should be replaced with appropriate blood products such as FFP and cryoprecipitate.
Platelet transfusions should be considered immediately prior to surgery for counts less than 100,000/ L.



Circulatory Manifestations

Cirrhosis is typically characterized by a hyperdynamic circulatory state. Cardiac output is often increased, and generalized peripheral vasodilation is present.
Arteriovenous shunting can occur in both the systemic and pulmonary circulations. The arteriovenous shunting together with the decrease in blood viscosity from anemia are partly responsible for the increased cardiac output, which is dependent upon above normal filling pressures and below normal systemic vascular resistance (cirrhotic cardiomyopathy).

Respiratory Manifestations

Disturbances in pulmonary gas exchange as well as ventilatory mechanics are often present.
Hyperventilation is common and results in a primary respiratory alkalosis.
Hypoxemia is frequently present and is due to right-to-left shunting (up to 40% of cardiac output). Shunting is due to an increase in both pulmonary arteriovenous communications (absolute) and ventilation/perfusion mismatching (relative).
Elevation of the diaphragm from ascites decreases lung volumes, particularly functional residual capacity, and predisposes to atelectasis.
Moreover, large amounts of ascites produce a restrictive ventilatory defect that increases the work of breathing.
Review of the chest film and arterial blood gas measurements is very useful preoperatively because atelectasis and hypoxemia are often not evident on clinical examination.
Paracentesis should be considered for patients with massive ascites and pulmonary compromise but should be done with caution because removal of too much fluid can lead to circulatory collapse.

Renal Manifestations and Fluid Balance


Derangements of fluid and electrolyte balance are manifested as ascites, edema, electrolyte disturbances, or the hepatorenal syndrome.
Important mechanisms thought to be responsible for ascites include (1) portal hypertension, which increases the 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 often water) retention.
patients with cirrhosis and ascites have decreased renal perfusion, altered intrarenal hemodynamics, enhanced proximal and distal sodium reabsorption, and often an impairment of free water clearance. Hyponatremia and hypokalemia are common. The former is dilutional, whereas the latter is due to excessive urinary potassium losses (from secondary hyperaldosteronism or diuretics). The most severe expression of these abnormalities is seen with development of the hepatorenal syndrome.

The hepatorenal syndrome is a functional renal defect in patients with cirrhosis that usually follows gastrointestinal bleeding, aggressive diuresis, sepsis, or major surgery. It is characterized by progressive oliguria with avid sodium retention, azotemia, intractable ascites, and a very high mortality rate. Treatment is supportive and often unsuccessful unless liver transplantation is undertaken.

Central Nervous System Manifestations
Hepatic encephalopathy is characterized by alterations in mental status with fluctuating neurological signs (asterixis, hyperreflexia, or an inverted plantar reflex) and characteristic electroencephalographic changes (symmetric high-voltage, slow-wave activity).
Metabolic encephalopathy appears to be related to both the amount of hepatocellular damage present as well as the degree of shunting of portal blood away from the liver and directly into the systemic circulation. The accumulation of substances originating in the gastrointestinal tract but normally metabolized by the liver has been implicated. These proposed toxins include ammonia, methionine metabolites (mercaptans), short-chain fatty acids, and phenols.

Factors known to precipitate hepatic encephalopathy include
• gastrointestinal bleeding,
• increased dietary protein intake,
• hypokalemic alkalosis (from vomiting or diuresis),
• infections, and
• worsening liver function.
Encephalopathy should be aggressively treated preoperatively.
Precipitating causes should be corrected.
Oral lactulose 30–50 mL every 8 h or neomycin 500 mg every 6 h is useful in reducing intestinal ammonia absorption.
Avoidance of sedatives in patients with encephalopathy is recommended.

Intraoperative Considerations

Drug Responses

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 blocking agents (NMBAs), is due to the expanded extracellular fluid compartment; an apparent resistance may be observed, requiring larger than normal loading doses.
• Smaller than normal maintenance doses of NMBAs dependent on hepatic elimination (pancuronium, rocuronium, and vecuronium) are needed.
• There may be a prolonged duration of action for succinylcholine as a result of reduced levels of pseudocholinesterase, but it is rarely of clinical consequence.

Anesthetic Technique

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 thrombocytopenia or coagulopathy, but more care than normal must be directed to avoid hypotension.
A barbiturate or propofol induction followed by isoflurane in oxygen or an oxygen–air mixture is most commonly employed for general anesthesia.
Opioid supplementation reduces the dose of the volatile agent required, but the half-lives of opioids are often significantly prolonged, leading to prolonged respiratory depression.
Cisatracurium may be the NMBA of choice because of its unique nonhepatic metabolism.

Preoperative nausea, vomiting, upper gastrointestinal bleeding, and abdominal distention due to massive ascites require a well-planned, methodical anesthetic induction. Preoxygenation and a rapid-sequence induction with cricoid pressure are most often performed. For unstable patients and those with active bleeding, either an awake intubation or a rapid-sequence induction with cricoid pressure using ketamine (or etomidate) and succinylcholine is best advised.

Monitoring

Close respiratory and cardiovascular monitoring is necessary for patients undergoing abdominal procedures.
Intraarterial pressure monitoring is generally indicated for most patients. Rapid changes in blood pressure occur as a result of excessive bleeding, rapid intercompartmental fluid shifts, and surgical manipulations.
Intravascular volume status is often difficult to assess without central venous or pulmonary artery pressure monitoring.
Urinary output must be followed closely; mannitol should be considered for persistently low urinary outputs in spite of adequate intravascular fluid replacement.


Fluid Replacement
The use of predominantly colloid intravenous fluids (albumin) may be preferable to avoid sodium overload 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.
Because most patients are anemic preoperatively and coagulopathic, red cell transfusions perioperatively are common.
Significant transfusions may result in citrate toxicity. Citrate, the anticoagulant in stored red blood cell preparations, is normally readily metabolized by the liver. Toxicity occurs in patients with cirrhosis because metabolism is impaired. Citrate binds with serum calcium leading to the sequelae of hypocalcemia.
Intravenous calcium is often necessary to reverse the negative inotropic effects of a decrease in the blood ionized calcium concentration.