**1. Introduction**

Patients with liver disease who undergo surgery have an increased risk of morbidity and mortality [1-3].

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The optimal management of such patients requires the following:


Impairment of the liver functions increases the risks of surgery and anesthesia in several ways, including the following [4-6]:


#### **1.1. Factors contributing decreased liver blood flow and hypoxia [7, 8]**


*Induction of anesthesia hypotension, intermittent positive-pressure ventilation, pneumoperitoneum during laparoscopic surgery, traction on abdominal viscera, hemorrhage, hypoxemia, vasoactive drugs, surgical maneuver, and even positioning of the patient may all result in intraoperative and perioperative hepatic hypoxemia and further increase in the hepatic dysfunction. Risk factors for hepatic hypoxemia include ascites, hepatic hydrothorax, and hepatopulmonary syndrome [7, 17]*

#### **1.2. Altered drug metabolism**

The duration of action of many drugs can be increased as a result of [10]

**1.** altered metabolism by cytochrome P450 enzymes,


The optimal management of such patients requires the following:

**5.** Hepatic hemodynamic evaluation and identification of the site of upper gastrointestinal

Impairment of the liver functions increases the risks of surgery and anesthesia in several ways,

**2.** Susceptibility to infection is increased due to altered functions of the hepatic reticuloen‐

**1.** Hyperdynamic circulation with increased cardiac output and decreased systemic vascular

**2.** Systemic and splanchnic vasodilation, with subsequent activation of the sympathetic nervous system and neurohormonal axis in an attempt to maintain arterial perfusion

**3.** Alterations in the systemic circulation due to arteriovenous shunting and reduced

**5.** The compensatory inotropic and chronotropic response to pharmacologic and physiologic

*Induction of anesthesia hypotension, intermittent positive-pressure ventilation, pneumoperitoneum during laparoscopic surgery, traction on abdominal viscera, hemorrhage, hypoxemia, vasoactive drugs, surgical maneuver, and even positioning of the patient may all result in intraoperative and perioperative hepatic hypoxemia and further increase in the hepatic dysfunction. Risk factors for hepatic hypoxemia*

dothelial cells and changes in the immune system and portal hypertension

**1.1. Factors contributing decreased liver blood flow and hypoxia [7, 8]**

*include ascites, hepatic hydrothorax, and hepatopulmonary syndrome [7, 17]*

The duration of action of many drugs can be increased as a result of [10]

**1.** Diagnosis of the underlying liver disease

**3.** Estimation of functional hepatic reserve

hemorrhage, if present

2 Recent Advances in Liver Diseases and Surgery

including the following [4-6]:

**3.** Reduced hepatic blood flow **4.** Altered drug metabolism

resistance

pressure

splanchnic inflow

**1.2. Altered drug metabolism**

**4.** Correction of underlying conditions if feasible

**2.** Assessment and stratification of the risk of surgery

**1.** Bleeding risk may increase because of coagulopathy

**4.** Anesthetic agents may reduce hepatic blood flow

**1.** altered metabolism by cytochrome P450 enzymes,

stress, including surgery, is blunted

Hepatic dysfunction can significantly impair the metabolism of certain medications. Examples are as follows [10, 11]:


### **2. Preoperative assessment**

If liver dysfunction is suspected, elective surgery should be deferred until extensive evaluation is made. Evaluation will include the following items [12].

#### **2.1. History and physical examination [1-3, 13]**

Thorough history and physical examination usually provide important informatation.


#### **2.2. Laboratory tests [1-18])**

The term "liver function tests" is a misnomer and can be misleading. Because of the complexity of liver functions, the ideal liver function test has not been invented yet. A successful liver function test, to assist with preoperative assessment of liver function, should be safe, repro‐ ducible, and easily performed.

The aims of the tests are as follows:

	- **•** Markers of hepatocellular injury include aminotransferases and lactate dehydrogenase
	- **•** Markers of cholestasis include alkaline phosphatase, gamma glutamyl transpeptidase, 5′-nucleotidase, and bilirubin
	- **•** Markers of synthetic functions of the liver are prothrombin time and albumin

#### **2.3. Aminotransferases**

Alanine aminotransferase (ALT) (normal range: 10-55 U/L)

Aspartate aminotransferase (AST) (normal range: 10-40 U/L)


#### **2.4. Alkaline phosphatase (AP)**


#### **2.5. Gamma Glutamyl Transpeptidase (GGTP)**


#### **2.6. 5′-Nucleotidase**

**1.** To determine the presence or absence of hepatic injury

Alanine aminotransferase (ALT) (normal range: 10-55 U/L) Aspartate aminotransferase (AST) (normal range: 10-40 U/L) **•** Serum level rises as a result of leakage from damaged tissue

**•** ALT is more specific than AST for hepatic injury

**•** Moderate rises occur in many liver diseases

liver neoplasms), and rarely alcoholic cirrhosis

**2.5. Gamma Glutamyl Transpeptidase (GGTP)**

**•** Mild to moderate elevations occur in many types of liver disease

**•** Marked elevations occur in hepatitis (viral, toxic, autoimmune, and ischemic)

**•** Serum level rises as a result of increased production and leaks into the serum

**•** Considerable rises occur in bone diseases (e.g., tumor, fracture, Paget's disease)

**•** It also originates from the intestine, placenta, and some neoplasms

**•** AST is nonspecific and can originate from skeletal muscle, red blood cell, kidney, pancreas,

**•** Marked rises occur in extra- and intrahepatic cholestasis, diffuse infiltrating disease (e.g.,

**•** Serum level rises as a result of overproduction and leakage into serum, as for AP; induced

**•** AST/ALT >2 suggests alcoholic liver disease or cirrhosis of any etiology

**3.** To specify the particular disease

4 Recent Advances in Liver Diseases and Surgery

5′-nucleotidase, and bilirubin

**4.** To determine its severity

**2.3. Aminotransferases**

brain, and myocardium

**•** Normal range 45-115 U/L

**•** Normal range: 0-30 U/L

by ethanol and drugs

**2.4. Alkaline phosphatase (AP)**

**2.** To decide whether the injury is cell necrosis or cholestasis

**•** Markers of hepatocellular injury include aminotransferases and lactate dehydrogenase **•** Markers of cholestasis include alkaline phosphatase, gamma glutamyl transpeptidase,

**•** Markers of synthetic functions of the liver are prothrombin time and albumin


#### **2.7. Bilirubin**


The mechanisms that result in elevation of serum unconjugated bilirubin levels include increased production (increased breakdown of hemoglobin (resulting from hemolysis, disordered erythropoiesis, and resorption of hematoma) or myoglobin (resulting from muscle injury)) and defects in hepatic uptake or conjugation.

**•** Conjugated hyperbilirubinemia

The mechanisms that result in the elevation of serum-conjugated bilirubin levels are hepato‐ biliary diseases, including extrahepatic and intrahepatic bile duct obstruction, viral, alcoholic or drug-induced hepatitis, and inherited hyperbilirubinemia.

#### **2.8. Prothrombin Time (PT) (10.9-12.5 s), International Normalized Ratio [INR]: (0.9-1.2)**

	- **1.** Decreased synthetic capacity as in acute or chronic liver failure (prolonged PT unre‐ sponsive to vitamin K)
	- **2.** Biliary obstruction (prolonged PT usually responsive to vitamin K administration)
	- **3.** Vitamin K deficiency (secondary to malabsorption, malnutrition, and antibiotics) and consumptive coagulopathy

#### **2.9. Albumin**

	- **1.** chronic liver failure
	- **2.** nephrotic syndrome, protein-losing enteropathy, and vascular leak

#### **2.10. Markers of viral hepatitis**

#### *2.10.1. Hepatitis A*

Acute infection is confirmed by detection of IgM anti-hepatitis A antibody (IgM HAV), which appears early in the course of infection and has high sensitivity and specificity. IgG anti-HAV predominates in convalescence and persists throughout life.

#### *2.10.2. Hepatitis B*


### *2.10.3. Hepatitis C*


#### **2.11. Liver function quantitative tests**

These tests offer attractive means to assess the liver functions. However, they have limitations, including expense, availability, invasiveness, and lack of validity.

#### *2.11.1. Indocyanine green clearance*

This dye is taken up almost exclusively by hepatocytes and excreted unchanged into the bile. It is measured photometrically in blood samples taken at regular intervals after a bolus intravenous injection (0.5 mg/kg). Clearance of the dye decreases with loss of hepatocyte mass.

### *2.11.2. Aminopyrine breath test*

**2.10. Markers of viral hepatitis**

6 Recent Advances in Liver Diseases and Surgery

Acute infection is confirmed by detection of IgM anti-hepatitis A antibody (IgM HAV), which appears early in the course of infection and has high sensitivity and specificity. IgG anti-HAV

**•** Acute infection is associated with the presence of hepatitis B surface antigen (HBsAg).

**•** Some time after HBsAg disappears; HBsAg antibody (anti-HBs) appears and persists for

**•** In the interval between disappearance of HBsAg and appearance of anti-HBs, hepatitis core antigen antibody (anti-HBc) is present and helps as a marker for current or recent HBV

**•** Hepatitis C antibodies are detected relatively late in the course of the HCV infection.

**•** Reverse transcriptase polymerase chain reaction and branched amplification assays are the

These tests offer attractive means to assess the liver functions. However, they have limitations,

This dye is taken up almost exclusively by hepatocytes and excreted unchanged into the bile. It is measured photometrically in blood samples taken at regular intervals after a bolus intravenous injection (0.5 mg/kg). Clearance of the dye decreases with loss of hepatocyte mass.

predominates in convalescence and persists throughout life.

**•** HBsAg becomes undetectable 1-3 months after jaundice.

**•** IgM anti-HBc distinguishes recent from remote infection

including expense, availability, invasiveness, and lack of validity.

**•** Detection of HBsAg precedes serum aminotransferase elevations.

**•** Anti-HBc may remain for years after infection longer than anti-HBs.

*2.10.1. Hepatitis A*

*2.10.2. Hepatitis B*

life.

infection.

*2.10.3. Hepatitis C*

**•** False-positive test is a problem.

most sensitive and specific.

*2.11.1. Indocyanine green clearance*

**2.11. Liver function quantitative tests**

Radioactivity (14CO2) is measured in breath at 15-min intervals for 2 h after oral or intravenous administration of 14C-labeled methyl aminopyrine. It may predict death and histology in chronic hepatitis.

### *2.11.3. Monoethylglycinexylidide (MEGX)*

This lidocaine metabolite is measured in blood samples 15 min after intravenous administra‐ tion of lidocaine (1 mg/kg). It may predict death and complications before and after liver transplantation

#### **2.12. Ultrasound**

Ultrasound is useful for assessing liver size, spleen size, intra- and extrahepatic biliary tree, and the presence of liver masses. It can also detect ascites in its earliest stages (≥100 mL). Doppler ultrasonography is helpful in assessment of portal venous patency, direction of portal flow.
