Anaesthesia in liver disease patient
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Anaesthesia in liver disease patient. Baharulhakim Said b Daliman Department of Anaesthesiology & Intensive Care Hospital Kuala Terengganu. www.anaesthesia.co.in [email protected] Objectives. It is an important topic? Physiology Pharmacology ~ Phase I & II metabolism

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Anaesthesia in liver disease patient

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Anaesthesia in liver disease patient

Baharulhakim Said b Daliman

Department of Anaesthesiology & Intensive Care

Hospital Kuala Terengganu

[email protected]


Objectives

  • It is an important topic?

  • Physiology

  • Pharmacology ~ Phase I & II metabolism

  • Perioperative Management

  • Discussion

  • Latest update


  • The literature contains several good reviews on the perioperative management of patients with liver disease, and much of the research is based on retrospective analyses (Conn, 1991; Patel, 1999; Friedman, 1987; Friedman, 1999; Gholson, 1990).

  • Approximately 1 of every 700 patients admitted for elective surgery has abnormal liver chemistry test results (Conn, 1991).

  • Up to 10% of patients with end-stage liver disease may have surgery during the last 2 years of their lives (Jackson, 1968).


HKT experience…cholecystectomy


General

  • The largest organ in the body is the liver

  • Involved with almost all of the biochemical pathways that allow growth, fight disease, supply nutrients, provide energy, and aid reproduction

  • Dual blood supply: portal-venous (75%) and hepatic-arterial (25%).

  • Surgery and anesthesia impact hepatic function primarily due to their impact on hepatic blood flow and not primarily as a result of the medications or anesthetic technique utilized


Physiology

  • Primarily made up of hepatocytes (80% of the cells in the liver).

  • Complex functions of the liver which include:

    • metabolism of carbohydrates

    • metabolism of fats

    • protein synthesis and metabolism

    • drug metabolism and the synthesis and

    • excretion of bilirubin.


Physiology ~ carbohydrate metabolism

  • Main role ~ storage of glycogen. Normally, about 75 grams of glycogen is found in the liver

  • Depleted by 24-48 hours of starvation

  • Poor nutrition or pre-existing liver disease may lower glycogen stores ~ prone to hypoglycemia


Physiology ~ fat & protein metabolism

  • Beta oxidation of fatty acids and the formation of lipoproteins.

  • Synthesis of plasma proteins ~ All proteins, except gamma globulins and antihemophiliac factor

  • Normally, 10-15 grams of albumin are produced daily (3.5-5.5 g/dl)


Important facts

albumin can be decreased with liver disease

colloid osmotic pressure will be reduced

+

fewer binding sites for drugs and the unbound, active portion of protein-bound drugs will be increased example : Thiopental.


Important facts

  • Increased drug sensitivity is usually not clinically relevant until the albumin drops below 2.5 g/dl

  • Acute liver dysfunction is unlikely to be associated with low levels of albumin since the elimination half-life of albumin is 14-21 days


Clotting factors V, VII, IX, X, prothrombin and fibrinogen are all dependent on the liver for synthesis ~ many of the factors require only 20-30% of normal levels to stop bleeding, significant impairment of liver function must occur before problems begin.

Important facts:

Plasma half-lives of clotting factors are measured in hours. Therefore, acute liver dysfunction can lead to coagulopathies.

Both severe parenchymal disease and biliary disease may lead to coagulopathy - the former due to impaired synthesis and the second by decreased vitamin K absorption due to the absence of bile salts secondary to biliary obstruction.

Physiology


Physiology ~ drug metabolism

  • Microsomal enzymes convert lipid-soluble drugs to more water-soluble and less active products.

  • Elimination is dependent on hepatic blood flow and the microsomal enzyme actvity.

  • Drugs with high hepatic extraction ratios depend more on blood flow as their limiting factor whereas drugs with lower extraction ratios depend on the enzyme activity and protein binding.


Physiology ~ drug metablism

Divided into 2 phase:

  • Phase I metabolism

    • Oxidation

    • Reduction / demethylation

  • Phase II metabolism

    • Conjugation


Physiology ~ drug metabolism

Factor affecting drug metabolism:

  • microsomal enzyme system

  • route of administration

  • liver blood flow

  • competitive inhibition


Physiology ~ drug metabolism

Pharmacokinetic changes cause by liver disease:

  • Metabolising capacity is reduced ~ liver cells sick @ functioning normally but reduced in number

  • Liver cell that metabolise drugs are bypassed ~ portal-systemic shunts in cirrhosis

  • Liver disease cause hypoproteinaemia; drug binding capacity ,  more unbound & pharmacologically active drug may circulate


Physiology ~ drug metabolism

Pharmacodynamic changes occur because:

  • Cellular responses to drugs may alter. CNS sensitivity to opioids & sedatives is increased; effect of oral anticoagulants  because synthesis of clotting factors is impaired

  • Fluid & electrolyte imbalanced; Na retention may more readily induced by NSAIDs / corticosteroids; ascites & oedema may be more resistant to diuretics


Important facts

  • Chronic liver disease can lead to decreased metabolism due to decreased number of enzymes or to decreased blood flow (or obviously a combination of both).

  • Cirrhosis may actually be associated with increased drug metabolism due to upregulation of enzyme activity (due to decreased number of hepatocytes exposed to drugs for metabolism).


Pre Operative ~ Sx

Classic symptoms are:

  • Poor appetite (anorexia)- a common symptom

  • Weight loss- poor appetite leads to loss of weight. Improper metabolism of fat, carbohydrates, and proteins complicates the situation.

  • Polyuria/polydipsia (PU/PD)- excess urinating and excess drinking of water. This can occur in several other important diseases; kidneydisease, Cushing's disease, pyometra, and diabetes mellitus (sugar diabetes).

  • Lethargy- Poor appetite and disruption in normal physiologic processes leads to this symptom. Anemia adds to this lethargy, along with ascites due to the discomfort it causes.


Pre Operative ~ Sx

  • Anemia- Improper nutrition from a poor appetite, along with disease in the hepatocytes will cause this.

  • Light colored stool- If the biliary tree is prevented from secreting normal bile pigments into the intestine the stool will lack pigmentation and appear lighter in color.

  • Bleeding disorders- The normal clotting system is impaired since it depends on a healthy liver.

  • Distended abdomen due to ascites or hepatomegaly. If the distention is severe enough breathing might be labored from pain or the pressure on the diaphragm.


Pre Operative ~ Sx

  • Vomiting (emesis) nausea, or diarrhea. Sometimes blood is present in the vomitus (hematemesis), especially if a gastric ulcer is present. The ulcer comes from a complex interaction of histamine, nitrogen, bile acids, Gastrin, portal hypertension, and altered mucous membrane lining the inside of the stomach.

  • Pain due to distention of a diseased liver.

  • Orange colored urine or mucous membranes due to jaundice.

  • Behavioral changes- circling, head tilt, heap pressing, and seizures, particularly right after a meal.


Diagnosis

  • A thorough approach is needed for a correct diagnosis of any liver problem

  • Take full history

  • Do thorough physical examination

  • Relevant laboratory investigation eg. Complete blood count, biochemistry panel, liver function test, coagulation profile, ascites fluid analysis, urinalysis, ultrasound


Clinical

Aberrations of physiology in chronic liver disease:

  • Increased cardiac output

  • Decreased systemic vascular resistance

  • Hepatopulmonary syndrome

  • Tissue hypoperfusion resulting from shunting

  • Pulmonary hypertension

  • Ascites or hepatic hydrothorax causing restrictive disease


Pre OP management

  • Electrolyte replacement or management of hyperkalemia resulting from potassium-sparing diuretics (eg, spironolactone) - Provide anemia correction, assess for ongoing gastrointestinal blood resulting from portal gastropathy or varices, and hydrate as needed, avoiding excess sodium load in patients with cirrhosis.


Pre OP management

  • Management of encephalopathy - briefly, administer lactulose, restrict protein without compromising nutrition, and avoid use of sedatives that may precipitate the process


Pre OP management

  • Management of coagulopathy - Administer fresh frozen plasma to correct the prothrombin time to within 3 seconds of normal. Also, provide vitamin K (eg, 10 mg IM), cryoprecipitate, deamino-8-D-arginine vasopressin (eg, 0.3 mcg/kg IV), and platelet transfusion (if platelet count mL) (Patel, 1999).


Child’s Classification of liver disease


Intra operative factors

  • Effect of anaesthesia

  • Effect of surgery


Effect of anaesthesia

  • Most inhalation agents decrease hepatic blood flow

  • Fatal hepatic necrosis resulting from halothane is rare (1 case in 35,000), but severe liver dysfunction may occur in 1 case in 6000

  • Isoflurane is a safer choice because the effect on hepatic blood flow and oxygenation is much less than that of halothane. In fact, isoflurane increases hepatic arterial blood flow.


Effect of anaesthesia

  • Nitrous oxide is not hepatotoxic

  • Hypotension resulting in "shock liver injury" is possible

  • Delayed clearance of drugs such as midazolam, fentanyl, and morphine

  • Hypercarbia causes decreased portal blood flow and must be avoided

    # clinical pearl is to decrease the drug dosage by half and modify as needed (Conn, 1991).


Effect of surgery

  • Splanchnic traction and exploratory laparotomy can reduce blood flow to the intestines and the liver

  • Upper abdominal surgery is associated with the greatest reduction in hepatic blood flow

  • Elevation of liver chemistry tests is more likely to occur after biliary tract procedures than after nonabdominal procedures


Post operative factors

  • Cause of acute liver disease after surgery ~ multifactorial; drug-induced problems, hypotension, blood loss, anesthetic-induced hepatitis, and intraoperative hepatic hypoxia

  • Close monitoring of renal function is necessary, especially if fluid shifts have occurred. Renal failure worsens outcome, as noted in patients with hepatorenal syndrome


Post operative factors

  • Monitor patients for hypoglycemia and for signs of hepatic decompensation, such as jaundice, ascites, and encephalopathy

  • Treat spontaneous bacterial peritonitis

  • Enteral or, rarely, parenteral nutrition may be necessary.


Discussion

  • Hepatorenal syndrome

  • Anaesthesia for patient with cirrhosis

  • Anaesthesia for cholecystectomy

  • Anaesthesia for liver transplant


Hepatorenal syndrome

  • Typically occur in advanced cirrhosis with jaundice & ascites

  • Low urine output with low urinary sodium concentration

  • Tubular function intact & almost normal renal histology

  • Renal failure ~ ‘functional’

  • Advanced cases progress beyond ‘functional stage’ ► acute tubular necrosis


Hepatorenal syndrome

Mechanism:

Extreme peripheral vasodilation ► extreme ↓ arterial blood volume & hypotension

Activates homeostatic mechanism ► vasoconstriction of renal vasculature

↓ GFR & plasma renin remains high with salt & water retention


Hepatorenal syndrome

Treatment:

  • Treated for prerenal failure

  • Stop diuretic therapy

    Prognosis is poor


Anaesthesia for patient with cirrhosis

  • Postoperative morbidity is increased.

  • Problems with wound healing, bleeding, infection, decreased hepatic function and development of encephalopathy

  • Divided into acute hepatic failure

     chronic failure


Anaesthesia for patient with cirrhosis (acute failure)

  • Acute hepatic failure, only truly emergency surgery should be undertaken

  • Fresh frozen plasma may be necessary to correct coagulation defects

  • More susceptible to sedatives - sedatives and depressant drugs are probably not needed and nitrous oxide may be sufficient for analgesia and amnesia


Anaesthesia for patient with cirrhosis (acute failure)

  • Use of succinylcholine is possible without risk of prolonged effect.

  • Muscle relaxants are appropriate

  • Avoid hypotension and maintain urine output & avoid hypoglycemia.

  • Patient also prone to acidosis, hypoxemia and electrolyte abnormalities - appropriate laboratory tests should be utilized to guide therapy


Anaesthesia for patient with cirrhosis (chronic liver disease)

  • No optimal anesthetic drug or technique - perfusion (i.e. blood pressure) and oxygenation must be maintained

  • Regional anesthetic techniques are acceptable as well assuming that coagulation is normal

  • Plasma proteins may be decreased lead to increased effects of protein-bound drugs ~ increased susceptibility to cardiac depression, decreased responsiveness to catecholamines, and alterations in anesthetic requirement


Anaesthesia for cholecystectomy

  • Open or laparoscopically ~ under general anesthesia with muscle relaxation

  • Use of opioids ~ theoretical concern; known to cause spasm of the sphincter of Oddi

  • PCA or intercostal blockade for post OP pain (Postoperative pain can limit ventilation)


Anaesthesia for cholecystectomy

  • A bilirubin level of more than 3 mg/dL, elevated creatinine level, and hypoalbuminemia are also known to be associated with increased mortality (Runyon, 1986).

  • The odds ratio for perioperative mortality in patients with liver disease who undergo cholecystectomy is 8.47.

  • Open cholecystectomy in patients with cirrhosis has been called a formidable operation, although more recent studies have reported lower, but still considerable, mortality rates in patients with cirrhosis who undergo abdominal surgery


Anaesthesia for liver transplant

  • Preoperatively already; hypoxemia, anemia, thrombocytopenia, coagulation defects, electrolyte disturbances (hypokalemia and hypocalcemia), heart failure and encephalopathy

  • Invasive monitoring is routinely utilized (arterial pressure, cardiac filling pressures) and large bore intravenous access is important


Anaesthesia for liver transplant

  • Avoid nitrous oxide ~ venous air embolism

  • Decreased venous return during cross-clamping often requires inotropic support

  • Hypothermia should be avoided

  • Co-existing pulmonary hypertension may require vasodilator therapy

  • Acid-base status, electrolytes, glucose levels, and urine output should all be closely monitored.

  • Postoperative ventilation is frequently necessary


Most of us will never take part in a transplant but the lessons learned can be applied each time we administer anesthesia to a patient with hepatic disease


Latest Update

  • 1st dedicated liver unit in SEA (liver ICU) ~ Gleneagles Hospital, Singapore

  • Equipped withi. Monitoring devices

    ii. Ventilator

    iii. Liver dialysis machine

    (molecular adsorbent recirculating system)

  • Pre-requisite; existing living donor liver transplant (LDLT) program


Bibliography

  • Conn M: Preoperative evaluation of the patient with liver disease. Mt Sinai J Med 1991 Jan; 58(1): 75-80

  • Sai Praveen Haranath: Perioperative management of the patient with liver disease. emedicine 2002

  • Laurence & Bennett: Clinical pharmacology 7th edition. Churchill livingstone, pg 543


Thank you

[email protected]


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