Anaesthetic management of Anaesthetic management of Liver diseaseLiver disease

SpeakerSpeaker Dr.K.Aditya vikramDr.K.Aditya vikram P.G. Dept of AnaesthesiologyP.G. Dept of AnaesthesiologyModeratorModerator Dr. MadhaviDr. Madhavi Asst. prof Dept of AnaesthesiologyAsst. prof Dept of AnaesthesiologyChair personChair person Dr. SatyanarayanaDr. Satyanarayana Prof Dept of Anaesthesiology.Prof Dept of Anaesthesiology.

Concerns of anaesthesiologist in Concerns of anaesthesiologist in chronic liver disease patients.chronic liver disease patients.

Optimisation of patient .Optimisation of patient .

1.coagulopathy.1.coagulopathy. 2.anaemia.2.anaemia. 3.hypoproteinaemia3.hypoproteinaemia

.. 4.ascitis.4.ascitis. 5.disturbed 5.disturbed

metabolism.metabolism. 6.encephalopathy.6.encephalopathy. 7.hyperbilirubinaem7.hyperbilirubinaem

ia.ia.

8.altered P-K of 8.altered P-K of drugs.drugs.

9.hepato-9.hepato-pulmonary pulmonary syndrome.syndrome.

10.hepatorenal 10.hepatorenal syndrome.syndrome.

11.hypersplenism.11.hypersplenism. 12.malnutriton12.malnutriton

Pre-operative risk factor assessment Pre-operative risk factor assessment and minimizing the risk factors.and minimizing the risk factors.

Anesthetic management proper.Anesthetic management proper.

Post operative jaundice.Post operative jaundice.

Anesthetic management of Anesthetic management of patients with moderate to severe patients with moderate to severe liver disease includes liver disease includes

Pre-op optimisation of condition Pre-op optimisation of condition Modifying and minimising the risk Modifying and minimising the risk

factors of mortalityfactors of mortality

COAGULOPATHYCOAGULOPATHY

Decreased synthesis.Decreased synthesis. Thrombocytopenia.Thrombocytopenia. Hypothermia.Hypothermia.

Coagulopathy :Coagulopathy : PT 2-3 sec control .PT 2-3 sec control .

FFP 2-6 units need to be transfused.FFP 2-6 units need to be transfused.

1FFP increases clotting factors by 2-5%.1FFP increases clotting factors by 2-5%.

250ml FFP increases fibrinogen by 10%.250ml FFP increases fibrinogen by 10%.

Platelets<40,000/ clinicallybleeding diathesis - Platelets<40,000/ clinicallybleeding diathesis - Platelet transfusion required. Platelet transfusion required.

Bleeding and clotting Bleeding and clotting abnormalitiesabnormalities

Decrease in Vit K dependent factors.Decrease in Vit K dependent factors. Decreased intrinsic factors.Decreased intrinsic factors. Decreased t1/2 of clotting factors due to Decreased t1/2 of clotting factors due to

consumptive coagulopathy. consumptive coagulopathy. Qualitative and quantitative platelet Qualitative and quantitative platelet defects, thrombocytopenia.defects, thrombocytopenia.

Goal: PT < 2.5 sec of controlGoal: PT < 2.5 sec of control

Fresh Frozen PlasmaFresh Frozen Plasma::

is collected as the supernatant after centrifuging a is collected as the supernatant after centrifuging a donation of whole blood.donation of whole blood.

It is frozen within 8 hours to maintain the activity of It is frozen within 8 hours to maintain the activity of factors V and VII. factors V and VII.

The main indication is deficiency of multiple The main indication is deficiency of multiple coagulation factors such as that found in massive coagulation factors such as that found in massive haemorrhage, DIC, liver disease, and occasionally for haemorrhage, DIC, liver disease, and occasionally for reversal of warfarin effect.reversal of warfarin effect.

Stored at -18 to-30 c, thawed before Stored at -18 to-30 c, thawed before

administeration,ABO compatibility must be doneadministeration,ABO compatibility must be done

Consider FFPs in:Consider FFPs in: microvascular bleeding due to cogulopathy.microvascular bleeding due to cogulopathy. after massive whole blood transfusion.after massive whole blood transfusion. APTT>1.5 times,I.N.R>2 times normal.APTT>1.5 times,I.N.R>2 times normal. 1 unit of FFP per 10 kg body weight will raise the 1 unit of FFP per 10 kg body weight will raise the

fibronogen level by 100mg/ml.fibronogen level by 100mg/ml. 1 unit of FFP to every 4units of PRBCS in actively 1 unit of FFP to every 4units of PRBCS in actively

bleeding patients guided by aPTTbleeding patients guided by aPTT

PlateletsPlatelets: A unit of platelets is prepared from a single whole : A unit of platelets is prepared from a single whole blood collection and contains at least 5.5 x 10blood collection and contains at least 5.5 x 1010 10 platelets in platelets in 50 ml plasma.50 ml plasma.

They are stored at 20-24°C under agitation and have a shelf They are stored at 20-24°C under agitation and have a shelf life of 5 days. Each unit can raise the platelet count by 5-10 x life of 5 days. Each unit can raise the platelet count by 5-10 x 109. 109.

6 units of random donor plates or 1 unit of single donor 6 units of random donor plates or 1 unit of single donor platelets raises the count by 20000-30000 per cubic mm.platelets raises the count by 20000-30000 per cubic mm.

Goal of platelet therapy to maintain a platelet count of 50000 Goal of platelet therapy to maintain a platelet count of 50000 to 100000per cubic mm .to 100000per cubic mm .

  

Hematologic Abnormalities :Hematologic Abnormalities :

Numerous hematologic manifestations of cirrhosis Numerous hematologic manifestations of cirrhosis are present, including anemia from a variety of are present, including anemia from a variety of causes including hypersplenism, hemolysis, iron causes including hypersplenism, hemolysis, iron deficiency, and perhaps folate deficiency from deficiency, and perhaps folate deficiency from malnutrition.malnutrition.

Macrocytosis is a common abnormality in red Macrocytosis is a common abnormality in red blood cell morphology seen in patients with blood cell morphology seen in patients with chronic liver disease, and neutropenia may be chronic liver disease, and neutropenia may be seen as a result of hypersplenism.seen as a result of hypersplenism.

Packed Red cellsPacked Red cells: : A bag of RBCs have a haematocrit of between 60-70%, A bag of RBCs have a haematocrit of between 60-70%,

and an average shelf life of 35 days if properly stored.and an average shelf life of 35 days if properly stored.

Their function is to act as carriers of oxygen and Their function is to act as carriers of oxygen and carbon dioxide in the blood.carbon dioxide in the blood.

The main indications for transfusion is the correction The main indications for transfusion is the correction of anaemia or replacement in acute haemorrhage, but of anaemia or replacement in acute haemorrhage, but there is no absolute level of Hb to trigger a there is no absolute level of Hb to trigger a transfusion.transfusion.

A single unit of red blood cells will typically increase A single unit of red blood cells will typically increase

the Hb by 1g/dl, 3%haematocrit.the Hb by 1g/dl, 3%haematocrit.

Management of various risk factorsManagement of various risk factors

AscitesAscites – indicates severe liver disease – indicates severe liver disease

Elective surgery:Elective surgery: carbohydrate and protein dietcarbohydrate and protein diet restrict sodium intake – 2gm/dayrestrict sodium intake – 2gm/day Not responding to salt restriction Not responding to salt restriction Use of potassium sparing diuretics alone/Use of potassium sparing diuretics alone/ loop diureticsloop diuretics

Tab. spironolactone 100mg/day max 400mg/dTab. spironolactone 100mg/day max 400mg/d

Tab. Amiloride 5-10 mg/dTab. Amiloride 5-10 mg/d

Frusemide 40-160 mg/dFrusemide 40-160 mg/d

if hyponatremia (<125meq/l) restrict fluid if hyponatremia (<125meq/l) restrict fluid intakeintake

800-1000ml/d 800-1000ml/d

Goal: Pre-op sodium level >130mmol/LGoal: Pre-op sodium level >130mmol/L

Large volume paracentesis:Large volume paracentesis:

tense ascites - wt.loss <0.5kg/dtense ascites - wt.loss <0.5kg/d

if >1lt/d supplement with salt free albumin if >1lt/d supplement with salt free albumin 10gm/d , dextran -70 8gm/d, gelatin 10gm/d , dextran -70 8gm/d, gelatin 125ml/d.125ml/d.

Definition Definition Refractory ascites Refractory ascites is defined as fluid overload that is non-is defined as fluid overload that is non-

responsive to restriction of dietary sodium to 88 mmol/day responsive to restriction of dietary sodium to 88 mmol/day and maximal-dose diuretic therapy (furosemide + and maximal-dose diuretic therapy (furosemide + spironolactone), in the absence of ingestion of spironolactone), in the absence of ingestion of prostaglandin inhibitors, such as non-steroidal anti-prostaglandin inhibitors, such as non-steroidal anti-inflammatory drugs.inflammatory drugs.

Ascites is also considered to be refractory when there is Ascites is also considered to be refractory when there is intolerance of diuretic therapy. intolerance of diuretic therapy.

Indications of failure of diuretic therapy include minimal or Indications of failure of diuretic therapy include minimal or no weight loss, together with inadequate urinary sodium no weight loss, together with inadequate urinary sodium excretion (< 78 mmol/day).excretion (< 78 mmol/day).

Less than 10% of patients with ascites complicating Less than 10% of patients with ascites complicating cirrhosis meet the criteria of the definition of refractory cirrhosis meet the criteria of the definition of refractory ascites. ascites.

Serum-ascites albumin gradient = serum albumin - Serum-ascites albumin gradient = serum albumin - ascitic fluid albumin ascitic fluid albumin

o if o if > > 1.1 g/dL portal hypertension is present; 1.1 g/dL portal hypertension is present; o if < 1.1 g/dL portal hypertension is not present o if < 1.1 g/dL portal hypertension is not present

(about 97% accurate). (about 97% accurate).

A high gradient is associated with diffuse parenchymal A high gradient is associated with diffuse parenchymal liver disease and occlusive portal and hepatic venous liver disease and occlusive portal and hepatic venous disease (as well as nephrotic syndrome, liver disease (as well as nephrotic syndrome, liver metastasis and hypothyroidism). metastasis and hypothyroidism).

Large volume paracentesis:Large volume paracentesis:

If tense ascites is causing clinically significant symptoms, a If tense ascites is causing clinically significant symptoms, a single large volume paracentesis (4–6 L) can be performed single large volume paracentesis (4–6 L) can be performed safely, without adversely affecting hemodynamics, and safely, without adversely affecting hemodynamics, and without the necessity of concomitant colloid infusion, as an without the necessity of concomitant colloid infusion, as an initial treatment to relieve the symptoms.initial treatment to relieve the symptoms.

If the paracentesis is > 6 L, intravenous infusion of albumin, If the paracentesis is > 6 L, intravenous infusion of albumin,

6–8 g/L removed, is recommended. 6–8 g/L removed, is recommended.

To prevent reaccumulation of fluid, dietary sodium restriction To prevent reaccumulation of fluid, dietary sodium restriction and diuretic therapy are instituted.and diuretic therapy are instituted.

Large volume paracentesis is not first line therapy for all Large volume paracentesis is not first line therapy for all patients with tense ascites.patients with tense ascites.

Albumin (5%)

6.4-7.4 130-160 130-160 < 1 0 0 0 309 50 g/L albumin

Albumin (25%)

6.4-7.4 130-160 130-160 < 1 0 0 0 312 250 g/L albumin

Solution pH Na+ Cl- K+ Ca++ Lactate GlucoseOsmolali

ty Other

Infusion rate: 25% vials: 2-3 ml/minute maximum. 5% solution: 5-10 ml/minute maximum. 

Discard unused solution after 4 hours.Dilute if necessary with D5W or NS. 

Hypoproteinemia (Usual dose): 0.5- 1 gram/kg/dose q1-2 days as calculated to replace ongoing losses. Maximum dose/day: 250 grams/48 hours. 

 Albumin is a highly soluble, globular protein (MW 66,500), accounting for 70-80% of the colloid osmotic pressure of plasma. 

Therefore, it is important in regulating the osmotic pressure of plasma. Human Albumin 25% supplies the oncotic equivalent of approximately 5 times its volume of human plasma.

It will increase the circulating plasma volume by an amount approximately 3.5 times the volume infused within 15 minutes, if the recipient is adequately hydrated.

This extra fluid reduces hemoconcentration and decreases blood viscosity.

Albumin is distributed throughout the extracellular water and more than 60% of the body albumin pool is located in the extravascular fluid compartment.

The total body albumin in a 70 kg man is approximately 320 g.

it has a circulating life span of 15-20 days, with a turnover of approximately 15 g per day. 

an albumin:electrolyte ratio of 1:3 or 1:4(it will expand the plasma volume if interstitial water is available for an inflow through the capillary walls.)

There is some evidence that a serum oncotic pressure near 20 mmHg – equaling a total serum protein (TSP) concentration of 5.2 g/100 mL – represents a threshold, below which the risk of complications increases.

The target organs of hypoproteinemia include the skin, the lungs, and the intestine.

Cutaneous edema lowers the oxygen tension of wounds and may thus impair the healing process.

An oncotic deficit favors the development of interstitial pulmonary edema and the intestinal accumulation of fluids, which may progress to a paralytic ileus. 

In acute liver failure, Albumin solution may serve the triple purpose:

1. of stabilizing the circulation.2. correcting an oncotic deficit3. binding excessive serum bilirubin.

In the absence of active hemorrhage, the total dose should at any rate not exceed the normal circulating albumin mass, i.e. 2 g per kg body weight.

SBP is a common and severe complication of SBP is a common and severe complication of ascites characterized by spontaneous ascites characterized by spontaneous infection of the ascitic fluid without an infection of the ascitic fluid without an intraabdominal source.intraabdominal source.

most common organisms are most common organisms are Escherichia Escherichia colicoli and other gut bacteria; however, gram- and other gut bacteria; however, gram-positive bacteria, including positive bacteria, including Streptococcus Streptococcus viridans, Staphococcus aureus, viridans, Staphococcus aureus, andand EnterococcusEnterococcus sp sp

diagnosis of SBP : absolute neutrophil count diagnosis of SBP : absolute neutrophil count >250/mm3 >250/mm3

Treatment :second-generation Treatment :second-generation cephalosporin, inj. cefotaxime 2gm tid x cephalosporin, inj. cefotaxime 2gm tid x 5d5d

ALTERED METABOLISMALTERED METABOLISM

Significant impact on drug metabolism and Significant impact on drug metabolism and pharmacokinetic as a result of alterations in:pharmacokinetic as a result of alterations in:

A.protein binding.A.protein binding. B.altered volume of distribution.B.altered volume of distribution. C.reduced metabolism.C.reduced metabolism. D.impact of chronic alcohol on enzyme induction.D.impact of chronic alcohol on enzyme induction. E.sedatives and opiods have exaggerated effects E.sedatives and opiods have exaggerated effects

in patents with ALD ----worsen encephalopathy . in patents with ALD ----worsen encephalopathy .

Efficacy of drug removal by the liver Efficacy of drug removal by the liver is determined by several factors :is determined by several factors :

A.hepatic blood flow.A.hepatic blood flow. B.hepatic enzyme activity and efficacy.B.hepatic enzyme activity and efficacy. C.extent of plasma protein binding.C.extent of plasma protein binding. D.cholestasis induced alteration in enterohepatic D.cholestasis induced alteration in enterohepatic

circulation.circulation. E.portosystemic shunts. E.portosystemic shunts.

High extraction High extraction –primarily –primarily dependent on hepatic blood flow …dependent on hepatic blood flow …

ex: lidocaine,meperidine.ex: lidocaine,meperidine.

Low extraction Low extraction ---mainly protein ---mainly protein binding.binding.

ex: benzodiazepines. ex: benzodiazepines.

Hepatic encephalopathy (also known as portosystemic encephalopathy) is the occurrence of confusion, altered level of consciousness, and coma as a result of liver failure. In the advanced stages it is called hepatic coma or coma hepaticum. It may ultimately lead to death.

West Haven Criteria

this is based on the level of impairment of autonomy, changes in consciousness, intellectual function, behavior, and the dependence on therapy.

Grade 1 - Trivial lack of awareness; euphoria or anxiety; shortened attention span; impaired performance of addition or subtraction

Grade 2 - Lethargy or apathy; minimal disorientation for time or place; subtle personality change; inappropriate behaviour

Grade 3 - Somnolence to semistupor, but responsive to verbal stimuli; confusion; gross disorientation

Grade 4 - Coma (unresponsive to verbal or noxious stimuli)

Hepatic EncephalopathyHepatic Encephalopathy::

Increased Ammonia conc., increased GABA activityIncreased Ammonia conc., increased GABA activity

Preventive measuresPreventive measures:: hydration and correction of electrolyte imbalance hydration and correction of electrolyte imbalance correcting precipitating factorscorrecting precipitating factors vegetable protein better than animal proteinvegetable protein better than animal protein use lactulose, a nonabsorbable disaccharideuse lactulose, a nonabsorbable disaccharide acute cases- 30 – 40ml tid x 7d, 2-3 soft stools/dacute cases- 30 – 40ml tid x 7d, 2-3 soft stools/d no response addno response add Poorly absorbed antibiotics Poorly absorbed antibiotics neomycin – 0.5 -1gm tid x 7dneomycin – 0.5 -1gm tid x 7d metronidazole –250mg tid x 7d metronidazole –250mg tid x 7d rifaximin - 1200mg od rifaximin - 1200mg od

Metabolic disturbances:Metabolic disturbances:

I.I. Metabolic alkalosis.Metabolic alkalosis.

II.II. Hypokalemia.Hypokalemia.

III.III. Hypocalcemia.Hypocalcemia.

IV.IV. Hyperglycemia.Hyperglycemia.

V.V. Hypoglycemia.Hypoglycemia.

EFFECTS OF EFFECTS OF HYPERBILIRUBINEMIAHYPERBILIRUBINEMIA

Unconjugated bilirubin more toxic than conjugated.Unconjugated bilirubin more toxic than conjugated.

Impairs myocardial contractility, reduces vagal Impairs myocardial contractility, reduces vagal tone - causing bradycardia (atropine double dose).tone - causing bradycardia (atropine double dose).

Blunts response to catecholamines, angiotensin II Blunts response to catecholamines, angiotensin II and isoprenaline - blunts stress response.and isoprenaline - blunts stress response.

Therefore tolerate blood loss badly - prompt and Therefore tolerate blood loss badly - prompt and

adequate replacement of blood volume required.adequate replacement of blood volume required. Binds to albumin: Relative Hypoalbuminemia Binds to albumin: Relative Hypoalbuminemia

results in increased free drug concentration. results in increased free drug concentration.

Toxic to enzymes of oxidative phosphorylation, Toxic to enzymes of oxidative phosphorylation, glycolysis, glycogenesis and TCA cycle, heme glycolysis, glycogenesis and TCA cycle, heme synthesis, amino acid and protein metabolism. synthesis, amino acid and protein metabolism.

Toxic to CNS - but cannot cross intact BBB. Toxic to CNS - but cannot cross intact BBB. Causes kernictus in premature infants – Causes kernictus in premature infants –

Sensitizes kidneys to hypoxia-induced injury.Sensitizes kidneys to hypoxia-induced injury.

Bilirubin casts precipitate in renal tubules causing Bilirubin casts precipitate in renal tubules causing acute tubular necrosis.acute tubular necrosis.

Artefactually lowers measured serum creatinine - Artefactually lowers measured serum creatinine - Therefore serum creatinine under estimates renal Therefore serum creatinine under estimates renal dysfunction. dysfunction.

Pulmonary functionPulmonary function Hypoxemia PaO2 <70mmHgHypoxemia PaO2 <70mmHg Decreased HPV responseDecreased HPV response Treat associated pul. disease Treat associated pul. disease

(smoker-COPD)(smoker-COPD) Chest physiotherapy Chest physiotherapy Pulmonary toileting Pulmonary toileting Bronchodilators Bronchodilators AntibioticsAntibiotics

Renal systemRenal system:: Pre renal Azotemia- correct by fluid administrationPre renal Azotemia- correct by fluid administration Renal failure- Gram –ve septicemia, Endotoxin Renal failure- Gram –ve septicemia, Endotoxin mediated, Bilirubin mediatedmediated, Bilirubin mediated Diuresis by mannitol Diuresis by mannitol Antibiotic coverage (non toxic)Antibiotic coverage (non toxic)

Asses for Hepatorenal syndrome (mortality 95%)Asses for Hepatorenal syndrome (mortality 95%) type I – doubled s.creatinine (2.5mg/dl) halved type I – doubled s.creatinine (2.5mg/dl) halved

creatinine clearance 20ml/min in 2wks.creatinine clearance 20ml/min in 2wks. type II – progressive , chronic, resistant to treatmenttype II – progressive , chronic, resistant to treatment

Hepatorenal failureHepatorenal failure

Pre and Peroperative dehydration.Pre and Peroperative dehydration.

Hypovolaemia.Hypovolaemia.

Fall in renal blood flow during surgery.Fall in renal blood flow during surgery.

Direct effect of the excess conjugated bilirubin on Direct effect of the excess conjugated bilirubin on the renal tubules .the renal tubules .

Increased absorption of endotoxin from the gut.Increased absorption of endotoxin from the gut.

Rx:Rx: i.v infusion of albumini.v infusion of albumin dopamine + long acting vassopressindopamine + long acting vassopressin ( ornipressin / terlipressin)( ornipressin / terlipressin) octreotideoctreotide midodrine, an alpha-agonist (under midodrine, an alpha-agonist (under

trail) trail) TIPSTIPS The best therapy for HRS is liver The best therapy for HRS is liver

transplantation transplantation Goal: Urine out put 50ml/hr Goal: Urine out put 50ml/hr

Obstructive jaundice Obstructive jaundice Elective surgery – Vit K can be given Elective surgery – Vit K can be given

preoperativelypreoperatively Dose: 5-10mg/day x 7 IMDose: 5-10mg/day x 7 IM 5-10mg TID x 3 IM5-10mg TID x 3 IM In emergency : 5-10mg 4In emergency : 5-10mg 4thth hourly hourly

Splenomegaly and Hypersplenism Splenomegaly and Hypersplenism :: Congestive splenomegaly is common in patients Congestive splenomegaly is common in patients

with portal hypertension. with portal hypertension.

Clinical features include the presence of an Clinical features include the presence of an enlarged spleen on physical examination and the enlarged spleen on physical examination and the development of thrombocytopenia and development of thrombocytopenia and leukopenia in patients who have cirrhosis.leukopenia in patients who have cirrhosis.

Some patients will have fairly significant left-Some patients will have fairly significant left-sided and left upper quadrant abdominal pain sided and left upper quadrant abdominal pain related to an enlarged and engorged spleen. related to an enlarged and engorged spleen.

Splenomegaly itself usually requires no specific Splenomegaly itself usually requires no specific treatment, although splenectomy can be treatment, although splenectomy can be successfully performed under very special successfully performed under very special circumstances.circumstances.

Hypersplenism with the development of Hypersplenism with the development of thrombocytopenia is a common feature of thrombocytopenia is a common feature of patients with cirrhosis and is usually the first patients with cirrhosis and is usually the first indication of portal hypertension.indication of portal hypertension.

Malnutrition :Malnutrition :

Because the liver is principally involved in the Because the liver is principally involved in the regulation of protein and energy metabolism in the regulation of protein and energy metabolism in the body, it is not surprising that patients with advanced body, it is not surprising that patients with advanced liver disease are commonly malnourished.liver disease are commonly malnourished.

Once patients become cirrhotic, they are more Once patients become cirrhotic, they are more

catabolic, and muscle protein is metabolizedcatabolic, and muscle protein is metabolized. .

multiple factors that contribute multiple factors that contribute ::

including poor dietary intake.including poor dietary intake.

alterations in gut nutrient absorption.alterations in gut nutrient absorption. alterations in protein metabolism. alterations in protein metabolism.

Dietary supplementation for patients with cirrhosis is Dietary supplementation for patients with cirrhosis is helpful in preventing patients from becoming helpful in preventing patients from becoming catabolic.catabolic.

Bone Disease :Bone Disease :

Osteoporosis is common in patients with chronic Osteoporosis is common in patients with chronic cholestatic liver disease because of malabsorption of cholestatic liver disease because of malabsorption of vitamin D and decreased calcium ingestion.vitamin D and decreased calcium ingestion.

The rate of bone resorption exceeds that of new bone The rate of bone resorption exceeds that of new bone formation in patients with cirrhosis resulting in bone loss.formation in patients with cirrhosis resulting in bone loss.

Dual x-ray absorptiometry Dual x-ray absorptiometry (DEXA) (DEXA) is a useful method for is a useful method for determining osteoporosis or osteopenia in patients with determining osteoporosis or osteopenia in patients with chronic liver disease. chronic liver disease.

When a DEXA scan shows decreased bone mass, When a DEXA scan shows decreased bone mass, treatment should be administered with bisphosphonates treatment should be administered with bisphosphonates that are effective at inhibiting resorption of bone and that are effective at inhibiting resorption of bone and efficacious in the treatment of osteoporosis.efficacious in the treatment of osteoporosis.

General measuresGeneral measures:: Acceptable sr.Albumin >3gm/dlAcceptable sr.Albumin >3gm/dl Acceptable Sr.Bilirubin (if >8mg/dl pre-op Acceptable Sr.Bilirubin (if >8mg/dl pre-op

mannitol to be given)mannitol to be given) Anemia : iron deficiency anemia ferrous Anemia : iron deficiency anemia ferrous

sulphate 300mg tidsulphate 300mg tid

megaloblastic folic acid 1mg/d , vit. B12megaloblastic folic acid 1mg/d , vit. B12 packed cell transfusion if Hct< 28%packed cell transfusion if Hct< 28% Nutrition : calories 25- 30 kcal/kg/dNutrition : calories 25- 30 kcal/kg/d protein 1-1.2gm/kg/dprotein 1-1.2gm/kg/d hepatic encephalopathy restrict to 60gm/dhepatic encephalopathy restrict to 60gm/d Other factors : stop alcohol, stop smoking, Other factors : stop alcohol, stop smoking,

correct electrolyte imbalance correct electrolyte imbalance

Type of AnesthesiaType of Anesthesia Major intra-abdominal surgeries – Major intra-abdominal surgeries – GAGA Monitoring: routine ASA monitoring Monitoring: routine ASA monitoring

spo2,ECG,NIBP,Etco2spo2,ECG,NIBP,Etco2

Severe disease/major surgerySevere disease/major surgery Invasive: IBP, CVPInvasive: IBP, CVP Periodic ABG analysisPeriodic ABG analysis RBS, Sr.electrolytes, HaematocritRBS, Sr.electrolytes, Haematocrit PT,APTT, Thromboelastography PT,APTT, Thromboelastography

GA:GA:

Pre-med: no/minimal sedative Pre-med: no/minimal sedative

Fentanyl (min dose)Fentanyl (min dose)

Metaclopromide (full stomach)Metaclopromide (full stomach)

Rapid sequence induction and intubationRapid sequence induction and intubation

Induction: Propofol 2mg/kg (best agent)Induction: Propofol 2mg/kg (best agent)

Thiopentone 3-5mg/kg (single Thiopentone 3-5mg/kg (single dose)dose)

Intubation: Suxamethonium (duration Intubation: Suxamethonium (duration slightlyslightly

prolonged)prolonged)

Opiods :Opiods : Morphine :Morphine : prolonged elimination t1/2 .prolonged elimination t1/2 . increased bioavailability.increased bioavailability. ↓↓protein binding.protein binding. Exaggerated sedative and resp depression effect Exaggerated sedative and resp depression effect

…….administraton interval ↑1.5-2 fold and oral …….administraton interval ↑1.5-2 fold and oral dosage be reduced.dosage be reduced.

Fentanyl :Fentanyl : Highly lipid soluble.Highly lipid soluble. Short acting synthetic.Short acting synthetic. Fentanyl elimination s not appreciably altered in Fentanyl elimination s not appreciably altered in

pt with cirrhosis.pt with cirrhosis. Sufentanil :Sufentanil : Extensively metabolized by liver and more Extensively metabolized by liver and more

protein bound.protein bound. Chronic infusion impact ill defined .Chronic infusion impact ill defined . Alfentanil :Alfentanil : T1/2 doubled.T1/2 doubled. High free fraction…..prolong duration and High free fraction…..prolong duration and

enhanced effects.enhanced effects. Remifentanil:Remifentanil:

Intravenous inducing agents:Intravenous inducing agents: i.v anaesthetics have modest impact on the hepatic i.v anaesthetics have modest impact on the hepatic

blood flow and no meaningful adverse influence on blood flow and no meaningful adverse influence on postop liver function when arterial blood pressure is postop liver function when arterial blood pressure is adequately maintained.adequately maintained.

TPS : TPS : small hepatic extraction .small hepatic extraction . Elimination t1/2 unchanged in cirrhotic pt becoz of Elimination t1/2 unchanged in cirrhotic pt becoz of

large Vd.large Vd. KETAMINE,PROPOFOL,ETOMIDATE,METHOHEXITAL:KETAMINE,PROPOFOL,ETOMIDATE,METHOHEXITAL: Highly lipid soluble.Highly lipid soluble. High extraction ratio.High extraction ratio. Propofol has a more favourable splanchnic and Propofol has a more favourable splanchnic and

hepatic oxygen delivery then halothane.hepatic oxygen delivery then halothane.

Neuromuscular blocking agents :Neuromuscular blocking agents : Succinyl choline :Succinyl choline : ↓↓cholinesterase and pseudocholinesterase.cholinesterase and pseudocholinesterase. Mivacurium :Mivacurium : Longer residence time in cirrhotic then normal Longer residence time in cirrhotic then normal

patients.patients.

Maintanance :Maintanance :

O2, N2O mixtureO2, N2O mixture

NDMR- Atracurium/Cis-Atracurium NDMR- Atracurium/Cis-Atracurium (safe)(safe)

large initial doses( inc. vd )large initial doses( inc. vd )

subsequent doses should be subsequent doses should be

decreased decreased

Avoid injury/ insult to LiverAvoid injury/ insult to Liver

Goal: maintain liver blood flow and Goal: maintain liver blood flow and O2 supply O2 supply

Hypoxia, V/Q mismatch- increase Fio2Hypoxia, V/Q mismatch- increase Fio2 Prevent arterial hypotension, fall in Prevent arterial hypotension, fall in

cardiac out putcardiac out put Inhalational agent: Isoflurane best Inhalational agent: Isoflurane best

agentagent

SevofluraneSevoflurane

Halothane better avoided in cases with Halothane better avoided in cases with liver disease. liver disease.

Fluid and blood products Fluid and blood products

Post-op JaundicePost-op Jaundice Incidence in abdominal procedures <1%Incidence in abdominal procedures <1% Manifestation: increased Manifestation: increased

ALT/AST/S.bilirubin/clinical jaundiceALT/AST/S.bilirubin/clinical jaundice Only bilirubinemiaOnly bilirubinemia::1.1. Resorption of large haematoma, multiple Resorption of large haematoma, multiple

blood transfusionsblood transfusions2.2. Congenital: Gilberts, Rotors, Dubin-johnson Congenital: Gilberts, Rotors, Dubin-johnson

(prognosis good), criggler-najjar syn.(prognosis good), criggler-najjar syn.3.3. Intravascular haemolysis- haemolytic Intravascular haemolysis- haemolytic

anaemia, G-6-PD deficiency, Sickle cell anaemia, G-6-PD deficiency, Sickle cell anaemiaanaemia

Bilirubinemia with mild – mod amino Bilirubinemia with mild – mod amino transferase increase:transferase increase:

post op intra hepatic cholestasis- mild fever , post op intra hepatic cholestasis- mild fever , jaundice, upper abdominal painjaundice, upper abdominal pain

<48hrs & recedes in 2-3wks<48hrs & recedes in 2-3wks

Biliary tract obstruction: retained stones in biliary Biliary tract obstruction: retained stones in biliary tract, duct injury, acute cholecystitis post op, acute tract, duct injury, acute cholecystitis post op, acute pancreatitis.pancreatitis.

Circulatory failure: open heart surgery/traumatic Circulatory failure: open heart surgery/traumatic circulatory shock, ischemic hepatic injury.circulatory shock, ischemic hepatic injury.

Sepsis – mainly obstructive type (high bilirubin Sepsis – mainly obstructive type (high bilirubin levels)levels)

Bilirubinemia with marked amino Bilirubinemia with marked amino transferase increasetransferase increase::

Shock liver- centrilobular necrosis due to Shock liver- centrilobular necrosis due to hypoxia, viral hepatitishypoxia, viral hepatitis

Drug induced hepatitis:Drug induced hepatitis: alcohol AST:ALT >2:1alcohol AST:ALT >2:1 isoniazid,phenytoin,methyl dopaisoniazid,phenytoin,methyl dopa tetracycline, oc pillstetracycline, oc pills asprin, acetaminophin.asprin, acetaminophin.

Halogenated inhalational agents:Halogenated inhalational agents:

halothane hepatitis- type 1halothane hepatitis- type 1

type 2( severe type 2( severe form)form)

Obesity: BMI >30 post op liver failure Obesity: BMI >30 post op liver failure likely in 30% cases.likely in 30% cases.

Time course of onset of post op Time course of onset of post op jaundicejaundice

0-1wk : intra hepatic cholestasis0-1wk : intra hepatic cholestasis

resorption of hematomaresorption of hematoma

hypotension- ischaemic hepatitishypotension- ischaemic hepatitis 1-2wks: above causes1-2wks: above causes

sepsis, biliary trauma, sepsis, biliary trauma, pancreatitispancreatitis

nonA,nonB hepatitisnonA,nonB hepatitis

halothane hepatitishalothane hepatitis

Pre op proper history taking:Pre op proper history taking:

h/o hepatitis(viral)h/o hepatitis(viral)

familial disease,drug history,familial disease,drug history,

alcohol overuse, h/o jaundice alcohol overuse, h/o jaundice pastpast

obesity, exposure to halothaneobesity, exposure to halothane Intra op: shock, retraction/major Intra op: shock, retraction/major

abdominal surgery, sepsis, biliary abdominal surgery, sepsis, biliary tract surgery.tract surgery.

FACTORS ASSOCIATED WITH FACTORS ASSOCIATED WITH INCREASED POST-OP INCREASED POST-OP

MORTALITYMORTALITY.. S.albumin < 3 gm/dlS.albumin < 3 gm/dl Presence of infectionPresence of infection WBC > 10,000 /mm3WBC > 10,000 /mm3 Treatment with > 2 antibioticsTreatment with > 2 antibiotics Prothrombin time > 1.5 sec. over controlProthrombin time > 1.5 sec. over control S.bilirubin > 50 µ mol/L (>3 mg/dl)S.bilirubin > 50 µ mol/L (>3 mg/dl) Presence of ascitesPresence of ascites MalnutritionMalnutrition Emergency surgery.Emergency surgery.

PREOPERATIVE MEDICATIONPREOPERATIVE MEDICATION

Phenothiazines are avoided - centrilobular Phenothiazines are avoided - centrilobular necrosis. necrosis.

Anticholinergics - as bradycardia may be Anticholinergics - as bradycardia may be present atropine preferred. present atropine preferred.

If patient is on steroids, continue till morning of If patient is on steroids, continue till morning of surgery, supplement during induction, surgery, supplement during induction, intraoperatively if required and post intraoperatively if required and post operatively. operatively.

INTRAOPERATIVE INTRAOPERATIVE COMPLICATIONSCOMPLICATIONS

Hypotension .Hypotension .

Oliguria .Oliguria .

Blood loss.Blood loss.

Hypoglycemia .Hypoglycemia .

Electrolyte abnormalities - hypocalcaemia may Electrolyte abnormalities - hypocalcaemia may occur when citrated blood or FFP transfused. occur when citrated blood or FFP transfused.

POST OPERATIVEPOST OPERATIVE Oxygen supplementation for at least 24 hrs. Oxygen supplementation for at least 24 hrs. Postoperative chest X-ray. Postoperative chest X-ray. Continue antibiotics, H2 receptor antagonists Continue antibiotics, H2 receptor antagonists

and fluid management. and fluid management. Adequate analgesia should be provided using Adequate analgesia should be provided using

epidural –CEA /PCEA, small intermittent doses of epidural –CEA /PCEA, small intermittent doses of opioids, local anaesthesia opioids, local anaesthesia

Maintain urine output > 1-2 ml/kg/hr. Maintain urine output > 1-2 ml/kg/hr. Continue mannitol and dopamine if used Continue mannitol and dopamine if used

intraoperatively intraoperatively

POST OPERATIVEPOST OPERATIVE

SAME MONITORING &CARESAME MONITORING &CARE ELECTIVE POST OPERATIVE VENTILATIONELECTIVE POST OPERATIVE VENTILATION

Severe liver diseaseSevere liver disease Extensive surgery Extensive surgery Associated pulmonary or cardiac diseaseAssociated pulmonary or cardiac disease Fluid or electrolyte imbalance Fluid or electrolyte imbalance Hypothermia Hypothermia Impaired consciousnessImpaired consciousness Saturation <90% with FiO2 > 0.4.Saturation <90% with FiO2 > 0.4.

POSTOPERATIVE POSTOPERATIVE COMPLICATIONSCOMPLICATIONS

Impaired consciousness due to over sedation .Impaired consciousness due to over sedation .

Impaired respiration due to opioid over dose.Impaired respiration due to opioid over dose.

Inadequate reversal .Inadequate reversal .

Chest infection .Chest infection .

Oliguria and renal failure. Oliguria and renal failure.

Deterioration of hepatic function.Deterioration of hepatic function. Post Operative Jaundice Post Operative Jaundice

Post Op JaundicePost Op Jaundice Classification – Classification – LaMont &IsselbacherLaMont &Isselbacher.. 1.Overproduction of Bilirubin1.Overproduction of Bilirubin

Hemolytic Anemia, Hemolysis of tranfused Hemolytic Anemia, Hemolysis of tranfused bld,Resorption of hematoma bld,Resorption of hematoma

2.Hepatocellular damage2.Hepatocellular damage Ischemic, Cholestatic, Drug induced, Preexisting Ischemic, Cholestatic, Drug induced, Preexisting

hepatitishepatitis Extrahepatic ObstructionExtrahepatic Obstruction

Stone, Duct injuryStone, Duct injury MiscellaneousMiscellaneous

Gilbert’s, Post Op CholecystitisGilbert’s, Post Op Cholecystitis

THANK YOUTHANK YOU

Central neuraxial blockadeCentral neuraxial blockade

The effect of regional anaesthesia on liver blood The effect of regional anaesthesia on liver blood flow and hepatic function is not clearly an flow and hepatic function is not clearly an anaesthetic drug induced alteration in hepatic anaesthetic drug induced alteration in hepatic function.function.

These changes can be reversed and hepatic These changes can be reversed and hepatic blood flow may be mantained with vasopressors blood flow may be mantained with vasopressors or fluid administration to maintain normal arterial or fluid administration to maintain normal arterial blood pressure. blood pressure.

Risk stratificationRisk stratification

Risk assessment for Anaesthesia in Risk assessment for Anaesthesia in patients with Liver diseasepatients with Liver disease

Assessment of risk factors in moderate to severe liver Assessment of risk factors in moderate to severe liver diseasedisease

CHILD-TURCOTT classification posted for major surgeryCHILD-TURCOTT classification posted for major surgery

FactorFactor Gr-AGr-A Gr-BGr-B Gr-CGr-C

Sr.bilirubin(mg/Sr.bilirubin(mg/dl)dl)

<2<2 2-32-3 >3>3

AscitesAscites NONO ModerateModerate TenseTense

EncephalopathyEncephalopathy NONO Gr 1-2Gr 1-2 Gr 3-4Gr 3-4

NutritionNutrition GoodGood UndernourishedUndernourished PoorPoor

S. ALBUMIN(gmS. ALBUMIN(gm%)%)

>3.5>3.5 2.8-3.52.8-3.5 <2.8<2.8

Risk(Mortality Risk(Mortality rate)rate)

<10%<10% 30%30% >40%>40%

Child-pughChild-pugh modification ( 1972 ) modification ( 1972 )FactorFactor 11 22 33

Sr.bilirubin(mg/Sr.bilirubin(mg/dl)dl)

<2<2 2-32-3 >3>3

AscitesAscites NONO ModerateModerate TenseTense

EncephalopathyEncephalopathy NONO Gr 1-2Gr 1-2 Gr 3-4Gr 3-4

PT (Sec PT (Sec prolonged)prolonged)

INR INR

<4<4

<1.7<1.74-64-6

1.7-2.31.7-2.3>6>6

>2.3>2.3

S. ALBUMIN(gmS. ALBUMIN(gm%)%)

>3.5>3.5 2.8-3.52.8-3.5 <2.8<2.8

MELD ScoreMELD ScoreModified end stage liver diseaseModified end stage liver disease

Sr.BilirubinSr.Bilirubin Sr.AlbuminSr.Albumin Sr.CreatinineSr.Creatinine

Meld commonly used for Meld commonly used for Transplantation and Shunt surgeriesTransplantation and Shunt surgeries

The The modified Maddrey's discriminant modified Maddrey's discriminant functionfunction) was originally described by Maddrey and ) was originally described by Maddrey and BoitnottBoitnott[1][1] to predict prognosis in alcoholic  to predict prognosis in alcoholic hepatitis. It is calculated by a simple formula:hepatitis. It is calculated by a simple formula:

(4.6 x (PT test - control))+ S.Bilirubin in mg/dl.(4.6 x (PT test - control))+ S.Bilirubin in mg/dl.

Prospective studies have shown that, it is useful in Prospective studies have shown that, it is useful in predicting short term prognosis especially predicting short term prognosis especially mortality within 30 days.mortality within 30 days.[2][2] A value more than 32  A value more than 32 implies poor outcome with one month mortality implies poor outcome with one month mortality ranging between 35% to 45%.ranging between 35% to 45%.[3][3]

To calculate Maddrey discriminant function using SI To calculate Maddrey discriminant function using SI units - micromol/l (i.e. not US) divide bilirubin value units - micromol/l (i.e. not US) divide bilirubin value by 17.by 17.

Pre op variables and peri op mortality rate in Pre op variables and peri op mortality rate in cirrhotic patients (Garrison etal)cirrhotic patients (Garrison etal)

Risk factor Mortality rateRisk factor Mortality rate Emergency surgery 57%Emergency surgery 57% S.albumin <3gm/dl 58%S.albumin <3gm/dl 58% S.bilirubin> 3mg/dl 62%S.bilirubin> 3mg/dl 62% PT >1.5 X control 63%PT >1.5 X control 63% Infection 64%Infection 64% Antibiotics >2 82%Antibiotics >2 82% Cardiac failure 92%Cardiac failure 92% Pulmonary failure 100%Pulmonary failure 100% WBC count > 10,000 cells/cummWBC count > 10,000 cells/cumm

Causes of mortality Causes of mortality (perioperatively)(perioperatively)

SepsisSepsis Renal failureRenal failure BleedingBleeding Hepatic failureHepatic failure EncephalopathyEncephalopathy Pulmonary failurePulmonary failure

PROCEDURAL PROCEDURAL ANAESTHESIAANAESTHESIA

TIPSSTIPSS

Indications • Complications of portal

hypertension » Variceal hemorrhage » Refractory ascites » Hepatic hydrothorax

TIPSSTIPSS

Preop Preop Considerations • Altered mental status from encephalopathy • Full stomach considerations due to ascites or GI bleeding • Poor drug clearance due to hepatic failure • Coexisting diseases: coagulopathy, renal insufficiency,

anemia

Physical Findings • Jaundice • Ascites • Asterixis • Bruising • Petechiae

Complications • Hepatic encephalopathy, decline in liver function. » Monitor for change in mental status. Keep sedatives

postop to a minimum. • Stents may occlude immediately or over a period of

time: stents are evaluated for patency w/ ultrasound the next morning & whenever signs of portal hypertension return.

• Bleeding: serial hematocrits are obtained for 24 hours as well as monitoring for change in abdominal girth & blood pressure. If severe, transfusions & return to the OR are possibilities.

• Pts are usually kept in the ICU overnight for monitoring.

• Independent predictors of short-term mortality. » Need for emergent TIPS. » ALT >1,000. » Bilirubin >3. » Encephalopathy pre-TIPS

TIPPSTIPPS

ERCPERCP

In contrast to upper gastrointestinal endoscopy, ERCP is a complex, often time consuming diagnostic and

therapeutic endoscopic procedure that requires a high degree of patient cooperation in order to facilitate an intervention requiring precision from the endoscopist.

Therefore, deep sedation is preferable in ERCP. General anesthesia should be considered in

patients difficult to sedate, or having difficulty in ventilation and intubation or in high risk for aspiration. Also, it should be considered in lengthy procedures.