9.1.09 ANAESTHESIA AND LIVER DISEASE Dr.Pratheeba Durairaj,M.D,D.A,

9109

ANAESTHESIA AND LIVER ANAESTHESIA AND LIVER DISEASEDISEASE

DrPratheeba Durairaj MDDADrPratheeba Durairaj MDDA

Liver FunctionsLiver Functions The liver conjugates bilirubin produced from the The liver conjugates bilirubin produced from the

degradation of the haemoglobindegradation of the haemoglobin - water-soluble form of bilirubin is then - water-soluble form of bilirubin is then

excreted into the bile ducts excreted into the bile ducts The bile salts produced by the liver are passed to The bile salts produced by the liver are passed to

the gut - necessary for the absorption of the fat-the gut - necessary for the absorption of the fat-soluble vitamins A D E and K soluble vitamins A D E and K

Synthesis of proteins - most clotting factors Synthesis of proteins - most clotting factors albumin albumin

Lipid metabolism - cholesterol and triglycerides Lipid metabolism - cholesterol and triglycerides synthesised here synthesised here

Carbohydrate metabolism - synthesis and Carbohydrate metabolism - synthesis and breakdown of glycogen It stores glycogen and breakdown of glycogen It stores glycogen and releases glucose into the blood when the blood releases glucose into the blood when the blood glucose falls for any reasonglucose falls for any reason

Biotransformation of drugs either by oxidation or Biotransformation of drugs either by oxidation or conjugation - render them water-soluble - more conjugation - render them water-soluble - more easily excreted easily excreted

Impaired liver functionImpaired liver function Direct effectsDirect effects Hypoglycemia Lactic acidosis Hyper metabolism Hypoglycemia Lactic acidosis Hyper metabolism

Azotemia and Impaired urea synthesisAzotemia and Impaired urea synthesis Jaundice appears when serum bilirubin exceeds 35 Jaundice appears when serum bilirubin exceeds 35

micromoll micromoll Defects in cholesterol metabolism together with intra-Defects in cholesterol metabolism together with intra-

hepatic cholestasis may lead to production of poor hepatic cholestasis may lead to production of poor quality bile and malabsorbtion of fat and fat-soluble quality bile and malabsorbtion of fat and fat-soluble vitamins vitamins

Reduced synthesis of proteins such as albumin clotting Reduced synthesis of proteins such as albumin clotting factors thyroid binding globulin and pseudo-factors thyroid binding globulin and pseudo-cholinesterasecholinesterase

Impaired hormone biotransformation reduced Impaired hormone biotransformation reduced production of modulator proteins and reduced protein production of modulator proteins and reduced protein binding lead to increased circulating levels of hormones binding lead to increased circulating levels of hormones such as insulin thyroxine T3 aldosterone and oestrogen such as insulin thyroxine T3 aldosterone and oestrogen

Indirect effectsIndirect effects Cardiovascular changesCardiovascular changes Vasodilatation and vascular shunting are Vasodilatation and vascular shunting are

almost invariable in ESLDalmost invariable in ESLD Low systemic vascular resistance (SVR) Low systemic vascular resistance (SVR)

results in high cardiac output and high results in high cardiac output and high mixed venous oxygen saturationsmixed venous oxygen saturations

Intrapulmonary amp arteriovenous shunting Intrapulmonary amp arteriovenous shunting Pulmonary hypertension may developPulmonary hypertension may develop Tachycardia bounding pulse Ejection Tachycardia bounding pulse Ejection

systolic murmur systolic murmur

Pulmonary problems are both vascular and mechanical Pulmonary problems are both vascular and mechanical Hepato-Pulmonary syndromeHepato-Pulmonary syndrome ndash triad of end ndash triad of end

stage liver disease A-a gradient gt2 kPa stage liver disease A-a gradient gt2 kPa intrapulmonary vascular dilationintrapulmonary vascular dilation

Impaired pulmonary function in absence of Impaired pulmonary function in absence of cardiopulmonary diseasecardiopulmonary disease

Impaired hypoxic vaso-constriction and ventilation Impaired hypoxic vaso-constriction and ventilation perfusion mismatch lead to arterial desaturation and perfusion mismatch lead to arterial desaturation and clubbing if chronicclubbing if chronic

Cyanosis dyspnoea platypnea orthodeoxia Cyanosis dyspnoea platypnea orthodeoxia [desaturation pronounced in upright position relieved by [desaturation pronounced in upright position relieved by recumbency ]recumbency ]

Pleural effusions together with ascites can cause Pleural effusions together with ascites can cause considerable mechanical embarrassment of respiration considerable mechanical embarrassment of respiration and a reduction in functional residual lung capacityand a reduction in functional residual lung capacity

Pulmonary changesPulmonary changes

HEPATORENAL SYNDROMEHEPATORENAL SYNDROME

1048708 1048708 Low GFRLow GFR 1048708 1048708 Low renal blood flowLow renal blood flow 1048708 1048708 No other cause for renal failureNo other cause for renal failure 1048708 ldquo1048708 ldquoFunctional renal failurerdquoFunctional renal failurerdquo Symptoms ndash water retention Symptoms ndash water retention

Azotemia hyponatremia amp oliguriaAzotemia hyponatremia amp oliguria

Hepatorenal failureHepatorenal failure

Causes may beCauses may be

Pre and peroperative dehydrationPre and peroperative dehydration

HypovolaemiaHypovolaemia

Falls in renal blood flow during surgery Falls in renal blood flow during surgery

Direct effect of the excess conjugated Direct effect of the excess conjugated bilirubin on the renal tubules or possibly an bilirubin on the renal tubules or possibly an increased absorption of endotoxin from the increased absorption of endotoxin from the gutgut

Not a major risk in patients with Prehepatic Not a major risk in patients with Prehepatic jaundice jaundice

ManagementManagementof Hepato renal syndromeof Hepato renal syndrome

Avoid it developing by ensuring adequate hydration Avoid it developing by ensuring adequate hydration and a urine flow of at least 50mlshr in the average and a urine flow of at least 50mlshr in the average adult patientadult patient

In moderately elevated bilirubin - simple fluid In moderately elevated bilirubin - simple fluid loading for 12 hours before surgery using 09 NaCl loading for 12 hours before surgery using 09 NaCl and during the operation and during the operation

If the urine output is not maintained - Mannitol If the urine output is not maintained - Mannitol 1010

Bilirubin greatly elevated (gt140 micromolslitre) - Bilirubin greatly elevated (gt140 micromolslitre) - intravenous fluids during the 24 hours before surgery intravenous fluids during the 24 hours before surgery and for 36 hours postoperatively and for 36 hours postoperatively

Mannitol 10 05-1gkg - prior to surgery Mannitol 10 05-1gkg - prior to surgery without making the patient dehydrated as a result of without making the patient dehydrated as a result of an over-zealous diuresisan over-zealous diuresis

Neurological problemsNeurological problems Mechanisms leading to deepening Mechanisms leading to deepening

encephalopathy -incompletely understood encephalopathy -incompletely understood Due to accumulation of neurotoxic Due to accumulation of neurotoxic

compounds penetrating an impaired blood-compounds penetrating an impaired blood-brain barrier brain barrier

Symptoms can occur in chronic as well as in Symptoms can occur in chronic as well as in acute disease may be rapid in onset acute disease may be rapid in onset

Precipitated by a gastrointestinal bleed Precipitated by a gastrointestinal bleed dietary protein overload or sepsis dietary protein overload or sepsis

Somnolence can be exacerbated by sedative Somnolence can be exacerbated by sedative drugs and narcoticsdrugs and narcotics

Rapid correction of hyponatraemia can lead Rapid correction of hyponatraemia can lead to osmotic demyelination and central to osmotic demyelination and central pontine myelinolysis and should be avoided pontine myelinolysis and should be avoided

HAEMATOLOGICAL PROBLEMS

Anaemia may be the result of nutritional Anaemia may be the result of nutritional deficiency toxic bone marrow depression or deficiency toxic bone marrow depression or gastrointestinal bleeding from varices or gastrointestinal bleeding from varices or erosions erosions

Coagulation defects arise from Coagulation defects arise from thrombocytopenia platelet dysfunction and thrombocytopenia platelet dysfunction and decreased levels of circulating clotting factors decreased levels of circulating clotting factors

Clotting factor levels fall because of impaired Clotting factor levels fall because of impaired synthesis vitamin K malabsorbtion and synthesis vitamin K malabsorbtion and intravascular consumption intravascular consumption

The short half-life of clotting factors means The short half-life of clotting factors means that INR or Prothrombin Ratio (PTR) can that INR or Prothrombin Ratio (PTR) can reliably be used to evaluate residual hepatic reliably be used to evaluate residual hepatic functionfunction

Treatment ndashVit K FFPTreatment ndashVit K FFP

GASTROINTESTINAL SYSTEMGASTROINTESTINAL SYSTEM Rupture of oesophageal varicesRupture of oesophageal varices Vassopressin amp octreotide ndashreduce portal Vassopressin amp octreotide ndashreduce portal

hypertensionhypertension Susceptibility to infection - increasedSusceptibility to infection - increasedDrug dispositionDrug disposition Cholestasis will reduce absorption of fat-Cholestasis will reduce absorption of fat-

soluble drugs after oral administrationsoluble drugs after oral administration Compartment changes and altered protein Compartment changes and altered protein

binding will affect volume of distribution binding will affect volume of distribution clearance and re-distribution clearance and re-distribution

Patients with liver dysfunction may be Patients with liver dysfunction may be particularly sensitive to opiates and particularly sensitive to opiates and benzodiazepines due to altered end-organ benzodiazepines due to altered end-organ sensitivitysensitivity

Effect of hepatic dysfunction on Effect of hepatic dysfunction on anaestheticsanaesthetics

darr darr Albumin -increased free fraction Albumin -increased free fraction Altered volume of distribution [Ascites amp increased Altered volume of distribution [Ascites amp increased

total body water compartment]total body water compartment] Reduced metabolism ndashalters drug pharmacodynamics Reduced metabolism ndashalters drug pharmacodynamics Opiods -Opiods - Morphine pethidine -uarr uarr respiratory depression amp Morphine pethidine -uarr uarr respiratory depression amp

sedationsedationSedative hypnotic drugsSedative hypnotic drugs Benzodiazepines ndash prolongedBenzodiazepines ndash prolongedNDMR NDMR Prolonged action for vecuronium and pancuroniumProlonged action for vecuronium and pancuroniumDMRDMR Decreased serum cholinesterase activity Decreased serum cholinesterase activity

The Effect of Anaesthetics on Liver The Effect of Anaesthetics on Liver FunctionFunction

VOLATILE AGENTSVOLATILE AGENTS Halothane -darr HABFPBF disturb HABR [hepatic Halothane -darr HABFPBF disturb HABR [hepatic

arterial buffer response]arterial buffer response] Sevoflurane isoflurane maintain HABR Sevoflurane isoflurane maintain HABR SEVO gt ISO gt DES gt HALOSEVO gt ISO gt DES gt HALO

IV ANAESTHETICSIV ANAESTHETICS Thiopentone etomidate -darrTHBFThiopentone etomidate -darrTHBF Propofol - uarrTHBF ndashsplanchnic vasodilatorPropofol - uarrTHBF ndashsplanchnic vasodilator Ketamine ndash no effectsKetamine ndash no effects

REGIONAL ANAESTHESIAREGIONAL ANAESTHESIA High epidural may reduce THBFHigh epidural may reduce THBF

Effect of General Anaesthesia on liver Effect of General Anaesthesia on liver functions in patients with preexisting functions in patients with preexisting

liver diseasesliver diseases Indian Journal of Anaesthesia 1989 Apr 37(2) 61-Indian Journal of Anaesthesia 1989 Apr 37(2) 61-

66 ABSTRACT Effects of anaesthetics on liver ABSTRACT Effects of anaesthetics on liver

functions were studies in 13 patients having no functions were studies in 13 patients having no liver disease (group I) and 11 patients having liver liver disease (group I) and 11 patients having liver disease (group II) disease (group II)

Serum cholinesterase increased significantly in Serum cholinesterase increased significantly in both the group Rise in SGOT levels was significant both the group Rise in SGOT levels was significant only in group I who had greater surgical trauma only in group I who had greater surgical trauma and not in the other group of patients (group II) and not in the other group of patients (group II)

Significant decrease in total serum proteins was Significant decrease in total serum proteins was seen on different postoperative days in group I but seen on different postoperative days in group I but only on 5th postoperative day in group II only on 5th postoperative day in group II

It was concluded that presence of liver disease It was concluded that presence of liver disease does not increase the adverse effect of anaesthesia does not increase the adverse effect of anaesthesia on liver function and that on liver function and that surgical trauma is surgical trauma is more important than anaesthesia in producingmore important than anaesthesia in producing liver dysfunction liver dysfunction

Signs of Liver DiseaseSigns of Liver Disease

JaundiceJaundice HepatomegalyHepatomegaly Spider NaeviSpider Naevi SplenomegalySplenomegaly Scratch MarksScratch Marks AscitesAscites Palmer ErythemaPalmer Erythema

Dilated Abdominal Dilated Abdominal VeinsVeins

Peripheral OedemaPeripheral Oedema Finger ClubbingFinger Clubbing Testicular AtrophyTesticular Atrophy BruisingBruising GynaecomastiaGynaecomastia ConfusionComa ConfusionComa

JaundiceJaundicePrehepatic jaundice [haemolysis]Prehepatic jaundice [haemolysis] Massive intravascular haemolysis - as in some Massive intravascular haemolysis - as in some

forms of malaria or in sickle cell anemiaforms of malaria or in sickle cell anemia Hepatocellular function is normal but Hepatocellular function is normal but

overwhelmed - increased unconjugated overwhelmed - increased unconjugated bilirubin bilirubin

Intact Protein and carbohydrate metabolism Intact Protein and carbohydrate metabolism No reduction in the absorption of Vitamin K No reduction in the absorption of Vitamin K

or production of clotting factorsor production of clotting factorsHepatocellular jaundiceHepatocellular jaundice Hepatitis or Cirrhosis Hepatitis or Cirrhosis decreased protein synthesis signs of delayed decreased protein synthesis signs of delayed

clotting and even encephalopathy clotting and even encephalopathy

CONTDhellipCONTDhellipObstructive JaundiceObstructive Jaundice Biliary obstruction - from a stone in the common Biliary obstruction - from a stone in the common

bile duct pancreatic tumour or ascending bile duct pancreatic tumour or ascending cholangitischolangitis

Hepatocellular function is normal Hepatocellular function is normal Excess plasma bilirubin is chiefly conjugated - Excess plasma bilirubin is chiefly conjugated -

excreted in the urine which becomes darkexcreted in the urine which becomes dark Stools are pale as a result of poor lipid Stools are pale as a result of poor lipid

absorption absorption Protein synthesis is normalProtein synthesis is normal Vitamin K dependant clotting factors reduced Vitamin K dependant clotting factors reduced as the absorption of vitamin K is as the absorption of vitamin K is

dependent on the excretion of bile salts into the dependent on the excretion of bile salts into the small intestine rarr clotting time prolonged small intestine rarr clotting time prolonged parenteral vitamin K parenteral vitamin K

Renal impairment in Renal impairment in JaundiceJaundice

Release of endotoxins into systemic Release of endotoxins into systemic circulationcirculation

following biliary obstruction ndash renal following biliary obstruction ndash renal failurefailure

Prevention Prevention

- in high srbilirubin levels ndash - in high srbilirubin levels ndash percutaneous drainage of biliary tree percutaneous drainage of biliary tree under antibiotic coverunder antibiotic cover

- pre op oral bile salts -- pre op oral bile salts -darr post op RFdarr post op RF

Liver Function TestsLiver Function Tests Indication of severity help to differentiate Indication of severity help to differentiate

between prehepatic hepatocellular and between prehepatic hepatocellular and obstructive jaundiceobstructive jaundice

Jaundice - sign of an elevation of serum Jaundice - sign of an elevation of serum bilirubin bilirubin

Protein and albumin levels are normal in Protein and albumin levels are normal in prehepatic or obstructive jaundice low prehepatic or obstructive jaundice low values indicate hepatocellular damagevalues indicate hepatocellular damage

clotting - Prothrombin Time clotting - Prothrombin Time An elevated INR may indicate impaired An elevated INR may indicate impaired

synthesis of clotting factors due to synthesis of clotting factors due to hepatocellular damage or malabsorption hepatocellular damage or malabsorption of vitamin K due to biliary obstruction of vitamin K due to biliary obstruction

ContdhellipContdhellip Prothrombin time[ half life - 6 -12 hrs ] ndash Prothrombin time[ half life - 6 -12 hrs ] ndash

best indicator than Albumin [ half life ndash 24 -best indicator than Albumin [ half life ndash 24 -48 days]48 days]

Alanine Transaminase (ALT) and Aspartate Alanine Transaminase (ALT) and Aspartate Transaminase (AST) are enzymes that are Transaminase (AST) are enzymes that are released into the circulation by damaged released into the circulation by damaged hepatocytes Raised levels indicate hepatocellular hepatocytes Raised levels indicate hepatocellular damagedamage

AST can also be elevated in other circumstances AST can also be elevated in other circumstances such as myocardial infarction such as myocardial infarction

Alkaline Phosphatase (ALP) is an enzyme localized Alkaline Phosphatase (ALP) is an enzyme localized near the bile cannaliculi and is elevated in biliary near the bile cannaliculi and is elevated in biliary obstruction Not specific to hepatobiliary disease[ obstruction Not specific to hepatobiliary disease[ raised in malignant bone disease]raised in malignant bone disease]

An accompanying rise in Gamma glutamyl An accompanying rise in Gamma glutamyl Transferase (Gamma GT) suggests that the ALP is Transferase (Gamma GT) suggests that the ALP is from the liverfrom the liver

ContdhellipContdhellip

Glutathione ndash S ndash transferase ndashto Glutathione ndash S ndash transferase ndashto assess damage assess damage

due to anaestheticsdue to anaesthetics ALP ndashEarly in biliary obstructionALP ndashEarly in biliary obstruction γγ - Glutamyl trans peptidase ndash rises - Glutamyl trans peptidase ndash rises

after alcohol amp drug induced liver after alcohol amp drug induced liver damagedamage

Plasma glucose should be measuredPlasma glucose should be measured

Risk and severity scoringRisk and severity scoring In 1964 Child and Turcotte classified risk for In 1964 Child and Turcotte classified risk for

patients with liver cirrhosis undergoing patients with liver cirrhosis undergoing porto-caval anastomosis for management of porto-caval anastomosis for management of portal hypertensionportal hypertension

Pugh et al at Kings College Hospital Pugh et al at Kings College Hospital published a severity scoring system for published a severity scoring system for patients undergoing oesophageal transection patients undergoing oesophageal transection for bleeding oesophageal varices for bleeding oesophageal varices

The two systems have been amalgamated and The two systems have been amalgamated and provide a disease severity assessment based provide a disease severity assessment based on two clinical and three laboratory variables on two clinical and three laboratory variables

PUGHlsquoS MODIFICATION OF CHILD GRADINGPUGHlsquoS MODIFICATION OF CHILD GRADING

Clinical amp Biochemical Clinical amp Biochemical variablesvariables

POINTS POINTS

11SCORESCOREDD

2233

Serum albumin (gL)Serum albumin (gL) gt35gt35 28-3528-35 lt28lt28

Serum bilirubin (micromolL)Serum bilirubin (micromolL)

[Mg dl][Mg dl]

lt35lt35

lt 2lt 235-6035-60

2 -32 -3gt60gt60

gt 3gt 3

PT (seconds) prolongedPT (seconds) prolonged

from controlfrom control1-41-4

INR [ lt INR [ lt 1 7]1 7]

4-104-10

INR [17 INR [17 -23]-23]

1010

INR gt23INR gt23

AscitesAscites NoneNone MildMild ModerateModerate

EncephalopathyEncephalopathy AbsentAbsent Grade I ndash Grade I ndash IIII

Grade III ndash Grade III ndash IVIV

POINTS 5- 6 ndash class A [5 Mortality] 7 -9 ndashClass B [10 mortality] 10 -15 ndashClass C [50 mortality]

Surgery in patients with liver Surgery in patients with liver dysfunctiondysfunction

The Child-Pugh classification is a useful method The Child-Pugh classification is a useful method of staging the progress of liver decompensation of staging the progress of liver decompensation

Limited predictive value in anaesthesia and Limited predictive value in anaesthesia and surgerysurgery

Group A patients are lower riskGroup A patients are lower risk and with and with sufficient care can be considered as candidates sufficient care can be considered as candidates for most types of surgeryfor most types of surgery

Group B patients ndash acceptable but correct Group B patients ndash acceptable but correct abnormalities abnormalities

Group C patientsGroup C patients present an extremely high present an extremely high operative risk - surgical procedures in these operative risk - surgical procedures in these patients should be avoided if possible- patients should be avoided if possible- only only emergency or life-saving proceduresemergency or life-saving procedures should should be undertakenbe undertaken

Preoperative assessmentPreoperative assessment Type and extent of liver diseaseType and extent of liver disease Extra hepatic effectsExtra hepatic effects Risk assessmentRisk assessment Patients general condition- hydration nutritionPatients general condition- hydration nutrition Associated co-morbid conditionsAssociated co-morbid conditions LFTLFT ConsentConsent Premedication-short acting temazepam in absence Premedication-short acting temazepam in absence

of neurological impairment orally ndashavoid of neurological impairment orally ndashavoid intramuscular injectionsintramuscular injections

H2 receptor antagonistsH2 receptor antagonists Preop Vit K optimal hydrationPreop Vit K optimal hydration

PREOP INVESTIGATIONSPREOP INVESTIGATIONS

Hematological ndashHb Platelet Hematological ndashHb Platelet countWBC Coagulation profilecountWBC Coagulation profile

Metabolic ndash sr Metabolic ndash sr glucose urea creatinine electrolytesglucose urea creatinine electrolytes

Cardio respiratory ndash chest x-rayECG Cardio respiratory ndash chest x-rayECG PFT ABGPFT ABG

Liver function ndash Liver function ndash srbilirubinalbuminliver enzymessrbilirubinalbuminliver enzymes

Pre-op risk factors Pre-op risk factors associated with associated with

postoperative mortalitypostoperative mortality Serum albumin lt3gLSerum albumin lt3gL Serum bilirubin gt50 micromolLSerum bilirubin gt50 micromolL PT gt15 s over controlPT gt15 s over control Presence of infectionPresence of infection WBC gt 10000WBC gt 10000 Treatment with more than two antibioticsTreatment with more than two antibiotics Presence of AscitesPresence of Ascites MalnutritionMalnutrition Emergency surgeryEmergency surgery

Anaesthetic TechniqueAnaesthetic Technique Avoid hypotensive techniquesmdashintra hepatic necrosisAvoid hypotensive techniquesmdashintra hepatic necrosis High conc of oxygen -- - due to intrapulmonary shuntsHigh conc of oxygen -- - due to intrapulmonary shunts Avoid hypotension amp hypoxemiaAvoid hypotension amp hypoxemia Meticulous fluid balance ndashMeticulous fluid balance ndash Ascites ndash may lose a large amount of fluid rapidlyAscites ndash may lose a large amount of fluid rapidly Concentrated albumin solutions ndashto correct Concentrated albumin solutions ndashto correct

hypoproteinemiahypoproteinemia Fresh blood ndashto prevent hypocalcemia due to Fresh blood ndashto prevent hypocalcemia due to

reduced metabolism of preservativesreduced metabolism of preservatives FFP 12 - 15 mlKg ndashCorrect dilutional FFP 12 - 15 mlKg ndashCorrect dilutional

coagulopathycoagulopathy 1 unit of FFP for every 1 unit of packed cells or 250 1 unit of FFP for every 1 unit of packed cells or 250

ml of 09 saline or colloid [500 ml of FFP - uarr ml of 09 saline or colloid [500 ml of FFP - uarr Clotting factors by 20 ]Clotting factors by 20 ]

Maintenance of temperature Maintenance of temperature

MonitoringMonitoring Monitoring of temperature Monitoring of temperature Coagulation status should be monitored ndashplatelet count fibrin Coagulation status should be monitored ndashplatelet count fibrin

degradation products prothrombin time activated clotting degradation products prothrombin time activated clotting time partial thromboplastin timetime partial thromboplastin time

Thromboelastography has been used as a tool in liver Thromboelastography has been used as a tool in liver transplantationtransplantation

Repeated BP cuff inflation ndashmay lead to bruising in patients Repeated BP cuff inflation ndashmay lead to bruising in patients with altered haemostatic functionwith altered haemostatic function

Insertion of Intra arterial line ndash care to prevent haematoma Insertion of Intra arterial line ndash care to prevent haematoma Jugular route is preferred in CVP monitoringJugular route is preferred in CVP monitoring OximetryOximetry Urine outputUrine output Blood lossBlood loss Monitor ionized calciumMonitor ionized calcium

DRUGSDRUGS

Thiopentone ndash intrinsic clearance delayed Thiopentone ndash intrinsic clearance delayed but recovery not delayed because of but recovery not delayed because of redistributionredistribution

Alcoholic cirrhosis ndash larger dose of thio ndash Alcoholic cirrhosis ndash larger dose of thio ndash cross tolerancecross tolerance

Halothane and enflurane reduce hepatic Halothane and enflurane reduce hepatic arterial flow (vasodilatation negative arterial flow (vasodilatation negative inotropic effects)inotropic effects)

Isoflurane increases hepatic blood flowIsoflurane increases hepatic blood flow

[preferred][preferred]

NEUROMUSCULAR BLOCKING NEUROMUSCULAR BLOCKING AGENTSAGENTS

Reduced plasma pseudo cholinesterase activityReduced plasma pseudo cholinesterase activity Prolonged action- vecuronium Prolonged action- vecuronium

pancruonium[16 fold]pancruonium[16 fold]

Decreased biliary excretionDecreased biliary excretion

Increased volume of distribution ndashlarger Increased volume of distribution ndashlarger initial dosesinitial doses

1048708 1048708 Recommended Atracurium ndash metabolism Recommended Atracurium ndash metabolism independent of liver and kidneysindependent of liver and kidneys

1048708 1048708 For transplantation ndash long acting agent such For transplantation ndash long acting agent such as doxacuriumas doxacurium

OPIODS amp SEDATIVESOPIODS amp SEDATIVES

NarcoticsNarcotics Reduced metabolism of morphine and Reduced metabolism of morphine and

pethidinepethidine Prefer fentanylPrefer fentanyl Remifentanyl - ideal Remifentanyl - ideal 1048708 1048708 BenzodiazepinesBenzodiazepines 1048708 1048708 Diazepam - prolonged half lifeDiazepam - prolonged half life 1048708 1048708 Oxazepam and lorazepam preferrred Oxazepam and lorazepam preferrred

ndashmetabolised by glucuronidation ndashmetabolised by glucuronidation without liver requirementwithout liver requirement

Regional Anaesthesia Regional Anaesthesia

Contraindicated if PT gt25 s above control Contraindicated if PT gt25 s above control platelet count lt 50000 cumm bleeding platelet count lt 50000 cumm bleeding time gt12 mtstime gt12 mts

Spinal and epidural anaesthesia carries the Spinal and epidural anaesthesia carries the risk of epidural haematoma and paralysis if risk of epidural haematoma and paralysis if there is abnormal clotting but there are there is abnormal clotting but there are otherwise no special precautionsotherwise no special precautions

The half-life of lignocaine is prolonged in The half-life of lignocaine is prolonged in liver failure but this is not significant when liver failure but this is not significant when used in regional anaesthesia used in regional anaesthesia

LA dose diminished in presence of AscitesLA dose diminished in presence of Ascites

Canadian Journal of Anesthesia Vol 45 452-Canadian Journal of Anesthesia Vol 45 452-459 459

Obstetrical anaesthesia for a parturient with Obstetrical anaesthesia for a parturient with preeclampsia HELLP syndrome and acute cortical preeclampsia HELLP syndrome and acute cortical

blindnessblindness A 39-yr-old woman with three past A 39-yr-old woman with three past uncomplicated pregnancies presented at 33 uncomplicated pregnancies presented at 33 wk with acute cortical blindnesswk with acute cortical blindness

Based on clinical and laboratory assessment Based on clinical and laboratory assessment a diagnosis of preeclampsia with HELLP a diagnosis of preeclampsia with HELLP syndrome was madesyndrome was made

A CT scan of her head demonstrated A CT scan of her head demonstrated ischaemic lesions of her basal ganglia ischaemic lesions of her basal ganglia extending superiorly to involve both posterior extending superiorly to involve both posterior parietal and occipital regionsparietal and occipital regions

Infusions of magnesium sulphate and Infusions of magnesium sulphate and hydralazine were started and an urgent hydralazine were started and an urgent Caesarean section was performed Caesarean section was performed under under subarachnoid anaesthesiasubarachnoid anaesthesia after insertion of after insertion of an arterial line and intravenous hydration an arterial line and intravenous hydration

ContdhellipContdhellip The course of anaesthesia and surgery was uneventful The course of anaesthesia and surgery was uneventful

and she delivered a live 1540 g female infantand she delivered a live 1540 g female infant By the following morning she had recovered some By the following morning she had recovered some

vision and visual recovery was complete by 72 hr vision and visual recovery was complete by 72 hr postpartum postpartum

Her postoperative course was uneventful Her postoperative course was uneventful CONCLUSIONCONCLUSION Provided that it is not Provided that it is not

contraindicated because of prohibitive risk to the contraindicated because of prohibitive risk to the mother mother regional anaesthesia has particular regional anaesthesia has particular advantage in these patientsadvantage in these patients

In particular the use of spinal anaesthesia which has In particular the use of spinal anaesthesia which has been discouraged by some for this patient population been discouraged by some for this patient population should be re-evaluated should be re-evaluated

Postoperative Postoperative managementmanagement

Oxygen enriched airOxygen enriched air Major surgery ndash elective post Major surgery ndash elective post

operative ventilationoperative ventilation Replace blood lossReplace blood loss Maintain adequate urine outputMaintain adequate urine output Dopamine and inotropes should be Dopamine and inotropes should be

continuedcontinued The principle complications are likely The principle complications are likely

to be continued bleeding sepsis and to be continued bleeding sepsis and hepatic decompensation hepatic decompensation

Peri-operative considerations in Child-Peri-operative considerations in Child-Pugh A patientsPugh A patients

Pre-operative Pre-operative Aetiology of condition - virology Aetiology of condition - virology Drug idiosyncrasy Drug idiosyncrasy

Blood count and platelets Blood count and platelets Clotting screen Clotting screen Assess renal function Assess renal function Previous anaesthetics Previous anaesthetics

Per-operative Per-operative Consider drug bio-availability issues Consider drug bio-availability issues Avoid drugs excreted via liverAvoid drugs excreted via liver Regional techniques acceptable if clotting Regional techniques acceptable if clotting

normalnormal Post-operativePost-operative Monitor for post-operative hepatic Monitor for post-operative hepatic

decompensationdecompensation Possible prolonged duration of action in Possible prolonged duration of action in opiates HDU ITU careopiates HDU ITU care

Child-Pugh Group BC patient Child-Pugh Group BC patient undergoing major surgeryundergoing major surgery

Previous upper abdominal surgery portal Previous upper abdominal surgery portal hypertension and coagulopathy dramatically hypertension and coagulopathy dramatically increase the potential for per-operative blood lossincrease the potential for per-operative blood loss

8-12 units of blood together fresh frozen plasma 8-12 units of blood together fresh frozen plasma and platelets should be available and platelets should be available

Pre-medicationPre-medication Sedative premedicants should be avoided in the Sedative premedicants should be avoided in the

encephalopathic patient encephalopathic patient Other drugs may be needed pre-operatively and Other drugs may be needed pre-operatively and

include antibiotics and H2 receptor antagonistsinclude antibiotics and H2 receptor antagonists The oral or intravenous route used - The oral or intravenous route used -

intramuscular injections should be avoidedintramuscular injections should be avoided Coagulopathy may require correction with fresh Coagulopathy may require correction with fresh

frozen plasma and platelets and renal frozen plasma and platelets and renal replacement therapy may need to be consideredreplacement therapy may need to be considered

Per-operative considerationsPer-operative considerations

Regional techniques -- considered carefully - Regional techniques -- considered carefully - coagulopathy epidural varices can pose an coagulopathy epidural varices can pose an additional risk additional risk

Vascular accessVascular access with a multi-lumen central with a multi-lumen central venous catheter together with at least one venous catheter together with at least one large bore central line large bore central line

Monitoring of arterial and central venous Monitoring of arterial and central venous pressures is mandatory pressures is mandatory

Pulmonary artery pulmonary capillary wedge Pulmonary artery pulmonary capillary wedge pressure and cardiac output measurements pressure and cardiac output measurements may be necessary in the sick patientmay be necessary in the sick patient

Trans-oesophageal echocardiography and Trans-oesophageal echocardiography and volumetric haemodynamic monitoring pulse volumetric haemodynamic monitoring pulse contour analysis can provide significant contour analysis can provide significant additional information for the strategic additional information for the strategic management of these patients management of these patients

CONTDhellipCONTDhellip Coagulation and fibrinolysisCoagulation and fibrinolysis are major are major

concerns concerns The potential for large volume blood replacement The potential for large volume blood replacement

means that temperature should be measured and means that temperature should be measured and a fluid warmer and warming mattress useda fluid warmer and warming mattress used

Regular per-operative estimation of INRPTR Regular per-operative estimation of INRPTR may be necessary - thromboelastography may be necessary - thromboelastography provides useful intra-operative evaluation of provides useful intra-operative evaluation of coagulationcoagulation

Blood conservationBlood conservation - considered - considered Preservation of hepatic function -Preservation of hepatic function - N- N-

acetylcysteine (NAC) is a sulphur-containing acetylcysteine (NAC) is a sulphur-containing antioxidant - benefit patients with fulminant antioxidant - benefit patients with fulminant hepatic failurehepatic failure

NAC appears to improve oxygen delivery NAC appears to improve oxygen delivery and consumption and reduce base deficitand consumption and reduce base deficit

Renal FunctionRenal Function - - Dopamine may be usefulDopamine may be useful

Bleeding oesophageal Bleeding oesophageal varicesvarices

Bleeding oesophageal varices - life-Bleeding oesophageal varices - life-threatening complication of - often occur threatening complication of - often occur against a background of abnormal clotting against a background of abnormal clotting thrombocytopenia encephalopathy and thrombocytopenia encephalopathy and AscitesAscites

Overall mortality is 30 Overall mortality is 30 The principles of anaesthetic managementThe principles of anaesthetic management Protect the airway Protect the airway Establish good vascular access Establish good vascular access Volume replacement - colloid blood fresh Volume replacement - colloid blood fresh

frozen plasma and platelets Avoid saline frozen plasma and platelets Avoid saline Check correct clotting Give Vitamin K Check correct clotting Give Vitamin K

correct fibrinolysis and review blood correct fibrinolysis and review blood chemistry chemistry

Intoxicated Alcoholic Intoxicated Alcoholic PatientsPatients

Requires less anaesthetic ndashadditive depressant Requires less anaesthetic ndashadditive depressant effect of alcohol amp anaestheticseffect of alcohol amp anaesthetics

Ill - equipped to withstand stress amp Acute blood Ill - equipped to withstand stress amp Acute blood lossloss

Alcohol decrease the tolerance of brain to hypoxiaAlcohol decrease the tolerance of brain to hypoxia uarr uarr Risk of regurgitation amp aspiration - alcohol Risk of regurgitation amp aspiration - alcohol

darrtone of lower oesophageal sphincter amp slows darrtone of lower oesophageal sphincter amp slows gastric emptyinggastric emptying

Alcohol Interferes with platelet aggregationAlcohol Interferes with platelet aggregation Causes uarrconc of plasma catecholamines rarr Causes uarrconc of plasma catecholamines rarr

Intraoperative dysarrhytmiasIntraoperative dysarrhytmias

POSTOPERATIVE JAUNDICEPOSTOPERATIVE JAUNDICE

Mild ndash 17 marked - 4Mild ndash 17 marked - 4

Patient factorsPatient factors Congenital Congenital

hemolytic disordershemolytic disorders Acquired hemolytic Acquired hemolytic

disordersdisorders Pre existing liver Pre existing liver

diseasedisease CoagulopathyCoagulopathy Gilberts syndromeGilberts syndrome SepsisSepsis

Perioperative Perioperative factorsfactors

Anaesthetic induced Anaesthetic induced darrHBFdarrHBF

BleedingBleeding HypotensionHypotension Blood transfusionBlood transfusion Biliary tree traumaBiliary tree trauma Viral hepatitisViral hepatitis DrugsDrugs Halothane antibioticsHalothane antibiotics Nonsteroidal agentsNonsteroidal agents

POSTOPERATIVE JAUNDICEPOSTOPERATIVE JAUNDICE Extravascular break down of haematoma [1 ltr] Extravascular break down of haematoma [1 ltr]

-5000mg Bilirubin-5000mg Bilirubin 500ml of blood transfusion ndash contains 250 mg 500ml of blood transfusion ndash contains 250 mg

bilirubinbilirubin Intravascular destruction of RBC can occur in Intravascular destruction of RBC can occur in

G6P-dehydrogenase defeciency G6P-dehydrogenase defeciency cardiopulmonary bypass Artificial valves cardiopulmonary bypass Artificial valves sickle cell disease multiple blood transfusionssickle cell disease multiple blood transfusions

Delayed transfusion reactions ndash hemolysis ndashDelayed transfusion reactions ndash hemolysis ndashpostop jaundicepostop jaundice

Biliary obstruction due to surgery -uarrbilirubin Biliary obstruction due to surgery -uarrbilirubin amp uarralkaline phosphatase within 3 days of amp uarralkaline phosphatase within 3 days of surgerysurgery


Postop cholecystitispancreatitis may follow Postop cholecystitispancreatitis may follow non biliary surgery 3- 30 days post opnon biliary surgery 3- 30 days post op

Post operative intrahepatic cholestasis Post operative intrahepatic cholestasis [benign] - associated with multiple blood [benign] - associated with multiple blood transfusions hypoxia hypotension - transfusions hypoxia hypotension - uarrbilirubin amp uarralkaline phosphatase within uarrbilirubin amp uarralkaline phosphatase within 2-7 days of surgery ndashresolution in 3 weeks2-7 days of surgery ndashresolution in 3 weeks

ManagementManagement Prevention is the best treatment Prevention is the best treatment Avoid precipitating factorsAvoid precipitating factors

Halothane HepatitisHalothane Hepatitis The incidence is 17000-30000 halothane The incidence is 17000-30000 halothane

anaesthetics - higher in women the middle anaesthetics - higher in women the middle aged and the obeseaged and the obese

Rarer in paediatric patients and with the Rarer in paediatric patients and with the newer volatile agents newer volatile agents

Commonest iatrogenic cause of fulminant Commonest iatrogenic cause of fulminant hepatic failurehepatic failure

ldquoldquoUnexplained liver damage within 28 days of Unexplained liver damage within 28 days of halothane exposure in previously normal halothane exposure in previously normal patientrdquo ndash idiosyncratic reactionpatientrdquo ndash idiosyncratic reaction

Clinical featuresClinical features malaise anorexiafever malaise anorexiafever within 7 days jaundice within days to 4 within 7 days jaundice within days to 4 weeks weeks

Halothane HepatitisHalothane Hepatitis

DIAGNOSISDIAGNOSIS Serum antibodies that react with specific liver Serum antibodies that react with specific liver

microsomal proteins that are altered by microsomal proteins that are altered by trifluroacetyl chloride metabolite of halothanetrifluroacetyl chloride metabolite of halothane

Gross rise of Transaminases [500 -2000 ul]Gross rise of Transaminases [500 -2000 ul]Risk factorsRisk factors High - recent previous exposure [ 78 ]High - recent previous exposure [ 78 ] previous adverse reactionprevious adverse reaction Uncertain - obesityUncertain - obesity Female [16 1 ]Female [16 1 ] Drug allergy [ 15 ]Drug allergy [ 15 ] Family historyFamily history Lymphocyte sensitivity to phenytoinLymphocyte sensitivity to phenytoin

ContdhellipContdhellip The cause not fully established - multifactorial The cause not fully established - multifactorial

- possible immunological cause - possible immunological cause Immune sensitization to trifluoracetylated Immune sensitization to trifluoracetylated

proteins produced by Cyt P450 2E1 in genetically proteins produced by Cyt P450 2E1 in genetically predisposed subjectspredisposed subjects

Reduced hepatic blood flow and hypoxia are also Reduced hepatic blood flow and hypoxia are also to blameto blame

Related to the degree of metabolism of the Related to the degree of metabolism of the volatile agent so toxic metabolites may be volatile agent so toxic metabolites may be involvedinvolved

The onset time of the jaundice is shorter with The onset time of the jaundice is shorter with increasing numbers of exposures to halothane increasing numbers of exposures to halothane

Nevertheless enflurane and isoflurane are Nevertheless enflurane and isoflurane are associated with hepatic dysfunction albeit associated with hepatic dysfunction albeit apparently at lower rates than halothane WHO apparently at lower rates than halothane WHO database holds 225 and 159 reports respectivelydatabase holds 225 and 159 reports respectively

Halothane exposure Halothane exposure guidelinesguidelines

Avoid Halothane ifAvoid Halothane if Within at least 3 months of a previous Within at least 3 months of a previous

exposure exposure Previous adverse reactions -jaundice or Previous adverse reactions -jaundice or

pyrexia pyrexia Family history of hepatic reactions to Family history of hepatic reactions to

halothanehalothane Pre - existing liver diseasePre - existing liver disease Adverse reactions to Other volatile Adverse reactions to Other volatile

anaesthetic agentsanaesthetic agents

Liver and PregnancyLiver and Pregnancy Normal in sizeNormal in size A decrease in total protein as well albumin A decrease in total protein as well albumin An increase of the liver dependent clotting An increase of the liver dependent clotting

factors such as fibrinogen factors such as fibrinogen An increase of alkaline phosphates 3-4 times An increase of alkaline phosphates 3-4 times

secondary to placental alkalinesecondary to placental alkaline Srcholinesterase Srcholinesterase darr 30darr 30 Normal transaminase [ASTALT] levels and Normal transaminase [ASTALT] levels and

bilirubinbilirubin Any increase in transaminase levels and Any increase in transaminase levels and

bilirubin ndash good indicator of pregnancy ndashbilirubin ndash good indicator of pregnancy ndashinduced liver disease induced liver disease

Intrahepatic Cholestasis of Intrahepatic Cholestasis of PregnancyPregnancy

Incidence 001 Mainly in the third Incidence 001 Mainly in the third trimester Rare in black patients trimester Rare in black patients

Strong family history Strong family history High recurrence in subsequent High recurrence in subsequent

pregnanacies 60-70pregnanacies 60-70 Pruritus alone - 80 percent Pruritus alone - 80 percent Jaundice develop in 20 percentJaundice develop in 20 percent Infrequent mild to moderate steatorrhea Infrequent mild to moderate steatorrhea Bilirubin level less than 5 mg dl minimal Bilirubin level less than 5 mg dl minimal

or no elevation in transaminasesor no elevation in transaminases

IChP ndashcontdhellipIChP ndashcontdhellip Incidence of fetal distress and death high if Incidence of fetal distress and death high if

early delivery is not induced (deliver at week 38 early delivery is not induced (deliver at week 38 if pruritus at week 36 in case of jaundice ) if pruritus at week 36 in case of jaundice )

Parenteral vitamin K Ursodeoxycholic acid 15 Parenteral vitamin K Ursodeoxycholic acid 15 mg kg Cholestyramine binds bile acid salts mg kg Cholestyramine binds bile acid salts Dexamethasone Dexamethasone

Pruritus resolve within two days of delivery but Pruritus resolve within two days of delivery but bilurubin within 4-6 weeks bilurubin within 4-6 weeks

Implications on Anaesthesia Implications on Anaesthesia Check coagulation profile Check coagulation profile Ask for vit K IV Ask for vit K IV take care of high incidence of fetal distress take care of high incidence of fetal distress

meconium-stained prematurity ( neonatologist meconium-stained prematurity ( neonatologist must attend with incubatormust attend with incubator

Preeclampsia amp EclampsiaPreeclampsia amp Eclampsia About 25 of patients with Severe pre-eclampsia About 25 of patients with Severe pre-eclampsia

and 90 of those with eclampsia will have elevated and 90 of those with eclampsia will have elevated AST and ALT gt 5 times and bilirubin lt 5 mgdl AST and ALT gt 5 times and bilirubin lt 5 mgdl

If not associated with other criteria of HELLP If not associated with other criteria of HELLP syndrome eg low platelets haemolysis we give syndrome eg low platelets haemolysis we give prophylactic dexamethasone 8mg12hrs beside prophylactic dexamethasone 8mg12hrs beside mgsulphate antihypertensive albumin 20 mgsulphate antihypertensive albumin 20 50mlday 50mlday

Implications on anaesthesiaImplications on anaesthesia Painless labour with epidural to reduce stress Painless labour with epidural to reduce stress

response which could continue to anaesthesia response which could continue to anaesthesia provided INR lt15 provided INR lt15

Difficult intubation because of edema - small cuffed Difficult intubation because of edema - small cuffed tube 6-7 mm tube 6-7 mm

Adequate analgesia Adequate analgesia Fluids restriction Fluids restriction Continue medications postoperative in ICU Continue medications postoperative in ICU

HELLP syndrome HELLP syndrome Hemolysis Elevated liver enzymes Low Hemolysis Elevated liver enzymes Low

plateletsplatelets Peripartum multiorgan damage with pre-Peripartum multiorgan damage with pre-

eclampsia result from very active platelets eclampsia result from very active platelets aggregation everywhere with end organ aggregation everywhere with end organ ischemia and congestion with deposition of ischemia and congestion with deposition of fibrous network and entraped haemolysed RBCs fibrous network and entraped haemolysed RBCs amp platelets ndashnecrosis amp periportal haemorrhage amp platelets ndashnecrosis amp periportal haemorrhage

Nausea vomiting headache and upper right Nausea vomiting headache and upper right abdominal pain hypotension shockabdominal pain hypotension shock

Best markers are the maternal lactate Best markers are the maternal lactate dehydrogenase level and the maternal platelet dehydrogenase level and the maternal platelet count count

Congested liver of HELLP Congested liver of HELLP syndromesyndrome

CONTDhellipCONTDhellip Perinatal administration of dexamethasone in a Perinatal administration of dexamethasone in a

high dosage of 10 mg intravenously every 12 hours high dosage of 10 mg intravenously every 12 hours has been shown to markedly improve the has been shown to markedly improve the laboratory abnormalities associated with HELLP laboratory abnormalities associated with HELLP syndrome syndrome

Magnesium sulfate to prevent seizures Magnesium sulfate to prevent seizures Antihypertensive therapy if blood pressure is Antihypertensive therapy if blood pressure is

greater than 160110 mmHg despite the use of greater than 160110 mmHg despite the use of magnesium sulfate magnesium sulfate

Anesthesia like severe preclampsia Anesthesia like severe preclampsia avoid trauma to liveravoid trauma to liver Vit K if INR gt15Vit K if INR gt15 FFP 4-6 if INR gt2 FFP 4-6 if INR gt2 Platelets 6-8 units if platelets lt50000 Platelets 6-8 units if platelets lt50000 Mortality ndash maternal 50 - 60foetal -60Mortality ndash maternal 50 - 60foetal -60

ACUTE FATTY LIVER OF ACUTE FATTY LIVER OF PREGNANCYPREGNANCY

Rare serious disorder unknown etiologyRare serious disorder unknown etiology Symptoms in third trimesterSymptoms in third trimester ndashabdominal

pain nausea vomiting anorexiafatique fever headache

Rapid progression ndashbleeding jaundice encephalopathy renal failure hepatic failure coagulopathy - PPH

uarrTransaminases hyperbilirubinemia uarrprothrombin time --- DIC

Prompt delivery is advisable

Hepatic Rupture and Hepatic Rupture and Infarction Infarction

Older multigravida mothers with preeclampsia (75 Older multigravida mothers with preeclampsia (75 to 85 percent) are at higher risk to 85 percent) are at higher risk

Extremely rare 140000 to 1 250000 Extremely rare 140000 to 1 250000 Patients with hepatic rupture typically present in Patients with hepatic rupture typically present in

shock with preceding right upper quadrant pain shock with preceding right upper quadrant pain hypertension elevated transaminase levels hypertension elevated transaminase levels (greater than 1000 IU per L) and coagulopathy (greater than 1000 IU per L) and coagulopathy

Therapy for hepatic rupture has included Therapy for hepatic rupture has included transfusion of blood products and intravenous transfusion of blood products and intravenous fluids surgical evacuation and arterial fluids surgical evacuation and arterial embolization with 75 percent perinatal mortality embolization with 75 percent perinatal mortality rate have been noted in hepatic rupture rate have been noted in hepatic rupture

Hepatic infarctionHepatic infarction was typically present with was typically present with fever and marked elevations in transaminase fever and marked elevations in transaminase levels In surviving patients liver function and levels In surviving patients liver function and histopathology are normal within six months of histopathology are normal within six months of delivery delivery

Anesthesia in pregnant women with Anesthesia in pregnant women with HELLP syndromeHELLP syndrome

Retrospective studyRetrospective study For the period of 1 July For the period of 1 July 1996 through 30 June 2000 1996 through 30 June 2000

RESULTS During the period of study 119 patients RESULTS During the period of study 119 patients had HELLP syndrome Eighty-five patients had had HELLP syndrome Eighty-five patients had cesarean delivery and 34 had vaginal deliverycesarean delivery and 34 had vaginal delivery

Seventy-one patients had diagnosed HELLP Seventy-one patients had diagnosed HELLP syndrome previous to the anesthesia and 14 syndrome previous to the anesthesia and 14 postcesarean delivery the range platelet count postcesarean delivery the range platelet count was 19000-143000microl was 19000-143000microl

Of these 71 58 had an epidural anesthesia 9 had Of these 71 58 had an epidural anesthesia 9 had general anesthesia and 4 had spinal anesthesia general anesthesia and 4 had spinal anesthesia

There were no neurologic complications or There were no neurologic complications or bleeding in the epidural spacebleeding in the epidural space

CONCLUSION We found no documentation of CONCLUSION We found no documentation of any neurologic or hematologic complications of any neurologic or hematologic complications of women with HELLP syndrome and neuraxial women with HELLP syndrome and neuraxial anesthesiaanesthesia

Subdural Hematoma following dural Subdural Hematoma following dural puncture in a parturient with HELLP puncture in a parturient with HELLP

syndromesyndrome This complication occurred following This complication occurred following accidental dural puncture in a parturient accidental dural puncture in a parturient with thrombocytopenia (99000bullmicroL-1) who with thrombocytopenia (99000bullmicroL-1) who subsequently developed the syndrome of subsequently developed the syndrome of hemolysis elevated liver enzymes and low hemolysis elevated liver enzymes and low plateletsplatelets

On the first postoperative day postdural On the first postoperative day postdural puncture headache (PDPH) developed puncture headache (PDPH) developed

An epidural blood patch (EBP) was An epidural blood patch (EBP) was deferred to the third postoperative day deferred to the third postoperative day because of a platelet count of 21000bullmicroL-1 because of a platelet count of 21000bullmicroL-1

Headache intensified from a typical PDPH Headache intensified from a typical PDPH to one which was not posturally related to one which was not posturally related

A second EBP was abandoned after the A second EBP was abandoned after the

injection of 5 mL of blood because of injection of 5 mL of blood because of increasing headache during the procedure increasing headache during the procedure

Magnetic resonance imaging revealed Magnetic resonance imaging revealed bilateral temporal subdural hematomas bilateral temporal subdural hematomas

The patient was managed conservatively and The patient was managed conservatively and discharged home without any sequelae discharged home without any sequelae

ConclusionConclusion It is conceivable that It is conceivable that thrombocytopenia together with possible thrombocytopenia together with possible abnormal platelet function increased the risk abnormal platelet function increased the risk of subdural hematoma of subdural hematoma

Alternative diagnoses to PDPH should be Alternative diagnoses to PDPH should be considered whenever headache is not considered whenever headache is not posturally related posturally related

OCUPATIONAL HAZARDOCUPATIONAL HAZARD Risk of transmission of HBV following Risk of transmission of HBV following

inoculation is 5 -30inoculation is 5 -30 May occur through needle prickcuts May occur through needle prickcuts

sharp injuriesmucous membranes- sharp injuriesmucous membranes- waterproof dressingwaterproof dressing

Wear gloves while inserting a Wear gloves while inserting a cannula airways intubation amp cannula airways intubation amp extubation extubation

Sharps should not be handed directly to Sharps should not be handed directly to othersothers

See to the sterilisation of other See to the sterilisation of other contaminated thingscontaminated things

Liver FunctionsLiver Functions The liver conjugates bilirubin produced from the The liver conjugates bilirubin produced from the

degradation of the haemoglobindegradation of the haemoglobin - water-soluble form of bilirubin is then - water-soluble form of bilirubin is then

excreted into the bile ducts excreted into the bile ducts The bile salts produced by the liver are passed to The bile salts produced by the liver are passed to

the gut - necessary for the absorption of the fat-the gut - necessary for the absorption of the fat-soluble vitamins A D E and K soluble vitamins A D E and K

Synthesis of proteins - most clotting factors Synthesis of proteins - most clotting factors albumin albumin

Lipid metabolism - cholesterol and triglycerides Lipid metabolism - cholesterol and triglycerides synthesised here synthesised here

Carbohydrate metabolism - synthesis and Carbohydrate metabolism - synthesis and breakdown of glycogen It stores glycogen and breakdown of glycogen It stores glycogen and releases glucose into the blood when the blood releases glucose into the blood when the blood glucose falls for any reasonglucose falls for any reason

Biotransformation of drugs either by oxidation or Biotransformation of drugs either by oxidation or conjugation - render them water-soluble - more conjugation - render them water-soluble - more easily excreted easily excreted


















































































































POINTS POINTS

11SCORESCOREDD

2233



[Mg dl][Mg dl]

lt35lt35

lt 2lt 235-6035-60

2 -32 -3gt60gt60

gt 3gt 3



INR [ lt INR [ lt 1 7]1 7]

4-104-10

INR [17 INR [17 -23]-23]

1010

INR gt23INR gt23
































DRUGSDRUGS
















































































































































































































































































































POINTS POINTS

11SCORESCOREDD

2233



[Mg dl][Mg dl]

lt35lt35

lt 2lt 235-6035-60

2 -32 -3gt60gt60

gt 3gt 3



INR [ lt INR [ lt 1 7]1 7]

4-104-10

INR [17 INR [17 -23]-23]

1010

INR gt23INR gt23
































DRUGSDRUGS


























































































































































































































DRUGSDRUGS































































































































































































9.1.09 ANAESTHESIA AND LIVER DISEASE Dr.Pratheeba Durairaj,M.D,D.A,

Documents

Transcript of 9.1.09 ANAESTHESIA AND LIVER DISEASE Dr.Pratheeba Durairaj,M.D,D.A,