ANAESTHESIA AND LIVER DISEASE

1
ANAESTHESIA AND LIVER DISEASE

• Dr.Pratheeba Durairaj ,M.D,D.A,

• HAPPY 2009

2
Liver Functions

• The liver conjugates bilirubin, produced from the
  degradation of the haemoglobin
• - water-soluble form of bilirubin is
  then excreted into the bile ducts
• The bile salts produced by the liver are passed
  to the gut - necessary for the absorption of the
  fat-soluble vitamins A, D, E and K.
• Synthesis of proteins - most clotting factors,
  albumin.
• Lipid metabolism - cholesterol and
  triglycerides synthesised here.
• Carbohydrate metabolism - synthesis and
  breakdown of glycogen . It stores glycogen and
  releases glucose into the blood when the blood
  glucose falls for any reason.
• Biotransformation of drugs either by oxidation or
  conjugation - render them water-soluble - more
  easily excreted. 

3
Impaired liver function

• Direct effects
• Hypoglycemia, Lactic acidosis , Hyper metabolism,
  Azotemia and Impaired urea synthesis.
• Jaundice appears when serum bilirubin exceeds 35
  µmol/l
• Defects in cholesterol metabolism together with
  intra-hepatic cholestasis may lead to production
  of poor quality bile and malabsorbtion of fat and
  fat-soluble vitamins.
• Reduced synthesis of proteins such as albumin,
  clotting factors, thyroid binding globulin and
  pseudo-cholinesterase.
• Impaired hormone biotransformation, reduced
  production of modulator proteins and reduced
  protein binding lead to increased circulating
  levels of hormones such as insulin, thyroxine,
  T3, aldosterone and oestrogen

4
Indirect effects

• Cardiovascular changes
• Vasodilatation and vascular shunting are almost
  invariable in ESLD.
• Low systemic vascular resistance (SVR) results
  in high cardiac output and high mixed venous
  oxygen saturations
• Intrapulmonary arteriovenous shunting
• Pulmonary hypertension may develop
• Tachycardia, bounding pulse ,Ejection systolic
  murmur

5
Pulmonary changes

• Pulmonary problems are both vascular and
  mechanical.
• Hepato-Pulmonary syndrome triad of end stage
  liver disease, A-a gradient gt2 kPa ,
  intrapulmonary vascular dilation
• Impaired pulmonary function in absence of
  cardiopulmonary disease
• Impaired hypoxic vaso-constriction and
  ventilation perfusion mismatch lead to arterial
  desaturation and clubbing if chronic.
• Cyanosis ,dyspnoea , platypnea, orthodeoxia
  desaturation pronounced in upright position
  relieved by recumbency
• Pleural effusions together with ascites can
  cause considerable mechanical embarrassment of
  respiration and a reduction in functional
  residual lung capacity.

6
HEPATORENAL SYNDROME

• ?? Low GFR
• ?? Low renal blood flow
• ?? No other cause for renal failure
• ?? Functional renal failure
• Symptoms water retention, Azotemia,
  hyponatremia, oliguria

7
Hepatorenal failure

• Causes may be
• Pre and peroperative dehydration
• Hypovolaemia
• Falls in renal blood flow during surgery,
  
• Direct effect of the excess conjugated
  bilirubin on the renal tubules or possibly an
  increased absorption of endotoxin from the gut.
• Not a major risk in patients with Prehepatic
  jaundice. 

8
Managementof Hepato renal syndrome

• Avoid it developing by ensuring adequate
  hydration and a urine flow of at least 50mls/hr
  in the average adult patient.
• In moderately elevated bilirubin - simple fluid
  loading for 12 hours before surgery using 0.9
  NaCl and during the operation.
• If the urine output is not
  maintained - Mannitol 10
• Bilirubin greatly elevated (gt140
  micromols/litre), - intravenous fluids during the
  24 hours before surgery and for 36 hours
  postoperatively.
• Mannitol 10 0.5-1g/kg - prior
  to surgery without making the patient dehydrated
  as a result of an over-zealous diuresis.

9
Neurological problems

• Mechanisms leading to deepening encephalopathy
  -incompletely understood.
• Due to accumulation of neurotoxic compounds
  penetrating an impaired blood-brain barrier.
• Symptoms can occur in chronic as well as in acute
  disease, may be rapid in onset
• Precipitated by a gastrointestinal bleed, dietary
  protein overload or sepsis.
• Somnolence can be exacerbated by sedative drugs
  and narcotics.
• Rapid correction of hyponatraemia can lead to
  osmotic demyelination and central pontine
  myelinolysis and should be avoided

10
HAEMATOLOGICAL PROBLEMS

• Anaemia may be the result of nutritional
  deficiency, toxic bone marrow depression or
  gastrointestinal bleeding from varices or
  erosions.
• Coagulation defects arise from thrombocytopenia,
  platelet dysfunction and decreased levels of
  circulating clotting factors.
• Clotting factor levels fall because of impaired
  synthesis, vitamin K malabsorbtion and
  intravascular consumption.
• The short half-life of clotting factors means
  that INR or Prothrombin Ratio (PTR) can reliably
  be used to evaluate residual hepatic function.
• Treatment Vit K ,FFP

11

• GASTROINTESTINAL SYSTEM
• Rupture of oesophageal varices
• Vassopressin octreotide reduce portal
  hypertension
• Susceptibility to infection - increased
• Drug disposition
• Cholestasis will reduce absorption of fat-soluble
  drugs after oral administration.
• Compartment changes and altered protein binding
  will affect volume of distribution, clearance and
  re-distribution.
• Patients with liver dysfunction may be
  particularly sensitive to opiates and
  benzodiazepines due to altered end-organ
  sensitivity

12
Effect of hepatic dysfunction on anaesthetics

• ? Albumin -increased free fraction
• Altered volume of distribution Ascites
  increased total body water compartment,
• Reduced metabolism alters drug pharmacodynamics
• Opiods -
• Morphine ,pethidine -? ? respiratory depression
  sedation
• Sedative /hypnotic drugs
• Benzodiazepines prolonged
• NDMR
• Prolonged action for vecuronium and pancuronium
• DMR
• Decreased serum cholinesterase activity

13
The Effect of Anaesthetics on Liver Function

• VOLATILE AGENTS
• Halothane -? HABF/PBF, disturb HABR hepatic
  arterial buffer response
• Sevoflurane ,isoflurane maintain HABR
• SEVO gt ISO gt DES gt HALO
• IV ANAESTHETICS
• Thiopentone /etomidate -?THBF
• Propofol - ?THBF splanchnic vasodilator
• Ketamine no effects
• REGIONAL ANAESTHESIA
• High epidural may reduce THBF

14
Effect of General Anaesthesia on liver functions
in patients with preexisting liver diseases

• Indian Journal of Anaesthesia. 1989 Apr 37(2)
  61-6
• ABSTRACT Effects of anaesthetics on liver
  functions were studies in 13 patients having no
  liver disease (group I) and 11 patients having
  liver disease (group II).
• Serum cholinesterase increased significantly in
  both the group. Rise in SGOT levels was
  significant only in group I, who had greater
  surgical trauma and not in the other group of
  patients (group II).
• Significant decrease in total serum proteins was
  seen on different postoperative days in group I
  but only on 5th postoperative day in group II.
• It was concluded that presence of liver disease
  does not increase the adverse effect of
  anaesthesia on liver function and that surgical
  trauma is more important than anaesthesia in
  producing liver dysfunction.

15
Signs of Liver Disease

• Jaundice
• Hepatomegaly
• Spider Naevi
• Splenomegaly
• Scratch Marks
• Ascites
• Palmer Erythema

• Dilated Abdominal Veins
• Peripheral Oedema
• Finger Clubbing
• Testicular Atrophy
• Bruising
• Gynaecomastia
• Confusion/Coma 

16
Jaundice

• Prehepatic jaundice haemolysis
• Massive intravascular haemolysis - as in some
  forms of malaria or in sickle cell anemia
• Hepatocellular function is normal but
  overwhelmed - increased unconjugated bilirubin
• Intact Protein and carbohydrate metabolism
• No reduction in the absorption of Vitamin K or
  production of clotting factors.
• Hepatocellular jaundice
• Hepatitis or Cirrhosis
• decreased protein synthesis, signs of delayed
  clotting, and even encephalopathy.

17
CONTD

• Obstructive Jaundice
• Biliary obstruction - from a stone in the common
  bile duct, pancreatic tumour or ascending
  cholangitis
• Hepatocellular function is normal
• Excess plasma bilirubin is chiefly conjugated -
  excreted in the urine which becomes dark.
• Stools are pale as a result of poor lipid
  absorption.
• Protein synthesis is normal
• Vitamin K dependant clotting factors reduced
• as the absorption of vitamin K
  is dependent on the excretion of bile salts into
  the small intestine ? clotting time prolonged
  parenteral vitamin K.

18
Renal impairment in Jaundice

• Release of endotoxins into systemic circulation
• following biliary obstruction renal failure
• Prevention
• - in high sr.bilirubin levels
  percutaneous drainage of biliary tree under
  antibiotic cover
• - pre op oral bile salts -? post op RF

19
Liver Function Tests

• Indication of severity, help to differentiate
  between prehepatic, hepatocellular and
  obstructive jaundice.
• Jaundice - sign of an elevation of serum
  bilirubin.
• Protein and albumin levels are normal in
  prehepatic or obstructive jaundice, low values
  indicate hepatocellular damage.
• clotting - Prothrombin Time
• An elevated INR may indicate impaired synthesis
  of clotting factors due to hepatocellular damage
  or malabsorption of vitamin K due to biliary
  obstruction.

20
Contd

• Prothrombin time half life - 6 -12 hrs best
  indicator than Albumin half life 24 -48
  days
• Alanine Transaminase (ALT) and Aspartate
  Transaminase (AST) are enzymes that are released
  into the circulation by damaged hepatocytes.
  Raised levels indicate hepatocellular damage.
• AST can also be elevated in other circumstances
  such as myocardial infarction
• Alkaline Phosphatase (ALP) is an enzyme localized
  near the bile cannaliculi and is elevated in
  biliary obstruction. Not specific to
  hepatobiliary disease, raised in malignant bone
  disease.
• An accompanying rise in Gamma glutamyl
  Transferase (Gamma GT) suggests that the ALP is
  from the liver.

21
Contd

• Glutathione S transferase to assess damage
• due to anaesthetics
• ALP Early in biliary obstruction
• ? - Glutamyl trans peptidase rises after
  alcohol drug induced liver damage
• Plasma glucose should be measured

22
Risk and severity scoring

• In 1964, Child and Turcotte classified risk for
  patients with liver cirrhosis undergoing
  porto-caval anastomosis for management of portal
  hypertension.
• Pugh et al at King's College Hospital published
  a severity scoring system for patients undergoing
  oesophageal transection for bleeding oesophageal
  varices.
• The two systems have been amalgamated and provide
  a disease severity assessment based on two
  clinical and three laboratory variables

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PUGHS MODIFICATION OF CHILD GRADING
Clinical Biochemical variables POINTS 1 SCORED 2 3
Serum albumin (g/L) gt35 28-35 lt28
Serum bilirubin (µmol/L) Mg /dl lt35 lt 2 35-60 2 -3 gt60 gt 3
PT (seconds) prolonged from control 1-4 INR lt 1 .7 4-10 INR 1.7 -2.3 10 INR gt2.3
Ascites None Mild Moderate
Encephalopathy Absent Grade I II Grade III IV
POINTS 5- 6 class A 5 Mortality , 7 -9
Class B 10 mortality, 10 -15 Class C 50
mortality
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25
Surgery in patients with liver dysfunction

• The Child-Pugh classification is a useful method
  of staging the progress of liver decompensation.
• Limited predictive value in anaesthesia and
  surgery
• Group A patients are lower risk and with
  sufficient care can be considered as candidates
  for most types of surgery.
• Group B patients acceptable but correct
  abnormalities
• Group C patients present an extremely high
  operative risk - surgical procedures in these
  patients should be avoided if possible.- only
  emergency or life-saving procedures should be
  undertaken

26
Preoperative assessment

• Type and extent of liver disease
• Extra hepatic effects
• Risk assessment
• Patients general condition- hydration ,nutrition
• Associated co-morbid conditions
• LFT
• Consent
• Premedication-short acting temazepam in absence
  of neurological impairment orally avoid
  intramuscular injections
• H2 receptor antagonists
• Preop Vit K ,optimal hydration

27
PREOP INVESTIGATIONS

• Hematological Hb , Platelet count,WBC
  Coagulation profile
• Metabolic sr. glucose ,urea ,creatinine
  electrolytes
• Cardio respiratory chest x-ray,ECG ,PFT, ABG
• Liver function sr.bilirubin,albumin,liver
  enzymes

28
Pre-op risk factors associated with postoperative
mortality

• Serum albumin lt3g/L
• Serum bilirubin gt50 µmol/L
• PT gt1.5 s over control
• Presence of infection
• WBC gt 10,000
• Treatment with more than two antibiotics
• Presence of Ascites
• Malnutrition
• Emergency surgery

29
Anaesthetic Technique

• Avoid hypotensive techniquesintra hepatic
  necrosis
• High conc of oxygen -- - due to intrapulmonary
  shunts
• Avoid hypotension hypoxemia
• Meticulous fluid balance
• Ascites may lose a large amount of
  fluid rapidly
• Concentrated albumin solutions to
  correct hypoproteinemia
• Fresh blood to prevent hypocalcemia due
  to reduced metabolism of preservatives
• FFP 12 - 15 ml/Kg Correct dilutional
  coagulopathy
• 1 unit of FFP for every 1 unit of packed cells or
  250 ml of 0.9 saline or colloid 500 ml of FFP -
  ? Clotting factors by 20
• Maintenance of temperature

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Monitoring

• Monitoring of temperature
• Coagulation status should be monitored platelet
  count ,fibrin degradation products , prothrombin
  time , activated clotting time, partial
  thromboplastin time
• Thromboelastography has been used as a
  tool in liver transplantation
• Repeated BP cuff inflation may lead to bruising
  in patients with altered haemostatic function
• Insertion of Intra arterial line care to
  prevent haematoma
• Jugular route is preferred in CVP monitoring
• Oximetry
• Urine output
• Blood loss
• Monitor ionized calcium

31
DRUGS

• Thiopentone intrinsic clearance delayed but
  recovery not delayed because of redistribution
• Alcoholic cirrhosis larger dose of thio cross
  tolerance
• Halothane and enflurane reduce hepatic arterial
  flow (vasodilatation, negative inotropic effects)
• Isoflurane increases hepatic blood flow
• preferred

32
NEUROMUSCULAR BLOCKING AGENTS

• Reduced plasma pseudo cholinesterase activity
• Prolonged action- vecuronium , pancruonium1.6
  fold
• Decreased biliary excretion
• Increased volume of distribution larger
  initial doses
• ?? Recommended Atracurium metabolism
  independent of liver and kidneys
• ?? For transplantation long acting agent such
  as doxacurium

33
OPIODS SEDATIVES

• Narcotics
• Reduced metabolism of morphine and pethidine
• Prefer fentanyl
• Remifentanyl - ideal
• ?? Benzodiazepines
• ?? Diazepam - prolonged half life
• ?? Oxazepam and lorazepam preferrred metabolised
  by glucuronidation without liver requirement

34
? Regional Anaesthesia

• Contraindicated if PT gt2.5 s above control,
  platelet count lt 50,000 /cu.mm, bleeding time gt12
  mts
• Spinal and epidural anaesthesia carries the risk
  of epidural haematoma and paralysis if there is
  abnormal clotting but there are otherwise no
  special precautions.
• The half-life of lignocaine is prolonged in
  liver failure but this is not significant when
  used in regional anaesthesia. 
• LA dose diminished in presence of Ascites

35
Canadian Journal of Anesthesia, Vol 45, 452-459,
Obstetrical anaesthesia for a parturient with
preeclampsia, HELLP syndrome and acute cortical
blindness

• A 39-yr-old woman, with three past uncomplicated
  pregnancies presented at 33 wk with acute
  cortical blindness.
• Based on clinical and laboratory assessment, a
  diagnosis of preeclampsia with HELLP syndrome was
  made.
• A CT scan of her head demonstrated ischaemic
  lesions of her basal ganglia, extending
  superiorly to involve both posterior parietal and
  occipital regions.
• Infusions of magnesium sulphate and hydralazine
  were started and an urgent Caesarean section was
  performed under subarachnoid anaesthesia after
  insertion of an arterial line and intravenous
  hydration.

36
Contd

• The course of anaesthesia and surgery was
  uneventful and she delivered a live 1540 g female
  infant.
• By the following morning, she had recovered some
  vision and visual recovery was complete by 72 hr
  postpartum.
• Her postoperative course was uneventful
• CONCLUSION Provided that it is not
  contraindicated because of prohibitive risk to
  the mother, regional anaesthesia has particular
  advantage in these patients.
• In particular, the use of spinal anaesthesia,
  which has been discouraged by some for this
  patient population, should be re-evaluated.

37
Postoperative management

• Oxygen enriched air
• Major surgery elective post operative
  ventilation
• Replace blood loss
• Maintain adequate urine output
• Dopamine and inotropes should be continued.
• The principle complications are likely to be
  continued bleeding, sepsis and hepatic
  decompensation

38
Peri-operative considerations in Child-Pugh A
patients

• Pre-operative
• Aetiology of condition -
  virology,
• Drug idiosyncrasy
  Blood count and platelets
  Clotting screen Assess renal
  function Previous anaesthetics
• Per-operative
• Consider drug bio-availability
  issues ?
• Avoid drugs excreted via liver
• Regional techniques acceptable
  if clotting normal
• Post-operative
• Monitor for post-operative
  hepatic decompensation Possible
  prolonged duration of action in opiates HDU / ITU
  care

39
Child-Pugh Group B/C patient undergoing major
surgery

• Previous upper abdominal surgery, portal
  hypertension and coagulopathy dramatically
  increase the potential for per-operative blood
  loss
• 8-12 units of blood, together fresh frozen
  plasma and platelets should be available.
• Pre-medication
• Sedative premedicants should be avoided in the
  encephalopathic patient.
• Other drugs may be needed pre-operatively and
  include antibiotics and H2 receptor antagonists.
• The oral or intravenous route used -
  intramuscular injections should be avoided.
• Coagulopathy may require correction with fresh
  frozen plasma and platelets and renal replacement
  therapy may need to be considered.

40
Per-operative considerations

• Regional techniques -- considered carefully -
  coagulopathy , epidural varices can pose an
  additional risk.
• Vascular access with a multi-lumen central venous
  catheter together with at least one large bore
  central line
• Monitoring of arterial and central venous
  pressures is mandatory.
• Pulmonary artery, pulmonary capillary wedge
  pressure and cardiac output measurements may be
  necessary in the sick patient.
• Trans-oesophageal echocardiography and volumetric
  haemodynamic monitoring / pulse contour analysis
  can provide significant additional information
  for the strategic management of these patients.

41
CONTD

• Coagulation and fibrinolysis are major concerns.
• The potential for large volume blood replacement
  means that temperature should be measured and a
  fluid warmer and warming mattress used.
• Regular per-operative estimation of INR/PTR may
  be necessary - thromboelastography provides
  useful intra-operative evaluation of coagulation.
• Blood conservation - considered
• Preservation of hepatic function -
  N-acetylcysteine (NAC) is a sulphur-containing
  antioxidant - benefit patients with fulminant
  hepatic failure.
• NAC appears to improve oxygen
  delivery and consumption, and reduce base
  deficit.
• Renal Function - Dopamine may be useful

42
Bleeding oesophageal varices

• Bleeding oesophageal varices - life-threatening
  complication of - often occur against a
  background of abnormal clotting,
  thrombocytopenia, encephalopathy and Ascites.
• Overall mortality is 30.
• The principles of anaesthetic management
• Protect the airway.
• Establish good vascular access.
• Volume replacement - colloid, blood, fresh frozen
  plasma and platelets. Avoid saline.
• Check / correct clotting. Give Vitamin K, correct
  fibrinolysis and review blood chemistry.

43
Intoxicated Alcoholic Patients

• Requires less anaesthetic additive depressant
  effect of alcohol anaesthetics
• Ill - equipped to withstand stress Acute blood
  loss
• Alcohol decrease the tolerance of brain to
  hypoxia
• ? Risk of regurgitation aspiration - alcohol
  ?tone of lower oesophageal sphincter slows
  gastric emptying
• Alcohol Interferes with platelet aggregation
• Causes ?conc. of plasma catecholamines ? ?
  Intraoperative dysarrhytmias

44
POSTOPERATIVE JAUNDICEMild 17, marked - 4

• Patient factors
• Congenital hemolytic disorders
• Acquired hemolytic disorders
• Pre existing liver disease
• Coagulopathy
• Gilberts syndrome
• Sepsis

• Perioperative factors
• Anaesthetic induced ?HBF
• Bleeding
• Hypotension
• Blood transfusion
• Biliary tree trauma
• Viral hepatitis
• Drugs
• Halothane ,antibiotics
• Nonsteroidal agents

45
POSTOPERATIVE JAUNDICE

• Extravascular break down of haematoma 1 ltr
  -5000mg Bilirubin
• 500ml of blood transfusion contains 250 mg
  bilirubin
• Intravascular destruction of RBC can occur in
  G6P-dehydrogenase defeciency, cardiopulmonary
  bypass, Artificial valves, sickle cell disease,
  multiple blood transfusions
• Delayed transfusion reactions hemolysis postop
  jaundice
• Biliary obstruction due to surgery -?bilirubin
  ?alkaline phosphatase within 3 days of surgery

46
Contd

• Postop cholecystitis/pancreatitis may follow non
  biliary surgery 3- 30 days post op
• Post operative intrahepatic cholestasis benign
  - associated with multiple blood transfusions,
  hypoxia ,hypotension - ?bilirubin ?alkaline
  phosphatase within 2-7 days of surgery
  resolution in 3 weeks
• Management
• Prevention is the best treatment
• Avoid precipitating factors

47
Halothane Hepatitis

• The incidence is 17000-30,000 halothane
  anaesthetics - higher in women, the middle aged
  and the obese
• Rarer in paediatric patients and with the newer
  volatile agents.
• Commonest iatrogenic cause of fulminant hepatic
  failure
• Unexplained liver damage within 28 days of
  halothane exposure in previously normal patient
  idiosyncratic reaction
• Clinical features malaise, anorexia,fever
  within 7 days ,jaundice within days to 4 weeks

48
Halothane Hepatitis

• DIAGNOSIS
• Serum antibodies that react with specific liver
  microsomal proteins that are altered by
  trifluroacetyl chloride metabolite of halothane
• Gross rise of Transaminases 500 -2000 u/l
• Risk factors
• High - recent previous exposure 78
• previous adverse reaction
• Uncertain - obesity
• Female 1.6 1
• Drug allergy 15
• Family history
• Lymphocyte sensitivity to
  phenytoin

49
Contd

• The cause not fully established -
  multifactorial - ? possible immunological cause
  .
• Immune sensitization to trifluoracetylated
  proteins produced by Cyt P450 2E1 in genetically
  predisposed subjects
• Reduced hepatic blood flow and hypoxia are also
  to blame
• Related to the degree of metabolism of the
  volatile agent, so toxic metabolites may be
  involved.
• The onset time of the jaundice is shorter with
  increasing numbers of exposures to halothane.
• Nevertheless, enflurane and isoflurane are
  associated with hepatic dysfunction, albeit
  apparently at lower rates than halothane. WHO
  database holds 225 and 159 reports respectively.

50
Halothane exposure guidelines

• Avoid Halothane if
• Within at least 3 months of a previous exposure
• Previous adverse reactions -jaundice or pyrexia
• Family history of hepatic reactions to halothane.
• Pre - existing liver disease
• Adverse reactions to Other volatile anaesthetic
  agents.

51
Liver and Pregnancy

• Normal in size
• A decrease in total protein as well albumin.
• An increase of the liver dependent clotting
  factors such as fibrinogen.
• An increase of alkaline phosphates 3-4 times
  secondary to placental alkaline.
• Sr.cholinesterase ? 30
• Normal transaminase AST,ALT levels and
  bilirubin
• Any increase in transaminase levels and bilirubin
  good indicator of pregnancy induced liver
  disease

52
Intrahepatic Cholestasis of Pregnancy

• Incidence 0.01. Mainly in the third trimester .
  Rare in black patients .
• Strong family history .
• High recurrence in subsequent pregnanacies
  60-70.
• Pruritus alone - 80 percent ,
• Jaundice develop in 20 percent
• Infrequent, mild to moderate steatorrhea.
• Bilirubin level less than 5 mg /dl , minimal or
  no elevation in transaminases

53
IChP contd

• Incidence of fetal distress and death high if
  early delivery is not induced (deliver at week 38
  if pruritus , at week 36 in case of jaundice )
• Parenteral vitamin K , Ursodeoxycholic acid , 15
  mg /kg , Cholestyramine binds bile acid salts ,
  Dexamethasone
• Pruritus resolve within two days of delivery but
  bilurubin within 4-6 weeks
• Implications on Anaesthesia
• Check coagulation profile
• Ask for vit K I.V
• take care of high incidence of fetal distress ,
  meconium-stained , prematurity ( neonatologist
  must attend with incubator

54
Preeclampsia Eclampsia

• About 25 of patients with Severe pre-eclampsia
  and 90 of those with eclampsia will have
  elevated AST and ALT gt 5 times and bilirubin lt 5
  mg/dl
• If not associated with other criteria of HELLP
  syndrome e.g. low platelets , haemolysis , we
  give prophylactic dexamethasone 8mg/12hrs. beside
  mg.sulphate , antihypertensive , albumin 20
  /50ml/day
• Implications on anaesthesia
• Painless labour with epidural to reduce stress
  response which could continue to anaesthesia
  provided INR lt1.5
• Difficult intubation because of edema - small
  cuffed tube 6-7 mm
• Adequate analgesia
• Fluids restriction
• Continue medications postoperative in ICU .

55
HELLP syndrome

• Hemolysis , Elevated liver enzymes, Low platelets
• Peripartum multiorgan damage with pre-eclampsia
  result from very active platelets aggregation
  everywhere with end organ ischemia and congestion
  with deposition of fibrous network and entraped
  haemolysed RBCs platelets necrosis
  periportal haemorrhage
• Nausea, vomiting , headache and upper right
  abdominal pain ,hypotension /shock
• Best markers are the maternal lactate
  dehydrogenase level and the maternal platelet
  count.

56
Congested liver of HELLP syndrome
57
CONTD

• Perinatal administration of dexamethasone in a
  high dosage of 10 mg intravenously every 12 hours
  has been shown to markedly improve the laboratory
  abnormalities associated with HELLP syndrome.
• Magnesium sulfate to prevent seizures.
• Antihypertensive therapy if blood pressure is
  greater than 160/110 mmHg despite the use of
  magnesium sulfate.
• Anesthesia like severe preclampsia
• avoid trauma to liver
• Vit. K if INR gt1.5
• FFP 4-6 if INR gt2
• Platelets 6-8 units if platelets
  lt50.000.
• Mortality maternal 50 - 60,foetal -60

58
ACUTE FATTY LIVER OF PREGNANCY

• Rare ,serious disorder ,unknown etiology
• Symptoms in third trimester abdominal pain
  ,nausea vomiting, anorexia,fatique , fever
  ,headache
• Rapid progression bleeding, jaundice,
  encephalopathy, renal failure, hepatic failure,
  coagulopathy - PPH
• ?Transaminases, hyperbilirubinemia, ?prothrombin
  time --- DIC
• Prompt delivery is advisable

59
Hepatic Rupture and Infarction

• Older multigravida mothers with preeclampsia (75
  to 85 percent) are at higher risk.
• Extremely rare, 140,000 to 1 250,000 .
• Patients with hepatic rupture typically present
  in shock, with preceding right upper quadrant
  pain, hypertension, elevated transaminase levels
  (greater than 1,000 IU per L) and coagulopathy.
• Therapy for hepatic rupture has included
  transfusion of blood products and intravenous
  fluids, surgical evacuation and arterial
  embolization with 75 percent perinatal mortality
  rate have been noted in hepatic rupture.
• Hepatic infarction was typically present with
  fever and marked elevations in transaminase
  levels. In surviving patients, liver function and
  histopathology are normal within six months of
  delivery

60
Anesthesia in pregnant women with HELLP syndrome.

• Retrospective study. For the period of 1 July
  1996, through 30 June 2000
• RESULTS During the period of study 119 patients
  had HELLP syndrome. Eighty-five patients had
  cesarean delivery and 34 had vaginal delivery.
• Seventy-one patients had diagnosed HELLP
  syndrome previous to the anesthesia and 14
  postcesarean delivery the range platelet count
  was 19000-143000/microl.
• Of these 71, 58 had an epidural anesthesia, 9 had
  general anesthesia and 4 had spinal anesthesia.
• There were no neurologic complications or
  bleeding in the epidural space.
• CONCLUSION We found no documentation of any
  neurologic or hematologic complications of women
  with HELLP syndrome and neuraxial anesthesia.

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Subdural Hematoma following dural puncture in a
parturient with HELLP syndrome

• This complication occurred following accidental
  dural puncture in a parturient with
  thrombocytopenia (99,000µL-1) who subsequently
  developed the syndrome of hemolysis, elevated
  liver enzymes and low platelets.
• On the first postoperative day, postdural
  puncture headache (PDPH) developed.
• An epidural blood patch (EBP) was deferred to the
  third postoperative day because of a platelet
  count of 21,000µL-1.
• Headache intensified from a typical PDPH to one
  which was not posturally related.

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• A second EBP was abandoned after the injection of
  5 mL of blood because of increasing headache
  during the procedure.
•  Magnetic resonance imaging revealed bilateral
  temporal subdural hematomas.
• The patient was managed conservatively and
  discharged home without any sequelae.
• Conclusion It is conceivable that
  thrombocytopenia together with possible abnormal
  platelet function increased the risk of subdural
  hematoma.
• Alternative diagnoses to PDPH should be
  considered whenever headache is not posturally
  related.

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OCUPATIONAL HAZARD

• Risk of transmission of HBV following inoculation
  is 5 -30
• May occur through needle prick/cuts/ sharp
  injuries/mucous membranes- waterproof dressing
• Wear gloves while inserting a cannula ,airways,
  intubation extubation
• Sharps should not be handed directly to others
• See to the sterilisation of other contaminated
  things

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• HAPPY NEW YEAR

• Thank you