This document discusses liver function and the impact of liver disease on anesthesia. It covers the key roles of the liver, signs of impaired function, and how disease affects drug metabolism, cardiovascular and pulmonary systems. Risk is assessed using Child-Pugh scoring. For patients undergoing surgery, careful fluid management, blood product administration, and hemodynamic stability are emphasized to reduce risk according to their liver disease severity.

1. 9.1.09
ANAESTHESIA AND LIVER
DISEASE
Dr.Pratheeba Durairaj ,M.D,D.A,

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 problems are both vascular and mechanical.
 Hepato-Pulmonary syndrome – triad of end stage liver
disease, A-a gradient >2 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.
Pulmonary changes

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. Management
of 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 (>140 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 > ISO > DES > 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
 γ - 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

23. PUGH‘S MODIFICATION OF CHILD GRADING
Clinical & Biochemical
variables
POINTS
1
SCORED
2 3
Serum albumin (g/L) >35 28-35 <28
Serum bilirubin (µmol/L)
[Mg /dl]
<35
< 2
35-60
2 -3
>60
> 3
PT (seconds) prolonged
from control
1-4
INR [ < 1 .7]
4-10
INR [1.7 -
2.3]
10
INR >2.3
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]

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 <3g/L
 Serum bilirubin >50 µmol/L
 PT >1.5 s over control
 Presence of infection
 WBC > 10,000
 Treatment with more than two antibiotics
 Presence of Ascites
 Malnutrition
 Emergency surgery

29. Anaesthetic Technique
 Avoid hypotensive techniques—intra 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

30. 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 , pancruonium[1.6 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 >2.5 s above control, platelet
count < 50,000 /cu.mm, bleeding time >12 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 JAUNDICE
Mild – 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 1:7000-30,000 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 > 5 times
and bilirubin < 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 <1.5
 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 >1.5
FFP 4-6 if INR >2
Platelets 6-8 units if platelets <50.000.
 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, 1:40,000 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.

61. Subdural Hematoma following dural puncture in a
parturient with HELLP syndrome
 This complication occurred following accidental dural
puncture in a parturient with thrombocytopenia
(99,000•µL-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
21,000•µL-1.
 Headache intensified from a typical PDPH to one
which was not posturally related.

62.  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.

63. 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