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Anaesthetic management in Obstructive jaundice
1. Presenter : Dr. M. Senthil Prakash
Dept Of Anaesthesiology
MAMC - Delhi
2. Patient details
Mr. X Age: 58 years Sex: male Occupation: Rickshaw coolie
Chief Complaints
▪ Pain abdomen – 20 days
▪ Generalised Itching – 10 days
▪ Nausea, fever – 3 days
CASE PRESENTATION
3. Pain abdomen
History of presenting illness
Right upper abdominal pain
20 days duration;
Dull aching; Insidious onset
Intermittent in nature
Non radiating
No aggravating/relieving
Generalised itching , 10
days duration
Progressive in nature
Relieved on medication
Low grade
Intermittent , 3 days duration
Not associated with chills and rigors
No diurnal variation
Relieved on medication
• Yellowish discoloration of eyes
• Dark coloured urine since 20 days
• Clay coloured stools
• Loss of Appetite and loss of Weight since last one month (has lost about 6 kgs)
• No h/o Malena, ascites & swelling of legs
Itching Fever
4. Past history
▪ No history of similar complaints in the past
▪ No history of previous surgery, Exposure to anaesthesia
▪ No Jaundice or contact with jaundiced patient
▪ No history of Diabetes Mellitus, Hypertension, Bronchial asthma or Epilepsy
▪ No history of drug intake
▪ No history of blood transfusions.
5. Family history
No history of similar complaints in the family was noted.
Personal history
Diet: Vegetarian
Sleep: disturbed (due to itching)
Habits: Smoker since 20 years ( 8 beedis/day). Not an alcoholic.
6. General Physical Examination
An elderly male patient moderately built and nourished.
Ht – 158cm, Wt – 42kg , BMI – 20.8
Pallor - +, Icterus - +, No cyanosis, oedema, clubbing, spidernavi, palmar erythema, Echymosis
Scratch marks - ++ over the abdomen and peripheries.
Airway Examination Pulse rate – 62/min;
MPC II, MO - Adequate Blood pressure – 110/70 mm of Hg
ROM Neck full Respiratory rate – 16/min
TMD > 6cms
7. Systemic Examination
▪ Inspection:
– Normal in shape.
– No dilated veins, scars and
sinuses.
– All quadrants move
correspondingly with respiration.
▪ Palpation:
– Soft. Tenderness in right hypochondrium
and epigastrium.
– Palpable hard mass of about 5 x 3 cms felt
in the epigastrium with an irregular border.
– Hepatomegaly +, 3 cms below the costal
margin
– No Splenomegaly/ free fluid
Per abdominal examination:
8. ▪ Percusion
– Liver dullness extent from 4th ICS to
3cm below the Rt subcostal margin
s/o hepatomegaly
– No other organomegaly
– No shifting dullness/ fluid thrill
▪ Auscultation
– Bowel Sound present
– No bruits hear
▪ CVS:
– S1 S2 hear
– No murmurs heard.
▪ RS:
– Normal Vesicular Breath Sounds heard,
– No added sounds.
▪ CNS:
– Normal, No focal neurological deficits
Systemic Examination
9. 58 yr male patient with pain abdomen, discolouration of eyes, urine, clay
coloured stools, itching, significant loss of weight and appetite with
hepatomegaly
Clinical Diagnosis :
Obstructive Jaundice with probably Peri-ampullary
carcinoma
Summary
14. ▪ Second largest organ
▪ Most vascular organ
▪ 30% of CO
▪ 100 – 120 ml/100gm/min
▪ Synthetic, Storage, Excretion
▪ Endocrine
15. Anatomy
▪ Four Lobes
– Right
– Left
– Caudate
– Quadrate
▪ Four Ligaments
– Rt/Lt Coronary
– Rt/Lt Triangular
– Falciform
– Teres/Round
16. Physiologic Segments
▪ Considerable variability
▪ Couinaud system
▪ Eight Segments
▪ 1st segment is caudate
▪ CE-Spiral CT
▪ Lower rates of perioperative
morbidity & mortality
17. Liver Lobule
▪ Anatomical unit
▪ 3mm in circumference
▪ 50k to 1lakh
▪ Hexagonal – portal canals
▪ Portal canal – Portal triad,
nerve fibers, lymphatics,
connective tissues
18. Liver Acinus
▪ Functional Microvascular
▪ Three Zones
– Z I -> Periportal -> High Po2
– Z II -> Midzone
– Z III -> Pericentral -> Low Po2
▪ Zone I – Highest Mitochondria
▪ Synthetic fn, Urea cycle
▪ Zone III – High SER, Cyt P450
▪ Xenobiotics
19.
20. Hepatic Blood Supply
▪ 25% to 30% of CO
▪ Dual supply
– Portal V (75%) 85% saturated
– Hepatic A (25%) 95% saturated
▪ Oxygen delivery is 50% by both
▪ 2/3 of oxygen used by liver
▪ Sinusoids can accommodate 400 –
600 ml of blood
21. Control of Liver Blood Flow
INTRINSIC
▪ AUTOREGULATION
– Myogenic
– Resistance to vascular bed
– Hepatic artery - 80 mmHg
– Portal vein – low pressure flow from spleen, intestine
– Anaesthesia abolish
▪ Hepatic Arterial Buffer response (HABR)
– Max doubles the H.Art flow
– Adenosine
▪ Metabolic
– O2 tension, pH of PV -> HABF
26. • Total bile flow- 600 ml/day(500-1000ml/day)
• Hepatocyte component is - 450ml/day
• Bile salt dependent due to biliary glutathione and ductular bicarbonate secretion
• Cholangiocyte component- 150ml/day
• It depends on secretin stimulation
• With conjugated bilirubin <15 %
PHYSIOLOGICAL FACTS BILE
27. BILE
▪ Heterogenous
– Bile acid, salts
– Conj. Bilirubin
– Cholesterol
– Phospholipids
– Electrolytes
▪ Bile Acid/salt
– 200mg – 500mg/day
– Primary / Secondary
– Entero-hepatic circulation
– Buffer system of the gut
Functions
‒ Absorption of Lipids, LCFA, FS Vitamins
‒ Excretion of lipid soluble wastes
exogenous/endogenous
‒ Regulate plasma lipid levels
29. Physiological functions of Liver
▪ Blood Reservoir
▪ Glucose Homeostasis
▪ Fat Metabolism
▪ Protein Synthesis
▪ Drug & Hormone Metabolism
▪ Bilirubin formation &excretion
▪ Anti bacterial action
30. Blood Reservoir
▪ 10% of total blood volume
▪ Available for Auto transfusion into central circulation
▪ Prevents profound hypotension after minimal blood loss
▪ Neural and Humoral control
32. Glucose Homeostasis
▪ Glycogen stores 75gm 24—48hrs
▪ Anesthesia inhibits gluconeogenesis
▪ Provide ext. source of glucose in long duration surgeries
33. Lipid metabolism
▪ Synthesis & Storage of FA – TGL , VLDL
▪ Synthesis of lipo-proteins & cholesterol
▪ β-Oxidation of FA to Acetyl-CoA TCA cycle / ketone bodies modulated by
Glucagon and Insulin
▪ Ketone bodies – Important extrahepatic energy source
34. Protein Metabolism
▪ Synthesis and Deamination of AA
▪ Formation of urea from ammonia
▪ All Plasma proteins – except γ-globulin & factor III, IV, VIII
▪ Albumin
– Daily prod. 12 - 15g/d (3.5-5.5gm%) Total pool – 500gm
– Negative acute phase reactant
– Liver disease Alb glob – Significance..?
▪ Function of Albumin
– Plasma O. P.
– Binding of drugs, FFA, UCB, Hormones
36. Drug binding
▪ Acidic Drugs reversibly combine with Albumin
▪ Albumin < 2.5gm%
▪ albumin bound form free drug
▪ Highly bound (>90%)
– Warfarin
– OHA - glimepiride, glipizide, glyburide,
– NSAID
– Cardiac: Loop diuretics, amiodarone, prazosin, nicardipine, digitoxin, ticlopidine, losartan
– Benzodiazepines: diazepam, midazolam
▪ Intermediate bound ( 60%)
– Anticonvulsant , Thiopental
37. Coagulation
▪ Coagulation :
– Vit K Dependent : Factor II, VII, IX, X, Protein C / S / Z
– Prothrombin
– fibrinogen
▪ 20%--30% activity required for normal coagulation
▪ LFT grossly deranged before coagulation abnormalities appear
▪ T½ of clotting factors produced in liver is very short ( 2 – 4 hrs F-VII )
▪ Ac. Hep dysfunction Coag. Abn
▪ Evaluate PT- INR/ aPTT
38. Drug metabolism
▪ Lipophilic, highly active → water soluble, less reactive
Enzymatic reaction
▪ Phase I
– oxidation
▪ Cyt P450 – Z III / reduced O₂ species / Free radicals / Down regulation
– reduction & hydrolysis (L.A)
▪ Phase II
– Conjugation glucuronidation,
– sulphation, methylation
– Acetylation
– UDP-GT ( Bilirubin, morphine, aminophylline)
39. Clearance of drugs from plasma
Rowland's Equation
▪ Hepatic Clearance: Cl(h) = Q [(f x Clint)/(Q+ f x Clint)]
▪ Q = hepatic blood flow
▪ f = fraction of free drug (not bound)
▪ Clint = intrinsic capacity of the hepatocytes to metabolize a drug
▪ High DER ∝ Rapid clearance
– Consider ER is 1, Now Cl = Q [ DER – Drug Extraction Ratio ]
▪ Low DER ∝ Low clearance
– Capacity limited / extract less avidly
– By protein binding , Hepatic enzymes
40. Clearance of drugs from plasma
High
HER
~ Hepatic Blood
Flow (HBF)
Opioids, Lidocaine,
Pethidine, CCB, 𝛽 blocker,
TCA
Low
HER
~ mic.enzymes
~ protein binding
BZD, Thio, Pancu’m, Asprin,
Warf, Acetaminophen,
Antoconvulsants
• Chronic liver disease drug metabolism d/t - ed no. of hepatocytes and HBF
• Repeated injection cumulative effect
• Volatile anesth. Agents ed clearance of drugs
41. Liver Function Tests
▪ Non specific, Large hepatic reserve
Detection of HC Injury
• Aminotransferases (SGOT/SGPT)
Hepatocyte damage - hypoxia/ drugs/viruses
Extrahepatic -heart/lungs/skeletal ms
Marked (3x)-ac. Hep damage
• LDH
• Hemolysis, rhabdomyolysis,tumor necrosis
• Pre-eclampsia, MI, CVA
• G-S-T
• Senitive/specific for DILI
• 90min
• Z III – Hypoxia, Drug
42. Liver Function Tests
▪ Synthetic Function
▪ Plasma proteins
▪ Serum Albumin
▪ PT
▪ Cholestatic Disorder
▪ S. Bilirubin
– Total 0.3 - 1.1mg%
– ID 0.2-0.7mg%, D 0.1 - 0.4mg%
▪ Alkaline phoshphatase
– Bile duct cells
– Slight obstruction (3x)
– Bone –extrahep source
▪ 5- Nucleotidase
▪ GGT
43. Hepatic
dysfunction
Bilirubin Transaminase
enzyme
Alkalinep
hosph.
Causes
Pre hepatic Unconjug
ated
(indirect)
Normal Normal Hemolysis/
hematoma
resorp./
bilirubin
overload-BT
Intrahepatic
(hepatocellu
lar)
Conjugated
(direct)
elevated Normal to
Slightly
Viral/drugs/s
epsis/hypoxi
a/cirrhosis
Posthepatic
(cholestatic)
conjugated Nomal to
slightly ed
(2x) Stones,
Sepsis,
tumor
45. JAUNDICE
Jaundice (derived from French word ‘jaune’ for yellow) or icterus (Latin
word for Jaundice)
Yellowing of sclera at 3 mg%
Bilirubin has got high affinity for elastin and sclera has high elastin
content
Yellowing of skin and mucous membrane at 6 mg%
Bilirubin level rise upto three weeks then stabilise
46.
47. Extrahepatic causes
▪ Benign
– Gallstone/ Choledocholithiasis - mc
– Clinical features - Previous history of
dyspepsia, Intermittent Pyrexia/ Rigors,
Pain, jaundice (Charcot’s triad), O/e –
positive Murphy’s sign
– Chronic pancreatitis, Strictures
– Parasitic infections – ascariasis,
clonorchiasis, Biliary atresia , Choledochal
cysts
▪ Malignant
– Carcinoma of pancreas/ampulla/bile
duct/gall bladder
– Clinical features – Painless,
progressive deep Jaundice, Weight
loss,
– Courvoisier’s sign - Palpable
Gallbladder (exception ampullary Ca-
intermittent jaundice d/t sloughing of
tumour cells)
49. Normal secretory pressure of bile is 15-25 cm of water
At 35 cm of water there is suppression of bile flow
High pressure leads to cholangiovenous and cholangiolymphatic reflux of bile
Dilatation of bile duct and intra hepatic biliary radicals(IHBR)
IHBR dilatation may be absent if there is secondary hepatic fibrosis or cirrhosis
PHYSIOLOGY OF OBSTRUCTION
50. Increase in biliary
pressure leads to
Disruption of tight junctions between hepatocytes
and bile duct cells with increased permeability
Reflux of bile contents in liver sinusoids
Neutrophil infiltration,increased fibrinogenesis and
deposition of reticulin fiberes in portal triad
Reticulin fibers gets converted in to type 1 collagen
Laying down of collagen fibers leads to hepatic
fibrosis obstruction of sinusoids and secondary
biliary cirrhosis and portal hypertension
Fibrosis can also lead to atrophy of obstructed liver
PATHOPHYSIOLOGY
52. • Acute obstruction
• increase in hepatic arterial blood flow
• No change in portal venous blood flow
• Chronic obstruction
• Decrease in total liver blood flow , dilatation of sinusoids and elevation of
portal pressure
CHANGES IN LIVER BLOOD FLOW
53. Circulating Bile salts leads to
Bradycardia due to direct effect on SA node.
Impaired cardiac contractability
Impaired response to beta agonist drugs
Decreased peripheral vascular resistance
Net result
• Hypotensive patient prone for circulatory collapse
• Exaggerated hypotensive response to bleeding
• More prone to perioperative shock - therefore replace volume losses immediately
in peri-operative period.
CARDIOVASCULAR EFFECTS
54. 10 % incidence with 70 % mortality
Factors responsible are
• Effect of bile salts, Endotoxins, inflammatory mediators on kidney
• Decresed cardic function - Hypotension
• Refractoriness of tubules to ADH
• Increased levels of ANP resulting in hypovolemia
Resulting in
• Renal vasoconstriction, hypoperfusion
• Shunting of blood from cortex
• Activation of complement system leading to tubular and cortical necrosis
EFFECT ON RENAL SYSTEM
55. Defects in cellular immunity
Depressed function of RE system i.e Kuffer cells
Impaired T cell proliferation
Decreased neutophil chemotaxis
Defective bacterial phagocytosis
Can lead to Sepsis
Associated cholangitis and bactibilia
Absence of bile salts in intestine Escape of endotoxins from intestine into
portal blood
IMMUNE SYSTEM
56. Deranged coagulation
▪ ed synthesis of Clotting factors Prolongation of Prothrombin time
▪ Vit. K deficiency d/t biliary obstruction Defective γ-carboxylation
▪ Endotoxin, Hyperspleenism Thrombocytopenia
▪ Endotoxin ed Fibrinolysis, Low grade DIC
▪ Loss of calcium
▪ Decreased absroption of fat solube vitamins A,D,E,K
57. Delayed wound healing
High incidence of wound dehiscence
Decresed activity of enzyme Propyl hydroxylase in the skin
This helps in incorporation of proline in collagen
Defective synthesis of collagen
WOUND HEALING
58. ENDOTOXEMIA
Bile salts are surfactants----disrupt endotoxins
▪ Absence of bile in intestine intest.bact. Flora
▪ Breakdown of GI mucos. Barrier bact. translocation
▪ Hepatic RES function clearance of endotoxins
62. RELATED TO SURGERY
▪ Whipple’s procedure Ca. Head of pancreas, Periampullary
▪ Distal gastrectomy, H-J, P-J, G-J
▪ Major surgery long duration
▪ Increased blood loss/fluid shifts
▪ Wide incision Roof top—warrants good postoperative analgesia
▪ Extensive monitoring reqd for favourable outcome
63. RISK stratification
▪ Age > 60yrs
▪ Albumin < 3.0gm%
▪ Preop. renal dysfunction
▪ Long standing biliary obstruction infection sepsis
▪ Weight loss
Serum creatinine & Sepsis—prognostic factors
Periop CVS collapse & renal failure
64. Child – Pugh Score
Mortality Rate for major
Abdominal Sx
Child A 10 %
Child B 30 %
Child C 80 %
66. Preoperative Assessment
OBJECTIVES
▪ Assess the type and degree of liver dysfunction.
▪ Assess effect on other system.
▪ To ensure – post operative facilities (High risk patient).
68. Preoperative Investigations
To judge the synthetic ability of liver
▪ Serum albumin – < 2·5 gm% - severe damage
▪ Albumin/globulin ratio – reversed.
▪ Prothrombin time – > 1·5 sec. Over control
▪ INR – > 1.3
Parenteral Vit. K use..?
76. IV Anaesthetics
▪ Ketamine
– Little or no effect on HBF
▪ Thiopentone
– Protein bound
– Titrated doses
▪ General rules
– Titrated dosage
– Maintain adequate MAP, CO
– IV Fluid volume
▪ Propofol
– THBF, splanchnic vasodilation
– Oxygen delivery
– Anti-oxidant
77. Opioids
▪ Well tolerated
▪ Smaller doses
▪ Morphine—ph-II reac.
▪ Fentanyl / Sufentanyl – continuous infusion
▪ Remifentanyl {DOC} – ester hydrolysis
Spasm of sphincter of Oddi
78. Spasm of sphincter of Oddi
▪ Interpretation of operative cholangiography & biliary pressures
▪ All patients do not show this response
▪ Incidence of spasm is very low
▪ Intraop manipulation of BD system spasm
79. Volatile Anesthetics
▪ Useful & well tolerated
▪ Can be entirely eliminated
▪ Halothane – Hepato toxicity
▪ CVS instability vasodilation perf. Press. blood velocity oxygen
extraction HBF & oxygen supply
▪ Isoflurane—best maint. of HBF & oxygen delivery
▪ Sevoflurane better than Iso
– HABR
– Suppresses H.Art vasoconstriction
– Ischemic-preconditioning
▪ Desflurane – Similar as ISO
84. Analgesia - TEA
▪ Patients undergoing upper
abdominal operations
(gastrectomy, hepatectomy
and Whipple’s operation)
▪ Recommended sites are at
T6-8 levels
▪ Midthoracic spinous
processes are acutely
angulated and the laminae
become more vertically
oriented – Paramedian
approach
88. Conclusion TEA
▪ Epidural analgesia provides favorable outcomes after upper
abdominal surgery
▪ The success and safety of the procedure rely on
– Expertise in the procedure
– Pharmacologic selection.