This document presents the case of a 68-year-old male with obstructive jaundice. He presents with pain in the right upper abdomen, itching, and fever for the past few weeks. On examination, he is jaundiced and has hepatomegaly. Investigations show elevated bilirubin and alkaline phosphatase. Imaging reveals dilatation of the intrahepatic and common bile ducts. The patient is diagnosed with obstructive jaundice likely due to carcinoma of the head of the pancreas and is planned for a Kausch-Whipple's procedure.

1. Obstructive Jaundice
Case Discussion
Speaker: Dr S.N.Bhagirath
Panelists: Dr Hemalatha.S
Dr Manjula.B.P.
Dr Krithika Devi

2. Case Presentation
Patient details
 Name: Puttasomachari
 Age: 68 years
 Sex: male
 I.P.No.: 216363
Chief Complaints
 Pain abdomen – 20 days
 Generalised Itching – 20 days
 Fever – 3 days

3. Case Presentation……..contd
History of presenting illness
Pain abdomen Itching Fever
Colicky type
Gradual in onset
Intermittent in nature
Over right upper part of
abdomen
Non radiating
No aggravating/relieving
factors
20 days duration
Gradual in onset
Progressive in
nature
Generalised in
extent
Relieved on
medication
20 days duration
Low grade
Intermittent in nature
Not associated with
chills and rigors
No diurnal variation
Relieved on
medication
3 days duration
History of yellowish discolouration of eyes and urine since 15 days
No history of Diabetes Mellitus, Hypertension, Bronchial asthma or Epilepsy

4. Case Presentation……..contd
Past history
No history of similar complaints in the past.
History of weight loss present since last three months (has lost
about 6 kgs).
No history of previous surgery, Jaundice or contact with jaundiced
patient.
No history of drug intake except for consumption of Tab. Atarax
(hydroxyzine – 25 mg) for itching and Tab. Crocin (Paracetamol –
500 mg) for fever.

5. Case Presentation……..contd
Family history
No history of similar complaints in the family was noted.
Personal history
Diet: Vegetarian
Appetite: reduced
Bowel & bladder habits: Normal. (pale stools)
Sleep: disturbed (due to itching)
Habits: Smoker since 20 years ( 8 beedis/day). Not an alcoholic.

6. Case Presentation……..contd
General Physical Examination
An elderly male patient moderately built and nourished. Conscious and oriented.
Pallor - +, Icterus - +, No cyanosis, oedema, clubbing
Scratch marks - ++ over the abdomen and peripheries.
Pulse rate – 62/min;
Blood pressure – 130/80 mm of hg;
Respiratory rate – 16/min;

7. Case Presentation……..contd
General Physical Examination
.
Per abdominal examination:
Inspection:
Normal in size and 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
No free fluid

8. Case Presentation……..contd
General Physical Examination
Cardiovascular system: S1 S2 heard, No murmurs heard.
Respiratory System: Normal Vesicular Breath Sounds heard, No added sounds.
Central Nervous System: Normal. No neurological deficits
Impression:
Obstructive Jaundice with probable carcinoma of head of pancreas

9. Case Presentation……..contd
Investigations
Hb: 10.4 gm%
Differential count: Neutrophils – 71
Lymphocytes – 24
Monocytes – 02
Eosinophils – 03
Total count – 9, 800
Platelets: 2.73 lakhs/mm3
PT INR: 1.0
BT: 3’ 00”
CT: 4’ 00”
RBS: 99 mg/dl
Urea: 30 mg/dl
Creatinine: 1.1 mg/dl
Na+: 135 mEq/l, K+: 3.9 mEq/l, Cl-: 104 mEq/l

10. Case Presentation……..contd
Investigations……ccontd
LFT: Total Bilirubin: 9.0 (0.1 – 1.0)
Direct Bilirubin: 5.3 (0.0 – 0.2)
Indirect Bilirubin: 3.7
Albumin: 2.8 (3.4 – 5.0)
A/G Ratio: 0.9 (1.2 – 2.5)
AST: 39 (0 – 40)
ALT: 32 (0 – 40)
Alkaline Phosphatase: 570 (37 – 147)
HIV 1 & 2: Not detected, HBsAg: Not detected
USG: Intra Hepatic Biliary radical dilatation in its entire length probably due to
stricture.

11. Case Presentation……..contd
Investigations……ccontd
ECG: Sinus rhythm. Within normal limits. Heart rate: 60/min.
2D ECHOCARDIOGRAPHY: Normal Left Ventricular systolic function
No Regional Wall Motion abnormalities
Ejection fraction: 59 %
Upper G.I. Endoscopy: bulging growth in Periampullary region.
C.T. Scan: Moderated dilatation of intrahepatic and common bile ducts.
Chest X – Ray: Hyperinflated lung fields (COPD changes)
Arterial Blood Gas Analysis: Mild hypoxia.

12. Case Presentation……..contd
Management Plan
Kausch – Whipple’s Procedure

13. Discussion with elaborations
History of presenting
illness
Pain abdomen
Colicky type
Gradual in onset
Intermittent in nature
Over right upper part of
abdomen
Non radiating
No aggravating/relieving
factors
20 days duration
Biliary colic
•Severe
• intermittent
•Colicky pain
Pancreatic Pain
•Dull, continous pain radiating to back
• aggravated by food
• relieved by sitting up or leaning
forward
Hepatomegaly
•Dull, continous dragging type of pain
in right hypochondrium – stretching of
Glisson’s capsule

14. Discussion with elaboration
History of presenting illness
Fever
Low grade
Intermittent in nature
Not associated with
chills and rigors
No diurnal variation
Relieved on
medication
3 days duration
Viral hepatitis
• Fever at onset
with
arthralgias
Cholangitis
• Fever with rigors
Neoplasm
• low grade fever

15. Discussion with elaboration
History of presenting illness
History of yellowish discolouration of eyes and urine since 15 days
Normal range of plasma bilirubin
•Total - 0.3 – 1.0 mg/dl
• Indirect – 0.2 – 0.7 mg/dl
• Direct – 0.1 – 0.4 mg/dl
Clinically
obvious
2 – 2.5 mg/dl
•Sclera
•Under surface
of tongue
•Palms
•Nails
•Skin
Bilirubin has
affinity to elastin
(collagenous
tissue) – scleral
icterus is more
sensitive.
Differential
diagnosis of
icterus
-Carotemia
(scleral icterus
is absent)

16. Discussion with elaboration
Past history
No history of similar complaints in the past.
History of weight loss present since last three months (has lost
about 6 kgs).
-suggestive of malignancy
No history of previous surgery
-retained or recurrent stone, biliary structure, recurrent obstruction
from enlarging tumor
-anaesthesia exposure (post operative hepatic dysfunction, halothane
hepatitis)
Jaundice
-relapsing hepatitis, choledocholithiasis

17. Discussion with elaboration
Family and personal history
Family history of Cholestasis
Progressive Familial Intrahepatic Cholestasis syndrome (Dubin Johnson
& Rotor syndrome)
α1 antitrypsin deficiency
Family history of jaundice
Wilson’s disease
Progressive Familial Intrahepatic Cholestasis syndrome (Dubin Johnson
& Rotor syndrome)
α1 antitrypsin deficiency
Alcohol – Alcoholic hepatitis can lead to cholestasis

18. Discussion with elaboration
General
Physical
examination
BMI
Vital signs
Pallor:
Gastrointestinal
bleeding
Icterus
Lemon yellow – Hemolytic
Greenish yellow – Obstructive
Orange yellow - Hepatocellular
Pedal edema -
hypoproteinemia
Scratch marks - pruritis
Xanthoma -
hypercholesterolemia
Bruises -
Coagulopathy
Fat Soluble vitamin deficiency
• Vitamin A deficiency – Bitot’s spot,
hyperpigmentation
• Vitamin K deficiency - Ecchymoses

19. Discussion with elaboration
Abdominal Examination
Inspection:
Abdominal distension -ascites
Dilated abdominal vessels- cirrhosis
Operative scar-previous surgery
Palpation
Right upper quadrant tenderness (Murphy’s sign)-cholecystitis, cholangitis
Hepatomegaly: tender-Right heart failure, acute hepatitis, obstruction in biliary
tract;
Non-tender nodular–malignancy or infiltrative process e.g. amyloidosis
Splenomegaly-infective hepatitis, portal HT due to cirrhosis, Right heart
failure, haemolytic anaemia
Distended palpable GB (Courvoisier’s law) - in malignant obstruction of distal
common bile duct
Free fluid: Malignant ascites or non malignant ascites

20. Discussion with elaboration
Différences between extrahepatic/ intrahepatic Cholestasis
Extrahepatic Intrahepatic
Abdominal Pain Present Absent
Fever Present Absent
Prodrome Absent Present
Drugs Absent Present
History of surgery Present Absent
Risk factors like transfusion Absent Present
Family History Absent Present
Stigma of cirrhosis Absent Present
Encephalopathy Absent Present
PT Normalizing with Vitamin K Present Absent

21. Clinical pointers
Nature of Jaundice
Progressively worsening jaundice - Malignant obstruction, primary biliary
cirrhosis, familial cholestasis, primary sclerosing cholangitis, advanced end stage
liver disease
Intermittent jaundice - choledocholithiasis, ampullary carcinoma, biliary
ascariasis, relapsing viral hepatitis
Association with drug intake
Cholestatic – oral contraceptives, anabolic steroid, chlorpromazine,
carbamazepine, antibiotics- erythromycin, rifampicin
Hepatitis- INH, halothane, phenytoin, methyldopa, acetaminophen
Fatty liver- tetracycline, valproate
Toxic necrosis- acetaminophen, CCl4

22. Clinical pointers
Why pruritis..?
Central mechanism: ↑central opioidoergic tone in patients with cholestasis
Peripheral Mechanism: accumulation of numerous substances e.g. bile
acids,
histamine, serotonin & endogenous opoids in the
systemic circulation subsequent to failure of
elimination
Treatment:
Opioid antagonists, Cholestyramine, Rifampicin (Induce CP450 which
inactivates pruritogen), Phenobarbitone, Oral guar gum, 5-HT antagonist,
UDCA (Urso deoxy cholic acid), Propofol, Lidocaine, Charcoal
hemofiltration, Plasmapheresis, Ileal diversion, Liver transplantation.

23. Bilirubin Metabolism
Reticuloendotheli
al system
Unconjugated
bilirubin +
Albumin
Bilirubin +
glucuronic acid 
bilirubin di/ mono
glucuronide
Conjugated
bilirubin is
hydrolyzed
and converted
to
urobilinogen
by intestinal
pathogens
Stercobili
n
Faeces
90% urobilinogen
back to liver
10% urobilinogen
into systemic
circulation
Urobilin

24. Clinical pointers
Obstructive Jaundice
Intrahepatic causes
Familial/ hereditary disorders –
•Dublin Johnson syndrome,
•Rotor syndrome,
•Cholestatic jaundice of pregnancy,
•Recurrent intrahepatic cholestasis
Acquired–
•Cholestatic drugs ,
•viral and alcoholic hepatitis,
•TPN induced,
•Biliary Cirrhosis,
•sclerosing cholangitis

25. Clinical pointers
Obstructive Jaundice
Extrahepatic causes
Benign
Gallstone/ Choledocholithiasis - most common cause
Clinical features - Previous history of dyspepsia, Intermittent Pyrexia/
Rigors, Pain, jaundice (Charcot’s triad), O/e – positive Murphy’s
sign
Chronic pancreatitis, Strictures – iatrogenic, trauma
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)

26. Clinical pointers
Obstructive Jaundice
Lab investigations –
• ↑ conj. plasma bilirubin,
•bilirubinuria,
•absent urobilinogen in urine,
•clay coloured stools,
•↑ - ALP
•5-NT

27. Biochemical differentiators
Prehepatic Jaundice Hepatic Jaundice Post hepatic
Jaundice
Serum bilirubin ↑ (mostly unconjugated) ↑ (conj. & unconj.) ↑
(conjugated.)
Urine Urobilinogen ++ + -
Urine Bile Salts absent + / +
Urine Bilirubin -- + / - ++ ↑↑
(high coloured)
Fecal stercobilinogen ↑↑ N or ↓ absent
(clay colour)
Faecal fat N N or ↑ ↑↑
Enzymes SGOT / PT N ↑↑ N or ↑
(AST / ALT) (> 800 IU/L) 50-100 IU/L
Alkaline PO4 N N or ↑ (x 1-2) ↑↑ (x 3-10)
Plasma albumin N ↓ N or ↓
Prothrombin Time N ↑↑ ↑↑

28. Clinical pointers
Consequences of Obstructive Jaundice
• Decreased hepatocyte function
• metabolic dysfunction of cyt450
• decreased synthesis of albumin and clotting factors
• decreased Kupffer cell activity
• bilirubinemia, pruritis, CVS depression, nephrotoxicity,
hypercholesterolemia, atheromas and xanthoma.
• With absence of bile, endotoxins escape into portal blood
• Malabsorption of fats and vitamin A, D, E and K
• Acholic stools.

29. Clinical pointers Investigative aids
Ultrasound
- determines level & presence of intra and extrahepatic biliary
dilatation
- More sensitive than CT in detecting gall stone
CT
- useful in obese and excessive bowel gas
- stages and assesses operability of tumor
ERCP
- allows biopsy, brush cytology
- therapeutic – Sphincterotomy, stone removal, stricture
dilatation.
PTC
- 22G chiba needle, - allows biliary drainage and stenting

30. Clinical pointers
Surgical procedures•Ca Gall Bladder: Radical Cholecystectomy with wedge resection and CBD
excision
•Choledocholithiasis: ERCP removal or CBD exploration/ bilio-enteric
anastamoses
•Cholangio Ca: Liver resection and or local excision of the lesion or
Whipple
•Biliary Stricture: Hepatico-jejunostomy/ liver resection
•Periampullary Ca: Whipple’s Procedure
•Chronic Pancreatitis with head Mass: Whipple/ bilio-enteric
anastamoses

31. Anaesthetic Perspectives
Cardiovascular system
circulating bile salts (cholemia) leads to
•Impaired myocardial contractility
•Bradycardia
•Vasodilatation ↓ ability to mobilise blood from splanchnic vasculature
during Hemmorhage
•↓ sensitivity to vasopressors
•Hypotension & circulatory collapse
• Small blood losses are poorly tolerated; therefore replace volume losses
immediately in peri-operative period.

32. Anaesthetic Perspectives
Renal System
Acute renal failure
•Etiology multifactorial
•Arterial hypotension-myocardial depression
•Reduction in intravascular volume
•Nephrotoxicity - bile salt, endotoxins & inflammatory mediators
•Incidence 5 -10%, mortality high 32 – 100%
•Level of hyperbilirubinemia correlates with postoperative decrease
in Creatinine clearance

33. Anaesthetic Perspectives
Sepsis
can be due to
•Associated cholangitis and bactibilia
•Absence of bile salts in intestine Escape of
endotoxins from intestine into portal
•blood
•Retention of bile solutes in liver ↓ Kupffer cell activity
•Prevention - Perioperative antibiotics and oral bile salts

34. Anaesthetic Perspectives
Coagulopathy
1.Absence of bile salts in intestine Vitamin. K malabsorption
(required for gamma carboxylation of glutamyl residues of factors II,
VII, IX, X) ↑ PT
Correction - pre-op. Vitamin. K 10 mg OD × 3 days
2. Long lasting biliary obstruction Sec. biliary cirrhosis ↓ syn. of
coagulation factors (poor prognosis) Correction - transfusion of FFP

35. Anaesthetic Perspectives
Multiple Vitamin Deficiency - A, D, E, K due to absence of bile salts
in intestine
(A- night blindness, D – osteoporosis and muscle weakness, E- leg
cramps, K-easy bruising)
Haemorrhagic gastritis and stress ulcer
Impaired wound healing
Altered drug handling due to cholestasis
Long standing extrahepatic biliary obstruction > 1yr → biliary
cirrhosis →
problems of liver dysfunction

36. Anaesthetic Perspectives
LIVER FUNCTION TESTS
A. Indices of hepatocellular damage
1. Transaminases SGOT/SGPT - 0 – 35 IU/L
• SGOT (AST) - extrahepatic sources- heart /skeletal muscle/ kidney/
brain, less specific
• SGPT (ALP) - primarily found in liver, more specific
Viral hepatitis - SGOT/SGPT
Alcoholic hepatitis - SGOT/SGPT > 2 (deficiency of pyridoxine-5-
PO4)
In advanced liver cell injury Transaminases level may actually be
normal or low due to massive loss of parenchymal tissue
How does one assess liver functions..?

37. Anaesthetic Perspectives
LDH – poor specificity
3. Glutathione- S – transferase (GST) isoenzyme B – sensitive
indicator of liver damage
B. Indices of Obstructed Bile Flow
1). Alkaline Phosphatase – 35 – 100 IU/L
Derived from plasma membrane of bile duct cells
Extrahepatic sources- bone, intestine, liver, placenta
2.) 5- Nucleotidase - confirms hepatic origin of ALP, specific for liver
disease
3). Gamma glutamyl transferase (GGT) – most sensitive indicator of
biliary tract disease, but limited usefulness due to poor specificity
How does one assess liver functions..? …..contd

38. Anaesthetic Perspectives
How does one assess liver functions..? …..contd
Aminotransferases Alkaline PO4 Diagnostic Likelihood
Viral hepatitis Obstructive
Jaundice
> X 6 < X 2.5 90% 10%
< X 6 > X 2.5 10% 80%
C. Indices of hepatic synthetic function
1. Prothrombin time – factors II, V, VII & X
Coagulation. Factors have a short t ½; therefore PT is good indicator of
liver function in both Acute & Chronic liver disease, good prognostic
indicator of outcome of surgery in patients with liver disease
Causes for prolonged PT independently of liver disease - Vit. K deficiency,
Antibiotic therapy, DIC, Fibrinolysis, Coumarin administration

39. Anaesthetic Perspectives
How does one assess liver functions..? …..contd
Serum albumin
Long t ½ - 14-20days,
Liver – substantial reserve for alb. syn., daily production 10—15g/d (3.5-
5.5gm %)
Functions - Plasma oncotic pressure, Transport vehicle, Drug binding
Not a good indicator for acute or mild liver damage
Indicator of severity of chronic. Liver disease (< 2·5 gm% - severe
damage)
D. Indices of hepatic blood flow and metabolic capacity
1. Indocyanine green (ICG) elimination test – for liver perfusion & function
ICG has high extraction ratio

40. Anaesthetic Perspectives
How does one assess liver functions..? …..contd
OTHER PREOPERATIVE INVESTIGATIONS
1. Haematological inv - Hb – decreased in concealed blood Loss,
haemolysis,
TLC, DLC - increased infection
Platelet Count, clotting studies - BT, PT
2. Urine analysis - Urobilinogen absent, Bilirubin & Bile Salts present
3. Metabolic - Serum proteins, glucose, Urea - ↓ syn. in liver disease,
Electrolyte
4. KFT – Urea, S. Creatinine,
5 Viral markers – HBV, HCV
6. Cardiorespiratory - Chest X-ray, ECG, blood gases

41. Anaesthetic Perspectives
RISK FACTORS for operative mortality in obstructive jaundice
patients
•Hematocrit < 30 %
•S. bilirubin > 11mg%
•Malignant cause of biliary obstruction
•Azotemia
•Hypoalbuminemia
•Cholangitis

42. Anaesthetic Perspectives
Maintain hepatic blood flow and oxygenation
AVOID:
1. Sympathetic stimulation
2. Hypotension (decreased venous return / cardiac output) caused by
* Haemorrhage
* Cardiac depressant drugs
* Regional anaesthesia e.g.; thoracic epidural analgesia
3. Hypocapnia & Hypoxemia
4. Pressure effects caused by
* Surgical retraction
* Tumors
* Ascites / Laparoscopy
5. Hepatic venous congestion caused by
* Head down position
* IPPV with PEEP, Rt. side heart failure
6. Hepatotoxic drugs e.g. halothane or acetaminophen
ANAESTHETIC GOALS in Obstructive Jaundice
patient

43. Anaesthetic Perspectives
2. Maintain Renal functions
Preoperatively
• Avoid NSAIDs and nephrotoxic antibiotics e.g.; (aminoglycosides)
•Oral bile salts to normalize gut flora
•Prophylactic antibiotics to prevent sepsis
•Drainage stent -↓ Hyperbilirubinemia
•PTC, ERCP or papillotomy
Intraoperatively
•avoid hypotension & hypoxemia
•avoid dehydration
•Renal does dopamine /Mannitol / furosemide.
ANAESTHETIC GOALS in Obstructive Jaundice
patient

44. Anaesthetic Perspectives
Choosing appropriate anaesthetic agent
No drug is contraindicated in Cholestatic liver disease. per se.
Other considerations
Coexisting hepatocellular disorder
Renal dysfunction
Hepatotoxic and Cholestatic drugs
Anaesthetic agent of choice
Not dependent on hepatic metabolism
Maintains hepatic O2 supply – demand relationship
PREOPERATIVE PREPARATION for Anaesthesia

45. Anaesthetic Perspectives
General anesthesia
Induction agent - Thiopentone/Propofol
slow titrated dose → avoid hypotension
gentle intubation → avoid sympathetic stimulation
Muscle relaxant
Suxamethonium – Rapid sequence Induction
Atracurium (drug of choice) - Hoffman’s elimination
Vecuronium 0.15mg/ kg body weight
PREOPERATIVE PREPARATION for Anaesthesia

46. Anaesthetic Perspectives
Opioids
•Fentanyl (DOC)- maintains hepatic oxygen supply – demand
•opioids can cause spasm of sphincter of Oddi (incidence < 3%) leading to
biliary colic , false + cholangiogram
•fentanyl> morphine> meperidine> butorphenol
•T/T naloxone, glucagon, atropine, nitroglycerine
Volatile Anesthetics
•Isoflurane - maintains hepatic blood flow & oxygen supply
•IPPV –- Maintain eucapnia, Avoid high airway pressures

47. Anaesthetic Perspectives
Regional anaesthesia (Epidural anaesthesia) as supplement to G.A.
Supplemental for intraoperative analgesia and for postoperative analgesia
Concerns – coagulopathy & hypotension
Intra Operative Monitoring
Routine
Pulse oximetry, ECG, NIBP
EtCO2
Urine output
Core temperature
NMJ monitoring
Longer & extensive surgeries
Intra arterial and CVP monitoring.
Biochemical – Blood Sugar, ABGs. Electrolytes.
Haematology -Hb, PT

48. Anaesthetic Perspectives
• Conscious, adequate neuromuscular recovery, vitals stable  extubate
 oxygen enriched air
•Else - Continue IPPV
• Correct Fluid & Electrolyte imbalance
• Correct hypothermia
• Achieve CVS stability
•Adequate analgesia & chest physiotherapy
•Antibiotics and H2 receptor antagonist
•Maintain urine output
•Replace blood and blood products
Post operative Management

49. References
Harrison’s Internal Medicine 16th Edition,
p1888 –p1889
Clinical Anesthesia by Paul.G.Barash, 6th
Edition, p1253

50. References
Miller’s Anaesthesia, 7th Edition, p411,
p1071
A Practice of anaesthesia, seventh
Edition, Wylie and Churchill Davidson,
p1253

51. References
Stoelting’s Anesthesia and co-existing
Disease
Clinical Anesthesiology,
Edward.G.Morgan, 4th Edition.