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Obstructive Jaundice
Case Discussion
Speaker: Dr S.N.Bhagirath
Panelists: Dr Hemalatha.S
Dr Manjula.B.P.
Dr Krithika Devi
Case Presentation
Patient details
 Name: Puttasomachari
 Age: 68 years
 Sex: male
 I.P.No.: 216363
Chief Complaints
 ...
Case Presentation……..contd
History of presenting illness
Pain abdomen Itching Fever
Colicky type
Gradual in onset
Intermit...
Case Presentation……..contd
Past history
No history of similar complaints in the past.
History of weight loss present since...
Case Presentation……..contd
Family history
No history of similar complaints in the family was noted.
Personal history
Diet:...
Case Presentation……..contd
General Physical Examination
An elderly male patient moderately built and nourished. Conscious ...
Case Presentation……..contd
General Physical Examination
.
Per abdominal examination:
Inspection:
Normal in size and shape....
Case Presentation……..contd
General Physical Examination
Cardiovascular system: S1 S2 heard, No murmurs heard.
Respiratory ...
Case Presentation……..contd
Investigations
Hb: 10.4 gm%
Differential count: Neutrophils – 71
Lymphocytes – 24
Monocytes – 0...
Case Presentation……..contd
Investigations……ccontd
LFT: Total Bilirubin: 9.0 (0.1 – 1.0)
Direct Bilirubin: 5.3 (0.0 – 0.2)
...
Case Presentation……..contd
Investigations……ccontd
ECG: Sinus rhythm. Within normal limits. Heart rate: 60/min.
2D ECHOCARD...
Case Presentation……..contd
Management Plan
Kausch – Whipple’s Procedure
Discussion with elaborations
History of presenting
illness
Pain abdomen
Colicky type
Gradual in onset
Intermittent in natu...
Discussion with elaboration
History of presenting illness
Fever
Low grade
Intermittent in nature
Not associated with
chill...
Discussion with elaboration
History of presenting illness
History of yellowish discolouration of eyes and urine since 15 d...
Discussion with elaboration
Past history
No history of similar complaints in the past.
History of weight loss present sinc...
Discussion with elaboration
Family and personal history
Family history of Cholestasis
Progressive Familial Intrahepatic Ch...
Discussion with elaboration
General
Physical
examination
BMI
Vital signs
Pallor:
Gastrointestinal
bleeding
Icterus
Lemon y...
Discussion with elaboration
Abdominal Examination
Inspection:
Abdominal distension -ascites
Dilated abdominal vessels- cir...
Discussion with elaboration
Différences between extrahepatic/ intrahepatic Cholestasis
Extrahepatic Intrahepatic
Abdominal...
Clinical pointers
Nature of Jaundice
Progressively worsening jaundice - Malignant obstruction, primary biliary
cirrhosis, ...
Clinical pointers
Why pruritis..?
Central mechanism: ↑central opioidoergic tone in patients with cholestasis
Peripheral Me...
Bilirubin Metabolism
Reticuloendotheli
al system
Unconjugated
bilirubin +
Albumin
Bilirubin +
glucuronic acid 
bilirubin ...
Clinical pointers
Obstructive Jaundice
Intrahepatic causes
Familial/ hereditary disorders –
•Dublin Johnson syndrome,
•Rot...
Clinical pointers
Obstructive Jaundice
Extrahepatic causes
Benign
Gallstone/ Choledocholithiasis - most common cause
Clini...
Clinical pointers
Obstructive Jaundice
Lab investigations –
• ↑ conj. plasma bilirubin,
•bilirubinuria,
•absent urobilinog...
Biochemical differentiators
Prehepatic Jaundice Hepatic Jaundice Post hepatic
Jaundice
Serum bilirubin ↑ (mostly unconjuga...
Clinical pointers
Consequences of Obstructive Jaundice
• Decreased hepatocyte function
• metabolic dysfunction of cyt450
•...
Clinical pointers Investigative aids
Ultrasound
- determines level & presence of intra and extrahepatic biliary
dilatation...
Clinical pointers
Surgical procedures•Ca Gall Bladder: Radical Cholecystectomy with wedge resection and CBD
excision
•Chol...
Anaesthetic Perspectives
Cardiovascular system
circulating bile salts (cholemia) leads to
•Impaired myocardial contractili...
Anaesthetic Perspectives
Renal System
Acute renal failure
•Etiology multifactorial
•Arterial hypotension-myocardial depres...
Anaesthetic Perspectives
Sepsis
can be due to
•Associated cholangitis and bactibilia
•Absence of bile salts in intestine E...
Anaesthetic Perspectives
Coagulopathy
1.Absence of bile salts in intestine Vitamin. K malabsorption
(required for gamma ca...
Anaesthetic Perspectives
Multiple Vitamin Deficiency - A, D, E, K due to absence of bile salts
in intestine
(A- night blin...
Anaesthetic Perspectives
LIVER FUNCTION TESTS
A. Indices of hepatocellular damage
1. Transaminases SGOT/SGPT - 0 – 35 IU/L...
Anaesthetic Perspectives
LDH – poor specificity
3. Glutathione- S – transferase (GST) isoenzyme B – sensitive
indicator of...
Anaesthetic Perspectives
How does one assess liver functions..? …..contd
Aminotransferases Alkaline PO4 Diagnostic Likelih...
Anaesthetic Perspectives
How does one assess liver functions..? …..contd
Serum albumin
Long t ½ - 14-20days,
Liver – subst...
Anaesthetic Perspectives
How does one assess liver functions..? …..contd
OTHER PREOPERATIVE INVESTIGATIONS
1. Haematologic...
Anaesthetic Perspectives
RISK FACTORS for operative mortality in obstructive jaundice
patients
•Hematocrit < 30 %
•S. bili...
Anaesthetic Perspectives
Maintain hepatic blood flow and oxygenation
AVOID:
1. Sympathetic stimulation
2. Hypotension (dec...
Anaesthetic Perspectives
2. Maintain Renal functions
Preoperatively
• Avoid NSAIDs and nephrotoxic antibiotics e.g.; (amin...
Anaesthetic Perspectives
Choosing appropriate anaesthetic agent
No drug is contraindicated in Cholestatic liver disease. p...
Anaesthetic Perspectives
General anesthesia
Induction agent - Thiopentone/Propofol
slow titrated dose → avoid hypotension
...
Anaesthetic Perspectives
Opioids
•Fentanyl (DOC)- maintains hepatic oxygen supply – demand
•opioids can cause spasm of sph...
Anaesthetic Perspectives
Regional anaesthesia (Epidural anaesthesia) as supplement to G.A.
Supplemental for intraoperative...
Anaesthetic Perspectives
• Conscious, adequate neuromuscular recovery, vitals stable  extubate
 oxygen enriched air
•Els...
References
Harrison’s Internal Medicine 16th Edition,
p1888 –p1889
Clinical Anesthesia by Paul.G.Barash, 6th
Edition, p1253
References
Miller’s Anaesthesia, 7th Edition, p411,
p1071
A Practice of anaesthesia, seventh
Edition, Wylie and Churchill ...
References
Stoelting’s Anesthesia and co-existing
Disease
Clinical Anesthesiology,
Edward.G.Morgan, 4th Edition.
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Obstructive Jaundice and Anesthesia

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A Case of Obstructive Jaundice and administration of Anesthesia in such a case

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Obstructive Jaundice and Anesthesia

  1. 1. Obstructive Jaundice Case Discussion Speaker: Dr S.N.Bhagirath Panelists: Dr Hemalatha.S Dr Manjula.B.P. Dr Krithika Devi
  2. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 12. Case Presentation……..contd Management Plan Kausch – Whipple’s Procedure
  13. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 26. Clinical pointers Obstructive Jaundice Lab investigations – • ↑ conj. plasma bilirubin, •bilirubinuria, •absent urobilinogen in urine, •clay coloured stools, •↑ - ALP •5-NT
  27. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 49. References Harrison’s Internal Medicine 16th Edition, p1888 –p1889 Clinical Anesthesia by Paul.G.Barash, 6th Edition, p1253
  50. 50. References Miller’s Anaesthesia, 7th Edition, p411, p1071 A Practice of anaesthesia, seventh Edition, Wylie and Churchill Davidson, p1253
  51. 51. References Stoelting’s Anesthesia and co-existing Disease Clinical Anesthesiology, Edward.G.Morgan, 4th Edition.

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