ANESTHETIC CONSIDERATION FOR

PATIENTS WITH OBSTRUCTIVE JAUNDICE

PREPARED BY: ALI YIMAM

ADVISOR:- S /r LEMLEM GETACHEW

April 2014

1
outline
 objective
 Introduction
 Anatomy and physiology of hepatobiliary system
 Etiology of obstructive jaundice
 pathophysilogy of obstructive jaundice
 Clinical manifestation
 Effect of obstructive jaundice in different body system
 diagnosis
 Medical and surgical management
 Anesthetic management
 summary
2
 objective
At the end of this topic we will be able to:
 Explain general overview of jaundice
 Identify pathophysiology of obstructive jaundice
 Explain pathophysiologic consequence of obstructive
jaundice in different body system and its management
 perform effective Anesthesia management

3
 DEFINTION OF JAUNDICE

 Jaundice is a yellowish staining of the skin, sclera and mucous

membranes by deposition of bilirubin (a yellow orange bile
pigment).

 It indicates excessive levels of conjugated or unconjugated

bilirubin in the blood and is clinically apparent when the bilirubin
level exceeds 2mg/dl (34.2 μmol per L).

4
 Anatomy of hepatobiliary system

The Intra-hepatic biliary tract

The secretory units of the liver (hepatocytes and biliary
epithelial cells, including the peribiliary glands),
 The bile canaliculi, bile ductules (canals of Hering), and
the intrahepatic bile duct
The Extrahepatic tract
 Extrahepatic bile ducts (right and left)
 common hepatic duct
 cystic duct
 gallbladder and the commen bile duct 5
 CONT’D
 The biliary tract is supplied by a complex vasculature
called the peribiliary vascular plexus.

 Afferent vessels of this plexus derive from hepatic

arterial branches, and this plexus drains into the portal
venous system or directly into hepatic sinusoids.

6
  

7
Physiology of bilirubin production and
metabolism
Stages of bilirubin metabolism
 Pre-hepatic
 Intra-hepatic
 Post-hepatic

8
9
 Bile Formation & Excretion
 The liver produce bile continously and excretes in to the
bile canaliculi.
 Normal liver produce 500-1000ml bile/day
 Bile is mainly composed of water, electrolytes,bile

salts,proteins,lipids and bile pigments.

Functions of bile:
 digestion and absorption of fats and fat-soluble vitamins
 Elimination waste products

10
 Cont’d
 In the fasting state, 80% of the bile secreted by the liver is
stored in the gall bladder
 After meal cholesystokinin(cck) is relased from the
duodenal mucosa in response to meal
 Gall bladder empties 50-70% of its contents within 30-
40min

11
 Classfication of jaundice
1. Pre-hepatic- Increased production of bilirubin due to
hemolysis.

2. Intra-hepatic-Hepatic impairment,of take up, conjugate, or

secrete bilirubin, or bile, or if bile stagnates within the liver
on the level of minute bile ducts

3. post (obstructive) hepatic jaundice- Reduction or

stopping of the drainage of bile due to mechanical
obstruction in extra hepatic bile pathways.

12
 Etiology of obstructive jaundice
  Intrahepatic :
Viral hepatitis
Alcohol
Drugs eg. Phenothiazine, Chlorpromazine
Primary biliary cirrhosis
Primary sclerosing cholangitis
Pregnancy
 Extrahepatic :
In the wall out side the wall
Ca head of the pancreas Biliary stricture
stone of CBD Cholangitis

Metastatic tumour Tumor in the bile duct

Pancreatitis Congenital atresia
Choledocal cyst 13
 Gall stone formation
 Bile duct stones are stones that have lodged in the
common bile duct.
 80% of gallstones and duct stones are made of
cholesterol in the bile.
 If the amount of cholesterol in the bile increases beyond
the ability of acids to keep a balance, the cholesterol
crystallizes and forms a stone.
 Stones usually form in the gallbladder, but they may
form in the common bile duct.

14
Cont’d
 Passage of gallstones into the common bile duct
occurs is approximately 10-15% of patients with
Gallstones.
 Pressure from stones blocking the duct makes it hard
for the liver and gallbladder to work normally.
 A blockage in the common bile duct will lead to
obstructive jaundice since there can be no outflow of
bile.

15
 Pathophysiology of obstructive
 jaundice jaundice is
Obstructive a particular type of jaundice and
occurs when the essential flow of bile to the intestine is
blocked and results an interruption to the drainage of bile in
the biliary system.

 This might be due to blocked bile ducts caused by

gallstones, or tumours of the bile duct which can block the
area where the bile duct meets the duodenum.

 The absence of bile in the intestines, and their backup,

causes spillage into the systemic circulation.

16
 cont’d
 Absenceof bile salts can produce malabsorption,leading to
steatorrhea and deficiencies of fat-soluble vitamins
(particularly A, K,E and D);

 Vitamin K deficiency can reduce prothrombin levels.

 In long-standing cholestasis,concomitant vitamin D and Ca

malabsorption can cause osteoporosis or osteomalacia.
 Impairment of liver antioxidant defense.

17
 Clinical manifestation of obstructive
jaundice

 Yellowish staining of the skin, sclera and mucous

membranes
 Dark urine  
 Pale stool
 Steatorrhoea
 Pruritis
 High fever

18
Cont’d
 Weight loss
 Xanthomata (fatty yellow nodules under eyes/on wrists
and hands)
 Episodic right upper abdominal pain
 Anorexia

19
Effect of obstructive jaundice in different body system

Retention of bile salt in liver

• Decreased hepatocyte function
• Dysfunction of Cyto -450
• Albumin & clotting factors synthesis decreased
• Decreased Kuffer cell activity

20
Cardiovascular Dysfunction
Hyperbilirubinemia
↓
Deposition in the myocardium
↓ ↓
Impaired myocardial contractility Bradycardia

21
CONT’D
Circulating bile salts (cholemia) also leads to:
1. ↓ ability to mobilize blood from splanchnic
circulation during hemorrhage.

2. ↓ sensitivity to vasopressors
↓
 Hypotension & circulatory collapse

22
 Renal Dysfunction
Renal hypoperfusion occcures due to:
1. ↓ Bile salt—-↑ Production of endotoxins by the intestinal
bacterial flora—↑ absorption of endotoxin into the
circulation—-Intra-renal vasospasm—-ARF
2. -Ve chronotropic, inotropic and diuretic effect of bile
salts→ ↓BP→Hypoperfusion of the kidneys.
3. Nephrotoxic bile pigments →Refractoriness of tubules to
ADH

23
Absence of bile in Intestine
 Septic complications
 Escape of endotoxins into portal blood
 Acute cholangitis is an ascending bacterial infection
in association with partial or complete obstruction of
the bile ducts.
 Multiple Vit. Deficiency - A, D, E, K due to
absence of bile salts in intestine, (A- night blindness,
D – osteoporosis and ms weakness, E- leg cramps, K-
easy bruising)

24
Coagulation disorder
 ↓Bile flow due to obstruction
↓
 ↓ intestinal bile salt

↓
 ↓ absorption of vit. K

↓
 ↓clotting factors ǁ, Vǁ, ǀX, X

↓
 ↑PT, aPTT

25
 CONT…
 Anaemia due to malnourished,bleeding disorder
 Impaired wound healing
 Long standing extrahepatic biliary obstruction >
1yr/intrahepatic obstruction
↓
biliary cirrhosis
↓
problems of liver dysfunction

26
 S. Bilirubin
Investigations

 Transaminase AST/ALT - 0 – 35 IU/L

AST -extrahepatic- heart/sk/ ms/kidney/brain:less specific
ALT - primarily found in liver, more specific
Alcoholic hepatitis AST/ALT >2

 Alkaline phosphatase – 35 – 100 IU/L

Extrahepatic- bone, intestine, liver, placenta
 5- Nucleotidase - confirms hepatic origin of ALP
 Gamma Glutamyl Transpeptidase – most sensitive
indicator of biliary tract disease

27
Assessment of Synthetic Ability of Liver

 Prothrombin time
Good Indicator of liver fn. in both Acute & Chronic
Liver disease.

 Serum albumin
Not a good indicator for acute or mild liver damage
Indicator of severity of chronic liver disease

28
 Other Preoperative Investigations

 HB, WBC, &Platelet Count

 Urine analysis
 KFT
Imaging
 A plain abdominal x ray
 CT
 ERCP & PTC
 Endoscopic ultrasound & MRCP

29
 Medical management of obstructive jaundice

 A = Broad Spectrum Antibiotic

 B= Complete bed rest, supplementary bile salt 
 C= Coagulopathy correction by inj. Vit. K 10mg i.v/i.m.
 D= Non fatty diet, High intake of glucose 
 Diuretic- inj. Mannitol 0.5-1.5mg/kg –to promote dieresis 
 Prevent dehydration 
 Nasogastric suction
 Opioid analgesic
 Correction of pruritus with 2 to 8 gm. orally of
cholestyramine bid.
30
 Surgical management
 If there is no improvement from medical treatment
 Decompression of extrahepatic biliary obstruction can be

achieved by:
 Surgical bypass,
 Resection of obstructing lesions,
 Percutaneous insertion of stents &
 Endoscopic insertion of stents 

31
Risk factors for operative mortality in obstructive jaundice
patients
 
 Hematocrit < 30 %
 S. bilirubin > 11mg% 
 Malignant cause of biliary obstruction
 Azotemia
 Hypoalbuminemia 
 Cholangitis

32
Anesthesia goals of obstructive jaundice

 Maintain hepatic oxygen supply – demand

 Maintain renal function

33
Preoperative preparation for Anaesthesia
 Anxiolytic – oral short acting Benzodiazepine 
 Oral H 2 antagonist 
 Broad spectrum antibiotics, oral bile salts 
 Beeding profile (PT, aPTT) should be done before

operation.
 Inj. Vit. K 10mg iv/im 3 times/day for 48 hours prior to

surgery.

 Patient may suffer from anaemia. So, Blood transfusion

may be considered.

34
 cont’d
 If persistent abnormality of coagulation secondary biliary
cirrhosis FFP prior to routine & emergent surgery.
 Drainage stent -↓ Hyperbilirubinaemia
PTC, ERCP or papillotomy.
 Avoid NSAIDs & nephrotoxic antibiotics e.g.
(aminoglycoside).
 Rehydration and adequate diuresis to maintain u/o 1ml/kg/
 Opioid: May cause biliary spasm, should avoided in
cholangiogram.

35
 Monitoring
 Pulse/BP (non invasive)
 ECG
 Etco2
 spo2
 core temperature
 urine output & blood loss,
 For severely ill patients or major operative procedures,
intra arterial,CVP, electrolytes, hematocrit,coagulation
study is essential.

36
 Intraoperative management

 Drugs primarily dependent on biliary excretion should

be avoided.
 Agents dependent on renal excretion preferreble
 Maintain renal perfusion & meticulous fluid balance
 Monitoring of u/o by indewelling catheter
 Small blood losses are poorly tolerated, replace volume
losses immediately .

37
 cont’d
AVOID :
 Sympathetic stimulation

 Hypotension
 Hypocapnia
 Pressure effects caused by Surgical retraction
 Hepatic venous congestion caused by

Head down position, IPPV

 Hepatotoxic drugs
 

38
 Cont’d
 Avoid hypothermia as it worsens coagulopathy.
 During IPPV
Maintain eucapnia
 since liver is low pressure tissue bed
Avoid large VT & high airway pressures
 Regional anaesthesia (Epidural anaesthesia)  as
supplement to G.A.
 Supplemental for intraoperative analgesia and for

postoperative analgesis
 Concerns –  coagulopathy & hypotension

39
Choosing appropriate anaesthetic agent

 In contrast to the patient with hepatocellular liver

disease, who may be quite sensitive to anaesthetic
agents, no such contraindications hold for patients with
cholestatic jaundice.

40
 Cont’d

Other consideration:
 Coexisting hepatocellular disorder
 Renal dysfunction
 Drugs ↑ cholestasis e.g.chlorpromazine

Anaesthetic agent of choice

 Not dependent on hepatic metabolism
 Maintains hepatic O2 supply – demand relationship

41
 cont’d
Induction agent:
 Thiopentone/Propofol
 Slow titrated dose → avoid hypotension
Volatile Anesthetics:
 Isoflurane is the agent of choice.
 Drugs causes hepatic insult should be avoided.eg. Halothane,
Enflurane
Maintenance: N2O, O2, Isoflurane. Opioid, Muscle relaxants.

42
 cont’d 
Opioids  
 Fentanyl - maintains hepatic oxygen supply – demand
 Opioids can cause spasm of sphincter of Oddi (incidence < 3%)
leading to biliary spasm.
Muscle relaxant
 Suxamethonium – RSI
 Cisatracurium- choice of relaxant due to liver independent
metabolism.  
 Atracurium -may also used

43
 Post operative management
 Sedative drugs should be discontinued early.
 Conscious, adequate NM recovery, vitals stable→
extubate → oxygen enriched air
 Correct Fluid & Electrolyte imbalance 
 Correct hypothermia
 Achieve CVS stability
 Adequate analgesia  
 Antibiotics and H 2 receptor antagonist
  Avoid NSAIDs
 Maintain urine output 
 Replace blood and blood products
44
 Summary
 Obstructive jaundice occurs when the flow of bile to the
intestine is blocked commonly due to CBD obstruction.

 Obstructive jaundice have an impact on multiple organ

systems, and causing a series of pathophysiological
changes during anesthesia.
 Careful preoperative evaluation is required to detect
coexisting liver disease and to identify important risk
factors for anesthesia.
 Coagulopathy, sepsis,and renal failure are main
challenges for the anesthetist.
 When postoperative complication occurs, the mainstay
of therapy is supportive. 45
 REFERENCE
1, Morgan,Mikhail&Murray,Clinical Anesthesiology,
2006, 4thed.
2, Ronald D. Miller,Miller’s Anesthesia,2009;7th ed.
3, Paul G. Barash,Clinical Anesthesia,2009,6th ed.
4, Schwartz’ principles of surgery;2007,9th ed.
5, Tinsley R. Harrison, Harrison’s principles of internal
medicine;2005, 16th ed.
6,www.sassit.co.za/.../09_management_of_malignant_
obstructive_jaundice...

46
Thank you

47