PATHOPHYSIOLOGY OF OBSTRUCTIVE

JAUNDICE

DR. VIGNESH KUMARAMBEDKAR HOSPITAL

ContentsMetabolismEffect on systemsSymptomatology The why behind it

Jaundice “jaune” in french = yellowNormal bile secretion 600-

1200ml/dayBilirubin 250-350mg/dayTypes of jaundiceVan der Bergh test /

PhotospectrometryScleral icterus is evident at

2.5mg/dl, and cutaneous/mucous membrane icterus at 6mg/dl

Hemoglobin catabolism

Bilirubin metabolism

Bile salt metabolism

Systemic effectsHepatobiliary

◦ Normal biliary pressures 7-14 cm H₂O◦ As the pressure in the biliary tree increase,

the cholangiolymphatic reflux and cholangiovenous reflux come into play l/t systemic toxicity

◦ As biliary pressure increases (30 cm H₂O), the bile secretion completely stops

◦ Reflux into space of disse and hepatic sinusoids resulting in an inflammatory response followed by increased fibrogenesis

Greenfield's surgery

Cholangiolymphatic and cholangiovenous reflux

Systemic effectsCardiovascular

◦decreased cardiac contractility; reduced left ventricular pressures; impaired response to β- agonistic drugs; decreased peripheral vascular resistance

Renal ◦depressed cardiac function;

hypovolemia; endotoxemia may l/t renal impairment

Systemic effectsImmunity

◦increased bacterial translocation from the gut in the setting of bile duct obstruction

Wound healing◦Delayed wound healing and a high

incidence of wound dehiscence and incisional hernia have been observed in patients undergoing surgery to relieve obstructive jaundice

Symptomatology PruritisClay coloured

stoolsHigh coloured

urineRUQ painIcterus Steatorrhoea Bleeding

tendencyf/o fat soluble

vitamin deficiency

AnorexiaFeverNausea /

vomitingHigh grade fever

with chillsWeight lossSystemic

endotoxemiaf/o liver cell

failure

The why behind it allPruritis

◦Bile salts reflux back into plasma, l/t mast cell degranulation in the skin

Clay coloured stools◦Conjugated bilirubin does not reach

the gut, no sterco/urobilin, stools devoid of yellow colour

High coloured urine◦Conjugated bilirubin (soluble) diffuses

into plasma, is filtered by kidney

The why behind it all (cont.)RUQ pain and tenderness

◦ Stasis of bile in ducts l/t inflammatory response causing pain

◦ Elicited as tenderness (irritation of parietal peritoneum) and palpable lump (omentum)

Biliary colic◦ A misnomer as CBD in most individuals

does not contain muscle layers◦ Stasis leads to release of inflammatory

mediators (phospholipase A₂ and prostaglandins)

The why behind it all (cont.)Steatorrhoea

◦Fat does not get absorbed without bile salt (micelle formation)

Bleeding tendency◦Vitamin K deficiency l/t prolonged PT

Deficiency of fat soluble vitamins◦Deficiency of vitamins A,D,E,K and

their manifestations

The why behind it all (cont.)Icterus

◦Bilirubin has a high affinity for elastin that is abundant in sclera and skin

Fever◦Release of TNF alpha and IL-1d/t

inflammatory response ◦Local PG activity in anterior

hypothalamusNausea / Vomiting

◦Gut irritation and vagal stimulation d/t pain

The why behind it all (cont.)Anorexia

◦IL-1 effects on satiety centreWeight loss

◦IL-1 increases production of IL-2 and TH-2 cells, l/t skeletal muscle proteolysis and thereby weight loss

The why behind it all (cont.)High grade fever with chills

◦Stasis leads to ascending bile infection

Systemic endotoxemia◦elevated intraductal pressure in the

bile duct allows translocation of bacteria or endotoxin into the vascular and lymphatic system (cholangio-venous/lymphatic reflux)

Courvoisier’s law

The why behind it all (cont.)Features of liver cell failure

◦Portal hypertension◦Ascitis◦Gynaecomastia ◦Vascular spider naevi◦Palmar erythema◦Testicular atrophy◦Dupuytrens contracture◦KF ring◦Flapping tremors◦Fetor hepaticus◦Hepatic encephalopathy