Jaundice

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JAUNDICE JAUNDICE By By Rajasri Rajasri Manimaran Manimaran Group 2 Group 2

Transcript of Jaundice

JAUNDICEJAUNDICE

By By Raja s r i Raja s r i

ManimaranManimaranGroup 2Group 2

What is jaundice?What is jaundice?O It is yellowish

discoloration of Skin, mucous membranes, sclera.. Due to excess plasma bilirubin.

Signs and symptoms Signs and symptoms O Skin and sclerae - yellowO Stool - light colour, clay colouredO Dark urineO Pain in abdomenO ItchingO Trouble with sleepingO Fatigue, swellingO AscitesO Mental confusion, comaO Bleeding

O The differential diagnosis for yellowing of the skin is limited. In addition to jaundice, it includes Carotenoderma.

O In carotenoderma the pigment is concentrated on the palms, soles, forehead, and nasolabial folds. Carotenoderma can be distinguished from jaundice by the sparing of the sclerae.

Carotenoderma vs jaundice Carotenoderma vs jaundice

Is it disease?Is it disease?O Is not a disease but rather a sign that

can occur in many different diseases.O Normal plasma bilirubin range 5-17 m

mol/l O Clinically obvious   50 mmol/l (2.5mg/dl)

Normal bilurubin production and Normal bilurubin production and metabolismmetabolism

Types of jaundiceTypes of jaundicecategory definit ion

Pre-hepatic/ hemolytic The pathology is occurring prior to the liver.

Hepatic/ hepatocellular The pathology is located within the liver.

Post-Hepatic/ cholestatic

The pathology is located after the conjugation of bilirubin in the liver.

Prehepatic jaundicePrehepatic jaundiceO Pre-hepatic jaundice is caused by

anything which causes an increased rate of hemolysis.

O In jaundice secondary to hemolysis, the increased production of bilirubin, leads to the increased production of urine-urobilinogen. Bilirubin is not usually found in the urine because unconjugated bilirubin is not water-soluble.

Hepatocellular jaundiceHepatocellular jaundiceO  Cell necrosis reduces the liver's ability

to metabolize and excrete bilirubin leading to a buildup of unconjugated bilirubin in the blood.

O Other causes include primary biliary cirrhosis leading to an increase in plasma conjugated bilirubin because there is impairment of excretion of conjugated bilirubin into the bile.

Posthepatic jaundicePosthepatic jaundiceO  is caused by an interruption to the

drainage of bile in the biliary systemO In complete obstruction of the bile

duct, no urobilinogen is found in the urine, since bilirubin has no access to the intestine and it is in the intestine that bilirubin gets converted to urobilinogen to be later released into the general circulation.

Differential diagnosis Differential diagnosis

Neonatal jaundiceNeonatal jaundiceO Yellowish staining of the skin and whites of

the newborn's eyes (sclerae) by pigment of bile (bilirubin)

O Breakdown of red blood cells (which release bilirubin into the blood) and immaturity of the newborn's liver (which cannot effectively metabolize bilirubin and prepare it for excretion into urine)

O Normal neonatal jaundice appears between the 2nd and 5th days of life and clears with time

O Kernicterus – brain damage - lifelong disability.

Bili light and sunbathBili light and sunbath

Diagnosis Diagnosis O HistoryO Physical examinationO Blood tests - laboratoryO UltrasonographyO CTO MRIO Liver biopsyO ERCP (Endoscopic retrograde

cholangiopancreatography) O Endoscopic ultrasound

Physical examination

Biliary tract dilation due to obstruction

Gall stone

Treatment Treatment O Treatment requires a precise diagnosis of the

specific cause and should be directed to the specific problem.

O Complications of jaundice include sepsis especially cholangitis, biliary cirrhosis, pancreatitis , coagulopathy, renal and liver failure.

O Cholangitis, especially the suppurative type (Charcot’s triad or Reynolds' pentad), is usually secondary to choledocholithiasis. It may also complicate procedures like ERCP.

O Treatment should include correction of coagulopathy, fluid/electrolyte anomaly, antibiotics and biliary drainage with ERCP where available or trans-hepatic drainage or surgery.