Jaundice - 1

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APPROACH TO

PATIENT WITH
JAUNDICE

Prepared by : AHMED SALEM BAMUHRIZ

Supervised by : Dr OMAR MOHAMMED BARAHMAN


Ahmed 10 year old student from fuwah
came to ER complaining of fever anorexia
nausea and vomiting
in the past few days

O/E he was ill febrile lethargic jaundiced


with RUQ tenderness no organomegaly no
abdominal distension

Laboratory tests
LFT raised both ALTand AST levels
bilirubin raised both total and direct .

Most probable diagnosis?

Further investigation to confirm type ?


Tutorial objectives

Discuss bilirubin metabolism


Define jaundice and clarify its types
Mention Causes of hepatocellular Jaundice
Discuss diagnostic Approach to a patient with
Jaundice
Discuss the treatment of jaundice
Recognize fulminant hepatic failure
Jaundice is defined as yellowing of body fluids and tissues due to an
increase in bilirubin.

Yellowing of sclerae is visible at serum concentrations 2.0−2.5 mg/dL and of


the skin at levels 3.0−4.0 mg/dL due to increased bilirubin production or
impaired liver function or reduced excretion

sources of bilirubin are senescent RBCs, myoglobin, cytochromes, other heme-


containing enzymes, and a small pool of free heme.

Approximately 300 mg (0.5 mmol) of bilirubin are formed daily .

It comes in two forms Unconjugated(indirect) bilirubin which is water insoluble


and ranges from 0.2 - 0.9 mg/dl and conjugated (direct) bilirubin which is the
processed form in liver and it's water soluble and ranges from 0.1-0.3mg/dl
and both forms together is called total bilirubin which range from 0.3 -1.2
mg/dl.
Mechanism of bilirubin metabolism
1. Red Blood Cell Breakdown:
- Old red blood cells are destroyed primarily in the spleen.
- Hemoglobin from these cells is released.

2. Conversion to Bilirubin:
- Hemoglobin is broken down into heme and globin.
- The heme is converted to biliverdin (green pigment) and then to
bilirubin (yellow pigment).

3. Transport to the Liver:


- Unconjugated bilirubin (water insoluble) binds to albumin in the
bloodstream and is transported to the liver.

4. Liver Processing:
- In the liver, unconjugated bilirubin is converted into conjugated
bilirubin (water-soluble) through a process called conjugation. This
involves adding glucuronic acid.

5. Excretion in Bile:
- Conjugated bilirubin is secreted into bile and stored in the
gallbladder. It then enters the intestine.

6. Intestinal Conversion:
- In the intestine, bacteria convert bilirubin into urobilinogen and
stercobilin. Stercobilin gives stool its brown color, while some
urobilinogen is reabsorbed into the bloodstream
Types of jaundice

According to
According to According to the
pathophysiolo
gy severity site of pathology

Mild<2-3mg/dl Pre hepatic


Pathological

Physiologic Moderate 3-10 Hepatic


al mg/dl
Severe > 10
Post hepatic
mg /dl
causes of jaundice according to severity
1. Mild Jaundice<2-3mg/dl
- Often asymptomatic or with minimal symptoms.
- Causes:
- Physiological Jaundice: Common in newborns due to immature liver
function.
- Gilbert's Syndrome: A benign genetic condition causing intermittent
elevation of unconjugated bilirubin.
- Mild Hemolysis: Conditions like minor blood group incompatibility or
certain anemias.

2. Moderate Jaundice 3-10 mg/dl


Symptoms may include fatigue, dark urine, and slight abdominal discomfort.
- Causes:
- Acute Hepatitis: Viral infections (e.g., Hepatitis A, B, C) leading to liver
inflammation.
- Alcoholic Liver Disease: Chronic alcohol consumption affecting liver
function.
- Non-Alcoholic Fatty Liver Disease (NAFLD): Fat accumulation in liver cells
causing inflammation.
- Hemolytic Anemias: More significant hemolysis due to conditions like sickle
cell disease or autoimmune hemolytic anemia.
3. Severe Jaundice > 10 mg /dl
More pronounced symptoms, including significant fatigue, severe pruritus, and
possible confusion (due to hepatic encephalopathy).
- Indicates serious underlying conditions and usually requires urgent medical
evaluation and intervention.
- Causes:
- Chronic Liver Diseases: Cirrhosis due to chronic hepatitis, alcohol abuse, or
metabolic disorders.
- Obstructive Jaundice: Biliary obstruction from gallstones, tumors, or
strictures.
- Acute Liver Failure: Rapid deterioration of liver function due to various
causes (e.g., drug overdose, viral hepatitis).
- Severe Hemolysis: Conditions like hemolytic crises or transfusion reactions
leading to significant bilirubin production.
- Biliary Atresia: Congenital condition in infants leading to bile duct
obstruction.

Understanding these causes helps in diagnosing the specific type of jaundice


and determining appropriate management strategies.
causes according to site of pathology
1. Pre-Hepatic Causes
These are conditions that
lead to increased
production of bilirubin:
- Hemolytic Anemia:
Increased breakdown of
red blood cells (e.g., in
conditions like sickle cell
disease, thalassemia).
- Hemolysis: Due to
infections, autoimmune
diseases, or certain
medications.
- Genetic Disorders Such
as Gilbert's syndrome or
Crigler-Najjar syndrome.
2. Hepatic Causes
These involve liver dysfunction
where the liver cannot adequately
process bilirubin:
- Hepatitis: Viral (e.g., hepatitis A, B,
C) or drug-induced liver injury.
- Cirrhosis: Chronic liver disease
leading to liver failure.
- Liver Tumors: Hepatocellular
carcinoma or metastatic liver
disease.
-

3.Post-Hepatic Causes
These occur when there is
obstruction in the biliary tract,
preventing bilirubin from being
excreted:
- Biliary Obstruction: Gallstones,
strictures, or tumors in the bile duct.
- Pancreatic Cancer: Causing
compression of the bile duct.
- Cholangiocarcinoma: Cancer of the
Other Causes of jaundice

Dietary causes :
1-Malnutrition
2-alcohol consumption
3- high fatty diets
4-excessive iron or copper intake
5-contaminnated food
6- excessive carrot intake *psuedo

Drugs :
1-acetaminophen overdose
2-methotrexate long term
3-Anti TB drugs: isoniazid rifampicin pyrazinamide
4- Antiepileptic drugs : phenytoin carbamazepine
Clinical Approach
History:
personal data

Onset duration site character relieved or


excrabating factors And Associated symptoms
urine and stool color

Past medical history of liver or hemolytic or


chronic or autoimmune diseases

Drug history

Family history

Dietary history

Travel history

Bad habits
Clinical Approach
Clinical Examination:
General look

Vital signs

Signs of acute or chronic liver


disease

Signs of autoimmune diseases

Signs of complications
Signs of liver disease
Laboratory investigations
1-COMPLETE BLOOD COUNT :
WBC >raised in INFECTION OR INFLAMMATION OF LIVER
or Biliary system or reduced due to BM suppression
HB ANEMIA FOR HEMOLYSIS
PLATELET COUNT IN CIRRHOSIS, HYPERSPLENISM

2-LIVER FUNCTION TEST :


Total and direct bilirubin : to differentiate between direct
and indirect hyperbilirubinemia
Liver enzymes:
Alanine aminotransferase ALT 7-56 U\L : primarily found
in liver and indicate hepatocellular injury
Aspartate aminotransferase AST 10-40 U\L : found in
liver,heart, muscles and indicates liver and muscle injury
Alkaline phosphatase ALP 44-147U\L : associated with
bile ducts and biliary system elevated levels suggest
cholestasis or biliary obstruction.
gamma-glutamyl transferase GGT 9-48U\L :mostly
elevated in liver disase and can confirm that ALP is raised
from hepatic origin

3-Coagulation profile : Albumin 3.5-5.0 g\dl and


Prothrombin time PT 11-13.5 seconds
BOTH of them USED TO ASSES LIVER FUNCTION
4-Hemolysis workup:

1 -Reticulocyte count 0.5%-2.0% of total blood


count :elevated levels suggest hemolysis

2- peripheral blood smear : positive findings of


abnormal RBC shapes suggest hemolysis like
spherocytes and schistocytes

3- haptoglobin 30-200 mg/dl: decreased levels


indicate hemolysis

4- lactate dehydrogenase LDH 140-280u\l : elevated


levels indicate hemolysis and tissue damage

5- direct coombs test : positive result indicate


autoimmune hemolytic anemia

5- viral hepatitis markers :


- Hepatitis A IgM Indicates recent infection with
hepatitis A.
- Hepatitis B Surface Antigen (HBsAg): Indicates
active hepatitis B infection.
- Hepatitis B Surface Antibody (anti-HBs): Indicates
recovery from hepatitis B or vaccination.
- Hepatitis C Antibody (anti-HCV): Indicates
exposure to hepatitis C virus.
6-Autoimmune Markers:
- Antinuclear Antibody (ANA): - Screens for
autoimmune diseases.

- Smooth Muscle Antibody (SMA): Specific


for autoimmune hepatitis.

- Liver/Kidney Microsomal Antibody (LKM):


Indicates autoimmune hepatitis type 2.

-Anti-Mitochondrial Antibody (AMA) is a


specific autoantibody often associated with
Primary Biliary Cholangitis (PBC), it can also
be present in other conditions, including:
- Autoimmune hepatitis (less common).
- Chronic hepatitis C.
- Certain drug-induced liver injuries
Radiological investigations
1-ultrasonography:
First line imaging for evaluating jaundice it asses liver
size ,texture,vascular structures .
Identify cholelithiasis , biliary obstruction, liver
tumors ,cysts , cirrhosis

2 - computed tomography scan :


Indicated when U/S findings is inconclusive or suggestive of
malignancy.
It evaluates liver masses, pancreatic pathology,vascular
structures
Identify liver tumors like HCC , metastasis and visualization
of dilated bile ducts
And pancreatic involvement if present
3- Magnetic resonance imaging MRI :
Indicated when further characterization of
liver lesions is needed and to asses biliary
tree anatomy and pathology through MRCP .
give detailed view of bile ducts and possiple
strictures and differentiate between beingn
and malignant tumors and asses liver fat
content

4- Endoscopic retrograde
cholangiopancreatography ERCP
Therapeutic and diagnostic evaluation of
biliary obstruction and for removal of common
bile duct Stones
Asses pancreatitis or tumors affecting the
pancreas
5- percutaneous transhepatic cholangiography PTC
Indicated when ERCP is not possible or unsuccessful
To relieve biliary obstruction e.g (placing a stent )

6-liver biopsy (imaging guided)

Indicated when liver pathology needs to be


assessed for cirrhosis, hepatitis,tumors
It provides definitive diagnosis related to liver
pathology
Management
The main principle is to treat the underlying cause either by medical or surgical intervention

Anemias : blood transfusion

antimicrobial for infections

Corticosteroids for autoimmune diaseses

Obstructive surgical intervention

Malignancy chemotherapy radiotherapy surgical

Symptomatic for associated symptoms


Fluid hydration and electrolyte balance
Dietry modification
Fulminant hepatic failure
Syndrome characterized by the rapid onset of liver failure typically defined
by the development of hepatic encephalopathy within 8 weeks of the onset
of jaundice in a patient with no
preexisting liver disease

Etiology: Hepatitis: A,B ,E

acetaminophen toxicity

Autoimmune hepatitis

Wilson's disease
Clinical features:
Jaundice
Hepatic encephalopathy: confusion, altered mental status, coma
Coagulopathy: prolonged PT and increased risk of bleeding
Multisystem involvement: possible renal failure, metabolic disturbances,
infections
Diagnosis :
hyperbilirubinaemia,
high serum aminotransferases
low levels of coagulation factors, including prothrombin and factor V.
hypoglycemia
electrolytes disturbance
electroencephalogram (EEG) is sometimes helpful in grading the
encephalopathy.
Ultrasound will define liver size and may indicate underlying liver pathology

lines of TTT
Treatment of the underlying cause
treatment of the associated abnormalities ( encephalopathy, coagulopathy,
etc)
treatment of complications
Hepatic transplantation
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