JAUNDICE DIAGNOSTIC APPROACH Leave a comment

Jaundice: refers to the yellow appearance of the skin that occurs with the deposition of bilirubin in the dermal and subcutaneous tissue. Normally in the body, bilirubin is processed through the liver, where it is conjugated to glucuronic acid by the enzyme uridine diphosphate glucuronyl transferase (UGT) 1A1. This conjugated form of bilirubin is then excreted into the bile and removed from the body via the gut. When this excretion process is low following birth, does not work efficiently, or is overwhelmed by the amount of endogenously produced bilirubin, the amount of bilirubin in the body increases, resulting in hyperbilirubinemia and jaundice.

Evidence-based medicine
American reference

Jaundice: is a Yellow discoloration of the sclerae and skin, as a result if raised serum bilirubin, and is usually detectable clinically when the bilirubin is greater than 3mg/dl.

Jaundice: yellowish discoloration of skin & mucous membrane due to increased serum bilirubin

Values:

Normal bilirubin:

TOTAL BILIRUBIN:

0.3 – 1.1 mg/dl or 5.1 – 17.0 mmol/L

DIRECT BILIRUBIN:

0.1-0.3 mg/dL or 1.7 – 5.1 mmol/L

Clinical jaundice: >3 mg/dl

Yellowing of sclera at 3 mg

(bilirubin has high affinity for elastin, sclera has high elastin content.

APPROACH TO A JAUNDICED PATIENT

TYPES OF JAUNDICE

Extrahepatic causes of obstructive jaundice

BILIRUBIN METABOLISM

The haem component of spent red cells is normally broken down to bilirubin (mainly in the spleen and bone marrow), bound to albumin and transported to the liver. This relatively stable protein-pigment complex is insoluble in water and is not excreted in the urine.
• In the liver, the complex is split and the bilirubin conjugated with glucuronic acid which makes it water-soluble, before it is excreted into the bile canaliculi. The normal concentration of both conjugated and unconjugated bilirubin in the blood is very low.
• Bacterial action in the bowel converts conjugated bilirubin into colourless urobilinogen & pigmented urobilin which gives the brown colour to normal faeces.
• Some urobilinogen is reabsorbed, passing to the liver in the portal blood, and is then re-excreted in the bile. The entire process is called an enterohepatic
circulation. A small amount of urobilinogen escapes into the systemic circulation and is excreted in the urine, colouring it yellow.
Bile acids (salts) are synthesised in the liver from cholesterol-based precursors. These are excreted in bile to the duodenum and facilitate lipid digestion and absorption in the small intestine. About 95% of the bile acids are reabsorbed in the distal ileum and returned to the liver via the portal vein, only to be re-excreted in the bileThus both bilirubin and bile acids are involved in enterohepatic circulations.

HISTORY OF PRESENTING ILLNESS

Specific Questions about the Jaundice itself:

• Onset of Jaundice (acute vs chronic).
• Duration (since when).
• Previous similar episodes.
• how the patient noticed the jaundice?
• Course (Progressive or intermittent) ?

Intermittent jaundice
Choledocholithiasis
Ampullary carcinoma
Relapsing viral hepatitis

Progressive jaundice
Malignant obstruction
Primary sclerosing cholangitis
End stage liver disease^

• Association of pain?

Painful jaundice: gallstones

Painless jaundice: tumers

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HISTORY OF PRESENTING ILLNESS Jaundice

The Differential diagnoses of Jaundice in the surgical context should include:

1. Obstructive Jaundice.
2. Cholangitis.
3. Malignancy (Pancreatic head tumor)
4. Liver disease and complications
5. Hepatitis
6. Primary liver or biliary malignancy.

Obstructive Jaundice

1. Pale stool
2. Dark urine.
3. Itching.
4. yellow sclera.

Cholangitis:

1.Fever.
2.RUQ pain.
3.Chills.

Liver disease complications (Colon cancer with liver Mets):

1. Change in Bowel habits (Constipation).
2. Nausea/Vomiting/Abd distention.
3. Melena/Hematemesis/Bleeding per Rectum.

Pancreatic head cancer:

1. Anorexia.
2. Weight loss.
3. Fatigue.
4. Bloating.
5. Steatorrhea.
6. Diarrhea.

Review of Systems: Jaundice

1.Confusion, Headache.
2.Shortmess of breath.
3.Lower limb swelling.
4.generalized weakness.

Then

Past medical and surgical history:
1.Gallbladder stones.
2.Hx of pancreatitis.
3.Biliary surgeries.
4.Any previous surgeries.

Then

Drug History:
1.Paracetamol.
2.Sulpha drugs.
3.OCPs.

Then

Family History:
Family Hx of hepatitis, Liver disease, Jaundice, Hemolytic Disease, Malignancies.

Then

Social History:
1.Hx of IV drug abuse.
2.Travel Hx. (endemic area)
3.Sexual Hx.
4.Alcohol/Smoking.
5.Blood transfusions.
6.Skin tattoos
7.Prior Hepatitis Immunizations.
8.Contact with jaundiced patients.

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Physical Examination Jaundice

General examination:

• Jaundice is first detectable in the frenulum of tongue.
SEQUENTIAL SITES OF JAUNDICE:

SEQUENTIAL SITES OF JAUNDICE:

1^ST STAGE: frenulum of tongue

2^ND STAGE: sclera of eye

3^RD STAGE: skin

Sites to be examined:

• Upper bulbar conjunctiva (contains elastin which has high affinity for bilirubin).

• frenulum of tongue.

• Mucous membrane of palate (specially soft palate).

• Palms and soles.

• General skin surface.

In bright natural day light ideally Infront of open window

• Scratch marks : In some cases of obstructive jaundice, the patient develops generalized itching (pruritus) and scratch marks

• Stigmata of liver disease: such as spider naevi are only found when jaundice is caused by primary liver disease

• Enlarged left supraclavicular node (Virchow’s node) or periumbilical nodule (Sister Mary Joseph’s nodule) suggests an abdominal malignancy.

• Jugular venous distention, a sign of right-sided heart failure, suggests hepatic congestion .

• Hepatomegaly •

Lab Test Jaundice

CBC Lab Test

WBC: infection, leukemia, neutrophils

RBC: anemia, polycythemia

HB: anemia, malignancy

MCV: thalassemia

PLT: bleeding and clotting disorders

KFT

BILE ACID/BILE CAST NEPHROPATHY

Cholemic nephrosis

Cholemic nephrosis has been attributed to the following:

1. Direct bile acid tubular toxicity
2. Systemic vasodilation with renal vasoconstriction and ischemic tubular injury

• Induce oxidative damage/oxidative stress to tubular cell membranes (apoptosis and necrosis).

Liver Function Test – Jaundice

Tests for liver functioning:

• Based on detoxification & excretory function
• Enzymes indicating liver injury: 1.Damage to hepatocytes – 2.Cholestasis
• Measure biosynthetic function

Bilirubin – Jaundice

Total, Direct & Indirect

Serum Aminotransferases – Jaundice

ALT is more liver specific than AST

serum aminotransferases (AST/ALT) are the sensitive markers of acute hepatocellular injury.

Causes of elevated levels of blood ALT & AST:

1- Viral, toxic or alcoholic hepatitis

ALT&AST are elevated even before appearance of clinical signs (jaundice) & symptoms.

marked increase in ALT & AST (up to 20-50 – may reach up to 100 folds).

in viral hepatitis ALT is much elevated than AST

2- Cirrhosis (chronic liver diseases)

ALT&AST are increased to levels depending on the status of the process (moderate increase (up to 4-5 folds)

in chronic cases, AST is much elevated than ALT

3- Obstructive jaundice:

ALT&AST are increased up to 3 folds (moderate increase)

4- After alcoholic or drug intake

transient slight to moderate increase

ALKALINE PHOSPHATASE (ALP) – Jaundice

present in most tissue, richest being in bone osteoblasts, bile canaliculi, proximal convoluted tubule of the kidneys, placenta and intestine.

ALP half life is 7 days

–Extrahepatic cholestiasis:

 (marked increase up to 10-12 folds)

-Intrahepatic cholestiasis:

(moderate increase 3-5 folds)

–Viral, toxic and alcoholic hepatitis:

(less than 3 folds)

GAMMA GLUTAMYL TRANSFERASE (GGT) – Jaundice

GGT present in blood originates primarily from hepatobiliary system

Causes of increased blood GGT:

1-By alcohol or dugs as anticonvulsants, phenobarbitone and phenytoin

2- Biliary obstruction:

GGT is markedly increased with obstructive jaundice (5-30 folds)

increase earlier (more sensitive) than ALP

persists longer than ALP

3- Viral, toxic and alcoholic hepatitis:

increase is only 2-5 folds ( less sensitive than ALT&AST)

4- Primary and secondary liver tumors:

GGT is elevated earlier than other enzymes in liver neoplasm.

secondaries of other organ tumors in the liver can be early detected by elevated GGT.

PT – PTT – INR

Serum albumin:

low serum albumin suggests a chronic process such as cirrhosis or cancer

Prothrombin time:

PT measures three out of four vitamin k-dependent factors (II, VII, X) and is prolonged in hepatocellular disease and in obstructive jaundice

deficient synthesis of vitamin K dependent factors occurs in hepatocellular jaundice.

In obstructive jaundice, vitamin K ( a fat-soluble vitamin) cannot be absorbed due to the absence of bile in the intestine.

Intramuscular injection of vitamin k correct prolonged PT in obstructive jaundice but not in hepatocellular jaundice.

SUBSEQUENT STUDIES – Jaundice

If there is no suggestion of biliary obstruction, screening studies should be performed to evaluate the potential causes of hepatocellular dysfunction; confirmation of the diagnosis is usually made by liver biopsy

• Serologic tests for viral hepatitis
• Measurement of antimitochondrial antibodies (for primary biliary cirrhosis)
• Measurement of antinuclear anti-smooth muscle (sm), and liver-kidney microsomal (LKM) antibodies (for autoimmune hepatitis)
• Serum levels of iron, transferrin, and ferritin (for hemochromatosis)
• Serum levels of ceruloplasmin (for Wilson’s disease)
• Measurement of alpha-1-antitrypsin activity (for alpha-1-antitrypsin deficiency)

RADIOLOGIC TOOLS – Jaundice

Ultrasonography

The sensitivity of abdominal ultrasound (US) for the detection of dilated bile ducts and biliary obstruction ranges in various studies from 55 to 91 percent.

US can also demonstrate cholelithiasis and gallbladder stones; however, common duct stones may not be well seen since gas in the duodenum can obscure visualization of the distal common duct.

The advantages of US are that it is noninvasive, portable, and relatively inexpensive.

Endoscopic ultrasound (EUS)

Mainly for pancreatico-biliary pathologies

Higher-frequency ultrasonic waves compared to traditional US and allows diagnostic tissue sampling via EUS-guided fine needle aspiration.

EUS has been reported to have up to 98% diagnostic accuracy in patients with obstructive jaundice

The sensitivity of EUS for the identification of focal mass lesions in pancreas has been reported to be superior to that of CT scanning

Compared to MRCP for diagnosis of biliary stricture, EUS has been reported to be more specific (100% vs 76%) and have much greater positive predictive value (100% vs 25%)

The positive yield of EUS-FNA for cytology in patients with malignant obstruction has been reported to be as high as 96%

Helical CT scan

Conventional computed tomography (CT) and US are equally effective for the recognition of obstruction and identification of the level of obstruction.

 However, helical (spiral) CT has improved the accuracy of CT and may emerge as the preferred technique for hepatobiliary imaging.

Compared to US, helical CT offers a more comprehensive analysis of the liver and extrahepatic abdomen and pelvis.

 CT is not as sensitive in detecting cholelithiasis because only calcified stones are visualized.

Endoscopic retrograde cholangiopancreatography (ERCP)

ACCURACY >90%

Complications of ERCP

Risk factors for PEP Post-Endoscopic Retrograde pancreatography pancreatitis

Patient-related factors	Procedure-related factors
Female gender	Difficult cannulation
Younger age	Cannulation or injection into the pancreatic duct
Sphincter of Oddi dysfunction	Biliary balloon sphincter dilation
Prior history of PEP
Normal serum bilirubin

ERCP showing double duct sign – dilated pancreatic duct (red arrow) and dilated CBD (black arrow)

Magnetic resonance cholangiopancreatography (MRCP)
Diagnostic only jaundice

That’s all Thanks for reading this

Prepared by:

DR. NIZAR ISMAIL ABU-ODDOUS

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jaundice specialists
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jaundice causes
JAUNDICE DIAGNOSTIC APPROACH
APPROACH TO A JAUNDICED PATIENT
Extrahepatic causes of obstructive jaundice
BILIRUBIN METABOLISM jaundice
HISTORY OF PRESENTING ILLNESS jaundice
HISTORY OF PRESENTING ILLNESS Jaundice
Physical Examination Jaundice
Lab Test Jaundice
Liver Function Test – Jaundice
Bilirubin – Jaundice
Serum Aminotransferases – Jaundice
ALKALINE PHOSPHATASE (ALP) – Jaundice
GAMMA GLUTAMYL TRANSFERASE (GGT) – Jaundice
Adult Jaundice
What is jaundice?
What causes jaundice?
What are the symptoms of jaundice?
How is jaundice diagnosed?
How is jaundice treated?
Can jaundice be prevented?
What is the risk you’ll develop jaundice?