APPROACH TO A CHILD WITH
JAUNDICE AND ASCITIS
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LEARNING OBJECTIVESWhat is jaundice
Basic patho -physiology of bilirubin
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metabolismCauses of jaundice
Approach to a child with jaundice
Ascites
INTRODUCTION
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Symptom of disease rather than a disease
In adults and older children sclera appears jaundiced when serum bilirubin is
increased
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Gives yel owish hue to the skin, sclera, and mucous membranes
Normal serum bilirubin <1mg%
It is not a visible til s. bilirubin exceeds 2 mg/dl.
In newborn->5 mg/dl
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However it is difficult to see sclera in newborn due to difficulty in opening eyeBILIRUBIN
End product of hemoglobin metabolism that is excreted in bile.
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It comes from?
from catabolism of circulating RBCs
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?
from ineffective erythropoiesis (bone marrow)
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?from turnover of heme proteins
What causes bilirubin?
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1. Overproduction by reticuloendothelial system2. Failure of hepatocyte uptake
3. Failure to conjugate or excrete
4. Obstruction of biliary excretion into intestine
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Normal Range of BilirubinIt is normal to have some bilirubin in your blood. Normal levels are:
?Direct (also cal ed conjugated) bilirubin: 0 to 0.3 mg/dL
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?Total bilirubin: 0.3 to 1.9 mg/dL
Causes of Jaundice
Jaundice occurs when there is:
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too much bilirubin being produced for the liver to remove
from the blood (for example, patients with hemolytic anemia
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have an abnormally rapid rate of destruction of their red bloodcells that releases large amounts of bilirubin into the blood)
a defect in the liver that prevents bilirubin from being
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removed from the blood, converted to bilirubin/glucuronic
acid (conjugated) or secreted in bile; or
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blockage of the bile ducts that decreases the flow of bileand bilirubin from the liver into the intestines. For
example, the bile ducts can be blocked by worms, cancer,
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gallstones, or inflammation of the bile ducts. The
decreased conjugation, secretion, or flow of bile that can
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result in jaundice is referred to as cholestasis: however,cholestasis does not always result in jaundice.
Obstructive Jaundice
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Obstructive jaundice is a condition in which there is blockage of the flow of bile out of theliver
INTRAHEPATIC
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EXTRAHEPATIC
CAUSES OF OBSTRUCTIVE JAUNDICE: INTRAHEPATIC
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Primary biliary cirrhosisSclerosing cholangitis (Inflammation/scarring)
Primary biliary cirrhosis
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Sclerosing cholangitis (Inflammation/scarring)CAUSES OF OBSTRUCTIVE JAUNDICE: EXTRAHEPATIC
? Choledocholithiasis
? Worms
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? Malignancy : neoplasia, L.N.Choledocholithiasis
Malignancy : Pancreatic (head of pancreas) carcinoma
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AN APPROACH TO A CHILDWITH JAUNDICE
CLASSIC APPROACH
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Proper detailed history
Proper physical examination
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Appropriate investigationsIDENTIFY
Acute
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Chronic (more than 6 months)IDENTIFY
Hemolytic
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Hepatocel ularCholestatic
TYPES OF JAUNDICE
TYPE
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PRE
HEPATIC
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POSTHEPATIC
HEPATIC
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Urine color
normal
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darkdark
Stool color
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normal
normal
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acholicPruritis
no
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No
yes
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Signs and Symptomsof Jaundice
1. yel ow discoloration of the skin, mucous
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membranes, sclera of the eyes
2. light-colored stools
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3. dark-colored urine4. itching of the skin.
5. nausea and vomiting
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6. abdominal pain
7. fever
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8. weakness9. loss of appetite
10. headache
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11. confusion
12. swel ing of the legs and abdomen
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13. Skin stigmataDiagnosis of Jaundice
The health care provider wil perform a physical exam. This may reveal liver
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swel ing.?A bilirubin blood test wil be done.
Other tests vary, but may include:
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?Hepatitis virus panel to look for infection of the liver
?Liver function tests to determine how wel the liver is working
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?Complete blood count to check for low blood count or anemia?Abdominal ultrasound
?Abdominal CT scan
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?Endoscopic retrograde cholangiopancreatography (ERCP)?Percutaneous transhepatic cholangiogram (PTCA)
?Liver biopsy
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?Cholesterol level
?Prothrombin time
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IN CHILDRENHepatocel ular (SGOT/SGPT more than twice of ALP)
Cholestatic (SGOT/SGPT less than twice of ALP)
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Table of diagnostic testsFunction test
Pre-hepatic Jaundice
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Hepatic Jaundice
Post-hepatic Jaundice
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Total bilirubinNormal / Increased
Increased
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Conjugated bilirubin
Normal
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IncreasedIncreased
Unconjugated bilirubin Normal / Increased
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Increased
Normal
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UrobilinogenNormal / Increased
Increased
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Decreased / Negative
Dark (urobilinogen +
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Dark (conjugatedUrine Color
Normal
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conjugated bilirubin)
bilirubin)
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Stool ColorNormal
Normal/Pale
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Pale
Alkaline phosphatase
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Increasedlevels
Normal
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Alanine transferase and
Aspartate transferase
Increased
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levels
Conjugated Bilirubin in Not Present
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PresentUrine
Splenomegaly
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PresentPresent
Absent
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REMEMBER
The prognostic value of
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AlbuminCoagulation profile
NEONATAL JAUNDICE
?Jaundice is clinical y detectable in the newborn when the serum
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bilirubin levels are greater than 5 mg/dl. This occurs in
approximately 60% of term infants and 80% of preterm infants.
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?Neonatal jaundice first becomes visible in the face and forehead.Blanching reveals the underlying color. Jaundice then gradual y
becomes visible on the trunk and extremities.
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Signs and Symptoms of Neonatal Jaundice
Newborns, as the bilirubin level rises, jaundice wil typically
progress from the head to the trunk, and then to the hands and
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feet. Additional signs and symptoms that may be seen in thenewborn include:
1. poor feeding
2. lethargy
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3. changes in muscle tone4. high-pitched crying
5. seizures.
ASCITES
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DEFINITIONAccumulation of serous fluid in peritoneal cavity
oAs a part of generalized edema- anasarca
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oIsolated collection or disproportionate
CAUSES
1. Isolated or disproportionate
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Cardiac
?Hepatic
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Constrictive pericarditisCirrhosis
Neoplastic
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Congenital hepatic fibrosis
Lymphoma
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Portal vein obstructionNeuroblastoma
Budd chiari syndrome
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Urinary
Neonatal cholestatis
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Perforation?Abdominal
Leakage from urinary tract
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Peritoneal Tuberculosis
Chylous ascites
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Acute pancreatitisGynecological
Renal
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Ovarian tumor
Peritoneal dialysis
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Ovarian ruptureObstructive uropathy
2. Ascitis with generalized edema
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?Renal- Nephrotic syndrome, AGN, renal failure?Cardiac- CHF, constrictive pericarditis
?Polyserositis- SLE, Dengue fever, sepsis
?Severe Malabsorption
CLINICAL FEATURE
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Abdominal distension-hal mark
Five classical signs
Bulging vein
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Flank dullness and fullnessShifting dullness
Fluid thrill
Puddle sign
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Umbilical laughing/ herniation with tense ascitesD/D
?Gaseous distention
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?Fecal retention?Masses
?Obesity
?Pregnancy
EVALUATION OF CAUSE
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?Generalized/ isolated or predominant
?Predominant- hepatic or intra-abdominal
?Age- Neonate- urinary, chylous
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Infancy- cholestatic?Look for signs and symptoms of hepatic disease
?H/o contact for TB with pulmonary findings
?Presence of L. N.
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ASCITIC FLUID ANALYSIS
?Transudative/ exudative ( by SAAG ?serum albumin-ascetic fluid albumin gradient)
?SAAG- 1.1g/dl-transudative
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<1.1g/dl- exudative
?Transudative- CLD and when ascites is a part of generalized edema
?Ascitic fluid- cytology, gram staining, culture
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characteeristic
disease
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Lymphocytic pleocytosistuberculosis
Polymorphic pleocytosis
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Bacterial perotonitis
hemorrhagic
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Malignancy, pancreatitis,tuberculosis
Milky white
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Chylous ascitis
OTHER INVESTIGATIONS
?Ultrasonography? quantity, etiology, L.N., hepatic echotexture, size of
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portal vein
?Portal venous Doppler studies
?CT Abdomen-intra abdominal mass, malignancy etc.
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?LFT?UGI endoscopy- CLD and PH
?Chest X-ray
?Mantoux test
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TREATMENT?Low salt diet
?Diuretics
?IV albumin
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?Repeated large volume paracentesis?Depend on cause of ascites
AT T- TB
Antibiotics- bacterial infection
Interferons- Heptitis B and C
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Steroids- autoimmune hepatitisSurgery or propranolol- PH and Varices
Liver transplantation- decompensated liver, cirrhosis, portal hypertension
MCQ 1
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Regarding bilirubin metabolism, whic h ofthe following is true?
a) Normal elimination is through the urine and the stool
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b) Serum bilirubin concentration is not influenced by medicationsc) Bilirubin is primarily free in circulation
d) Heme protein is primarily broken down in circulation
MCQ 2
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Followings are alarming signs in a patient with jaundice, except:
a) Altered sensorium
b) Raised INR
c) Raised ALT
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d) Persistent vomiting