Download MBBS (Bachelor of Medicine, Bachelor of Surgery) Pediatric PPT 6 Jaundice In Children Lecture Notes
APPROACH TO A CHILD WITH
JAUNDICE AND ASCITIS
LEARNING OBJECTIVES
What is jaundice
Basic patho -physiology of bilirubin
metabolism
Causes of jaundice
Approach to a child with jaundice
Ascites
INTRODUCTION
Symptom of disease rather than a disease
In adults and older children sclera appears jaundiced when serum bilirubin is
increased
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
However it is difficult to see sclera in newborn due to difficulty in opening eye
BILIRUBIN
End product of hemoglobin metabolism that is excreted in bile.
It comes from
?
from catabolism of circulating RBCs
?
from ineffective erythropoiesis (bone marrow)
?
from turnover of heme proteins
What causes bilirubin?
1. Overproduction by reticuloendothelial system
2. Failure of hepatocyte uptake
3. Failure to conjugate or excrete
4. Obstruction of biliary excretion into intestine
Normal Range of Bilirubin
It is normal to have some bilirubin in your blood. Normal levels are:
?Direct (also cal ed conjugated) bilirubin: 0 to 0.3 mg/dL
?Total bilirubin: 0.3 to 1.9 mg/dL
Causes of Jaundice
Jaundice occurs when there is:
too much bilirubin being produced for the liver to remove
from the blood (for example, patients with hemolytic anemia
have an abnormally rapid rate of destruction of their red blood
cells that releases large amounts of bilirubin into the blood)
a defect in the liver that prevents bilirubin from being
removed from the blood, converted to bilirubin/glucuronic
acid (conjugated) or secreted in bile; or
blockage of the bile ducts that decreases the flow of bile
and bilirubin from the liver into the intestines. For
example, the bile ducts can be blocked by worms, cancer,
gallstones, or inflammation of the bile ducts. The
decreased conjugation, secretion, or flow of bile that can
result in jaundice is referred to as cholestasis: however,
cholestasis does not always result in jaundice.
Obstructive Jaundice
Obstructive jaundice is a condition in which there is blockage of the flow of bile out of the
liver
INTRAHEPATIC
EXTRAHEPATIC
CAUSES OF OBSTRUCTIVE JAUNDICE: INTRAHEPATIC
Primary biliary cirrhosis
Sclerosing cholangitis (Inflammation/scarring)
Primary biliary cirrhosis
Sclerosing cholangitis (Inflammation/scarring)
CAUSES OF OBSTRUCTIVE JAUNDICE: EXTRAHEPATIC
? Choledocholithiasis
? Worms
? Malignancy : neoplasia, L.N.
Choledocholithiasis
Malignancy : Pancreatic (head of pancreas) carcinoma
AN APPROACH TO A CHILD
WITH JAUNDICE
CLASSIC APPROACH
Proper detailed history
Proper physical examination
Appropriate investigations
IDENTIFY
Acute
Chronic (more than 6 months)
IDENTIFY
Hemolytic
Hepatocel ular
Cholestatic
TYPES OF JAUNDICE
TYPE
PRE
HEPATIC
POST
HEPATIC
HEPATIC
Urine color
normal
dark
dark
Stool color
normal
normal
acholic
Pruritis
no
No
yes
Signs and Symptoms
of Jaundice
1. yel ow discoloration of the skin, mucous
membranes, sclera of the eyes
2. light-colored stools
3. dark-colored urine
4. itching of the skin.
5. nausea and vomiting
6. abdominal pain
7. fever
8. weakness
9. loss of appetite
10. headache
11. confusion
12. swel ing of the legs and abdomen
13. Skin stigmata
Diagnosis of Jaundice
The health care provider wil perform a physical exam. This may reveal liver
swel ing.
?A bilirubin blood test wil be done.
Other tests vary, but may include:
?Hepatitis virus panel to look for infection of the liver
?Liver function tests to determine how wel the liver is working
?Complete blood count to check for low blood count or anemia
?Abdominal ultrasound
?Abdominal CT scan
?Endoscopic retrograde cholangiopancreatography (ERCP)
?Percutaneous transhepatic cholangiogram (PTCA)
?Liver biopsy
?Cholesterol level
?Prothrombin time
IN CHILDREN
Hepatocel ular (SGOT/SGPT more than twice of ALP)
Cholestatic (SGOT/SGPT less than twice of ALP)
Table of diagnostic tests
Function test
Pre-hepatic Jaundice
Hepatic Jaundice
Post-hepatic Jaundice
Total bilirubin
Normal / Increased
Increased
Conjugated bilirubin
Normal
Increased
Increased
Unconjugated bilirubin Normal / Increased
Increased
Normal
Urobilinogen
Normal / Increased
Increased
Decreased / Negative
Dark (urobilinogen +
Dark (conjugated
Urine Color
Normal
conjugated bilirubin)
bilirubin)
Stool Color
Normal
Normal/Pale
Pale
Alkaline phosphatase
Increased
levels
Normal
Alanine transferase and
Aspartate transferase
Increased
levels
Conjugated Bilirubin in Not Present
Present
Urine
Splenomegaly
Present
Present
Absent
REMEMBER
The prognostic value of
Albumin
Coagulation profile
NEONATAL JAUNDICE
?Jaundice is clinical y detectable in the newborn when the serum
bilirubin levels are greater than 5 mg/dl. This occurs in
approximately 60% of term infants and 80% of preterm infants.
?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.
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
feet. Additional signs and symptoms that may be seen in the
newborn include:
1. poor feeding
2. lethargy
3. changes in muscle tone
4. high-pitched crying
5. seizures.
ASCITES
DEFINITION
Accumulation of serous fluid in peritoneal cavity
oAs a part of generalized edema- anasarca
oIsolated collection or disproportionate
CAUSES
1. Isolated or disproportionate
Cardiac
?Hepatic
Constrictive pericarditis
Cirrhosis
Neoplastic
Congenital hepatic fibrosis
Lymphoma
Portal vein obstruction
Neuroblastoma
Budd chiari syndrome
Urinary
Neonatal cholestatis
Perforation
?Abdominal
Leakage from urinary tract
Peritoneal Tuberculosis
Chylous ascites
Acute pancreatitis
Gynecological
Renal
Ovarian tumor
Peritoneal dialysis
Ovarian rupture
Obstructive uropathy
2. Ascitis with generalized edema
?Renal- Nephrotic syndrome, AGN, renal failure
?Cardiac- CHF, constrictive pericarditis
?Polyserositis- SLE, Dengue fever, sepsis
?Severe Malabsorption
CLINICAL FEATURE
Abdominal distension-hal mark
Five classical signs
Bulging vein
Flank dullness and fullness
Shifting dullness
Fluid thrill
Puddle sign
Umbilical laughing/ herniation with tense ascites
D/D
?Gaseous distention
?Fecal retention
?Masses
?Obesity
?Pregnancy
EVALUATION OF CAUSE
?Generalized/ isolated or predominant
?Predominant- hepatic or intra-abdominal
?Age- Neonate- urinary, chylous
Infancy- cholestatic
?Look for signs and symptoms of hepatic disease
?H/o contact for TB with pulmonary findings
?Presence of L. N.
ASCITIC FLUID ANALYSIS
?Transudative/ exudative ( by SAAG ?serum albumin-ascetic fluid albumin gradient)
?SAAG- 1.1g/dl-transudative
<1.1g/dl- exudative
?Transudative- CLD and when ascites is a part of generalized edema
?Ascitic fluid- cytology, gram staining, culture
characteeristic
disease
Lymphocytic pleocytosis
tuberculosis
Polymorphic pleocytosis
Bacterial perotonitis
hemorrhagic
Malignancy, pancreatitis,
tuberculosis
Milky white
Chylous ascitis
OTHER INVESTIGATIONS
?Ultrasonography? quantity, etiology, L.N., hepatic echotexture, size of
portal vein
?Portal venous Doppler studies
?CT Abdomen-intra abdominal mass, malignancy etc.
?LFT
?UGI endoscopy- CLD and PH
?Chest X-ray
?Mantoux test
TREATMENT
?Low salt diet
?Diuretics
?IV albumin
?Repeated large volume paracentesis
?Depend on cause of ascites
AT T- TB
Antibiotics- bacterial infection
Interferons- Heptitis B and C
Steroids- autoimmune hepatitis
Surgery or propranolol- PH and Varices
Liver transplantation- decompensated liver, cirrhosis, portal hypertension
MCQ 1
Regarding bilirubin metabolism, whic h of
the following is true?
a) Normal elimination is through the urine and the stool
b) Serum bilirubin concentration is not influenced by medications
c) Bilirubin is primarily free in circulation
d) Heme protein is primarily broken down in circulation
MCQ 2
Followings are alarming signs in a patient with jaundice, except:
a) Altered sensorium
b) Raised INR
c) Raised ALT
d) Persistent vomiting
This post was last modified on 07 April 2022