neonatal jaundice

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Slide 1 : Powerpoint Templates NEONATAL JAUNDICE
Slide 2 : Learning outcome Describe bilirubin metabolism Discuss the causes of unconjugated hyperbilirubinaemia Discuss the causes of conjugated hyperbilirubinaemia Define prolong jaundice and list the causes Plan systemic diagnostic approach to a neonate with a jaundic from a history, physical examination and appropriate laboratoryinvestigations Discuss the complication of severe uncnjugated hyperbilirubinaemia Discuss the various method of treatment : a. phototheraphy-mechanism of tx,principle of tx and cx b. exchange tranfusion- principle and cx
Slide 3 : DEFINITION Yellowish staining of the skin and whites of the newborn's eyes (sclerae) by pigment of bilirubin Can be detected clinically when the level of bilirubin in the serum rises above 85umol/L
Slide 4 : PHYSIOLOGIC JAUNDICE Physiologic jaundice is a common cause of hyperbilirubinemia among newborns Increase RBC mass Shortened RBC lifespan (70days) Hepatic immaturity of ligandin and glucuronosyltransferase
Slide 5 : Normal metabolism Of bilirubin Normal metabolism Of bilirubin
Slide 6 : Transport of bilirubin to the liver: Bilirubin is formed outside the liver and released bound to serum albumin because bilirubin is insoluble in aqueous solutions, hence, impossible to transport in blood. Then occurs carrier-mediated hepatic uptake of bilirubin Liver uptake and conjugation of bilirubin Conjugation is the coupling of two or more biomolecules. Bilirubin is conjugated with one or two molecules of glucuronic acid with the action of bilirubin UDP-glucuronyltransferase. Liver is conjugated to make it water soluble inside the liver. Once in the liver, bilirubin is secreted by liver cells into bile. Intestinal bacterial action on conjugated bilirubin: Intestinal bacteria convert conjugated bilirubin back into unconjugated bilirubin, which is then excreted in feces.
Slide 7 : Some urobilinogen is absorbed back into blood and converted into a yellow pigment called urobilin and excreted in urine. • Most urobilinogen is excreted in feces in the form of a brown pigment called stercobilin.
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Slide 10 : Causes of neonatal jaundice
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Slide 12 : Causes of unconjugated bilirubin Physiological jaundice In almost every newborn infant, particularly premature infants, a physiologic elevation of serum unconjugated bilirubin develops during the 1st week of life, usually in the 2nd or 3rd day and resolves spontaneously. Hb is higher than required Bilirubin production is elevated because of increased breakdown of fetal erythrocytes. Shorter life of RBC This is the result of the shortened lifespan of fetal erythrocytes and the higher erythrocyte mass in neonates. Hepatic immaturity Hepatic excretory capacity is low because of low concentrations of the binding protein ligandin in the hepatocytes and because of low activity of glucuronyl transferase
Slide 13 : It is diagnosis of exclusion Unconjugated bilirubin level >12.9mg/dL in term infant Unconjugated bilirubin level >15mg/dL in preterm infant Bilirubin level increasing at a rate >5mg/dL/day Jaundice in the first 24 hours of life Conjugated bilirubin level>2mg/dL Clinical jaundice persisting >1week in full-term infant or >2weeks in preterm infant
Slide 14 : Haemolytic disorder Rhesus haemolytic disease -usually identified antenatally and monitored if necessary - frequently occurs when an Rh negative mother has a baby with an Rh positive father. - When the baby's Rh factor is positive, like the father's, problems can develop if the baby's red blood cells cross to the Rh negative mother. - This usually happens at delivery when the placenta detaches.
Slide 15 : ABO incompatibility More common than rhesus incompatibility Most ABO antibodies are IgM and do not cross the placenta HOWEVER, some group of O women have IgG anti A haemolysin in blood which can cross the placenta and haemolysis the red cell of a group A infant Group B infant will be affected by anti-b haemolysin Hepatomegally absent Diagnose by Coombs test which demontrate antibody on the surface of red cell
Slide 16 : G6PD deficiency Mainly affect the male infants an inherited disorder of the red blood cell Parents of the affected infants should be given a list of drug to be avoided as they may precipitate haemolysis In G6PD deficiency the red blood cells are prone to haemolysis when exposed to oxidants or when certain foods or herbs are ingested
Slide 17 : Polycythemia The liver may not have the capacity to metabolize the increased bilirubin load presented by the increased blood volume increased blood volume ? increased bilirubin load ? beyond liver capacity Cephalhaematoma (internal haemolysis)
Slide 18 : Breast milk Bilirubin is rarely increase more than 20mg/dL Breast milk may contain an inhibitor of bilirubin conjugation or may increase enterohepatic recirculation of bilirubin because of breast milk glucuronidase Breast-milk fed is higher (unconjugated) compare to formula fed infant(reduce fluid intake)
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Slide 20 : Congenital deficiency of glucoronyl transferase - Crigler-Najjar syndrome type I. A severe of UDP-glucoronyl transferase deficiency that is inherited as an autosomal recessive disorder. - Crigler-Najjar syndrome type II. Moderate deficiency of UDP-glucoronyl transferase. It is responsive to phenobarbital therapy. - Gilbert syndrome. A mild form of UDP-glucoronyl transferase deficiency inherited as an autosomal dominant condition which is benign and relatively common.
Slide 21 : Conjugated bilirubin (direct bilirubin >2mg/dL) Never physiologic
Slide 22 : Causes of conjugated bilirubin Neonatal hepatitis Perinatal congenital infection ( TORCH) Intestinal obstruction Biliary atresia Dubin-Johnson Syndrome Rotor's Syndrome Choledochal cyst
Slide 23 : Neonatal hepatitis inflammation of the liver that occurs only in early infancy, usually between one and two months after birth. About 20 percent of the infants - infected by a virus that caused the inflammation before birth by their mother or shortly after birth Cytomegalovirus rubella (measles) hepatitis A, B or C viruses. In the remaining 80 percent of the cases no specific virus can be identified as the cause Occur at one to two months of age, is not gaining weight and growing normally, and has an enlarged liver and spleen
Slide 24 : Intestinal obstruction Biliary atresia
Slide 25 : Biliary atresia characterized by obliteration or discontinuity of the extrahepatic biliary system, resulting in obstruction to bile flow Typical symptoms include variable degrees of jaundice, dark urine, and light stools. Biliary atresia occurs when the bile ducts inside or outside the liver do not develop normally. It is not known why the biliary system fails to develop normally
Slide 26 : Investigation Alkaline phosphatase (AP), 5' nucleotidase, gamma-glutamyl transpeptidase (GGTP), serum aminotransferases, serum bile acids ultrasound
Slide 27 : Choledochal cyst congenital bile duct anomalies. These cystic dilatations of the biliary tree can involve the extrahepatic biliary radicles, the intrahepatic biliary Clinical presentation Infants Infants frequently present with jaundice and acholic stools. In early infancy, this may prompt a workup for biliary atresia. In addition, infants with choledochal cysts often have a palpable mass in the right upper quadrant of the abdomen, accompanied with hepatomegaly.
Slide 28 : Choledochal cyst
Slide 29 : Prolong jaundice
Slide 30 : Prolonged jaundice is defined as hyperbilirubinaemia beyond age 14 days (termed) or 21 days (full termed) and must be investigated to exclude pathological causes
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Slide 32 : HISTORY
Slide 33 : History of Present Illness Onset and progression of jaundiced skin Feeding: breast milk or formula? Current weight compared to birth weight. Gaining weight appropriately? Number of wet diapers per day? (Indicator of hydration status) Consistency and colour of stool?(pale stool implies poor bilirubin excretion) Infections or fever? Medications? (newborn or mother) General activity: irritable? lethargic? Gender & ethnicity? (Males, Asians, and Blacks have some increased risk) Perinatal History Maternal blood group Maternal illnesses or infections Results of antenatal screening tests Maternal medicine or drug intake Birth trauma with bruising Results of newborn screening tests Family History: Previous siblings with neonatal jaundice Other family members with jaundice Anemia or blood disorders Splenectomy Bile stones or gallbladder removal
Slide 34 : PHYSICAL EXAMINATION
Slide 35 : General: Does the child look well or unwell?  You may be able to observe the child feeding – is the baby having difficulty feeding? Is the baby consolable? Vitals: If febrile, the newborn will require a full septic work-up.  In hemolytic states, there can be an increase in heart rate and respiration rate as well as poor perfusion. Growth Parameters: Obtain length, weight and head circumference and compare to measurements taken at birth.  Depending on the newborn’s age, excessive weight loss or insufficient weight gain may point to dehydration. HEENT: Is there pallor? Sclerae and mucous membranes should be closely inspected for jaundice. Look for cephalohematoma or bruising.
Slide 36 : Cardiovascular: Heart rate, pulse volume, blood pressure, apex location,  perfusion.  Severe haemolytic processes can result in heart failure. Respiratory: Respiration rate and rhythm and oxygen saturation.  If the neonate is in heart failure, there may be respiratory signs. Abdomen: Is the abdomen distended? Is there caput medusa (evidence of portal hypertension)? Are there any masses? Check for hepatomegaly and splenomegaly. Are there any areas of tenderness? Neurologic: Level of consciousness. Cranial nerves, tone, gross motor movements, quality of the cry, and primitive reflexes (Moro, grasps, tonic-neck, step).
Slide 37 : LAB INVESTIGATION
Slide 38 : Hemolytic work-up Serum bilirubin: conjugated and unconjugated CBC (mainly for Hb and Hct but also WBC as a non-specific marker of infection) Peripheral blood smear (for RBC morphology) Maternal blood group and Rh status Infant blood group and Rh status Coomb’s test Also consider: Septic work-up if clinically indicated G6PD (Glucose-6-Phosphate Dehydrogenase) screen (especially if male and of Asian or Middle Eastern ethnicity) Other red cell enzyme studies if hemolysis remains undefined Liver enzymes (AST, ALT, GGT, Alk Phos) and liver function tests (PT, PTT, albumin, ammonia) if conjugated hyperbilirubinemia Imaging studies consider abdominal Ultrasound if conjugated hyperbilirubinemia
Slide 39 : COMPLICATION OF SEVERE UNCONJUGATED HYPERBILIRUBINAEMIA
Slide 40 : Unconjugated bilirubin 2 form: Tightly complexed to serum albumin Free unconjugated bilirubin Water insoluble Cannot be excreted in urine
Slide 41 : Bilirubin encaphalopathy
Slide 42 : Bilirubin Encephalopathy bilirubin level > 20mg/dL(345umol/L) Acute Phase 1 Phase 2 Phase 3 Chronic Kernicterus
Slide 43 : Acute Bilirubin Encephalopathy Phase 1 (first few days) poor sucking, hypotonia, stupor and depressed sensorium Phase 2 Hypertonia (retrocollis – backward arching of neck, opisthotonus – arching of trunk) and fever. All infants who develop these symptoms, will develop chronic encephalopathy. Phase 3 (after first week) Gradual disappearance of the hypertonia, high pitched cry, hearing and visual abnormalities, poor feeding, athetosis -Up to years after the first week
Slide 44 : Kernicterus First year: Poor feeding, high pitched cry. Hypotonia but good deep tendon reflexes. Tonic neck reflex, righting reflex persist. Slow motor skills (up to 5 years to walk). After first year: Main clinical features are: extrapyramidal disorder (athetosis, ballismus, tremor, dysarthria) hearing loss (damage to cochlear nuclei in brainstem) gaze abnormalities (limitation of upward gaze) Athetosis normally develops 18 months- 8 years of age. Hearing loss may be the only symptom in some children.
Slide 45 : Long term sequelae: Chorioathetoid cerebral palsy Sensorineural hearing loss Upward gaze palsy Dental-enamel dysplasia Mental retardation Speech disturbance
Slide 46 : MANAGEMENT Aim: ? unconjugated(indirect) bilirubin level Methods of treatment: Phototherapy Exchange transfusion
Slide 47 : PHOTOTHERAPY
Slide 48 : TYPE OF PHOTOTHERAPY Conventional phototherapy in cases of mild to Fibre optic phototherapy moderate jaundice Intensive phototherapy for jaundice which significantly high ( eg : > 300 umol/L in 5 days old / 250 umol/L in 24h old infant )
Slide 49 : Conventional phototherapy Use one or more tungsten halogen bulb, a metal halide gas discharge tube, long or compact (or folded) fluorescent lamps, or most recently, light emitting diodes (leds). The light source is positioned above or below the baby and the irradiance is dependent on the distance between the baby and the lights. Fibre optic phototherapy Use a standard light source, usually a quartz halogen bulb. The light from the bulb may then be passed through a filter before being channelled down a fibreoptic bundle into a pad of woven optic fibres. The pad can then be placed next to the neonate’s skin
Slide 50 : PHOTOTHERAPY
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Slide 52 : MECHANISM Absorption of light by dermal and subcutaneous bilirubin induces a fraction of the pigment to undergo several photochemical reactions. Normal form of bilirubin (4Z,15Z-bilirubin) generates transient excited-state bilirubin molecules that can react with oxygen to produce colorless products of lower molecular weight, OR they can undergo rearrangement to become structural isomers (lumirubins) or isomers in which the configuration of at least one of the two Z-configuration double bonds has changed to an E configuration.
Slide 53 : The photoisomers are less lipophilic than the 4Z,15Z form of bilirubin and can be excreted unchanged in bile without undergoing glucuronidation.
Slide 54 : PRINCIPLE OF TREATMENT Prevent potential dangerous indirect bilirubin levels because phototherapy can change the indirect bilirubin into more soluble forms to be excreted Decreased the need for exchange transfusion
Slide 55 : COMPLICATION Retinal effects Unknown in human but animal studies showed retinal degeneration may occur. Thus, use eye shields. 2) ? insensible fluid loss ? fluid requirements by 25 % Stools become looser & more frequent Thus, use fiberoptic phototherapy ? lesser insensible loss.
Slide 56 : 3) Bronze baby syndrome With conjugated hyperbilirubinaemia ? photodestruction of copper porphyrins ? urine & skin bronze.
Slide 57 : 4) Congenital erythropoietic porphyria Rare C/I phototherapy Exposure to moderate-high intensity of visible light ? severe bullous lesions on skin ?death
Slide 58 : EXCHANGE TRANSFUSION
Slide 59 : Exchange transfusion (ET) is indicated for severe hyperbilirubinaemia (if infants show signs of acute bilirubin encephalopathy -hypertonia, retrocollis, opisthotonus, fever, high pitch cry or if TSB is = 5 mg/dL (85 umol/L) above the exchange levels) Aims: - To reduce the serum bilirubin level and reduce the risk of brain damage and kernictures - To remove the infant’s sensitised red blood cells and the circulating antibodies, reduce the degree of red cell destruction.
Slide 60 : INDICATIONS Blood exchange transfusion to lower the serum bilirubin level and reduce the risk of kernicterus Partial exchange transfusion is either increasing or decreasing an infant’s hematocrit, while maintaining a constant blood volume. Aims: - to correct polycythaemia with hyperviscosity - to correct severe anaemia without hypovolaemia.
Slide 61 : TECHNIQUE 1. Two Catheter Push-pull Technique Blood is removed from the artery while infusing fresh blood through a vein at the same rate. In Out Umbilical vein Peripheral artery Umbilical vein Umbilical artery  Peripheral vein Peripheral artery Peripheral vein Umbilical artery 2. One Catheter Push-pull Technique This can be done through an umbilical venous catheter. Exceptionally, an umbilical artery catheter can be used. Ideally, the tip of the UVC should be in the IVC/right atrium (at or just above the diaphragm) but can be used if it is in the portal sinus. For ‘high’ UVC placement, position should be checked by an X-ray. This is not always necessary for a low position. A low positioned catheter is usually removed after each exchange. Withdraw blood over 2 minutes, infuse slightly faster.
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Slide 64 : COMPLICATION Catheter related infection haemorrhage necrolizing enterocolitis air embolism portal and splenic vein thrombosis (late sequelae) Haemodynamic problems overload cardiac failure hypovolaemic shock arrhythmia (catheter tip near sinus node in right atrium) bradycardia with calcium bolus Electrolyte imbalance hyperkalemia hypocalcemia hyper- and hypo-glycaemia metabolic acidosis, alkalosis (late breakdown of citrate)
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