Lecture- 09. Neonatal jaundice
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La ictericia neonatal es una condición común en recién nacidos, que se manifiesta como una coloración amarillenta de la piel y los ojos debido a niveles elevados de bilirrubina. Factores como el nacimiento prematuro, hematomas al nacer y la incompatibilidad de grupos sanguíneos pueden aumentar el riesgo de ictericia. Esta condición puede clasificarse como fisiológica o patológica, con diferentes mecanismos y tratamientos necesarios según la causa subyacente.
Lecture- 09. Neonatal jaundice
- 2. Lecture-08 Neonatal Jaundice Prof. Dr. Sunil Natha Mhaske Dean Dr. Vithalrao Vikhe Patil Foundation’s Medical College and Hospital, Ahmednagar (M.S.) India-414111 Mo- 7588024773 Mail-sunilmhaske1970@gmail.com
- 3. History • The term jaundice is from the French word "jaune” • Neonatal jaundice may have first been described in a Chinese textbook 1000 years ago. • Earliest work on jaundice from Baumes-1785 and Hervieux-1847 • Medical theses, essays, and textbooks from the 18th and 19th centuries contain discussions about the causes and treatment of neonatal jaundice. • Kernicterus was first described by Johannes Orth, 1875, He postulated that jaundice might have hematologic origins. He noted that the brain in jaundiced adults wasn’t affected. • Christian Schmorl coined the term in 1904, Translated, Kernicterus means jaundice of the “kern” or nuclear region of the brain.
- 4. • It is a yellowish discoloration of the white part of the eyes and skin in a newborn baby due to high bilirubin levels. • About 60% of full term newborn and 80% of premature babies are jaundiced. • 3% of normal term infant show bilirubin level more than 15mg/dl • Jaundice is the most common condition that requires medical attention and hospital readmission in newborns. Neonatal jaundice or Neonatal Hyperbilirubinemia-
- 5. Bilirubin • Non-polar, water insoluble compound requiring conjugation with glucuronic acid to form a water soluble product that can be excreted. • It circulates to the liver reversibly bound to albumin
- 6. Pathophysiology • Bilirubin comes from the breakdown in heme, which is produced from the breakdown of hemoglobin. • Heme is converted to biliverdin, iron, and carbon monoxide by the enzyme heme oxygenase. • biliverdin is then converted to bilirubin by biliverdin reductase. • The conversion of heme to bilirubin takes place in the reticuloendothelial system. • The unconjugated bilirubin is hydrophobic and is transported to the liver bound to albumin where it is conjugated by the enzyme uridine diphosphate- glucuronosyltransferase (UGT). • Conjugated bilirubin, which is water-soluble, is excreted in bile and into the gastrointestinal (GI) tract and mostly excreted in feces after being metabolized by bacterial flora. • Some conjugated bilirubin is deconjugated to unconjugated bilirubin and reabsorbed through the enterohepatic circulation.
- 8. • Ligandins{y} responsible for transport from plasma membrane to endoplasmic reticulum. • Bilirubin conjugated in presence of UDPGT (uridine diphosphate glucuronyl transferase) to mono and diglucoronides, which are then excreted into bile canaliculi. • Phenobarbitol Increases the conc. of Ligandin and also induces UDPGT. • Conjugated” bilirubin is water soluble and is secreted by the hepatocytes into the biliary canaliculi. • Converted to stercobilinogen (urobilinogen) (colorless) by bacteria in the gut. • Oxidized to stercobilin which is colored, Excreted in feces. • Some stercobilin may be re-adsorbed by the gut and re-excreted by either the liver or kidney.
- 9. Enterohepatic circulation- • Meconium contains 100-200mg of conjugated bilirubin at birth. • Conjugated bilirubin is unstable and easily hydrolyzed to unconjugated bilirubin. • This process occurs non-enzymatically in the duodenum and jejunum and also occurs in the presence of beta- glucuronidase, an enteric mucosal enzyme, which is found in high concentration in newborn infants and in human milk. Factors enhancing enterhepatic circulation - Decrease entral intake - Intestinal atresia - Meconium ileus - Hiruschsrung disease
- 10. Jaundice is visible- - in adults at STB > 2mg/dl - in neonates if STB> 5 mg/dl Physiological Mechanisms of Neonatal Jaundice- •Increased synthesis •Less efficient binding and transport •Less efficient hepatic conjugation and excretion •Enhanced absorption via enterohepatic circulation
- 11. Risk factors for Neonatal Jaundice Premature birth. A baby born before 38 weeks of gestation may not be able to process bilirubin as quickly as full-term babies do. Premature babies also may feed less and have fewer bowel movements, resulting in less bilirubin eliminated through stool. Significant bruising during birth. Newborns who become bruised during delivery gets bruises from the delivery may have higher levels of bilirubin from the breakdown of more red blood cells. Blood type. If the mother's blood type is different from her baby's, the baby may have received antibodies through the placenta that cause abnormally rapid breakdown of red blood cells. Breast-feeding. Breast-fed babies, particularly those who have difficulty nursing or getting enough nutrition from breast-feeding, are at higher risk of jaundice. Dehydration or a low caloric intake may contribute to the onset of jaundice. However, because of the benefits of breast-feeding It's important to breast feed. Race. Studies show that babies of East Asian ancestry have an increased risk of developing jaundice.
- 12. Classification Neonatal Hyperbilirubinemia Based on Mechanism of Accumulation Increased bilirubin load (prehepatic) 1. Haemolytic- • coomb positive • coomb negative:- 2. Non haemolytic • Extravascular source • Polycythemia • Exaggerated enterohepatic circulation Decreased bilirubin conjugation (Hepatic) 1. Physiologic jaundice 2. Crigler-Najjar syndrome 1 and 2 3. Gilbert syndrome 4. Hypothyroidism 5. Breast milk jaundice Impaired bilirubin Excretion (post hepatic) 1. Biliary obstruction: 2. Metabolic disorder 3. Chromosomal abnormality: 4. Infection 5. Drugs
- 13. Classification
- 16. • Pathologic jaundice may occur in the first 24 hours of life and • It is characterized by a rapid rate of rising in the bilirubin level more than 0.2 mg/dl per hour or 5 mg/dl per day. • Causes - due to increased bilirubin production, decreased bilirubin clearance, and increased enterohepatic circulation. a. Immune-mediated hemolysis - ABO and rhesus incompatibility. b. Non-immune mediated - cephalhematoma, red blood cell membrane defects like hereditary spherocytosis and elliptocytosis, enzyme defects like glucose-6-phosphate dehydrogenase (G6PD) deficiency and pyruvate kinase. Pathological jaundice (Pathologic unconjugated Hyperbilirubinemia.)
- 17. Signs of Pathological Jaundice – • Intrauterine growth restriction • Stigma of intrauterine infections (e.G. Cataracts, small head, and enlargement of the liver and spleen) • Cephalohematoma • Bruising • Signs of bleeding in the brain's ventricles • Family history of jaundice and anemia • Family history of neonatal or early infant death due to liver disease, maternal illness suggestive of viral infection • Maternal drugs (e.G. Sulphonamides, anti-malarials causing red blood cell destruction in G6PD deficiency)
- 18. Red flags for pathologic jaundice •Jaundice in first 24 hours •Rapidly rising total bilirubin concentration (>86umol/L/day) •Early gestational age •Previous sibling with jaundice •Significant bruising •Jaundice persisting for more than 2-3 weeks •East Asian ethnicity
- 19. Physiological jaundice • It is also referred to as non-pathologic jaundice. • It is mild and transient. • This occurs because of differences in the metabolism of bilirubin in the neonatal period leading to an increased bilirubin load. • The increased bilirubin load in the newborn arises from increased production of bilirubin due to a higher mass of red blood cells with a decreased lifespan in the neonate, a decreased bilirubin clearance from a deficiency of the uridine diphosphate glucuronosyltransferase (UGT) enzyme, which in the newborn has the activity of about 1% of the adult liver and increased enterohepatic circulation. • Physiologic jaundice usually occurs on days 2 to 4, peaks between 4 to 5 days, and resolves in 2two weeks. Physiologic jaundice never occurs in the first 24 hours. • Visible jaundice due to elevation of unconjugated bilirubin during first week.
- 20. • Phase one- - Term infants - jaundice lasts for about 10 days with a rapid rise of serum bilirubin up to 204 μmol/l (12 mg/dL). - Preterm infants - jaundice lasts for about two weeks, with a rapid rise of serum bilirubin up to 255 μmol/l (15 mg/dL). • Phase two – - bilirubin levels decline to about 34 μmol/l (2 mg/dL) for two weeks, eventually mimicking adult values. • Preterm infants - phase two can last more than one month. • Exclusively breastfed infants - phase two can last more than one month.
- 21. 1) Increase bilirubin load over liver cell • Increase RBC volume/kg as compared to adult • Decrease RBC survival:-90 dayS • Increase early labelled bilirubin from haem,haem proteins , myoglobin, haem containing liver enzyme or ineffective erythropoesis,. • Increase enterohepatic circulation of bilirubin: - No bactericidal activity in gut ,bilirubin can not converted into urobillinogen. - Beta glucronidase which unconjugate bilirubin diglucronide present in intestine and helps in reabsoportion of bilirubin in portal circulation. 2) Defective hepatic uptake of bilirubin from plasma Decrease ligandin (Y protein) Binding of Y & Zn protein by other anions 3) Defective bilirubin conjugation- Decrease UDP Glucronyl transferase activity and decrease UDP glucose dehydrogenase activity. 4) Defective Bilirubin excretion.
- 23. ABO incompatibility ABO incompatibility occurs in mother’s with blood group O who have anti-A and anti-B IgG antibodies that cross the placenta and cause hemolysis in newborns with blood group A or B. ABO incompatibility Type O mothers Type A or B fetuses Presence of IgG anti-A or Anti-B antibodies in type O mother Frequently occurring during the first pregnancy without prior sensitization
- 24. Rhesus (Rh) incompatibility • Pathophysiology of alloimmune hemolysis resulting from Rh incompatibility An Rh-negative mother An Rh-positive fetus Leakage of fetal RBC into maternal circulation Maternal sensitization to D antigen on fetal RBC Production and transplacental passage of maternal anti-D antibodies into fetal circulation Attachment of maternal antibodies to Rh-positive fetal RBC Destruction of antibody-coated fetal RBC Rh hemolytic disease was rare during the first pregnancy involving an Rh-positive fetus. • Once sensitization has occurred, re-exposure to Rh D RBC in subsequent pregnancies leads to an anamnestic response, with an increase in the maternal anti- Rh D antibody titer. • The likelihood of an infant being affected increased significantly with each subsequent pregnancy. • Using Rhogam (anti-D gamma globulin) as prophylaxis in a mother with prior exposure has decreased the incidence of Rh hemolysis.
- 25. Clinical Features Rh ABO` Frequency Unusual Common Anemia Marked Minimal Jaundice Marked Minimal to moderate Hydrops Common Rare Hepatosplenomegaly Marked Minimal Kernicterus Common Rare
- 26. Laboratory Features Rh ABO blood type of Mother Rh negative O blood type of Infant Rh positive A or B Anemia Marked Minimal Direct Commb’s test Positive Negative Indirect Commb’s test Positive Usually positive Hyperbilirubinemia marked Variable RBC morphology Nucleated RBC Spherocytes
- 27. G6PD enzyme deficiency • The G6PD enzyme, found in red blood cells (RBCs), protects against oxidative injury by the production of NADPH (nicotinamide adenine dinucleotide phosphate hydrogenase) from NADP (nicotinamide adenine dinucleotide phosphate). • With its deficiency, and in the presence of oxidant stressors like illness, certain drugs, dyes, and foods like fava beans, there is hemolysis of RBCs. • The clinical presentation is varied depending on the variant of the GGPD, and some newborns may present with neonatal jaundice with severe hyperbilirubinemia or kernicterus. • G6PD is an X-linked disorder leading to males mostly being affected and females mostly being asymptomatic carriers.
- 28. Crigler- Najjar syndrome • In Crigler-Najjar syndrome, there is either an absence of UGT activity (type 1) or low UGT activity (type 2), which leads to severe hyperbilirubinemia in the first days of life or less severe disease respectively. • Neonates with Crigler-Najar 1 need liver transplantation or long-term use of phototherapy. • Phenobarbital may be used in type 2 Crigler-Najjar.
- 29. Gilbert syndrome • There is a mutation of the UGT1A1 gene in Gilbert syndrome. • Causing decreased UGT production and unconjugated hyperbilirubinemia. • Gilbert is usually diagnosed in the adolescent period, although presentation in the neonatal period may occur and is mostly inherited as an autosomal dominant condition. • It can be diagnosed with genetic testing.
- 30. Breastfeeding jaundice (breastfeeding failure jaundice) • occurs in the first week of life. • It is due to failure of adequate intake of breast milk leading to dehydration and hypernatremia. • Breastfeeding failure leads to decreased intestinal motility and decreases the elimination of bilirubin in the stool or meconium. • This leads to increased enterohepatic circulation, resulting in increased reabsorption of bilirubin from the intestines. • most cases can be ameliorated by frequent breastfeeding sessions of sufficient duration to stimulate adequate milk production
- 31. Breast milk jaundice • occurs late in the first week, peaks in the second, and usually resolves by 12 weeks of age. • It is due to inhibition of UGT activity and a factor in breast milk with a beta-glucuronidase-like activity that deconjugates conjugated bilirubin in the intestines leading to increased enterohepatic circulation. • It is a biochemical occurrence. • bilirubin uptake in the gut (enterohepatic circulation) is increased in breast fed babies, possibly as the result of increased levels of epidermal growth factor (EGF) in breast milk. Breast milk also contains glucoronidase which will increase deconjugation and enterohepatic recirculation of bilirubin. • inhibition of bilirubin conjugation leads to increased levels of bilirubin in the blood. • enzyme in breast milk (lipoprotein lipase) produces increased concentration of nonesterified free fatty acids that inhibit hepatic glucuronyl transferase, which again leads to decreased conjugation and subsequent excretion of bilirubin.
- 32. Conjugated hyperbilirubinemia Conjugated hyperbilirubinemia is always pathologic and is due to defects in bile formation or transport, obstruction to its flow, or to systemic conditions that may affect the liver. Conditions causing conjugated hyperbilirubinemia due to hepatobiliary disease include- biliary atresia Inborn errors of metabolism like galactosemia choledochal cysts genetic disorders like a-1 antitrypsin deficiency idiopathic neonatal hepatitis. metabolic disorders such as tyrosinemia. Alagille syndrome. Urinary tract infections TORCH” (toxoplasmosis, other- syphilis, varicella-zoster, rubella, cytomegalovirus, and herpes simplex) Systemic infections like “infections and systemic conditions like sepsis, shock, and birth asphyxia
- 33. Biliary atresia • Biliary atresia is the most common cause of conjugated neonatal hyperbilirubinemia. • It involves both intra-hepatic and extra-hepatic bile ducts. • classically presents around 2 to 4 weeks of life with pale stools. • The initial evaluation is by ultrasonography that may show an absent gallbladder and the classic "triangular cord" sign. • percutaneous liver biopsy • open cholangiogram • surgical intervention-Kasai procedure (hepatoportoenterostomy) - performed before eight weeks.
- 34. Choledochal cysts • Choledochal cysts involve dilation of the intrahepatic and extra-hepatic bile duct. • Ultrasonography
- 35. Alagille syndrome • Alagille syndrome is caused by a genetic mutation leading to a paucity of interlobular bile ducts and hepatic manifestations, including jaundice and cirrhosis. • Other clinical features are butterfly vertebrae, peripheral pulmonic stenosis, renal involvement, dysmorphic features, and posterior embryotoxon of the eye. • Alagille syndrome is inherited in an autosomal dominant pattern
- 36. • Alpha-1-antitrypsin deficiency is a common genetic disorder that presents with cholestatic jaundice in infants who are homozygous for the PiZZ genotype. • Accumulation of anti-trypsin polymers in the endoplasmic reticulum of hepatocytes of a patient with the PiZZ genotype leads to apoptosis, neonatal cholestasis, and cirrhosis later in childhood. Alpha-1-antitrypsin deficiency
- 37. • Newborns with galactosemia present with jaundice, cataracts, hepatomegaly, failure to thrive, renal tubular acidosis, and Escherichia coli sepsis after the ingestion of milk. • Galactosemia is due to galactose-1-phosphate uridyltransferase (GALT) deficiency leading to the accumulation of toxic metabolites in multiple organs. • The presence of reducing substances in urine suggests galactosemia, and GALT activity in the liver or erythrocytes confirms the diagnosis. Galactosemia
- 39. • Originally described by Kramer. • Dermal staining of bilirubin may be used as a clinical guide to the level of jaundice. • Dermal staining in newborns progresses in a cephalo-caudal direction. • The newborn should be examined in good daylight. • The physician should pale the skin by digital pressure and the underlying color of skin and subcutaneous tissue should be noted. • Newborns who are detected the yellow skin beyond the thighs should have an urgent laboratory confirmation for bilirubin levels. • Clinical assessment is unreliable if a newborn has been receiving phototherapy and has dark skin. Clinical Examination of Neonatal Jaundice
- 42. Diagnosis 1. Biochemical: The gold standard method for bilirubin estimation is the total and conjugated bilirubin assessment based on the van den Bergh reaction. 2. Bilimeter: Spectrophotometry is the base of Bilimeter and it assesses total bilirubin in the serum. Because of the predominant unconjugated form of bilirubin, this method has been found a useful method in neonates. 3. Transcutaneous Bilirubinometer: This method is noninvasive and is based on the principle of multi wavelength spectral reflectance from the bilirubin staining in the skin. The accuracy of the instrument may be affected by variation of skin pigmentation and its thickness 4. Blood grouping and Rh typing 5. Hematocrit, Reticulocyte count, PBS 6. Direct Coomb’s test on baby 7. Sepsis screen 8. Liver function and Thyroid tests 9. Torch assay
- 43. Complications 1. Kernicterus- - occurs if acute bilirubin encephalopathy causes permanent damage to the brain. - Involuntary and uncontrolled movements (athetoid cerebral palsy) - Permanent upward gaze - Hearing loss - Improper development of tooth enamel
- 44. 2. Acute Bilirubin Encephalopathy 1st phase: hypotonia, poor suck-present in the first few days 2nd phase: Hypertonia (retrocollis and opisthotonos), fever 3rd phase: Gradual disappearance of the hypertonia-Up to years after the first week 3. Chronic Encephalopathy: • Perlstein’s Tetrad: Extrapyramidal Abnormalities, Hearing Loss, Gaze abnormality, and Dental Dysplasia • Extrapyramidal abnormalities: Facial grimacing, drooling, dysarthria, and athetosis--may develop by 18mo or delayed to 8or9 years. • Hearing loss is usually due to injury of the cochlear nuclei in the brainstem. It may be the only manifestation • Gaze abnormalities: Limitation of upward gaze, palsies • Cerebral cortex is relatively spared, so intelligence is often close to normal.
- 45. Physiological Jaundice- • Benign in nature. • mother should be encouraged to breast-feed her baby frequently and exclusively. • Mother should be told to bring the baby to the hospital if the color on the legs looks as yellow as the face. • Any newborn discharged before 48 h of life should be evaluated again in the next 48 h for breastfeeding sufficiency and development of jaundice. Treatment
- 46. • It is a portable phototherapy device for the treatment of neonatal jaundice The name is a combination of bilirubin and blanket. • Biliblankets offer the possibility of treating some degrees of jaundice at home. • The baby is tied to the machine, unless they can wheel it around, and there is a stiff pad between the mother and baby. • Phototherapy for jaundice involves a blue/white light of varying intensity placed close to the skin or touching it through a special, light-permeable fabric. • The whole setup consists of the light generator, termed the light box, the fibre-optic cable through which the light is carried and the light pad, which is a 25cm x13cm (10"x5") pad that's attached to the baby. Biliblanket
- 47. Phototherapy
- 48. • 1950- The use of phototherapy was first discovered, accidentally, at Rochford Hospital in Essex, England, when a nurse, Sister Jean Ward, noticed that babies exposed to sunlight had reduced jaundice. • Dr. Perryman- a pathologist, who noticed that a vial of blood left in the sun had turned green. • Dr. Cremer, Richards and Dobbs put together these observations, leading to a landmark randomized clinical trial which was published in Pediatrics in 1968; it took another ten years for the practice to become established. • Niels Ryberg Finsen- Danish physician, founder of modern phototherapy.
- 49. • Bilirubin absorbs light optimally in the blue-green range (460 to 490 nm) • Mechanism: Bilirubin is photoisomerized and excreted in the bile or converted into lumirubin and excreted in the urine. - Eyes and genitalias (Boy) of the newborn must be covered and the maximum body surface area exposed to the light. - It is important to maintain hydration and urine output as most of the bilirubin is excreted in the urine as lumirubin. - The use of phototherapy is not indicated in conjugated Hyperbilirubinemia and may lead to the “bronze baby syndrome” with grayish-brown discoloration of the skin, serum, and urine. - After phototherapy is discontinued, there is an increase in the total serum bilirubin level known as the" rebound bilirubin." - The phototherapy involved is not ultraviolet light therapy. - Distance - 45 cm. - The penetration power of phototherapy is 2mm
- 50. Preferable to use either daylight (provides enhanced clinical observation and adequate efficacy) or blue light (better efficacy) Not green light which provides neither
- 51. • The baby is turned every 2 hrs or after each feed • Temp is monitored every 2-4 hrs • Weight is taken daily • More frequent breast feeds or 10-20% extra IV fluids are provided • STB is measured every 12 hrs • Phototherapy is discontinued if 2 STB values are < 10 mg/dl Side effects- Increased insensible water loss Loose green stools Hyperthermia / Hypothermia Rashes (erythema) Oxidative injury UV light irradiation Bronze baby syndrome
- 52. • Used for any newborn with a total serum bilirubin of greater than 25 mg/dl • Indicated if there is a risk of neurologic dysfunction with or without an attempt at phototherapy. • It is used to removed bilirubin from the circulation, and in iso-immune hemolysis removes circulating antibodies and sensitized red blood cells as well. • A double volume exchange blood transfusion (160 to 180 ml/kg) is performed, replacing the neonate’s blood in aliquots with crossed-matched blood. • Complications - electrolyte abnormalities like hypocalcemia and hyperkalemia, cardiac arrhythmias, thrombocytopenia, blood-borne infections, portal vein thrombosis, graft versus host disease, and necrotizing enterocolitis (nec) Exchange transfusions
- 53. N.B: Blood Volume = 70-90 ml/kg for term and 85-110 ml/kg for preterm infants One blood volume removes 65% of baby’s red cells. Two blood volumes removes 88% of baby’s red cells. <1000gms Use 5ml aliquots 1000-2000gm 10ml aliquots >2000gms 15ml aliquots
- 54. Maisel’s Chart STB (mg/dl) Birth Wt <24 hrs 24-48 hrs 49-72 hrs >72 hrs <5` All 5-9 All Phototherap y if hemolysis 10-14 <2500G -------------- >2500 G Exchange if hemolysis Phototherapy -------------------------------------------------- Investigate if STB > 12 mg/dl 15-19 <2500 g -------------- >2500 g Exchange Transfusion Consider exchange -------------------------------- Phototherapy 20 and More All Exchange Transfusion
- 56. Pharmacological Treatment 1. Phenobarbitone: Bilirubin processing including hepatic uptake, conjugation and its excretion are ameliorated by this agent thus helps in decreasing level of bilirubin. When used for 3–5 days in a dose of 5 mg/kg after birth prophylactically, it has shown to be effective in babies with hemolytic disease, extravasated blood and in pre-term without any significant side effects. 2. Intravenous Immunoglobulin (IVIG): High dose IVIG (0.5–1 gr/kg) has shown to be effective in decreasing the needs of exchange transfusion and phototherapy in babies with Rh hemolytic disease. 3. Metalloporphyrins: These compounds are still experimental but showing promising results in various hemolytic and non-hemolytic settings without significant side effects. 4. Administration of agar has been tried in an attempt to decrease the enterohepatic recirculation of conjugated bilirubin. It has not proved to be clinically useful and may cause intestinal obstruction. 5. Administration of glycerin suppositories to facilitate stooling has been evaluated as a potential method of preventing hyperbilirubinemia 6. Enteral prebiotics- Enterohepatic recirculation and delayed stooling contribute to perpetuation of hyperbilirubinemia. 7. L-aspartic acid and enzymatically hydrolyzed casein are known inhibitors of beta glucuronidase, the enzyme that promotes enterohepatic recirculation of conjugated bilirubin in the neonatal intestine.
- 57. Prevention • Early and frequent feeding • Adequate hydration • Administration of Anti-D injection to Rh negative mother Follow-up • Babies having roughly 20 mg/dl serum bilirubin and that requiring exchange transfusion should be kept under follow-up in the high risk clinic for neurodevelopmental outcome. • Hearing assessment (Brainstem Evoked Response Audiometry (BAER)) should be done at 3 months of corrected age.
- 58. Prognosis • With treatment, the prognosis is excellent. • In those with delayed treatment, brain damage is a major complication.
- 59. Thanks a lot