Neonatal jaundice
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This document discusses neonatal jaundice, including the physiology of bilirubin metabolism, causes of neonatal hyperbilirubinemia, clinical features of bilirubin encephalopathy, and management. It notes that degradation of red blood cells leads to bilirubin production, which is transported to the liver and conjugated by uridine diphosphate glucuronyl transferase. Neonatal jaundice can be physiologic or pathologic due to increased bilirubin production or impaired clearance. High bilirubin levels can cause acute or chronic bilirubin encephalopathy. Management involves evaluation, phototherapy, and exchange transfusion if needed to prevent neurological damage.
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This document discusses the pathophysiology of bilirubin-induced neurological dysfunction (BIND), commonly known as kernicterus. It begins with a brief history of kernicterus and describes the areas of the brain that are most intensely stained by bilirubin, including the basal ganglia. It then explains bilirubin chemistry and solubility, how the blood-brain barrier influences bilirubin entry into the brain, and various cellular mechanisms by which high bilirubin levels can damage neurons. Specifically, bilirubin can uncouple oxidative phosphorylation, interact with and damage membranes, and alter neurotransmitter metabolism. The document concludes by outlining the clinical spectrum of BIND, from acute
Neonatal jaundice
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A 22 month old male patient presented with loose stools, vomiting and yellowing of the skin. Laboratory tests found elevated bilirubin levels and decreased thyroid levels. The patient was diagnosed with neonatal jaundice likely caused by hypothyroidism and acute gastroenteritis. Treatment included antibiotics, antacids, antiemetics, probiotics and phototherapy to reduce bilirubin levels. The parents were advised to monitor for worsening jaundice using a bilirubin meter or skin color tests and seek medical care if additional symptoms developed.
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The document discusses jaundice in newborns. After birth, infants begin breaking down excess red blood cells produced before birth to cope with low oxygen levels in the womb. This releases bilirubin, which the liver normally converts to a water-soluble form excreted in urine. In jaundiced newborns, the liver is not yet mature enough to clear bilirubin quickly enough, allowing levels to rise and potentially cause brain damage if severe. Treatment focuses on phototherapy to convert bilirubin to a form the body can remove, with exchange transfusions in rare severe cases.
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This document summarizes neonatal jaundice. It notes that a bilirubin level over 5mg/dl causes clinical jaundice in newborns, typically progressing from head to toe. About 50-60% of babies are affected in the first week of life. Physiological jaundice is most common, caused by immature liver pathways and the breakdown of fetal hemoglobin. It describes the typical phases and timelines of physiological jaundice. Pathological jaundice has specific criteria for onset, rise in bilirubin levels, and total bilirubin levels. Causes, clinical assessment, treatment with phototherapy or exchange transfusions, and complications like kernicterus are also outlined
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This document provides an overview of hyperbilirubinemia in newborns. It begins with a brief introduction and outline. It then covers topics like bilirubin physiology including heme catabolism, transport, hepatic uptake, and conjugation. It discusses bilirubin toxicity and the factors that influence the rate of bilirubin production and elimination. It also covers differential diagnosis, "vigintiphobia" or fear of bilirubin levels reaching 20, workup, treatment including phototherapy, and breast milk jaundice. Key points emphasized are the importance of interpreting bilirubin levels based on an infant's age in hours, major and minor risk factors, and indications for phototherapy in
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Jaundice is the most common condition that requires medical attention in newborns. The yellow coloration of the skin and sclera in newborns with jaundice is the result of accumulation of unconjugated bilirubin.
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Neonatal jaundice
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A 22 month old male patient presented with loose stools, vomiting and yellowing of the skin. Laboratory tests found elevated bilirubin levels and decreased thyroid levels. The patient was diagnosed with neonatal jaundice likely caused by hypothyroidism and acute gastroenteritis. Treatment included antibiotics, antacids, antiemetics, probiotics and phototherapy to reduce bilirubin levels. The parents were advised to monitor for worsening jaundice using a bilirubin meter or skin color tests and seek medical care if additional symptoms developed.
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- Feeding may begin with intravenous fluids or a nasogastric tube and progress to breastfeeding. Nutritional needs for protein, carbohydrates, fats, vitamins and minerals must be met.
- Ongoing monitoring of vital signs and development is needed to detect any issues and provide appropriate treatment and care. Immunizations should also be given according to schedule.
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The document discusses jaundice in newborns. After birth, infants begin breaking down excess red blood cells produced before birth to cope with low oxygen levels in the womb. This releases bilirubin, which the liver normally converts to a water-soluble form excreted in urine. In jaundiced newborns, the liver is not yet mature enough to clear bilirubin quickly enough, allowing levels to rise and potentially cause brain damage if severe. Treatment focuses on phototherapy to convert bilirubin to a form the body can remove, with exchange transfusions in rare severe cases.
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This document summarizes neonatal jaundice. It notes that a bilirubin level over 5mg/dl causes clinical jaundice in newborns, typically progressing from head to toe. About 50-60% of babies are affected in the first week of life. Physiological jaundice is most common, caused by immature liver pathways and the breakdown of fetal hemoglobin. It describes the typical phases and timelines of physiological jaundice. Pathological jaundice has specific criteria for onset, rise in bilirubin levels, and total bilirubin levels. Causes, clinical assessment, treatment with phototherapy or exchange transfusions, and complications like kernicterus are also outlined
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This document provides an overview of hyperbilirubinemia in newborns. It begins with a brief introduction and outline. It then covers topics like bilirubin physiology including heme catabolism, transport, hepatic uptake, and conjugation. It discusses bilirubin toxicity and the factors that influence the rate of bilirubin production and elimination. It also covers differential diagnosis, "vigintiphobia" or fear of bilirubin levels reaching 20, workup, treatment including phototherapy, and breast milk jaundice. Key points emphasized are the importance of interpreting bilirubin levels based on an infant's age in hours, major and minor risk factors, and indications for phototherapy in
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Neonatal jaundice is a yellowish discoloration of the skin due to high bilirubin levels in newborns. Nearly 60% of term newborns experience jaundice in the first week of life. High bilirubin levels can be toxic to the developing brain. Jaundice is caused by physiological or pathological factors like blood incompatibilities or liver diseases. It is important to monitor bilirubin levels closely in newborns as severe jaundice can lead to kernicterus, a neurological condition causing cerebral palsy or hearing loss.
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Neonatal jaundice is one of the most common conditions in newborns. It is caused by high levels of bilirubin in the blood which causes yellowing of the skin. Physiological jaundice is common and appears after 24 hours, peaks by days 3-5, and resolves by 14 days without treatment. Pathological jaundice appears within 24 hours and requires treatment. Proper assessment includes history, physical exam, and lab tests to determine severity and risk of complications like acute bilirubin encephalopathy. Treatment may include phototherapy or exchange transfusion in severe cases. Close monitoring is important to prevent bilirubin neurotoxicity in newborns.
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NEONATAL JAUNDICE 8/12/2015(HOWRAH)
MY NAME IS DR.M.SUDARSHAN REDDY,DNB(PAEDS) POSTGRADUATE TRAINEE,HOWRAH GENERAL HOSPITAL,HOWRAH,WEST-BENGAL.
Jaundice in newborn
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NEONATAL JAUNDICE
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neonatal jaundice
Neonatal jaundice is common, affecting 60% of term and 80% of preterm infants. It can signal illness but may also cause neurological damage if bilirubin levels are too high. Jaundice is either physiological, appearing after 24-72 hours and resolving by 2 weeks, or pathological, appearing within 24 hours with rapidly rising bilirubin or lasting over 2 weeks. Pathological jaundice requires treatment while physiological jaundice needs monitoring. Breast milk jaundice causes mild jaundice persisting up to 3 months. Conditions like Rh and ABO incompatibility can cause pathological jaundice through hemolysis. Very high unconjugated bilirubin levels can cross the blood
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This document discusses neonatal jaundice and hyperbilirubinemia. It notes that jaundice is common in newborns, occurring in 60% of term and 80% of preterm infants. While usually benign, high bilirubin levels can be toxic to the brain. The document reviews causes of jaundice, risk factors, methods of assessing bilirubin levels like transcutaneous bilirubin monitoring, and treatments including phototherapy, fluid therapy, exchange transfusions. It provides guidelines for treatment thresholds and follow-up based on gestational age and risk level.
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This document provides information on neonatal hyperbilirubinemia or jaundice. It defines jaundice and discusses the mechanisms and risk factors for both physiologic and pathologic hyperbilirubinemia in newborns. It outlines the evaluation, management, and treatment of hyperbilirubinemia including phototherapy and exchange transfusion. The major points covered are the definition of jaundice, causes of increased and decreased bilirubin levels in newborns, clinical assessment and lab evaluation of hyperbilirubinemia, guidelines for phototherapy and exchange transfusion, and methods to optimize phototherapy treatment.
Neonatal jaundice cpg
This document summarizes information about neonatal jaundice from the Neonatology Department at Hadi Clinic. It discusses the definition of neonatal jaundice as a high bilirubin level in the blood. It describes physiological and pathological jaundice and their causes. It also outlines risk factors for jaundice, evaluation and treatment methods like phototherapy and exchange transfusion, and references guidelines on the treatment of hyperbilirubinemia in infants.
Approach to neonatal jaundice
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references : Cloherty And Stark's Manual Of Neonatal Care
AIIMS Protocol In Neonatology
Care Of The Newborn – Meherban Singh
Hyperbilirubinemia
This document discusses hyperbilirubinemia (excess bilirubin in the blood), including its definition, causes, pathophysiology, complications, management, and a plan of care for babies with the condition. It defines hyperbilirubinemia as jaundice caused by a yellowish discoloration. Risk factors and two types - physiological and pathological - are outlined. Management involves assessing jaundice clinically, intensive phototherapy, and exchange blood transfusions if necessary. A nursing procedure for exchange transfusions is also detailed.
Neonatalcasepresentation 131018051020-phpapp01 (1)
A 22 day old male baby was brought to the hospital with complaints of fever for 2 days, fits for 2 days, and reluctance to feed for 1 day. The baby's birth history included delivery via normal vaginal delivery at 38 weeks gestation with delayed and weak crying, peripheral cyanosis, and no jaundice. On examination, the baby had decreased tone and hyperactive reflexes. Investigations revealed ischemic encephalopathy involving multiple regions of the brain. The baby was diagnosed with hypoxic ischemic encephalopathy secondary to birth asphyxia and treated accordingly.
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Physiologic jaundice is a common cause of hyperbilirubinemia in newborns resulting from increased bilirubin production, shortened RBC lifespan, and hepatic immaturity. It presents between 2-10 days of life with indirect bilirubin levels <12 mg/dL in term infants peaking on day 3. Kernicterus is a neurological syndrome caused by bilirubin deposition in the brain and can be prevented by avoiding excessively high indirect bilirubin levels >25 mg/dL. Diagnosis of hyperbilirubinemia involves history, physical exam, and laboratory tests including total, direct and indirect bilirubin levels as well as blood typing if levels are
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This document discusses neonatal jaundice (hyperbilirubinemia) in infants. It covers the definition, causes, types (physiological vs pathological), investigations, management including phototherapy and exchange transfusion, and prevention of kernicterus. Key points include:
- Jaundice is caused by high bilirubin levels which cause yellowing of the skin and eyes. Bilirubin is produced from the breakdown of red blood cells.
- Physiological jaundice appears after 24-72 hours and is common, while pathological jaundice appears within 24 hours and requires treatment.
- Management involves phototherapy to reduce bilirubin levels or exchange transfusion for severe
Neonatal jaundice
This document discusses neonatal jaundice, also known as hyperbilirubinemia. It defines jaundice as an excessive level of bilirubin in the blood characterized by yellowing of the skin. It distinguishes between physiological jaundice, which occurs in most newborns and resolves on its own, and pathological jaundice, which requires treatment. The causes, diagnostic evaluation, therapeutic management including phototherapy, and nursing considerations for babies with hyperbilirubinemia are described in detail. The goals of treatment are to reduce bilirubin levels and prevent complications like bilirubin toxicity.
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This document provides an outline and overview of neonatal jaundice (NNJ). It begins with an introduction defining NNJ and noting that it is one of the most common conditions in newborns. It then covers the pathophysiology of jaundice, classifications of jaundice, assessment of patients including history, physical exam and investigations. It discusses complications of NNJ including acute and chronic bilirubin encephalopathy. Finally, it outlines the management of NNJ including phototherapy, exchange transfusion and pharmacological interventions.
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Neonatal jaundice
Neonatal jaundice is a yellowish discoloration of the skin due to high bilirubin levels in newborns. Nearly 60% of term newborns experience jaundice in the first week of life. High bilirubin levels can be toxic to the developing brain. Jaundice is caused by physiological or pathological factors like blood incompatibilities or liver diseases. It is important to monitor bilirubin levels closely in newborns as severe jaundice can lead to kernicterus, a neurological condition causing cerebral palsy or hearing loss.
Neonatal jaundice(reference msia cpg)
Neonatal jaundice is one of the most common conditions in newborns. It is caused by high levels of bilirubin in the blood which causes yellowing of the skin. Physiological jaundice is common and appears after 24 hours, peaks by days 3-5, and resolves by 14 days without treatment. Pathological jaundice appears within 24 hours and requires treatment. Proper assessment includes history, physical exam, and lab tests to determine severity and risk of complications like acute bilirubin encephalopathy. Treatment may include phototherapy or exchange transfusion in severe cases. Close monitoring is important to prevent bilirubin neurotoxicity in newborns.
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This document discusses neonatal jaundice (hyperbilirubinemia). It defines jaundice as an excessive level of bilirubin in the blood characterized by yellowing of the skin. It distinguishes between physiological and pathological jaundice. The causes, pathophysiology, complications, diagnostic evaluation and management including phototherapy, exchange transfusion and drugs are described in detail over multiple pages.
NEONATAL JAUNDICE 8/12/2015(HOWRAH)
MY NAME IS DR.M.SUDARSHAN REDDY,DNB(PAEDS) POSTGRADUATE TRAINEE,HOWRAH GENERAL HOSPITAL,HOWRAH,WEST-BENGAL.
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Jaundice in newborns, also known as neonatal jaundice, is caused by high levels of bilirubin in the bloodstream and tissues. It can be either physiological, appearing 2-3 days after birth due to the normal breakdown of red blood cells, or pathological, caused by excessive red cell breakdown or liver/bilirubin processing issues. Pathological jaundice is diagnosed based on bilirubin levels and may require treatment like phototherapy or exchange transfusions to prevent kernicterus, a potentially serious brain condition caused by high bilirubin levels. Treatment aims to lower bilirubin through phototherapy or medications while monitoring for complications.
NEONATAL JAUNDICE
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neonatal jaundice
Neonatal jaundice is common, affecting 60% of term and 80% of preterm infants. It can signal illness but may also cause neurological damage if bilirubin levels are too high. Jaundice is either physiological, appearing after 24-72 hours and resolving by 2 weeks, or pathological, appearing within 24 hours with rapidly rising bilirubin or lasting over 2 weeks. Pathological jaundice requires treatment while physiological jaundice needs monitoring. Breast milk jaundice causes mild jaundice persisting up to 3 months. Conditions like Rh and ABO incompatibility can cause pathological jaundice through hemolysis. Very high unconjugated bilirubin levels can cross the blood
Jaundice
This document discusses neonatal jaundice and hyperbilirubinemia. It notes that jaundice is common in newborns, occurring in 60% of term and 80% of preterm infants. While usually benign, high bilirubin levels can be toxic to the brain. The document reviews causes of jaundice, risk factors, methods of assessing bilirubin levels like transcutaneous bilirubin monitoring, and treatments including phototherapy, fluid therapy, exchange transfusions. It provides guidelines for treatment thresholds and follow-up based on gestational age and risk level.
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introduction, physiology, pathology, causes, clinical features, predisposing factors of neonatal jaundice.
Physiological Neonatal Jaundice
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Neonatal hyperbilirubinemia
This document provides information on neonatal hyperbilirubinemia or jaundice. It defines jaundice and discusses the mechanisms and risk factors for both physiologic and pathologic hyperbilirubinemia in newborns. It outlines the evaluation, management, and treatment of hyperbilirubinemia including phototherapy and exchange transfusion. The major points covered are the definition of jaundice, causes of increased and decreased bilirubin levels in newborns, clinical assessment and lab evaluation of hyperbilirubinemia, guidelines for phototherapy and exchange transfusion, and methods to optimize phototherapy treatment.
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This document summarizes information about neonatal jaundice from the Neonatology Department at Hadi Clinic. It discusses the definition of neonatal jaundice as a high bilirubin level in the blood. It describes physiological and pathological jaundice and their causes. It also outlines risk factors for jaundice, evaluation and treatment methods like phototherapy and exchange transfusion, and references guidelines on the treatment of hyperbilirubinemia in infants.
Approach to neonatal jaundice
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references : Cloherty And Stark's Manual Of Neonatal Care
AIIMS Protocol In Neonatology
Care Of The Newborn – Meherban Singh
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This document discusses hyperbilirubinemia (excess bilirubin in the blood), including its definition, causes, pathophysiology, complications, management, and a plan of care for babies with the condition. It defines hyperbilirubinemia as jaundice caused by a yellowish discoloration. Risk factors and two types - physiological and pathological - are outlined. Management involves assessing jaundice clinically, intensive phototherapy, and exchange blood transfusions if necessary. A nursing procedure for exchange transfusions is also detailed.
Neonatalcasepresentation 131018051020-phpapp01 (1)
A 22 day old male baby was brought to the hospital with complaints of fever for 2 days, fits for 2 days, and reluctance to feed for 1 day. The baby's birth history included delivery via normal vaginal delivery at 38 weeks gestation with delayed and weak crying, peripheral cyanosis, and no jaundice. On examination, the baby had decreased tone and hyperactive reflexes. Investigations revealed ischemic encephalopathy involving multiple regions of the brain. The baby was diagnosed with hypoxic ischemic encephalopathy secondary to birth asphyxia and treated accordingly.
Neonatal jaundice
Physiologic jaundice is a common cause of hyperbilirubinemia in newborns resulting from increased bilirubin production, shortened RBC lifespan, and hepatic immaturity. It presents between 2-10 days of life with indirect bilirubin levels <12 mg/dL in term infants peaking on day 3. Kernicterus is a neurological syndrome caused by bilirubin deposition in the brain and can be prevented by avoiding excessively high indirect bilirubin levels >25 mg/dL. Diagnosis of hyperbilirubinemia involves history, physical exam, and laboratory tests including total, direct and indirect bilirubin levels as well as blood typing if levels are
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This document discusses neonatal hyperbilirubinemia and provides guidelines for phototherapy treatment. It outlines various risk factors that can increase the risk of significant jaundice in infants, such as gestational age, race, family history of jaundice, and conditions that can cause hemolysis like ABO incompatibility. It also discusses the potential consequences of untreated high bilirubin levels, known as kernicterus, which can lead to neurological damage or death. Guidelines are provided on assessing jaundice risk based on bilirubin levels and thresholds for phototherapy treatment in hospitalized infants 35 weeks or more gestation.
Neonatal jaundice
This document discusses neonatal jaundice (hyperbilirubinemia) in infants. It covers the definition, causes, types (physiological vs pathological), investigations, management including phototherapy and exchange transfusion, and prevention of kernicterus. Key points include:
- Jaundice is caused by high bilirubin levels which cause yellowing of the skin and eyes. Bilirubin is produced from the breakdown of red blood cells.
- Physiological jaundice appears after 24-72 hours and is common, while pathological jaundice appears within 24 hours and requires treatment.
- Management involves phototherapy to reduce bilirubin levels or exchange transfusion for severe
Neonatal jaundice
This document discusses neonatal jaundice, also known as hyperbilirubinemia. It defines jaundice as an excessive level of bilirubin in the blood characterized by yellowing of the skin. It distinguishes between physiological jaundice, which occurs in most newborns and resolves on its own, and pathological jaundice, which requires treatment. The causes, diagnostic evaluation, therapeutic management including phototherapy, and nursing considerations for babies with hyperbilirubinemia are described in detail. The goals of treatment are to reduce bilirubin levels and prevent complications like bilirubin toxicity.
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This document provides an outline and overview of neonatal jaundice (NNJ). It begins with an introduction defining NNJ and noting that it is one of the most common conditions in newborns. It then covers the pathophysiology of jaundice, classifications of jaundice, assessment of patients including history, physical exam and investigations. It discusses complications of NNJ including acute and chronic bilirubin encephalopathy. Finally, it outlines the management of NNJ including phototherapy, exchange transfusion and pharmacological interventions.
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This document discusses neonatal jaundice, including its definition, etiology, bilirubin production and metabolism, types of hyperbilirubinemia, causes, clinical features, kernicterus, and treatment options. Neonatal jaundice is caused by increased bilirubin levels and results in a yellowish skin and eye discoloration. Bilirubin is produced from the breakdown of hemoglobin. Treatment depends on the type and severity of hyperbilirubinemia, and may include phototherapy, exchange blood transfusions, or medications to increase bilirubin clearance from the liver.
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This document summarizes the findings of a systematic review examining the effects of various treatments for unconjugated hyperbilirubinemia in term and preterm infants. The review assessed outcomes such as mortality, neurological effects, and serum bilirubin levels. The review found that hospital phototherapy reduces serum bilirubin levels compared to no treatment. It also found that low threshold phototherapy may reduce neurodevelopmental impairment compared to high threshold phototherapy in some populations, though it increases the duration of phototherapy. Exchange transfusion and immunoglobulin also show benefits, but their effects on long-term outcomes are unclear from the available evidence. The effectiveness of other interventions like albumin infusion and home phototherapy remain uncertain based
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This document summarizes evidence from a systematic review on treatments for neonatal jaundice. The main points are:
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- Exchange transfusion is likely effective at reducing serum bilirubin levels, though direct evidence is lacking. It carries risks of mortality and permanent sequelae.
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This document summarizes evidence from a systematic review on treatments for neonatal jaundice. The main points are:
- Hospital phototherapy is effective at reducing jaundice compared to no treatment, as measured by serum bilirubin levels. Low threshold phototherapy may reduce neurodevelopmental impairment compared to high threshold phototherapy.
- Exchange transfusion is likely effective at reducing serum bilirubin levels, though direct evidence is limited. Immunoglobulin may reduce the need for exchange transfusion in infants with hemolytic jaundice.
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Over 60% of newborns experience jaundice due to the normal physiological breakdown of red blood cells in the first few days after birth. Unconjugated bilirubin can potentially be deposited in the brain, causing kernicterus. The liver's ability to conjugate and excrete bilirubin is impaired in preterm and ill newborns compared to healthy full term babies. Conditions like sepsis, hemolytic disease, or liver dysfunction can also cause pathological jaundice beyond the first 2 weeks of life. Timely diagnosis and treatments like phototherapy and exchange transfusion are important to prevent bilirubin encephalopathy.
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The document discusses neonatal jaundice, including physiological jaundice in babies. It describes jaundice as yellow discoloration of the skin and eyes caused by high bilirubin levels. Physiological jaundice is common and due to liver immaturity in newborns. It typically appears 2-4 days after birth and resolves within 1-2 weeks. The document also outlines risk factors for severe neonatal jaundice, methods for detecting and assessing jaundice severity, management approaches like phototherapy and exchange transfusion, as well as complications.
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Neonatal jaundice, or hyperbilirubinemia, refers to the yellowing of the skin and eyes in newborn babies due to high levels of bilirubin. It is common and usually harmless, but can become a medical emergency if bilirubin levels get too high. The document discusses the causes, presentation, risk factors, evaluation, and management of physiological and pathological neonatal jaundice. Key points include that physiological jaundice is due to liver immaturity and resolves by 2 weeks, while pathological jaundice requires further workup and may necessitate phototherapy or exchange transfusion to prevent complications like kernicterus.
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This document provides information about neonatal jaundice and retinopathy of prematurity (ROP). It defines these conditions and discusses their risk factors, etiology, types, diagnostic evaluation, and management. For neonatal jaundice, the document covers bilirubin metabolism, risk factors, types of jaundice, evaluation, complications like kernicterus, and treatment methods like phototherapy and exchange transfusion. For ROP, it describes the abnormal blood vessel growth in the retina that can lead to blindness if left untreated.
Newborn hyperbilirubinemia
Breast milk jaundice.
The key features that point to breast milk jaundice in this case are:
- Jaundice onset after the first week of life
- Progressive deepening of jaundice over 1 week
- Exclusively breastfed
- Pale/gray stool color indicating reduced bilirubin conjugation
Breast milk jaundice results from high levels of beta-glucuronidase in breast milk interfering with bilirubin conjugation in the infant's liver and gut. It typically presents after the first week of life and can persist for several weeks if breastfeeding continues.
Icterus neonatorum presentation for students
Introduction
Definition
Metabolism and excretion of bilirubin
Causes
Symptoms
Types
Physiological jaundice
Pathological jaundice
Breast milk jaundice
Neo natal jaundice is a yellow discoloration of the white part of the eyes and skin in a newborn baby due to high bilirubin level.
Neo natal jaundice becomes apparent at serum bilirubin concentration of 5-7mg / dL.
Shoulder and trunk 8-10mg/dl
Lower body – 10-12mg/dl.
Entire body 12-15 mg /DL
Jaundice presentation
This document defines jaundice as hyperbilirubinemia, an excessive level of bilirubin in the blood, and differentiates between physiological and pathological jaundice. It states that kernicterus, caused by unconjugated bilirubin deposits in the brain, is the most dangerous complication. An approach to evaluating a jaundiced baby includes assessing age, risk factors, and signs of kernicterus, and determining if jaundice is physiological or pathological by considering time of onset and duration. Workup may include bilirubin levels, blood typing, and additional tests depending on the situation. Treatment options include increasing feeding, phototherapy, and exchange transfusion for more severe cases.
Copy of 2,Neonatal_Jaundice.pptx
Neonatal jaundice is caused by an accumulation of unconjugated bilirubin in the blood and tissues. Physiological jaundice appears between 2-4 days of life, peaks at 5-6 mg/dL by days 2-4, and resolves by days 5-7. Pathological jaundice appears within 24 hours, bilirubin increases more than 5 mg/dL per day, persists past 14 days, or direct bilirubin is elevated. Causes include hemolytic diseases, breastfeeding, infections, and genetic disorders affecting bilirubin metabolism. Timely diagnosis and treatment are important to prevent neurotoxicity and kernicterus.
PHYSIOLOGICAL JAUNDICE.ppt
Physiological jaundice is common in newborns and results from the breakdown of excess red blood cells. It peaks between 48-72 hours of life and usually resolves by 1 week. The bilirubin produced is initially unconjugated and insoluble, but is converted in the liver to conjugated bilirubin which is water soluble and excreted in bile and urine. For some infants, phototherapy may be needed to prevent bilirubin levels from rising too high and posing a risk of kernicterus, or permanent brain damage from bilirubin toxicity. Proper feeding and care can help resolve physiological jaundice, while monitoring bilirubin levels helps guide treatment and management
jaundice.pptx
This document discusses neonatal jaundice, including its causes, types, and treatments. It notes that nearly all newborns develop transient hyperbilirubinemia and nearly 65% are clinically jaundiced. Jaundice in the first 24 hours is always pathological. Kernicterus results from deposition of unconjugated bilirubin in brain cells and can be prevented by treatments like phototherapy and exchange transfusion when bilirubin levels are high. The document outlines the mechanisms, types, and management of both unconjugated and conjugated hyperbilirubinemia.
Neonatal icterus.pptx
This document discusses neonatal jaundice, also known as neonatal icterus. Some key points:
- Neonatal jaundice is very common, affecting 25-60% of full term and 75-85% of preterm newborns. It is characterized by elevated bilirubin levels in the blood.
- Jaundice can be physiological (due to normal newborn processes) or pathological (due to underlying conditions). The causes, signs, diagnosis, complications and various treatment methods like phototherapy are described.
- Kernicterus, a type of brain damage caused by high bilirubin levels, is a serious potential complication if jaundice is not properly managed.
Neonatal Jaundice
This document provides an overview of neonatal jaundice presented by Dr. Binaya Dhakal of Shree Birendra Hospital. It discusses the metabolism of bilirubin, types of neonatal jaundice including physiological, pathological, breastfeeding and breast milk jaundice. It also covers the evaluation, causes, approach and management of hyperbilirubinemia as well as prolonged hyperbilirubinemia. Management options discussed include phototherapy, intravenous immunoglobulins, exchange transfusion and metalloporphyrins. The document concludes with information on kernicterus.
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Neonatal jaundice
- 2. Physiology of bilirubin metabolism Mechanisms of neonatal jaundice Risk factors for neonatal jaundice Causes of neonatal hyperbilirubinaemia Clinical features of bilirubin encephalopathy Key elements in management of neonatal jaundice
- 3. Degradation of RBCs leads to release of haemoglobin Heme part degraded to biliverdin and carbon monoxide Enzyme biliverdin reductase reduces biliverdin to unconjugated bilirubin Unconjugated bilirubin binds to albumin and is transported to the liver(enzyme responsible for this is urudine diphosphate glucuronyl transferase/ UGT1A1)
- 5. a) Physiologic jaundice: Commonly occurs in newborns Occurs after day 1 and may persist up to 2 weeks in preterms Usually resolves without sequelae b) Pathologic jaundice: Increased bilirubin production Deficiency of hepatic uptake Impaired conjugation of bilirubin Increased entero-hepatic circulation
- 6. a. Increased bilirubin production: newborns have a high Hb and short life span of RBC. This translates to a high rate of bilirubin production. b. Impaired ability to extract bilirubin from the body c. Immature glucuronyl transferase activity
- 7. Increased bilirubin production: Haemolytic disease due to: ABO isoimmunisation, Rh, enzyme defects and structural defects Birth trauma: Cephalohaematoma, excessive bruising Polycaethemia Impaired bilirubin conjugation: Gilbert syndrome Crigler-Najjar syndrome l and ll Human milk jaundice
- 8. Decreased bilirubin production: as a result of biliary obstruction. Causes of obstruction include: Biliary atresia, choledochal cysts…….. Other causes: Prematurity Maternal diabetes Infections like sepsis, UTI Drugs eg streptomycin, chloramphenicol…..
- 9. Acute bilirubin encephalopathy occurs in three phases in the first few weeks after birth The three phases include: Phase 1: poor suck, high pitched cry, stupor, hypotonia and seizures. This occurs in the first 1 to 2 days Phase 2: Hypertonia of extensor muscles, opisthotonus, retrocollis and fever. This occurs in the middle of the first postnatal week Phase 3: Occurs after the first post natal week. Presents with hypertonia
- 11. If bilirubin levels remain high, long term morbidity can result Unconjugated bilirubin easily crosses the BBB causing neuronal injury This injury occurs primarily in the basal ganglia and brainstem nuclei. In severe forms, the hippocampus and cerebellum may be affected
- 12. The long term morbidity after neuronal injury is referred to as kernicterus This occurs in two phases: ◦ Phase 1: first post natal year: hypotonia, active deep tendon reflexes, obligatory tonic neck reflex, delayed motor skills ◦ Phase 2: choreoathetotic CP, ballismus, tremor, upward gaze, dental dysplasia, sensorineural hearing loss and cognitive impairment
- 15. Evaluation: ◦ Blood group and Rh determination for pregnant women ◦ Infant’s blood group and Rh, Coomb’s test ◦ Clinical examination: Cephalocaudal progression ◦ Total serum bilirubin(TSB), CBC ◦ Infection screen ◦ Abdominal ultrasound ◦ TSB concentration should be rechecked every 4-24 hours depending on risk factors
- 16. Main aim is to prevent bilirubin encephalopathy Phototherapy and exchange transfusion are the mainstays of management All newborns with jaundice MUST receive phototherapy Important to treat underlying cause as well. Eg if there’s infection
- 19. Indicated in toxic levels of bilirubin Removes bilirubin and antibodies. Double volume used Corrects anaemia Mortality 1% Complications 12% Takes 1-2 hours
- 20. Infection Portal venous thrombosis Thrombocytopenia Necrotizing enterocolitis Electrolyte imbalance Graft versus host disease Death!!