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neonatology

neonatology. BIRTH ASPHYXIA. DEFINITION. Birth asphyxia is defined as interrupted gas exchange from either placental or lung dysfunction resulting in failure of a newborn to initiate and establish spontaneous respiration after birth. The evidence of birth asphyxia at birth is delayed cry.

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neonatology

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  1. neonatology

  2. BIRTH ASPHYXIA

  3. DEFINITION • Birth asphyxia is defined as interrupted gas exchange from either placental or lung dysfunction resulting in failure of a newborn to initiate and establish spontaneous respiration after birth. • The evidence of birth asphyxia at birth is delayed cry

  4. Classification of birth asphyxia USING THE APGAR SCORE Severe birth asphyxia (<3) Moderate birth asphyxia (4-5) Mild birth asphyxia (6-7) Normal APGAR Score (>7)

  5. Aetiology of birth asphyxia • ANTEPARTUM CAUSES • Maternal diabetes mellitus • Pregnancy indused hypertension • Chronic hypertension • APH • Prematurity and post maturity

  6. Intrapartum causes • Cephalopelvic disproportion • Cord accidents • Prolonged labour • Precipitate labour • Prolonged rupture of membrane

  7. Postpartum • Cerebral defect • Narcotics the depresses respiratory centre • RDS • Choanal atresia • Laryngeal webs • etc

  8. complications • Short term complications • CNS- HYPOXIC ISCHAEMIC ENCEPHALOPATHY • CVS- CONGESTIVE CARDIAC FAILURE • RENAL- RENAL FAILURE • PULMONARY-PULMONARY HYPERTENSION AND HAEMORRHAGE • HAEM-DIC • METABOLIC –SIADH,HYPOGLYCAEMIA, HYPOCAL.., HYPONA… • INTEGUMENT SUBCUTANOUS FAT NECROSIS • GIT-NEC

  9. LONG TERM COMPLICATION • Asphyxia neonatorum is the most important avoidable cause of permanent neurological injury affecting the newborn

  10. SPASTIC CEREBRAL PALSY • MENTAL RETARDATION • HYDROCEPHALUS • MICROCEPHALY • DELAYED DEVELOPMENTAL MILESTONE • CORTICAL BLINDNESS • HEARING DEFICITS • EPILEPSY

  11. TREATMENT • There is no specific treatment for birth asphyxia- hence supportative care • Induction of hypothermia (selective brain cooling)

  12. prognosis • Severe birth asphyxia • 50% mortality • 80% of survivors are left with serious sequelae • Moderate birth asphyxia, 30-50% of survivors have serious long term deficits

  13. prevention • General health promotion • Specific intervention • Early diagnosis and prompt treatment • Limitation of disability • rehabilitation

  14. QUESTION

  15. NEONATAL JaUNDICE

  16. DEFINITION • Jaundice is the yellow discolouration of the skin, mucous membranes and sclera. • Jaundice is a sign of hyperbilirubinaemia • There are 3 principal mechanisms through which jaundice may arise • increased bilirubin load (from a high rate of Hb catabolism) • defective conjugation(e.g in hepatic disease) • defective excretion(e.g from intra or extra hepatic block)

  17. Neonatal jaundice could be 1.Physiological jaundice 2.Pathological jaundice

  18. Physiological jaundice • Jaundice appearing on the 2nd or 3rd day of life • Peak in the 3-5day of life and disappear within 10days in term infant or 14 days in preterm infants • Serum bilirubin level usually never exceed 12mg/dl in term infant or 15mg in preterm • The rate of rise of bilirubin is <5mg/dl per day or 0.5mg/dl per house • The baby is otherwise normal(no anaemia, or hepatosplenomegaly)

  19. Pathological jaundice ? • 1.jaundice appearing on the first day of life • 2.Total serum bilirubin concentration >12mg/dl • 3.The rate of rise of serum bilirubin is >0.5mg/dl/hour or >5mg/dl/day • 4.conjugated bilirubin of >2mg/dl • 5.clinical jaundice persisting for more than 2weeks • 6.evidence of haemolysis

  20. A diagnosis of physiological jaundice should rarely be made in preterm infants

  21. Aetiology -AGIP • ABO INCOMPATIBILITY • G6PD DEFICIENCY • INFECTION • PREMATURITY

  22. THE COMMON CAUSES OF PROLONGED JAUNDICE UTI Down syn Cretinism Neonatal hepatitis Hypothyroidism Galactosaemia Biliary atresia Inborn error Crigler Najjar and gilbert syn

  23. Mention one drug associated with jaundice Differentiate between breastmilk jaundice and breastfeeding jaundice List 10 investigations you will order in the mgt of NNJ

  24. kernicterus • Kernicterus or bilirubin encephalopathy is a neurologic syndrome resulting from the deposition of unconjugated (indirect) bilirubin in the basal ganglia and brainstem nuclei • The development of kernicterus is dependent on 1.Level of unconjugated bilirubin 2.Duration of exposure to elevated level 3.The cause of the jaundice 4.Infant’s well being

  25. Factors that potentiate the movement of bilirubin across the bbb and into brain cell • Hypoproteinaemia • Acidosis • Hypothermia • Hypoglycaemia • Prematurity • Infection • dehydration

  26. Modalities of management of nnj • Phototherapy • Exchange blood transfusion • Pharmacotherapy • immunotherapy

  27. phot0therapy

  28. Indications for phototherapy • Prevention of hyperbilirubinaemia in preterm LBW infants • Treatment of moderate hyperbilirubinaemia • Post EBT to accelerate excretion and prevent rebound hyperbilirubinaemia

  29. Mechanisms of action • Photooxidation • Photo isomerization(4z, 15z -4z,15E) • Structural isomerization- lumirubin

  30. Facts to note • The standard phototherapy is 8-10mW/cm2/nm • Intensive phototherapy >30mW/cm/nm • Phototherapy lowers bilirubin by 1-2mg/dl over 4-6hours • The bilirubin should be monitored every 12-24hrs

  31. Factors influencing efficacy of phototherapy • The spectral qualities of the light delivered( the wavelength range and peak) • The intensity of the light i.e the irradiance-The irradiance depends on the distance blw the baby and the light. this is the critical determinant of the effectiveness of phototherapy • The surface area of infant exposed to phototherapy • The total bilirubin at presentation • The aetiology of jaundice • Duration of exposure

  32. Exchange blood transfusion • Serum bilirubin level of 10mg/dl by 24hrs of live • Serum bilirubin level of 15mg/dl by 48hours of life • Serum bilirubin 20mg/dl @ any age • Rate of rise of serum bilirubin >5mg/dl/day or >0.5mg/dl/hour • The appearance of clinical signs suggesting kernicterus is indication for EBT at any level of SB

  33. question

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