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 ID: 1009746
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1. neonatology
2. BIRTH ASPHYXIA
3. DEFINITIONBirth 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 asphyxiaUSING THE APGAR SCORESevere birth asphyxia (<3)Moderate birth asphyxia (4-5)Mild birth asphyxia (6-7)Normal APGAR Score (>7)
5. Aetiology of birth asphyxiaANTEPARTUM CAUSESMaternal diabetes mellitusPregnancy indused hypertensionChronic hypertensionAPHPrematurity and post maturity
6. Intrapartum causesCephalopelvic disproportionCord accidentsProlonged labourPrecipitate labourProlonged rupture of membrane
7. PostpartumCerebral defectNarcotics the depresses respiratory centreRDSChoanal atresiaLaryngeal websetc
8. complicationsShort term complicationsCNS- HYPOXIC ISCHAEMIC ENCEPHALOPATHYCVS- CONGESTIVE CARDIAC FAILURERENAL- RENAL FAILUREPULMONARY-PULMONARY HYPERTENSION AND HAEMORRHAGEHAEM-DICMETABOLIC –SIADH,HYPOGLYCAEMIA, HYPOCAL.., HYPONA…INTEGUMENT SUBCUTANOUS FAT NECROSISGIT-NEC
9. LONG TERM COMPLICATIONAsphyxia neonatorum is the most important avoidable cause of permanent neurological injury affecting the newborn
10. SPASTIC CEREBRAL PALSYMENTAL RETARDATIONHYDROCEPHALUSMICROCEPHALYDELAYED DEVELOPMENTAL MILESTONECORTICAL BLINDNESSHEARING DEFICITSEPILEPSY
11. TREATMENTThere is no specific treatment for birth asphyxia- hence supportative careInduction of hypothermia (selective brain cooling)
12. prognosisSevere birth asphyxia 50% mortality80% of survivors are left with serious sequelaeModerate birth asphyxia, 30-50% of survivors have serious long term deficits
13. preventionGeneral health promotionSpecific interventionEarly diagnosis and prompt treatmentLimitation of disabilityrehabilitation
14. QUESTION
15. NEONATAL JaUNDICE
16. DEFINITIONJaundice is the yellow discolouration of the skin, mucous membranes and sclera.Jaundice is a sign of hyperbilirubinaemiaThere 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 jaundice2.Pathological jaundice
18. Physiological jaundiceJaundice appearing on the 2nd or 3rd day of lifePeak in the 3-5day of life and disappear within 10days in term infant or 14 days in preterm infantsSerum bilirubin level usually never exceed 12mg/dl in term infant or 15mg in pretermThe rate of rise of bilirubin is <5mg/dl per day or 0.5mg/dl per houseThe baby is otherwise normal(no anaemia, or hepatosplenomegaly)
19. Pathological jaundice ?1.jaundice appearing on the first day of life2.Total serum bilirubin concentration >12mg/dl3.The rate of rise of serum bilirubin is >0.5mg/dl/hour or >5mg/dl/day4.conjugated bilirubin of >2mg/dl5.clinical jaundice persisting for more than 2weeks6.evidence of haemolysis
20. A diagnosis of physiological jaundice should rarely be made in preterm infants
21. Aetiology -AGIPABO INCOMPATIBILITYG6PD DEFICIENCYINFECTIONPREMATURITY
22. THE COMMON CAUSES OF PROLONGED JAUNDICEUTIDown synCretinismNeonatal hepatitisHypothyroidismGalactosaemiaBiliary atresiaInborn error Crigler Najjar and gilbert syn
23. Mention one drug associated with jaundiceDifferentiate between breastmilk jaundice and breastfeeding jaundiceList 10 investigations you will order in the mgt of NNJ
24. kernicterusKernicterus or bilirubin encephalopathy is a neurologic syndrome resulting from the deposition of unconjugated (indirect) bilirubin in the basal ganglia and brainstem nucleiThe 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 cellHypoproteinaemiaAcidosisHypothermiaHypoglycaemiaPrematurityInfectiondehydration
26. Modalities of management of nnjPhototherapyExchange blood transfusionPharmacotherapyimmunotherapy
27. phot0therapy
28. Indications for phototherapyPrevention of hyperbilirubinaemia in preterm LBW infantsTreatment of moderate hyperbilirubinaemiaPost EBT to accelerate excretion and prevent rebound hyperbilirubinaemia
29. Mechanisms of actionPhotooxidationPhoto isomerization(4z, 15z -4z,15E)Structural isomerization- lumirubin
30. Facts to noteThe standard phototherapy is 8-10mW/cm2/nmIntensive phototherapy >30mW/cm/nmPhototherapy lowers bilirubin by 1-2mg/dl over 4-6hoursThe bilirubin should be monitored every 12-24hrs
31. Factors influencing efficacy of phototherapyThe 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 phototherapyThe surface area of infant exposed to phototherapyThe total bilirubin at presentationThe aetiology of jaundiceDuration of exposure
32. Exchange blood transfusionSerum bilirubin level of 10mg/dl by 24hrs of liveSerum bilirubin level of 15mg/dl by 48hours of lifeSerum bilirubin 20mg/dl @ any ageRate of rise of serum bilirubin >5mg/dl/day or >0.5mg/dl/hourThe appearance of clinical signs suggesting kernicterus is indication for EBT at any level of SB
33. question