Common Neonatal Problems.pptx

Common Neonatal Problems Clinical Science Lecture Dr T Martin (MBChB, FC Paed, DCH) 13 March 2014 Overview Introduction Complications of Prematurity Meconium aspiration syndrome Neonatal Encephalopathy/Asphyxia Birth Trauma Congenital Abnormalities Genetic Abnormalities...

Common Neonatal Problems Clinical Science Lecture Dr T Martin (MBChB, FC Paed, DCH) 13 March 2014 Overview Introduction Complications of Prematurity Meconium aspiration syndrome Neonatal Encephalopathy/Asphyxia Birth Trauma Congenital Abnormalities Genetic Abnormalities Feeding Difficulties Hearing Loss Visual Impairment Discharge Planning What is a neonate? First 28 days of life Transitionfrom foetal circulation to neonatal circulation Mostrapid period of cerebral and somatic growth A vulnerable time and things can go wrong Relevance MDG to decrease under 5 mortality by 2/3’s in 2015 Infant mortality rate a major contributing factor NMR 2/3 of infant mortality rate Main causes: Prematurity, asphyxia, sepsis, congenital abnormalities The High Risk Neonate Maternal Characteristics ( medical conditions, demographics, obstetric risk factors) Foetal Characteristics ( anomalies, presentation) Placental Characteristics Gestation and Birthweight Intrapartum – labour, instrumentation Complications of Prematurity  Complications of Prematurity Respiratory : Neurologic: HMD / Apnoea / BPD IVH / PVL Cardiovascular: Haematologic : Hypotension/PDA Anaemia/ Jaundice Gastrointestinal : Metabolic : NEC/ Feed intolerance Glucose / calcium Renal : Bicarb losses Temp regulation Immunologic Ophthalmologic : ROP  Respiratory Distress Syndrome HMD = Surfactant Deficiency May require ventilation (IPPV/HFOV/CPAP) Complications of ventilation: - mucous plugging - lobar collapse - VAP/BPD - Secretions Apneoa Definition: The cessation of respiratory effort for > 20 seconds associated with bradycardia Causes: Respiratory or Central causes Management: Supportive, treat underlying cause, respiratory stimulants Hypothermia Definition: Hypothermia < 37 degrees Severe Hypothermia < 35 degrees Neonatal cold injury < 32.2 degrees Hypothermia Causes: Heat loss occurs through 4 basic mechanisms: 1. Evaporation 2. Convection 3. Conduction 4. Radiation Hypothermia Management: 1. Dry baby as soon as possible 2. Wrap in warm dry towel 3. Place under heater / put to breast 4. Move to incubator 5. Limit procedures/ exposure Neonatal Jaundice Alsoknown as hyperbilirubinaemia Yellow-greenish discolouration of skin and sclera Potentially toxic to the CNS Neonatal Jaundice Causes: Increased Decreased Decreased Production Excretion enzyme activity Haemolytic Enterohepatic Drugs amaemia circulation Polycythemia Obstructive Free fatty acids Shortened Hydrogen RBC ions life span 90d vs 120d Infection Genetic defects Kernicterus Brain damage due to deposition of bilirubin in the basal ganglia and brainstem nuclei Lipid soluble,unconjugated bilirubin is toxic to the developing CNS Occurs when levels are high and exceed binding capacity of albumin Crosses the blood brain Kernicterus Characterized by the clinical tetrad: 1. Choreoathetoid cerebral palsy 2. High-frequency central neural hearing loss, 3. Palsy of vertical gaze, 4. Dental enamel hypoplasia All the result of bilirubin-induced cell toxicity Kernicterus Rarely seen in the decades following the introduction of phototherapy and exchange transfusion However, recent reports suggest it is re - emerging Since 1990, the Pilot Kernicterus Registry id kernicterus in more than 120 infants who had been d/c and readmitted Kernicterus Many who progress to the severe neurological signs die Survivors may initially appear to recover Show few abnormalities for 2- 3 months But by 3 yrs display the fill clinical syndrome IVH Grade 1 - germinal matrix bleed Grade 2 - Bleeding extends into the ventricle Grade 3 - Grade 2 with enlargement of the ventricles Grade 4 – Grade 3 with parenchymal haemorrhage  IVH GRADE 3 GRADE 4 PVL “Classic” focal PVL : Easily detectable on CUS. Characterized by regions of coagulation necrosis and liquefaction in the periventricular white matter with loss of all cellular elements. Diffuse PVL characterized by central cerebral white matter injury with loss of premyelinating oligodendrocytes, astrogliosis, and microglial infiltration. Atrisk for motor and cognitive impairment, as well as behavioral problems  Long Term Outcomes US TEST RESULT PRE TEST LR 95%CI POST TEST PROBABILIT PROBABILITY Y NORMAL 9% 0.5(0.4-0.7) 5% (4-6) GR 1 OR 2 IVH 9% 1 (0.4-3) 9% (4-22) GR 3 IVH 9% 4 (2-8) 26% (13-45) GR 4 IVH 9% 11 (4-31) 53% (29-76) CYSTIC PVL 9% 29 (7-116) 74% (42-92) VE 9% 3 (2-4) 22% (17-28) HYDROCEPHALUS 9% 4 ( 1-13) 27% (10-56) Osteopenia of Prematurity Nutritional Needs not met to allow for optimal mineralization Accelerated Growth Drugs : diuretics , steroids, TPN Management: High dose Vit D Passive limb therapy  Long Term Problems: Neuro-developmental Disability ( CP) Cognitive + language impairments (ADHD, learning disability) Sensory impairments ROP Chronic lung disease Increased rates of readmission Meconium Aspiration Syndrome  Meconium Aspiration Syndrome Risk of Airleak Syndrome therefore gentle physio required Neonatal Encephalopathy/Asphyxia Neonatal Encephalopathy/Asphyxia Conditions known to reduce uteroplacental blood flow or interfere with spontaneous respiration lead to perinatal hypoxia Reduced bloodflow > decreased glucose and oxygen> accumulation of lactate and ischaemic Causes Impairment of maternal oxygenation Decreased blood flow from mother to placenta Decreased blood flow from placenta to foetus Impaired gaseous exchange from placenta to foetus Increased foetal oxygen requirements Clinical Exam Low apgars Decreased tone Lethargic > poorly responsive Seizures Apneoa Absent primitive reflexes Complications: Seizures Feeding difficulties Aspiration pneumonia Contractures Sensory impairment Motor impairment ( spastic CP) HIE Outcome Birth Trauma Birth Trauma Definition: An impairment of the infant’s body function or structure due to adverse influences that occurred at birth Injurycan occur antenatal , intrapartum or during resuscitation Avoidable / unavoidable Birth Trauma RISK FACTORS :  Primiparity  Small maternal stature  Maternal pelvic anomalies  Prolonged or precipitous labour  Oligohydramnios, malpresentation  Instrumental deliveries  Fetal anomalies  Macrosomia/macrocephaly Head Injuries Head Injuries Cephalohaematoma Brachial Plexis Injuries Erbs Palsy Clinical Appearance: Motor Loss:  Adducted Shoulder  Medially Rotated Arm  Extended Elbow Sensory Loss: Lateral aspect of Upper Limb (uncommon) Waiters tip position Characteristic position - adduction and internal rotation of the arm with forearm pronated Forearm extension normal Biceps reflex absent Klumpke Palsy Injury to Inferior part of Plexus. Occurrence: Excessive abduction of arm. Less common then Injury to Superior part of Plexus. Roots Involved:  C8 and T1 Klumpke’s Palsy Clinical Appearance: Motor Loss:  Small muscles of Hand Sensory Loss:  Medial aspect of Upper Limb Fractures Clavicle:analgesia, limit movement to allow callus formation Humerus: splint for 2 weeks Femoral: traction, suspension with spica cast analgesia, immobilization for 14 days  Cranial Nerve, Spinal Cord and Peripheral nerve injury CRANIAL Nerve injuries – Facial , recurrent laryngeal Spinal Cord – haematoma, vertebral injuries, transection, occlusion Phrenic Nerve Injury Congenital Abnormalities Neural Tube Defects Neural tube defects Causes : Folic acid deficiency , maternal anticonvulsants ,maternal diabetes, irradiation, maternal hyperthermia, amniotic band syndrome Primary NTD MENINGOMYELOCOELE Primary NTD ENCEPHALOCOELE Primary NTD ANENCEPHALY Secondary NTD Meningocoele – skin and dura,not neural elements Prognosis Depends on level of lesion Surgery does not reverse insult Association with renal tract anomalies Shunting for associated hydrocephalus Requires ongoing physio,OT,psych Cleft Lip and palate Commonest craniofacial anomaly Cleft lip twice as common on L vs R Cleft lip more common in males, cleft palate in females Syndromic/ maternal phenytoin/ familial Cleft lip and palate Multidisciplinary team – surgeon, speech therapist, psychologist, geneticist, paediatrician Surgery – according to lesion Assistance with feeding specialized teats Cleft Lip and palate Hydrocephalus Causes: Congenital Malformations: Aqueduct stenosis, Chiari Malformation, Dandy Walker Malformation Post- Haemorrhagic: IVH, SAB, trauma, Vit K def Post Infective: Neonatal Meningitis , Intrauterine viral infection Neoplastic Lesions Vascular Malformations Choroid Plexus Papilloma Genetics Trisomy 21 Trisomy 21 Epicanthic folds Upslanting palperbral fissures Brushfield spots on the iris Flat nasal bridge Protruding tongue Brachycephaly Single palmer crease Hypotonia Saddle gap 5th finger clinodactaly  Genetics Trisomy 18 1/1/3000 conceptions 1/6000 live births 95% non dysjunction, 5% translocatio or mosaics May be diagnosed prenatally 50% live to 2 months 5% live to 1 year Genetics Trisomy 13 1/9500 live births Median survival is 7 – 10 days 90% die within 1st year of life  Teratogens Drugs and Heavy Radiatio Maternal Intrauterin Other Metals n Condition e Exposure s Infections s Warfarin Cancer IDDM CMV Gasoline Therapy fumes Anticonvulsants Graves Herpes Heat Simplex Alcohol,recreatio SLE Rubella Hypoxia nal Drugs Antipsychotics Myasthen Syphilis Maternal ia Gravis Smoking Lead,Mercury Myotonic Varicella, Dystroph Toxo y Feeding Problems CleftLip and Palate Micrognathia TOF Premature Asphyxiated babies Other congenital abnormalities Post surgery Visual Impairment Visual Impairment ROP (