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Published byJaniya Morley Modified over 9 years ago
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William 2001
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Hyperbilirubinemia Nonimmune hydrops Cardiac arrhythmias Hemorrhagic disease of the newborn Thrombocytopenia Polycythemia Necrotizing entrocolitis
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Unconjugated bilirubin: Not excreted in bile and urine Pass the placenta to the mother Conjugated bilirubin: Water soluble Excreted in bile and urine Kernicterus: ↑ unconjugated bilirubin > 18 – 20 mg/dL - < 18 in preterm
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Clinical picture: Spasticity MR Muscle incoordination Causes of kernicterus: Hypoxia Hypoglycemia hypothermia Acidosis sepsis
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Drugs : Furosemide Gentamicin Salicylates Sulfonamides Diazepam Na benzoate ↑ vitamin K 1
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Brest milk jaundice: - Due to excretion of: pregnane – 3 α, 20 β–diol in the milk inhibit conjugation of bilirubin by inhibiting glucuronyl transferase activity - Jaundice starts 4 th to 15 th day - No encephalopathy
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Physiological jaundice: Starts 3 rd to 4 th day Bilirubin level < 10 mg/dL Phototherapy: For treatment of hyperbilirubinemia Mechanism: Ligh oxidation of bilirubin ↓ ↑ peripheral blood flow ↑ photooxidation
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Method: Eyes covered Skin exposed Appropriate fluorescent wavelength Baby turned /2 hours Bilirubin measured after 24 hours Monitor temperature to prevent dehydration
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Definition: Abnormal fluid accumulation in ≥ sites Incidence: 0.6 % 77% of them are known 1.7 % 95% of them are known Incidence of hydrops: 13% immune 1.3% extrinsic 21% idiopathic 64% intrinsic
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Intrinsic causes: 41% cystic hygroma 27% cardiac anomalies 21% multiple malformations 11% others Causes of nonimmune hydrops: 1 – Cardiac: = 20 – 45%
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½ structural anomalies ½ cardiac arrhythmia 2 – Chromosomal anomalies: = 35% - earlier - extensive space suite hydrops 87% with anencephaly 3 – Severe anemia: Parvovirus Acute fetal - maternal Hg α - thalassemia
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4 – Twin-to-twin transfusion: Recipient HF Donor hydrops after the death of the recipient 5 - Inborn errors of metabolism: - Gaucher disease - GM 1 gangliosidosis - Sialidosis All recurrent hydrops
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6 – Lymph system anomalies: - Chylothorax - Chylous ascites Prognosis: < 24 weeks 95% mortality ≥ 24 weeks 80% mortality Diagnosis: Maternal tests – cordocentesis - US
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Maternal tests: Hb electrophoresis Indirect Coombs test Kleihauer – Batke test Serological tests for: Rubella Toxoplasmosis Syphilis Cytomegalovirus Parvovirus B - 19
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Cordocentesis: karyotyping Hb% Hb electrophoresis Direct Coombs test Liver transaminases Serological test for Ig M specific Abs
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Most important predictor tests for prognosis: Karyotyping Fetal ECG Management: - Blood transfusion for anemia - Amniocentesis for twin-to-twin transfusion may spontaneous cure If persistent exclude cardiac anomalies and anencephaly
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Deliver if near term Expectant treatment if very preterm Maternal complications: Mirror syndrome: Edema and preeclampsia due to vascular changes in the fetus Others: Overdistension PTL – PP Hg -- retained placenta
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Usually transient and benign Some tacchycardia if sustained may hydrops, HF and fetal death Sustained bradicardia is caused by: Congenital anomalies Myocarditis And is less often associated with hydrops
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Isolated extrasystoles: Atrial extrasystoles Ventricular extrasystoles Sustained arrhythmias: Supraventricular tacchycardia Ventricular tacchycardia Complete heart block 2 degree heart block Atrial flatter, fibrillation Sinus bradicardia
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Premature atrial contractions: = 64% of cardiac arrhythmia Usually benign and transient Rarely supraventricular tacchycardia and if > 200 b/m may HF Bradicardia: Poor prognosis Caused by:
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Structure anomalies as A-V canal Heart block Congenital heart block : - Caused by Abs against fetal myometrium in 50% of the cases - Most common Abs: Anti-SS-A (Anti Ro) Abs - Inflammation and permanent damage to the myocardial tissue
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- Neonate may require pacemaker - Only 1 : 20 of the cases are affected - Mothers usually have: SLE or other CT disease or subsequently develop it Fetotherapy : By corticosteroids to the mother
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Characterized by: Hypoprothrombinemia ↓ factor V, VII, IX, X ↑ prothrombin time ↑ PTT Spontaneous internal or ext Hgs May occur at any time Usually delayed 1 – 2 days
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Causes: ↓ vit k 1 Hemophilia Sepsis Syphilis Thrombocytopenia Erythroblastosis ICH
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Vit K 1 : ↓ during pregnancy # nonpregnant ↓ placental transmission ↓ in milk Anticonvulsive drugs prevent hepatic synthesis of factor VII, IX, X ↓ vit K 1 A phenotype similar to Chondrodysplasia punctata = Conradi – Hunermann syndrome =inherited disease characterized by bone dystrophy and facial anomalies
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Types: 1 – Immune thrombocytopenia: - Maternal antiplatelet Ig G fetal/ neonatal thrombocytopenia - Usually associated with maternal autoimmune disease and maternal thrombocytopenia - Corticosteroid therapy ↑ maternal platelet count but does not improve fetal condition
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2 -- Alloimmune thrombocytopenia (ATP): - Fetal platelet Ag pass the placenta to the mother isoimmunization - Usually discovered after the delivery of an affected child - May IC Hg - 98% of the population are HPA 1a +ve 2 % of the population are HPA 1a –ve - % = 1 : 5000 – 10000 live birth - 1 : 50 of pregnancies are at risk
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- Significant fetal – maternal Hg must occur provoke immune respond - Affect offspring of women with HLA type DR - 3 or B - 8 Diagnosis: - Maternal platelet count normal + no autoimmune disease - Fetal platelets count ↓ + no other autoimmune D
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- IV injection of Ig in a large dose to the mother recurrent fetal thrombocytopenia by cordocentesis Recurrence = 70 – 90% More severe and earlier in subsequent pregnancies
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Predisposing factors: Chronic hypoxia Placental transfusion ( maternal or twin) Clinical picture: Plethora Cyanosis Neurological impairment
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Laboratory: ↑ bilirubin ↓ platelet Hypoglycemia Fragmented RBCs Treatment: plasma
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Bowel disorder affects mainly premature neonates due to intestinal immaturity Clinical picture: Distension Illus Bloody stools X ray: Gas in intestine = pneumatosis intestinalis May perforation
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% 5.7 of preterm infants Causes: Perinatal hypotension hypoxia Sepsis Umbilical catheters Exchange transfusion Hypertonic fluids
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Cow milk Coronovirus infection Treatment: Ig administration orally
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