William 2001

 Hyperbilirubinemia  Nonimmune hydrops  Cardiac arrhythmias  Hemorrhagic disease of the newborn  Thrombocytopenia  Polycythemia  Necrotizing entrocolitis

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

Clinical picture:  Spasticity  MR  Muscle incoordination Causes of kernicterus:  Hypoxia  Hypoglycemia  hypothermia  Acidosis  sepsis

 Drugs : Furosemide Gentamicin Salicylates Sulfonamides Diazepam Na benzoate ↑ vitamin K 1

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

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

Method:  Eyes covered  Skin exposed  Appropriate fluorescent wavelength  Baby turned /2 hours  Bilirubin measured after 24 hours  Monitor temperature to prevent dehydration

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

Intrinsic causes: 41% cystic hygroma 27% cardiac anomalies 21% multiple malformations 11% others Causes of nonimmune hydrops: 1 – Cardiac: = 20 – 45%

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

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

6 – Lymph system anomalies: - Chylothorax - Chylous ascites Prognosis: < 24 weeks  95% mortality ≥ 24 weeks  80% mortality Diagnosis: Maternal tests – cordocentesis - US

Maternal tests:  Hb electrophoresis  Indirect Coombs test  Kleihauer – Batke test  Serological tests for: Rubella Toxoplasmosis Syphilis Cytomegalovirus Parvovirus B - 19

Cordocentesis:  karyotyping  Hb%  Hb electrophoresis  Direct Coombs test  Liver transaminases  Serological test for Ig M specific Abs

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

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

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

Isolated extrasystoles:  Atrial extrasystoles  Ventricular extrasystoles Sustained arrhythmias:  Supraventricular tacchycardia  Ventricular tacchycardia  Complete heart block  2 degree heart block  Atrial flatter, fibrillation  Sinus bradicardia

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:

 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

- 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

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

Causes:  ↓ vit k 1  Hemophilia  Sepsis  Syphilis  Thrombocytopenia  Erythroblastosis  ICH

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

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

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 – live birth - 1 : 50 of pregnancies are at risk

- 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

- 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

Predisposing factors:  Chronic hypoxia  Placental transfusion ( maternal or twin) Clinical picture:  Plethora  Cyanosis  Neurological impairment

Laboratory:  ↑ bilirubin  ↓ platelet  Hypoglycemia  Fragmented RBCs Treatment: plasma

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

% 5.7 of preterm infants Causes:  Perinatal hypotension  hypoxia  Sepsis  Umbilical catheters  Exchange transfusion  Hypertonic fluids

 Cow milk  Coronovirus infection Treatment: Ig administration orally