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Bleedingneonate sandip1

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  • 1. Bleeding neonate Dr.Sandip Gupta PGT,PEDIATRICS B.S.M.C.H.
  • 2. Introduction • Neonates are susceptible to bleeding for various reasons Immaturity of the haemostatic system because of quantitative and qualitative deficiency of coagulation factors Maternal disease and drugs Birth trauma Other conditions - sepsis and asphyxia
  • 3. Clinical presentation • Bleeding in neonates may present with Oozing from the umbilical stump Cephalhaematoma Bruising , Petechiae Bleeding from peripheral venipuncture or procedure sites Bleeding following circumcision Intracranial haemorrhage Bleeding from mucous membranes Unexplained anemia and hypotension
  • 4. Etiology A.Deficiency of clotting factors: 1.Transitory deficienciesDeficiency of vitamin K dependent C.F- II, VII, IX, X.  Deficiency of anticoagulant proteins C & S.
  • 5. Causes: a. Total parenteral nutrition or antibiotics b. Lack of administration of vitamin K . c. Drug intake in pregnancy eg.i. Phenytoin, Phenobarbital, Salicylates . (Interferes with the synthesis of vit. K dependent c.f. ) ii. Calmodulin compounds
  • 6. • The incidence among babies born to mothers on these drugs have varied between 6-12%*. In a recent series on children born to mothers on anticonvulsants, abnormal PT was documented in 14 out of 105 babies (13%) , no overt bleeding was observed*.
  • 7. 2. Disturbances of clotting - Related to DIC due to infection, shock, anoxia, NEC, renal vein thrombosis, use of IV canula. 3. Inherited abnormalities of C.F. a. X-Linked recessive diseasesi. Hemophilia-A : Factor VIII deficiency. ii. Hemophilia-B : Factor IX deficiency.
  • 8. b. Autosomal dominant diseases: i. Von Willebrand disease – Deficiency of VWF which is a carrier of factor VIII & as a platelet aggregation agent. c. Autosomal recessive diseases: i. Severe factor VII & factor XIII deficiency – intracranial hemorrhage in neonates ii. Factor XI deficiency – unpredictable bleeding during surgery/trauma.
  • 9. iii. VWD Type III B. Platelet problems: 1. Qualitative disorders: - Glanzman’s thrombasthenia. - Bernard-Soulier syndrome - Platelet type VWD
  • 10. 2. Quantitive disorders: - Immune thrombocytopenia - Matrnal Preeclampsia, HELLP syndrome or severe uteroplacental insuffuciency. - DIC due to infection or asphyxia. - Inherited marrow failure syndromes : Fanconi anemia & congenital amegakaryocytic thrombocytopenia
  • 11. - Congenital leukemia - Inherited thrombocytopenia syndromes : gray platelet syndrome - Macrothrombocytopenias : MayHegglin syndr. - Platelet consumption in clots/ vascular disorders eg. Vascular malformations, NEC.
  • 12. C. Vascular origin: - Pulmonary haemorrhage - A-V malformations - CNS haemorrhage - Hemangiomas.
  • 13. Diagnostic workup • HISTORY: A detailed history and examination essential in the assessment of bleeding neonate History includes • Maternal diseases as ITP, preeclampsia . • Maternal exposure to drugs as aspirin, anticonvulsants, rifampicin and isoniazid • Family history of bleeding disorders • Previous affected sibling
  • 14. B. Examination: First diagnose whether the infant is Sick or Well 1. Sick infant: - DIC - Bacterial/ viral infections. 2. Well infant: - Vit K deficiency - Isolated C.F. deficiencies - Immune thrombocytopenia - Maternal blood in infant’s GIT.
  • 15. 3. Patchiae, ecchymosis, mucosal bleeding: Platelet problem 4. Large bruises: DIC, C.F deficiencies, liver diseases 5. Enlarged spleen : Possible congenital infections or erythroblastosis. 6. Jaundice : Sepsis, liver diseases, resorption of large hematoma.
  • 16. C. Laboratory tests: 1. Apt test : - To rule out maternal blood in infant’s GIT - Done in otherwise well infant with only GI bleeding. 2. PBS : - DIC- fragmented RBCs - Congenital macrothrombocytopenias – large platelets.
  • 17. 3. PT 4. APTT 5. D-Dimer assays: Measure fibrin degradation products in DIC & Liver diseases causing defective clearing of fibrin split products. 6. Specific factor assays & Von Willebrand assay: For patients with + ve family h/o.
  • 18. Laboratory findings Laboratory Studies Other useful tests DIC Platelets PT Likely Diagnosis Fibrinogen, FDP, Sepsis screen Platelet consumption (NEC, Renal vein thrombosis, marrow infiltration, Sepsis) LFT, Albumin APTT SICK INFANTS N N Liver disease N N N N Compromised vascular integrity (hypoxia, prematurity, acidosis)
  • 19. Laboratory Studies Platelets PT Likely Diagnosis Other useful tests Immune thrombocytopenia Bone marrow hypoplasia Maternal platelet count, Platelet antigen typing, Bone marrow, Fibrinogen, FDP, Factor VII & IX assays APTT HEALTHY INFANTS N N N N N Vitamin K Deficiency N Heriditory C.F. deficiencies N Bleeding d/t local factors, Plt function anomalies, Factor XIII deficiency(rare) N Platelet aggregometry Urea clot solubility
  • 20. Treatment Of Bleeding A. Inj Vitamin K1 (Aquaminophyton) - 1 mg IV or IM if not given at birth. - Infants on TPN - Infants on Antibiotics > 2 weeks: at least 0.5mg Vit K weekly. - Preferred rather than FFP for prolonged PT & PTT, FFP should be reserved for emergencies.
  • 21. B. FFP: - 10ml/kg IV for active bleeding - Repeated 8-12 hrly as needed. - Replaces C.F. immediately. C. Platelets: - 1 Unit of platelet raises count by 50,000-100,000/mm3 in a 3kg newborn. - Platelet count slowly decreases if stores 3-5 days.
  • 22. D. Fresh whole blood: - 10ml/kg - Can be repeated after 6-8 hrs as needed. E. Clotting factor concetrates - Severe VWD : - VWF containing plasma derived factor VIII concetrate. - Known deficiency of factor VIII or IX : Recombinent DNA derived factor VIII and IX concetrate
  • 23. F. Disorders due to problems other than hemostatic proteins : - Rule out the underlying possibilities - eg. Infection, Liver rupture, catheter, NEC. G. T/t of specific disorders : 1. DIC : - Treat the underlying cause i.e. sepsis, NEC - Make sure that Vit K1 has been given.
  • 24. - Platelets/ FFP to keep platelet counts > 50,000/ml and to stop bleeding. - If bleeding persists, i. Exchange transfusion with fresh whole blood /Packed RBC/Platelets/FFP ii. Continuous transfusion with platelets, packed RBCs or FFP as needed. iii. For hypofibrinogenemia : Cryoprecipitate (10ml/kg)
  • 25. VKDB • • • • Early , Classic, and Late forms Early VKDB – in first day Severe bleeding – GI and ICH Cause – Maternal drug intake Phenytoin, phenobarb, ATT, warfarin
  • 26. VKDB Classical form: 2-7 days of age • 0.25-1.7% of all babies • Cause – not received prophylaxis on breast feeds, sterile gut, lack of placental transfer Late form : 2-8 weeks of age • Boys > girls, 5-10/1 lac • Well , breastfed, term baby • Liver disease • Malabsorption
  • 27. Management of VKDB • Prolonged PT , APTT (if severe) • Normal platelets and fibrinogen • Factor assays of vit K dependent factors • Treatment – 1mg iv or sc • FFP in severe cases
  • 28. Prophylaxis of VKDB • Early VKDB- single IM inj of vit K at birth and oral Vit K to mother for last 4 weeks • Classical and Late forms – IM Vit K at birth oral Vit K at 0 , 4 days and 4 weeks In preterms – Weekly iv Vit K
  • 29. Hemophilia in the Newborn • Factor VIII or XI deficiency – A good family history goes a long way
  • 30. Hemophilia A Most common inherited clotting factor def X linked recessive, 1 in 4000 males 1/3rd of cases present in newborn period ICH(25%), cephalhematoma(10-15%) Post circumcision bleed is characteristic Family history – absent in 30% Inv – prolonged APTT, normal PT, normal platelets. • Factor VIIIc assay level <2% severe, 2-10% moderate, >10% mild • • • • • • •
  • 31. Hemophilia B • • • • • • XLR Deficiency of Factor IX Less common than the classical form Prolonged APTT and low Factor IX Rx- 100u/k iv OD , to raise levels to 100% Avoid lumbar punctures, IM injections
  • 32. Thrombocytopenia • • • • • Less than 150,000/uL Incidence in newborns: 1-5% Incidence in NICU – 15-30% In VLBW and preterms – 50% Causes of thrombocytopenia in newborn: Neonatal megakaryocytes are smaller Inadequate production of thrombopoietin
  • 33. Causes of thrombocytopenia • Immune-mediated • Associated with infection - Bacterial or Nonbacterial • Drug-Related • Increased peripheral consumption of platelets – Disseminated Intravascular Coagulation, Necrotizing enterocolitis, hypersplenism • Genetic and Congenital Anomalies • Miscellaneous – asphyxia, IUGR, PIH, GDM
  • 34. Early thrombocytopenia • • • • • • • Placental insufficiency (PIH, IUGR,DM) NAITP Birth asphyxia Perinatal infection Maternal autoimmune causes( ITP, SLE) Congenital infection Inherited – TAR, Wiskott- Aldrich
  • 35. Late Thrombocytopenia • • • • Late onset sepsis and NEC Congenital infection Maternal ITP, SLE Congenital / Inherited conditions
  • 36. Immune Thrombocytopenia • Neonatal allo-immune thrombocytopenia (NAIT) • Incidental thrombocytopenia of pregnancy or Gestational thrombocytopenia • Autoimmune thrombocytopenic purpura
  • 37. Neonatal allo-immune thrombocytopenia (NAIT ) • • • • • • Incompatibility between mother and baby Similar to Rh disease Antibodies against HPA – 1 (most common) In utero bleed can occur Manifests with first pregnancy in 50% Postnatal : petechiae, purpura ICH in 10% with sequelae
  • 38. NAIT • Management – fetal blood sampling and platelet transfusion or maternal IVIG • If previous sibling had a significant bleed • Caesarian section • In newborn – maternal platelets or HPA compatible platelets • IVIG 1gm/k for 2 days or 0.5g/k for 4 days
  • 39. Congenital causes • • • • • TAR , Fanconis anemia, Congenital amegakaryocytic anemia Trisomy 21, 18,13 Wiskott Aldrich syndrome Noonan’s and Apert’s Syndromes
  • 40. TAR (Thrombocytopenia & Absent Radii) • Congenital • Findings – – – – – Thrombocytopenia Absent radii bilaterally Small shoulders Abnormal knees Malabsorption • History – Platelets stabilize – ? Leukemia
  • 41. PT and APTT • PT: measures extrinsic pathway • VII, X, II, V • Normal range : preterm:(14-22S) term : (13-20s) • APTT: Measures intrinsic pathway • VIII, IX,XI,XII, X,II, V • Uses a contact activator like kaolin , silica • Normal values: Term-(30s-45s) Preterm – ( 35 – 55s)
  • 42. Thank You…

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