Hemorrhagic Conditions in

Neonates
Dr Hodan Ahmed,
Department of Pediatrics and Child Health,
Amoud Medical School, AU
 Introduction
• Bleeding in neonate is a frequent problem encountered in all
newborn nurseries especially in premature units and NICU’s,
requring rapid diagnosis and immediate institution of
therapy.
• It is estimated that 1% of all nursery admissions and 25-30%
of neonatal intensive care unit admissions are complicated
by disorder
of bleeding.
• It is one of the important cause of morbidity and mortality
and is a life threatening situation
• It is accentuated in preterms and low birth weight babies.
 Aetiology of bleeding in neonate
• Vascular defect
• Platelet defect
• Coagulation defect
1. Vascular abnormalities
• prematurity – intracranial hemorrhage.
2. Platelets abnormalities:
• Immune thrombocytopenic purpura - child born to mother with SLE or ITP.
• Drugs like aspirin given to mother and inherited disorders of platelet dysfunction
3. Deficiency of coagulation factors
• Hemorrhagic disease of newborn.
• Transitory
• sepsis, liver disease, DIC etc.
• Inherited
• Hemophilia A & B, Von Willebrand disease etc.
4.Trauma
• cephalhematoma etc.
 Clinical presentations
• Oozing from umbilicus
• Cephalohaematomas
• Post circumcision bleeding
• Venepuncture site bleeding
• Bleeding into skin
• Intracranial haemorrhage (few) in sick infants:
• Mucous membranes
• Git
• Urinary bladder
• Venepuncture / invasive procedure sites
• Common causes
• Healthy neonate
– Thrombocytopaenia secondary to transplacental
passage of maternal antiplatelet antibody
– Vitamin k deficiency
– Congenital deficiency of coagulation proteins
• Sick neonate
– Acquired deficit – DIC, liver failure, vitamin k deficiency
– Congenital deficit
Disease states associated with neonatal
thrombocytopaenia
•Increased destruction
–Immune-mediated
•Maternal idiopathic thrombocytopenic purpura
•Maternal SLE
•Maternal hyperthyroidism
•Maternal drugs – quinine, hydralazine, tolbutamide, thiazide diuretics
•Maternal preeclampsia
•Neonatal alloimmune thrombocytopaenia
– Nonimmune – probably related to DIC
• Asphyxia
• Perinatal aspiration
• Necrotizing enterocolitis
• Hemangiomas
• Neonatal thrombosis
• Respiratory distress syndrome
– Unknown
• Hyperbilirubinemia
• Phototherapy
• Polycythemia
• Rh hemolytic disease
• Congenital thrombotic thrombocytopenic purpura
• Total parenteral nutrition
• Inborn errors of metabolism
• Wiskott-aldrich syndrome
• Multiple congenital anomalies
– Hypersplenism
• Decreased production of platelets (5%)
• Bone marrow replacement disorders
• Congenital leukaemia
• Congenital leukemoid reactions
• Neuroblastoma
• Histiocytosis
• Osteopetrosis
• Bone marrow aplasia
• Thrombocytopenia with the absence of the radius
• Amegakaryocytic thrombocytopenia
• Fanconi’s anemia
• Other marrow hypoplastic or aplastic disorders
• Alloimmune thrombocytopaenia
• Analogous to haemolytic disease of the new born
•  
• Mother: normal platelet count
– No bleeding history
– + previously thrombocytopaenic infants
– Maternal IgG alloantibody directed against specific
paternally derived antigens on infant’s platelets
which are absent from mother’s platelets
• Clinical presentation
– Severe isolated thrombocytopaenia in healthy full - term infant
– Minor bleeding petechiae git haematuria haemoptysis
– Intracranial heamorrhage in up to 15% prenatally or postnatally can cause hydrocephalus,
porencephalic cysts, epilepsy
– High probability that subsequent infants will be affected.
•  
• Diagnosis
– Clinical presentation
– Severe thrombocytopaenia
– Serology
– Missing platelet alloantigen in mother
– Alloantibody in maternal serum (not infrequently none is detected)
– Test maternal serum against paternal platelets to detect alloantibody
– Elevated platelet – activated IgG on newborn’s platelets.
•  
•  
• Woman with previously affected neonate
– In utero ultrasound monitoring for each beginning 20
weeks.
– Cordocentesis to confirm presence of thrombocytopaenia
and provide route for regular administration of compatible
platelets to treat affected foetuses.
– Less invasive approach – iv IgG + dexamethasone to
mother in latter part of pregnancy. Not effective in all
foetuses.
– Elective c.s. at foetal maturity 
•  
• Management of neonate
• Washed irradiated maternal platelets.
• Washed - to remove maternal alloantibody.
• Irradiated - to prevent gvhd caused by maternal lymphocytes
• Maternal - certain compatibility availability safety
• Frozen maternal platelets
• Random donor platelets
• Iv ig g with or without maternal platelets
• Corticosteroids prednisone 1mg / kg / day
• Exchange transfusions to remove maternal alloantibody
• Autoimmune neonatal thrombocytopaenia
– Autoimmune platelet consumption
– Antibody directed against antigen common to
maternal and neonatal platelets.
– Milder clinical course
– Platelet count nadir occurs several days after birth.
– Majority are born with normal platelet count
therefore monitor for postnatal drop.
 
• Diagnosis
– Clinical presentation of mother and infant
– Exclude other causes of thrombocytopaenia
•  
• Treatment
– Irradiated platelet transfusion
– Exchange transfusion + platelet transfusion
– Corticosteroids
– Iv ig g + steroids – 80% response rate
 Regimen:
– Iv IgG on 2 consecutive days
– If no response – add prednisone
– Platelet transfusion if infant bleeding
– If no response and has evidence of bleeding –
methylprednisolone may be substituted for
predisone and iv IgG repeated
• Infections and thrombocytopaenia
– In utero rubella, herpes, echovirus, toxoplasma, cmv, hiv
– Postnatally acquired infections
– Mechanism of thrombocytopaenia in neonatal bacterial and viral
sepsis is multifactorial: -
• Consumption secondary to dic
• Endothelial damage by bacteria or bacterial products leading to platelet
adhesion and aggregation.
• Binding of bacterial products to platelet membranes leading to platelet
aggregation.
• Immune – mediated thrombocytopaenia
• Decreased production due to marrow infection
• Giant haemangioma
• ACQUIRED HAEMOSTATIC DISORDERS
• Disseminated intravascular coagulation
• Vitamin k deficiency
• Liver disease
• Pathologic processes:
• Hypoxia
• Acidosis
• Tissue necrosis
• Endotoxic shock
• Endothelial damage
 
• DIC
• Diagnosis:
• Prolonged PT TT and APTT
• Elevated fdp
• Thrombocytopaenia
• Rbc fragmentation
• Low levels of fibrinogen; factors v and viii; inhibitors
• Antithrombin iii, heparin cofactor ii, protein c 
Treatment:
• Underlying disease
• Coagulation factor replacement
• Platelet transfusion
• Anticoagulant drugs
• Exchange transfusion
• VITAMIN K DEFICIENCY
• Three clinical patterns:
• Classic form (Hemolytic disease of the newborn)
• Usually in breastfed, full term, healthy infants
• Presentation on day 2 to 5 of life
• GIT, into skin, venepuncture site, intracranial hemorrhage
• Contributing factors: -
– Low placental transfer of vitamin k
– Low concentration of vitamin k in breast milk.
– Low intake of breast milk during first days of life
– Sterile gut 
•  
• Pattern two
• Presentation in 1st 24 hours of life with serious bleeding, including
intracranial haemorrhage
• Often mothers have been on drugs e.g. warfarin, anticonvulsants,
rifampin, isoniazid that interfere with vitamin k stores or function
in newborn
• Pattern three
• Present beyond first weeks of life in breast-fed babies
• Compromise of vitamin k supply e.g. chronic diarrhoea, cystic
fibrosis, alpha 1 - antitrypsin deficiency, hepatitis, coeliac disease 
 Management
• General prophylaxis at birth
• Additional vitamin K prophylaxis in risk groups
• Pregnant women on anticonvulsants - give oral vitamin K during 3rd
trimester
• Slow iv or sc vitamin k - Takes 2 hours to increase vitamin K dependent
factors to safe levels
• Plasma
• Factor ix concentrates
• In life threatening haemorrhage
– Immediately increase levels of vitamin K dependent factors to safe levels
– High risk of hepatitis and DIC therefore give hepatitis B immunoglobulin and
vaccine. 
• LIVER DISEASE
• Conditions:-
• Viral hepatitis
• Hypoxic liver damage
• Shock
• Foetal hydrops
• Cirrhosis
 
• Mechanism:-
• Failure of hepatic synthetic function
• Activation of coagulation and fibrinolytic
systems
• Poor clearance of the products of haemostasis
• Loss of haemostatic proteins into ascitic fluid
• Abnormally glycosylated proteins
 
• Management:-
• Replacement of coagulation proteins
• Platelets
• Exchange transfusion in more severe cases