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Approach to Bleeding newborn

Dr Somnath pal
MD(pediatrics) DM(neonatology)
Assistant professor
Department of Neonatology, IPGMER
Introduction
• The normal range for the newborn PT and aPTT extend above
than those for a healthy adult.
• But there is NO increased risk of bleeding in a healthy newborn.
• Platelet counts is the same as the normal range for the adult
(150,000–400,000/mm3).
• Bleeding disorders may present during the neonatal period but
several factors make it difficult to establish a diagnosis.
• Therefore evaluation of the neonatal haemostatic system with
the intention of identifying bleeding diathesis should be
performed similarly to any other clinical problem in the neonatal
period.
Neonatal haemostatic system- how is
it different?
• At birth, concentrations of the vitamin K dependent factors
(FII, FVII, FIX, FX) and FXI, FXII are reduced to about 50% of
normal adult values and are further reduced in preterm
infants.
• Concentrations of the naturally occurring
anticoagulants(e.g- antithrombin, protein C, and protein S)
are low at birth
• As a consequence, both thrombin generation and thrombin
inhibition are reduced in the newborn period.
• Plasminogen is also low in neonatal period resulting in a
relatively hypofibrinolytic state.
• Despite this there seems to be relatively few clinical
bleeding problems for the healthy term infant.
• The haemostatic system matures after birth reaching
adult values by 6 months of age.
• Platelet count is within the normal adult range in both
term and preterm infants but are hyporeactive
compared with adult platelets.
• Despite this bleeding time is shortened in neonates
owing to increased concentrations of vWF and high
neonatal packed cell volume.
Coagulation pathway
Causes of bleeding in newborn
• Coagulopathy
• Platelet Quantitative/ Qualitative defects
• Combined defect
• Vascular causes
• Miscellaneous
Platelet disorder Coagulation disorder
• Skin, mucous membrane • Deep in soft tissue, joints,
bleeding muscle bleeding
• Petechiae ++ • No petechiae
• Ecchymosis- small, • Ecchymosis- deep, large
superficial • Post surgical bleeding –
• Post surgical bleeding – delayed, severe
immediate, mild
Coagulopathy
Inherited Acquired
• Hemophilia A • Vitamin K deficiency
• Hemophilia B bleeding
• vWD • Liver disease
• Dysfibrinogenemia • Transplacental exposure to
• Congenital coagulation warfarin, phenytoin
factor deficiency
Platelet defect
Early onset (<72 h) Late onset(>72 h)
• Placental insufficiency • NEC
• Sepsis • Late onset sepsis
• NAIT • Fungal infection
• Autoimmune (maternal SLE, • DIC
ITP)
• DIC
• Congenital infection
• Syndromic
Vasculopathy MISC
• Hemangioma • Trauma (subgaleal
• Vascular malformation hemorrhage,
retroperitoneal
hemorrhage, adrenal
hemorrhage etc )
• Common in breech delivery,
large for date baby
• Swallowed blood
Clinical approach to the bleeding neonate

• Was the baby sick or well at the onset of bleeding?


• Was Vitamin K given to the baby?
• Is the bleeding generalized or localized?
• Is there a family history of bleeding/ coagulation
defects?
• Is there a H/o maternal thrombocytopenia,
connective tissue disease, PIH ,intake of drugs
(barbiturates, phenytoin, aspirin, rifampin, INH,
warfarin)
• What was the age of onset of bleeding?
• Is the bleeding petechial with small mucosal
hemorrhages or are the bleeds deep/ large?
• Is there any coexisting signs like conjugated
hyperbilirubinemia, organomegaly, signs of
sepsis?
Excessive bleeding may present as Sick neonate may present as
• Expanded • Hematuria
cephalhematoma. • Mucous membrane bleed
• Prolonged bleeding after • Intracranial bleed
circumcision. • Pulmonary hemorrhage
• Oozing from venipuncture
site and line placement site.
• Bleeding from umbilicus
Swallowed blood syndrome
• Blood or bloody stools are passed during the 2nd or 3rd
day of life due to swallowing of maternal blood during
delivery or from a fissure in the mother’s nipple .
• It may be confused with hemorrhage from GIT of the
newborn .
• The Apt test is used to rule out maternal blood, based
on the fact that the infant’s blood containing mostly
HbF is alkali-resistant where as the maternal blood (Hb
A) forms alkaline haematin on addition of alkali .
Apt test
• If the child is well and only GI bleeding is noted, it is
performed on gastric aspirate or stool to rule out
presence of maternal blood.
• Mix 1 part bloody stool/ vomitus + 5 parts of water.
• Centrifuge and separate clear pink supernatant.
• Add 1 ml 1% Na hydroxide to 4 ml supernatant.
• HbA changes from pink to yellow brown (maternal)
• HbF stays pink (fetal).
Investigation
First line Second line
• CBC with PBS • Thrombin time
• aPTT • Platelet aggregation study
• PT with INR • Platelet function analysis
• Platelet count • Human platelet antigen
analysis
• Fibrinogen level
• Clotting factor assay
• D –dimer assay
• PIVKA
• Mixing study
Normal Coagulation parameters in
Healthy Term and Preterm Infants
MANAGEMENT OF BLEEDING
Definite etiology unknown
• Vitamin K -1 mg IM/IV (if not received at birth)
• Vitamin K-1 mg every weekly (prolonged TPN
or antibiotic therapy)
• FFP-10 ml/kg (for active bleed , repeat 8-12
hourly, replaces all clotting factors)
• Platelet -10 ml/kg
• PRBC- for severe blood loss. Take pre-
transfusion sample for diagnostic testing.
Specific etiology known
• NAIT
• Autoimmune thrombocytopenia
• VKDB
• Hemophilia
• DIC
NAIT
• Should be considered in any neonate who
presents with severe thrombocytopenia at
birth or shortly thereafter, particularly in the
absence of other risk factors, clinical signs, or
abnormalities in the physical examination.
• A platelet count of <50 × 103/μL on the first day
of life with a parenchymal (rather than
intraventricular) intracranial hemorrhage is
highly suggestive of NAIT.
• Human platelet antigen (HPA) analysis is done,
where antiplatelet antibodies are detected in
maternal or neonatal plasma against HPA of
father or newborn ( HPA 1,3,5,9,15,4)
• low antibody concentration in the neonate
coupled with binding of the antibodies to the
infant’s platelets can lead to false-negative
results.
• Brain imaging studies (cranial ultrasound)
should be performed as soon as NAIT is
suspected, regardless of the presence or
absence of neurologic manifestations
• The clinical course of NAIT is short in most
cases, often resolving almost entirely within 2
weeks
Antenatal management of NAIT

• Maternal treatment with IVIG (1 to 2


g/kg/week) ± steroids (0.5 to 1.0 mg/kg/day
prednisone), weekly starting at 12 or at 20 to
26 weeks’ gestation, depending on whether
the previously affected fetus suffered an ICH,
and if so, at what time during pregnancy.
• Elective cesarean section is recommended in
most countries, regardless of the ICH status, to
avoid ICH.
Postnatal management of NAIT
• Antigen negative platelet transfusion if already
diagnosed in previous pregnancy
• Random donor platelet transfusion in
suspected cases.
• IVIG to protect the transfused platelet
• Steroid in refractory cases
NAIT
Platelet count Treatment dose
<25000/ml in asymptomatic neonate with no family RDP 10 ml/kg
history of ICH
<50000/ml in preterm or with family history of ICH RDP 10ml/kg
<100000/ml with ICH RDP 10ml/kg
<50000/ml in asymptomatic neonate immediately IVIG 1g/kg/d for
following platelet transfusion 2 days
Thrombocytopenia refractory to platelet transfusion Methyl 1 mg/kg/BD
and IVIG prednisolone for 3-5 days
Autoimmune thrombocytopenia
• Platelet count on Day 1 or cord blood
• If normal, recheck on Day 3. If normal on Day
3 no further evaluation
• If platelet 100000-150000/ml , recheck
between D3-D5
• If platelet<100000/ml, recheck daily or more
frequently if <50000/ml
• Cranial USG if platelet <50000/ml
Autoimmune thrombocytpoenia
• Platelet <30000/ml :
- Random donor platelet transfusion + IVIG(1
gm/kg/day for 2 days)

• Platelet 30000-50000/ml : IVIG alone


VKDB
Type Time of onset Etiology Site of bleeding
early <24 h Maternal drugs Cephalhematoma FFP
(warfarin, phenytoin, Umbilical stump Vit K
ATD) ICH
Classic 1-7 days Lack of Vitamin K at GI Vit K
birth Muco- cutaneous FFP
Umbilical stump
Post- circumcision
Late 1-12 weeks Cholestasis GI, Vit K
Muco-cutaneous FFP
Intracranial Recombina
nat FVIIa
Hemophilia
• ICH is common in moderate/severe cases
• Factor replacement therapy is the treatment
of choice
• Formation of inhibitors
Hemophilia
• FFP/cryoprecipitate
• Factor VIII concentrate in hemophilia A-
1U/kg increases factor by 2%
• Factor IX concentrate in hemophilia A- 1U/kg
increases factor by 1%
THANK YOU

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