This document discusses the approach to managing bleeding in children. It covers various causes of bleeding including platelet disorders like thrombocytopenia from conditions like ITP, coagulation disorders, and dysfunctional fibrinolysis. It provides details on evaluating the clinical history and performing examinations and lab tests to identify the underlying cause. Specific conditions discussed in more depth include ITP, hemophilia, vitamin K deficiency, and DIC. Treatment approaches are described for replacing coagulation factors, corticosteroids, IVIG, platelet transfusions, and managing thrombotic disorders.

1. APPROACH TO ABLEEDING CHILD
JISHNU.K.R
FINAL MBBS

2. • Bleeding may occur due to:
1)Defects in platelet
a)Thrombocytopenia
b)Qualitative disorders of function
2)Coagulation disorders
3)Dysfunctional fibrinolysis

3. CAUSES OF THROMBOCYTOPENIA
• ITP
• Infections: DIC, malaria, kala-azar, DHF, hepatitis B & C
• Medications : valproate, penicillin, heparin
• Thrombotic microangiopathy: TTP, HUS
• Malignancies: leukemia, lymphoma
• Autoimmune or related disorders: SLE, APL syndrome
• Immunodeficiency
• Bone marrow failure and marrow replacement
• Others: hypersplenism

4. QUALITATIVE DISORDERS OF
PLATELET FUNCTION
• INHERITED DISORDERS
Glanzmann thrombasthenia
Bernard Soulier syndrome
Gray platelet syndrome
Dense body deficiency
• ACQUIRED DISORDERS
Medications
c/c renal failure
Cardioulmonary bypass

5. COMMON COAGULATION
DISORDERS
• INHERITED DISORDERS
Hemophilia A and B
von Willebrand disease
Specific factor deficiencies
Factor VII, X, XIII deficiency
Afibrinogenemia
• ACQUIRED DISORDERS
Liver disease
Vit K deficiency
Warfarin overdose
DIC

6. • The process of hemostasis involves platelets, vessel wall and plasma
proteins in a fine balance b/w blood flow and local response to
vascular injury
• Extrinsic pathway is the primary initiating pathway for coagulation
& is measured by PT
• Intrinsic system works as a regulatory amplification loop, measured
by APTT

8. CLINICAL EVALUATION
• Age of onset of bleeding
• Type of bleeding
• Precipitating factors
• Recent onset bleeding – h/o antecedent infection, rash
(Henoch-Schonlein purpura, varicella), icterus (liver failure),
prodromal diarrhoea & associated renal failure(HUS)
• Medications
• Family history – X linked (hemophilia) –only boys are affected,
girls may have bleeding in autosomal dominant (von
willibrand)
• Poor wound healing & prolonged bleeding from umbilical
stump – factor XIII deficiency

9. Examination
• Ecchymoses, petechia, vascular malformations (hemangioma,
telengiectasia), rashes
• Splenomegaly infections, malignancy, collagen vascular dis. or
hypersplenism

11. ITP / IMMUNE THROMBOCYTOPENIA
CLINICAL EVALUATION
• Antecedent h/o febrile illness
• Sudden appearance of bruises & mucosal bleeding, epistaxis, oral
oozing & prolonged bleeds with superficial trauma
• Presence of petechie & ecchymoses

12. LABORATORY EVALUATION
• CBC – low platelet count
• Peripheral smear – for abnormal cells or malarial parasites
• LFT, RFT & LDH to rule out hepatitis, occult malignancy, hemolysis &
HUS
• Appropriate evaluation of infections
• Screening tests for DIC if sepsis is suspected
• Bone marrow – increased megakaryocytes

13. MANAGEMENT
• Minimising the risk of h’ge & decreasing the long term side effects
of treatment
• Active bleeding – IV Ig (1g/kg/day) for 1-2days or Anti- D Ig (50-
75mg/kg) in Rh +ve children
• Corticosteroids – Prednisolone (1-4mg/kg/day) for 2-4 weeks and
tapered.
• Severe h’ge – platelet transfusions under cover of steroids
• Chronic ITP – prednisone at low dose on alternate days ,
combination of danazol , vincristine , cyclosporine, azathioprine ,
rituximab , splenectomy , thrombopoetin receptor binding agents.

14. NEONATAL ALLOIMMUNE
THROMBOCYTOPENIA
• Fetal platelets are destroyed by maternal Abs against paternally
inherited Ags on fetal platelets
• H’gic complications including intracranial h’ge may occur within hrs
after birth
• Specific tests are limited – diagnosed by excluding sepsis,
meconium aspiration, IU infections, effect of maternal medications,
maternal SLE

15. • Postnatal Mx – transfusion of washed maternal platelets & close
monitoring until the platelet counts normalize
• Fetus requires serial USG for intracranial h’ge
• IV Ig during pregnancy & at birth along with dexamethasone

16. HEMOPHILIA
• Hemophilia A – factor VIII
• Hemophilia B – factor IX
• C/F of A & B are indistinguishable
• Managed at specialized centres
• Appropriate factor replacement
• Dose of factors required :
VIII = % desired rise in F VIII * bdwt(kg) * 0.5
IX = % desired rise in F IX * bdwt(kg) *1.4
• Judicious physiotherapy to prevent c/c joint d/s, counselling for
injury prevention & monitoring for development of F VIII & IX
inhibitors

17. VITAMIN K DEFICIENCY
• Factors II, VII, IX , X Protein C & S
• Prolonged PT & aPTT
• Vit. K 1 mg s/c at birth to prevent h’gic disease of newborn
• Symptomatic neonates who didn’t receive prophylaxis or have
anticoagulant overdose – vit.K 2-10 mg, repeated till coagulation
studies are normal
• Overt bleeding / suspected liver dysfunction – fresh frozen plasma

18. DIC
SCREENING TESTS
• Peripheral blood film & hemogram – schistocytes &
thrombocytopenia
• PT, aPTT, thrombin time – prolonged
SUPPORTIVE TESTS
• D – dimer – increased
• DIC scoring system based on recommendations of Scientific
Standardization Committee of the International Society on
Thrombosis & Hemostasis

19. Algorithm for diagnosis of DIC using
DIC score
• Risk assessment
? Does patient have an underlying disorder known to be asso. with
DIC? (if yes proceed)
• Order global coagulation tests
Score test results
1)Platelet count Score
• >1,00,000/mm3 0
• 50,000- 1,00,000 1
• <50,000 2

20. 2)Elevated fibrin related marker Score
• no increase 0
• moderate increase 1
• strong increase 2
3)Prothrombin time
• <3s 0
• >3 but <6 1
• >6 2
4)Fibrinogen level
• >1g/L 0
• <1g/L 1
SCORE >/= 5 IS DIAGNOSTIC

21. TREATMENT
1)Hemostatic support(replacement therapy)
• Blood components used in DIC are : fresh frozen plasma,
cryoprecipitate, platelet concentrate, packed red cells
2)Heparin therapy
• Indication – arterial or large vessel venous thrombosis

22. THROMBOTIC DISORDERS
CLINICAL EVALUATION
• Predisposing factors : CHD, recent cardiac catheterization, recent sx,
trauma, use of central venous catheter, nephrotic syndrome,
dehydration, sepsis, collagen vascular diseases
• Limb edema, erythema & tenderness on dorsiflexion of foot (+VE
HOMAN SIGN) –DVT
• Diminished / absent arterial pulses & cool extremities – arterial
thrombosis

23. • Pulmonary embolism – anxiety, breathlessness, pleuritic chest pain,
fever, tachypnoea & cough
• CNS thrombosis – vomiting, lethargy, seizures, weakness
• In-utero stroke – seizures & lethargy
• Renal vein thrombosis – flank pain & hematuria
LABORATORY EVALUATION
• Rule out DIC
• Colour doppler – thrombosed vessels
• Echocardiography – for venacaval & proximal subclavian vein
thrombosis

24. • MRI in conjunction with magnetic resonance venography – cerebral
venous thrombosis
• CXR & ventilation- perfusion scanning– pulmonary embolism
MANAGEMENT
• Unfractionated / LMW Heparin followed by oral warfarin

25. THANK YOU