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approch to bleeding by R

The document outlines the approach to managing bleeding in children, detailing the phases of hemostasis, types of bleeding disorders (acquired and inherited), and their symptoms. It emphasizes the importance of history, physical examination, and laboratory investigations in diagnosing and managing these conditions. Key laboratory tests include platelet count, bleeding time, prothrombin time, and activated partial thromboplastin time, among others.

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samritt022
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15 views27 pages

approch to bleeding by R

The document outlines the approach to managing bleeding in children, detailing the phases of hemostasis, types of bleeding disorders (acquired and inherited), and their symptoms. It emphasizes the importance of history, physical examination, and laboratory investigations in diagnosing and managing these conditions. Key laboratory tests include platelet count, bleeding time, prothrombin time, and activated partial thromboplastin time, among others.

Uploaded by

samritt022
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPTX, PDF, TXT or read online on Scribd
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APPROACH TO BLEEDING CHILD

Outline
Introduction
Approach
History
Physical examination
Investgations
Bleeding disorder and their management
Introduction
Hemostasis is the dynamic process of
coagulation as it occurs in areas of vascular
injury, involving interaction of platelets,
vascular wall, and pro- coagulant and
anticoagulant proteins to prevent or arrest
bleeding.
Phases of Hemostasis

 Vascular Phase
 Platelet Phase
 Coagulation Phase
 Fibrinolytic Phase
Primary hemostasis: role of blood vessels and
platelets in the initial formation platelet plug
Activated by vascular injury
Secondary hemostasis:Is the activation of a
series of plasma proteins in the coagulation
system to form a fibrin clot
Primary hemostasis Secondary hemostasis

Activated by desquamation By large injuries to BV and


and small injuries to BV surrounding tissue

Involves vascular intima & Platelets and coagulation


platelets system

Rapid and short lived Delayed & long term


Sub. Released by endothlial Tissue factors exposed on cm
cells
Coagulation phase
Major types of disorders
1)Acquired
 Thrombocytopenia: Autoimmune/drug-induced,HUS
Liver diseases: Cirrhosis, acute hepatic failure
Vitamin K deficiency: Malabsorption/ malnutrition
Hematologic disorders: leukemias
DIC: sepsis, malignancies, trauma
Drugs
2)INHERITED
 Deficiencies of coagulation factors: Hemophilia A and
B
 Platelet disorders: Glanzmann thrombasthenia,
Bernard-Soulier
 Fibrinolytic disorders: Antiplasmin deficiency,
plasminogen activator inhibitor-1 deficiency
 Connective tissue disorder: Ehlers-Danlos syndrome
Platelet disorders Coagulation factor
disorders

Site of bleeding Skin, Mucous membranes Deep in soft tissues


(epistaxis, gum, vaginal, GI (joints, muscles)
tract)

Petechiae yes no
Ecchymoses (“bruises”) Small, superficial Large, deep

Bleeding after cuts & yes no


scratches

Bleeding after surgery or Immediate,usually mild Delayed(1-2D) often severe


trauma
symptoms
• Petechia
• Pupura and ecchymosis
• Blood in stool
• Blood In gingiva
• Nose bleeds
Approach
Age at the onset of bleeding
An inherited bleeding is strongly considered when
the onset is in infancy or early childhood & is
associated with a positive family Hx.
However, a negative family history does not
exclude an inherited coagulation disorder.
Some typical presentations
 M infant who is starting to walk and presents with a
painful swollen joint after a fall: hemophilia
 An adolescent girl with excessive menstrual bleeding,
recurrent nosebleeds: vWD
 5 yrs old child with moderate mucocutaneous purpura
in the wake of a viral infection :has acute post-
infectious immune thrombocytopenia (ITP, previously
known as idiopathic thrombocytopenic purpura)
 A teenage girl: easy bruising + mild pallor with a
strong family Hx of autoimmune disorders may have
chronic ITP
 1O day old infant with bleeding from the umbilical
stump should be evaluated for factor XIII deficiency

 Site, severity and duration of bleeding


 Hx of trama/surgery
 SS of CLD, nutritional histories……
Medication :
aspirin and NSAID’s, use of such drugs within one
to two weeks of platelet function testing may
cause abnormalities.
Family Hx
Bleeding only in male siblings and maternal uncles
is suggestive: X-linked recessive (hemophilia A/B).
In contrast, AD such as hereditary hemorrhagic
telangiectasia will affect individuals of both sexes
Physical examination

mucous membranes or skin (mucocutaneous


bleeding) or with the muscles and joints

Skin stigmata :
 petechiae
Purpura
Ecchymosis
hematoma
 Individuals with hemophilia A/B: deep bleeding into
muscles/joints, with more ecchymoses & hematoma formation
 Patients with VWD or platelet function defects have epistaxis,
menorrhagia, petechiae, ecchymoses, occasional hematomas
 Disorders of the collagen matrix and vessel wall may have loose
joints and lax skin associated with easy bruising
 Arterial thrombi usually cause an or a painful, white, cold
extremity
Laboratory Investigations
Platelet Count
 thrombocytopenia is the most common
acquired cause of a bleeding diathesis in
children.
platelet count of >50,000/ml rarely have
significant clinical bleeding unless its
<10,000/ml
Bleeding time
 Tests vascular integrity and platelet function
 Normal < 8 minutes,ussually 1-6 mins
 Borderline 8-10 minutes
 Abnormal 10 + minutes
 Affected by drugs
 Use of the bleeding time is declining in many centres.
Prothrombine time(Pt)
 measures extrinisic & Common pathway
the normal PT value is 10-13 sec. PT has been
standardized using INR & the ratio is used to
determine similar degrees of anticoagulation
with warfarin (Coumadin)–like medications.
 PT is prolonged with deficiencies of factors I,II
V, VII, X
Partial Thromboplastin Time(PTT)
 Tests intrinsic and common pathway
 Average normal 26-34 seconds
 PTT can be abnormally prolonged by numerical or
functional deficiencies in factors VIII, IX, X, XI, and XII.
 Affected by heparin
 Can be effected by coumadin at supra-therapeutic levels
due to effects on the common pathway
 Activated partial thromboplastin time
(aPTT)

 It is called "partial" because clotting is initiated in vitro


with agents that are only partial thromboplastins (ie, they
are incapable of activating the extrinsic pathway)
 The aPTT is sensitive to deficiencies of factors XII, XI, IX,
VIII and heparin
 It is less sensitive than the PT to deficiencies within the
common pathway (eg, factors X, V, prothrombin, and
fibrinogen) and is unaffected by alterations in factors VII
and XIII.
Thrombin time
 final step in the clotting cascade
 usually 11-15 sec.
 Prolongation of thrombin
 hypofibrinogenemia
 dysfibrinogenemia
 in the presence of heparin and fibrin split products
 If heparin contamination is cause of prolonged PT,
a reptilase time is usually ordered.
Reptilase Time
 uses snake venom to clot fibrinogen.
 Unlike thrombin time, Rt is not sensitive to heparin
and is prolonged only by reduced or
dysfibrinogemia and fibrin split products.
Therefore, if thrombin time is prolonged but
reptilase time is normal, the prolonged thrombin
time is due to heparin and does not indicate the
presence of fibrin split products or reduced
concentration or function of fibrinogen.
Mixing Studies
 Done when there is unexplained prolongation of PT, PTT, or TT
 Normal plasma is added to the patient's plasma, and the PT or
PTT is repeated. Correction of PT or PTT => def. of a clotting
factor, (because a 50% level of individual clotting proteins is
sufficient to produce normal PT or PTT.)
 If the clotting time is not corrected or only partially corrected,
an inhibitor is usually present.
D-Dimer
produced when fibrinogen is clotted by
thrombin and is specific for fibrinolysis
elevated in patients with DIC or DVT
Is useful to exclude venous thrombosis and
pulmonary embolus because of its high
negative predictive value; for example, a
patient with a normal D-dimer value is unlikely
to have an acute thrombosis
Antiphospholipid antibodies :lupus
anticoagulants also can result in a prolonged
aPTT that is not correctable by the addition of
normal plasma.
Blood smear
BM biopsy

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