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Approach To Bleeding Neonate

1. Bleeding in neonates can be life-threatening and requires immediate attention. Common causes are platelet or coagulation disorders. 2. Hemostasis involves vessel walls, platelets, coagulation proteins, and fibrinolytic systems working together to stop bleeding at the site of injury. 3. Disorders can occur from deficiencies in coagulation factors, platelets, or natural anticoagulants, leading to bleeding or thrombosis. Acquired disorders may involve multiple interacting problems.

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Indranil Dutta
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149 views20 pages

Approach To Bleeding Neonate

1. Bleeding in neonates can be life-threatening and requires immediate attention. Common causes are platelet or coagulation disorders. 2. Hemostasis involves vessel walls, platelets, coagulation proteins, and fibrinolytic systems working together to stop bleeding at the site of injury. 3. Disorders can occur from deficiencies in coagulation factors, platelets, or natural anticoagulants, leading to bleeding or thrombosis. Acquired disorders may involve multiple interacting problems.

Uploaded by

Indranil Dutta
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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APPROACH TO A BLEEDING

NEONATE
INTRODUCTION
• Bleeding syndromes of newborn are not
uncommon and they may be life threatening and
demand immediate attentions .
• Neonatal bleeding include skin and mucosal
bleedings, retroperitonial, GI, parenchymal or
intracranial hemorrhages.
• Petechie are pathgnomonic of platelet disorders ;
• Hematomas are common in coagulation
disorders.
INTRODUCTION
• A moderate decrease in factors II, VII, IX, and X
normally occurs in all newborn infants by 48-
72 hr after birth, with a gradual return to birth
levels by 7-10 days of age.
• Caused by lack of free vitamin K from the
mother .
• Absence of the bacterial intestinal flora
normally responsible for the synthesis of
vitamin K.
• In neonates diminished platelets function and
suboptimal defence against clot formation.
• Increase in vascular permeability and fragility
in preterm.
• Accentuation and prolongation of this
deficiency between the 2nd and 7th days of
life result in spontaneous and prolonged
bleeding.
• Must be distinguished from disseminated
intravascular coagulopathy and some
infrequent congenital deficiencies of one or
more of other factors that are unresponsive to
vitamin K.
PATHOPHYSIOLOGY
HEMOSTASIS :
• Hemostasis is the active process that clots
blood in areas of blood vessel injury yet
simultaneously limits the clot size only to the
areas of injury.
• The main components of the hemostatic
process are the vessel wall, platelets,
coagulation proteins, anticoagulant proteins,
and fibrinolytic system
THE PROCESS
• The intact vascular endothelium is the primary
barrier against hemorrhage.
• The endothelial cells that line the vessel wall
normally inhibit coagulation
• Provide a smooth surface that permits rapid
blood flow.
• After vascular injury, vasoconstriction occurs
and flowing blood comes in contact with the
subendothelial matrix.
HEMOSTATIC MECHANISM
CLOTTING CASCADE: ACTIVATION AND
AMPLIFICATION
[1] THE ROLE OF PLATELETS
• Von Willebrand factor (VWF) changes
conformation and provides the glue to which the
platelet VWF receptor, the glycoprotein Ib
complex binds,
• Tethering platelets to sites of injury.
• During the process of platelet activation platelet
phospholipids interact at 2 specific, rate-limiting
steps in the clotting process—
• Factor VIII(X-ase complex)
• Factor V (prothrombinase complex)
Activating the platelets and triggering secretion of storage
granules containing adenosine diphosphate (ADP),
serotonin, and stored plasma and platelet membrane
proteins.
ACTIVATION OF X COMPLEX
• Exposed tissue factor binds
to factor VII and activates
the extrinsic clotting
cascade.

• The activated clotting factor


then initiates the activation
of the next sequential
clotting factor in a
systematic manner.
ACTIVATION OF X COMPLEX
• Factor XII will activate
factor XI, thus initiating
the intrinsic mechanism.
• Both VIIa and active
factor XIa will promote
cascade reactions,
eventually activating
factor X.
ACTIVATION THROMBIN
• Active factor X, along with
factor III, factor V, Ca++, and
PF3, will activate
prothrombin activator.

• Prothrombin activator
converts prothrombin to
thrombin.
• Thrombin converts
fibrinogen to fibrin.
• Fibrin initially forms a loose
mesh,
• Factor XIII causes the
formation of covalent cross
links, which convert fibrin
to a dense aggregation of
fibers.
• Platelets and red blood
cells become caught in this
mesh of fiber, thus the
formation of a blood clot.
ANTICOAGULANTS
• Virtually all procoagulant proteins are
balanced by an anticoagulant protein that
regulates or inhibits procoagulant function.
• Four clinically important, naturally occurring
anticoagulants regulate the extension of the
clotting process: antithrombin III (AT-III),
protein C, protein S, and tissue factor pathway
inhibitor.
FIBRINOLYSIS
• Once a stable fibrin-platelet plug is formed, the
fibrinolytic system limits its extension and also
lyses the clot to re-establish vascular integrity.
• Plasmin, generated from plasminogen by either
urokinase-like or tissue-type plasminogen
activator, degrades the fibrin clot.
• The fibrinolytic pathway is regulated by
plasminogen activator inhibitors and α-
antiplasmin, as well as by the thrombin-
activatable fibrinolysis inhibitor.
• Finally, the flow of blood in and around the
clot is crucial, because flowing blood returns
to the liver, where activated clotting factor
complexes are removed and
• New procoagulant and anticoagulant proteins
are synthesized to maintain homeostasis of
the hemostatic system.
PATHOLOGY
• Congenital deficiency of an individual procoagulant
protein leads to a bleeding disorder, whereas
deficiency of an anticoagulant (clotting factor
inhibitor) predisposes the patient to thrombosis.
• In acquired hemostatic disorders, there are
frequently multiple problems.
• A primary illness (sepsis) and its secondary effects
(shock and acidosis) activate coagulation and
fibrinolysis and impair the host’s ability to restore
normal hemostatic function.
• Disseminated intravascular coagulation,
platelets, procoagulant clotting factors and
anticoagulant proteins are consumed,
• Leaving the hemostatic system unbalanced
and prone to bleeding or clotting.
• Newborn infants and patients with severe liver
disease have impaired synthesis of both
procoagulant and anticoagulant proteins.
• Such dysregulation predisposes to
hemorrhage or thrombosis with mild or
moderate triggers.

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