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.