Hemorrhage

Pre by lect : MR ZAHID REHMAN

IPMS (KMU)
Hemostasis
Hemostasis is a precisely orchestrated process
involving platelets clotting factors and endothelium
that occur at the site of vascular injury and culminate
in the formation of blood clot which serves to prevent
or limit the extent of bleeding
Hemostasis means blood in a fluid, clot free state in
normal state vessel while inducing the rapid formation
of a localised hemostatic plug ( clots) at the site of
vascular injury.
Mechanism of cloting formation
Vascular injury due to endothelin small
peroid of vassoconstriction.
Platelates adhere to exposed extracellular
matrix (ECM) by binding to von
willibrand factor (VWF) then lead to
palateltes aggregates to form the
primary plug.
Local activation of the coaglative casades
result in “cementing” the palatelets into a
definitive secondry hemostatic plug.
Hemorrhage
Rupture or laceration of blood vessel with
extravasation of blood is called
hemorrhage .
OR
the Extravasation of blood from the
vessel due to vessel rupture or clot
formation
ETIOLOGY
Localised causes:
 Truama
 Abnormality of vessel due to anuerysm
 Atheroscelorosis
 Diapedesis
Enlarged interendothelial gap
(basement membrane injury).
Generalized causes :

Defect of coaglation mechanism in disease

such as hemophilia ,
Hyperprothrombinemia , and
hypofibrinogenemia.

Palatelets abnormalities such purpura and

thrombocytopenia.

Leukemia

deficiency of Vit. K
Different terminology related to hemorrage
 Hematoma:
 accumulation of blood within tissue.
 Petechiae:
 Minute 1- to 2-mm hemorrhages into
skin, mucous membranes.
 Purpura:
 Slightly larger (≥3 mm) hemorrhages.
 Ecchymoses:
 Larger (>1 to 2 cm) subcutaneous
hematomas (i.e., bruises).
 Large accumulations of blood in the
body cavities are called hemothorax,
hemopericardium,
hemoperitoneum, or
hemarthrosis (in joints).
Hematemesis:
Blood during vomiting
Hemoptysis:
Blood with cough
Melena:
Blood in feces
Hematuria :
Blood in urine
Clinical features:
Hypovolumic shock due to rapidly and
more blood loose
Small amount of blood is lethal in brain
Chronic blood loss may cause iron
deficiency anemia.
 Thrombosis
Thrombosis is the formation of a blood clot inside
a blood vessel, obstructing the flow of blood through
the circulatory system. When a blood vessel is injured,
the body uses platelets (thrombocytes) and fibrin to
form a blood clot to prevent blood loss. Even when a
blood vessel is not injured, blood clots may form in
the body under certain conditions. A clot that breaks
free and begins to travel around the body is known as
an embolus
 A thrombus is a solid mass of blood constituents which
developes in artery or vein.
 Is intravascular coagulation of blood often causing sinificant
interuption to blood flow.
 When a thrombus is significantly large enough to reduce the
blood flow to a tissue, hypoxia (oxygen deprivation) can occur
and metabolic products such as lactic acid can accumulate. A
larger thrombus causing a much greater obstruction to the blood
flow may result in anoxia, the complete deprivation of oxygen
and infarction, tissue death. There are also a number of other
conditions that can arise according to the location of the
thrombus and the organs affected.
Pathogenesis
Three primary influences predispose to
thrombus formation, the so-called
Virchow triad:
(1) endothelial injury
(2) stasis or turbulence of blood flow
(3) blood hypercoagulability
In other words it results from interaction
platelets, damaged endothelial cells
and the coagulation cascade.
Vascular endothelial injury :
Injury to endothelial exposes subsendothelial collagen
to palatelets which initiate clotting mechanism to form
thrombus. Vascular endothelial injury is particulary
important in thrombus formation in the heart and
arterial circulation.
Endothelial layer protect flowing blood from the
thrombogenic effect of subendothelial
tissue.Endothelial cell release some Heparin like
antithrombotic factor which prevent throbosis. Heparin
like substances are (thrombomudulin, Tissue
plasminogen activator(t.PA), inhibitor of platelates
aggregation PGI2)
Heparin like subs accelerate antithrombine 3
which inhibit the clotting factor.
Thrombomudulin convert thrombin into activator
of protein C which have anti thrombotic effect.
Inhibition plateltes aggregation include PGI2
and postacyclin.
Tissue plasminogen activator which activate
tissue plasminogen and help fibrinolytic
activity which prevent thrombosis.

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Endothelial cell also secrete prothrombolic substances
these are thromboplastin, VWF(VON WILLIBRAND
FACTOR) inhibition of tissue plasminogen.
When the endothelial surface damage the
antithrombotic porperty is lost and the subendothelial
surface expose which result thrombosis.
Imbalancing occur between antithrombotic and
prothromobotic acitivity.
Causes:
Truama
Inflammatory injury
hypertension
Bacterial toxin

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Alteration in normal blood flow :
Turbulence :
It contributes to arterial and cardaic
thrombosis by causing endothelial
injury.Turbulence means unequal blood
flow or the disruption of the axial blood
flow lead to turbulence.
Stasis :
Slowing of blood flow is the major factor in
the development of venous thrombi.
Causes :
Atherosclerosis
Aneurysms (abnormal aortic and arterial
dilatation) causes local stasis and are
common site of thrombosis .
Mural thrombi
Hyperviscosity syndrome result stasis.
Hypercoagulability :
Any alteration of the coaglation pathway
that predisposes to thrombosis.
Hypercoaglibility can be divided into primary(genetic) and
secondry(acquired) disorder.
primary (genetic)common causes are
Factor V mutation
Prothrombin mutation
Increased levels of factor VIII, IX, OR XI or fibrinogen
Rare causes due to defect in fibrinolysis
Secondry (acquired) common causes are
Prolong bed rest or immobilization
MI
Tissue injury
Disseminated intravascular coagulation

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Classification

 Venous thrombosis
 Venous thrombosis is the formation of a thrombus (blood clot)
within a vein There are several diseases which can be classified .
 Deep vein thrombosis
 Deep vein thrombosis (DVT) is the formation of a blood clot
within a deep vein. It most commonly affects leg veins, such as
the femoral vein. Three factors are important in the formation of a
blood clot within a deep vein—these are the rate of blood flow,
the thickness of the blood and qualities of the vessel wall.
Classical signs of DVT include swelling, pain and redness of the
affected area.
 Portal vein thrombosis
 Portal vein thrombosis affects the hepatic portal vein, which can
lead to portal hypertension and reduction of the blood supply to
the liver. It usually has a pathological cause such
as pancreatitis, cirrhosis, diverticulitis or cholangiocarcinoma.
 Renal vein thrombosis
 Renal vein thrombosis is the obstruction of the renal
vein by a thrombus. This tends to lead to reduced
drainage from the kidney. Anticoagulation therapy is
the treatment of choice.
 Jugular vein thrombosis
 Jugular vein thrombosis is a condition that may occur
due to infection, intravenous drug use or malignancy.
Jugular vein thrombosis can have a varying list of
complications, including: systemic sepsis, pulmonary
embolism.Though characterized by a sharp pain at
the site of the vein.
 Arterial thrombosis
 Arterial thrombosis is the formation of a thrombus
within an artery. In most cases, arterial thrombosis
follows rupture of atheroma, and is therefore referred
to as atherothrombosis.
 Stroke
 A stroke is the rapid decline of brain function due to a
disturbance in the supply of blood to the brain. This
can be due to ischemia, thrombus, embolus (a lodged
particle) or hemorrhage (a bleed). In thrombotic stroke,
a thrombus (blood clot) usually forms
around atherosclerotic plaques.
 Myocardial infarction
 Myocardial infarction (MI) or heart attack,
is caused by ischemia, (restriction in the
blood supply), often due to the
obstruction of a coronary artery by a
thrombus. This restriction gives an
insufficient supply of oxygen to the heart
muscle which then results in tissue
death,(infarction). A lesion is then
formed which is the infarct
Morphology
 Arterial thrombi(pale thrombi)
 Originate from injury sites
They are dry easliy breakeble granular
Masses manily composed of palateltes
And fibrin with few entrapped RBCs.
Pale thrombi typically develop in arterail
Circulation and are attached to vessel
Wall.
Thrombi occur in the heart chamber or
aortic lumen is called mural thrombi.
Abnormal myocardial contraction
(arrythmias, cardiomayopathy, MI ,
myocarditis) promote cardaic mural
thrombi.
Thrombi on the heart valve are called
vegetation.
Venous thrombi (phlebothrombi)
Originate from the sites of stasis 2/6/2020
These thrombi are composed of palateletes ,
fibrin and large number of RBCs entrapped in
fibrin mesh. Red thrombi typically develop in
venous circulation .slow blood flow in veins
enourageds entrapment of red cells.
Propagation of thrombosis
The thrombus enlarge through the accretion of
additional platelets and fibrin, increasing the
odds of vascular occulusion or embolization.
Resolution of thrombosis
If the thrombus is newly formed ,
activation of fibrinolytic factors may lead
to it,s rapid shrinkage and complete
dissolution.

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