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A blood clot within a blood vessel or within the heart

Pathogenesis is given by Virchow’s triad
endothelial injury
stasis or turbulence of blood flow
blood hypercoagulability

Endothelial Injury

The dominant of the three
Dysfunctional endothelium may elaborate greater amount of pro-coagulant factors or may synthesize lesser amount of anti-coagulant effectors.
Seen commonly in
HTN, trauma, lesions likeMS and VSD causing jet lesion, homocysteinuria, radiotherapy, smoke


any alteration of the coagulation pathways that predisposes to thrombosis
Hyper-coagulable states
Primary (Genetic)

COMMONEST: Mutations like –
- Factor V
- Mutation in prothrombin gene
- Mutation in methyl tetrahydrofolate gene

Rare: Deficiencies like –
- Antithrombin III deficiency
- Protein C deficiency
- Protein S deficiency 
Very rare: Fibrinolysis defects

Secondary (Acquired)

High risk for thrombosis

Prolonged bed rest or immobilization
Myocardial infarction  
Atrial fibrillation
Tissue damage (surgery, fracture, burns)
Cancer (TROUSSEAU syndrome, i.e., migratory thrombophlebitis)     
Disseminated intravascular coagulation
Heparin-induced thrombocytopenia (HIT)
Antiphospholipid antibody syndrome (lupus anticoagulant syndrome)

Low Risk for thrombosis

Nephrotic syndrome 
Hyperestrogenic states (pregnancy)
Oral contraceptive use    
Smoking, Obesity
Morphology of thrombus:

Differs according to the site of thrombosis
In heart and aorta: mural thrombi have lines of Zahn due to layers of RBC alternating with layers of platelet and fibrin

Arterial thrombi: usually superimposed on a plaque rupture or due to trauma or vasculitis: appears gray white and friable due to less RBC in the clot

Commonest sites are coronary, carotid and femoral

Venous thrombi or phlebothrombosis: forms a long cast due to slow blood flow, red due to RBC collection

Commonest sites are DVT of lower legs, upper limbs, peroprostatic plexus, ovarian and periuterine veins, dural sinus of brain, portal and hepatic vein.

Fate of a thrombus

Infection forming mycotic aneurysm and septic embolisation


A detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin
99% of the emboli are dislodged thrombi, hence, the term THROMBOEMBOLISM
Potential consequence of embolism is INFARCTION of the tissue distal to it.


Fat embolism eg after fractures
Air embolism, eg in open carotid injury, angiographic procedures, Caisson’s disease in deep sea divers
Amniotic fluid embolism in abruptio placenta of pregnancy

Pulmonary thromboembolism

In greater than 95% of cases, pulmonary emboli originate from deep leg vein thrombi above the level of the knee.

Saddle embolus- A large pulmonary thromboembolus impacting across the bifurcation of pulmonary artery.

Paradoxical embolism – A rare condition where an venous thromoembolus may pass through an interatrial (more common) or interventricular defect to gain access to the systemic circulation.

Frequently, pulmonary thromboemboli are multiple, sequential emboli.
In general, a patient who has had one pulmonary embolus is at high risk of having more.

When 60% of the pulmonary circulation is obstructed sudden DEATH , Right heart failure , (cor pulmonale) or cardiovascular collapse occurs.

With left sided cardiac failure & sluggish bronchial artery flow a pulmonary embolus may cause a large infarct. But, with normal cardiac function these emboli in medium size pulmonary artery will cause pulmonary hemorrhage but no infarct.

Emboli into small end-arteries cause infarct.
Multiple emboli over time will cause Pulmonary Hypertension and Right Heart Failure.
Most pulmonary emboli (60-80%) ARE CLINICALLY SILENT.


Embolism in arterial circulation


80% are intra cardiac mural thrombi.
Rest- are from ulcerated atherosclerotic plaque or vascular vegetation or aortic aneurysm.
These can lodge anywhere in the body (as opposed to venous emboli, which can ONLY lodge in lungs with exception of PARADOXICAL EMBOLI).
COMMON SITES: 75% - L. Limbs. 10% - Brain.
Rest - Intestine, Kidneys, Spleen, upper extremities.


Happens in 90% case; but, ONLY 1% have clinical findings.


Pulmonary insufficiency, neurologic symptoms.
Fatal in about 10 % case.
Symptoms appear 1-3 days after injury with sudden onset of tachypnea, dyspnea, and tachycardia.
Neurologic symptoms are irritability, restlessness with progression to delirium and coma.


BOTH mechanical obstruction & Chemical injury

MECHANICAL: Neutral fat-Micro-emboli-Occlusion of pulmonary or cerebral micro-circulation.

CHEMICAL: Free fatty acids released from fat globules also cause toxic injury to endothelium.
Also, Platelets adhere to fat globules and get removed from circulation-THROMBOCYTOPENIA- Petechial hemorrhage.


Air may enter the circulation during obstetric procedure or chest wall trauma
More than 100 ml air is required to produce clinical effects


Expossure to sudden changes in atmospheric pressure.
Scuba and deep sea divers, under water construction workers, people in unpressurized air craft in rapid ascent are at risk.
Characterised by
bends – painful condition due to rapid formation of gas bubbles within skeletal muscles and supporting tissues in and about joints (derived from Grecian bend)
Chokes – edema, hemorrhages, and focal atelectasis or emphysema in lungs leading to respiratory distress
Caisson Disease – a chronic form of decompression sickness in which the vascular obstruction causes multiple foci of ischemic necrosis of bone, particularly affecting the head of the femur, tibia and humerus


CAUSE: Tear in placental membrane and rupture of uterine veins.

S/S:Suden onset of SOB (Shortness of breath),
Cyanosis, Shock.

If the patient survives the initial crisis, pulmonary edema typically develops, along with DIC, due to release of thrombogenic substances from amniotic fluid.
FINDINGS: In lungs: Squamous cells, shed from fetal skin, lanugo hair, fat from vernix caseosa.

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