thrombosis, embolism, infarction

1. Virchow’s Triad:::
Endothelial Injury
Stasis or Blood turbulence
Hypercoagulability

2.  Loss of endothelium exposes Subendothelial collagen
Etiology:
Hypertension
Endotoxins
Scarred valves
Hyperhomocystinemia
Hypercholesterolemia
Smoking
Radiation
1. ENDOTHELIAL INJURY

3.  Turbulence Arterial thrombus
 Stasis Venous thrombus
 Alteration in Flow causes….
 Disrupt the laminar blood flow
 Cause concentration of Clotting factors
 Permit build of thrombi
 Promote endothelial cell activation

4.  PRIMARY/ GENETIC:
 Factor V Leiden mutation
 Prothrombin mutation
 Antithrombin III deficiency
 Protein C & Protein S deficiency
 ACQUIRED CAUSES:
 Prolonged bed rest- Immobilization
 Myocardial Infarction
 Surgery, Fracture, Burns
 Cancer, Cardiac valves,
 DIC, SLE
 Hyperestrogen states, Smoking, Sickle cell anemia, Nephrotic
syndrome.

5. Previous extensive
transmural
myocardial
infarction.
The stasis of blood
in the aneurysm
predisposes to
mural thrombosis.

6.  Deep thrombi occur in large veins of leg
 DVT are asymptomatic in 50 % of patients
 Trousseau Syndrome: Tumor associated
procoagulant release Increased risk of Thromboembolic
phenomenon in disseminated cancers.
 Also known as migratory thrombophlebitis
 Ca Pancreas, Prostate, Stomach, Breast, Lung, Osteosarcoma,
AML- M3.

7. Propagation
Embolization
Dissolution
Recanalization
Organization

10.  “Detached Intravascular Solid, Liquid or gas mass carried
by blood to a distant site.”
 99% are Thrombo-embolus
 Consequences of embolus is ischemic necrosis of affected
tissue.

11.  Venous Embolism/ Pulmonary (DVT)
 Arterial Embolism (Post MI)
 Paradoxical Embolism (Venous will become arterial: due to
ASD/ VSD)
 Fat embolism
 Amniotic fluid embolism
 Air embolism
 Septic embolism
 Foreign body embolism.
Types of Embolism:

12.  Most commonly from venous emboli from leg veins (DVT)
 “Saddle embolus” obstructs main Pulmonary artery
 Once a Pulmonary embolus occurs, patient will be prone for
recurrent emboli episodes.
 Multiple emboli or shower of small emboli in small pulmonary
arteries.

13.  Most arise from Intra cardiac mural thrombi
 Left ventricular wall infarction and Mitral stenosis
predisposes to thrombi and embolus
 Arterial emboli travel to wide variety of sites
 Lower limbs, Brain, intestines, kidney, spleen…….any organ.

14.  Microscopic fat globules enter circulation following fracture of
long bones
 Fat embolism syndrome:: Symptoms appear 1- 3 days after
injury
 Pulmonary insufficiency: Tachypnea, Dyspnea, Tachycardia
 Neurologic symptoms: Irritability, Restlessness, Delirium, Coma
 Low platelets: Petechial skin rash
 Fatal in 10% of individuals

15.  Fracture long bones: Imp.
 Soft tissue trauma
 Burns
 Parenteral lipid infusion
 Sickle cell crisis
 Acute pancreatitis
 Liposuction
 Decompression sickness

16.  Gas bubbles in circulation
 100 ml of air is needed to produce clinical effect
 Chest wall injury, Neck injury, Therapeutic, Intra-operative
 Decompression sickness seen in Deep sea divers

17.  Amniotic fluid into ruptured uterine veins
 Grave, but uncommon complication
 Important obstetric complication
 Sudden onset of severe dyspnea, Cyanosis,
Hypotension, Shock, Seizures, Coma.
 If survives… Pulmonary edema, DIC
AMNIOTIC FLUID EMBOLISM

19.  An infarct is an area of ischemic necrosis caused by
occlusion of arterial supply or venous drainage
 Can be due to Thrombus, embolus, vasospasm, atheroma,
compression of vessels, etc.,
 Venous blockade Congestion

20.  Classified based on the color
1. Red (Hemorrhagic) infarct
2. White (Anemic) infarct
 Red infarcts are seen in::
- Dual blood supply.. Lung, Small intestine
- Loose tissues.. Lung
- With venous occlusions (ovarian torsion)
- Previously congested tissue

21.  White Infarcts::
- Arterial occlusions
- Organs with end arterial blood supply
- Solid organs.. Heart, Spleen, Kidneys, Brain
 Microscopy::
- Coagulative necrosis
- Liquefactive necrosis