Pathology of Thrombosis

Thrombosis and Embolism

• Hypercoagulability states can lead to thrombosis and embolism, including:
  • Hyperestrogenic states (pregnancy and postpartum)
  • Oral contraceptive use
  • Sickle cell anemia
  • Smoking
• Thrombus morphology:
  • Lines of Zahn: alternating pale platelet and fibrin layers with darker red cell-rich layers
• Fate of the thrombus:
  • Propagation: enlargement
  • Embolization: transported elsewhere
  • Dissolution: fibrinolysis
  • Organization and recanalization: ingrowth of endothelial cells, smooth muscle cells, and fibroblasts

Clinical Features

• Venous thrombosis (phlebothrombosis):
  • Most common in superficial or deep veins of legs
  • Deep vein thrombosis (DVT): causes localize pain and edema; associated with stasis or hypercoagulable state
• Arterial and cardiac thrombosis:
  • Atherosclerosis, myocardial infarction, and rheumatic heart disease can lead to thrombosis, which can embolize to brain, kidneys, and spleen
• Disseminated intravascular coagulation (DIC):
  • Pathologic activation of coagulation cascade, leading to widespread thrombi formation in microcirculation
  • Consumptive coagulopathy: uses up platelets and coagulation factors, which can evolve into bleeding catastrophe
  • Secondary to obstetric complications, advanced malignancy, or sepsis

Embolism

• An embolus is a detached intravascular solid, liquid, or gaseous mass that travels through the blood to a distant site, causing tissue dysfunction or infarction
• Emboli can travel through the bloodstream until they encounter vessels too small to permit further passage, causing partial or complete vascular occlusion

Pulmonary Embolism

• Originate from deep venous thromboses and are the most common form of thromboembolic lesions
• Can occlude the main pulmonary artery, lodge at the pulmonary artery bifurcation (saddle embolus), or pass out into smaller branching arteries
• Rarely, a venous embolus can pass through an interatrial or interventricular defect and gain access to the systemic arterial circulation (paradoxical embolism)

Systemic Thromboembolism

• Mostly arise from intracardiac mural thrombi
• Most commonly involve the lower extremities (75%) or brain (10%)
• Consequences depend on the vulnerability of the affected tissues to ischemia, the caliber of the occluded vessel, and the presence of collateral blood supply

Fat and Marrow Embolism

• Microscopic fat globules and hematopoietic bone marrow can be found in the pulmonary vasculature after fractures of long bones or soft tissue trauma

Air Embolism

• Gas bubbles within the circulation can coalesce to form frothy masses that obstruct vascular flow and cause distal ischemic injury
• Decompression sickness: nitrogen dissolved in the blood and tissues during high-pressure breathing (e.g., scuba diving) can come out of solution during rapid decompression, causing gas bubbles to form

Infarction

• Ischemic necrosis caused by occlusion of either the arterial supply or venous drainage
• Arterial thrombosis or arterial embolism underlies the vast majority of infarctions
• Venous thrombosis most commonly leads to congestion
• Infarcts caused by venous thrombosis are more likely in organs with a single efferent vein (e.g., testis and ovary)

Morphology of Infarction

• Red (hemorrhagic) or white (anemic) and may be septic or bland
• Red infarcts: occur with venous occlusions (e.g., testicular or ovarian torsion) or in tissues with dual circulations (e.g., lung and small intestine)
• White infarcts: occur with arterial occlusions in solid organs with end-arterial circulation (e.g., heart, spleen, and kidney)