Pulmonary Pathology Online
Pathology of Pulmonary Thromboembolism
The most common
lesion of the pulmonary vasculature is pulmonary embolism, and the most
common emboli are thrombi derived from the leg veins.
The embolism of thrombi to the lung is considered to be both underdiagnosed and overdiagnosed by clinicians.
Thrombi can be found in pulmonary arteries in 20 to 60% of adult autopsies, though many of these are small and probably not of clinical consequence.
Thrombi forming anywhere in the venous circulation can embolize in the lung.
In practice more than 90% of clinically significant emboli arise in the deep veins of the legs and thighs and are associated with venous stasis.
The clinical effects of thromboembolism vary depending on the volume of emboli and on the condition of both the pulmonary and systemic circulations.
Some but not all of the physiologic consequences of thromboembolism can be explained by mechanical obstruction of the vascular bed.
The effects of embolism on gas exchange are :
(1) increased dead space ventilation,
(2) pneumoconstriction, and
(3) impaired synthesis of pulmonary surfactant.
The ventilation of unprefused lung adds to the work of breathing and produces tachypnea and a sense of dyspnea.
Transient constriction of smooth muscle in airways and alveolar ducts occurs in response to vagal reflexes and humoral mediators such as serotonin, adenosine diphosphate , and thromboxane released from platelets.
The hypoxemia that commonly follows pulmonary embolism is attributable to the production of areas of low ventilation/perfusion ratio by the constriction of small airways in well-perfused lung tissue surrounding an occluded area.
Some patients manifest asthma-like wheezing.
Impaired surfactant production is a delayed effect that produces edema and atelectasis.
The hemodynamic effects of embolism are slight unless more than 50% of the vascular bed is occluded.
They include a rise in pulmonary artery pressure and in severe cases congestive heart failure and shock.
Massive pulmonary embolism is a well-recognized cause of sudden death, which may be virtually instantaneous or extend over a period of a few minutes.
The major pulmonary arteries are distended with clots that are often coiled or twisted and bear the imprint of venous valves.
The lung parenchyma shows little change except congestion, which presumably comes by way of the bronchial circulation.
Sublethal thromboemboli are often recurrent.
Consequently, it is common to find emboli of varied age at autopsy.
Fresh emboli are poorly adherent to the vessel wall but can be distinguished from postmortem clots because they distend the artery, have a drier, more granular surface, and seem less elastic.
Lines of Zahn and imprints of valves are diagnostic.
Older thrombi are adherent and retracted to varying degrees.
The fate of nonfatal emboli is variable.
Fibrinolytic mechanisms produce dissolution of the embolus within a few days, as demonstrated by serial angiograms and lung scans.
Organization of emboli and recanalization restore the vascular lumen more slowly, within weeks.
The embolus becomes invaded by myofibroblasts from the vascular intima, whilst endothelial cells migrate out over the surface of the clot and invade the thrombotic material to form new vascular channels within it.
Gradually the clot is transformed into a ridge or into a web with multiple points of attachment to the intima.
The core of the web is fibrous tissue, perhaps containing a few siderophages, and the surface is endothelialized.
Occasionally such webs can be detected angiographically.
Clinically, diagnosis of pulmonary emboli is difficult, even in fatal cases and with infarction.
Even without treatment, there is usually improvement in perfusion within the first day due to fibrinolysis and contraction of the thrombus.
The embolus may completely resolve or be reduced to mural plaque within weeks or months and infarct is converted to a fibrous scar.
With diagnosis and use of fibrinolytic agents, mortality rate may be reduced.
Occlusion of pulmonary arteries, are almost always embolic.
Thrombosis of pulmonary arteries, are rare and occurs only in pulmonary hypertension and pulmonary atherosclerosis.
More than 95 % of pulmonary emboli arise in deep veins of legs.
Frequency of pulmonary embolism correlates with a predisposition to thrombosis in the legs. 30% of the patients with severe burns, trauma or fractures show pulmonary embolism at autopsy.
Large emboli impact in the major pulmonary artery or astride the bifurcation of the pulmonary artery (saddle embolus).
Emboli may cause instantaneous death.
Emboli may cause cardiovascular collapse (Example: Acute cor pulmonale, right-sided heart failure).
Hemodynamic compromise is secondary, not only to vascular obstruction, but also to reflex vasoconstriction caused by such agents as thromboxane A2+.
Small emboli may be clinically silent in patients without cardiovascular failure.
Emboli may cause transient chest pain and sometimes haemoptysis due to pulmonary hemorrhage.
Pulmonary hemorrhage is characterized by blood in the alveoli, but there is no ischemic necrosis of the pulmonary parenchyma.
In patients with compromised pulmonary circulation (Example: Cardiac failure), emboli may give rise to infarction.
Middle sized emboli occlude moderate-sized peripheral pulmonary branches.
In rare cases, multiple small emboli may produce chronic cor-pulmonale and eventually pulmonary hypertension and vascular sclerosis.
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