Fig. 4.15 ). Frequently, multiple emboli occur, either sequentially or as a shower of smaller emboli from a single large thrombus; a patient who has had one pulmonary embolus is at increased risk for having more. Rarely, an embolus passes through an atrial or ventricular defect and enters the systemic circulation (paradoxical embolism). A more complete discussion of PE is found in Chapter 13; the major clinical and pathologic features are the following:
Most pulmonary emboli (60%–80%) are small and clinically silent. With time, they undergo organization and become incorporated into the vascular wall; in some cases, organization of thromboemboli leaves behind bridging fibrous webs.
At the other end of the spectrum, a large embolus that blocks a major pulmonary artery can cause sudden death.
Embolic obstruction of medium-sized arteries and subsequent rupture of downstream capillaries rendered anoxic can cause pulmonary hemorrhage. Such emboli do not usually cause pulmonary infarction because the
Fig. 4.15 Embolusderivedfromalower-extremitydeepvenousthrombuslodgedinapulmonaryarterybranch.
area also receives blood through an intact bronchial circulation (dual circulation). However, a similar embolus in the setting of left-sided cardiac failure (and diminished bronchial artery perfusion) can lead to a pulmonary infarct.
Embolism to small end-arteriolar pulmonary branches usually causes infarction.
Multiple emboli occurring through time can cause pulmonary hypertension and right ventricular failure (cor pulmonale).
Most systemic emboli (80%) arise from intracardiac mural thrombi; two-thirds of these are associated with left ventricular infarcts and another 25% with dilated left atria (e.g., secondary to mitral valve disease). The remainder originate from aortic aneurysms, thrombi overlying ulcerated atherosclerotic plaques, fragmented valvular vegetations (Chapter 11), or the venous system (paradoxical emboli); 10% to 15% of systemic emboli are of unknown origin.
By contrast with venous emboli, which lodge primarily in the lung, arterial emboli can travel virtually anywhere; their final resting place understandably depends on their point of origin and the relative flow rates of blood to the downstream tissues. Common arteriolar embolization sites include the lower extremities (75%) and central nervous system (10%); intestines, kidneys, and spleen are less common targets. The consequences of embolization depend on the caliber of the occluded vessel, the collateral supply, and the affected tissue’s vulnerability to anoxia; arterial emboli often lodge in end arteries and cause infarction.
Soft tissue crush injury or rupture of marrow vascular sinusoids (eg, due to a long bone fracture) release microscopic fat globules into the circulation. Fat and marrow emboli are common incidental findings after vigorous cardiopulmonary resuscitation but probably are of little clinical significance. Similarly, although fat and marrow embolism occurs in some 90% of individuals with severe skeletal injuries (
Fig. 4.16A ), less than 10% show any clinical findings. However, a minority of patients develop a http://ebooksmedicine.net