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5 embolism
An embolus is a solid, liquid, or gaseous mass that breaks off and travels through the bloodstream, lodging in and blocking smaller blood vessels. Pulmonary embolisms originate from deep leg vein thrombi in 95% of cases and can cause infarction or blockage of lung tissue. Systemic embolisms originate from heart mural thrombi in 80% of cases and commonly impact the brain or lower extremities. Fat embolisms occur after bone fractures and burns, causing pulmonary insufficiency, neurological issues, and thrombocytopenia. Air embolisms enter the circulation through chest or obstetric injuries and can block major blood vessels. Amniotic fluid embolisms are a rare
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5 embolism
- 1.
- 2. Def: An embolusis a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin.
- 3. Almost all embolirepresent some part of a dislodged thrombus Unless specified embolism means Thromboembolism
- 4. Rare forms ofemboli droplets of fat bubbles of air or nitrogen Cholesterol emboli from AS debri tumor fragments bits of bone marrow, or even foreign bodies such as bullets
- 5. Effect of embolus Occlusion Embolilodge in vessels too small to permit further passage, resulting in partial or complete vascular occlusion
- 6. Consequences Infarction The potential consequenceof such thromboembolic events is the ischemic necrosis of distal tissue, known as infarction
- 7. Clinical outcome Depends on:the site of origin & the site of lodgment The clinical outcomes are best understood from the standpoint of whether emboli lodge in the pulmonary or systemic circulations.
- 8.
- 9. PULMONARY THROMBOEMBOLISM •Incidence of 20to 25 per 100,000 hospitalized patients •In more than 95% of instances, venous emboli originate from deep leg vein thrombi •Depending on the size of the embolus, it may occlude the main pulmonary artery, impact across the bifurcation (saddle embolus), or pass out into the smaller, branching arterioles •in general, the patient who has had one pulmonary embolus is at high risk of having more. •Rarely, an embolus may pass through an interatrial or interventricular defect to gain access to the systemic circulation (paradoxical embolism)
- 10. • Most pulmonaryemboli (60% to 80%) are clinically silent because they are small. With time, they undergo organization and are incorporated into the vascular wall in some cases, organization of the thromboembolus leaves behind a delicate, bridging fibrous web. • Sudden death, right heart failure (cor pulmonale). or cardiovascular collapse occurs when 60% or more of the pulmonary circulation is obstructed with emboli. • Embolic obstruction of medium-sized arteries may result in pulmonary hemorrhage but usually does not cause pulmonary infarction because of the dual blood flow into the area from the bronchial circulation. A similar embolus in the setting of left-sided cardiac failure (i.e., with sluggish bronchial artery flow), however, may result in a large infarct. • Embolic obstruction of small end-arteriolar pulmonary branches usually does result in associated infarction. • Multiple emboli over time may cause pulmonary hypertension with right heart failure. PULMONARY THROMBOEMBOLISM
- 11. Consequences of Pul.embolism •The morphologic consequences depend on the size of the embolic mass and the general state of the circulation • Large emboli - Sudden death often ensues - acute cor pulmonale (ECG-elecromechanical dissociation) • Smaller emboli – with good CVS – hemorrhages resorption & reconstitution of the preexisting architecture – with CVS compromise - 10% infarction
- 12. Here is largepulmonary thromboembolus seen in cross section of this lung. The typical source for such thromboemboli is from large veins in the legs and pelvis.
- 14. Figure 4-17 Large embolusderived from a lower extremity deep venous thrombosis and now impacted in a pulmonary artery branch
- 15.
- 17. Recent, small, roughly wedge-shapedhemorrhagic pulmonary infarct
- 18. Non thrombotic formsof pul.emboli • uncommon but potentially lethal • air (may be iatrogenic) • bone marrow (after trauma and bone marrow necrosis in sickle cell patients) • fat (trauma and surgery) • amniotic fluid (during parturition) and • foreign bodies (in I/V drug abusers)
- 19. SYSTEMIC THROMBOEMBOLISM • refersto emboli travelling within the arterial circulation • Common source: Mural thrombi in heart (80%) • Less common source: Aorta (AS, Aneurysm)
- 20.
- 21. SYSTEMIC THROMBOEMBOLISM The majorsites for arteriolar embolization • Lower extremities (75%) and • Brain (10%) • the intestines, kidneys, spleen, and upper extremities involved to a lesser extent
- 22. SYSTEMIC THROMBOEMBOLISM The consequencesof systemic emboli depend on: the extent of collateral vascular supply in the affected tissue the tissue's vulnerability to ischemia and the caliber of the vessel occluded in general, arterial emboli cause infarction of tissues downstream of the obstructed vessel
- 23. Tissues supplied byend-arteries without significant collateral supplies will be the most susceptible. Obstruction of blood supply leads to ischemia which when prolonged leads to necrosis and atrophy. Where there is reperfusion after ischemic necrosis the tissues will show a hemorrhagic necrosis. Where there is infection by Clostridia (gram positive bacilli), gangrene sets in.
- 24. FAT EMBOLISM • Presenceof microscopic fat globules in the circulation • Causes: # of long bones Soft tissue trauma Burns
- 25. FAT EMBOLISM Fat embolismsyndrome is characterized by pulmonary insufficiency, neurologic symptoms, anemia, and Thrombocytopenia Symptoms: typically begin 1 to 3 days after injury, sudden onset of tachypnea, dyspnea, and tachycardia
- 26. FAT EMBOLISM Fat embolismsyndrome: Pathogenesis mechanical obstruction and biochemical injury Fat globule platelet complexes Fat globule RBC complexes Release of FFA > toxic injury to endothelium > inflammation > further damage to the vessels
- 27. FAT EMBOLISM Demonstration offat embolism in specimens: By means of frozen sections Routine processing dissolves fat
- 28. Figure 4-18 Bonemarrow embolus in the pulmonary circulation. The cleared vacuoles represent marrow fat that is now impacted in a distal vessel along with the cellular hematopoietic precursors.
- 29. AIR EMBOLISM • Gasbubbles within the circulation can obstruct vascular flow • Entry of gas into circulation occurs during Obstetric procedures Chest wall injury
- 30. AIR EMBOLISM Dose: shouldbe > 100ml to produce any clinical effect Bubbles act like physical obstructions and may coalesce to form frothy masses sufficiently large to occlude major vessels
- 31. AIR EMBOLISM Decompression sickness: Scubaand deep sea divers, underwater construction workers, and individuals in unpressurized aircraft Gas: Nitrogen Clinically: bends, chokes, ischemia, infarction Treatment: slow decompression Caisson disease: chronic form of decompression sickness
- 32. AMNIOTIC FLUID EMBOLISM Uncommoncomplication of laborUncommon complication of labor Has a mortality rate of 20% to 40% Clinically: sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures and coma Pathogenesis: DIC The underlying cause: infusion of amniotic fluid or fetal tissue into the maternal circulation via a tear in the placental membranes or rupture of uterine veins The classic findings: the presence in the pulmonary microcirculation of squamous cells shed from fetal skin, lanugo hair, fat from vernix caseosa, and mucin derived from the fetal respiratory or gastrointestinal tract
- 33.
Editor's Notes
- #8 Depending on the site of origin, emboli may lodge anywhere in the vascular tree; the clinical outcomes are best understood from the standpoint of whether emboli lodge in the pulmonary or systemic circulations.
- #10 PULMONARY THROMBOEMBOLISM: Incidence of 20 to 25 per 100,000 hospitalized patients Although the rate of fatal pulmonary emboli (as assessed at autopsy) has declined from 6% to 2% over the last quarter century pulmonary embolism still causes about 200,000 deaths per year in the United States. In more than 95% of instances, venous emboli originate from deep leg vein thrombi They are carried through progressively larger channels and usually pass through the right side of the heart into the pulmonary vasculature. Depending on the size of the embolus, it may occlude the main pulmonary artery, impact across the bifurcation (saddle embolus), or pass out into the smaller, branching arterioles ( Fig. 4-17 ). Frequently, there are multiple emboli, perhaps sequentially or as a shower of smaller emboli from a single large mass; in general, the patient who has had one pulmonary embolus is at high risk of having more. Rarely, an embolus may pass through an interatrial or interventricular defect to gain access to the systemic circulation (paradoxical embolism). A more complete discussion of pulmonary emboli is presented in Chapter 15 ; an overview is offered here.[43][44]
- #12 The morphologic consequences of embolic occlusion of the pulmonary arteries depend on the size of the embolic mass and the general state of the circulation. Large emboli may impact in the main pulmonary artery or its major branches or lodge at the bifurcation as a saddle embolus ( Fig. 15-27 ). Sudden death often ensues, owing largely to the blockage of blood flow through the lungs. Death may also be caused by acute failure of the right side of the heart (acute cor pulmonale). Smaller emboli can travel out into the more peripheral vessels, where they may cause infarction. In patients with adequate cardiovascular function, the bronchial arterial supply can often sustain the lung parenchyma despite obstruction to the pulmonary arterial system. Under these circumstances, hemorrhages may occur, but there is no infarction of the underlying lung parenchyma. Only about 10% of emboli actually cause infarction. Although the underlying pulmonary architecture may be obscured by the suffusion of blood, hemorrhages are distinguished by the preservation of the pulmonary alveolar architecture; in such cases, resorption of the blood permits reconstitution of the preexisting architecture ==================== A large pulmonary embolus is one of the few causes of virtually instantaneous death. During cardiopulmonary resuscitation in such instances, the patient frequently is said to have electromechanical dissociation, in which the electrocardiogram has a rhythm but no pulses are palpated because of the massive blockage of blood in the systemic venous circulation.
- #13 Here is another large pulmonary thromboembolus seen in cross section of this lung. The typical source for such thromboemboli is from large veins in the legs and pelvis.
- #14 This pulmonary thromboembolus is occluding the main pulmonary artery. Persons who are immobilized for weeks are at greatest risk. The patient can experience sudden onset of shortness of breath. Death may occur within minutes.
- #15 Figure 4-17 Large embolus derived from a lower extremity deep venous thrombosis and now impacted in a pulmonary artery branch
- #16 A pulmonary thromboembolus travels from a large vein in the leg up the inferior vena cava to the main pulmonary arteries as they branch. Such thrombi embolize most often from large veins in the legs and pelvis where thrombi form with stasis.
- #17 This is the microscopic appearance of a pulmonary embolus (PE) in a major pulmonary artery branch
- #18 Figure 15-28 Recent, small, roughly wedge-shaped hemorrhagic pulmonary infarct.
- #21 Figure 4-14 Mural thrombi. A, Thrombus in the left and right ventricular apices, overlying a white fibrous scar. B, Laminated thrombus in a dilated abdominal aortic aneurysm.
- #22 The major sites for arteriolar embolization are the lower extremities (75%) and the brain (10%), with the intestines, kidneys, spleen, and upper extremities involved to a lesser extent.
- #23 The major sites for arteriolar embolization are the lower extremities (75%) and the brain (10%), with the intestines, kidneys, spleen, and upper extremities involved to a lesser extent.
- #29 Figure 4-18 Bone marrow embolus in the pulmonary circulation. The cleared vacuoles represent marrow fat that is now impacted in a distal vessel along with the cellular hematopoietic precursors
- #33 AMNIOTIC FLUID EMBOLISM : Amniotic fluid embolism is a grave but fortunately uncommon complication of labor and the immediate postpartum period (1 in 50,000 deliveries). It has a mortality rate of 20% to 40%, and as other obstetric complications (e.g., eclampsia, pulmonary embolism) have been better managed, amniotic fluid embolism has become an important cause of maternal mortality. The onset is characterized by sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures and coma. If the patient survives the initial crisis, pulmonary edema typically develops, along with (in half the patients) DIC, owing to release of thrombogenic substances from amniotic fluid.[51][52] The underlying cause is the infusion of amniotic fluid or fetal tissue into the maternal circulation via a tear in the placental membranes or rupture of uterine veins. The classic findings are therefore the presence in the pulmonary microcirculation of squamous cells shed from fetal skin, lanugo hair, fat from vernix caseosa, and mucin derived from the fetal respiratory or gastrointestinal tract. There is also marked pulmonary edema and changes of diffuse alveolar damage ( Chapter 15 ) as well as systemic fibrin thrombi indicative of DIC.