1. thromboemboli

2. liquid emboli

3. gaseous emboli

4. solid particle emboli

these represent fragments of thrombi carried by venous or arterial blood. Infected thrombi give rise to septic emboli.

*these account for most of the emboli in the clinical practice, are classified on the basis of the vessels through which they are carried in the blood.

like cholesterol crystals can detach from atherosclerotic plaques, as well as from tumor cells, bone marrow emboli, or bullets

*The clinical significance of embloi lies in the fact that all emboli can occlude blood vessels

anatomical classification of embooli

originate in the left atrium or ventricle, aorta, and the major arteries

they are carried by arterial blood and are important causes of infarction resulting from the occlusion of peripheral arteries

the most important complication of venous emboli that typically originate in the deep veins of the lower extremities and are carried by venous blood to the vena cava, through the right atrium and ventricle and then into the pulmonary artery

A massive thromboembolus may occlude the amin pulmonary artery or its branches

are common causes of ischemia in various organs and most originate from the endocardium or from valvar thrombi

in cases of bacterial endocarditis, the emboli may be infected

other sources are thrombi from ulcerated atherosclerotic plaques of the aorta and its major branches

• splenic infarcts (sharp subcostal pain)

• renal infarcts (assoc w hematuria)

• intestinal infarcts (results from an embolus that lodges in one of the major intestinal arteris, causing gangrene and necrosis of the bowel)

also characterized by mental changes, thrombocytopenia, and widespread petechiae.

the lungs typically exhibit cahnges of ARDS and microscopically show numerous fat globules within the microvasculature

the lesions in the brain include cerebral edema, red petechiae and microinfarcts, with fat globules also seen in the microvasculature

(brain and lungs are the two organ systems involved)

the transformation of the fluid blood into a solid aggregate encompassing blood cells and fibrin

fibrin is polymerized fibrinogen and forms a meshwork of thin filaments that bind together the cellular elements of the blood

1. Intramural thrombi

2.Arterial thrombi

3. Venous thrombi

4. Microvascular thrombi

Intramural Thrombi

• carotid and cerebral arteries
• aortic atherosclerosis
• aortic aneurysm
• coronary arteries
• varicose veins
• valvular thrombi (vegetations)
• thrombus over myocardial infarct

how are thrombi classified pathologically?

Red thrombi

Layered thrombi

Typically arterial occlusion in solid organs (heart, kidneys)

The area of ischemic necrosis caused by the arterial obstruction is typically paler than the surrounding tissue. It is often rimmed by a thin red zone containing extravasated blood that was destined to reach the ischemic zone from surrounded anastomotic blood vessels.

Typically venous obstruction involving the intestines (volvulus) or testes (torsion). The venous circulation may be interrupted as a result of twisting of the organ around its supporting structure.

Twisting of the sigmoid colon (volvulus) causes compression of the blood vessels in the mesentary. As the veins have thin walls, they are compressed much more easily than arteries

Red Infarcts

What happens as a result of venous compression?

Typical of organs that have a dual blood supply, such as the liver or lungs.

1. pump failure of the heart (cardiogenic shock)

2. loss of fluid from the circulation (hypovolemic shock)

3. severe gram negative bacteremia (septic shock)* most common

septic shock

gram-negative endotoxic shock resulting from the spread of bacteria from a severe localized infection into the blood stream (abscesses, pneumonia, or peritonitis)

can also occur with gram-positive and fungal infections

currently the most common cause of death in ICUs

1. Nonprogressive stage

2.progressive stage

3. Irreversible stage

Stages of shock

Nonprogressive Stage

an initial phase during which reflex compensatory mechanism are activated and perfusion of vital organs is maintained.

The cardiac failure and the resultant hypoperfusion are initially compensated for by peripherl vasoconstriction. This redirects blood to vital organs such as the brain and preserves their critical fxn

Stages of Shock

Nonprogressive Stage features

central pooling of blood in the abdominal organs and the lungs accompanied bu pallor of the skin which is also clammy.

Vasoconstriction of the renal blood vessels results in renal hypoperfusion and a decreased GFR. This activated the RAS for conservation of fluid, increasing the cardiac output and blood pressure. The early stage is reversible and treatable.

Stages of Shock

Progressive Stage

characterized by tissue hypoperfusion and the onset of worsening circulatory and metabolic imbalances (acidosis)

Results in widespread tissue hypoxia and impairment of intracellular aerobic respiration by which anearobic respiration follows, resulting in lactic acidosis.

this low pH dilates the arterioles and blood begins to pool in the microcirculation, which worsens the cardiac output.

Metabolic acidosis also has a depressive effect on the heart, further potentiating pump failure. Left ventricular insufficiency raises the intrapulmonary venous pressure, causing stagnation of blood in the pulmonary circulation, and favors the formation of pulmonary edema and ARDS (shock lungs)

Stages of Shock:

Progressive shock

changes seen in the lungs

the capillaries are congested and leaky owing to anoxia. The alveolar capillaries necrotize and slough off, and are covered and lined by fibrin (hyaline membranes)

Stages of Shock

Progressive shock:

Changes seen in kidneys

Stages of shock:

Irreversible stage of shock

sets in after the body has incurred cellular and tissue injury so sever that even if treatment is instituted, survival is not possible.

The cellular injury is widespread, affecting all organs, the kidneys being th most serious with renal shutdown. The intestines exhibit necrosis, perforation, and peritonitis

Stages of shock

Irreversible stage of shock:

characteristic changes seen

the brain exhibits ischemic encephalopathy, confusion and coma

Typically, pts are in great distress or are unconscious

There is marked hypotension, respiratory distress, acidosis, and anuria

Multiple organ failure is usually present and DIC is common

on gross examination, the body is usually edematous (anasarca), and the body cavities contain fluid (effusions and ascites)

On internal examination, the organs appear congested and wet from edema, most prominent in the lungs (2-3 xs normal wt)

The liver is congested and enlarged, with blood oozing from the cut surface

the intestines are dark due to pooling of blood in their vessels, and the walls are swollen from the edema.

the kidneys are swollen with a pale cortex on cut surface, due to the constriction of the cortical blood vessels with cortical-tubular necrosis.

the brain is edematous with flattening of the gyri

• ARDS
• centrilobar hemorrhagic necorsis of liver
• acute tubular necrosis of kidney
• superficial hemorrhagic necrosis of intestine
• focal myocardial necrosis
• congestion and hyperplasia of spleen
• stress (steroid) ulcers of stomach
• vasodilation and splanchnic pooling