How shock and pulmonary embolism can be devastating

Embolism and their types

An embolus is a separated intravascular mass in various forms that travels by blood to a distant site from its place of origin. They appear in solid, liquid and gaseous forms & are becoming silent killers because of their insidious onsets, elusive natures, & very drastic consequences.

Pulmonary embolism has been reported in over 95 percent of cases, due to deep vein thrombosis. Pulmonary embolus can occlude main pulmonary artery causing sudden death. It may also occlude medium-sized branches to cause lung infarction if bronchial artery is compromised. Pulmonary infarction and hemorrhage are common in small pulmonary arteries. 

Fat embolism occurs after a severe skeletal and soft tissue injury from trauma and burn respectively. Bone marrow ruptures & then releases fat embolus into vein through bone marrow vascular sinusoids. Fat embolus then travels to pulmonary artery branches to cause pulmonary insufficiency. Other signs include: thrombocytopenia, anemia, delirium and possibly coma.

Amniotic fluid embolism is a postpartum complication in which amniotic fluid embolus enters the vein through ruptured placenta membrane. Sings include: pulmonary insufficiency, shock, seizure & coma. 

Systemic thromboembolism is an embolus in arterial circulation. Mural thrombi, aortic aneurysm, ruptured atherosclerotic plaque, & valvular vegetation produce this embolus. They occur in conditions such as left ventricular failure, arrhythmia, atrial dilation, & hypertension. Ischemic organ damage including lower limbs, brain, kidney, intestine, spleen are consequences of this embolus.

Air embolism occurs due to entrapment of air or gas bubbles in blood vessels. A quick change from high to low pressure environment among astronauts & others may result in air embolism.  An example is nitrogen bubbles in blood of scuba divers who rapidly depressurize after deep sea activities. Air can be introduced during surgery which may cause organ damage.

What to know about tissue infarction

A tissue Infarction is the necrotic death of tissues from arterial or venous occlusions. This necrotic tissue resulting from ischemia is called an infarct. There are 3 kinds of infarcts: red, white & septic infarcts.

Red infarcts are reddish-brown in color due to hemorrhage & are seen in venous obstructions and ischemic reperfusion injuries. E.g. in ovaries and lungs, liver (nut meg liver). They can also be seen in organs with multiple blood supplies e.g (intestine and lungs)

White infarcts are pale due to blockage of arterial blood supply to solid organs like heart, spleen, kidney.

Septic infarcts are infected cardiac valve vegetations or necrotic tissues. In general, it takes 4 to 12 hours to histologically confirm tissue necrosis after ischemic coagulative necrosis. Brain tissues die 4 minutes after blood supply is compromised. Heart tissues die 30 minutes after blood supply is compromised.

The mechanism of shock

Shock is a systemic response to low cardiac output & hypotension, which causes tissue hypoperfusion and injury. Let’s briefly discuss the types:

Cardiogenic shock results in low cardiac output due cardiac pump failure. Caused by myocardial infarction, pulmonary embolism, sepsis, cardiac tamponade, ventricular arrythmias.

Septic shock results from vasodilation & peripheral pooling of blood caused by   infections with fungi & gram positive, negative microbes. Inflammatory cytokines, endothelial injury, metabolic abnormalities, & immune suppression are important mediators of septic shock.

Including other organs, the lungs are severely affected leading to respiratory distress syndrome in septic shock. In septic shock, pro-inflammatory cytokines decrease myocardial contractility. Sepsis causes production of glucagon, growth hormone glucocorticoids, and catecholamines which cause hyperglycemia.

Hyperglycemia impairs neutrophils activity further worsening sepsis. TNF, IL-I also suppress insulin secretion and promote insulin resistance in liver and peripheral tissues. Toxic shock syndrome is another subtype of septic shock caused by superantigen toxin of bacteria. Toxic shock syndrome results in hypotension, skins rash, vasodilation and death.

Hypovolemic shock is the loss of plasma volume caused by large hemorrhage, burns or trauma. This indirectly reduces cardiac output.

Neurogenic shock results from loss of vascular tone resulting from spinal cord injury or anesthetic overdose.

Anaphylactic shock is a shock due to systemic vasodilation and permeability caused by IgE.

Clinical implications of shock include the followings:

1. Tissue injury of the lungs, brain, kidney, adrenals, G.I tract and others.
2. Metabolic lactic acidosis, low PH, electrolyte imbalance
3. Tachycardia, tachypnea, hypotension
4. Cyanosis, cool skin
5. Warm and flushed skin in septic shock
6. Disseminated Intravascular Coagulation (DIC)
7. Diffused alveolar damage in septic shock
8. Adrenal insufficiency following glucocorticoid surge
9. Kidney tubular necrosis