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PA5.3-5 | Thrombosis, Embolism, Infarction & Shock — SDL Guide (Part 2)

Embolism: Types, Sources & Consequences

Embolism is the lodgement of an abnormal mass (embolus) within the vascular system at a site distant from its origin, carried there by the bloodstream. An embolus may be solid, liquid, or gaseous.

Type	Source	Destination	Key clinical scenario
Thromboembolism (most common)	DVT of lower limb	Pulmonary arteries	Post-op PE, sudden dyspnoea
Systemic arterial	Mural thrombus (MI, AF, dilated CMP)	Brain, spleen, kidney, limbs	Stroke, splenic/renal infarct
Fat embolism	Long-bone fracture (femur, tibia) — marrow fat	Pulmonary + cerebral capillaries	Hypoxia + petechiae + confusion 24-72 hr post-fracture
Air embolism	IV line, chest trauma, neck surgery	Right heart / pulmonary	Churning 'mill-wheel' murmur; >100 mL fatal
Amniotic fluid embolism	Amniotic fluid enters maternal veins at delivery	Pulmonary vessels	Acute dyspnoea, DIC, cardiovascular collapse; rare but highly fatal
Atherosclerotic (cholesterol crystal)	Ruptured plaque	Distal arterioles	Blue toe syndrome, livedo reticularis
Tumour embolism	Tumour cells invading vessels	Pulmonary, systemic	Haematogenous metastasis mechanism
Septic embolism	Infected thrombus (endocarditis, septic thrombophlebitis)	Distal organs	Pulmonary abscesses from right-sided endocarditis

Pulmonary thromboembolism (PTE): 95% arise from DVT of lower limb veins. A saddle embolus straddles the bifurcation of the main pulmonary artery → sudden death from acute cor pulmonale. Smaller emboli → pulmonary infarction (haemorrhagic, wedge-shaped, pleural surface). Smaller still → transient dyspnoea without infarction. Repeated small emboli → pulmonary hypertension.

A five-panel medical diagram explains embolism as a travelling intravascular mass and compares pulmonary thromboembolism, systemic thromboembolism, fat embolism, and air or gas embolism. — **Panel A:** General embolism mechanism: embolus, site of origin, bloodstream transport, distant lodgement, downstream ischemia or infarction.. **Panel B:** Pulmonary thromboembolism: deep vein thrombosis of lower limb, inferior vena cava, right heart, pulmonary artery, pulmonary infarction, sudden death risk.. **Panel C:** Systemic thromboembolism: mural cardiac thrombus, left heart, aorta, brain embolus, renal infarct, splenic infarct, limb ischemia.. **Panel D:** Fat embolism: long bone fracture, marrow fat globules, torn venous sinusoids, pulmonary capillaries, respiratory distress, petechial rash.. **Panel E:** Air or gas embolism: intravascular air bubbles, decompression sickness, nitrogen bubbles, intravenous air, vascular obstruction..

SELF-CHECK

A 24-year-old male sustains a closed femoral shaft fracture. 36 hours later he develops confusion, petechiae on the chest wall, and oxygen saturation of 85%. The MOST likely diagnosis is:

A. Pulmonary thromboembolism from DVT

B. Fat embolism syndrome

C. Air embolism from IV line insertion

D. Septic embolism from wound infection

Reveal Answer

Answer: B. Fat embolism syndrome

The triad of hypoxia + neurological features + petechiae appearing 24-72 hours after long-bone (especially femoral) fracture is classic fat embolism syndrome. Bone marrow fat globules enter torn venous sinusoids, travel to pulmonary and cerebral capillaries, and cause mechanical obstruction plus toxic fatty acid release. Petechiae result from fat globules in dermal capillaries — a pathognomonic finding not seen in PE.

Infarction: Red vs White

Infarction is an area of ischaemic coagulative necrosis caused by occlusion of arterial supply or venous drainage. Most infarcts result from thrombosis or embolism.

Red (haemorrhagic) infarcts occur when blood re-enters the necrotic zone:
• Venous occlusion (ovarian, mesenteric vein thrombosis) — arterial blood flows in but cannot drain.
• Loose (spongy) tissue architecture — lung has dual blood supply (bronchial + pulmonary); blood floods the necrotic area.
• Reperfusion after restoration of arterial supply.
• Examples: lung, small intestine, ovary, testis.
• Morphology: red-blue, haemorrhagic, wedge-shaped (base on pleura/serosa), coagulative necrosis with ghost alveolar outlines on histology.

White (anaemic) infarcts occur in solid organs with end-arterial supply:
• Single arterial supply with no effective collaterals; dense tissue resists blood re-entry into the necrotic zone.
• Examples: spleen, kidney, heart (myocardial infarction), brain (pale infarct in some zones).
• Morphology: pale yellow-white, wedge-shaped (apex toward hilum), firm; surrounded by a hyperaemic rim of viable congested tissue.

Factors influencing infarct development:
1. Nature of vascular supply (end-artery vs dual/collateral) — most important.
2. Rate of occlusion — gradual → collaterals develop; sudden → no compensation.
3. Tissue vulnerability — neurons: 3-5 min; myocardium: 20-30 min; skeletal muscle: hours.
4. Oxygen-carrying capacity — anaemia and hypoxia worsen infarct size.

Evolution (e.g., renal infarct): 0-24 hr — ill-defined area; 24-48 hr — pale, distinct border with hyperaemic rim; days to weeks — scar (fibrosis replaces necrotic tissue).

A three-panel medical diagram compares the mechanisms and morphology of red haemorrhagic and white anaemic infarcts with key factors influencing infarct development. — **Panel A:** Generic organ wedge, arterial supply, venous drainage, thrombus or embolus, ischaemic coagulative necrosis, arterial occlusion, venous occlusion, vascular supply, rate of occlusion, tissue vulnerability, oxygen-carrying capacity. **Panel B:** Red haemorrhagic infarct, venous occlusion, dual blood supply, reperfusion, loose spongy tissue, lung or intestinal segment, red-blue wedge-shaped infarct, base toward pleura or serosa, necrotic zone, ghost alveolar outlines, red blood cells, coagulative necrosis. **Panel C:** White anaemic infarct, end-arterial supply, arterial occlusion, no effective collaterals, dense solid organ tissue, kidney or spleen cut surface, pale yellow-white wedge-shaped infarct, apex toward hilum, base toward capsule, hyperaemic rim, viable congested tissue.

SELF-CHECK

A patient with mitral stenosis and atrial fibrillation suddenly develops severe left loin pain. Imaging shows a pale wedge-shaped lesion in the kidney with a hyperaemic rim. This is BEST explained by:

A. Red infarct due to renal venous occlusion

B. Red infarct due to dual blood supply of the kidney

C. Abscess formation from a septic embolus

D. White infarct due to arterial embolism to a solid end-arterial organ

Reveal Answer

Answer: D. White infarct due to arterial embolism to a solid end-arterial organ

AF with mitral stenosis creates left atrial stasis → mural thrombus → systemic arterial embolism. The kidney has an end-arterial supply with no effective collaterals, so occlusion of a renal artery branch produces a white (anaemic) infarct — pale, firm, and wedge-shaped. The hyperaemic rim is reactive congestion in the surviving tissue at the margin. A venous cause would produce a red infarct; the kidney does not have a dual blood supply comparable to the lung.

Shock: Definition, Types & Pathogenesis of Septic Shock

A four-panel medical diagram explains shock as systemic tissue hypoperfusion, classifies major shock types, and illustrates septic shock pathogenesis from infection to vasodilation, capillary leak, microthrombi, and cellular hypoxia. — **Panel A:** Shock, systemic circulatory failure, reduced cardiac output/effective circulating volume, tissue hypoperfusion, cellular hypoxia, anaerobic metabolism. **Panel B:** Hypovolemic shock, cardiogenic shock, septic shock, anaphylactic shock, neurogenic shock, vasodilation, pump failure, blood/fluid loss. **Panel C:** Infection focus, bacteria, LPS/microbial products, macrophage activation, TNF, IL-1, nitric oxide, vasodilation, endothelial activation, capillary leak, DIC/microthrombi, reduced tissue perfusion. **Panel D:** Dilated arteriole, leaky capillary endothelium, edema, activated neutrophils, fibrin microthrombus, impaired oxygen delivery, hypoxic tissue cells.

Shock is a state of systemic hypoperfusion of tissues resulting in cellular hypoxia and dysfunction, which if uncorrected leads to irreversible cell injury and death. It is not simply low blood pressure — it is a failure of oxygen delivery relative to demand.

Classification by mechanism:

Type	Primary mechanism	Classic example
Hypovolaemic	Decreased circulating volume	Haemorrhage, burns, severe dehydration
Cardiogenic	Pump failure (↓ cardiac output)	Massive MI, severe arrhythmia, cardiac tamponade
Distributive — Septic	Massive vasodilation + flow maldistribution	Gram-negative/gram-positive sepsis, fungal
Distributive — Anaphylactic	IgE-mediated vasodilation + ↑ vascular permeability	Bee sting, penicillin reaction
Distributive — Neurogenic	Loss of vasomotor tone	Spinal cord injury, high spinal anaesthesia
Obstructive	Mechanical obstruction to flow	Massive PE, tension pneumothorax, cardiac tamponade

Septic shock pathogenesis:

1. Infection → bacteraemia. Gram-negative: LPS (lipopolysaccharide/endotoxin); gram-positive: lipoteichoic acid, peptidoglycan.
2. LPS binds TLR4/CD14 on monocytes/macrophages → massive cytokine release: TNF-α, IL-1, IL-6, IL-8 (cytokine storm).
3. Cytokine storm effects:
• Endothelial activation → iNOS → excess nitric oxide → profound vasodilation → hypotension.
• ↑ Vascular permeability → 'third spacing' → functional hypovolaemia.
• Neutrophil activation → tissue injury (ROS, proteases).
• Endothelial damage → procoagulant state → DIC.
4. DIC — widespread microvascular thrombosis consumes clotting factors + platelets → paradoxical bleeding. Microthrombi in kidneys, lungs, adrenals → multi-organ dysfunction.
5. Compensatory anti-inflammatory response (CARS) follows SIRS — immunosuppression → risk of secondary infections.