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Oedema, thrombosis, embolism, infarction and shock — haemodynamic disorders
Thrombosis forms when one or more elements of Virchow's triad is present — endothelial injury, abnormal flow and hypercoagulability — and the thrombus can detach as an embolus and cause infarction, whose colour and appearance depend on the organ and the type of occlusion; shock leads to characteristic changes in many organs.
Why it matters in the exam
The bank asks where emboli come from, how to distinguish a thrombus from a postmortem clot and which infarct is red. The most common source of emboli in the systemic circulation is intracardiac thrombi — after infarction of the left ventricle or in the left atrium in atrial fibrillation. Pulmonary emboli come mainly from deep leg veins. A thrombus formed in life is attached to the wall, dry and friable, and shows "lines of Zahn" — alternating layers of platelets and fibrin with red cells; a postmortem clot is not attached, is rubbery and glistening, with a dark red lower part and a yellowish upper "chicken fat" part.
Emboli that are not thrombus: fat embolism after long-bone fractures — breathlessness, confusion and petechiae 1–3 days after injury, with fat droplets in lung and brain vessels; amniotic fluid embolism during labour — fetal squames, mucin and lanugo in maternal pulmonary vessels, with disseminated intravascular coagulation; and air embolism, in which usually more than 100 millilitres are needed to cause death.
A white (anaemic) infarct follows arterial occlusion in a solid organ that has a single blood supply — heart, spleen, kidney. A red (haemorrhagic) infarct forms with venous occlusion, in loose tissue, in an organ with dual supply (lung, liver) and with reperfusion. Oedema results from raised hydrostatic pressure, reduced oncotic pressure, lymphatic obstruction and sodium retention. In shock there is acute tubular necrosis in the kidney, diffuse alveolar damage in the lung, centrilobular necrosis in the liver, mucosal haemorrhages in the gut and lipid depletion of the adrenal cortex.
Key points
- Virchow's triad: endothelium, flow, coagulability.
- Source of systemic emboli: intracardiac thrombi.
- Lines of Zahn distinguish a thrombus from a postmortem clot.
- Fat embolism after fracture; amniotic fluid embolism in labour.
- White infarct in arterial solid organ; red in lung, liver and venous occlusion.
Summary table
| Topic | Fact | Finding | Pitfall |
|---|---|---|---|
| Source of systemic emboli | Intracardiac thrombus | After infarction or in atrial fibrillation | Thinking of leg veins |
| Thrombus in life versus postmortem clot | Lines of Zahn, attached and dry versus rubbery and unattached | "Chicken fat" in the postmortem clot | Reading a postmortem clot as an embolus |
| Fat embolism | 1–3 days after a long-bone fracture | Petechiae, confusion | Looking for a thrombus |
| Amniotic fluid embolism | During labour | Fetal squames in maternal lung vessels | Not doing suitable stains |
| Red versus white infarct | Venous, loose, dual supply versus arterial in solid organ | Lung versus kidney | Swapping them |
A free exam question
הממצא האופייני לבלוטות יותרת הכליה במצב של הלם( shock )הוא: (the question as examined, in Hebrew)
- א. ירידה(depletion) בשומן בתאי המדולה
- ב. ירידה(depletion) בשומן בתאי הקורטקס
- ג. הצטברות( accumulation )של ליפופוקסין בתאי הקורטס
- ד. הצטברות( accumulation )של גופיפי ראסל בתאי הקורטקס
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Sources
- Robbins and Cotran Pathologic Basis of Disease, 10th edition (2021) — Hemodynamic disorders, thromboembolism and shock
- Rubin's Pathology: Mechanisms of Human Disease, 8th edition (2020) — Hemodynamic disorders
- Knight's Forensic Pathology, 4th edition (2016) — Embolism and the distinction between thrombus and postmortem clot
Sources are given for further reading; the text is written afresh and not copied from them.
Reviewed by the Examqo AI Professor · 2026-11-06. The text may contain errors; when in doubt, check the source.