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PA5.6 | Infarction & Thrombus Morphology — Practical — SDL Guide

Learning Objectives

Distinguish pale (anaemic) from red (haemorrhagic) infarcts on gross examination, citing the organ and mechanism responsible for each type.
Describe the systematic gross features of an infarct: shape, colour, consistency, and margin changes across early, established, and healed stages.
Identify coagulative necrosis on H&E sections and list the cellular sequence from neutrophil infiltration through to fibrous scar formation.
Recognise lines of Zahn in a thrombus and explain why their presence confirms antemortem formation.
Differentiate an antemortem thrombus from a postmortem clot on gross inspection.

INSTRUCTIONS

Pathology practicals test pattern recognition under time pressure. The ability to look at a pot specimen or a glass slide and immediately articulate 'pale wedge-shaped infarct, renal cortex, arterial occlusion' separates a pass from a distinction. This module trains you to read infarcts and thrombi systematically — colour, shape, necrosis type, age, and antemortem vs postmortem — using the exact mental framework examiners expect.

References

Robbins & Cotran Pathologic Basis of Disease, 10th ed., Ch. 4 (Hemodynamic Disorders) (textbook)
Harsh Mohan Textbook of Pathology, 8th ed., Ch. 4 (textbook)
Underwood's General and Systematic Pathology, 6th ed., Ch. 6 (textbook)

Version 2.0 | NMC CBUC 2024

CLINICAL SCENARIO

A 60-year-old man with atrial fibrillation collapses at home. At autopsy, the left kidney shows a pale, wedge-shaped area with its apex pointing toward the hilum, and the heart shows a soft, yellow zone in the posterior left ventricular wall. A glass slide from the posterior wall shows ghost cells — nuclei gone, but cell outlines preserved.

Two different organs. Two infarcts. One word — ischaemic death — but the appearances are strikingly different. Your job today is to read these differences fluently, the way a radiologist reads a chest X-ray: systematically, then confidently.

WHY THIS MATTERS

PA5.6 appears on every MBBS Part II practical examination that involves a museum pot or a histology slide labelled 'infarct.' Examiners award marks for:

Naming the type (pale vs haemorrhagic) with justification.
Stating the organ and naming the occluded vessel.
Estimating age from histological features.
Distinguishing antemortem thrombus from postmortem clot.

Clinically, recognising infarct patterns on imaging is a direct extension of this morphological literacy — the wedge on CT correlates exactly with the wedge in the pot.

RECALL

Before you begin, check your Year-1 groundwork:

Coagulative necrosis — the dominant necrosis type in most solid organs (exception: brain).
Ischaemia — reduced arterial supply causing cell death downstream of an occlusion.
Oedema vs congestion — passive venous engorgement produces haemorrhagic zones; arterial cut-off produces pale zones.
Fibrin — the protein scaffold linking platelets in a thrombus, staining pink on H&E.

If any of these feel uncertain, spend 5 minutes with Robbins Ch. 2 before continuing.

Classifying Infarcts: The Two-Colour Rule

Every infarct is classified first by colour because colour encodes the mechanism.

Pale (anaemic/white) infarct — occurs in solid organs with end-arterial supply and little collateral circulation: heart, kidney, spleen. When the artery is blocked, no blood reaches the tissue. The zone dies and turns pale grey-white. It is firm and well-demarcated.

Red (haemorrhagic) infarct — occurs when blood re-enters a dead zone after the occlusion, filling the necrotic tissue. This happens in three settings:
• Organs with dual blood supply (lung has pulmonary artery + bronchial artery).
• Organs with venous occlusion (intestine — the artery keeps pushing blood in, the vein cannot drain it).
• Loose, spongy tissue (lung parenchyma) that accommodates seeping blood.

Memory rule: Solid + arterial = pale. Loose/dual/venous = red.

Side-by-side schematic comparing pale infarction in a kidney after end-arterial occlusion with red haemorrhagic infarction in lung tissue after vascular blockage and collateral refilling. — **Panel A:** Kidney cross-section, blocked end artery, absent downstream blood flow, pale grey-white wedge-shaped infarct, firm well-demarcated margin, solid end-arterial organ.. **Panel B:** Lung parenchyma, blocked pulmonary artery, intact bronchial collateral supply, blood re-entering necrotic tissue, dark red haemorrhagic wedge-shaped infarct, loose dual-supply organ.. **Top Banner:** The Two-Colour Rule: Solid + arterial = pale; Loose / dual / venous = red..

Gross Features: Reading the Shape and Margin

Shape is the second key read after colour.

Wedge-shaped infarct — the hallmark of end-arterial occlusion in a fan-distributed organ (kidney, spleen). The base faces the capsule (subcapsular), the apex points toward the hilum (toward the occluded vessel). Think of a pie slice with the narrow end at the blocked vessel.

In the intestine, infarcts are segmental — a loop of bowel goes dark red-purple, then black-green as gangrene supervenes. The shape follows the mesenteric vessel territory.

In the heart, the distribution follows coronary artery territories — posterior wall infarcts (right coronary), lateral wall (circumflex), anterior wall/septum (LAD).

Margin changes with age:
• Early (0–24 hours): barely visible; the zone is slightly pale and swollen with a hyperaemic rim (reactive red border from surrounding viable tissue).
• 1–3 days: pale/yellow-white centre becomes distinct; soft, may be slightly depressed.
• 1–2 weeks: yellow, soft, liquefying in centre; granulation tissue visible at margin.
• Weeks to months: replaced by a fibrous scar — grey-white, firm, shrunken, permanently depressed.

A multi-panel medical diagram showing wedge, segmental, and coronary infarct patterns with a four-stage timeline of renal infarct margin evolution. — **Panel A:** Renal capsule, subcapsular base of wedge infarct, pale wedge-shaped infarct, apex toward hilum, occluded interlobar artery, renal hilum. **Panel B:** Fan-distributed end-arterial organ, capsule-facing base, apex toward occluded end artery, wedge-shaped infarct. **Panel C:** Mesenteric artery territory, segmental bowel infarct, dark red-purple ischemic bowel, black-green gangrenous segment, viable adjacent bowel. **Panel D:** LAD territory anterior wall/septum, right coronary artery territory posterior wall, circumflex territory lateral wall, coronary artery distribution. **Panel E:** 0-24 h pale swollen wedge with hyperaemic rim, 1-3 days pale yellow-white distinct wedge, 1-2 weeks liquefying yellow centre with granulation margin, weeks-months grey-white shrunken fibrous scar.

SELF-CHECK

A pot specimen shows the left kidney with a grey-white, wedge-shaped lesion, base facing the cortical surface, apex pointing toward the renal pelvis. The most likely cause is:

A. Renal vein thrombosis

B. Embolism to an interlobar artery

C. Acute tubular necrosis from hypotension

D. Renal abscess formation

Reveal Answer

Answer: B. Embolism to an interlobar artery

A pale wedge infarct with apex toward the hilum indicates end-arterial occlusion — classically an embolus lodging in an interlobar or arcuate artery. Renal vein thrombosis would produce a red (haemorrhagic) infarct because venous congestion allows blood to re-enter the tissue. Acute tubular necrosis is diffuse, not wedge-shaped. An abscess is creamy/suppurative, not pale and wedge-shaped.

Spot Specimens: Four Key Examples

Learn these four — they cover the entire spectrum the examiner can ask:

1. Renal infarct (pale wedge)
Organ: kidney. Cut surface: pale, firm, grey-white wedge. Base at capsule (may be depressed/scarred if old). Apex at hilum. Cause: embolism (commonest — left heart thrombus, AF). Type: pale (end-arterial).

2. Splenic infarct (pale wedge)
Organ: spleen. Similar pale wedge, base at capsule. Often incidental in haematological disease (leukaemia, myelofibrosis) or endocarditis emboli. Healed = capsular fibrous tag.

3. Pulmonary infarct (red/haemorrhagic)
Organ: lung. Haemorrhagic, wedge-shaped (wedge base at pleura). Dark red-brown, firm, raised above surrounding parenchyma (congested). Cause: pulmonary embolism (DVT). Type: red (dual supply — bronchial artery re-fills the dead zone).

4. Myocardial infarct (pale, then yellow)
Organ: heart. Early: barely visible. 24–48 h: yellow-white, soft zone. Healed: grey-white fibrous scar, thinned wall. Location encodes artery: posterior wall = RCA. Type: pale (end-arterial; no collaterals in normal heart).

Four-panel medical diagram comparing renal, splenic, pulmonary, and myocardial infarcts with classic gross specimen appearances and cause/type labels. — **Panel A:** Kidney cut surface, pale grey-white wedge infarct, base at renal capsule, apex toward renal pelvis/hilum, depressed old capsular scar, embolic cause, pale end-arterial infarct.. **Panel B:** Spleen cut surface, pale wedge infarct, base at splenic capsule, apex inward, healed capsular fibrous tag, association with endocarditis emboli or haematological disease.. **Panel C:** Lung section, pleural surface, dark red-brown haemorrhagic wedge infarct, raised firm infarct zone, congested surrounding parenchyma, pulmonary embolus from DVT, dual blood supply.. **Panel D:** Heart wall cross-section, early barely visible infarct, 24-48 h yellow-white soft infarct, healed grey-white fibrous scar with thinned wall, coronary artery territory note including posterior wall equals RCA..