A 58-year-old man with poorly controlled atrial fibrillation and subtherapeutic anticoagulation presents with acute left upper quadrant pain radiating to the left shoulder. CT imaging and subsequent pathology confirm splenic infarction. The resected spleen shows a sharply demarcated, pale yellow-white lesion with its broad base abutting the capsule and apex pointing toward the hilum, as marked **A** in the diagram. Which of the following best describes the pathological process occurring within the structure marked **A**?
A. Liquefactive necrosis with suppurative inflammation and abscess formation
B. Coagulative necrosis with preserved ghost outlines of splenic architecture (anaemic infarct)
C. Fibrinoid necrosis of splenic arterioles with immune complex deposition
D. Caseous necrosis with epithelioid granulomas and acid-fast bacilli
Explanation
Why Coagulative necrosis with preserved ghost outlines of splenic architecture (anaemic infarct) is right
The structure marked A represents an acute splenic infarct secondary to thromboembolism from the left atrial appendage in atrial fibrillation. The pale, wedge-shaped appearance with capsular base and hilar apex is pathognomonic for an anaemic (white) infarct, which occurs in end-organ tissues with limited collateral circulation. Histologically, anaemic infarcts are characterized by coagulative necrosis—the hallmark pattern where the tissue architecture (ghost outlines of splenic follicles and cords) is preserved despite cell death, as confirmed in this case. This is the classic pathological definition of anaemic infarction in Robbins and Cotran.
Why each distractor is wrong
Liquefactive necrosis with suppurative inflammation and abscess formation: Liquefactive necrosis occurs in tissues rich in hydrolytic enzymes (brain, bacterial infections). While this patient later developed abscess complicating a second infarct, the primary infarct itself shows coagulative, not liquefactive, necrosis. Abscess is a secondary complication, not the defining pathology of the acute infarct.
Caseous necrosis with epithelioid granulomas and acid-fast bacilli: Caseous necrosis is characteristic of tuberculosis and some fungal infections. There is no clinical or pathological evidence of TB or mycobacterial infection in this case; the infarct is purely ischaemic in origin.
Fibrinoid necrosis of splenic arterioles with immune complex deposition: Fibrinoid necrosis occurs in vasculitis and immune-mediated conditions (SLE, polyarteritis nodosa). This patient has thromboembolism from AF, not vasculitis; the pathology is ischaemic necrosis, not immune-mediated vessel wall injury.
High-YieldNEET PG
Pale, wedge-shaped splenic infarcts = anaemic infarcts = coagulative necrosis with preserved architecture; red infarcts occur in organs with dual blood supply (lungs, liver).
Robbins and Cotran Pathologic Basis of Disease, 10th ed., Ch. The Spleen
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