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Question:

A 73-year-old man comes to the emergency department due to right-sided weakness and difficulty speaking.  The patient woke up with the symptoms an hour before arriving but felt well when he went to bed last night.  He has a history of paroxysmal atrial fibrillation but is not adherent with medical therapy.  Temperature is 98.6 F (37 C), blood pressure is 130/70 mm Hg, and pulse is 110/min and irregularly irregular.  Physical examination shows right-sided hemiplegia, hemisensory loss, and aphasia.  Despite appropriate treatment, the patient's symptoms fail to improve.  Over the next week, which of the following processes is most likely to occur in the affected brain region?

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Explanation:

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Patterns of tissue necrosis

Type

Etiology

Morphology

Liquefactive necrosis

  • Severe bacterial infections (eg, gangrene)
  • CNS infarcts
  • Necrotic tissue is digested by hydrolytic enzymes into a viscous fluid:
    • Infected abscess fluid is creamy yellow due to dead leukocytes (pus)
    • Brain infarcts resolve into CSF-filled spaces

Fibrinoid necrosis

  • Hypertension
  • Vasculitis
  • Damaged vessels leak fibrin/immune complexes
  • Eosinophilic layer of proteinaceous material in vessel walls

Fat necrosis

  • Acute pancreatitis
  • Trauma (subcutaneous adipose tissue)
  • Free fatty acids released by active enzymes (eg, lipases) or mechanical damage
  • Fatty acids combine with calcium, forming chalky-white deposits (saponification)

Caseous necrosis

  • Mycobacterial infections
  • Fungal infections (eg, Histoplasma, Cryptococcus, Coccidioides)
  • Friable, cheeselike material composed of cell fragments & amorphous proteinaceous debris
  • Surrounded by epithelioid macrophages & giant cells (granuloma)

Coagulative necrosis

  • Irreversible ischemic injury outside CNS
  • Tissue architecture is preserved due to denaturation of lytic enzymes:
    • Cells are anucleate with eosinophilic cytoplasm
    • Leukocytes eventually infiltrate & digest necrotic tissue

CSF = cerebrospinal fluid.

This patient's symptoms are consistent with an ischemic stroke involving the left middle cerebral artery territory.  An embolism is the most likely cause given his history of atrial fibrillation in the absence of anticoagulation therapy.  The resulting irreversible neural cell injury initiates immune cell migration and hydrolytic enzyme release, leading to necrosis of damaged neural tissue.  Although ischemic cell death in most organs results in coagulative necrosis, in the brain such injury causes liquefactive necrosis within 10 days of the infarction due to the brain's lack of supporting architecture.

The infarcted CNS tissue is then digested by microglia and replaced with a cystic space surrounded by a dense astroglial scar (gliosis) over the ensuing months to years.

(Choice A)  Fibrinoid necrosis is a pattern of injury that results in accumulation of fibrin-like material in the walls of blood vessels affected by vasculitis syndromes (eg, polyarteritis nodosa) or malignant hypertension.  Although fibrinoid necrosis in cerebral arteries can predispose a patient to hemorrhagic stroke, this change would not be an expected complication of acute ischemic stroke.

(Choice B)  Focal tuberculous infection can occur in the CNS and cause granulomas with caseous necrosis (epithelioid macrophages around a necrotic focus) within the affected parenchyma.  However, the onset of neurologic symptoms in patients with tuberculous brain abscesses tends to be more chronic and progressive than this patient's acute presentation.

(Choice C)  Breakdown of adipose tissue (ie, fat necrosis) due to mechanical trauma or pancreatic enzyme release (eg, acute pancreatitis) is characterized by infiltrating foamy macrophages containing engulfed lipid debris and release of free fatty acids that combine with calcium to form basophilic deposits.

(Choice E)  Coagulative necrosis occurs following hypoxic cell death in all tissues except the CNS.  It results in the acute denaturation of structural and enzymatic cellular proteins.  Cell nuclei disappear, but the basic architecture of the affected tissue is preserved because intracellular proteolytic enzymes are inactivated during the injury process.

Educational objective:
Irreversible ischemic injury to brain tissue causes tissue digestion by hydrolytic enzymes (liquefactive necrosis).  The infarcted CNS tissue is eventually replaced with a cystic astroglial scar.  In other organs, lethal ischemic injury results in coagulative necrosis.