watershed infarct

**Definition:** Infarction of "watershed" areas, the distal border zones between two arterial territories. These regions receive blood from the most distal branches of each artery, so they are the first to fail when perfusion pressure drops.

**Pathophysiology:** - Cause: systemic hypoperfusion, such as severe hypotension, cardiac arrest, hemorrhagic or septic shock, cardiac surgery (especially CABG with bypass), or severe carotid stenosis with a hemodynamic drop. It is not caused by a single occluded vessel. - Mechanism: when mean arterial pressure falls, the distal fields of adjacent arteries have no collateral reserve, so ischemia is worst at the border. - Often bilateral and symmetric with global hypoperfusion. It can be unilateral if there is severe ipsilateral internal carotid stenosis or occlusion.

**Brain watershed zones:** 1. **ACA–MCA border zone** (parasagittal, superior frontal and parietal cortex) - Causes "man in a barrel" syndrome: bilateral proximal arm and shoulder weakness (brachiofacial diplegia) with relative sparing of the distal arms and the legs. - Can cause proximal leg weakness, and sometimes transcortical motor or sensory aphasia if it is in the dominant hemisphere. 2. **MCA–PCA border zone** (parieto-occipito-temporal junction) - Causes visual disturbances such as homonymous quadrantanopia or hemianopia, Balint syndrome (simultanagnosia, optic ataxia, oculomotor apraxia), and visual agnosia. 3. **Internal (deep) border zone:** deep white matter between the superficial (cortical) and deep (lenticulostriate) branches of the MCA, seen on imaging as a "string of pearls" pattern in the centrum semiovale and corona radiata.

**Other classic watershed sites (high-yield for pathology):** - **Splenic flexure** of the colon (SMA/IMA border, Griffiths point) → ischemic colitis. The **rectosigmoid junction** (Sudeck point) is another site. - **Hippocampus (CA1 pyramidal cells), cerebellar Purkinje cells, and neocortex layers 3, 5, and 6** are selectively vulnerable to hypoxia. These are selective vulnerability sites rather than true arterial watersheds. - **Kidney:** the renal medulla and the proximal tubule/thick ascending limb are vulnerable to ischemic acute tubular necrosis. - **Heart:** the subendocardium is vulnerable because it is the farthest from the epicardial coronary arteries.

**Imaging:** - MRI DWI shows restricted diffusion in a wedge or linear (band-like) pattern along the border zones. - Pathology: the "red neurons" of acute hypoxic injury appear 12–24 hours after the insult. Coagulative necrosis follows, then macrophage infiltration, then liquefactive necrosis and a gliotic scar.

**Management:** - Restore perfusion pressure by treating the underlying cause (volume resuscitation, vasopressors, cardiac output support) and avoiding hypotension. - Evaluate carotid disease with CTA, MRA, or duplex ultrasound. Revascularize (carotid endarterectomy or stenting) if there is symptomatic high-grade stenosis. - Thrombolysis is not helpful when there is no occlusive thrombus.

**Board pearls:** - Bilateral proximal arm weakness after cardiac arrest or hypotension → ACA/MCA watershed ("man in a barrel"). - Visual deficits after hypotension → MCA/PCA watershed. - Abdominal pain and bloody diarrhea after hypotension in an older adult → ischemic colitis at the splenic flexure. - Contrast with embolic stroke, which has a sudden onset in a single vascular territory (wedge-shaped cortical infarct) and is often from atrial fibrillation or carotid plaque. - Contrast with lacunar infarct, which is a small-vessel lipohyalinosis from hypertension. It affects deep structures (internal capsule, basal ganglia, thalamus, pons) and causes pure motor or sensory syndromes.