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Patients with hypertensive emergencies frequently present with chest pain (27%), dyspnea (22%), and neurologic deficits (21%). Cerebral infarction is found in about 24% of patients, with about 22% having pulmonary edema, 16% hypertensive encephalopathy, and 12% heart failure.

Acute coronary syndromes, aortic dissection, subarachnoid hemorrhage, and pulmonary edema are discussed in other chapters. This section focuses on hypertensive encephalopathy.


Patients present with the acute or subacute development of lethargy, confusion, headache, and visual disturbances, sometimes followed by seizures (focal or generalized) and coma. The syndrome can occur with or without proteinuria and retinopathy.


  1. Cerebral blood flow is autoregulated within specific limits.

    1. In normotensive people, cerebral blood flow is unchanged between mean arterial pressures (MAP) of 50–150 mm Hg (MAP = [(2 × diastolic) + systolic]/3)

      1. Cerebral vasoconstriction limits hyperperfusion up to a MAP of ~ 150 mm Hg.

      2. Above a MAP of 150 mm Hg, autoregulation is overwhelmed.

    2. In hypertensive patients, cerebral blood flow can be maintained at higher MAPs.

      1. Thought to be due to arteriolar thickening

      2. Such patients also need higher MAPs to maintain adequate cerebral blood flow (ie, abrupt lowering of the BP to a MAP of < 100–110 mm Hg can potentially lead to cerebral ischemia).

  2. Failure of autoregulation leads to cerebral vasodilation, endothelial dysfunction, and cerebral edema.

  3. Vasogenic edema in the posterior parietal and/or occipital lobes

    1. Classic MRI finding in hypertensive encephalopathy, although a wide range of findings is possible

    2. Also called posterior reversible encephalopathy syndrome

    3. Generally seen in the posterior regions of the brain due to relatively sparse sympathetic innervation of the vertebrobasilar territory leading to more disruption of autoregulatory mechanisms, increased perfusion, and edema

    4. Also seen with eclampsia and use of some immunosuppressive agents and cytotoxic drugs; in 1 series, 68% of patients with posterior reversible encephalopathy syndrome had hypertension, 11% eclampsia, 11% immunosuppressive use, and 11% other causes

    5. Reversible with treatment of hypertension or removal of inciting agent, with MRI findings resolving in days to weeks; long-term antiepileptic therapy is not necessary.


  1. Hypertensive encephalopathy is primarily a clinical diagnosis; imaging is required to rule out CNS abnormalities.

  2. A head CT should be done to exclude intracranial hemorrhage (intracerebral or subarachnoid bleeding).

  3. An MRI should be done to exclude acute ischemic stroke and to look for posterior reversible encephalopathy syndrome.

    image MRI is much more sensitive than CT (83% vs 16% sensitivity; specificity of both > 95%) for the diagnosis of acute ischemic stroke.


  1. Hypertensive encephalopathy and other hypertensive emergencies should be treated in the ICU with parenteral, titratable antihypertensive agents.

  2. There is little evidence to guide the choice of agents; commonly used medications include labetalol, esmolol, fenoldopam, clevidipine, nitroprusside, and nicardipine.

  3. Generally, the BP should be reduced by no more than 25% in the first hour, then to 160/100 mm ...

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