Published online Dec 28, 2017. doi: 10.4329/wjr.v9.i12.448
Peer-review started: February 12, 2017
First decision: May 17, 2017
Revised: August 22, 2017
Accepted: November 29, 2017
Article in press: November 29, 2017
Published online: December 28, 2017
This case illustrates diffuse border zone infarcts caused by rapid and dramatic reduction in blood pressure in a patient presenting with intracerebral hemorrhage and chronic uncontrolled hypertension.
Stroke, sudden onset of slurred speech, right-sided hemiparesis, dysarthria, lethargy, blood pressure of 264/218.
Ischemic stroke, hemorrhagic stroke, transient ischemic attack, hypoglycemia, Todd’s paralysis, intracerebral aneurysm rupture.
No laboratory test was diagnostic; the patient, however, presented with very elevated blood pressure levels, and normal blood sugar levels.
Non-contrast computed tomography (CT) scan of the head showed left thalamic hemorrhage with intraventricular extension and developing hydrocephalus. Follow-up non-contrast CT scan of the head at 96 h showed a cerebellar hypodensity. Electrocardiogram revealed normal sinus rhythm. Echocardiogram did not reveal any cardioembolic etiology, except for left ventricular hypertrophy. Magnetic resonance imaging of the brain showed areas of restricted diffusion consistent with acute ischemia in multiple internal border zone areas of bilateral cerebral and cerebellar hemispheres; the location in the border zone areas makes embolic etiology of the ischemia unlikely. Magnetic resonance angiography of the brain and neck revealed no significant stenosis that could have contributed to the cerebral ischemia.
Blood pressure control with intravenous labetalol boluses and nitroprusside infusion. For the management of hydrocephalus and monitoring of intracranial and cerebral perfusion pressures, external ventricular drain was placed. Intraventricular thrombolytics were given to prevent clot formation in the ventricles and facilitate the cerebrospinal fluid drainage.
There are several randomized controlled trials that have focused on blood pressure control in the setting of intracerebral hemorrhage; however, strong evidence-based guidelines for the management of blood pressure in patients with spontaneous intracerebral hemorrhage and systolic blood pressure more than 220 mmHg are not clearly established.
Hematoma expansion: An increase in size of the initial intracerebral hemorrhage that occurs in up to one-third of the patients, usually within the first 24 h. Borderline or watershed infarctions: Those that occur in areas shared by two vascular territories; those areas are more susceptible to perfusion reduction as it happens with blood pressure reduction and/or shifted cerebral autoregulation. Cerebral autoregulation: A physiological mechanism that maintains cerebral blood flow at different blood pressure levels. In patients with chronic hypertension, the curve shifts to the right (“right shifted”); autoregulation is used for higher blood pressure levels, and it is more protective to elevated blood pressure but fails to react in case of lower blood pressure levels.
Caution should be advised when blood pressure reduction is considered in patients with intracerebral hemorrhage, especially if arriving with very elevated blood pressure and known to have untreated chronic hypertension. In addition, the presence of concomitant increased intracranial pressure due to the mass effect and/or hydrocephalus after intraventricular extension increases the intracranial pressure and thus decreases the cerebral perfusion pressure. Cerebral autoregulation shifts to the right in patients with chronic untreated hypertension and a reduction in blood pressure may not be tolerated leading to ischemia; therefore, such intervention in certain cases may be unsafe, as described in the article.