Critical care for patients with massive ischemic stroke

Abstract

Malignant cerebral edema following ischemic stroke is life threatening, as it can cause inadequate blood flow and perfusion leading to irreversible tissue hypoxia and metabolic crisis. Increased intracranial pressure and brain shift can cause herniation syndrome and finally brain death. Multiple randomized clinical trials have shown that preemptive decompressive hemicraniectomy effectively reduces mortality and morbidity in patients with malignant middle cerebral artery infarction. Another life-saving decompressive surgery is suboccipital craniectomy for patients with brainstem compression by edematous cerebellar infarction. In addition to decompressive surgery, cerebrospinal fluid drainage by ventriculostomy should be considered for patients with acute hydrocephalus following stroke. Medical treatment begins with sedation, analgesia, and general measures including ventilatory support, head elevation, maintaining a neutral neck position, and avoiding conditions associated with intracranial hypertension. Optimization of cerebral perfusion pressure and reduction of intracranial pressure should always be pursued simultaneously. Osmotherapy with mannitol is the standard treatment for intracranial hypertension, but hypertonic saline is also an effective alternative. Therapeutic hypothermia may also be considered for treatment of brain edema and intracranial hypertension, but its neuroprotective effects have not been demonstrated in stroke. Barbiturate coma therapy has been used to reduce metabolic demand, but has become less popular because of its systemic adverse effects. Furthermore, general medical care is critical because of the complex interactions between the brain and other organ systems. Some challenging aspects of critical care, including ventilator support, sedation and analgesia, and performing neurological examinations in the setting of a minimal stimulation protocol, are addressed in this review.

Keywords: Coma; Critical care; Stroke.

Figure 1

Measurement of ICP and herniation. (A) The distance (orange lines) from the ICP probe (black arrow) to the herniation site may contribute to the discrepancy between measured ICP and clinical deterioration. (B) Variations in the morphometric relationship between the tentorial aperture and the brainstem. Note the differences between the brainstem and the tentorial notches. The patient on the left is more susceptible to herniation syndromes and Kernohan's notch than the one on the right.

Figure 2

Decompressive hemicraniectomy for malignant MCA infarction. Computed tomography images from a 63-years-old male with atrial fibrillation and hypertension who presented with left-sided weakness. Images were obtained pre- (A) and post- (B) hemicraniectomy on post-stroke day 1, on post-stroke day 4 (C) and post-cranioplasty on post-stroke day 120 (D). The day after symptom onset, the patient became drowsy and his right pupil dilated. He recovered alertness and pupillary isocoria hours after the decompressive hemicraniectomy. Brain computed topography performed 3 days after the hemicraniectomy did not show a midline shift (C) and the patient was transferred to the general ward. Cranioplasty was performed 4 months after the hemicraniectomy.

Figure 3

Suboccipital craniectomy, cerebrospinal fluid drainage, and therapeutic hypothermia for cerebellar infarction. Computed tomography images from a 50-years-old male with a history of hypertension and 30 pack-years of smoking who presented with sudden onset of vertigo. Images were obtained pre- (A) and post- (B) craniectomy on post-stroke day 2, during hypothermia on post-stroke day 5 (C), and after hypothermia on post-stroke day 23 (D). Computed tomography obtained prior to craniectomy showed a massive infarct in the territory of the posterior inferior cerebellar artery and hydrocephalus (A). At this time, the patient's mental status had deteriorated to stupor. Suboccipital craniectomy was performed and the patient was comatose after the surgery. Cerebrospinal fluid was drained through an extraventricular drain but there was no prompt improvement in clinical condition. Therapeutic hypothermia with a target temperature of 33℃ was performed for 3 days, and the patient became alert without significant deficits other than bilateral limb ataxia. At post-stroke day 23, the patient was discharged without neurological deficits except subtle truncal ataxia.