At this time, it should be assumed that the patient has an elevated ICP and midline shift, and repeat a head CT to evaluate midline shift or the presence of hemorrhagic transformation. It has remained difficult to establish which patients with a complete MCA infarction will progress to have a malignant course (Figure 5-9), but it appears that those with first stroke, female gender, young age, heart failure,
Osmotherapy Complete MCA infarction
Medical management of elevated ICP Clinical monitoring
Normothermia Awake and symmetric
reactive pupils Difficult to arouse, symmetric reactive pupils
Neurosurgery consultation for hemicraniectomy
Stupor, dilated but reactive pupil
30 mL of 23.4% NaCl through a central line followed by continuous
infusion of 3% NaCl Mannitol 1-1.5 g/kg
Intubation, hyperventilation for
<30 min Elevated head of bed
to 30 degrees Sedation with propofol or benzodiazepine
Figure 5- . Proposed clinical pathway for management of elevated ICP due to ischemic stroke. ICP, intracranial pressure; MCA, middle cerebral artery.
Before hemicraniectomy, 72 h after stroke
Day 2 after hemicraniectomy
Figure 5-9. Computed tomographic scan of the head before and after hemicraniectomy in a patient with malig-nant middle cerebral artery infarction.
care greater than 50% involvement of the MCA region, carotid occlusion and an abnormal ipsilateral circle of Willis, insufficient leptomeningeal vessels, involvement of the anterior choroidal artery region, and serum biomarkers correlating with infarct volume (such as S100B greater than 1.03 μg/L) are at higher risk.145-148 The most important predictor may be the overall size of the infarct, and identifica-tion of the other factors should not be used to select candidates for hemicraniectomy before there is transtentorial herniation.149
The treatment options remain the same before the patient becomes somnolent. In this case, the clin-ical trial data clearly support the use of hemicraniectomy. A pooled analysis of three separate European clinical trials required the previously noted inclusion criteria, as well as greater than 50% involvement of the MCA distribution. In the trials, patients aged 18 to 60 years were randomized to early hemicraniec-tomy versus maximal medical management and followed for 1 year for the main clinical outcomes of a favorable mRS (0 to 4), as well as mRS of 3 or less and death. The surgical arm had an overwhelming benefit in all of the clinical outcomes. The number needed to treat in these studies was two, and there was a benefit regardless of which side the infarct was on.144 The trial did not require an absolute cutoff of midline shift, and using an absolute cutoff to trigger hemicraniectomy is potentially dangerous. Pre-dicting the outcome of surgical decompression remains difficult, and there have been no clear associa-tions between outcome and size of the infarct, although in one case series age older than 50 years was a poor prognostic sign.150 The trials leave many open questions, including the timing of when to operate and whether their outcomes are clinically meaningful to patients and their families. Depending on the patient’s age, atrophy, and involvement of the medial temporal lobe, surprisingly small amounts of mid-line shift can be associated with injury to the thalamus and midbrain.
While awaiting surgery, the patient becomes unresponsive and his left pupil is dilated (but still reactive). What are the treatment options now?
Medical treatment has been advocated by many clinicians, but the clinical evidence is not particularly strong, and clinical trials and case series demonstrate no change in the high mortality rate in medically treated patients.142 Treatment strategies in lieu of hemicraniectomy that have been suggested include osmotherapy (with mannitol, glycerol, or hypertonic saline), steroids, barbiturate coma, hyperventi-lation, and head elevation.151-153 All of these therapies remain unproven (and transient in effect) in clinical trials, hold the potential for harm,142 and should only be used as temporizing measures before surgery. Animal models and early studies indicate that hypothermia remains a promising medical treatment for patients with malignant MCA infarction, although it has yet to be tested in a blinded prospective clinical trial.142
The most effective treatment in this condition is emergent surgical decompression, with all other medical interventions being aimed at stabilizing the patient in preparation for the operating room.
Rapid intubation is advised, both to prevent pneumonia as well as to help manage ICP. Hyperven-tilation can be effective at reducing ICP by reducing CBV via vasoconstriction of distal arterioles, although in the long-term this same process could precipitate cerebral injury. Hyperventilation is car-ried out with the help of an end-tidal CO2 monitor, with a goal of 30 mm Hg, and for no longer than 30 minutes. After intubation the head of the bed should be maintained at 30 degrees, and sedation should be used to minimize agitation that might increase ICP; use of propofol may be helpful owing to its short half-life, although in select cases dexmedetomidine or midazolam may be considered. If surgery will not be carried out, sedation should be maintained, but at this point an ICP monitor is advisable. Discussion of the type of monitor is beyond the scope of this chapter.
Normothermia is an important component of medical treatment in preparation for surgery, although hypothermia may be necessary for intractable cases of high ICP; prevention of shivering in that case may be important to reduce ICP as well. Strategies to treat shivering will be covered in more detail in other chapters. For rapid lowering of ICP, osmotherapy is carried out at the same time as all of the above interventions. It is advisable to use either (or combination of) a 30-mL bolus of IV 23.4% sodium chloride given through a central line over 5 minutes or 1.0 to 1.5 g/kg of 10% mannitol
solution, depending on the volume status. Hypertonic saline in the acute setting may be safer and per-haps more effective based on the trauma literature,154 and has been associated with improvements in multimodality intracranial monitoring parameters155,156 as well as reversal of transtentorial hernia-tion.157 Hypertonic saline may be preferable because of a more rapid infusion time; how quickly each agent can be obtained and whether the patient has a central line frequently are the deciding factors in choosing one over the other.
The management of space-occupying infarcts in the posterior fossa is not as clear as in those with middle cerebral artery infarcts. Case series have pointed to a similar risk of cerebellar tonsilar herniation for infarcts of greater than 3 cm in size or those that involve the entire posterior-inferior cerebellar artery distribution, as in cerebellar hemorrhage. However, whether these patients should undergo prophylactic suboccipital decompression is unknown, but the differences in the herniation syndromes between cerebellar and cerebral edema should be considered.
A 61-year-old man with hypertension and coronary artery disease with a coronary bypass graft performed last year presents to the ED 12 hours after onset of left-sided weakness.
Three days before he had developed transient visual loss in the right eye. His blood pres-sure on arrival at the ED was 168/78 mm Hg, heart rate 68 bpm, and respiratory rate 16 breaths/min. His examination revealed mild-left hemineglect, left hemiparesis, and a left visual field cut. His cardiac and pulmonary examinations were normal, and the electrocardiogram (ECG) showed normal sinus rhythm with no ischemic changes. The NIHSS was 12. CT head scan revealed small infarcts in the internal border zone region. Brain CTA showed complete occlusion of the right internal carotid artery. He was placed in Trendelenburg position and given 500 mL of intravenous saline. His examination improved to an NIHSS of 4. However, in the next few days he continued to worsen, despite treatment with pressors, up to a blood pressure of 220/120 mm Hg, and he developed a right middle cerebral artery infarction.