Intensive Care Management in Space-Occupying Middle Cerebral Artery Stroke

Figure 48.1. Diffusion-weighted MRI (A) and corresponding ADC map (B) of a 53-year-old patient with aphasia and right-sided hemiparesis (NIHSS 19) show signs of cytotoxic edema indicating acute left-sided MCA infarction on admission. MRI-based thrombolysis was performed with 80 mg rt-PA 1 hour after symptom onset. (C) The follow-up CT scan at 24 hours shows signs of raised ICP with midline shift, compression of the lateral ventricles, and impending subfalcial herniation (arrows). Hemicraniectomy was performed 30 hours after symptom onset. (D) Postoperative CT scan: the vector of brain extension is reverted to the newly created compensatory space to relieve the pressure on midline structures. Follow-up diffusion weighted MRI scan (E) and ADC map (F) 16 days after hemicraniectomy show signal normalization and reduction of mass effect of the MCA infarction. The patient was transferred to a rehabilitation clinic 21 days after the infarction. At that time he was awake, had nonfluent aphasia, and brachio-facial hemiparesis on the right side (NIHSS 13). [Courtesy of M. Blatow, Department of Neuro-Radiology, University of Heidelberg].

48.3 Decompressive Surgery

Decompressive hemicraniectomy represents the treatment of choice in malignant MCA infarction. Evidence for the benefical effect of decompressive surgery in patients between 18 to 60 years in malignant MCA stroke has been provided by three randomized trials including 93 patients (52 surgery with 48 hours, 41 conservative treatment) [6]. The primary outcome measure in these trials was the modified Rankin scale (mRS) at one year. The distribution of the mRS at one year differed significantly between the conservative and the operative group: 75% of patients in the surgery group had a mRS ≤4 compared to 24% in the conservative group. 43% of patients attained a mRS ≤3 in the surgery group versus 21% in the conservative arm. Mortality at one year was significantly different between groups: 78% of patients who underwent surgery versus 29% in the conservative group survived (p<0.0001). The number needed to treat (NNT) was 2 for survival with mRS ≤4, 4 for survival with mRS ≤3, and 2 for survival irrespective of functional outcome. However, despite a level 1A evidence recommendation in European guidelines, the potential neurological deficits should be discussed with the patient and/or the family and one should always consider the individual opinion of a patient facing survival with a severe neurological deficit.

Based on these persuading results, the DESTINY II study had been undertaken, assessing the benefits of decompressive surery in patients older than 60 years. The study has not been published yet, however, the preliminary results clearly suggest that also elderly patients may benefit from decompressive surgery.

Above mentioned studies have performed surgery within the first 48 hours after ictus. While several studies had suggested that early hemicraniectomy may be preferable, in a larger case series of 138 patients, age however has been the only factor relevant for outcome, while time to surgery had no effect [7]. Still, it seems advisable to identify patients at risk for maligant stroke as early as possible in order to minimize the risk of further brain injury. If a malignant course seems predictable and a consent regarding surgery is gained, the operation should be performed rapidly since waiting for further clinical deterioration carries no benefit.

48.4 Hypothermia

Due to the evidence from randomized trials for the benefit of decompressive surgery, application of mild (>33°C) or moderate hypothermia (29-33°C) for malignant brain edema following ischemic stroke has so far been abandoned. This is in line with the result of one study comparing decompressive surgery and hypothermia, concluding that hemicraniectomy was associated with lower mortality rates and complications than hypothermia [8]. The combination of hemicraniectomy with hypothermia is recently under investigation (DEPTH-SOS).

In contrast, the neuroprotective effects of mild hypothermia in the early phase after stroke have not been properly explored. Data from patients following cardiac arrest seem promising [9]. It is unknown and subject of current studies if early application of hypothermia may impede the development of malignant brain edema. At the moment, the use in awake stroke patients is being assessed.

References

1. Hacke W, Schwab S, Horn M, et al. ‘Malignant’ middle cerebral artery territory infarction: Clinical course and prognostic signs. Arch Neurol 1996; 53: 309-15

2. Lauritzen M, Dreier JP, Fabricius M, et al. Clinical relevance of cortical spreading depression in neurological disorders: migraine, malignant stroke, subarachnoid and intracranial hemorrhage, and traumatic brain injury. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 2011; 31: 17-35

3. Hofmeijer J, Algra A, Kappelle LJ, et al. Predictors of life-threatening brain edema in middle cerebral artery infarction. Cerebrovasc Dis 2008; 25: 176-84

4. Thomalla G, Hartmann F, Juettler E, et al. Prediction of malignant middle cerebral artery infarction by magnetic resonance imaging within 6 hours of symptom onset: A prospective multicenter observational study. Ann Neurol 2010; 68: 435-45

5. Guidelines for management of ischaemic stroke and transient ischaemic attack 2008. Cerebrovasc Dis 2008; 25: 457-507

6. Vahedi K, Hofmeijer J, Juettler E, et al. Early decompressive surgery in malignant infarction of the middle cerebral artery: A pooled analysis of three randomised controlled trials. Lancet Neurol 2007; 6: 215-22

7. Gupta R, Connolly ES, Mayer S, et al. Hemicraniectomy for massive middle cerebral artery territory infarction: a systematic review. Stroke 2004; 35: 539-43

8. Georgiadis D, Schwarz S, Aschoff A, et al. Hemicraniectomy and moderate hypothermia in patients with severe ischemic stroke. Stroke 2002; 33: 1584-8

9. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002; 346: 549-56

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