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IntroductionSubarachnoid hemorrhage (SAH) repre-

sents a dramatic event with a substantial rate of morbidity and mortality (1,2). No clinical and radiological variables have been identified as reliable and faultless pre-dictors of poor outcome. Although global cerebral edema occurring after SAH and as-sessed on computed tomography (CT) has been described as an independent risk fac-tor for poor functional and survival progno-sis following SAH (3), this finding might wrongly orient treatment-level aggressive-ness in critically ill patients. We describe a patient with aneurysmal SAH having de-veloped extensive hemispheric cytotoxic edema that progressively resolved with re-markable clinical improvement. We discuss the importance of recognizing the possible

Practical Pearl

AbstractIntroduction: Cerebral edema, as assessed by computer-assisted tomography, has been proposed as a prognosis factor of poor outcome following aneurysmal subarachnoid hemorrhage. However, this radiological finding might wrongly influence the decision to maintain or withdraw treatment in critically ill patients.

Case Report: We present the case of a 63-year-old female presenting with poor clinical grade after an aneurysmal rupture that developed extensive right hemispheric cytotoxic edema. With appropriate treatment, the brain edema progressively resolved and the clinical state improved.

Conclusion: We discuss the importance of recognizing the possible reversibility of such extensive hemispheric edema and its relevance to patient management.

Key Words: Subarachnoid hemorrhage; cerebral edema; cytotoxic edema; ischemia; poor clinical grade; prognosis factor.

(Neurocrit. Care 2006;04:143–146)

Neurocritical CareCopyright © 2006 Humana Press Inc.All rights of any nature whatsoever are reserved.ISSN 1541-6933/06/4:143–146 ISSN 1556-0961 (Online)DOI: 10.1385/Neurocrit. Care 2006;04:143–146

Reversibility of Extensive Hemispheric Cytotoxic Cerebral Edema Following Subarachnoid HemorrhageNancy McLaughlin and Michel W. Bojanowski*

Division of Neurosurgery, Department of Surgery, Centre Hospitalier de l’Université de Montréal – Hôpital Notre-Dame, Montreal, QC, Canada

*Correspondence and reprint request to:

Michel W. Bojanowski, Division of Neurosurgery, Department of Surgery, CHUM-Hôpital Notre-Dame, 1560 Sherbrooke Est, Montreal, QC, Canada, H2L 4M1.

E-mail: michel.bojanowski.chum@ssss.gouv.qc.ca

reversibility of extensive hemispheric cyto-toxic edema on CT and its implication on patient management.

Case ReportFor the past 2 years, a 63-year-old female

had been followed by means of serial imag-ing in another institution for an unruptured right middle cerebral artery (MCA) aneu-rysm. She suddenly complained of a severe headache. On arrival at a local hospital, the patient was drowsy but could obey simple commands after insistence. Later on, the pa-tient presented a generalized tonic seizure and postictal obnubilation rendering intuba-tion mandatory. Cerebral CT showed a 2-cm right MCA partially thrombosed aneurysm surrounded by a small hematoma and edema resulting in a 7-mm midline shift.

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During transfer, her neurological state further deterio-rated with a fixed and dilated right pupil and bilateral decerebration movements. Immediate cerebral CT revealed rebleeding with diffuse SAH and subdural and intraparen-chymal hematomas involving the right temporo-insular region (Figure 1). The patient was brought immediately to the operating room.

Through a large right craniotomy, subdural and intraparen-chymal hematomas were drained. Intermittent temporary clipping of less than 10 minutes was used during aneurysmal dissection and clipping of two aneurysms on the MCA. Throughout surgery, patient was maintained normovolemic and normotensive. At the end of the surgery, the brain was relaxed and the bone flap was not replaced.

Immediately after surgery, pupils were equal and reactive but extensor posturing persisted. Cerebral CT performed at this time revealed right hemispheric cytotoxic edema. Optimal medical treatment was maintained. Three days after SAH, neurological deterioration was observed and follow-up cere-bral CT documented progression of the extensive edema with complete disruption of the gray-white matter differentiation (Figure 2). No hypotensive or hypoxemic episode occurred post-operatively. CT-angiography documented adequate exclusion of aneurysm and no evidence of vessel occlusion. One week after SAH, the attending neurosurgeon and the patient’s family discussed the prognosis and aggressiveness of treatments. It was proposed to maintain maximal treatment given the initial rapid response of the elevated intracranial

Fig. 1. Cerebral CT performed after neurological deterioration revealing rebleeding with diffuse SAH and subdural and intraparenchymal hematomas involving the right temporo-insular region.

Fig. 2. Cerebral CT done 3 days after SAH and aneurysm surgical treatment demonstrating significant right hemispheric edema with com-plete disruption of the gray-white matter differentiation and an increase of midline shift.

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pressure to medical and surgical treatments, the short period of time elapsed since the hemorrhage, and the right side loca-tion of tissue damage. Progressively, the patient improved. Follow-up CT revealed significant resolution of hemispheric hypodensity with reappearance of gray-white matter differen-tiation and important reduction of the mass effect (Figure 3). One month later, the patient was awake and oriented, spoke fluently, moved adequately right upper and lower extremities, and was directed towards a rehabilitation center.

DiscussionCerebral parenchymal edema resulting from an ischemic

process presents on cerebral CT as an hypodensity taking many different patterns. Cerebral hypodensity may be single or multiple, involve cortical or subcortical regions, or present a diffuse distribution (3,4). Whereas a delayed focal hypoden-sity is most often related to vasospasm (4,5), early diffuse edema is commonly attributed to microcirculatory dysfunc-tion after acutely increased intracranial pressure following SAH (6). Cerebral edema occurring in the setting of aneurys-mal SAH may also be the result of iatrogenic factors such as prolonged temporary arterial clipping, perforator or large-vessel occlusion caused by clip placement, thromboembolic event, or brain tissue retraction (7). In our case, neuroprotec-tion by anesthetic agents contributed to a decrease in the metabolic demand of cerebral tissue. Intermittent temporary clipping lasted less than 10 minutes, a duration that has been associated with a low risk of subsequent infarction (8).

Even though global cerebral edema assessed on CT has been described as an independent risk factor for poor func-tional and survival prognosis following SAH (3), this is not always the case. Although extensive hemispheric edema occurring after aneurysmal SAH has been observed by other clinicians (9), it has rarely been described in the literature. Ini-tially believed to represent the extent of infarct and indicate irreversible damage (10), early CT signs have only been of a moderate predictive value. Lesion volume on acute diffusion-weighted imaging (DWI), but not on acute CT, correlated

strongly with final infarct volume (11). Mismatch between early DWI and early CT signal abnormalities suggests that CT findings might not enable to reliably differentiate between reversible ischemia and completed infarct (12). Complemen-tary investigation of cerebral perfusion (13) might be clini-cally relevant in the management of patients presenting with poor clinical grade after SAH and developing extensive hemi-spheric cerebral cytotoxic edema. Despite the poor clinical state and radiological findings, the recommendation to maintain or withdraw treatment should be made on an indi-vidual basis, taking into account the time elapsed from hemorrhage.

ConclusionThe presence of extensive cerebral hypodensity on CT

following SAH is not reliably associated with poor neurologi-cal outcome. Extensive hemispheric cytotoxic edema might be reversible and its resolution might correlate with clinical improvement. Other imaging modalities might help recognize reversible ischemic damage, orient management and nuance treatment discussions that clinicians share with families of critically ill patients.

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Fig. 3. Cerebral CT performed 2 weeks following hemorrhage showing significant improvement of hemispheric hypodensity with reappear-ance of gray-white matter differentiation and significant reduction of the mass effect.

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