Hemorrhagic transformation and cerebral edema in acute ischemic stroke: Link to cerebral autoregulation

Abstract

Background Hemorrhagic transformation and cerebral edema are feared complications of acute ischemic stroke but mechanisms are poorly understood and reliable early markers are lacking. Early assessment of cerebrovascular hemodynamics may advance our knowledge in both areas. We examined the relationship between dynamic cerebral autoregulation (CA) in the early hours post ischemia, and the risk of developing hemorrhagic transformation and cerebral edema at 24 h post stroke Methods We prospectively enrolled 46 patients from our center with acute ischemic stroke in the middle cerebral artery territory. Cerebrovascular resistance index was calculated. Dynamic CA was assessed by transfer function analysis (coherence, phase and gain) of the spontaneous blood flow velocity and blood pressure oscillations. Infarct volume, hemorrhagic transformation, cerebral edema, and white matter changes were collected from computed tomography performed at presentation and 24 h. Results At admission, phase was lower (worse CA) in patients with hemorrhagic transformation [6.6 ± 30 versus 45 ± 38°; adjusted odds ratio 0.95 (95% confidence internal 0.94–0.98), p = 0.023] and with cerebral edema [6.6 ± 30 versus 45 ± 38°, adjusted odds ratio 0.96 (0.92–0.999), p = 0.044]. Progression to edema was associated with lower cerebrovascular resistance (1.4 ± 0.2 versus 2.3 ± 1.5 mm Hg/cm/s, p = 0.033) and increased cerebral blood flow velocity (51 ± 25 versus 42 ± 17 cm/s, p = 0.033) at presentation. All hemodynamic differences resolved at 3 months Conclusions Less effective CA in the early hour post ischemic stroke is associated with increased risk of hemorrhagic transformation and cerebral edema, possibly reflecting breakthrough hyperperfusion and microvascular injury. Early assessment of dynamic CA could be useful in identifying individuals at risk for these complications.

Cerebral autoregulation in hemorrhagic stroke: A systematic review and meta‐analysis of transcranial Doppler ultrasonography studies

“…The hypothesized relationship between autoregulation, cerebral blood flow, and clinical outcome is summarized in Figure . This concurs with similar findings in ischemic stroke, where worsening CA is associated with adverse prognostic features, such as hemorrhagic transformation and cerebral edema …”

Assessment of cerebral autoregulation in stroke: A systematic review and meta-analysis of studies at rest

“…25,30,33,50 Eleven studies presented the modified Rankin Scale (mRS). 13, 24, 27, 29, 32, 35-38, 43, 46 Moreover, the majority of participants were recruited within 6 to 72 hours from stroke onset, 2, 12, 13, 24-27, 29, 34-40, 42, 43, 45-47, 49, 51 including within 48 hours (n = 8), 2, 25, 34-36, 39, 47, 49 five studies assessed dCA at 72 hours, 24,29,40,45,51 twenty-four hours were studied in four studies, 37,42,43,46 three studies examined dCA between 30 to 37 hours, 12,13,38 dCA was assessed at 6 hours (n = 2), 26,27 one study assessed between onset to 16 days, 52 other three studies recruited participants after first week of stroke onset 32,33,48 and one study examined recovery at 6 months. 49 The location of the lesion was identified in the MCA (n = 13), 23, 26-28, 33-37, 40, 41, 49, 51 posterior cerebral artery (n = 3), 31,32,49 and anterior cerebral artery territories (n = 3), 2, 25, 52 though eight studies did not specify the precise localization of the lesion.…”

Acute characterization of tissue and functional deficits in a clinically translatable pig model of ischemic stroke

“…For example, ICH in the cerebellum was associated with ataxia whereas ICH in basal ganglia structures were associated with limb weakness. In previous studies, early neurologic deterioration was attributed primarily to cerebral edema and lesion volume; however, recent clinical pathological, MR, and CT studies suggest hemorrhage into ischemic tissues is a major contributor to poor clinical outcome, making ICH a novel target of pre-clinical studies (126–129). By replicating both tissue-level and neurological presentations unique to ICH, our model presents an exciting new platform for testing hemostatic therapies and surgical interventions.…”