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Management of Large Hemispheric Infarction

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Management of Large Hemispheric Infarction Management of Large Hemispheric Infarction K.E. Wartenberg and S.A. Mayer z Introduction: Natural History of Large Hemispheric Infarction Large hemispheric infarctions due to middle cerebral artery (MCA) or internal car- otid artery (ICA) occlusion are an important cause of morbidity and mortality in the neurological intensive care unit (ICU). Neurological deterioration occurs as a consequence of malignant cerebral edema in approximately 5±10% of hemispheric ischemic strokes [1±3], but in over two-thirds of patients when the complete MCA territory is infarcted [1, 3]. The reported mortality of these `malignant' hemispheric infarctions varies between 42 and 80% [1±5]. Patients with complete MCA infarction are generally 10 years younger (mean age 56 years) than the average stroke patient [1]. The initial presentation usually in- cludes contralateral conjugate gaze paresis, hemineglect, and reduced level of con- sciousness in addition to the expected sensorimotor and language deficits [1, 6, 7]. Most patients experience neurological decline within 48 hours [1, 3]. Of those who deteriorate, worsening occurs within 24 hours in 36% and within 48 hours in 68% [3]. The first sign of transtentorial herniation is usually drowsiness, followed by pupillary asymmetry, hyperventilation, and contralateral motor posturing [8, 9]. Autonomic abnormalities may include hyper- or hypoventilation, bradycardia, and sustained hypertension or blood pressure lability [1, 3, 5, 7]. Bilateral motor pos- turing and lower extremity rigidity then follows as the midbrain and diencephalon are subjected to physical distortion and compression [8]. Without life support, death typically occurs within five days [1, 3, 5] as a result of brain death, respirato- ry failure, cardiac arrhythmia, or pneumonia [1±3]. Infarction of the brain parenchyma and the vasculature results in a delayed break down of the blood brain barrier with extravasation of serum proteases and worsening of brain edema 24 to 72 hours after the initial infarct signs [9]. Hemi- spheric brain swelling leads to brain tissue shifting with subsequent brain stem distortion, bihemispheric dysfunction through mechanical displacement, vascular compression, uncal and transtentorial herniation (Fig. 1). Intracranial pressure (ICP) is usually not elevated early in the process of transtentorial hermiation from large hemispheric infarction, but increases later as severe cytotoxic edema ensues. Ongoing ischemia is usually not the cause of neurological deterioration beyond 24 hours of onset, but this can result from vascular compression of the anterior and posterior cerebral arteries against the falx or tentorium, and is a universal finding in patients who become brain dead [4]. 648 K.E. Wartenberg and S. A. Mayer Fig. 1. Schematic diagram of the importance of tissue shifts and hypothetical significance of pressure dif- ferentials in clinical worsening from large hemispheric infarction with edema. P1 represents the pressure in the injured hemisphere and P2 the pressure in the uninjured hemisphere. As edema ensues, pressure differentials occur and accentuate, leading to tissue shifts and clinical worsening. From [4] with permis- sion z Etiology of Large Hemispheric Infarctions Large hemispheric infarctions occur as the consequence of an occlusion of the dis- tal ICA or proximal MCA trunk without sufficient collateral flow (Figs. 2 and 3). Total ICA occlusions lead to infarction of the anterior cerebral artery (ACA) and MCA territories [7]. Most patients have risk factors for vascular disease such as hypertension, dia- betes, hypercholesteremia, tobacco abuse, history of transient ischemic attacks or ischemic strokes, congestive heart failure (CHF), and coronary artery disease. Atrial fibrillation is more frequent in patients with MCA and ICA territory strokes com- pared to the remaining stroke population [1±3, 6]. ICA dissection is a significant cause of large territory infarctions in younger patients (12%) [6]. In one series of 610 patients with large hemispheric strokes 42% were attributed to focal or general atherosclerosis and 33% to a cardioembolic source [6]. z Diagnosis of Early MCA Infarction Computed tomography (CT) of the brain obtained within 6 hours of symptom on- set has a sensitivity of 82% for ischemic hemispheric infarctions [10]. Early infarct signs on CT include: z Hyperdense MCA sign (high contrast in the MCA that is brighter than the adja- cent brain tissue and other intracranial arteries in the absence of calcification) (Fig. 4) Management of Large Hemispheric Infarction 649 Fig. 2. a ICA occlusion after the bifurcation demonstrated by cerebral angiography with a common caro- tid artery injection. b MR Angiogram of the Circle of Willis shows no flow signal in the left ICA and cross- filling of the left MCA via the anterior communicating artery z Hyperdense ICA sign distinguishable from the opposite ICA and the surround- ing bone z Obscuration of the lentiform nucleus defined by decreased density compared to the contralateral nucleus z Effacement of the sylvian fissure with loss of grey-white matter distinction com- pared to the contralateral side z Involvement of other vascular territories seen as hypodensity in the ACA, ante- rior choroidal and posterior cerebral arteries (PCA) z Complete sylvian fissure obscuration and extensive effacement of the hemisphere as well as compression of the lateral ventricle demonstrating mass effect z Midline shift at the level of the pineal gland and the septum pellucidum (antero- septal shift) [2, 10] z Predictors of Fatal Deterioration Several studies have identified risk factors for secondary fatal neurological dete- rioration after MCA infarction. A multivariate analysis of 201 patients with large hemispheric strokes [2] identified the following predictors of fatal brain swelling: z History of hypertension z History of CHF z An elevated white blood count (WBC) 650 K.E. Wartenberg and S. A. Mayer Fig. 3. MCA main stem occlusion by cerebral angiogram with left common carotid injection z CT involvement of > 50% of MCA territory (Fig. 5), and z CT involvement of additional territories [1, 2, 10, 11]. In a series of 37 patients with MCA stroke and proximal vessel occlusion a National Institute of Health Stroke Scale (NIHSS) on admission of 19 or greater was found to be highly predictive of severe neurological deterioration (sensitivity 96%, speci- ficity 72%) [12]. Several studies have found that radiographic evidence of a large initial infarction volume can reliably identify those at greatest risk for neurological deterioration. In a case control study of 31 patients studied with contrast CT, attenuated corticome- dullary contrast enhancement involving the entire MCA territory within 18 hours of onset was found to be the most reliable neuroradiological predictor of neurologi- cal deterioration, with a sensitivity of 87% and specificity of 97% [13]. In another study horizontal pineal displacement greater than 4 mm on CT performed within 48 hours of stroke onset was highly predictive of mortality with a specificity of 89% and a sensitivity of 46% in 127 patients [14]. In an analysis of magnetic reso- nance imaging (MRI) predictors, a reduction in the apparent diffusion coefficient (ADC) of greater than 82 ml was the most accurate predictor of deterioration, with Management of Large Hemispheric Infarction 651 Fig. 4. a Hyperdense MCA sign (right) on CT surrounded by hypoattenuation in the right frontal and tem- poral regions with loss of sulci and grey-white matter differention. b The Fluid Attenuated Inversion Re- covery (FLAIR) sequence reveals high signal in the right MCA consistent with a thrombus a sensitivity of 87% and specificity of 91% [12]. This finding is supported by a ret- rospective analysis that identified a diffusion weighted imaging (DWI) lesion vol- ume exceeding 145 ml within 14 hours of symptom onset as the best predictor of a malignant clinical course, with a sensitivity and specificity of 100% in a multivari- ate model [15]. Krieger et al. identified nausea and vomiting within 24 hours of stroke onset, systolic blood pressure (SBP) >180 mmHg after 12 hours, and involvement of >50% of the MCA territory on CT as independent predictors of fatal brain swelling in a multivariate analysis of 135 patients [16]. Carotid ªTº occlusion was signifi- cantly associated with a fatal outcome in 74 MCA infarction patients with acute carotid artery distribution stroke [17]. Severe cerebral blood flow (CBF) reductions in the MCA territory, detected by Xenon-CT (mean CBF 8.6 ml/100 gm/minute) [18] or single photon emission CT (SPECT) [19] can also identify patients at risk for fatal brain edema. Neurochemical monitoring with cerebral microdialysis is another interesting tool to monitor the course of MCA infarction. An increase in extracellular glutamate, glycerin and lactate concentration and an augmentation of the lactate/pyruvate ra- tio in peri-infarct areas was thought to reflect developing brain edema with subse- quent secondary neuronal ischemia as those changes of neurochemicals preceded an increase in ICP [20±22]. Bosche et al. found significantly lower non-transmitter amino acid concentrations in the areas adjacent to the infarct in patients who de- veloped malignant brain edema [23]. In summary, the CT criteria involvement of >50% of the MCA territory and other vascular territories, and the presence of a midline shift at the level of the pineal gland of septum pellucidum represent the most reliable predictors of fatal neurological deterioration.
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