Treatment of right hemispheric cerebral infarction by hemicraniectomy.

Delashaw, Johnny B.; Broaddus, William C.; Kassell, Neal F.; Haley, E. Clarke; Pendleton, G. A.; Vollmer, Dennis G.; Maggio, William W.; Grady, M. Sean

doi:10.1161/01.str.21.6.874

Cited by 211 publications

(148 citation statements)

References 17 publications

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“…24,27 A significant improvement in aphasia and a better overall outcome, however, have been observed with longer follow-ups. 5,16 Involvement of the dominant cerebral hemisphere should not preclude surgical decompression because long-term differences in clinical outcome after DH are not significantly different from those seen in patients with nondominant-hemisphere infarctions. 9,27,29 Intravenous tPA administration was not a significant predictor of poor outcome after DH.…”

Section: Discussionmentioning

confidence: 99%

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Decompressive hemicraniectomy: predictors of functional outcome in patients with ischemic stroke

Daou

Kent

Montaño

et al. 2016

JNS

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P atients presenting with large ischemic strokes may develop uncontrollable, progressive brain edema that puts them at risk for compression of brain parenchyma and cerebral herniation. 23 There are a limited number of therapeutic options, but research has shown that operative procedures, such as decompressive hemicraniectomy (DH), decrease patient mortality.32 Malignant infarction treated only by conservative approaches results in a mortality rate of 80% within the 1st week of the stroke. 15Edema that does not respond to medical treatment necessitates DH as a life-saving procedure. Studies have demonstrated that DH surgery can result in a reduction of mortality rate to 30% and, if decompression is performed within 24 hours of stroke onset, to 10%. 7,12,18,24,32 While DH imabbreviatioNs BMI = body mass index; DH = decompressive hemicraniectomy; DVT = deep vein thrombosis; ICA = internal carotid artery; IVC = inferior vena cava; MCA = middle cerebral artery; MI = myocardial infarction; MLS = midline shift; mRS = modified Rankin Scale; NIHSS = National Institutes of Health Stroke Scale; tPA = tissue plasminogen activator. obJective Patients presenting with large-territory ischemic strokes may develop intractable cerebral edema that puts them at risk of death unless intervention is performed. The purpose of this study was to identify predictors of outcome for decompressive hemicraniectomy (DH) in ischemic stroke. methods The authors conducted a retrospective electronic medical record review of 1624 patients from 2006 to 2014. Subjects were screened for DH secondary to ischemic stroke involving the middle cerebral artery, internal carotid artery, or both. Ninety-five individuals were identified. Univariate and multivariate analyses were performed for an array of clinical variables in relationship to functional outcome according to the modified Rankin Scale (mRS). Clinical outcome was assessed at 90 days and at the latest follow-up (mean duration 16.5 months). results The mean mRS score at 90 days and at the latest follow-up post-DH was 4. Good functional outcome was observed in 40% of patients at 90 days and in 48% of patient at the latest follow-up. The mortality rate at 90 days was 18% and at the last follow-up 20%. Univariate analysis identified a greater likelihood of poor functional outcome (mRS scores of 4-6) in patients with a history of stroke .66]; p = 0.017), peak midline shift (MLS) > 10 mm ]; p = 0.011), or a history of myocardial infarction ]; p = 0.04). Multivariate analysis demonstrated elevated odds of poor functional outcome associated with a history of stroke .05]; p = 0.008), MLS > 10 mm ; p = 0.007), a history of diabetes .88]; p = 0.01), delayed time from onset of stroke to DH (OR 1.32 [95% CI 1.02-1.72]; p = 0.037), and evidence of pupillary dilation prior to DH .51]; p = 0.04). Patients with infarction involving the dominant hemisphere had higher odds of unfavorable functional outcome at 90 days ]; p = 0.014), but at the latest follow-up, cerebral dominance was not significantly related to outc...

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Section: Discussionmentioning

confidence: 99%

“…The mRS ranges from 0 (no symptoms) to 6 (death), with intermediate values (1)(2)(3)(4)(5) representing increasing functional and cognitive disability. Poor functional outcome was defined as an mRS score of 4 (moderately severe disability), 5 (severe disability), or 6 (death).…”

Section: Outcomementioning

confidence: 99%

Decompressive hemicraniectomy: predictors of functional outcome in patients with ischemic stroke

Daou

Kent

Montaño

et al. 2016

JNS

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“…Historically, there has been reluctance to perform this operation because of a high rate of mortality and profound morbidity in survivors. Until recently, only case series and nonrandomized case-control studies suggested any benefit of decompressive craniectomy [39][40][41][42][43]. Several recent randomized controlled trials have demonstrated improved survival after decompressive craniectomy in certain stroke populations [6,[44][45][46].…”

Section: Osmotherapymentioning

confidence: 99%

Novel Treatment Targets for Cerebral Edema

2012

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Cerebral edema is a common finding in a variety of neurological conditions, including ischemic stroke, traumatic brain injury, ruptured cerebral aneurysm, and neoplasia. With the possible exception of neoplasia, most pathological processes leading to edema seem to share similar molecular mechanisms of edema formation. Challenges to brain-cell volume homeostasis can have dramatic consequences, given the fixed volume of the rigid skull and the effect of swelling on secondary neuronal injury. With even small changes in cellular and extracellular volume, cerebral edema can compromise regional or global cerebral blood flow and metabolism or result in compression of vital brain structures. Osmotherapy has been the mainstay of pharmacologic therapy and is typically administered as part of an escalating medical treatment algorithm that can include corticosteroids, diuretics, and pharmacological cerebral metabolic suppression. Novel treatment targets for cerebral edema include the Na(+)-K(+)-2Cl(−) co-transporter (NKCC1) and the SUR1-regulated NC Ca-ATP (SUR1/TRPM4) channel. These two ion channels have been demonstrated to be critical mediators of edema formation in brain-injured states. Their specific inhibitors, bumetanide and glibenclamide, respectively, are well-characterized Food and Drug Administration-approved drugs with excellent safety profiles. Directed inhibition of these ion transporters has the potential to reduce the development of cerebral edema and is currently being investigated in human clinical trials. Another class of treatment agents for cerebral edema is vasopressin receptor antagonists. Euvolemic hyponatremia is present in a myriad of neurological conditions resulting in cerebral edema. A specific antagonist of the vasopressin V1A-and V2-receptor, conivaptan, promotes water excretion while sparing electrolytes through a process known as aquaresis.Keywords Cerebral edema . Hyponatraemia . Osmotherapy . NKCC1 . SUR1/TRPM4 . Vaptan . Glyburide Overview of Perturbations in Brain Fluid HomeostasisCerebral edema in the neurointensive care setting can occur with a heterogenous group of neurological diseases, which typically fall under the categories of metabolic [1, 2], infectious [3], neoplastic [4], cerebrovascular [5][6][7], and traumatic [8,9] brain injury. Irrespective of the inciting process, cerebral edema results in the pathological accumulation of fluid in the brain's intracellular and extracellular spaces. This occurs secondary to alterations in the complex interplay between 4 distinct fluid compartments within the cranium; fluid is present within: 1) the blood in the cerebral blood vessels, 2) the cerebrospinal fluid in the ventricular system and subarachnoid space, 3) the interstitial fluid of the brain parenchyma, and 4) the intracellular fluid of the neurons and glia. These fluid compartments are not isolated, and specific movements of solutes and water from one compartment to another occur under normal conditions. When dysregulation of this normally tightly controlled fluid balance...

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“…The technique for decompressive haemicraniectomy is already well established 10,11 . It includes the A B remotion of a large (≥ 12 cm) bone flap with a circular or oval shape including the frontal, parietal, temporal and parts of the occipital squamae (with special care to avoid producing sharp bone edges); fixation of the dura at the edge of the craniectomy to prevent epidural bleeding; opening of the dura (usually one longitudinal and three radial incisions almost reaching the osseous rim) and placement of a dural patch made of lyophilised cadaver dura or more recently microporic poliester-uretane (Neuro-Patch ® ) in the incision.…”

Section: Discussionmentioning

confidence: 99%

Temporal muscle haematoma as a cause of suboptimal haemicraniectomy: case report

André

Niemeyer-Filho

2003

Arq. Neuro-Psiquiatr.

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-Objective: To call attention to an unusual complication of decompressive haemicraniectomy in the treatment of malignant haemispheric infarction. Method: We describe a case in which partial decompression occurred despite large craniectomy. Complete decompression followed resection of the temporal muscle. Pertinent literature is briefly reviewed. Case description: A 55-year old woman developed massive right middle cerebral artery infarction evolving to cerebral haerniation in 40 hours. Decompressive haemicraniectomy without cortical excision was unable to revert coma and decerebrate posturing because of a massive temporal muscle haemorrhage with persistent contralateral deviation of midline structures. Muscle resection was followed by adequate external haerniation of the affected haemisphere and fast recovery. Cranioplasty was succesfully performed 22 days later, following gradual regression of cerebral oedema. Conclusion: There is an increasing perception of the need to operate patients with massive middle cerebral or internal carotid artery territory infarctions before the development of coma and cerebral haerniation. The most common factor leading to inadequate surgical decompression is small size craniectomy. The case reported calls attention to temporal muscle bleeding as an additional complication of craniectomy.KEY WORDS: ischaemic stroke, acute cerebral infarct, craniectomy. Hematoma de músculo temporal como causa de inadequada descompressão após hemicraniectomia descompressiva: relato de casoRESUMO -Objetivo: Alertar para o risco de descompressão cirúrgica subótima após hemicraniectomia descompressiva. Método: Revisão da literatura pertinente após descrição de caso clínico exemplificador. Resultados -Descrição do caso: Mulher de 55 anos, com instalação rápida de infarto cerebral no território da artéria cerebral média à direita. Evolução em 40 horas para coma e síndrome de herniação uncal. Tratada com salina hipertônica, hiperventilação e hemicraniectomia descompressiva (sem excisão de tecido cerebral), mantendo, porém, coma e decerebração persistentes. Exame de controle demonstrando volumoso hematoma de músculo temporal, levando a persistente desvio contralateral do segmento anterior do hemisfério afetado. Reoperação após 72 horas (exérese de músculo temporal), com rápida recuperação do nível de consciência e extubação. Controles neurorradiológicos mostrando adequada herniação externa do hemisfério, seguida de lenta regressão do edema cerebral, permitindo cranioplastia após 22 dias da primeira cirurgia. Conclusão: Progressivamente torna-se clara a importância potencial da cirurgia descompressiva. Estudos recentes sugerem maior benefício em casos de cirurgia precoce (de preferência antes da instalação de herniação cerebral) e de grandes craniectomias com descompressão completa para a evolução favorável de pacientes com infarto cerebral maciço. Hematoma de músculo temporal pode constituir causa não rara de descompressão incompleta. PALAVRAS-CHAVE: acidente vascular cerebral agudo, craniectomia de...

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Treatment of right hemispheric cerebral infarction by hemicraniectomy.

Cited by 211 publications

References 17 publications

Decompressive hemicraniectomy: predictors of functional outcome in patients with ischemic stroke

Decompressive hemicraniectomy: predictors of functional outcome in patients with ischemic stroke

Novel Treatment Targets for Cerebral Edema

Temporal muscle haematoma as a cause of suboptimal haemicraniectomy: case report

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