Decompressive Hemicraniectomy for Space-occupying Cerebral Infarction

E, Uhl

doi:10.1055/s-0029-1216362

Cited by 80 publications

(132 citation statements)

References 75 publications

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“…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. Several other studies have failed to find a significant effect of tPA administration on poor outcome and mortality after surgery as well.…”

Section: Discussionmentioning

confidence: 85%

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: 85%

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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“…(Mori et al, 2004) On the other hand, there are other studies which do not confirm the effect of timely " preventive " operations and these studies encourage clinicians to be more conservative and to wait for the time of developing the mass effect and midline shift. (Uhl et al, 2004;Rabinstein et al, 2006) Bar et al demonstrated in his studies that the size of ischemia does not have any influence on the favourable outcome (mRankine 0-4) assessed 3 months after the operation. He also did not identify the timing as an important variable affecting the outcome but in his work only a few patients were indicated early and this masked the benefit of early versus late surgery.…”

Section: Indicationsmentioning

confidence: 99%