Effect Of Decompressive Craniectomy Research Articles

Effect of Decompressive Craniectomy on Perihematomal Edema in Patients with Intracerebral Hemorrhage

Effect of Decompressive Craniectomy on Perihematomal Edema in Patients with Intracerebral Hemorrhage

Effect of decompressive craniectomy on outcome following subarachnoid hemorrhage in mice.

Elevated intracranial pressure (ICP) is a key feature of subarachnoid hemorrhage (SAH). Here, we examined the role of elevated ICP in the pathophysiology of SAH, and we investigated whether decreasing ICP by performing decompressive craniectomy (DC) can improve outcome. SAH was induced in male C57BL/6 mice via endovascular Circle of Willis perforation in the following 4 groups: sham surgery, SAH, DC after SAH, and DC before SAH. DC was performed either 15 minutes before or after SAH induction. ICP, cerebral blood flow, heart rate, oxygen saturation, and end-tidal PCO2 were monitored for 45 minutes. After surgery, neurological function was evaluated daily for 7 days. After killing, hippocampal neurons, corpus callosum thickness, and ventricular volume were evaluated on paraformaldehyde-fixed coronal brain sections. Although DC reduced SAH-induced ICP, it yielded no beneficial effect with respect to posthemorrhagic hypoperfusion; moreover, DC increased the incidence of rebleeding, induced more severe neurological impairments, and caused higher mortality. Post SAH, mice that survived 7 days had no histopathologic differences, regardless of whether DC was performed. Performing DC to reduce ICP either during or acutely after SAH resulted in more severe bleeding, a higher incidence of rebleeding, and poorer outcome. Thus, elevated post-hemorrhagic ICP plays an important role in controlling bleeding after SAH and should therefore not be reduced acutely. If DC is considered for treating a patient with SAH, the timing of decompression should take these effects into consideration.

Effects of decompressive craniectomy, hypertonic saline solution and mannitol on an experimental model of cerebral ischemia.

Cerebral ischemia is a cause of serious morbidity and mortality. Strategies that would protect cerebral tissue against ischemic injury are important. The present study aimed to evaluate effects of surgical and medical treatments, either alone or in combination, on infarction area in an experimental rat model of cerebral ischemia. Adult male Sprague-Dawley rats (n=30) were divided into 6 groups, each including 5 experimental animals. Cerebral ischemia was created by right common carotid artery occlusion (CCAO) under anesthesia. Decompressive craniectomy (DC) was performed in the relevant groups at the 12th hour following CCAO, whereas medical treatments were performed in the relevant groups at the 1st, 12th, and 24th hours following CCAO. After CCAO, the control group received 1 mL/kg physiological saline, hypertonic saline (HS) group received 3% hypertonic saline (1 mL/kg), and mannitol (MAN) group received 20% mannitol (1 g/kg). While only DC was performed following CCAO in the DC group, DC+HS group underwent DC together with hypertonic saline treatment and DC+MAN group underwent DC together with mannitol treatment. The rats were decapitated at the end of the 24th hour following ischemia. Cerebral sections were stained with 2% 2,3,5-triphenyltetrazolium chloride (TTC). The ratio of infarction area to the total area of section was calculated as percentage. Mean infarction areas were 27.9% in the control group, 13.7% in the HS group, 15.1% in the MAN group, 10.6% in the DC group, 8.1% in the DC+HS group, and 9.7% in the DC+MAN group. Mean infarction areas were significantly lower in all groups than in the control group. While the mean infarction area did not differ between the HS and MAN groups, it was lower in the groups undergoing DC as compared to these two groups. The best outcome was observed in the DC+HS group. Both medical and surgical treatments were effective in decreasing cerebral ischemic infarction. There was no difference between medical treatments groups in terms of efficacy, whereas DC led to a substantial decrease in ischemic infarction volume as compared with the medical treatment groups. Combined treatment approaches performed to decrease infarction volume also resulted in favorable outcomes.

Decompressive craniectomy after intravenous tissue plasminogen activator administration for stroke

ObjectiveIntravenous tissue plasminogen activator (IV tPA) is an approved treatment for acute ischemic stroke. However, the effects of decompressive craniectomy (DC) after IV tPA administration for ischemic stroke are still largely unknown. The aim of this study was to investigate the safety and outcomes of DC after IV tPA administration. MethodsWe retrospectively reviewed patients who underwent DC for malignant hemispheric infarction. We compared 20 patients who underwent DC after IV tPA administration with another 20 patients who underwent DC without prior IV tPA administration. ResultsThe patient characteristics did not differ between the DC patients with and without prior IV tPA administration. New intracranial bleeding or worsening of pre-existing ICH occurred in two patients (10%) in each group. Furthermore, the rates of an mRS score of 4–6, 5 or 6, and 6 did not differ significantly between the two groups. ConclusionDC may be a safe and useful surgical procedure for space-occupying edema after IV tPA administration for acute stroke.

Effect of Decompressive Craniectomy on Aquaporin-4 Expression after Lateral Fluid Percussion Injury in Rats

Decompressive craniectomy is one therapeutic option for severe traumatic brain injury (TBI), and it has long been used for the treatment of patients with malignant post-traumatic brain edema. A lack of definitive evidence, however, prevents physicians from drawing any conclusions about the effects of decompressive craniectomy for the treatment of TBI. Therefore, the aim of the present study was to investigate the influence of decompressive craniectomy on post-traumatic brain edema formation. The aquaporin-4 (AQP4) water channel is predominantly expressed in astrocytes, and it plays an important role in the regulation of brain water homeostasis. In the present study, we investigated the time course of AQP4 expression and the water content of traumatized cortex following decompressive craniectomy after TBI. Adult male Sprague-Dawley rats (300-400 g) were subjected to lateral fluid percussion injury using the Dragonfly device. The effect of decompressive craniectomy was studied in traumatized rats without craniectomy (closed skull, DC-), and in rats craniectomized immediately after trauma (DC+). AQP4 expression was investigated with a Western blot analysis and immunohistochemistry. Brain edema was measured using the wet weight/dry weight method. At 48 h after TBI, AQP4 expression of the DC- group was significantly increased compared with the DC+ group (p < 0.01). In addition, the cortical water content of the DC- group was significantly increased compared to the DC+ group at the same time point (p < 0.05). The present results suggest that decompressive craniectomy may affect AQP4 expression and reduce brain edema formation after TBI.

The effects of decompressive craniectomy on cerebral blood flow volume and brain metabolism in different aged patients with severe traumatic brain injury

Objective To explore the effects of decompressive craniectomy on cerebral blood flow volume and brain metabolism in different aged patients with severe traumatic brain injury.Method 71 cases were divided into three groups according age：group A（ ＜30 years） ,group B（30 ～50 years） ,group C （ ＞ 50 years）.Each group was divided into decompressive craniectomy （ DC ） treatment group and control group.Monitor dynamically blood gas analysis, glucose, lactic acid, hemoglobin in radial artery and internal jugular venous bulb, accounting the cerebral oxygen extraction （ CEO2 ） and the D - values of glucose and lactic acid respectively between radial artery and internal jugular venous bulb.Color doppler ultrasonography was used to determine the cerebral blood flow volume（CBFV）.Results From the 1 st to 7th day, the CBFV and CEO2 of DC group were significantly greater than control group in group A and group B.The CBFV was significantly greater than control group while the CEO2 was lower than control group in group C （ P ＜ 0.05 ）.From third day, the D - values of glucose of DC group was significantly higher than control group while the D - values of lactic acid was lower than control group in group A and group B, the D - values of glucose of DC group was significantly lower than control group while the D - values of lactic acid was higher than control group in group C（ P ＜ 0.05 ）.Conclusions Decompression craniectomy can increase the CBFV and brain oxygen metabolism in STBI patients before age 50 and increase the CBFV in patients after age 50 whereas decrease the brain oxygeon metabolism. Key words: Decompressive craniectomy; Craniocerebral trauma; Cerebral blood flow volume; Brain metabolism; Cerebral oxygen extraction

Comment on the article “Comparison of the effects of decompressive craniectomy on different neurosurgical diseases”, by Kim K.T. et al.

Comment on the article “Comparison of the effects of decompressive craniectomy on different neurosurgical diseases”, by Kim K.T. et al.

The effect of decompressive craniectomy on CSF pulsatility in experimental communicating hydrocephalus

Background It has been well established that intracranial pulsatility, whether measured as parenchymal/intraventricular pressure or as cerebrospinal fluid (CSF) flow in the cerebral aqueduct, is often markedly elevated in patients with hydrocephalus. Attempts have been made to use this measure to predict outcome from shunt surgery, but its specificity is still questionable. The question of whether or not intracranial pulsatility plays a causative role in hydrocephalus or is merely an epiphenomenon related to intracranial compliance is similarly an unanswered question. As a first step toward answering this question, we hypothesized that aqueductal pulsatility would be reduced after increasing compliance following decompressive craniectomy. Materials and methods Communicating hydrocephalus was induced by injection of kaolin into the basal cisterns in five (n = 5) adult Sprague-Dawley rats; controls received similar saline injections. Flow pulsatility was studied at two weeks post-injection by cine phase contrast MRI prior to and immediately following bilateral craniectomy. Aqueductal stroke volume before and after craniectomy were compared. To minimize effects of extended anesthesia, the craniectomy was started prior to the first imaging scan without breaking through the bone completely. Animals were then moved to the scanner, imaged for the precraniectomy pulsatility measurements, and returned to the bench to complete the craniectomy. A bone flap (4 x 10 mm) was taken from each side over the parietal lobe. The dura mater was left intact, although small tears in the dura were noticed in some cases. A second scan was then obtained to measure post-craniectomy pulsatility. To ensure similar physiological state for the two scans, animals were intubated throughout and ventilated on O2/isoflurane. Following the second scan, the animals were euthanized.

The Surgical Approach to the Management of Increased Intracranial Pressure After Traumatic Brain Injury

Increased intracranial pressure occurring after severe traumatic brain injury is a common and potentially devastating phenomenon. It has been clearly demonstrated that increased intracranial pressure that is refractory to initial medical measures is a poor prognostic sign. Current optimal management is based on a sequential, target-driven approach combining both medical and surgical treatment strategies. The surgical measures in current common practice include external ventricular drain insertion and decompressive craniectomy. There is evidence that both of these measures reduce intracranial pressure but the effect on outcome, particularly in the long term, is equivocal. Current Brain Trauma Foundation guidelines recommend timely evacuation of mass lesions and there is clear guidance regarding the indications for intracranial pressure monitoring; however, decompressive craniectomy is only cautiously recommended as a possible option for selected patients. In this review, we highlight the ongoing debate about the use of decompressive craniectomy to control intracranial pressure after traumatic brain injury; included is a summary of review of the most recent literature on the effect of decompressive craniectomy on increased intracranial pressure after traumatic brain injury and associated long-term outcome. The RESCUEicp and DECRA studies are discussed in detail. It is hoped that these 2 randomized controlled trials, which are evaluating the short- and longer-term outcomes of decompressive craniectomy, will provide conclusive evidence regarding the role of decompressive craniectomy in managing increased intracranial pressure after trauma.

Decompressive craniectomy for the treatment of traumatic brain injury: does an age limit exist?

It is generally believed that the outcome of traumatic brain injury is not improved by decompressive craniectomy in patients older than 30-50 years. A literature search was performed to assess the level of evidence with respect to the effect of age on outcome in these cases. References were identified by PubMed searches of journal articles published between 1995 and December 2008. The inclusion criteria were as follows: 1) clinical series including adults; and 2) focus on age as a prognostic factor. Technical notes and laboratory investigations were excluded. Fourteen English-language articles were finally selected. In 5 of the 14 studies, the authors performed no statistical analysis. In 6 studies they concluded that age was not significantly related to outcome (with 1 of these studies showing a correlation between age and outcome only after 65 years). Three studies showed a correlation between age and outcome. With respect to age and effectiveness of decompressive craniectomy, there are no robust data to establish any degree of core evidence and the referred age thresholds are arbitrary.

The effect of decompressive craniectomy on Bispectral Index and memory

The effect of decompressive craniectomy on Bispectral Index and memory

The effects of decompressive craniectomy or barbiturates on cerebral metabolism after severe TBI

The effects of decompressive craniectomy or barbiturates on cerebral metabolism after severe TBI

Effect of decompressive craniectomy on expression of NF-κB and apoptosis in brain of rats with hypoxic-ischemic brain damage

Objective To investigate the effect of decompressive craniectomy on the expression of NF-κB and apoptosis in the brain of rats with hypoxic-ischemic brain damage.Methods Sixty adult sprague-dawley rats were randomly divided into 3 groups(n=20,each):cerebral isehemia group(IS),cerebral ischemia and decompressive cranieetomy group(IS+DC),and decompressive craniectomy group (DC).The brains were collected to observe the scope of cerebral infarction by TTC staining,to examine the uhrastrueture of ischemic penumbra by an electronic microscope,to detect the expression of NF-κB by immunohistochemistry and to test the apoptosis by TUNEL.Results Compared with the other groups,the infarction volume was decreased,the damage of ischemic penumbra neurons was relieved.the expression of NF-κB was attenuated remarkably(0.0621±0.0101,P＜0.05),and the apoptotie cells were decreased significantly(0.0621±0.0101,P＜0.05)in IS+DC group.Conclusion Deeompressive craniectomy may protect the brain by increasing the expression of NF-κB and decreasing the apoptotie cells in cerebral iscbemie penumbra. Key words: Brain isehemia; Decompression,snrsical; NF-κB; Apoptosis

Effect of Decompressive Craniectomy and Hypothermia on the Expression of c-Fos and Heat Shock Proteins Following Fluid Percussion Brain Injury in the Rat

FPI model treated with hypothermia 9) , an association between Corresponding Author: Young-Min Han, M.D. Department of Neurosugery, Our Lady of Mercy Hospital, 665 Bupyung-Dong, Bupyung-Gu, Incheon, 403-720 Korea Tel: 82-32-510-5515, Fax: 82-32-511-2370 E-mail: hymns@medimail.co.kr Effect of Decompressive Craniectomy and Hypothermia on the Expression of c-Fos and Heat Shock Proteins Following Fluid Percussion Brain Injury in the Rat

The effect of decompressive craniectomy on ICP in patients with traumatic brain injuries

The effect of decompressive craniectomy on ICP in patients with traumatic brain injuries

Effect of Decompressive Craniectomy on Massive Brain Swelling Patients According to the Diseases

Methods: Eighty patients with massive brain swelling, with Glasgow Coma Scale (GCS) less than 8 scores and midline shift more than 10 mm on CT were included in this study. 38 cases of traumatic brain injury (TBI), 24 cases of hypertensive intracerebral hematoma (H-ICH), 12 cases of major infarction and 6 cases of vasospasm after subarachnoid hemorrhage (SAH) were analyzed. In all patients, bilateral or unilateral craniectomy with dura expansion were performed, and the ventricular pressure was monitored through the operation. Results: The mean GCS scores that evaluated 3 months after the decompressive surgery were 9.4 in TBI, 9.5 in H-ICH, 3.1 in major infarction and 4.3 in vasospasm patients group. The mortality was 24% in TBI, 21% in H-ICH, 75% in major infarction and 66% in vasospasm patients group. Conclusions: Bilateral decompression with dura expansion is a effective therapeutic modality in intracranial pressure (ICP) control. To obtain favorable clinical outcome in patients with major stroke and vasospasm, early decision making should be done compare with the TBI and H-ICH patients.

Effects of decompressive craniectomy, hypothermia and their combination in a permanent focal cerebral ischemia model

AbstractHypothermia has a neuroprotective effect in cerebral ischemia and reduces brain edema, and decompressive craniectomy (DC) can prevent brain herniation caused by massive brain edema. Thus, combination of the two therapies may be more effective in large hemispheric infarctions, by exerting an additive effect. We investigated the effects of DC, hypothermia, and their combination in experimental cerebral ischemia. Seventy rats received focal cerebral ischemia for 72 hours and were allocated to one of four groups: untreated control (n=29), DC (n=21), hypothermia (n=10), and DC plus hypothermia (n=10). Hypothermia (34°C) and/or DC were performed 6 hours after ischemia. Mortality was 44.8% (control), 28.6% (DC), 10.0% (hypothermia), and 0% (DC plus hypothermia), respectively (p&lt;0.05). Compared to control (260.2±100.8 mm3), the size of the infarction was not reduced by DC (236.3±94.3 mm3), p&gt;0.1) but was by hypothermia (117.8±50.7 mm3), p&lt;0.01). Although hypothermia combined with DC reduced the size of the infarction significantly (99.6±71.2 mm3), no additional effect was observed versus hypothermia alone.

Effect of decompressive craniectomy on brain tissue oxygenation and intracranial pressure in patients with intracranial hypertension

Effect of decompressive craniectomy on brain tissue oxygenation and intracranial pressure in patients with intracranial hypertension

Decompressive Craniectomy for Cerebral Infarction

Acute ischemia in the territory of the carotid artery can lead to massive cerebral edema with raised intracranial pressure and progression to coma and death due to uncal, cingulate, or tonsillar herniation. Thus far, only anecdotal experience with supratentorial ischemia treated by decompressive craniectomy has been reported; and there are no published experimental data dealing with this kind of therapy in acute supratentorial stroke. In this study, we present our results on the effect of decompressive craniectomy in an endovascular model of cerebral infarction in rats. Focal cerebral ischemia was induced in 50 rats using an endovascular occlusion technique of the middle cerebral artery. Decompressive craniectomy was performed in 30 animals: in 15 animals after 1 hour and in the remaining 15 animals 24 hours after vessel occlusion. Twenty animals were not treated by decompressive craniectomy (control group). Mortality in the nontreated group was 35%, whereas none of the animals treated by decompressive craniectomy died. Neurological behavior, weight loss, and infarction size were all significantly better in the animals treated by decompressive craniectomy, regardless of whether they had been treated after 1 or 24 hours (P < .01). Our results suggest that decompressive craniectomy for cerebral ischemia not only reduces mortality but also significantly improves outcome and reduces infarction size, probably because of increased perfusion pressure through leptomeningeal collaterals. This experimental study suggests that a controlled study of decompressive craniectomy in patients with acute internal carotid or middle cerebral artery occlusion would be worthwhile. By performing decompressive craniectomy in a small, selected group of patients, neurosurgeons may play an important role in the management of these patients.

Effects of decompressive craniectomy on regional cerebral blood flow in severe head trauma patients.

The effect of decompressive craniectomy on regional cerebral blood flow (rCBF) was investigated in five patients with severe head trauma who underwent decompressive craniectomy. Repeated rCBF studies using single photon emission computed tomography with 99mtechnetium-hexamethylpropyleneamine oxime observed that a hyperperfusion area (focal CBF increase) occurred in the decompressed brain within 24 hours after decompressive craniectomy. The hyperperfusion area in the decompressed brain enlarged and increased in severity by 1 week after surgery. However, it attenuated and disappeared by 1 month after surgery. The chronology of the hyperperfusion area corresponded to the change in the swelling of decompressed brain observed by x-ray computed tomography. Patient consciousness showed a significant and progressive improvement in the postoperative 1 month period. Decompressive craniectomy may cause a focal CBF increase in the decompressed brain related to the beneficial effect in patients with acute severe head trauma.