Decompressive craniectomy for the treatment of high intracranial pressure in closed traumatic brain injury.
Ontology highlight
ABSTRACT:
SUBMITTER: Sahuquillo J
PROVIDER: S-EPMC6953357 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Traumatic brain injury (TBI) causes brain edema that induces increased intracranial pressure and decreased cerebral perfusion. Decompressive craniectomy has been recommended as a surgical procedure for the management of swollen brain and intracranial hypertension. Proper location and size of a decompressive craniectomy, however, remain controversial and no clinical guidelines are available. Mathematical and computational (in silico) models can predict the optimum geometric conditions and provide insights for the brain mechanical response following a decompressive craniectomy. In this work, we present a finite element model of post-traumatic brain injury and decompressive craniectomy that incorporates a biphasic, nonlinear biomechanical model of the brain. A homogenous pressure is applied in the brain to represent the intracranial pressure loading caused by the tissue swelling and the models calculate the deformations and stresses in the brain as well as the herniated volume of the brain tissue that exits the skull following craniectomy. Simulations for different craniectomy geometries (unilateral, bifrontal and bifrontal with midline bar) and sizes are employed to identify optimal clinical conditions of decompressive craniectomy. The reported results for the herniated volume of the brain tissue as a function of the intracranial pressure loading under a specific geometry and size of craniectomy are exceptionally relevant for decompressive craniectomy planning.
| S-EPMC7596483 | biostudies-literature
Project description:In the context of traumatic brain injury (TBI), decompressive craniectomy (DC) is used as part of tiered therapeutic protocols for patients with intracranial hypertension (secondary or protocol-driven DC). In addition, the bone flap can be left out when evacuating a mass lesion, usually an acute subdural haematoma (ASDH), in the acute phase (primary DC). Even though, the principle of "opening the skull" in order to control brain oedema and raised intracranial pressure has been practised since the beginning of the 20th century, the last 20 years have been marked by efforts to develop the evidence base with the conduct of randomised trials. This article discusses the merits and challenges of this approach and provides an overview of randomised trials of DC following TBI. An update on the RESCUEicp study, a randomised trial of DC versus advanced medical management (including barbiturates) for severe and refractory post-traumatic intracranial hypertension is provided. In addition, the rationale for the RESCUE-ASDH study, the first randomised trial of primary DC versus craniotomy for adult head-injured patients with an ASDH, is presented.
| S-EPMC4841020 | biostudies-literature
Project description:We aim to perform a systematic review and meta-analysis to examine the prognostic value of decompressive craniectomy (DC) in patients with traumatic intracranial hypertension. PubMed, EMBASE, Cochrane Controlled Trials Register, Web of Science, http://clinicaltrials.gov/ were searched for eligible studies. Ten studies were included in the systematic review, with four randomized controlled trials involved in the meta-analysis, where compared with medical therapies, DC could significantly reduce mortality rate [risk ratio (RR), 0.59; 95% confidence interval (CI), 0.47-0.74, P?<?0.001], lower intracranial pressure (ICP) [mean difference (MD), -2.12?mmHg; 95% CI, -2.81 to -1.43, P?<?0.001], decrease the length of ICU stay (MD, -4.63 days; 95% CI, -6.62 to -2.65, P?<?0.001) and hospital stay (MD, -14.39 days; 95% CI, -26.00 to -2.78, P?=?0.02), but increase complications rate (RR, 1.94; 95% CI, 1.31-2.87, P?<?0.001). No significant difference was detected for Glasgow Outcome Scale at six months (RR, 0.85; 95% CI, 0.61-1.18, P?=?0.33), while in subgroup analysis, early DC would possibly result in improved prognosis (P?=?0.04). Results from observational studies supported pooled results except prolonged length of ICU and hospital stay. Conclusively, DC seemed to effectively lower ICP, reduce mortality rate but increase complications rate, while its benefit on functional outcomes was not statistically significant.
| S-EPMC5562822 | biostudies-literature
Project description:ObjectiveDecompressive craniectomy (DC) is one of the treatment modalities in severe traumatic brain injury (TBI), however, there was a lack of evidence for optimal craniectomy size. The authors aimed to investigate optimal DC size and analyze clinical outcome according to craniectomy size.MethodsWe retrospectively reviewed the medical data of 87 patients with a space occupying lesion following TBI who underwent unilateral DC. Craniectomy size was measured by anterior-posterior (AP) diameter and surface estimate (SE). Mortality, clinical outcome, and complications were collected and analyzed according to craniectomy size.ResultsNineteen patients (21.8%) died and 35 patients (40.2%) had a favorable outcome at last follow-up (a mean duration, 30.3±39.4 months; range, 0.2-132.6 months). Receiver operating curve analyses identified AP diameter more than 12.5 cm (area under the curve [AUC]=0.740; p=0.002) and SE more than 98.0 cm2 (AUC=0.752; p=0.001) as cut-off values for survival, and AP diameter more than 13.4 cm (AUC=0.650; p=0.018) and SE more than 107.3 cm2 (AUC=0.685; p=0.003) for favorable outcome. Large craniectomy resulted in a significantly lower mortality rate and a higher rate of favorable outcome than small craniectomy (p=0.005 and p=0.014, respectively). However, procedure related bleeding occurred more frequently in the large craniectomy group (p=0.044).ConclusionUnilateral DC size is associated with clinical outcome of patients with a space occupying lesion following severe TBI. Large craniectomy is needed for survival and favorable outcome.
| S-EPMC8093026 | biostudies-literature
Project description:BackgroundDecompressive craniectomy is an important surgical treatment for patients with severe traumatic brain injury (TBI). Several reports have been published on the efficacy of non-watertight sutures in duraplasty performed in decompressive craniectomy. This study sought to determine the safety and feasibility of the non-suture dural closure technique in decompressive craniectomy.MethodsA total of 106 patients were enrolled at a single trauma center between January 2017 and December 2018. We retrospectively collected data and classified the patients into non-suture and suture duraplasty craniectomy groups. We compared the characteristics of patients and their intra/postoperative findings such as operative time, blood loss, imaging findings, complications, and Glasgow Outcome Scale scores.ResultsThere were 37 and 69 patients in the non-suture and suture duraplasty groups, respectively. There were no significant differences between the two groups concerning general characteristics. The operative time was significantly lower in the non-suture duraplasty group than in the suture duraplasty group (150 min vs. 205 min; p = 0.002). Furthermore, blood loss was significantly less severe in the non-suture duraplasty group than in the suture duraplasty group (1000 mL vs. 1500 mL; p = 0.028). There were no other significant differences.ConclusionNon-suture duraplasty involved shorter operative times and less severe blood losses than suture duraplasty. Other complications and prognoses were similar across groups. Therefore, the non-suture duraplasty in decompressive craniectomy is a safe and feasible surgical technique.
| S-EPMC7544056 | biostudies-literature
Project description:Decompressive craniectomy (DC) in traumatic brain injury (TBI) has been suggested to influence cerebrovascular reactivity. We aimed to determine if the statistical properties of vascular reactivity metrics and slow-wave relationships were impacted after DC, as such information would allow us to comment on whether vascular reactivity monitoring remains reliable after craniectomy. Using the CENTER-TBI High Resolution Intensive Care Unit (ICU) Sub-Study cohort, we selected those secondary DC patients with high-frequency physiological data for both at least 24 h pre-DC, and more than 48 h post-DC. Data for all physiology measures were separated into the 24 h pre-DC, the first 48 h post-DC, and beyond 48 h post-DC. We produced slow-wave data sheets for intracranial pressure (ICP) and mean arterial pressure (MAP) per patient. We also derived a Pressure Reactivity Index (PRx) as a continuous cerebrovascular reactivity metric updated every minute. The time-series behavior of the PRx was modeled for each time period per patient. Finally, the relationship between ICP and MAP during these three time periods was assessed using time-series vector autoregressive integrative moving average (VARIMA) models, impulse response function (IRF) plots, and Granger causality testing. Ten patients were included in this study. Mean PRx and proportion of time above PRx thresholds were not affected by craniectomy. Similarly, PRx time-series structure was not affected by DC, when assessed in each individual patient. This was confirmed with Granger causality testing, and VARIMA IRF plotting for the MAP/ICP slow-wave relationship. PRx metrics and statistical time-series behavior appear not to be substantially influenced by DC. Similarly, there is little change in the relationship between slow waves of ICP and MAP before and after DC. This may suggest that cerebrovascular reactivity monitoring in the setting of DC may still provide valuable information regarding autoregulation.
| S-EPMC7249464 | biostudies-literature
Project description:BackgroundThe use of decompressive craniectomy in traumatic brain injury (TBI) remains a matter of debate. According to the DECRA trial, craniectomy may have a negative impact on functional outcome, while the RescueICP trial revealed a positive effect of surgical decompression, which is evolving over time. This ambivalence of craniectomy has not been studied extensively in controlled laboratory experiments.ObjectiveThe goal of the current study was to investigate the prolonged effects of decompressive craniectomy (both positive and negative) in an animal model.MethodsMale mice were assigned to the following groups: sham, decompressive craniectomy, TBI and TBI followed by craniectomy. The analysis of functional outcome was performed at time points 3d, 7d, 14d and 28d post trauma according to the Neurological Severity Score and Beam Balance Score. At the same time points, magnetic resonance imaging was performed, and brain edema was analyzed.ResultsAnimals subjected to both trauma and craniectomy presented the exacerbation of the neurological impairment that was apparent mostly in the early course (up to 7d) after injury. Decompressive craniectomy also caused a significant increase in brain edema volume (initially cytotoxic with a secondary shift to vasogenic edema and gliosis). Notably, delayed edema plus gliosis appeared also after decompression even without preceding trauma.ConclusionIn prolonged outcomes, craniectomy applied after closed head injury in mice aggravates posttraumatic brain edema, leading to additional functional impairment. This effect is, however, transient. Treatment options that reduce brain swelling after decompression may accelerate neurological recovery and should be explored in future experiments.
| S-EPMC10694459 | biostudies-literature
Project description:Hyperelastic finite element models, with either an idealized cylindrical geometry or with realistic craniectomy geometries, were used to explore clinical issues relating to decompressive craniectomy. The potential damage in the brain tissue was estimated by calculating the volume of material exceeding a critical shear strain. Results from the idealized model showed how the potentially damaged volume of brain tissue increased with an increasing volume of brain tissue herniating from the skull cavity and with a reduction in craniectomy area. For a given herniated volume, there was a critical craniectomy diameter where the volume exceeding a critical shear strain fell to zero. The effects of details at the craniectomy edge, specifically a fillet radius and a chamfer on the bone margin, were found to be relatively slight, assuming that the dura is retained to provide effective protection. The location in the brain associated with volume expansion and details of the material modeling were found to have a relatively modest effect on the predicted damage volume. The volume of highly sheared material in the realistic models of the craniectomy varied roughly in line with differences in the craniectomy area.
| S-EPMC5112297 | biostudies-literature
Project description:Decompressive craniectomy (DC) is often performed as an empirical lifesaving measure to protect the injured brain from the damaging effects of propagating oedema and intracranial hypertension. However, there are no clearly defined indications or specified guidelines for patient selection for the procedure.To evaluate outcome determinants and factors important in patient selection for the procedure.We reviewed the literature on DC, including single case reports and reported case series, to identify factors affecting outcome following the procedure, as well as its pitfalls and associated complications.Glasgow coma score of 8 and above, age less than 50 years and early intervention were found to be among the most significant determinants of prognosis.Improving patient selection for DC may be expected to further improve the outcome following the procedure in severely brain-injured patients.
| S-EPMC3066780 | biostudies-other
Project description:BackgroundIntracranial-pressure monitoring is considered the standard of care for severe traumatic brain injury and is used frequently, but the efficacy of treatment based on monitoring in improving the outcome has not been rigorously assessed.MethodsWe conducted a multicenter, controlled trial in which 324 patients 13 years of age or older who had severe traumatic brain injury and were being treated in intensive care units (ICUs) in Bolivia or Ecuador were randomly assigned to one of two specific protocols: guidelines-based management in which a protocol for monitoring intraparenchymal intracranial pressure was used (pressure-monitoring group) or a protocol in which treatment was based on imaging and clinical examination (imaging-clinical examination group). The primary outcome was a composite of survival time, impaired consciousness, and functional status at 3 months and 6 months and neuropsychological status at 6 months; neuropsychological status was assessed by an examiner who was unaware of protocol assignment. This composite measure was based on performance across 21 measures of functional and cognitive status and calculated as a percentile (with 0 indicating the worst performance, and 100 the best performance).ResultsThere was no significant between-group difference in the primary outcome, a composite measure based on percentile performance across 21 measures of functional and cognitive status (score, 56 in the pressure-monitoring group vs. 53 in the imaging-clinical examination group; P=0.49). Six-month mortality was 39% in the pressure-monitoring group and 41% in the imaging-clinical examination group (P=0.60). The median length of stay in the ICU was similar in the two groups (12 days in the pressure-monitoring group and 9 days in the imaging-clinical examination group; P=0.25), although the number of days of brain-specific treatments (e.g., administration of hyperosmolar fluids and the use of hyperventilation) in the ICU was higher in the imaging-clinical examination group than in the pressure-monitoring group (4.8 vs. 3.4, P=0.002). The distribution of serious adverse events was similar in the two groups.ConclusionsFor patients with severe traumatic brain injury, care focused on maintaining monitored intracranial pressure at 20 mm Hg or less was not shown to be superior to care based on imaging and clinical examination. (Funded by the National Institutes of Health and others; ClinicalTrials.gov number, NCT01068522.).
| S-EPMC3565432 | biostudies-literature