Patients with brain contusions: predictors of outcome and relationship between radiological and clinical evolution

Abstract

Object Traumatic parenchymal mass lesions are common sequelae of traumatic brain injuries (TBIs). They occur in up to 8.2% of all TBI cases and 13%–35% of severe TBI cases, and they account for up to 20% of surgical intracranial lesions. Controversy exists concerning the association between radiological and clinical evolution of brain contusions. The aim of this study was to identify predictors of unfavorable outcome, analyze the evolution of brain contusions, and evaluate specific indications for surgery. Methods In a retrospective, multicenter study, patients with brain contusions were identified in separate patient cohorts from 11 hospitals over a 4-year period (2008–2011). Data on clinical parameters and course of the contusion were collected. Radiological parameters were registered by using CT images taken at the time of hospital admission and at subsequent follow-up times. Patients who underwent surgical procedures were identified. Outcomes were evaluated 6 months after trauma by using the Glasgow Outcome Scale-Extended. Results Multivariate analysis revealed the following reliable predictors of unfavorable outcome: 1) increased patient age, 2) lower Glasgow Coma Scale score at first evaluation, 3) clinical deterioration in the first hours after trauma, and 4) onset or increase of midline shift on follow-up CT images. Further multivariate analysis identified the following as statistically significant predictors of clinical deterioration during the first hours after trauma: 1) onset of or increase in midline shift on follow-up CT images (p < 0.001) and 2) increased effacement of basal cisterns on follow-up CT images (p < 0.001). Conclusions In TBI patients with cerebral contusion, the onset of clinical deterioration is predictably associated with the onset or increase of midline shift and worsened status of basal cisterns but not with hematoma or edema volume increase. A combination of clinical deterioration and increased midline shift/basal cistern compression is the most reasonable indicator for surgery.

Derivation of a Predictive Score for Hemorrhagic Progression of Cerebral Contusions in Moderate and Severe Traumatic Brain Injury

“…As in previously published reports, we identified presence of SAH [4, 5, 7], skull fracture [7], and SDH [3, 6, 12] as major risk factors for HPC. SAH, skull fracture, and SDH may be markers of the overall severity of head trauma, or they may represent injury to the cortical veins, bridging veins, and venous sinuses that could contribute to venous congestion of the brain and increased risk of hematoma expansion [1].…”

“…The first two brain CT scans were retrospectively evaluated by a board-certified neurointensivist for identification of HPC. Parenchymal hematoma volume was estimated using the ABC/2 method, which has been utilized in prior studies of spontaneous and traumatic hematoma volume [2, 3, 6, 18, 19]. Heterogeneous lesions, defined as mixed high and low density, were measured using the entire length of the hyperdense portion of the lesion.…”

“…Commonly called contusion “blossoming,” HPC can result in neurological worsening from mass effect, cerebral edema, and parenchymal tissue necrosis [2, 3]. Prior case series have reported an incidence of HPC in TBI patients that ranges from 18 to 51 % [4–10].…”

Sulfonylurea Receptor 1 in Humans with Post-Traumatic Brain Contusions

“…Contusions are frequently associated with volumetric expansion during the first 48 h post-trauma. 1,2 In most patients, there is a progressive increase in pericontusional edema (edema progression), and in nearly half of patients, there is an increase in the hemorrhagic component itself (secondary hemorrhage or hemorrhagic progression). 1,2 Until recently, the underlying molecular pathophysiology of contusion-induced brain edema and hemorrhagic progression was poorly understood.…”

“…1,2 In most patients, there is a progressive increase in pericontusional edema (edema progression), and in nearly half of patients, there is an increase in the hemorrhagic component itself (secondary hemorrhage or hemorrhagic progression). 1,2 Until recently, the underlying molecular pathophysiology of contusion-induced brain edema and hemorrhagic progression was poorly understood. However, new evidence has accumulated in the last decade that has shed light on the complex cellular and molecular mechanisms underlying volumetric increases resulting from edema and secondary hemorrhage in PTBCs.…”