Impact of a posttraumatic cerebral infarction on outcome in patients with TBI: the Italian multicenter cohort INCEPT study

Abstract

Background: Post-traumatic cerebral infarction (PTCI) is common after traumatic brain injury (TBI). It is unclear what the occurrence of a PTCI is, how it impacts the long-term outcome, and whether it adds incremental prognostic value to established outcome predictors.

Methods: This was a prospective multicenter cohort study of moderate and severe TBI patients. The primary objective was to evaluate if PTCI was an independent risk factor for the 6-month outcome assessed with the Glasgow Outcome Scale (GOS). We also assessed the PTCI occurrence and if it adds incremental value to the International Mission for Prognosis and Clinical Trial design in TBI (IMPACT) core and extended models.

Results: We enrolled 143 patients, of whom 47 (32.9%) developed a PTCI. In the multiple ordered logistic regression, PTCI was retained in both the core and extended IMPACT models as an independent predictor of the GOS. The predictive performances increased significantly when PTCI was added to the IMPACT core model (AUC = 0.73, 95% C.I. 0.66-0.82; increased to AUC = 0.79, 95% CI 0.71-0.83, p = 0.0007) and extended model (AUC = 0.74, 95% C.I. 0.65-0.81 increased to AUC = 0.80, 95% C.I. 0.69-0.85; p = 0.00008). Patients with PTCI showed higher ICU mortality and 6-month mortality, whereas hospital mortality did not differ between the two groups.

Conclusions: PTCI is a common complication in patients suffering from a moderate or severe TBI and is an independent risk factor for long-term disability. The addition of PTCI to the IMPACT core and extended predictive models significantly increased their performance in predicting the GOS.

Trial registration: The present study was registered in ClinicalTrial.gov with the ID number NCT02430324.

Keywords: Disability; Long term outcome; Posttraumatic cerebral infarction; Traumatic brain injury.

Fig. 1

Study flow chart

Fig. 2

CT scan showing posttraumatic cerebral infarction (PTCI). A1 MCA PTCI: acute parietal subdural hematoma on the right side (long arrow), extending to the falx (short arrow). A2 CT scan 9 days later showed an acute ischemic lesion in the superficial territory of the right MCA (preserved right lenticular nucleus, white *). B2 PCA PTCI: acute subdural hematoma along the right side of the tentorium (empty arrow), extra-axial blood in the prepontine cistern (short arrow), and small para sellar bubble air (long arrow) on admission brain CT. B2 Brain CT scan at 15 days showed complete effacement of the basal cisterns and bilateral temporo-occipital hypodensities (*), consistent with acute ischemic lesions in the territory of both PCA. C1 ACA PTCI: hemorrhagic contusions of the right frontal lobe mixed with air and perilesional vasogenic edema, intraventricular hemorrhage, a thick left frontoparietal acute subdural hematoma (long arrow) with midline shift to the right, and a thin acute subdural hematoma along the posterior falx (double arrows). C2 Left frontoparietal craniectomy and hematoma evacuation showed multifocal hypodensities in the anterior and posterior portion of the left cingulate gyrus (white outlined arrows), consistent with acute ischemic lesions in the territory of the left ACA. The small hypodensity in the genu of the corpus callosum (short arrow), barely visible in the first exam, is consistent with a shear-strain injury. D1 Superficial watershed PTCI: thick acute subdural hematomas along the whole tentorium and the left frontotemporal convexity. Diffuse subarachnoid hemorrhage is also visible at the vertex (long white arrows). D2 Bilateral cortical hypodensities in the posterior parasagittal regions (black arrows), consistent with acute watershed ischemia at the boundary zone between the MCA and ACA territories. Note the probe for the intracranial pressure monitoring in the left frontal lobe (short white arrow)

Fig. 3

ROC curves for the core and extended IMPACT models with the addition of PTCI. Comparison of ROC curves and AUCs with and without the addition of PTCI, for both the core and extended models (p values for the difference in AUC: p = 0.05 for core model, p = 0.049 for the extended model). IMPACT: International Mission on Prognosis Analysis of Clinical Trials in Traumatic Brain Injury

Fig. 4

Correction for optimism of AUC for both core and extended models. Auc.boot is the distribution of the AUC value in the bootstrap sample, which represents “an estimation of the apparent performance.” “auc.orig” is the distribution of the AUC value deriving from the model fitted to the bootstrap samples and evaluated on the original sample, which represents the model performance on independent data. At the bottom of the chart, the apparent AUC (i.e., the value deriving from the model fitted to the original dataset) and the AUC adjusted for optimism are reported on the box plot respectively with the blue line and red line [25]