HEAD TRAUMA / TRAUMATIC BRAIN INJURY (TBI)

J Trauma Acute Care Surg. 2018 Aug;85(2):380-386

A clinical prediction model for raised intracranial pressure in patients with traumatic brain injury.

Pace J, Parry N, Vogt K, Hilsden R, Leeper R, Markova Z, Priestap F, Younan J, Ball I.

BACKGROUND: Intracranial hypertension is believed to contribute to secondary brain insult in traumatically brain injured patients. Currently, the diagnosis of intracranial hypertension requires intracranial monitoring or advanced imaging. Unfortunately, prehospital transport times can be prolonged, delaying time to the initial radiographic assessment. The aim of this study was to identify clinical variables associated with raised intracranial pressure (ICP) prior to the completion of neuroimaging.

METHODS: We performed a retrospective cohort study of head injured patients over a 3-year period. Patients were labeled as having increased ICP if they had a single reading of ICP greater than 20 mm Hg within 1 hour of ICP monitor insertion or computed tomography findings suggestive of raised ICP. Patient and clinical characteristics were analyzed using stepwise multivariable logistic regression with ICP as the dependent variable.

RESULTS: Of 701 head injured patients identified, 580 patients met inclusion criteria. Mean age was 48.65 ± 21 years, 73.3% were male. The mean Injury Severity Score was 22.71 ± 12.38, and the mean Abbreviated Injury Scale for body region head was 3.34 ± 1.06. Overall mortality was 14.7%. Only 46 (7.9%) patients had an ICP monitor inserted; however, a total of 107 (18%) patients met the definition of raised ICP. The mortality rate for patients with raised ICP was 50.4%. Independent predictors of raised ICP were as follows: age, older than 55 years (odds ratio [OR], 2.26; 95% confidence interval [CI], 1.35-3.76), pupillary fixation (OR, 5.76; 95% CI, 3.16-10.50), signs of significant head trauma (OR, 2.431; 95% CI, 1.39-4.26), and need for intubation (OR, 3.589; 95% CI, 2.10-6.14).

CONCLUSION: This study identified four independent variables associated with raised ICP and incorporated these findings into a preliminary risk assessment scale that can be implemented at the bedside to identify patients at significant risk of raised ICP. Future work is needed to prospectively validate these findings prior to clinical implementation.

LEVEL OF EVIDENCE: Prognostic, Epidemiological, level III.

Lancet. 2018 May 26;391(10135):2107-2115

Tranexamic acid for hyperacute primary intracerebral haemorrhage (TICH-2): an international randomised, placebo-controlled, phase 3 superiority trial.

Sprigg N, Flaherty K, Appleton J, Al-Shahi Salman R, Bereczki D, Beridze M, Christensen H, Ciccone A, Collins R, Czlonkowska A, Dineen R, Duley L, Egea-Guerrero J, England T, Krishnan K, Laska A, Law Z, Ozturk S, Pocock S, Roberts I, Robinson T, Roffe C, Seiffge D, Scutt P, Thanabalan J, Werring D, Whynes D, Bath P; TICH-2 Investigators.

BACKGROUND: Tranexamic acid can prevent death due to bleeding after trauma and post-partum haemorrhage. We aimed to assess whether tranexamic acid reduces haematoma expansion and improves outcome in adults with stroke due to intracerebral haemorrhage.

METHODS: We did an international, randomised placebo-controlled trial in adults with intracerebral haemorrhage from acute stroke units at 124 hospital sites in 12 countries. Participants were randomly assigned (1:1) to receive 1 g intravenous tranexamic acid bolus followed by an 8 h infusion of 1 g tranexamic acid or a matching placebo, within 8 h of symptom onset. Randomisation was done centrally in real time via a secure website, with stratification by country and minimisation on key prognostic factors. Treatment allocation was concealed from patients, outcome assessors, and all other health-care workers involved in the trial. The primary outcome was functional status at day 90, measured by shift in the modified Rankin Scale, using ordinal logistic regression with adjustment for stratification and minimisation criteria. All analyses were done on an intention-to-treat basis. This trial is registered with the ISRCTN registry, number ISRCTN93732214.

FINDINGS: We recruited 2325 participants between March 1, 2013, and Sept 30, 2017. 1161 patients received tranexamic acid and 1164 received placebo; the treatment groups were well balanced at baseline. The primary outcome was assessed for 2307 (99%) participants. The primary outcome, functional status at day 90, did not differ significantly between the groups (adjusted odds ratio [aOR] 0·88, 95% CI 0·76-1·03, p=0·11). Although there were fewer deaths by day 7 in the tranexamic acid group (101 [9%] deaths in the tranexamic acid group vs 123 [11%] deaths in the placebo group; aOR 0·73, 0·53-0·99, p=0·0406), there was no difference in case fatality at 90 days (250 [22%] vs 249 [21%]; adjusted hazard ratio 0·92, 95% CI 0·77-1·10, p=0·37). Fewer patients had serious adverse events after tranexamic acid than after placebo by days 2 (379 [33%] patients vs 417 [36%] patients), 7 (456 [39%] vs 497 [43%]), and 90 (521 [45%] vs 556 [48%]).

INTERPRETATION: Functional status 90 days after intracerebral haemorrhage did not differ significantly between patients who received tranexamic acid and those who received placebo, despite a reduction in early deaths and serious adverse events. Larger randomised trials are needed to confirm or refute a clinically significant treatment effect.

FUNDING: National Institute of Health Research Health Technology Assessment Programme and Swiss Heart Foundation.