BackgroundTo assess whether circadian patterns of temperature correlate with further values of intracranial pressure (ICP) in severe brain injury treated with hypothermia.MethodsWe retrospectively analyzed temperature values in subarachnoid hemorrhage patients treated with hypothermia by endovascular cooling. The circadian patterns of temperature were correlated with the mean ICP across the following day (ICP24).ResultsWe analyzed data from 17 days of monitoring of three subarachnoid hemorrhage patients that underwent aneurysm coiling, sedation and hypothermia due to refractory intracranial hypertension and/or cerebral vasospasm. ICP24 ranged from 11.5 ± 3.1 to 24.2 ± 6.2 mmHg. The ratio between the coefficient of variation of temperature during the nocturnal period (18:00–6:00) and the preceding diurnal period (6:00–18:00) [temperature variability (TV)] ranged from 0.274 to 1.97. Regression analysis showed that TV correlated with ICP24 (Pearson correlation = −0.861, adjusted R square = 0.725, p < 0.001), and that ICP24 = 6 (4–TV) mmHg or, for 80% prediction interval,  mmHg. The results indicate that the occurrence of ICP24 higher than 20 mmHg is unlikely after a day with TV ≥1.0.ConclusionsTV correlates with further ICP during hypothermia regardless the strict range that temperature is maintained. Further studies with larger series could clarify whether intracranial hypertension in severe brain injury can be predicted by analysis of oscillation patterns of autonomic parameters across a period of 24 h or its harmonics.Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-017-1272-y) contains supplementary material, which is available to authorized users.

We present the case of a 7-year old boy with traumatic brain injury who received propofol during 38 h. Thirty-six hours after cessation of propofol infusion asystole occurred. After immediate mechanical and medical resuscitation, unreactive dilated pupils were observed. The following computed tomography scan revealed a generalized brain edema with transtentorial herniation. Prolonged bradyarrhythmia, rhabdomyolysis, and peracute renal failure were observed. Despite immediate craniectomy, barbiturate treatment, hemofiltration, and recovery of appropriate cardiac function, the patient died four days after discontinuation of propofol. In this case, metabolic acidosis, cardiac failure, rhabdomyolysis, and renal failure are in accordance with the symptoms of propofol infusion syndrome (PRIS), while seizure, brain edema, and transtentorial herniation could be caused by traumatic brain injury. However, it may be assumed that the entire clinical picture was caused by PRIS. This view could be explained by a common loss of function of ryanodine receptors in patients presenting with PRIS.