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Background: Headache is the most common presenting symptom of spontaneous subarachnoid hemorrhage and managing this acute pain can be challenging. The aim of this study was to describe the course of headaches and factors associated with analgesic failure in patients with spontaneous subarachnoid hemorrhage., Methods: We conducted a prospective observational study in patients admitted to a neurocritical care unit (between April 2016 and March 2017) within 48 hours of spontaneous subarachnoid hemorrhage. Headache intensity was assessed using a Numerical Pain Rating Scale (NPRS) ranging from 0 to 10. Analgesic failure was defined as any day average NPRS score >3 after 72 hours of hospitalization despite analgesic treatment., Results: Sixty-three patients were included in the analysis. Thirty-six (56.25%) patients experienced at least 1 episode of severe headache (NPRS ≥7), and 40 (63.5%) patients still reported moderate to severe headache on the final day of the study (day 12). Forty-six (73.0%) patients required treatment with opioids and 37 (58.7%) experienced analgesic failure. Multivariable analysis showed that analgesic failure was associated with smoking history (odds ratio [OR]=4.31, 95% confidence interval [CI]: 1.23-17.07; P =0.027), subarachnoid blood load (OR=1.11, 95% CI: 1.01-1.24; P =0.032) and secondary complications, including rebleeding, hydrocephalus, delayed cerebral ischemia, hyponatremia, or death (OR=4.06, 95% CI: 1.17-15.77; P =0.032)., Conclusions: Headaches following spontaneous subarachnoid hemorrhage are severe and persist during hospitalization despite standard pain-reducing strategies. We identified risk factors for analgesic failure in this population., Competing Interests: The authors have no conflicts of interest to declare., (Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.)

Introduction: Brain injuries can cause systemic immunosuppression, which in turn can lead to infections that adversely affect the injured brain and worsen clinical outcomes. This study aimed to investigate whether systemic infection, such as ventilator-associated pneumonia (VAP), induce intracranial inflammation in patients with subarachnoid hemorrhage (SAH)., Methods: This prospective, observational study included 16 adults with SAH treated in the neuro-intensive care unit. Three paired cerebrospinal fluid samples (obtained from an external ventricular drain) and peripheral blood samples were obtained on days 1 to 3, 4 to 5, and 6 to 7 after SAH onset. Cell counts, cell phenotypes (monocyte HLA-DR, T regulatory cells, lymphocytes, and neutrophils), and inflammatory mediator levels were monitored., Results: Six patients developed VAP in the context of systemic immunosuppression demonstrated by a reduction in monocyte HLA-DR expression, lymphopenia, increased percentages of circulating T regulatory cells, and increased proportions of immature and immunosuppressive neutrophil subsets. During VAP, there was de novo recruitment of leukocytes into the cerebrospinal fluid, preferentially neutrophils, which exacerbated intracranial inflammation., Conclusions: VAP increased intracranial inflammatory responses in patients with SAH despite the occurrence of systemic immunosuppression. A better understanding of cell trafficking and their pleiotropic functions in brain injury is needed to define the optimal strategies for preventing infections in patients with SAH., Competing Interests: The authors have no funding or conflicts of interest to disclose., (Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.)

Levels of jugular blood oxygen saturation (SjvO2) and lactate have been proposed as indicators of cerebral ischemia and prognosis. However, sensitivity and specificity of these markers remain unknown. We retrospectively analyzed records of a series of 43 comatose patients at risk for cerebral ischemia, mainly after head injuries or subarachnoidal hemorrhage. Their SjvO2, jugulo-arterial lactate difference (VADLactate), and lactate-oxygen index (LOI) were determined every 8 hours. An increase in VADLactate and LOI was found, indicative of ischemia on CT scan, with threshold values of 0.30 mmol/L and 0.15, respectively. Sensitivity and specificity were 100% and 64%, respectively, for the VADLactate threshold, and 90% and 55%, respectively, for the LOI threshold. Regarding prediction of a poor outcome, only an increase in VADLactate had a predictive value with a sensitivity of 100% and specificity of 67%. No threshold value with sufficient sensitivity and specificity was found for SjvO2, as indicator of either ischemia or outcome. During progression to brain death, VADLactate and LOI reached abnormal levels earlier than cerebral perfusion pressure or SjvO2. They reacted markedly to focal ischemia due to vasospasm. Hyperlactacidemia rendered VADLactate and LOI uninterpretable by causing a brain lactate influx. Present data, if confirmed by a prospective study, would justify inclusion of intermittent VADLactate and LOI determinations in the multimodal cerebral monitoring.