The safety of sportive chokes: a cross-sectional survey-based study.

Objectives: Sportive choking or strangling, known as a 'choke' in the combat sports community, is the practice of compressing the jugular veins and carotid arteries to threaten unconsciousness by lowering cerebral perfusion pressure. This is commonly practiced within combat sports and police/military combatives. The safety profile of sportive choking is underrepresented in the literature. The authors sought to explore the safety of sportive chokes. Methods: A convenience sample of visitors to two combat sports internet forums completed an anonymous web-based survey on choking experience and related symptoms. Descriptive statistics were used to describe the obtained data. Bivariate analysis was performed to elaborate on relationships between grappling experience and the number of times choked, between the number of times choked with pre-syncope/syncope, and between the duration of symptoms and the number of times choked with pre-syncope/syncope. Results: Overall, 4421 individuals completed the survey. One hundred and fourteen were excluded, leaving 4307 analyzed respondents. Ninety-four percent were male, 89.2% were ages 18-44 years. Seventy-nine percent had >1 year of grappling experience and 30% had >5 years. Of the 4307, 1443 (33.5%) reported being choked >500 times, 3257 (75.7%) have been choked to near-syncope, and 1198 (27.8%) have been choked unconscious. Two of the 4307 (0.05%) reported ongoing symptoms from chokes. Of the respondents, 94.3% felt applying a choke would be a safe and effective way to control a street fight; 83.6% felt that vascular neck restraint, the police combative equivalent of sportive choking, would be appropriate as an alternative escalation of force option. Conclusion: Based on a convenience sample of 4307 respondents' self-reported data, sportive choking appears to be safe. Only 0.05% experienced ongoing symptoms, which were likely not related to brain ischemia.

Conivaptan for the Reduction of Cerebral Edema in Intracerebral Hemorrhage: A Safety and Tolerability Study.

BACKGROUND: Perihematomal edema (PHE) growth in intracranial hemorrhage (ICH) is a biomarker for worse outcomes. Although the management of PHE is potentially beneficial for ICH patients, there is currently no proven clinical therapy that both reduces PHE and improves outcomes in this population. OBJECTIVE: To examine the safety and tolerability of conivaptan, a non-peptide vasopressin (AVP) receptor antagonist, for the management of PHE in ICH patients. METHODS: We performed a single-center, open-label, phase I study in seven patients with ICH at risk for developing PHE. Conivaptan (20 mg) was administered every 12 h for 2 days, along with the standard ICH management. Electrolyte levels, renal and cardiac function, and vital signs were monitored throughout treatment. Neurological status, ICH, and PHE volumes were assessed at study baseline, 24 h, 72 h, and 7 days from the first conivaptan administration, as well as at the 3-month follow-up. RESULTS: Conivaptan was well tolerated in our patients. We observed the expected increase in sodium levels following conivaptan administration (p = 0.01), with no change in cardiac or renal function. All patients survived to follow-up, and adverse event rates were comparable with those of the neurocritical care unit overall. CONCLUSIONS: These data indicate that conivaptan can be safely administered to ICH patients and support further clinical investigation into the efficacy of this drug for ICH treatment. CLINICAL TRIAL REGISTRATION: clinicaltrials.gov; NCT03000283, 22 December 2016.

There is more to the mechanism of unconsciousness from vascular neck restraint than simply carotid compression.

Vascular neck restraint (VNR), an effective technique practiced within police and military combatives and in mixed martial arts and grappling sports, is of both interest and controversy. In any context the goal of VNR (referred to as a choke within combat sports) is to restrict brain blood flow enough to threaten or result in unconsciousness. The physiologic basis for the resultant unconsciousness has been depicted as being solely because of restriction of carotid blood flow due to direct external compression. This view is likely simpler than what is actually going on, but it's an area not well explored in the medical literature. Brain blood flow is maintained through mechanisms that allow for a relatively wide acceptable cerebral perfusion pressure (CPP). If CPP drops below the threshold of this auto-regulation, blood flow and brain oxygen delivery begin to decline. CPP is the difference of the mean arterial pressure (MAP) coming into the brain and the intracranial pressure (ICP). Lowering the MAP and/or raising the ICP reduce the CPP. The best literature-established physiologic component of VNR is carotid compression and resultant reduction in functional carotid MAP, thus lowering the CPP. Most studies have looked at this essentially to the exclusion of two other contributing entities: jugular compression resulting in increased ICP from reduction of outflow, and reduction of actual whole body MAP due to reduced cardiac output from vagal stimulation coming from a pressure affected carotid body. This article fleshes out some of these physiologic variables and discusses the related available literature.

Utility of procalcitonin for diagnosis of bacterial infection-related systemic inflammatory response in the acute neurologic injury population.

OBJECTIVE: Inflammation and bacterial infection are common complicating factors in the treatment of patients with stroke. Inflammatory responses can manifest as systemic inflammatory response syndrome (SIRS), a condition with both infectious and non-infectious etiologies. Accurately identifying patients with infection-related SIRS is important for determining the correct treatment plan. Here, we investigated the use of the glycopeptide procalcitonin (PCT) as a potential biomarker for identifying patients with bacterial infections in the setting of SIRS. PATIENTS AND METHODS: A retrospective chart review was performed for adult patients admitted to United Hospital with an admission or discharge diagnosis of stroke for whom PCT testing was ordered between January 2011 and December 2014. Medical records were searched for the timing of PCT tests, and the previous 24 h was assessed for markers of SIRS, inflammation, and disease severity. RESULTS: PCT levels were negatively correlated with Glasgow Coma Scale scores (ρ=-0.27, p < 0.0001) and glomerular filtration rates (ρ=-0.22, p < 0.001), but demonstrated a positive correlation with white blood cell (WBC) count (ρ = 0.13, p = 0.031) and creatinine levels (ρ = 0.33, p < 0.0001). PCT levels were significantly higher in samples that corresponded to the presence of at least one infection (p < 0.0001) and in SIRS + samples (p < 0.001). However, even with the addition of a SIRS + diagnosis, the predictive value of PCT did not reach levels that would indicate clinical utility for the identification of patients with bacterial infections. CONCLUSIONS: PCT was not a viable biomarker for distinguishing between infectious and non-infections etiologies of SIRS in acute brain injury in this population. However, our results do indicate potential utility for PCT as an indicator for the cessation of antibiotic use in acute brain injury patients with bacterial infections.

Variable change in renal function by hypertonic saline.

AIM: To investigate the effects of hypertonic saline in the neurocritical care population. METHODS: We retrospectively reviewed our hospital's use of hypertonic saline (HS) since March of 2005, and prospectively since October 2010. Comparisons were made between admission diagnoses, creatinine change (Cr), and HS formulation (3% NaCl, 3% NaCl/sodium acetate mix, and 23.4% NaCl) to patients receiving normal saline or lactated ringers. The patients (n = 1329) of the retrospective portion were identified. The data presented represents the first 230 patients with data. RESULTS: Significant differences in Acute Physiology and Chronic Health Evaluation II scores and Glasgow Coma Scale scores occurred between different saline formulations. No significant correlation of Cl(-) or Na(+) with Cr, nor with saline types, occurred. When dichotomized by diagnosis, significant correlations appear. Traumatic brain injury (TBI) patients demonstrated moderate correlation between Na(+) and Cr of 0.45. Stroke patients demonstrated weak correlations between Na(+) and Cr, and Cl(-) and Cr (0.19 for both). Patients receiving HS and not diagnosed with intracerebral hemorrhage, stroke, subarachnoid hemorrhage, or TBI demonstrated a weak but significant correlation between Cl(-) and Cr at 0.29. CONCLUSION: Cr directly correlates with Na(+) or Cl(-) in stroke, Na(+) in TBI, and Cl(-) in other populations. Prospective comparison of HS and renal function is needed.

The use of targeted temperature management for elevated intracranial pressure.

The use of hypothermia for treatment of intracranial hypertension is controversial, despite no other medical therapy demonstrating consistent improvements in morbidity or mortality. Much of this may be the result of negative results from randomized controlled trials. However, the patients selected for these trials may have obscured the results in the populations most likely to benefit. Further, brain injury does not behave uniformly, not even within a diagnosis. Therefore, therapies may have more benefit in some diseases, less in others. This review focuses on the effect on outcome of intracranial hypertension in common disease processes in the neurocritical care unit, and identifies who is most likely to benefit from the use of hypothermia.

Clevidipine for acute hypertension in patients with subarachnoid hemorrhage: a pilot study.

PURPOSE: Clevidipine is a novel, ultra-short acting dihydropyridine. We hypothesized that clevidipine would rapidly control elevated blood pressure (BP) in patients with aneurysmal subarachnoid hemorrhage (SAH). MATERIALS AND METHODS: This prospective open-label pilot study evaluated the efficacy and safety of clevidipine in reducing blood pressure (BP) to a pre-specified range and within 30 min before or after clipping or coiling of the aneurysm. RESULTS: We enrolled five patients who received eight clevidipine infusions, including 1587 systolic or diastolic BP data points. The mean SBP upper and lower goals were set at 154 and 122 mmHg. The primary end point of achieving SBP control within <30 min was reached in all patients within 14.2 ± 6.4 min at an infusion rate of 10.8 ± 9.1 mg/h. The mean pre-infusion, during infusion and post-infusion SBP measurements were 165.5 ± 2.55, 146.4 ± 2.48 and 159.3 ± 11.5 mmHg ( p < 0.05 for pre- vs infusion comparison), respectively. After reaching the primary end point and during the clevidipine infusion, 17.5% and 11.8% of SBP readings were above the upper and below the lower goals, respectively. No patients re-bled. In one patient, the infusion had to be stopped temporarily three times due to SBP decrease below the lower goal. CONCLUSION: Clevidipine controlled SBP in all patients with aneurysmal SAH in <22 min and kept it within the elective range 70% of the time without major complications.

Use of hypothermia in the intensive care unit.

Used for over 3600 years, hypothermia, or targeted temperature management (TTM), remains an ill defined medical therapy. Currently, the strongest evidence for TTM in adults are for out-of-hospital ventricular tachycardia/ventricular fibrillation cardiac arrest, intracerebral pressure control, and normothermia in the neurocritical care population. Even in these disease processes, a number of questions exist. Data on disease specific therapeutic markers, therapeutic depth and duration, and prognostication are limited. Despite ample experimental data, clinical evidence for stroke, refractory status epilepticus, hepatic encephalopathy, and intensive care unit is only at the safety and proof-of-concept stage. This review explores the deleterious nature of fever, the theoretical role of TTM in the critically ill, and summarizes the clinical evidence for TTM in adults.

Single brain death examination is equivalent to dual brain death examinations.

BACKGROUND: Although the new Practice Parameters for brain death support a single examination, there is paucity of data comparing its impact to dual brain death (DBD) examinations. METHODS: We reviewed all brain deaths in our hospital over a 39-month period and compared the optional single brain death (SBD) exam requiring an apnea and a mandatory confirmatory blood flow test to the DBD for organ function at the time of death, rate of donation, and cost. RESULTS: Thirty-six patients had a SBD and 59 DBD exams, without any of them regaining neurological functioning. There was no difference in serum electrolytes (except for higher Na(+) and Cl(-) in the SBD group), blood urea nitrogen, creatinine, blood gases, incidence of diabetes insipidus, apnea completion, consent for donation, and organs recovered and transplanted. During the second BD exam, 35% of patients with DBD were on higher dose of vasopressors, but had lower systolic blood pressure (P = 0.046). For DBD patients, the mean interval between the two exams was 14.4 h, which contributed to a higher cost of $43,707.67 compared to SBD. There was a trend for increased consent rates (adjusted for age, race, and type of exam) when patients were declared by the neurointensivist service following a strict family approach protocol (P = 0.06). CONCLUSION: SBD exam is easier, faster to perform, with no brain function recovery and leads to similar donation rates, equivalent or better organ function status at the time of BD and lower cost than conventional DBD exams.

Hypothermia for refractory status epilepticus.

INTRODUCTION: Status epilepticus (SE) can be refractory to conventional anticonvulsants, requiring anesthetic doses of medications to suppress seizures. This approach carries significant morbidity, is associated with a high fatality rate, and may not always control SE. Hypothermia has been shown to suppress epileptiform activity experimentally, but has not previously been used as a primary modality to control SE in humans. METHODS: Four patients with SE refractory to benzodiazepine and/or barbiturate infusions were treated with hypothermia (target temperature: 31-35 degrees C) using an endovascular cooling system. All received continuous EEG monitoring, three were on midazolam infusions and one had recurrent seizures on weaning from pentobarbital. RESULTS: Therapeutic hypothermia was successful in aborting seizure activity in all four patients, allowing midazolam infusions to be discontinued; three achieved a burst-suppression pattern on EEG. After controlled rewarming, two patients remained seizure-free, and all four demonstrated a marked reduction in seizure frequency. Adverse events included shivering, coagulopathy without bleeding, and venous thromboembolism. Two death occurred, neither directly related to hypothermia; however, immunosuppression related to the use of barbiturates and hypothermia may have contributed to an episode of fatal sepsis in one patient. CONCLUSIONS: Hypothermia was able to suppress seizure activity in patients with SE refractory to traditional therapies with minimal morbidity. It appears promising as an alternative or an adjunct to anesthetic doses of other agents, but requires further study to better evaluate its safety and efficacy.

Clinical and experimental applications of NIR-LED photobiomodulation.

This review presents current research on the use of far-red to near-infrared (NIR) light treatment in various in vitro and in vivo models. Low-intensity light therapy, commonly referred to as "photobiomodulation," uses light in the far-red to near-infrared region of the spectrum (630-1000 nm) and modulates numerous cellular functions. Positive effects of NIR-light-emitting diode (LED) light treatment include acceleration of wound healing, improved recovery from ischemic injury of the heart, and attenuated degeneration of injured optic nerves by improving mitochondrial energy metabolism and production. Various in vitro and in vivo models of mitochondrial dysfunction were treated with a variety of wavelengths of NIR-LED light. These studies were performed to determine the effect of NIR-LED light treatment on physiologic and pathologic processes. NIRLED light treatment stimulates the photoacceptor cytochrome c oxidase, resulting in increased energy metabolism and production. NIR-LED light treatment accelerates wound healing in ischemic rat and murine diabetic wound healing models, attenuates the retinotoxic effects of methanol-derived formic acid in rat models, and attenuates the developmental toxicity of dioxin in chicken embryos. Furthermore, NIR-LED light treatment prevents the development of oral mucositis in pediatric bone marrow transplant patients. The experimental results demonstrate that NIR-LED light treatment stimulates mitochondrial oxidative metabolism in vitro, and accelerates cell and tissue repair in vivo. NIR-LED light represents a novel, noninvasive, therapeutic intervention for the treatment of numerous diseases linked to mitochondrial dysfunction.