Emergency Department Ceiling Collapse: Response to an Internal Emergency.

Hospital disaster resilience is often conceived as the ability to respond to external disasters. However, internal disasters appear to be more common events in hospitals than external events. This report describes the aftermath of a ceiling collapse in the emergency department of VieCuri Medical Center in Venlo, the Netherlands, on May 18, 2017. By designating the acute medical unit as a temporary emergency department, standard emergency care could be resumed within 8 hours. This unique approach might be transferrable to other hospitals in the developed world. In general, it is vital that hospital disaster plans focus on both external and internal disasters, including specific scenarios that disrupt vital hospital departments such as the emergency department. (Disaster Med Public Health Preparedness. 2019;13:829-830).

The impact of exercise-induced core body temperature elevations on coagulation responses.

OBJECTIVES: Exercise induces changes in haemostatic parameters and core body temperature (CBT). We aimed to assess whether exercise-induced elevations in CBT induce pro-thrombotic changes in a dose-dependent manner. DESIGN: Observational study. METHODS: CBT and haemostatic responses were measured in 62 participants of a 15-km road race at baseline and immediately after finishing. As haemostasis assays are routinely performed at 37°C, we corrected the assay temperature for the individual's actual CBT at baseline and finish in a subgroup of n=25. RESULTS: All subjects (44±11 years, 69% male) completed the race at a speed of 12.1±1.8km/h. CBT increased significantly from 37.6±0.4°C to 39.4±0.8°C (p<0.001). Post-exercise, haemostatic activity was increased, as expressed by accelerated thrombin generation and an attenuated plasmin response. Synchronizing assay temperature to the subjects' actual CBT resulted in additional differences and stronger acceleration of thrombin generation parameters. CONCLUSIONS: This study demonstrates that exercise induces a prothrombotic state, which might be partially dependent on the magnitude of the exercise-induced CBT rise. Synchronizing the assay temperature to approximate the subject's CBT is essential to obtain more accurate insight in the haemostatic balance during thermoregulatory challenging situations. Finally, this study shows that short-lasting exposure to a CBT of 41.2°C does not result in clinical symptoms of severe coagulation. We therefore hypothesize that prolonged exposure to a high CBT or an individual-specific CBT threshold needs to be exceeded before derailment of the haemostatic balance occurs.

The Impact of Central and Peripheral Cyclooxygenase Enzyme Inhibition on Exercise-Induced Elevations in Core Body Temperature.

PURPOSE: Exercise increases core body temperature (TC) due to metabolic heat production. However, the exercise-induced release of inflammatory cytokines including interleukin-6 (IL-6) may also contribute to the rise in TC by increasing the hypothalamic temperature set point. This study investigated whether the exercise-induced increase in TC is partly caused by an altered hypothalamic temperature set point. METHODS: Fifteen healthy, active men age 36 ± 14 y were recruited. Subjects performed submaximal treadmill exercise in 3 randomized test conditions: (1) 400 mg ibuprofen and 1000 mg acetaminophen (IBU/APAP), (2) 1000 mg acetaminophen (APAP), and (3) a control condition (CTRL). Acetaminophen and ibuprofen were used to block the effect of IL-6 at a central and peripheral level, respectively. TC, skin temperature, and heart rate were measured continuously during the submaximal exercise tests. RESULTS: Baseline values of TC, skin temperature, and heart rate did not differ across conditions. Serum IL-6 concentrations increased in all 3 conditions. A significantly lower peak TC was observed in IBU/APAP (38.8°C ± 0.4°C) vs CTRL (39.2°C ± 0.5°C, P = .02) but not in APAP (38.9°C ± 0.4°C) vs CTRL. Similarly, a lower ΔTC was observed in IBU/APAP (1.7°C ± 0.3°C) vs CTRL (2.0°C ± 0.5°C, P < .02) but not in APAP (1.7°C ± 0.5°C) vs CTRL. No differences were observed in skin temperature and heart-rate responses across conditions. CONCLUSIONS: The combined administration of acetaminophen and ibuprofen resulted in an attenuated increase in TC during exercise compared with a CTRL. This observation suggests that a prostaglandin-E2-induced elevated hypothalamic temperature set point may contribute to the exercise-induced rise in TC.

Precooling and percooling (cooling during exercise) both improve performance in the heat: a meta-analytical review.

BACKGROUND: Exercise increases core body temperature (Tc), which is necessary to optimise physiological processes. However, excessive increase in Tc may impair performance and places participants at risk for the development of heat-related illnesses. Cooling is an effective strategy to attenuate the increase in Tc. This meta-analysis compares the effects of cooling before (precooling) and during exercise (percooling) on performance and physiological outcomes. METHODS: A computerised literature search, citation tracking and hand search were performed up to May 2013. 28 studies met the inclusion criteria, which were trials that examined the effects of cooling strategies on exercise performance in men, while exercise was performed in the heat (>30°C). 20 studies used precooling, while 8 studies used percooling. RESULTS: The overall effect of precooling and percooling interventions on exercise performance was +6.7±0.9% (effect size (ES)=0.43). We found a comparable effect (p=0.82) of precooling (+5.7±1.0% (ES=0.44)) and percooling (+9.9±1.9% (ES=0.40)) to improve exercise performance. A lower finishing Tc was found in precooling (38.9°C) compared with control condition (39.1°C, p=0.03), while Tc was comparable between conditions in percooling studies. No correlation between Tc and performance was found. We found significant differences between cooling strategies, with a combination of multiple techniques being most effective for precooling (p<0.01) and ice vest for percooling (p=0.02). CONCLUSIONS: Cooling can significantly improve exercise performance in the heat. We found a comparable ES for precooling and percooling on exercise performance, while the type of cooling technique importantly impacts the effects. Precooling lowered the finishing core temperature, while there was no correlation between Tc and performance.

Incidence and predictors of exertional hyperthermia after a 15-km road race in cool environmental conditions.

OBJECTIVES: Current knowledge about the incidence and risk factors for exertional hyperthermia (core body temperature ≥40°C) is predominantly based on military populations or small-sized studies in athletes. We assessed the incidence of exertional hyperthermia in 227 participants of a 15-km running race, and identified predictors for exertional hyperthermia. DESIGN: Observational study. METHODS: We measured intestinal core body temperature before and immediately after the race. To identify predictive factors of maximum core body temperature, we entered sex, age, BMI, post-finish dehydration, number of training weeks, fluid intake before and during the race, finish time, and core body temperature change during warming-up into a backward linear regression analysis. Additionally, two subgroups of hyperthermic and non-hyperthermic participants were compared. RESULTS: In a WBGT of 11°C, core body temperature increased from 37.6±0.4°C at baseline to 37.8±0.4°C after warming-up, and 39.2±0.7°C at the finish. A total of 15% of all participants had exertional hyperthermia at the finish. Age, BMI, fluid intake before the race and the core body temperature change during warming-up significantly predicted maximal core body temperature (p<0.001). Participants with hyperthermia at the finish line had a significantly greater core body temperature rise (p<0.01) during the warming-up compared to non-hyperthermic peers, but similar race times (p=0.46). CONCLUSIONS: 15% of the recreational runners developed exertional hyperthermia, whilst core body temperature change during the warming-up was identified as strongest predictor for core body temperature at the finish. This study emphasizes that exertional hyperthermia is a common phenomenon in recreational athletes, and can be partially predicted.

Thermoregulation and fluid balance during a 30-km march in 60- versus 80-year-old subjects.

The presence of impaired thermoregulatory and fluid balance responses to exercise in older individuals is well established. To improve our understanding on thermoregulation and fluid balance during exercise in older individuals, we compared thermoregulatory and fluid balance responses between sexagenarians and octogenarians during prolonged exercise. Forty sexagenarians (60 ± 1 year) and 36 octogenarians (81 ± 2 year) volunteered to participate in a 30-km march at a self-selected pace. Intestinal temperature (T in) and heart rate were recorded every 5 km. Subjects reported fluid intake, while urine output was measured and sweat rate was calculated. Octogenarians demonstrated a lower baseline T in and a larger exercise-induced increase in T in compared to sexagenarians (1.2 ± 0.5 °C versus 0.7 ± 0.4 °C, p < 0.01), while maximum T in tended to be higher in octogenarians (38.4 ± 0.4 °C versus 38.2 ± 0.3 °C, p = 0.09). Exercise intensity (70 ± 11 % versus 70 ± 9 %) and exercise duration (7 h 45 min ± 0 h 57 min versus 7 h 24 min ± 0 h 58 min) were not different between octogenarians and sexagenarians. Octogenarians demonstrated lower fluid intake (251 ± 97 mL/h versus 325 ± 125 mL/h, p = 0.01) and urine output (28 ± 22 mL/h versus 52 ± 40 mL/h, p < 0.01) compared to sexagenarians. Furthermore, the sweat rate tended to be lower (294 ± 150 mL/h versus 364 ± 148 mL/h, p = 0.07) in the octogenarian group. Sodium levels and plasma volume changes were not different between sexagenarians and octogenarians (all p > 0.05). These results suggest that thermoregulatory responses deteriorate with advancing age, while fluid balance is regulated appropriately during a 30-km walking march under moderate ambient conditions.

The impact of obesity on cardiac troponin levels after prolonged exercise in humans.

Elevated cardiac troponin I (cTnI), a marker for cardiac damage, has been reported after high-intensity exercise in healthy subjects. Currently, little is known about the impact of prolonged moderate-intensity exercise on cTnI release, but also the impact of obesity on this response. 97 volunteers (55 men and 42 women), stratified for BMI, performed a single bout of walking exercise (30-50 km). We examined cTnI-levels before and immediately after the exercise bout in lean (BMI < 25 kg/m(2), n = 30, 57 ± 19 years), overweight (25 ≤ BMI < 30 kg/m(2), n = 29, 56 ± 11 years), and obese subjects (BMI ≥ 30 kg/m(2), n = 28, 53 ± 9 years). Walking was performed at a self-selected pace. cTnI was assessed using a high-sensitive cTnI-assay (Centaur; clinical cut-off value ≥ 0.04 µg/L). We recorded subject characteristics (body weight, blood pressure, presence of cardiovascular risk) and examined exercise intensity by recording heart rate. Mean cTnI-levels increased significantly from 0.010 ± 0.006 to 0.024 ± 0.046 µg/L (P < 0.001). The exercise-induced increase in cTnI was not different between lean, overweight and obese subjects (two-way ANOVA interaction; P = 0.27). In 11 participants, cTnI was elevated above the clinical cut-off value for myocardial infarction. Logistic regression analysis identified exercise intensity (P < 0.001), but not BMI, body fat percentage or waist circumference to significantly relate to positive troponin tests. In conclusion, prolonged, moderate-intensity exercise results in a comparable increase in cTnI-levels in lean, overweight and obese subjects. Therefore, measures of obesity unlikely relate to the magnitude of the post-exercise elevation in cTnI.