Yuval Heled

Exertional heat stroke (EHS) is a clinical syndrome of hyperthermia, encephalopathy and multi-organ dysfunction that can be irreversible and fatal. Prompt recognition and immediate, aggressive total body cooling can prevent progression of the clinical syndrome, but even a short delay can exacerbate the effects of hyperthermic-induced changes. EHS is linked to an inflammatory response that is akin to the systemic inflammatory response syndrome (SIRS). However, because EHS is not a common problem in most hospital intensive care units and is not in the usual list of SIRS causes, it may easily be overlooked. The present case report will highlight the preliminary clinical manifestations of the syndrome, the initial optimal treatment, and its clinical sequelae.

During exercise certain metabolic and physiological processes influence fluid and electrolyte balance. Fluid loss, mostly through sweating, that is not properly compensated for by drinking, may result in dehydration. Clinical manifestations of dehydration depend on the amount of fluid lost. The more severe the level of dehydration is, the greater the reduction in physical and cognitive performance. It is recommended to drink water frequently and in small amounts. In order to encourage drinking, the fluid should be cool, palatable, readily available, and not carbonated. During exercise the ability of the kidney to excrete water is restricted, and therefore, there is a risk of hyperhydration and hyponatremia, mainly under conditions of overdrinking. Sodium loss through sweating and the development of hyponatremia will primarily occur during strenuous exercise lasting more than 4 hours. Symptoms of hyponatremia will generally appear at sodium concentrations below 130 mmol/l. In order to avoid hyponatremia one must avoid overdrinking, and during prolonged physical activity (> 4 hours) sodium intake must match the amount lost by sweating. Proper electrolyte and carbohydrate consumption through a normal diet is preferable to sport beverages or exogenous sodium supplements. In order to avoid dehydration, on one hand, and hyponatremia due to hyperhydration, on the other hand, the amount of fluid consumed should complement the amount of fluid lost during exercise. Given that there is intra- (depending on the type of activity and environmental conditions) and interindividual variability in the rate of fluid and salt loss, fluid and salt intake should be determined on an individual basis, as outlined in this standpoint.

Rhabdomyolysis is defined as a syndrome resulting from skeletal muscle injury with release of muscle cell contents into the plasma. One of the main causes of rhabdomyolysis is eccentric exercise against high resistance. There are mechanical as well as metabolic causes in exercise induced rhabdomyolysis. The mechanical aspect includes high physical tension on the muscle fiber and the metabolic causes include lack of available ATP and disturbance in intracellular electrolyte balance, especially calcium. The clinical picture of rhabdomyolysis may include muscle soreness, reduction of the range of motion, decreased muscle strength, black urine and, in severe cases, acute renal failure. Laboratory results may include delayed high levels of muscle enzymes in the plasma, myoglobinemia and myoglobinuria, disturbance in blood electrolyte balance, and in severe cases, disturbance in coagulatory function and DIC. Compartment syndrome may also be part of severe rhabdomyolyis. The main treatment for rhabdomyolysis is fluids administration and maintaining urination, in order to preserve renal function. In severe compartment syndrome fasciotomy may be necessary. There is a wide variability in the severity of rhabdomyolysis. This variability is not completely understood but may be related to the level of physical fitness, morphometrical characteristics and gender. In order to prevent exercise induced rhabdomyolysis, a gradual training program should be maintained providing enough recovery time, preserving fluid balance, and avoiding extreme eccentric exercise and exercise in high heat load.

A novel actigraphy method, the proportional integral mode, was used for monitoring metabolic rate and energy expenditure during different levels of exercise intensity. 13 young (24+/-3 yrs) male subjects, clothed in T-shirts, shorts and athletic shoes, ran/walked for 30 min on a level treadmill at different speeds (3, 5, 2, 6, 4, and 7 mph), 5 min at each speed. The following variables were continuously measured: Actigraphy (PCD, USA) data at three different modes (proportional integral mode, zero crossing, and time above threshold) from the wrist; oxygen consumption (Sensor Medics, USA), and heart rate (Polar, Finland). Analysis of the measured data revealed with low correlation between oxygen consumption and zero crossing or time above threshold (R=0.364 and 0.384, respectively), but with high correlation between oxygen consumption and proportional integral mode (R=0.843). The proportional integral mode, which is unlike the other modes, followed the oxygen consumption and the heart rate curves, showing a potential unique method to predict oxygen consumption and energy expenditure.

We hypothesized that there is an association between the angiotensin I-converting enzyme (ACE) insertion (I)/deletion (D) polymorphism with the variability in exercise heat tolerance in humans. Fifty-eight Caucasian men were exposed to a 2-h exercise heat-tolerance test. We analyzed the association between their heat-tolerance levels with the ACE DD ( n = 25) and I+ ( n = 33) genotypes and with various anthropometrical parameters and aerobic fitness. It was found that the relative changes in body core temperature, heat storage, and heart rate during the 120-min exposure to exercise heat stress was consistently lower in the I+ genotype group compared with the DD genotype group (0.8 ± 0.2 vs. 1 ± 0.1°C, P < 0.05; 17.7 ± 1.8 vs. 19.8 ± 1.3 W/M², P < 0.05; and 33 ± 7 vs. 44 ± 5 beats/min, respectively, P = 0.06). No significant association was found between heat strain response and the anthropometrical measurements or aerobic fitness in the various genotype groups. We suggest that the ACE I+ polymorphism may be considered as a possible candidate marker for increased heat tolerance.

The aim of this study was to evaluate the heat tolerance test, which was performed by individuals with high risk for heat injuries, for exposure duration and climatic conditions. Nineteen young (19+/-1 yr) post heat stroke males performed 2 separate tolerance tests consisting of identical treadmill walking (5km.h-1, 2% grade) for 120 min during hot (40 degrees C, 40%RH) and comfort (20 degrees C, 50%RH) climate conditions. Physiological monitoring included rectal temperature (Tre), heart rate (HR), skin temperature and sweat rate (msw). Concomitantly, strain evaluation was assessed by the physiological strain index (PSI) and the cumulative heat strain index (CHSI). 14 subjects were categorized as heat tolerant (HT) and 5 subjects as heat intolerant (HI). The comfort tolerance test was found as irrelevant for heat intolerance assessment. PSI after 60 min (PSI60) was unable to predict PSI after 120 min (PSI120) whereas there was not a high enough correlation between CHSI60 and CHSI120. It was concluded that tolerance to heat must be tested during heat stress and the test duration cannot be shorter than 120 min.

While wearing impermeable nuclear, biological, and chemical (NBC) clothing, reduction of thermal stress is of primary importance. We compared the effect between two cooling methods on the attenuation of heat strain. There were six male subjects who were divided into two groups of three and exposed on two consecutive days to 125 min of exercise in a high heat load (40 degrees C, 40% RH) wearing NBC clothing. They were cooled by one of two different cooling methods: an active cooling vest (CV) based on the sublimation of dry ice, or tap water spraying (TP). After 2 h, rectal temperature (Tre) was significantly higher for the CV compared with the TP (38.1 +/- 0.04 degrees C vs. 37.7 +/- 0.10 degrees C, respectively). Skin temperature (Tsk) was significantly higher for the CV compared with the TP (36.60 +/- 0.54 degrees C vs. 34.90 +/- 0.35 degrees C, respectively). In the second hour, heart rate (HR) was significantly higher for CV compared with TP (118 +/- 13 bpm vs. 104 +/- 64 bpm, respectively). Heat storage was significantly higher after the first and second hours for the CV compared with the TP. The physiological strain index (PSI) was higher for CV compared with TP in the second hour. Sweat rate (msw) was significantly higher for CV compared with TP (560 +/- 45 g x h(-1) vs. 409 +/- 84 g x h(-1), respectively). Subjective thermal comfort was not significantly different. TP was more effective than the CV in reducing heat strain under the conditions used in the study. Until a significant breakthrough in reducing heat strain while wearing NBC clothing in field conditions can be found, TP appears to be an effective and recommended cooling method.

A normal water-electrolyte balance is essential for normal function of body systems during physical activity. During recent years, awareness of the importance of drinking amongst athletes and Israeli Defense Force (IDF) soldiers, in particular, has been highlighted. A large number of athletes tend to drink prior to, during and after their exercise in order to enhance physical abilities and to prevent heat casualties and dehydration. However, excessive water consumption combined with sweat induced electrolytes loss during physical activity, may cause hyponatremia in extreme cases. Recently, several cases of exercise induced hyponatremia were reported in the IDF, resulting from improper water consumption. In this article, we describe a clinical case of exercise-induced hyponatremia in a soldier and a review of the literature, including the etiology, clinical characterization and recommended treatment. Moreover, water consumption recommendations with regard to physical activity are presented. The application of such recommendations may prevent future events of exercise-induced hyponatremia.

Various methods exist for rewarming hypothermia casualties. Most of these methods necessitate sophisticated medical equipment or vigorous hemodynamic and electrolytic monitoring. Therefore, only a few methods remain suitable for pre-hospital scenarios. The current work reviews the literature regarding these pre-hospital rewarming methods, focusing on their efficacy and compatibility to the cold pre-hospital environment with its limited resources. By relying on endogenous heat producing mechanisms and by isolating the victim, one can achieve fairly efficient rewarming for mild hypothermia (rectal temperature of 32 degrees C-35 degrees C) casualties. Many consider this as an independent rewarming method (passive or endogeneous rewarming method), advisable for mild hypothermia cases. There are also many active rewarming methods, suitable for pre-hospital treatment. These methods, however, suppress the endogenous heat producing mechanisms, and therefore are not more efficient than passive rewarming for mild hypothermia cases. In moderate or severe hypothermia casualties, hypothermia (rectal temperature below 32 degrees C) however, is characterized by suppressed or deficient endogenous heat producing mechanisms. Passive rewarming is not enough in these cases, necessitating the addition of active, central or peripheral rewarming methods. Studies regarding the use of various active rewarming methods in severe hypothermia casualties revealed low rewarming efficacy for the low heat capacity methods, such as warm air inhalation, and a high rewarming efficacy for the high heat capacity methods, such as forced air methods.