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At least 19 recordsLinked to original sources
PubMed1991

Heat stress disorders. Old problems, new implications.

Occupational health nurses must always be aware of changing job tasks that create new classes of employees at risk for developing heat stress disorders. Examples include chemical handlers or asbestos containment specialists who must wear non-permeable protective clothing. Heat induced occupational illnesses and injuries, and reduced productivity occur in situations in which the total heat load (environment plus metabolic heat) exceeds the capacities of the body to maintain normal body functions without strain. Health screening should include evaluation of an employee's age, sex, body size, level of fitness, chronic diseases, use of medications, drugs and alcohol, and ability to acclimate. Prevention of heat stress disorders is a team effort. The occupational health nurse, plant engineer, safety/industrial hygienist, and the employee all impact on the success of any heat stress disorder prevention program. Without cooperation, the possibility for harm exists.

Body Temperature Regulation↗
PubMed1989

Heat stroke and related heat stress disorders.

Medical disorders related to environmental heat exposure are exceptionally common in persons who perform hard work in hot climates. They are also common in competitive athletes as well as in persons who participate in casual exercise to maintain health. The important issue of salt and water disturbances consequent to heavy sweating in hot climates is discussed in detail as are mechanisms of potassium deficiency and its implications. The major forms of environmental heat illness including heat syncope, heat cramp, heat exhaustion, and heat stroke are presented in detail with relevant clinical examples. A discussion of the differential diagnosis of hyperthermia and rhabdomyolysis follows. Because of the difference in treatment and complications, heat stroke is subdivided into the classic variety that affects the elderly and very young and that form that follows heavy physical work and is always associated with rhabdomyolysis. Because severe heat exhaustion and heat stroke are life-threatening disorders, the chapter includes a detailed discussion of complications and plans for treatment.

Animals↗
PubMed1984

Heat disorders in industry. A reevaluation of diagnostic criteria.

Morbidity rates associated with occupationally induced heat syndromes have been infrequently reported. In part this results from the inconsistency of diagnostic criteria for heat syncopy, exhaustion, and cramps. This problem is augmented by inconstant administration and completion of population survey instruments. With due regard for these shortcomings, we can provide only estimates of heat-induced morbidity, ranging between 0.12 and 1.4 cases per 1,000 man-years. To facilitate diagnosis of occupational heat stress disorders, a series of algorithms is presented for diagnosis of heat-induced syncopy, exhaustion, and cramps. A differentiation between heat-induced and heat-aggravated clinical states is proposed, and a heat disorder questionnaire with instructions for use is presented.

Heat Exhaustion↗
PubMed2004

Heat-related illness.

Heat-related illness represents a continuum of disorders from minor syndromes such as heat cramps, heat syncope, and heat exhaustion to the severely life-threatening disorder known as heat stroke. It represents an important cause of wilderness-related morbidity and mortality.

Acclimatization↗
PubMed1998

Fluid and electrolyte disturbances in heat illness.

Three exercise-related heat illnesses are described in the literature -- heat cramps, heat exhaustion or heat syncope, and heat stroke. Of these, only exercise-induced heat stroke, which occurs infrequently, is definitely a heat illness caused by an increased rate of heat production unmatched by adequate heat loss causing progressive heat retention with the body temperature rising to dangerously high levels (> 41 degrees C). The terms heat cramps and heat exhaustion are misleading as neither is caused by an elevated body temperature; nor is there evidence that either is caused by specific fluid or electrolyte abnormalities. Cramps occur during or after exercise regardless of whether the exercise is performed in the heat or the cold, or in water. Current evidence suggests that a spinal neural mechanism may induce cramping that is unrelated to biochemical changes in either blood or in the affected skeletal muscles. Historically, heat exhaustion has been described as a condition of postural hypotension that develops immediately on termination of exercise especially when performed in the heat by unacclimatised persons. No modern evidence conflicts with this historical interpretation. Nor have more modern studies shown that exercise-related heat exhaustion is necessarily caused by specific fluid or electrolyte abnormalities. Similarly, there is no published evidence that fluid and electrolyte abnormalities are critical determinants of exercise-related heat stroke. This does not negate firm evidence that dehydration has important physiological effects that impair heat loss and exercise performance especially in the heat. Rather, it shows that exercise-induced heat stroke requires powerful initiating factors, in addition to dehydration which occurs commonly during prolonged exercise, whereas heat stroke is an extremely rare event. The purpose of this review is to provide an alternate, more critical review of the conditions that are considered to be exercise-related heat disorders and to evaluate the aetiological role of fluid and electrolyte disturbances. There is a need to better understand these conditions so that their clinical management can be based on modern information rather than on dated ideas, many of which have survived unchallenged for more than 50 years.

Athletic Injuries↗
PubMed2004

[Disorders caused by prolonged exposure to heat].

France has suffered last summer an unprecedented heat wave that led to an exceptional short-term surge of mortality. Cumulative deaths between August 1st to 14th are estimated at 14,800. Epidemiological studies carried out by the Institute de Veille Sanitaire will show the circumstances and risk factors leading to heat-related pathologies. A literature review already shows the principles of prevention, the circumstances of occurrences during similar past heat waves, the risk factors and the principles of treatment. Prolonged exposure to heat can be the initial cause of death, mainly in the elderly. The subject thus dies of an overload of his natural defenses, unable to preserve his thermal homeostasis. This is then a heat shock that reaches the central nervous system. Heat shocks could kill every second patient and leads to severe neurological sequel. During a heat wave, high temperatures can also trigger or worsen other illnesses or be responsible for other so called heat-related syndromes. It is crucially important to identify subjects at risk, situations of risk, and preventive measures, knowing that heat shock leads 25% of patients to develop multi-organ failure, even when appropriately treated.

Age Factors↗
PubMed2000

Differential effects of in vitro and in vivo hyperthermia on the production of interleukin-10.

OBJECTIVE: To determine whether hyperthermia activates an anti-inflammatory response. DESIGN: A prospective study. SETTING: Heatstroke Center, Makkah, and King Faisal Specialist Hospital, Riyadh, Saudi Arabia. PATIENTS: Twenty-five heatstroke patients pre-cooling (rectal temperature 42.4 +/- 0.8 degrees C) (group 1) and 13 normothermic heat-stressed subjects were studied (group 2). Twelve of the 25 heatstroke patients were also studied post-cooling (group 3). Mononuclear cells from six healthy blood donors resting at 24 degrees C were used for in vitro study. INTERVENTIONS: Mononuclear cells were cultured at a concentration of 1 x 10(6)/ml without and with lipopolysaccharide (LPS) added at concentration of 10, 100, and 1000 ng/ml. The cells were incubated for 24 h at 37, 39, 41, and 43 degrees C. ELISA was used to measure IL-10 in the supernatant and plasma from heatstroke and heat-stressed subjects. RESULTS: All patients in group 1, 40% of group 2, and 37% of group 3, showed elevation of IL-10 (1289 +/- 2519, 248 +/- 393, and 172 +/- 226 pg/ml, respectively) compared with normal control levels, (< 100 pg/ml) P < 0.05. IL-10 level on admission did not correlate with degree of hyperthermia. During 24 h incubation at 37 degrees C without LPS, no IL-10 was detected, whereas with 10 ng/ml LPS, monocytes released 658 +/- 291 pg IL-10/10(6) cells. At 39 degrees C and 41 degrees C IL-10 release was decreased to 225 +/- 114, and 245 +/- 90 pg/10(6) cells, respectively; and was completely inhibited at 43 degrees C (67 +/- 10 pg/10(6) cells), P < 0.0001. CONCLUSION: Heat-stress with and without hyperthermia is associated with anti-inflammatory response in vivo. However, it does not seem to be the direct effect of heat on monocytes, suggesting that other environmental or genetic factors may be involved.

Analysis of Variance↗
PubMed2026

Spermidine and melatonin ameliorate heat stress-induced decline in sheep semen quality.

Heat stress impairs reproductive performance in sheep through endocrine disruption and oxidative stress. This study evaluated the protective effects of spermidine (SPD) and melatonin (MT) supplementation on semen quality in Dorper rams during summer. Twenty-four rams were randomly assigned to a control group, an SPD group (5&#x202f;mg/kg, dietary supplementation), or an MT group (60&#x202f;mg, subcutaneous implantation) and treated for 60 days. The temperature-humidity index (THI) was monitored throughout the experimental period. Compared with the control group, MT significantly reduced serum cortisol concentration on day 30 (P&#x202f;<&#x202f;0.05), whereas no significant differences were observed at the other sampling time points. Serum testosterone, spermidine, and melatonin concentrations remained unchanged throughout the study (P&#x202f;>&#x202f;0.05). SPD supplementation significantly increased ejaculate volume on day 35 and sperm motility on day 42 (P&#x202f;<&#x202f;0.05), whereas MT did not significantly affect these parameters. Neither treatment reduced the overall sperm abnormality rate. However, both SPD and MT significantly decreased the proportion of acephalic and decaudated sperm on day 56 (P&#x202f;<&#x202f;0.05). Neither treatment significantly affected pregnancy rate, delivery rate, or the expression of PMFBP1 and SUN5 proteins in semen (P&#x202f;>&#x202f;0.05). Regarding oxidative stress, MT significantly downregulated CAT protein expression (P&#x202f;<&#x202f;0.05), whereas SPD significantly reduced MDA content and SOD1 protein expression (P&#x202f;<&#x202f;0.05); MT showed similar but non-significant trends for these two markers (P&#x202f;>&#x202f;0.05). Collectively, these findings demonstrate that SPD and MT exert distinct protective effects against heat stress, with SPD improving selected semen quality traits and both treatments reducing sperm head-tail separation, although these benefits did not translate into improved reproductive performance.

Animals↗
PubMed1999

Heat-related illnesses.

The majority of clinicians will encounter patients with heat-related illness in one form or the other. Early recognition and management are important to prevent morbidity and mortality. In children and elderly, the clinical signs may be subtle and in such situations a sound knowledge of heat-related illnesses is crucial. Besides diagnosing and treating heat-related illnesses, it is equally important to know how to prevent them as they are easily preventable.

Acclimatization↗
PubMed1998

Treatment of suspected heat illness.

1. Despite advances in the art and science of fluid balance, exertional heat illness -- even life-threatening heat stroke -- remains a threat for some athletes today. 2. Risk factors for heat illness include: being unacclimatized, unfit, or hypohydrated; certain illnesses or drugs; not drinking in long events; and a fast finishing pace. 3. Heat cramps typically occur in conditioned athletes who compete for hours in the sun. They can be prevented by increasing dietary salt and staying hydrated. 4. Early diagnosis of heat exhaustion can be vital. Early warning signs include: flushed face, hyperventilation, headache, dizziness, nausea, tingling arms, piloerection, chilliness, incoordination, and confusion. 5. Pitfalls in the diagnosis of heat illness include: confusion preventing self-diagnosis; the lack of trained spotters; rectal temperature not taken promptly; the problem of "seek not, find not;" and the mimicry of heat illness. 6. Heat stroke is a medical emergency. Mainstays of therapy include: emergency on-site cooling; intravenous fluids; treating hypoglycemia as needed; intravenous diazepam for seizures or severe cramping or shivering; and hospitalizing if response is slow or atypical. 7. The best treatment is prevention. Tips to avoiding heat illness include: rely not on thirst; drink on schedule; favor sports drinks; monitor weight; watch urine; shun caffeine and alcohol; key on meals for fluids and salt; stay cool when you can; and know the early warning signs of heat illness.

Acclimatization↗
PubMed2002

Heat stroke.

Explore the source record for details and available documents.

Acute-Phase Reaction↗
PubMed1998

Lymphocyte subsets and adhesion molecules expression in heatstroke and heat stress.

We examined the specificity of the recently reported alterations in circulating lymphocytes in heatstroke by determining lymphocyte subsets in 14 consecutive heatstroke patients before and after cooling and in 7 heat-stressed controls using single- or two-color immunofluorescence flow cytometry. The relationship with catecholamine levels was also studied. In heatstroke, percentages of T (CD3(+)/CD19(-)), T-helper (CD4(+)/CD8(-)), T-inactive [CD3(+)/human leukocyte antigen-DR-], CD11a+, CD11c+, and CD44(+) lymphocytes were significantly decreased, whereas percentages of T-suppressor-cytotoxic (CD8(+)/CD4(-)), natural killer (NK; CD3(-)/CD16(+) or CD56(+)), CD3(+)/CD16(+) or CD56(+), and CD54(+) lymphocytes were significantly increased, compared with 11 normal controls. The changes in the absolute numbers of lymphocyte subsets were in the same direction and were significant for T-helper, T-suppressor-cytotoxic, NK, CD3(+)/CD16(+) or CD56(+), and CD11c+ lymphocytes. Milder but significant changes in percentages of T-helper, T-suppressor-cytotoxic, CD11c+, and CD44(+) lymphocytes were seen in heat stress. Cooling was associated with partial or complete normalization, further derangement (CD11a+, CD11c+), or overcorrection (NK, T-suppressor-cytotoxic, CD11b+) of abnormal percentages of lymphocyte subsets. Norepinephrine levels were significantly elevated in heatstroke (4.7-fold) and heat stress (3.2-fold), but did not significantly correlate with lymphocyte subsets. We conclude that heatstroke is associated with significant changes in percentages and in absolute numbers of a wide range of circulating lymphocyte subsets that are not related to elevated catecholamine levels or totally normalized by cooling. Similar, albeit milder, changes are seen in heat stress, suggesting that the two syndromes represent a continuum.

Antigens, CD↗
PubMed2006

Heat shock protein 72 overexpression protects against hyperthermia, circulatory shock, and cerebral ischemia during heatstroke.

This study extends our earlier studies in rats by applying our heatstroke model to a new species. Additionally, transgenic mice are used to examine the role of heat shock protein (HSP) 72 in experimental heatstroke. Transgenic mice that were heterozygous for a porcine HSP70i gene ([+]HSP72), transgene-negative littermate controls ([-]HSP72), and normal Institute of Cancer Research strain mice (ICR) under pentobarbital sodium anesthesia were subjected to heat stress (40 degrees C) to induce heatstroke. In [-]HSP72 or ICR, the values for mean arterial pressure, the striatal blood flow, and the striatal PO2 after the onset of heatstroke were significantly lower than those in preheat controls. The core and brain temperatures, the extracellular concentrations of ischemic and injury markers in the striatum, and the striatal neuronal damage scores were significantly greater than those in the preheat controls. In [-]HSP72 or ICR, the body temperatures, cell ischemia content, and injury marker in the striatum were significantly higher, and the mean arterial pressure, striatal blood flow, and striatal PO2 concentration were significantly lower during heatstroke than in [+]HSP72. Accordingly, the latency and the survival times for [+]HSP72 significantly exceeded those of [-]HSP72 or ICR. These results demonstrate that the overexpression of HSP72 in multiple organs improves survival during heatstroke by reducing hyperthermia, circulatory shock, and cerebral ischemia and damage in mice.

Animals↗
PubMed2001

Presence of antibody against the inducible Hsp71 in patients with acute heat-induced illness.

Antibodies against heat shock or stress proteins (Hsps) have been reported in a number of diseases in which they may be involved in the pathogenesis of the disease or may be of use for prognosis. Heat-induced diseases, such as heat cramps, heat exhaustion, or heat stroke, are frequent in hot working or living environments. There are still few investigations on the presence and possible significance of autoantibodies against Hsps in heat-induced illnesses. Using an immunoblotting technique with recombinant human Hsps, we analyzed the presence and titers of antibodies against Hsp60, Hsp71, and Hsp90alpha, and Hsp90beta in a group of 42 young male patients who presented with acute heat-induced illness during training. We also examined the presence of antibody against Hsp71 in a second group of 57 patients with acute heat-induced illness and measured the changes in titers of anti-Hsp71 antibodies in 9 patients hospitalized by emergency physicians. In the first group of young persons exercising in a hot environment, the occurrence of antibodies against Hsp71 and Hsp90alpha was significantly higher among individuals with symptoms of heat-induced illness (P < 0.05) than in the matched group of nonaffected exercising individuals. Moreover titers of antibody against Hsp71 were higher in individuals of the severe and mild heat-induced illness groups, the highest titer being found in the most severe cases. The results from the second group of 57 heat-affected patients exposed to extreme heat were similar. Again, patients with the more severe heat-induced symptoms showed a significantly higher incidence of antibodies to Hsp71 than controls and the titer of anti-Hsp71 was higher in the severely affected group. Finally, in a study of 9 patients, it was observed that the titer of anti-Hsp71 decreased during recovery from severe heat symptoms. These results suggest that measurement of antibodies to Hsps may be useful in assessing how individuals are responding to abnormal stress within their living and working environment and may be used as one biomarker to evaluate their susceptibility to heat-induced diseases.

Adolescent↗
PubMed1996

Experimental approaches to therapy and prophylaxis for heat stress and heatstroke.

New developments in the fields of biochemistry, physiology, sepsis, cancer therapy, and molecular genetics have led to opportunities for the development of new therapies and prophylaxes for heat illnesses and for improving human performance during conditions of environmental stress. These include antilipopolysaccharide agents, anticytokines, potassium channel agents, a diet rich in omega-3 fatty acids, and psychological conditioning. This review summarizes the backgrounds and recent findings in the above fields and provides specific suggestions for potential therapy and prophylaxis for classic and exertional heatstroke and for improving athletic performance.

Animals↗
PubMed2002

Heat wave morbidity and mortality, Milwaukee, Wis, 1999 vs 1995: an improved response?

OBJECTIVES: This study examined whether differences in heat alone, as opposed to public health interventions or other factors, accounted for the reduction in heat-related deaths and paramedic emergency medical service (EMS) runs between 1995 and 1999 during 2 heat waves occurring in Milwaukee, Wis. METHODS: Two previously described prediction models were adapted to compare expected and observed heat-related morbidity and mortality in 1999 based on the city's 1995 experience. RESULTS: Both models showed that heat-related deaths and EMS runs in 1999 were at least 49% lower than levels predicted by the 1995 relation between heat and heat-related deaths or EMS runs. CONCLUSIONS: Reductions in heat-related morbidity and mortality in 1999 were not attributable to differences in heat levels alone. Changes in public health preparedness and response may also have contributed to these reductions.

Age Distribution↗
PubMed1998

Heat-related illness. Plan ahead to protect your patients.

Environmental heat illnesses range from irksome to devastating. People at particular risk are the elderly, the chronically mentally ill, the community-dwelling developmentally delayed, people without social contacts, athletes, and those without access to air-conditioning. Because heat-related deaths are preventable, community-wide response to heat emergencies, together with individual and community education programs, could greatly decrease morbidity and mortality.

Heat Exhaustion↗