Introduction
Heat wave and heat stress disorders were frequently reported in the country since the 70s and 80s and more frequently in 1990s when global warming started to have an adverse impact on climate and health. The author was born and bred in Pakokku and lived till the schooling finished in 1963; posted as assistant surgeon of the district hospital and the station medical officer of a rural hospital in the district; posted as Epidemiologist and Deputy Director and responsible for disaster and emergency management stationed at central epidemiology Unit of Department of Health. I would like to share my personal experience and training acquired from these positions interlaced with information from local medical journal.
Heat waves and Hot environment was a chapter in the book,” The Public Health Consequences of Disasters,” edited by Eric Noji, National Centre for Environmental Health, Centre for Disease Control and Prevention, 1997. The book was shared in the local training conducted by international disaster training groups. The topic on Heat waves and Hot environment was excerpted from the chapter” Heat waves and Hot environment”
Hot weather is an important determinant of human mortality. In the United States, a major heat wave can cause literally thousands of excess mortalities in a given summer. Yet, for purpose of public health the term “heat wave” is not easily defined. “Hot” is a relative term, and periods of hot weather (heat waves) vary greatly in intensity and duration. Ambient temperature changes rapidly and they have marked diurnal fluctuations. Their effect on human beings is not the same in different geographical areas. Moreover, the microclimates, behaviours and preexisting medical conditions of individual human beings dramatically affect the biological consequences of macroenvironmental heat. Thus, at the present time, a precise definition of hot weather conditions constituting a heat wave of public health importance eludes description. Determining the precise hot weather conditions leading to an adverse impact on public health remains an important area for scientific investigation.
Thermodynamics
Although there may be considerable fluctuation of the temperature of the extremities and outer body surface of human beings, thermal homeostatic mechanisms attempt to maintain a relatively constant inner body or “core” temperature. There are four physical processes involved in thermodynamics (1) heat gain from metabolism (2) heat loss from evaporation (3) heat gain or loss from conduction and convection and (4) gain from radiant heat energy. The body gains metabolic heat from myriad biochemical reactions that are essential to life. The body loses heat, however when perspiration evaporates from the skin or secretion evaporates from the respiratory epithelium. If the temperature of the body surface is different from the temperature from that of substances with which it is in contact then body gain or lose by means by conduction. If the substance with which it is in contact, is a fluid medium, air or water then conduction is hastened by the flow of fluid over body surfaces (conduction). Finally, regardless of ambient temperature if a person in the presence of objects or surfaces hotter than the body, then the body heat is gained from radiation.
Four meteorological variables significantly determine the physical processes affecting thermal homeostasis Those are (1) air temperature (measured by shaded dry -bulb thermometer) (2) humidity (measured by dew point temperature or comparison of dry-bulb and wet-bub temperature), (3) air motion or wind speed and (4) solar radiant heat energy. When dry-bulb temperature is low, metabolically generated heat is more easily lost from the body to the air by conduction/convection. As air temperature increases convective heat loss occur less readily until, at temperature above body temperature convection heat loss no longer possible and heat may be gained from the air. High humidity limits the cooling effect of evaporation of perspiration and secretions, therefore lead to increased heat stress. Increased air speed facilitates convective heat transfer and the evaporation of sweat. Radiant heat energy adds to heat stress, independent of other variables. For example, radiant heat causes one to feel hotter in direct sunlight than in the shade, even under identical air temperature, humidity and air speed.
Health Effects of Heat
The spectrum of illness recognized as heat-related illnesses as the direct result of exposure to prolonged periods of high environmental temperature are heat stroke, heat exhaustion, heat syncope, and heat cramps. Heat wave can increase the morbidity and mortality of other diseases that occur even in the absence of heat wave e.g myocardial infarction. Heat stroke occurs when perspiration and vasomotor, haemodynamic and adaptive behavior responses in a heat stress are insufficient to prevent in substantial rise in core temperature. Some authors distinguish between “classical” and “exertional” heat stroke. Classical heat stroke is said to occur largely in sedentary elderly people who are exposed to prolonged (days to weeks) period of heat stress. Exertional heat stroke affects younger, relatively fit person by exertion in a hot environment (as in a summer road race) beyond their capacity to maintain thermal equilibrium. Anhidrosis (absent or diminished perspiration) is reportedly more common in the presentation of classical heat stroke. Classical and exertional heat stroke are not distinct clinical entities. Rather they represent two ends of a spectrum of circumstances under which heat stroke occurs. Anyone, young or old, can develop heat stroke if subjected to sufficiently prolonged and intense heat stress. Exercise increases production of the metabolic heat, predisposing persons of all ages to the development of heat stroke.
Although standardized diagnostic criteria do not exist, heat stroke is usually designated when the rectal temperature rises to ≥105° F (40.6 °C) as a result of high environmental temperature. Mental status is affected and patient may be delirious, stuporous or comatose. Anhidrosis may or may not be present. It is a medical emergency. Rapid cooling is usually by means of ice massage, ice water bath or special facilities for evaporative cooling is essential to prevent permanent neurological damage or death. Further treatment is supportive and admission to intensive care unit is often required. Outcome is often fatal even in expert hands. The death to case ratio in reported case series generally varies from 0 % to 40 %, averaging about 15%.
Heat exhaustion is a much less severe condition, presenting with dizziness, weakness and fatigue. Body temperature is normal or slightly to moderately elevated. The cause of heat exhaustion is caused by fluid and electrolyte imbalance due to increased perspiration in response to intense heat. Therefore, the treatment is directed towards normalization of fluid and electrolytes status and the prognosis is generally good.
Heat syncope refers to sudden loss of consciousness in persons unacclimatized to weather. Consciousness returns with assumption of recumbent position. The cause is thought to be circulatory instabilities due to superficial vasodilatation in response to the heat and the disorder is benign.
Heat cramps occur as a result of fluid and electrolyte imbalance following strenuous exercise done in the heat. Cramps tend to occur in muscles that have been most. They are common in athletes who must perform in the heat or in workers who work in “active” industries. Such person may be highly acclimatized to weather and therefore able to lose a great quantity of fluids and electrolytes in their perspiration. Disproportionate repletion of fluids and electrolytes leads to imbalances.
Public Health Impacts
Heat wave-associated mortality
In the United States, approximately 270 deaths are recorded on death certificates as having caused by heat in years during which no major heat wave had occured. A few such deaths occur during winter and cooler month of the year indicating that not all are caused by meteorologic conditions. However, the great majority occurs during summer. In years in which prolonged periods of abnormally high temperature (heat waves) affected large areas of the country, the number of deaths attributed to heat wave rose greatly. In 1980, when summer temperatures reached all-time high levels in much of the central and southern United States, some 1,700 deaths were diagnosed as heat-related, over six times the number expected if there had been no heat wave.
Such figures however, do not reflect the full extent of the problem. In July 1980, 5000 deaths over the number expected occurred in the United States, far more than 1,700 documented having been caused by the heat. Excess mortality and excess death during a heat wave refer to the difference between the number of deaths observed and the number expected based on crude death rate in the same geographic areas during some appropriate control period during which neither heat wave or any epidemic was present.
Causes of Death
Of the syndromes whose sole cause is environmental heat, heatstroke is the only one with substantial death-to-case ratio. Thus, one might suppose that the great majority diagnosed as caused by heat represent majority due to heat stroke. Henschel and others reviewed the hospital charts of 120 persons whose deaths had been certified as heat-related during the 1966 heat wave in St.Louis. They found that virtually all had a temperature of 103° F (39.4 C), upon hospital admission, a fact that they interpret as showing that most of these deaths are due to heat stroke.
During the heat wave in Detroit in May 1962 and June-July 1963 in Birmingham no death had been classified as having been caused by the heat despite substantial excess mortality of 17 to 32 %.
Mortality associated with a heat wave is often so great that it appears as a sudden and substantial increase in the total number of deaths occurring in a given area. Increase of over 50% in crude mortality rate are not uncommon. Moreover, despite the use of air-conditioning there has been no clear and substantial decrease in death toll taken by heat wave in recent years.
Schuman and others found stroke (brain infarction and haemorrhage) to be an important cause of heat wave associated deaths; they found that deaths due to cerebrovascular accident rose 82 % and accounted for 52 % of excess mortality caused by heat wave in Detroit and Michigan in 1963. During another heat wave in previous year they observed 104 % rise in mortality from stroke (26% of all heat wave associated deaths). When Schuman studied the July 1966 in New York City he found far less dramatic increase of 27 %, accounting or a little over 6% of an estimated 1,181 excess deaths caused by the heat. He felt however that coding system in New York was different from other city and tended to be underestimate the problem. The variability in the magnitude of heat-waved related increases in stroke mortality related to other cause suggests some deaths attributed to stroke are misclassified. However, there are evidence of increased coagulability of blood in heat-stressed person and such increase coagulability may be biological basis for thrombotic and embolic stroke in hot weather. The relative consistency of excess stroke mortality during heat waves in different locations argues that the association is a real one.
The frequency of deaths attributed to heart diseases also increases during heat waves mainly due to increase in deaths attributed to ischaemic heart disease. The cause-specific death rate has increased in different heat waves by amount ranging from 7 % to 55% accounting for 10-40% of heat wave associated deaths.
A recent investigation of heat-wave associated mortality during the July 1993 heat wave in Philadelphia showed that cardiovascular deaths increased more than 100% over the baseline.Interestingly the investigators found no increase in cerebrovascular(stroke) deaths. This investigation underlines the importance of heat as an exacerbating factor for persons with preexisting heart diseases and reinforce the point that heat stroke is not always the principal cause of excess deaths during a heat wave.
The evidence mentioned above regarding increased coagulability of blood in heat stressed person lends plausibility to the idea that hot weather causes an increase in death from ischaemic heart disease, since thrombosis or embolism may exacerbate cardiac ischaemia. Moreover, increase in cardiac deaths occur consistently during heat waves. Thus, the link between heat and death from ischaemic heart disease is strong.
The recognition of heat stroke in a living patient who have characteristics neurologic finding and very high temperature present few difficulties in average clinicians, especially anhidrosis (greatly diminished sweating is present. However, heat stroke progress rapidly to deaths often in a few hours of the onset of symptoms. In 90 fatal cases the duration of illness was less than 24 hours in 70 % of cases. Thus, many persons who developed heat stroke die before they can be found and brought in for medical attention.
Post-mortem temperature measurements can be useful in the diagnosis of heatstroke. A post-mortem temperature of ≥106° F measured soon after death is a useful indicator of heat stroke because core temperature of the body changes relatively little during the first one to three hours after death especially if the ambient temperature is not particularly low.
Stroke or other types of cardiovascular mortality taken together accounted for as much as 90 % of excess mortality during a heat wave. Clearly defined period of excess deaths due to respiratory causes corresponding to July 1966 heat wave in the United States was apparent from national mortality statistics. Currently there is no pathophysiologic explanation for how an increase in respiratory deaths could occur from a heat wave.
Heat wave-associated morbidity
During heat wave in St. Louis and Kansas hospitals admitted 229 and 276 patients, respectively with non-fatal illness thought by attending physician due to the heat. Loss of consciousness was the most frequent complaint, affecting almost half of the common symptoms seen as city hospital in Memphis. Dizziness, nausea and vomiting and cramps are other common symptoms. The proportion of illness diagnosed for 417 patients for whom the diagnosis was known were as follows: heat stroke 47%; heat exhaustion 58%; heat syncope, 4%; heat cramps, 6% and other heat-related 15%. In July 1980 in St. Louis and Kansas emergency room visit rose 14% and 8% respectively.
Factors influencing morbidity and mortality and determinants of risk
Variation in heat-related health effects over time
The public health impact of heat at any given time depends not only on the weather conditions at the time but also on previously existing conditions. That this is true can be seen from the fact that that there is a delay between the onset of heat wave and the appearance of substantial adverse effects on public health. Unusually high temperature on several days in succession required to produce noticeable increase in mortality and heat wave lasting less than a week result in relatively few deaths. The importance of sustained heat is also illustrated by the observation that heat waves in which relatively little night time cooling occurs (i.e those in which daily minimum temperatures are elevated) are particularly lethal. Over a period time, however, hot weather seems to lose some of its virulence. Acclimatization of individuals to heat stress is a phenomenon that has been well-documented by means of physiologic experimentation. Populations seem to acclimatize to the heat over the course of the summer. During a sustained heat wave, after initial dramatic increase, the number of deaths tend to return toward the base line, even though the temperature may remain elevated. This fall in crude mortality may result not only from acclimatization but also from earlier deaths of susceptible persons, decreasing in number from the population at risk.
Urbanization and risk
Heat waves cause disproportionately severe health impact in cites, to a large extent sparing more rural and suburban areas. In July 1980 death in in St. Louis and Kansas were 57% and 55% higher respectively than in July 1979. In contrast, there is excess mortality of only 10% in the remainder of Missouri which is largely suburban and rural. In a review of deaths caused by heat and registered in United States from 1900 to 1928, Shattuck and Hillary noted that the rate of heat related deaths were substantially higher in urban than rural areas. In the later work the same investigator found that the effect of heat on death rates increased with the increase in the size of the city suggesting the dose-response effect of urbanization. The concept of urban “heat islands” has also been invoked to explain the disproportionate severity of health impact of heat in cities. The mass of stones, brick, concrete, asphalt and cement that are typical of urban architecture absorb radiant energy from the sun during the day and radiate that heat during the nights that would otherwise be cooler. In many there are few trees to provide shade. Tall city buildings may effectively decrease wind velocity thereby decreasing the contribution of moving air to evaporative and convective cooling. The relative poverty of some urban areas is another factor that may contributed to the severity of heat-related effects. Poor people are less able to afford cooling devices and the energy needed to run them.
High risk groups
Overall mortality increases observed during heat waves disproportionate by affect elderly people. During heat waves in July 1983, deaths in Rome increased 23 % overall but increased 35% among persons more than 64 years of age. The increase in mortality in Greater London resulting in heat wave in 1975 occurred almost exclusively among 65 years of age or older. Deaths specifically designated by physicians having been caused by the heat occur with disproportionately higher frequency among elderly. The trend is easily seen in the graph of age-specific mortality in the United States in the period 1979-91. Infancy and early childhood are relative sensitivity of heat. The rate of heat-related mortality is the lowest in late childhood. Then it increased monotonically throughout the teen age and adult years with the slope of the curve increasing rapidly as old age is approached.
The predisposition of the elderly to health effects of the heat may partially reflect impaired physiologic responses to heat stress. Vasodilatation in response to the heat requires increased cardiac output and decrease systemic vascular resistance during hot weather. Moreover, the body temperature at which sweating begins increases with increasing age. The elderly is more likely than younger persons to have chronic diseases or to be taking medicines (e.g. major tranquillizer and anticholinergic) that can increase the risk of heat stroke. Finally, old people perceive differences in temperature less well than do younger persons. They may therefore, less effectively regulate their thermal environment
At the other extreme of age, the rate of physician-diagnosed heat-related deaths is higher for babies and young children. However, the magnitude of this increased risk is nowhere near as great as it is for elderly persons. There was no detectable mortality for the age group 0-4 years in Greater London during the June-July 1975 heat wave Only one of the 83 persons who died of heat-related cases in Memphis in July 1980 was less than 20 years of age (a baby in the first year of life). No cases of fatal or non-fatal heatstroke was found to have occurred among persons aged 0-18 years in St. Louis or Kansas City during July 1980 heat wave, despite careful case finding efforts in peadiatric hospitals and medical examiners’ offices. Nevertheless, Henschel and others found that four of 182 person who dies of heat-related illness during the July 1966 heat wave in St.Louis were babies less than 1 year of age. The small but definitely increased risk of death for babies and young children is most clearly seen in summaries of state and national data compiled over a number of years than in studies of specific heat waves in individuals.
Other observations document the sensitivity to heat of the very young. Healthy babies kept in hot areas have been found to run temperature as high as 103° F and mild fever causing illness of babies may be tipped over frank heatstroke by heat stress. Children with central nervous system abnormalities with diarrhoeal illness appear to be particularly vulnerable. Parents may contribute to the risk by failing to give enough hypotonic fluid during heatwave and by dressing the child too warmly.
US national figures show that in the teenage years and during early and middle adult life males have an increased an increased risk of heat-related compared with females.This difference may reflect tendency toward greater heat exposure and exertional heat exposure among males from occupational and leisure activities but definitive epidemiologic data on this point are lacking. At extremes of age there is less difference between the sexes in rates of heat-related deaths. heat-related health effects are disproportionately severe in areas of low socioeconomic status. In areas of low median family income there was substantial crowding high number of persons/rooms. Relatively low incidence of heat-related health effects in well to do areas may include availability of air-conditioning, abundance of trees and shrub that provide shading and access to health care.
Obesity is the important factor affecting heat tolerance. Obese subjects exercising in hot environment showed a greater increase in rectal temperature and heart rate than do lean subjects. This insulating effect of subcutaneous fat impedes the transfer of metabolic heat from core to the surface. Soldiers in US army who have died of heat stroke in basic training during World War II are much more than their peers. However, obesity may not importantly influence the rate of heatstroke for the largely sedentary elderly population that is at the greatest risk during a heat wave.Persons with less common conditions may also tolerate heat poorly. These conditions include congenital absence of sweat glands and scleroderma with diffuse cutaneous involvement. In both conditions perspiration is markedly diminished, resulting in impaired thermoregulation in a hot environment.
Some drugs predispose to heat stroke. Neuroleptic drugs (e.g. phenothiazines, butyrophenones and thiozenthenes) have been particularly strongly implicated. In laboratory tests of human volunteers, anticholinergic decrease heat tolerance. Persons treated with anticholinergic while exposed to heat have been reported to have a decrease or cessation of sweating and a rise in temperature. Many commonly used prescription drugs ( e.g tricyclic anti-depressant, some antiparkinsonian agents and non- prescription drugs, antihistamines, sleeping pills have prominent anticholinergic effect and in one study the use of such drugs was more common among cases than controls. The likely mechanism of action appears to be inhibition of the ability to perspire. Certain stimulants and antidepressant drugs taken in combination or in overdose situations may induce the syndrome of heat stroke.
Whether a heatstroke damages the brain’s thermoregulatory apparatus or thermoregulatory abnormalities antedate the first heat stroke is not known. However, persons with a history of heat stroke should be considered at risk of a recurrence.Persons with other less common conditions may also tolerate the heat poorly. These conditions include congenital absence of sweat glands and scleroderma with diffuse cutaneous involvement. In both conditions perspiration is markedly diminished resulting in impaired thermoregulation in a hot environment.
Variation among physicians regarding the determination of heat relatedness continues to complete studies of heat-related health effects. In an effort to limit part of the investigation to a study of clean-cut illness caused by heat, researchers investigating the effects of the 1980 heat wave in St. Louis and Kansas City in Missouri defined the following people having heat stroke:
Patients with a presenting temperature (measured anywhere on the body) greater than or equal to 41.1 C : patients with documented temperature greater than or equal to 40.6 C (105 F) if altered mental status or anhidrosis was also present ; and those pronounced dead on arrival at hospital or medical examiner’s office if the body temperature was greater than or equal to 41.1 C(106 F )
Strict definitions could also be developed for the study of other outcomes whose direct cause is the heat (i.e heat exhaustion, heat syncope, heat cramps) Such definitions do not necessarily help the clinician attempting to diagnose the case of an individual patient. Their usefulness lies in their value as entry criteria for epidemiologic studies of groups of patients, enabling the investigator to explain precisely which clinical entities have been studied when heat-related illness is the subject of study. In this manner future investigators will be better able to clarify and quantify the health consequences of heat.
Prevention of Adverse Health effects Caused by Heat
Timing of Preventive Measures
In most parts of the United States heat wave severe enough to threaten health do not occur every year, and several relatively mild summers may intervene between major heat waves. The erratic occurrence of heat waves hindered the effective planning of preventive efforts. It may be administratively difficult for health department to plan for adequate resources that will be available if needed but that will not be wasted if no heat wave occurs.
Although long-term weather forecasts (those done some months in advance of events) cannot reliably predict the periods of severe heat, near-terms of forecast of several days in advance are becoming increasingly accurate. Could one also forecast the extent of morbidity and mortality expected to result from anticipated hot weather? Even the extent of 1 or 2 days of advanced warning regarding the probable extent of heat-related adverse effects would be of use in planning for the prevention.
Apparent temperature also known as heat index one of the indies of human heat stress discussed above has been proposed as a guide to classifying how hazardous to health the anticipated weather may be. However, this index was not developed for this specific use. The hazard posed by heat stress depends not only its magnitude at a given moment but also on how it has varied over time. Moreover, the index in no way takes into action the variation in heat sensitivity of different region. Thus, apparent temperature by itself independent of geographical location and antecedent weather conditions, will probably not to be found to be a useful predictor of the extent of heat related health effects to be expected in a population at risk.
Several authors have attempted to develop mathematical models to be quantified the increase in number of deaths to be expected for a given degree of temperature increase These formulae have taken into account such factors as the usual seasonal trends in mortality, acclimatization, and age structure and previous hot weather exposure of the population at risk. Currently available mathematical models have been fitted retrospectively to past mortality and meteorological data. These are reasonably in accord with the observations from which they are developed. However, none of these models has yet demonstrated its usefulness in the prospective prediction of heat-related adverse effects. This is an important area for further research.
In the absence of reliable prediction early detection of important adverse health consequences of heat could provide public health professional with useful information, allowing them to mobilize resources for prevention relatively early in an epidemic of heat-related illness. A large increase in caseloads of medical examiner that is unexplained by any other disaster that have been proposed as an early indicator of severe heat-related health effect in the community.There are as yet no firm criteria regarding just how much of the increase in case load should trigger implementation of prevention program.
Content of Prevention Programmes
Programmes to prevent heat-related illness should concentrate on measures whose efficiency is supported by empirical data. Many heat-illness preventions efforts have centred around distribution of electric fans to persons at risk. However, study of 1980 heat wave in Missouri did not show a protective effect of fans. This finding is consistent with theoretical predictions and empirical data showing that air temperature rises toward about 99° F the exact value depends on humidity and other factors increased air movement ceases to lessen heat stress. At even higher temperature increased movement of air may actually exacerbate heat stress. Although further epidemiologic studies are required to evaluate the preventive efficacy of fans, fan probably should not be used in situations in which established indices of heat stress suggest they might be harmful.
Air-conditioning effectively prevents heat stroke and may decrease the incidence of other adverse health effects of heat waves. In one study the presence of 24-hour air-conditioning in the home reduce heat stroke risk by 98%. In addition, just spending more time in air-conditioned places regardless of whether there was a home air conditioning) was associated with a 4-fold reduction in heat stroke. These findings suggest that air-conditioned shelters are an effective means of preventing heatstroke. Persons at high risk who do not have home air conditioning may benefit from spending a few hours each day in an air-conditioned environment.
The maintenance of adequate hydration is important in preventing heat-related illness. Increase in body temperature of heat-stressed volunteers were lessened when fluid losses were replaced. Moreover, taking extra liquids has been associated with decreased risk of heatstroke. More fluids than the amount dictated by thirst may be required to fully offset the increased fluid losses that occur during hot weather. Thus, unless there is a medical contraindication, person at risk from the heat should be advised to make a special effort to increase the amount of liquid they consume.
“Adequate intake of salt with meals is important. Although salt supplementation with tablets may be important in preventing electrolytes imbalances for carefully selected individuals who must tolerate intense heat for prolonged periods, it is of doubtful benefit in preventing heat-related illness in the general population. Furthermore, such supplementation may be harmful for persons with chronic illnesses in which a sodium intake is undesirable (persons with hypertension, congestive heart failure). Therefore, salt tablet should not be recommended for consumption by general population during a heat wave.
Persons at high risk should be advised to reduce activity in the heat, since such behavior appears to have protected against heatstroke in one study. Conversely athletic exertion in the heat substantially increase risk, although risk does not increase as much for persons who have become acclimatized by training in a hot environment
Target Groups
To be maximally effective programmes for the prevention of heat related illness should be directed toward groups known to be at particularly high risk. Cities – especially low socioeconomic status inner cities areas are particularly appropriate for prevention efforts. The elderly should receive special attention, since old age is one of the factors most strongly associated the increased risk of heatstroke or death from other causes during a heat wave. As much as possible special living facilities and special institutions such as nursing homes and hospitals in which many elderly persons are to be found should be air-conditioned during severely hot weather. The elderly living at home should not be forgotten, however, since they may be at even greater risk than those in institution. Parents should be made aware of the increased heat sensitivity of babies and children less than 5 years of age. Patients taking neuroleptic or anticholinergic drugs should be counseled regarding their possible increased sensitivity to heat.
Experience encountered in two major hospitals in both upper and lower Myanmar was gathered during the heat waves in the year 2010.
Heat stroke in Medical Unit II of Mandalay General Hospital
During the summer of 2010 Medical Unit II of Mandalay General hospital reported heat stroke cases of a total of 224 while the ambient temperature around Mandalay reaching 45° C following weeks of Water Festival, in April up to the end of May, breaking the record of the high temperature ever recorded and heat-related impact extending to second and third week of May when monsoon may set in. The peak in ward admission on 15th May was 112 and 16th May being 71 patients. Male constituted 65 % and age range was 40 to 80 years. Commonest age group of 50-59 years. The youngest was 13-year student and oldest 94 year both recovered completely. Risk groups identified were those who have occupational heat exposure like farmers working in the fields, drivers, trishaw-peddlers, cooks, blacksmith etc. Unrelated occupations were civil service person, teachers, students and shops keepers and can be classifiable either classical or exertional heat stroke. Associated morbidities were hypertension found in 27 %, in chronic alcoholism 25% and diabetes in 11% of total patients. COPD, CVD and psychiatric disorders were seen in a minority. All the cases met the case definition of heat stroke, high body temperature with or without central nervous system dysfunction. Axillary temperature was recorded mostly 102-over 104 F reaching the highest of 108 F. Some patients could not be taken body temperature as cooling was done before admission by volunteers or NGO.
Central nervous system dysfunction ranged from irritability, confusion, delirium, convulsions to deep coma. Those CNS symptoms are the criteria for diagnosis of heat stroke. Most patients had history of heat exhaustion prior to the heat stroke, which may present as malaise, weakness, headache and dizziness. Those cases of heat exhaustion progressed to heat stroke without receiving proper management.
Being a specialist teaching hospital, laboratory investigation could be carried out whichever necessary. Full blood count, urea and electrolytes and liver function tests can be done. Clotting screening was done to detect coagulopathy. Blood glucose and ECG and chest X ay was taken to exclude comorbidity and other complications. Brain imaging (CT or MR) was done for any neurological complications.
Severe hypotension and shock with tachycardia were detected in 14 %, which is the feature of heat exhaustion.
The most common abnormal finding in electrolytes was hyponatremias and hypokalaemia. Hyponatraemia (serum Na < 135 mmol /L) was found in 57% of patients checked. Hypokalemia (serum potassium < 3.5 mmol/L) was found in 62% of cases. These abnormalities might be attributed to sweat loss and ingestion of large amount of hypotonic solution (i.e. water) during heat exhaustion stage. Renal function assessment indicated slightly increased serum urea and creatinine but classical features of acute renal failure with oliguria and uraemia were not found in any of the patients. Thrombocytopaenia (platelet count <100x 103 / mm3) was seen in 56 % of patients with lowest platelet of 4 x 103 / mm3. Coagulation screening (OSPT, INR, APT, FTP) in severely ill patients platelet count <50x 103 / mm3 was abnormal. Disseminated Intravacular Coagulation was not detected in any of the patients. Regarding cardiovascular complications pulmonary oedema was seen in five patients. Full blown cerebellar syndrome with nystagmus, dysarthria, intention tremors, ataxia gait was detected during recovery in four stroke patients. Most of the patients regained consciousness after 6-12 hours of management. Mortality was 8.5 %.
Another episode of heat wave recorded in a private clinic had the patients checked for electrolyte status among 22 patients and the majority were 76 years old on the average and most of them has underlying hypertension or diabetes mellitus. Hyponatremia of sodium < 135 mmol /L was found in 19 out of 22 patients and hypokalaemia in 13 patients. Outbreaks of heatstroke and its sequelae have been described and prevalence of hyponatraemia has not been described. Author hypothesized that development of hyponatraemia was most probably due to be excessive ingestion of electrolyte free water. In our observation, heat-related illnesses occur in two phases. On daily exposure to intense heat the body responds by excessive sweating. Replacement of Na-containing sweat by drinking water alone results in hyponatraemia. Hyponatraemia is characterized by lassitude, malaise, lethargy, loss of appetite, confusion, dizziness and headache. In elderly patients the appetite loss is so marked that they refuse to take fluids. Most of them lie in stuporous state.
It is the first phase. Because of failure to take fluid and ongoing sweating there is dehydration and oliguria. Because of dehydration, a point is reached where the body cannot defend against the environmental heat by sweating. External heat enters the body by direct convection and body temperature rises to dangerous levels rapidly. At that time hyponatraemia is also marked. Patient develop delirium, confusion, seizures and coma. Circulatory collapse is common. It is the second stage we call “heatstroke”.
Heatstroke occurs in previously healthy younger patients on exposure to heat. Hyponatraemia also occur in this group similar to marathon runners. It is possible that cerebral involvement in heatstroke may be due to hyponatraemic encephalopathy. It is very similar to exercise-associated hyponatremia which is a well-established entity.
We noted similar pathogenesis and presentation in heatstroke and believe they represent the same spectrum of a disease.
In addition to lowering body temperature, correction of hyponatraemia-hypochloraemia by infusion of at least 1 litre of normal saline should be emphasized. In our series the mortality is just 10 per cent (2 /22 patients).
Serum electrolytes are examined at the outpatient department who suffered from heat-related patients. Most are elderly and diabetics or hypertensive patients. Symptoms of metal impairment disappeared after fluid replacement. (ORS or intravenous fluids). None of them progressed to the illness of heatstroke.
High prevalence of hyponatremia was observed among cases tested and electrolyte imbalances are appropriately corrected and further progress to heat stroke is prevented. Electrolyte imbalances are due to combination of water and salt loss from heat exposure and inappropriate replacement by drinking of hypotonic solutions.
Heatstroke experience from ward 1, and 2 of Yangon General Hospital
In Yangon ambient temperature reached 108 °F in the periods of 75 years on 27th May 2010. Following Nargis storm the trees fell down and less shade and less cloud cover at that time aggravated the heat of the environment and people are exposed to intense heat and suffered negative impacts on human health. From early May to the middle of June 2010, a total of 35 patients suffered from heat related stress or disorders, the proportion of heat exhaustion 5 cases and heat stroke 30 cases. The central epidemiology unit (CEU) collected the country data on heat stress disorders and there were 1482 cases and 260 deaths and the case to death ratio was %. The highest was from Magway region (39%), Yangon 32.3% and Mandalay 18%). Heat stroke is defined clinically as core temperature that rises above 40 C (106°F) and is accompanied by hot, dry skin and central nervous system abnormalities such as delirium, convulsion and coma. Among 30 heatstroke cases author classifies 18 cases as pure heat strokes and remaining with comorbidity. Pure type cases were healthy persons previous to the heat stress and high body temperature was due to exposure to environmental heat. Some cases were alcoholics, some elderly. They were mostly trishaw peddlers, taxi drivers, and street vendors, too much exposed. So called secondary cases are those with minor illnesses which usually lead to low-grade fever, but which after exposure to environmental heat resulted in hyperpyrexia. Common comorbidities are diabetes with skin infections, CVA and meningitis, chest infections and malaria which predisposed to secondary heat stroke.
Presentations
History of exposures and clinical presentations related to patient’s occupation or work are recorded. Exposure period was two or more hours to the ambient temperature ranging from 106° to 109° F. By occupation one was a seller of crispy snacks fried in oil over the fire for hours. One patient was a water distributor or donor carrying water buckets on a yoke, exposing himself to the direct sun light. One patient was a policeman or guard on duty on a bridge and he was sober and slept on the platform for 5-6 hours. One patient had pneumonia coming from Ma-U-bin transported in Van car and since there was no air-conditioning in the car the body temperature rose to 106F at the arrival.
Some patients had loose motion and hyponatraemia on investigation and some showed features of Disseminated Intravascular Coagulation (DIC). No other abnormalities of rhabdomyolysis, hyperphosphatemia, or hypocalcemia were not encountered. Post mortem findings of East Yangon Hospital reveal diffuse punctate cerebellar hemorrhages typical of textbook descriptions.
Personal experiences
My first training on the management of heat stress disorder was the training at Tropical Medicine Unit of Rangoon General Hospital in the month of rain season of the year, probably in 1980. Topics and points that I still remember were generic terms “heat stress disorders” comprising the terms hyperpyrexia, heat exhaustion, heat stroke, heat syncope and heat cramps. Heat miliaria are the skin manifestations. The intravenous fluids to be replaced are half-strength normal saline and one precaution is not to infuse dextrose saline or dextrose solution as those may cause hemoconcentration in the face of dehydration from water and electrolytes loss. The then biochemist of RGH recommended the infusion of half-strength normal saline.
Professor Ko Ko Hla reported the heat stress disorder cases admitted to Monywa Regional hospital. The event was reported in BMJ issued around that time and professor mentioned clinical aspects as well as general or preventive management. He mentioned the daily ambient temperature around that heat wave period. What I remembered was presenting symptoms covering multi-systems which included the renal system involvement of polyuria, polydipsia and oliguria. At this point, I would like to mention the locally prevalent symptoms of thirst and passing large volume of urine especially among children. Myanmar description of ရေငတ်ကျင်မျော” was made by native folks of Pakokku and practising doctors recognized. For rapid cooling the ice block shop was opened in the premises of the hospital. Erecting the shelter of thatch-roof can reduce the temperature of the inner building by 1- or 2-degree C. The incident was a real and serious medical emergency and red cross and other volunteers gave support. During the heat wave of that time at the onset, extremes of ages were affected and subsequently all age groups.
I was born and bred in Pakokku area and so was exposed to heat since my childhood. I remember the habits and practices from my childhood. The summer or hot season was very hot and long. Old persons could die in the summer because of age and long-standing illness. My house was two-story brickhouse and in the evening the temperature inside the building was so hot and stuffy and everything we touched were so hot that we needed to sleep in the beds placed on the verandah and come inside only past midnight. During hot seasons, we needed to take a bath at certain fixed times of the day. Natives were afraid of using fans and avoided them as there were many instances of heat stroke following the use of fans while sleeping. People avoided having baths at very hot times of the day. Folks were prohibited taking bath on the Irrawaddy banks. The water had dried up on the side of the bank where people lived and the needed to go for a bath to the thin narrow strip of water crossing the sandy white shore of quite a long distance and after having a bath of cold Irrawaddy water which may be the melted snow of Himalayan Mountain at its origin. The cold body absorbed heat by convection from the hot sandy shore and the radiant heat from the sun in the open unshaded space. From that experience the people were warned or prohibited of taking bath in the river. At that time district health director was honorary weather man or meteorologist and temperature and other measurement were made at the premises of the hospital. Anecdote said that vital registration staff quit as he was alarmed at daily death tolls from heat strokes or may be other strokes as the local folks could not differentiate.
Case study
I was posted as Assistant Surgeon at the District Hospital, Pakokku. It was a very hot afternoon in the hottest month of May (most probably in 1977) and I saw mirages-like waves in the open space in the distance, though I never know the ambient temperature while I was on emergency duty, a young girl around 14 or 15 years of age was brought in totally unconscious and gasping. Axillary temperature was 108-degree Fahrenheit and at that time ambient temperature was 110 F. The patient was accompanied by Pakokku a native doctor. And I asked what happened and took the history of illness. The General Practitioner said, “I have given her the progstigmine injection because she complained of amenorrhoea.” And “as antidote I gave atropine injection. “What is the dosage? “I give a small dose of atropine as much the size of match stick head.” He said, “Atropine powder was dissolved in distilled water and boiled and cooled “(used to be called hypodermic tablet,)
The General Practitioner was asked to stay and myself and senior nurse started emergency treatment. She was placed in an air-conditioned room. Ceiling fan may not be adequate and we put four side fans around her. The whole body was covered by ice-soaked bed sheet. Ice compress was applied over the temple, axilla and groin on big vessels. The temperature was so high that iced cloth needs to be replaced so frequently. Ice enema was given. Normal saline was only electrolyte solution available and infused. Hydrocortisone was given as last resort medicine. Only after four hours’ effort to lower down the high temperature that it went down to 100-degree F. Temperature was brought down to 100° F after cooling of about an hour. She was saved from hyperpyrexia and heat stroke. After a week she developed ataxia and fortunately recovered after two weeks.
To sum up, the heat stroke was provoked by the inappropriate treatment of the general practitioner, iatrogenic, giving anticholinergic drug, atropine, by hypodermic tablet and the patient was admitted to district hospital with hyperpyrexia and loss of consciousness, typical of heat stroke. She was treated by rapid cooling, intravenous infusion of electrolytes and hydrocortisone. The temperature was cooled down from 108° F to 100° F within two hours. After a week she developed cerebellar ataxia which recovered in the following two weeks. Recent literature review mentioned the extreme heat exposure of heat stroke can cause brain damage, especially Purkinje cells.
The rapid cooling was made by isolating the patient in the air-conditioned room and fanning made by ceiling fans and two side fans. The whole body was covered by the ice blanket or the bedsheet and ice packs on the areas on big vessels of neck, axilla and groin. Ice enema was given. The procedure of rapid cooling was learnt from a case of hyperpyrexia resulting from pontine haemorrhage after car accident, in the surgical ward of NOGH in 1971.
Cases of hyperpyrexia following military exercise was admitted to district hospital from local regiment and can be labelled as exertional heat stroke or hyperpyrexia without neurological symptoms and temperature remained elevated and needed to be referred. So the outcome is not known. Similar cases were seen among civilian and temperature was elevated and other possible causes are investigated like typhoid or tuberculosis and other illnesses. Or trial antibiotics and some steroids were given and did not respond. Other causes of fever cannot be detected with limited facilities in district hospital at that time. Those cases should be thoroughly investigated and outcome be followed up with the definite history of exposure to heat.
Conclusion
Reminiscence and review of heat stress disorders in the country was made for the heat waves during past decades and up to the present. Standard reference of the book, The Public Health Consequences of Disasters” published by CDC USA was referred which describes the heat waves in the past decades in States, and Europe. Recent observations in hospitalized patients in Yangon and Mandalay hospitals are reviewed and updates on clinical presentations, risk groups or risk factors, laboratory and other investigations’ results which gave more scientific information which served as the background for the media or public education message for prevention of heat strokes especially in dry zones and elsewhere, as no other areas are immune. Standard treatment protocol should be made for rapid cooling and replacement of water and electrolytes. Case definition be made for epidemiological and research studies which should be further carried out, at least core temperature for a heat stroke patient.
Author Information
Ye Hla
Director (Retired),
Department of Medical Research (Central Myanmar)
