78-year-old male.
Surgical medical history of laryngectomy and heart disease.
Pharmacological treatment with non-confirmed fever, acetyl salicylic acid, acenocoumarol, diltiazem and pravastatin.
The previous days had not manifested any type of prodromal symptoms.
He was found at 19 hours in cardiorespiratory arrest in an orchard where he had been working.
The room temperature was 43.5°C. The rectal temperature at 20 hours (forensic medical intervention hour) was 43°C. Lesions in the region were observed and the lower extremities were bullous type.
Autopsy findings were cerebral edema (encephalon weight of 1625 grams), pathological cardiac hypertrophy of proliferative origin, mild atheromatous atheromatous disease, generalized vascular congestion of pulmonary origin and with generalized coronary stenosis.
The histological study of the lesions on the external surface showed findings similar to those of case 1.
The vitreous humor biochemical study showed normal values.
The toxicological chemical study detected only the drug diltiazem at therapeutic concentrations.
1.
In both cases it was concluded that the cause of death was hyperthermia (heat condition) due to exposure to very high environmental temperature.
DISCUSSION:
Heat stroke is a situation in which a person subjected to high environmental temperatures experiences a potentially lethal failure of the body thermoregulation system.
During heat waves mortality can markedly increase, sometimes reaching epidemic proportions, as occurred in France this summer.
The forensic system has the duty to properly diagnose heat stroke deaths when they occur in its research area.
This would help to provide reliable epidemiological data on mortality and thus contribute to the establishment of preventive measures against alarm episodes [6], as experienced in the latter summer in some parts of Europe.
However, official figures so far have not taken into account (at least according to Bizkaia's experience) forensic mortality.
Among people at risk of death due to heatstroke are the elderly (especially those living socially isolated); people with previous diseases such as congestive heart failure, cerebrovascular diseases and alcohol consumption; patients undergoing certain pharmacological treatments
Overexercise and clothing can contribute to the severe effects of heat [8].
The two cases presented in this work presented risk factors: chronic alcoholism with massive steatosis and acute intoxication by ethyl alcohol in one and hypertensive heart disease and possible overexercise in the other.
Heat stroke patients who arrive alive at an emergency department present a characteristic clinical picture with severe hyperthermia, altered level of consciousness and anhidrosis [7].
The exclusion of other causes of hyperthermia is essential to make the diagnosis.
The death of these patients usually does not present diagnostic or certification problems.
The diagnosis of heat stroke in dead people is more difficult, and it is even more complicated when the body is in an advanced stage of putative condition.
Autopsy findings are minimal and nonspecific and difficult to interpret.
When surviving less than 12 hours, the findings are small or absent: petechial hemorrhages can be observed on the surface of the lungs, heart and other serous.
Subsequently, pulmonary oedema and cerebral oedema may occur.
A series has described the existence of severe pulmonary hemorrhage or subendocardial hemorrhage in the left ventricle in several cases.
When survival is longer, hepatic centrolobular necrosis, acute renal tubular necrosis, neuronal degeneration, acute pancreatitis and disseminated intravascular coagulation fibrin thrombi in small blood vessels can be observed.
Other findings described have been epidermal detachment and thermal fixation lesions [5,8-10].
Our cases showed few findings, probably due to their short survival.
In both cases thermal lesions were observed due to maturation and in one of them pulmonary hemorrhage and cerebral edema.
Biochemical analysis in vitreous humor can show parameters of distortion [8], although the results are not very interesting in cadavers with prolonged postmortem period.
In case 1, the increase in chlorides, urea and creatinine is compatible with the biochemical pattern of postmortem lesions defined by several authors.
Similar patterns of biochemical alterations have been observed in hospital patients.
In a clinical series of 78 cases of heat stroke, elevated urea concentration was observed in 86% and hypernatremia in 46% [7].
The initial suspicion of heat stroke should be considered in any person exposed to high temperatures.
The final diagnosis should be based on an overall assessment of all data: a) history of exposure to high environmental temperatures (> 37.8 o C); b) exclusion of other causes of death; c) exclusion of other causes of pathological temperature; d
In subjects who are initially found alive and subsequently diagnosed with death by heat stroke, it is reached when antemortem body temperature (at the time of collapse) is higher than 40.6oC [5].
The lack of knowledge of heat stroke by the forensic physician may contribute to the disperse and misdiagnosed condition.
One of the main data is early rectal temperature measurement.
Unfortunately, this measurement is only rarely taken in people found cadaver, so the diagnosis should be based almost exclusively on circumstantial data.
At a time when clinical medicine, and also increasingly forensic medicine, has become increasingly popular with sophisticated diagnostic instruments of high economic cost, we seem to forget that procedures can be very simple and costly.
The thermometer is one of them, and its use should be mandatory in every situation in which you can suspect a heat stroke in view of the circumstantial data: days of high environmental temperatures, children left behind with a roadmap
