In diathermasia he considers that we have so great a strain on the thermotaxic mechanism that there is loss of balance between the heat discharge and heat producing centers, while in phoebism there is primarily an acute cerebral or cerebro-spinal congestion followed by a chronic inflammatory condition of the meninges and due to damage from the actinic or ultra-violet rays of the sun.
While admitting that there may be cases where the effects of certain rays of the sun are responsible for clinical manifestations varying from death of striking suddenness to vague complaints of irritability, headache and defective memory, yet the generally accepted views are that high temperature, high relative humidity and lack of evaporation from the skin, whether from excessive humidity or from lack of circulation of the surrounding air, can and do produce at one time heat stroke and at another heat prostration. Such factors as muscular exertion, disease conditions, alcoholism and dietary indiscretions undoubtedly play a part in the production of and variance in the clinical manifestations brought about by the effects of heat.
Sambon has suggested that there is a possibility that heat stroke or, as it is also designated thermic fever or siriasis, is due to a germ infection, but without advancing any particular evidence in favor of such an hypothesis.
There is undoubtedly, however, much in favor of the views of those who regard heat stroke and heat prostration as due to an auto-intoxication from the accumulation of toxic substances resulting from increased metabolic activity due to excessive heat retention and having a selective action on the nerve cells.
Others think that as the result of more active metabolism there is a retention of carbonic and lactic acid with a demand on the alkali content of the blood resulting in an acidosis. As a matter of fact treatment of heat stroke cases with intravenous or rectal injections of sodium bicarbonate seems to be of marked value.
It would seem advisable to take the ground that heat retention resulting from lack of heat radiation and insufficient skin evaporation causes various manifestations of discomfort or bodily injury. Aron in Manila showed that monkeys exposed to the sun died in about one hour but that a control monkey, similarly placed, but kept in a current of air from an electric fan, suffered little or no injury. The reason that monkey and man react differently to exposure to the sun is on account of the more numerous and more active sweat glands possessed by man which give rise to increased evaporation and resulting loss of heat of the body.
High relative humidity is a potent factor in checking evaporation. The rectal temperature in Haldane’s experiments showed a rise of a little over 1°F. when the wet bulb was at 90°F., 2°F. when at 94°F. while at 98°F. it was about 4°F. per hour. Leonard Hill has noted that the air surrounding the victims of the Black Hole of Calcutta became saturated with water vapour and heated to the temperature of the body so that it was heat stroke and not suffocation that caused death. The power of air to hold water vapour and its evaporative power increase rapidly with rising temperature; thus at 50°F. a cubic foot of air holds 4.08 grains water, at 80°F. 10.9 and at 100°F. 19.7 grains. Hill states that the limit of an Englishman’s power to keep cool is passed when the wet bulb exceeds 88°F. in the still air of a room even when stripped to the waist and resting. If muscular work is performed the limit may be 80°F. Walking in a tropical climate, wet bulb 75° to 80°F., dry bulb 80° to 90°F. may raise the temperature 2° to 3°F. and send the pulse up to 140 to 160. All the students of ventilation stress the importance of circulation of the air in promoting evaporation and comfort. According to Hill with the air saturated and the wet bulb reading 89°F. the wet ‘Kata’ readings would be 3.3 with still air, 8.0 with the wind moving 1 meter a second and 15.1 with a velocity of 9 meters per second. In tropical parts of the world when the wet bulb not infrequently reaches 90°F. the circulation of air by punkahs or electric fans becomes a necessity. There is great variation in capacity for sweating which, according to Hearne, is the basis of heat stroke. He notes that sweating is suppressed from 1 to 48 hours before the attack. With sweating suppressed the body temperature rises until, when 108°F. or more is reached, unconsciousness and convulsions develop. Hearne thinks that the inhibition of sweating is local in the sweat glands, and not central, as diaphoretics fail to cause sweating once it has stopped. As a practical point Hearne watched subjects for dryness of the skin and when discovered they were stripped, covered with a wet sheet and evaporation promoted by a current of air from an electric fan. Doctor Leonard Hill has noted the inefficiency of the application of pieces of ice to the hyperpyrexial body as compared with evaporation. Thus water evaporation at body temperature abstracts 0.59 calories per gram while melting ice only takes away 0.08 calories. Furthermore the application of ice constricts the capillaries and interferes with evaporation. He also notes that 70 grams of water evaporated from the skin takes away as much heat as 1000 grams of ice water used as an enema.
Pathology
Pathologically, there is usually congestion of the brain and meninges, that of the brain being particularly marked about the region of the medulla. There may even be punctate haemorrhages and the nerve cells show chromatolysis. These changes are much more evident in heat stroke than in heat prostration.