by the want of a continuous sufficiently elevated temperature, and fatally injured by direct exposure to cold.
It now remains to show that organs undergoing pathological evolution (conservative structural modification) are affected exactly in the same manner by exposure to cold. Speaking, first, theoretically, we find organs thus circumstanced are the seat of an exalted rate of tissue-transformation, of a change additional to that which belongs to the ordinary process of waste and repair, and therefore we should a priori expect to find in them the same liability to inflammation, on exposure, as was observed in organs being rapidly developed physiologically. Speaking practically, we find, a fortiori, that this is actually the case. What is more common, with a patient who is the subject of some chronic organic disease, than to be suddenly cut off by the occurrence of acute inflammation in the affected organ after exposure to cold? Every medical practitioner can answer. In remarking upon the influence of cold as a cause of mortality. Dr. Carpenter, in his "Human Physiology,"[1] refers to the Report of the Registrar-General for March, 1855, in which it appears that the rate of mortality, not only in infants and aged persons, but also in those affected with chronic disease, increases during the winter months, and diminishes in summer. The deaths in many instances (in old persons) were due to pneumonia, bronchitis, asthma, and various chronic diseases; so that Dr. Carpenter is led to observe that "cold brings quickly to a fatal termination many maladies which it does not directly induce." Nay, the acute inflammatory attack, under such circumstances, is often enough the first intimation, to the patient, and perhaps to the physician, of the existence of organic change in the affected organ. A most common error, and, as far as I know, a universal one, is to date the real beginning of the disease from the acute inflammation, and ascribe any recognizable lingering symptoms to the acute attack having "lapsed into the chronic form;" when, in fact, the slow, chronic changes of structure were present only in their naturally-designed latent form,[2] long before, and were only made manifest to the patient by the disturbing action of cold.
As we have seen that, in organisms undergoing physiological development, those organs are most liable to be attacked with inflammation after exposure, whose rate of growth happens to be at the time most rapid, so in after-life it is not all the organs in the body that are liable to inflame after exposure, but only those in which pathological evolution is taking place. And this explains why it is, when several persons have been equally exposed, that one suffers from acute pneumonia, another from acute nephritis (kidney-inflammation), another from acute arthritis (joint-inflammation), while some altogether escape
