Clinical Geriatrics

Introduction

Summer heat waves are among the deadliest environmental events, often accompanied by stories of heat-related deaths, usually involving the elderly. In the United States, an average of 400 Americans die each year from excessive heat. Last summer, newspaper headlines in the Southwest described the problem concisely. For example, the Los Angeles Times declared “Elderly, Isolated Are Heat’s Quiet Victims” after a week-long unprecedented heat wave in California that resulted in the deaths of 72 people.1 In the summer of 2003, August temperatures in France reached unexpected and unprecedented highs, resulting in the deaths of more than 10,000 people. The largest single heat-related disaster occurred in 1995 when an extreme heat wave in Chicago resulted in more than 700 deaths. The elderly and those who live alone or are unable to care for themselves represent the vast majority of these heat-related deaths. Thus, at-risk individuals can be readily identified and could be targets of effective preventive strategies. This article reviews the pathophysiology of heat regulation; the medical, environmental, and social components of heat-related illness in the elderly population; and the essential elements of early identification and proper treatment of these conditions.

Pathophysiology

Hyperthermia is an increase in body temperature due to an imbalance between heat production and dissipation. It also describes a group of heat-related emergencies in which the hypothalamus fails to regulate the balance between heat dissipation and heat accumulation. This failure may manifest itself as minor ailments such as heat cramps or heat edema, or as the more serious, life-threatening condition of heat stroke.

Decreased heat dissipation occurs with age due to a decline in lean body mass (greater barrier to heat exchange) and reduced superficial microvasculature (decreased circulation to cooler external body surfaces). Evaporation accounts for 20-30% of heat loss at rest and essentially all heat loss at air temperatures above 95 degrees F. Significant atrophy of sweat glands in the elderly makes heat dissipation by evaporation far less effective.2

The physiologic basis of thermoregulation is not completely understood. Current understanding is that homeostatic temperature control is maintained by a triad of thermosensors, a central integrative area, and thermoregulatory effectors. Thermosensors are temperature-sensitive collections of specialized neurons located peripherally in skin and centrally in the preoptic area of the anterior hypothalamus and the spinal cord that interpret changes in body temperature and regulate heat-dissipating responses.3 With increasing age, individual thermosensors, both central and peripheral, become less effective in responding to temperature changes. Whether this is due to a decrease in sensitivity or in overall number is unknown, but the effect is the same: a decreased perception of heat in the elderly with associated reduction in heat-dissipation mechanisms.

It is unclear whether the setpoint that keeps body temperature within a narrow range is a property of a specific autonomic structure within the central nervous system (CNS) or the result of a complex system lacking a central control center.4 Evidence suggests the existence of a central integrative mechanism at the hypothalamic or spinal cord level.

Thermoregulatory effectors are physiologic mechanisms that accelerate heat loss and are triggered by thermosensors via the central integrative area. The two primary effectors are sweat production and peripheral vasodilatation. In a warm environment, evaporation of sweat from the skin is the most important mechanism of heat dissipation.