• If the problem is a continuing condition (e.g. enlarged spleen due to malaria), then prevalence is the appropriate measurement and is calculated by dividing the number of people with the condition at a specified time by the number of people in the population at risk at that time. Prevalence tends to be higher if the problem is common (many new cases) and/or if it is of longer duration. • If the problem is an event that occurs at a clear point in time (e.g. fever due to malaria), then incidence is used. Incidence is a measure of the rate at which new cases occur (e.g. confirmed pyrexia with malaria parasites on a blood film) in the population at risk during a defined period of time. The term ‘homeostasis’ describes the capacity to maintain the internal milieu by adapting to increases or decreases in a given environmental factor. However, there are limits to the coping abilities of any system, at which ‘too much’ or ‘too little’ of a given environmental factor will result in ill health. Too many calories lead to obesity, while too few lead to malnutrition. Either involuntarily or deliberately, we expose ourselves to many poisons and hazards. Examples discussed elsewhere include industrial/occupational hazards, such as asbestos (p. 718) and other carcinogens (p. 266). ‘Social’ poisons, such as tobacco, alcohol and drugs of misuse, also need to be considered (p. 240). The World Health Organization (WHO) estimates that the harmful use of alcohol results in the death of 2.5 million people annually. Rates of alcohol-related harm vary by place and time but have risen dramatically in the UK, with Scotland showing the highest rates. (Fig. 5.2 demonstrates the climbing rates during the 1990s, since when rates have stabilised at very high levels.) Why did Scotland experience this dramatic increase in alcohol deaths? The most likely explanation is that the environment changed. The price of alcohol fell in real terms and availability increased (more supermarkets sold alcohol and the opening times of public houses were extended). Also, the culture changed in a way that fostered higher levels of consumption and more binge drinking. These changes have caused a trebling of male and a doubling of female deaths due to alcohol. Public, professional and governmental concern has now led to a minimum price being charged for a unit of alcohol, tightening of licensing regulations and curtailment of some promotional activity (e.g. two-for-one offers in bars). Many experts judge that even more aggressive public health measures will be needed to reverse the levels of harm in the community. The approach for individual patients suffering adverse effects of alcohol is described on pages 240 and 252. The adverse health and social consequences of poverty are well documented: high birth rates, high death rates and short life expectancy (Box 5.5). Typically, with industrialisation, the pattern changes: low birth rates, low death rates and longer life expectancy (Box 5.6). Instead of infections, chronic conditions such as heart disease dominate in an older population. Adverse health consequences of excessive affluence are also becoming apparent. Despite experiencing sustained economic growth for the last 50 years, people in many industrialised countries are not growing any happier and the litany of socioeconomic problems – crime, congestion, inequality – persists. Living in societies that give pride of place to economic growth means that there is constant pressure to contribute by performing ever harder at work and by consuming as much as – or more than – we can afford. As a result, people become stressed and may adopt unhealthy strategies to mitigate their discomfort; they overeat, overshop, or use sex or drugs (legal and illegal) as ‘pain-killers’. These behaviours often lead to the problems listed in Box 5.5. Body heat is generated by basal metabolic activity and muscle movement, and lost by conduction (which is more effective in water than in air), convection, evaporation and radiation (most important at lower temperatures when other mechanisms conserve heat) (Box 5.8). Body temperature is controlled in the hypothalamus, which is directly sensitive to changes in core temperature and indirectly responds to temperature-sensitive neurons in the skin. The normal ‘set-point’ of core temperature is tightly regulated within 37 ± 0.5°C, which is necessary to preserve the normal function of many enzymes and other metabolic processes. The temperature set-point is increased in response to infection (p. 296). Blood gases, a full blood count, electrolytes, chest X-ray and electrocardiogram (ECG) are all essential investigations. Haemoconcentration and metabolic acidosis are common, and the ECG may show characteristic J waves, which occur at the junction of the QRS complex and the ST segment (Fig. 5.4). Cardiac dysrhythmias, including ventricular fibrillation, may occur. Although the arterial oxygen tension may be normal when measured at room temperature, the arterial PO2 in the blood falls by 7% for each 1°C fall in core temperature. Serum aspartate aminotransferase and creatine kinase may be elevated secondary to muscle damage and the serum amylase is often high due to subclinical pancreatitis. If the cause of hypothermia is not obvious, additional investigations for thyroid and pituitary dysfunction (p. 737), hypoglycaemia (p. 807) and the possibility of drug intoxication (p. 209) should be performed. Reduction in oxygen tension results in a fall in arterial oxygen saturation (see Fig. 5.6). This varies widely between individuals, depending on the shape of the sigmoid oxygen–haemoglobin dissociation curve (see Fig. 8.3, p. 183) and the ventilatory response. Acclimatisation to hypoxaemia at high altitude involves a shift in this dissociation curve (dependent on 2,3-diphosphoglycerate (DPG)), erythropoiesis, haemoconcentration, and hyperventilation resulting from hypoxic drive (which is then sustained despite hypocapnia by restoration of cerebrospinal fluid pH to normal in prolonged hypoxia). This process takes several days, so travellers need to plan accordingly. Drowning is defined as death due to asphyxiation following immersion in a fluid, whilst near-drowning is defined as survival for longer than 24 hours after suffocation by immersion. Drowning remains a common cause of accidental death throughout the world and is particularly common in young children (Box 5.11). In about 10% of cases, no water enters the lungs and death follows intense laryngospasm (‘dry’ drowning). Prolonged immersion in cold water, with or without water inhalation, results in a rapid fall in core body temperature and hypothermia (p. 104). Those rescued alive (near-drowning) are often unconscious and not breathing. Hypoxaemia and metabolic acidosis are inevitable features. Acute lung injury usually resolves rapidly over 48–72 hours, unless infection occurs (Fig. 5.7). Complications include dehydration, hypotension, haemoptysis, rhabdomyolysis, renal failure and cardiac dysrhythmias. A small number of patients, mainly the more severely ill, progress to develop the acute respiratory distress syndrome (ARDS; p. 192). Initial management requires cardiopulmonary resuscitation with administration of oxygen and maintenance of the circulation (p. 558). It is important to clear the airway of foreign bodies and protect the cervical spine. Continuous positive airways pressure (CPAP; p. 193) should be considered for spontaneously breathing patients with oxygen saturations below 94%. Observation is required for a minimum of 24 hours. Prophylactic antibiotics are only required if exposure was to obviously contaminated water. Exposure of individuals to increased partial pressures of nitrogen results in additional nitrogen being dissolved in body tissues; the amount dissolved depends on the depth/pressure and on the duration of the dive. On ascent, the tissues become supersaturated with nitrogen, and this places the diver at risk of producing a critical quantity of gas (bubbles) in tissues if the ascent is too fast. The gas so formed may cause symptoms locally, by bubbles passing through the pulmonary vascular bed (Box 5.13) or by embolisation elsewhere. Arterial embolisation may occur if the gas load in the venous system exceeds the lungs’ abilities to excrete nitrogen, or when bubbles pass through a patent foramen ovale (present asymptomatically in 25–30% of adults; p. 528). Although DCS and AGE can be indistinguishable, their early treatment is the same.
Environmental and nutritional factors in disease
Principles and investigation of environmental factors in disease
Environmental effects on health
Investigations in environmental health
Incidence and prevalence
Environmental diseases
Alcohol
Poverty and affluence
Extremes of temperature
Thermoregulation
Hypothermia
The hypothalamus normally maintains core temperature at 37°C, but this set-point is altered – for example, in fever (pyrexia, p. 296) – and may be lost in hypothalamic disease (p. 785). In these circumstances, the clinical picture at a given core temperature may be different.
Investigations
High altitude
The blue curve shows changes in oxygen availability at altitude and the red curve shows the typical resultant changes in arterial oxygen saturation in a healthy person. Oxygen saturation varies between individuals according to the shape of the oxygen–haemoglobin dissociation curve and the ventilatory response to hypoxaemia. (To convert kPa to mmHg, multiply by 7.5.)
Physiological effects of high altitude
Under water
Drowning and near-drowning
Clinical features
Chest X-ray of a 39-year-old farmer, 2 weeks after immersion in a polluted freshwater ditch for 5 minutes before rescue. Airspace consolidation and cavities in the left lower lobe reflect secondary staphylococcal pneumonia and abscess formation.
Management
Diving-related illness
Clinical features
Decompression illness