Environmental and nutritional factors in disease

Environmental and nutritional factors in disease

P. Hanlon

M. Byers

J.P.H. Wilding

H.M. Macdonald

Principles and investigation of environmental factors in disease

Environmental effects on health

Health emerges from a highly complex interaction between factors intrinsic to the patient and his or her environment. Many factors within the environment influence health, including aspects of the physical environment, biological environment (bacteria, viruses), built environment and social environment, but these also encompass more distant influences such as the global ecosystem (Fig. 5.1). Environmental changes affect many physiological systems and do not respect boundaries between medical specialties. The specialty of ‘public health’ in the UK is concerned with the investigation and management of health in communities and populations, but the principles apply in all specialties.

Exposure to infectious agents is a major environmental determinant of health and is described in detail in Chapter 6. This chapter describes the approach to other common environmental factors that influence health.

The hierarchy of systems – from molecules to ecologies

When assessing a patient, a clinician subconsciously considers many levels at which problems may be occurring, including molecular, cellular, tissue, organ and body systems. When the environment’s influence on health is being considered, this ‘hierarchy of systems’ extends beyond the individual to include the family, community, population and ecology. Box 5.1 shows an example of the utility of this concept in describing determinants of coronary heart disease operating at each level of a hierarchy.

Interactions between people and their environment

The hierarchy of systems demonstrates that the clinician should not focus too quickly on the disease process without considering the context. Health is an emergent quality of a complex interaction between many determinants, including genetic inheritance, the physical circumstances in which people live (e.g. housing, air quality, working environment), the social environment (e.g. levels of friendship, support and trust), personal behaviour (smoking, diet, exercise), and access to money and the other resources that give people control over their lives. Health care is not the only determinant – and is usually not the major determinant – of health status in the population.

These systems do not operate in isolation in separate communities. When one group responds to ill health by manipulating its environment, the consequences may be global. For example, an Afghan farmer who starts growing opium for money in order to feed his children influences the environment of a teenager in Europe; in turn, drug misuse in Europe has fostered higher prevalence of blood-borne infectious diseases such as human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS); in turn, these have spilled out into sexually transmitted disease. This process contributes significantly to the tragedy of the epidemic of HIV/AIDS.

The life course

The determinants of health operate over the whole lifespan. Values and behaviours acquired during childhood and adolescence have a profound influence on educational outcomes, job prospects and risk of disease. Attributes such as the ability to form empathetic relationships or assess risk have a strong influence on whether a young person takes up damaging behaviour like smoking, risky sexual activity and drug misuse. Influences on health can even operate before birth.

Individuals with low birth weight have been shown to have a higher prevalence of conditions such as hypertension and type 2 diabetes as young adults and of cardiovascular disease in middle age. It has been suggested that under-nutrition during middle to late gestation permanently ‘programmes’ cardiovascular and metabolic responses.

This ‘life course’ perspective highlights the cumulative effect on health of exposures to episodes of illness, adverse environmental conditions and behaviours that damage health. In this way, biological and social risk factors at each stage of life link to form pathways to disease and health.

Investigations in environmental health

Incidence and prevalence

The first task is to establish how common a problem is within the population. This is expressed in two ways (Box 5.2).

Measuring risk

Epidemiology is also concerned with the numerical estimation of risk. This is best illustrated by a simple example. In a rural African town with a population of 5000, disease ‘d’ is under investigation. The majority of the cases of disease ‘d’ (300 out of 360) occurred among women and children who use the river, which recently had its flow of water reduced because of a new irrigation scheme. A formal experiment is established to measure risk. The 1000 women and children who use the river are followed up for 1 year and compared to a cohort with a similar age and sex distribution who use standpipes as their source of water.

The incidence (new cases) of disease ‘d’ in the 1000 exposed to risk ‘r’ (river water) was 300. The incidence (new cases) of disease ‘d’ in the 1000 not exposed to risk ‘r’ was 60. The relative risk is the incidence in the exposed population (300 per 1000 per year) divided by the incidence in the non-exposed population (60 per 1000 per year); 300/60 = 5, meaning that those exposed to the river water are 5 times more likely to contract the disease – their relative risk is 5. The attributable risk of exposure ‘r’ for disease ‘d’ is the incidence in the exposed population (300) minus the incidence in the non-exposed population (60), which is 240 per 1000 per year. The fraction, or proportion, of the disease in the exposed population which can be attributed to risk (r) is called the attributable fraction, in this case (300−60)/300 = 0.8. This means that 80% of the disease can be attributed to exposure to river water.

Preventive medicine

There are many examples of epidemiological associations defining causative factors in disease, e.g. the association between cigarette smoking and lung cancer (p. 699). However, as illustrated above, the complexity of the interactions between physical, social and economic determinants of health means that successful prevention is often difficult. Moreover, the life course perspective illustrates that it may be necessary to intervene early in life or even before birth, to prevent important disease in later life. Successful prevention is likely to require many interventions across the life course and at several levels in the hierarchy of systems. The examples below illustrate this principle.

Environmental diseases

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.


Smoking tobacco dramatically increases the risk of developing many diseases. It is responsible for a substantial majority of cases of lung cancer and chronic obstructive pulmonary disease, and most smokers die either from these respiratory diseases or from ischaemic heart disease. Smoking also causes cancers of the upper respiratory and gastrointestinal tracts, pancreas, bladder and kidney, and increases risks of peripheral vascular disease, stroke and peptic ulceration. Maternal smoking is an important cause of fetal growth retardation. Moreover, there is increasing evidence that passive (or ‘secondhand’) smoking has adverse effects on cardiovascular and respiratory health.

When the ill-health effects of smoking were first discovered, doctors imagined that warning people about the dangers of smoking would result in them giving up. However, it also took increased taxation of tobacco, banning of advertising and support for smoking cessation to maintain a decline in smoking rates. In several European countries (including the UK), this has culminated in a complete ban on smoking in all public places – legislation that only became possible as the public became convinced of the dangers of secondhand smoke. However, smoking rates remain high in many poorer areas and are increasing amongst young women. In many developing countries, tobacco companies have found new markets and rates are rising. Worldwide, there are approximately 1 billion smokers, and it is estimated by WHO that 6 million die prematurely each year as a result of their habit.

In reality, there is a complex hierarchy of systems that interact to cause smokers to initiate and maintain their habit. At the molecular and cellular levels, nicotine acts on the nervous system to create dependence, so that smokers experience unpleasant effects when they attempt to quit. So, even if they know it is harmful, the role of addiction in maintaining the habit is important. Influences at the personal and social level are just as important. Many individuals bolster their denial of the harmful effects of smoking by focusing on someone they knew personally who smoked until he or she was very old and died peacefully in bed. Such strong counter-examples help smokers to maintain internal beliefs that comfort them when presented with statistical evidence. Young female smokers are often motivated more by the desire to ‘stay thin’ or ‘look cool’ than to avoid an illness in middle life.

Even if a smoker decides to quit, there are a variety of influences in the wider environment that reduce the chances of sustained success, including peer pressure, cigarette advertising, and finding oneself in circumstances where one previously smoked. The tobacco industry works very hard to maintain and expand the smoking habit, and its advertising budget is much greater than that available to health promoters.

Strategies to help individuals quit smoking are outlined in Boxes 5.3 and 5.4. Although the success rates are modest, these interventions are cost-effective and form an important part of the overall anti-tobacco strategy.


Obesity is a condition characterised by an excess of body fat. In its simplest terms, obesity can be considered to result from an imbalance between the amount of energy consumed in the diet and the amount of energy expended through exercise and bodily functions. People who are obese are more likely to develop a range of chronic conditions. In 2006, the number of obese and overweight people in the world overtook the numbers who are malnourished and underweight. It would, however, be wrong to focus only on those who are obese because, in countries like the USA and the UK, fat deposition is affecting almost the entire population. The weight distribution of almost the whole population is shifting upwards – the slim are becoming less slim while the fat are getting fatter. In the UK, this translates into a 1-kilogram increase in weight per adult per year (on average over the adult population). It is now widely accepted that we cannot blame the current obesity epidemic on individual behaviour and poor choice, although many current approaches still focus on individuals. The best way, therefore, to understand the current obesity epidemic is to consider humans as ‘obesogenic organisms’ who, for the first time in their history, find themselves in an obesogenic environment – that is, one where people’s circumstances encourage them to eat more and exercise less. This includes the availability of cheap and heavily marketed energy-rich foods, the increase in labour-saving devices (e.g. lifts and remote controls) and the increase in passive transport (cars as opposed to walking, cycling, or walking to public transport hubs). Our physiology was formed a long time ago when food was scarce and we needed large amounts of energy in order to find food and stay alive. We are stuck with the metabolic and behavioural legacy of our evolutionary history – we are organisms that are programmed to eat when we can and preserve energy whenever possible. It is not surprising that we have problems coping with an environment that exerts constant pressure to increase energy intake and to decrease energy expenditure. The rise in obesity suggests that the effects of our obesogenic environment are overriding the biological regulatory mechanisms in more and more people. To combat the health impact of obesity, therefore, we need to help those who are already obese but also develop strategies that impact on the whole population and reverse the obesogenic environment.

Poverty and affluence

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.

Many countries are now experiencing a ‘double burden’. They have large populations still living in poverty who are suffering from problems such as diarrhoea and malnutrition, alongside affluent populations (often in cities) who suffer from chronic illness such as diabetes and heart disease. Recent research suggests that uneven distribution of wealth is a more important determinant of health than the absolute level of wealth; countries with a more even distribution of wealth enjoy longer life expectancies than countries with similar or higher gross domestic products (GDPs) but wider distributions of wealth.

Atmospheric pollution

Emissions from industry, power plants and motor vehicles of sulphur oxides, nitrogen oxides, respirable particles and metals are severely polluting cities and towns in Asia, Africa, Latin America and Eastern Europe. Increased death rates from respiratory and cardiovascular disease occur in vulnerable adults, such as those with established respiratory disease and the elderly, while children experience an increase in bronchitic symptoms. In nations like the UK that have reduced their primary emissions, the new issue of greenhouse gases has emerged. Developing countries also suffer high rates of respiratory disease as a result of indoor pollution caused mainly by heating and cooking combustion.

Carbon dioxide and global warming

Climate change is arguably the world’s most important environmental health issue. A combination of increased production of carbon dioxide and habitat destruction, both caused primarily by human activity, seems to be the main cause. The temperature of the globe is rising, climate is being affected, and if the trend continues, sea levels will rise and rainfall patterns will be altered so that both droughts and floods will become more common. These have already claimed millions of lives during the past 20 years and have adversely affected the lives of many more. The economic costs of property damage and the impact on agriculture, food supplies and prosperity have also been substantial. The health impacts of global warming will also include changes in the geographical range of some vector-borne infectious diseases.

Currently, politicians cannot agree on an effective framework of actions to tackle the problem. Meanwhile, the industrialised world continues with lifestyles and levels of waste that are beyond the planet’s ability to sustain. Rapidly growing economies in the world’s two most populous states, India and China, are going to be a vital part of the unfolding problem or solution.

Radiation exposure

Radiation includes ionising (Box 5.7) and non-ionising radiations (ultraviolet (UV), visible light, laser, infrared and microwave). Whilst global industrialisation and the generation of fluorocarbons have raised concerns about loss of the ozone layer, leading to an increased exposure to UV rays, and disasters such as the Chernobyl and Fukushima nuclear power station explosions have demonstrated the harm of ionising radiation, it is important to remember that it can be harnessed for medical benefit. Ionising radiation is used in X-rays, computed tomography (CT), radionucleotide scans and radiotherapy, and non-ionising UV for therapy in skin diseases and laser therapy for diabetic retinopathy.

Effects of radiation exposure

Effects on the individual are classified as either deterministic or stochastic.

Deterministic effects

Deterministic (threshold) effects occur with increasing severity as the dose of radiation rises above a threshold level. Tissues with actively dividing cells, such as bone marrow and gastrointestinal mucosa, are particularly sensitive to ionising radiation. Lymphocyte depletion is the most sensitive marker of bone marrow injury, and after exposure to a fatal dose, marrow aplasia is a common cause of death. However, gastrointestinal mucosal toxicity may cause earlier death due to profound diarrhoea, vomiting, dehydration and sepsis. The gonads are highly radiosensitive and radiation may result in temporary or permanent sterility. Eye exposure can lead to cataracts and the skin is susceptible to radiation burns. Irradiation of the lung and central nervous system may induce acute inflammatory reactions, pulmonary fibrosis and permanent neurological deficit respectively. Bone necrosis and lymphatic fibrosis are characteristic following regional irradiation, particularly for breast cancer. The thyroid gland is not inherently sensitive but its ability to concentrate iodine makes it susceptible to damage after exposure to relatively low doses of radioactive iodine isotopes, such as were released from Chernobyl.

Extremes of temperature


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).

In a cold environment, protective mechanisms include cutaneous vasoconstriction and shivering; however, any muscle activity that involves movement may promote heat loss by increasing convective loss from the skin, and respiratory heat loss by stimulating ventilation. In a hot environment, sweating is the main mechanism for increasing heat loss. This usually occurs when the ambient temperature rises above 32.5°C or during exercise.


Hypothermia exists when the body’s normal thermal regulatory mechanisms are unable to maintain heat in a cold environment and core temperature falls below 35°C (Fig. 5.3).

Fig. 5.3 Clinical features of abnormal core temperature.
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.

Whilst infants are susceptible to hypothermia because of their poor thermoregulation and high body surface area to weight ratio, it is the elderly who are at highest risk (Box 5.9). Hypothyroidism is often a contributory factor in old age, while alcohol and other drugs (e.g. phenothiazines) commonly impede the thermoregulatory response in younger people. More rarely, hypothermia is secondary to glucocorticoid insufficiency, stroke, hepatic failure or hypoglycaemia.

Hypothermia also occurs in healthy individuals whose thermoregulatory mechanisms are intact but insufficient to cope with the intensity of the thermal stress. Typical examples include immersion in cold water, when core temperature may fall rapidly (acute hypothermia), exposure to extreme climates such as during hill walking (subacute hypothermia), and slow-onset hypothermia, as develops in an immobilised older individual (subchronic hypothermia). This classification is important, as it determines the method of rewarming.


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.


Following resuscitation, the objectives of management are to rewarm the patient in a controlled manner while treating associated hypoxia (by oxygenation and ventilation if necessary), fluid and electrolyte disturbance, and cardiovascular abnormalities, particularly dysrhythmias. Careful handling is essential to avoid precipitating the latter. The method of rewarming is dependent not on the absolute core temperature, but on haemodynamic stability and the presence or absence of an effective cardiac output.

Cold injury

Freezing cold injury (frostbite)

This represents the direct freezing of body tissues and usually affects the extremities: in particular, the fingers, toes, ears and face. Risk factors include smoking, peripheral vascular disease, dehydration and alcohol consumption. The tissues may become anaesthetised before freezing and, as a result, the injury often goes unrecognised at first. Frostbitten tissue is initially pale and doughy to the touch and insensitive to pain (Fig. 5.5). Once frozen, the tissue is hard.

Rewarming should not occur until it can be achieved rapidly in a water bath. Give oxygen and aspirin 300 mg as soon as possible. Frostbitten extremities should be rewarmed in warm water at 37–39°C, with antiseptic added. Adequate analgesia is necessary, as rewarming is very painful. Vasodilators such as pentoxifylline (a phosphodiesterase inhibitor) have been shown to improve tissue survival. Once it has thawed, the injured part must not be re-exposed to the cold, and should be dressed and rested. Whilst wound débridement may be necessary, amputations should be delayed for 60–90 days, as good recovery may occur over an extended period.

Heat-related illness

When generation of heat exceeds the body’s capacity for heat loss, core temperature rises. Non-exertional heat illness (NEHI) occurs with high environmental temperature in those with attenuated thermoregulatory control mechanisms: the elderly, the young, those with comorbidity or those taking drugs that affect thermoregulation (particularly phenothiazines, diuretics and alcohol). Exertional heat illness (EHI), on the other hand, typically develops in athletes when heat production exceeds the body’s ability to dissipate it.

Acclimatisation mechanisms to environmental heat include stimulation of the sweat mechanism with increased sweat volume, reduced sweat sodium content and secondary hyperaldosteronism to maintain body sodium balance. The risk of heat-related illness falls as acclimatisation occurs. Heat illness can be prevented to a large extent by adequate replacement of salt and water, although excessive water intake alone should be avoided because of the risk of dilutional hyponatraemia (p. 437).

A spectrum of illnesses occurs in the heat (see Fig. 5.3). The cause is usually obvious but the differential diagnosis should be considered (Box 5.10).

Heat syncope

This is similar to a vasovagal faint (p. 555) and is related to peripheral vasodilatation in hot weather.

Heat exhaustion

Heat exhaustion occurs with prolonged exertion in hot and humid weather, profuse sweating and inadequate salt and water replacement. There is an elevation in core (rectal) temperature to between 37°C and 40°C, leading to the clinical features shown in Figure 5.3. Blood analyses may show evidence of dehydration with mild elevation of the blood urea, sodium and haematocrit. Treatment involves removal of the patient from the heat, and active evaporative cooling using tepid sprays and fanning (strip–spray–fan). Fluid losses are replaced with either oral rehydration mixtures or intravenous isotonic saline. Up to 5 L positive fluid balance may be required in the first 24 hours. Untreated, heat exhaustion may progress to heat stroke.

Heat stroke

Heat stroke occurs when the core body temperature rises above 40°C and is a life-threatening condition. The symptoms of heat exhaustion progress to include headache, nausea and vomiting. Neurological manifestations include a coarse muscle tremor and confusion, aggression or loss of consciousness. The patient’s skin feels very hot, and sweating is often absent due to failure of thermoregulatory mechanisms. Complications include hypovolaemic shock, lactic acidosis, disseminated intravascular coagulation, rhabdomyolysis, hepatic and renal failure, and pulmonary and cerebral oedema.

The patient should be resuscitated with rapid cooling by spraying with water, fanning and ice packs in the axillae and groins. Cold crystalloid intravenous fluids are given but solutions containing potassium should be avoided. Over-aggressive fluid replacement must be avoided, as it may precipitate pulmonary oedema or further metabolic disturbance. Appropriate monitoring of fluid balance, including central venous pressure, is important. Investigations for complications include routine haematology and biochemistry, coagulation screen, hepatic transaminases (aspartate aminotransferase and alanine aminotransferase), creatine kinase and chest X-ray. Once emergency treatment is established, heat stroke patients are best managed in intensive care.

With appropriate treatment, recovery from heat stroke can be rapid (within 1–2 hours) but patients who have had core temperatures higher than 40°C should be monitored carefully for later onset of rhabdomyolysis, renal damage and other complications before discharge from hospital. Clear advice to avoid heat and heavy exercise during recovery is important.

High altitude

The physiological effects of high altitude are significant. On Everest, the barometric pressure of the atmosphere falls from sea level by approximately 50% at base camp (5400 m) and approximately 70% at the summit (8848 m). The proportions of oxygen, nitrogen and carbon dioxide in air do not change with the fall in pressure but their partial pressure falls in proportion to barometric pressure (Fig. 5.6). Oxygen tension within the pulmonary alveoli is further reduced at altitude because the partial pressure of water vapour is related to body temperature and not barometric pressure, and so is proportionately greater at altitude, accounting for only 6% of barometric pressure at sea level, but 19% at 8848 m.

Physiological effects of high altitude

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.

Illnesses at high altitude

Ascent to altitudes up to 2500 m or travel in a pressurised aircraft cabin is harmless to healthy people. Above 2500 m high-altitude illnesses may occur in previously healthy people, and above 3500 m these become common. Sudden ascent to altitudes above 6000 m, as experienced by aviators, balloonists and astronauts, may result in decompression illness with the same clinical features as seen in divers (see below), or even loss of consciousness. However, most altitude illness occurs in travellers and mountaineers.

Acute mountain sickness

Acute mountain sickness (AMS) is a syndrome comprised principally of headache, together with fatigue, anorexia, nausea and vomiting, difficulty sleeping or dizziness. Ataxia and peripheral oedema may be present. Its aetiology is not fully understood but it is thought that hypoxaemia increases cerebral blood flow and hence intracranial pressure. Symptoms occur within 6–12 hours of an ascent and vary in severity from trivial to completely incapacitating. The incidence in travellers to 3000 m may be 40–50%, depending on the rate of ascent.

Treatment of mild cases consists of rest and simple analgesia; symptoms usually resolve after 1–3 days at a stable altitude, but may recur with further ascent. Occasionally there is progression to cerebral oedema. Persistent symptoms indicate the need to descend but may respond to acetazolamide, a carbonic anhydrase inhibitor that induces a metabolic acidosis and stimulates ventilation; acetazolamide may also be used as prophylaxis if a rapid ascent is planned.

High-altitude pulmonary oedema

High-altitude pulmonary oedema (HAPE) is a life-threatening condition that usually occurs in the first 4 days after ascent above 2500 m. Unlike HACE, HAPE may occur de novo without the preceding signs of AMS. Presentation is with symptoms of dry cough, exertional dyspnoea and extreme fatigue. Later, the cough becomes wet and sputum may be blood-stained. Tachycardia and tachypnoea occur at rest and crepitations may often be heard in both lung fields. There may be profound hypoxaemia, pulmonary hypertension and radiological evidence of diffuse alveolar oedema. It is not known whether the alveolar oedema is a result of mechanical stress on the pulmonary capillaries associated with the high pulmonary arterial pressure, or an effect of hypoxia on capillary permeability. Reduced arterial oxygen saturation is not diagnostic but is a marker for disease progression.

Treatment is directed at reversal of hypoxia with immediate descent and oxygen administration. Nifedipine (20 mg 4 times daily) should be given to reduce pulmonary arterial pressure, and oxygen therapy in a portable pressurised bag should be used if descent is delayed.

Air travel

Commercial aircraft usually cruise at 10 000–12 000 m, with the cabin pressurised to an equivalent of around 2400 m. At this altitude, the partial pressure of oxygen is 16 kPa (120 mmHg), leading to a PaO2 in healthy people of 7.0–8.5 kPa (53–64 mmHg). Oxygen saturation is also reduced, but to a lesser degree (see Fig. 5.6). Although well tolerated by healthy people, this degree of hypoxia may be dangerous in patients with respiratory disease.

Advice for other patients

Other circumstances in which patients are more susceptible to hypoxia require individual assessment. These include cardiac dysrhythmia, sickle-cell disease and ischaemic heart disease. Most airlines decline to carry pregnant women after the 36th week of gestation. In complicated pregnancies it may be advisable to avoid air travel at an earlier stage. Patients who have had recent abdominal surgery, including laparoscopy, should avoid flying until all intraperitoneal gas is reabsorbed. Divers should not fly for 24 hours after a dive requiring decompression stops.

Ear and sinus pain due to changes in gas volume are common but usually mild, although patients with chronic sinusitis and otitis media may need specialist assessment. A healthy mobile tympanic membrane visualised during a Valsalva manœuvre usually suggests a patent Eustachian tube.

On long-haul flights, patients with diabetes mellitus may need to adjust their insulin or oral hypoglycaemic dosing according to the timing of in-flight and subsequent meals (p. 825). Advice is available from Diabetes UK and other websites. Patients should be able to provide documentary evidence of the need to carry needles and insulin.

Deep venous thrombosis

Air travellers have an increased risk of venous thrombosis (p. 1008), due to a combination of factors, including loss of venous emptying because of prolonged immobilisation (lack of muscular activity) and reduced barometric pressure on the tissues, together with haemoconcentration as a result of oedema and perhaps a degree of hypoxia-induced diuresis.

Venous thrombosis can probably be prevented by avoiding dehydration and excess alcohol, and exercising muscles during the flight. Without a clear cost–benefit analysis, prophylaxis with aspirin or heparin cannot be recommended routinely, but may be considered in high-risk cases.

Under water

Drowning and near-drowning

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).

Following inhalation of water, there is a rapid onset of ventilation–perfusion imbalance with hypoxaemia, and the development of diffuse pulmonary oedema. Fresh water is hypotonic and, although rapidly absorbed across alveolar membranes, impairs surfactant function, which leads to alveolar collapse and right-to-left shunting of unoxygenated blood. Absorption of large amounts of hypotonic fluid can result in haemolysis. Salt water is hypertonic and inhalation provokes alveolar oedema, but the overall clinical effect is similar to that of freshwater drowning.

Clinical features

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).

Survival is possible after immersion for up to 30 minutes in very cold water, as the rapid development of hypothermia after immersion may be protective, particularly in children. Long-term outcome depends on the severity of the cerebral hypoxic injury and is predicted by the duration of immersion, delay in resuscitation, intensity of acidosis and the presence of cardiac arrest.


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.

Diving-related illness

The underwater environment is extremely hostile. Other than drowning, most diving illness is related to changes in barometric pressure and its effect on gas behaviour.

Ambient pressure under water increases by 101 kPa (1 atmosphere) for every 10 metres of seawater (msw) depth. As divers descend, the partial pressures of the gases they are breathing increase (Box 5.12), and the blood and tissue concentrations of dissolved gases rise accordingly. Nitrogen is a weak anaesthetic agent, and if the inspiratory pressure of nitrogen is allowed to increase above −320 kPa (i.e. a depth of approximately 30 msw), it produces ‘narcosis’, resulting in impairment of cognitive function and manual dexterity, not unlike alcohol intoxication. For this reason, compressed air can only be used for shallow diving. Oxygen is also toxic at inspired pressures above approximately 40 kPa (inducing apprehension, muscle twitching, euphoria, sweating, tinnitus, nausea and vertigo), so 100% oxygen cannot be used as an alternative. For dives deeper than approximately 30 msw, mixtures of oxygen with nitrogen and/or helium are used.

Whilst drowning remains the most common diving-related cause of death, another important group of disorders usually present once the diver returns to the surface: decompression illness (DCI) and barotrauma.

Clinical features

Decompression illness

This includes decompression sickness (DCS) and arterial gas embolism (AGE). Whilst the vast majority of symptoms of decompression illness present within 6 hours of a dive, they can also be provoked by flying and thus patients may present to medical services at sites far removed from the dive.

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.

image 5.13   Assessment of a patient with decompression illness*


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Apr 9, 2017 | Posted by in GENERAL SURGERY | Comments Off on Environmental and nutritional factors in disease

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