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.

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

Alcohol

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

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

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.

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.

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

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).

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.

 5.9   Thermoregulation in old age

• Age-associated changes: impairments in vasomotor function, skeletal muscle response and sweating mean that older people react more slowly to changes in temperature.

• Increased comorbidity: thermoregulatory problems are more likely in the presence of pathology such as atherosclerosis and hypothyroidism, and medication such as sedatives and hypnotics.

• Hypothermia: may arise as a primary event, but more commonly complicates other acute illness, e.g. pneumonia, stroke or fracture.

• Ambient temperature: financial pressures and older equipment may result in inadequate heating during cold weather.

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.

Clinical features

Diagnosis is dependent on recognition of the environmental circumstances and measurement of core (rectal) body temperature. Clinical features depend on the degree of hypothermia (see Fig. 5.3).

In a cold patient, it is very difficult to diagnose death reliably by clinical means. It has been suggested that, in extreme environmental conditions, irreversible hypothermia is probably present if there is asystole (no carotid pulse for 1 minute), the chest and abdomen are rigid, the core temperature is below 13°C and serum potassium is > 12 mmol/L. However, in general, resuscitative measures should continue until the core temperature is normal and only then should a diagnosis of brain death be considered (p. 1161).

Investigations

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.

Management

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.

Mild hypothermia

Outdoors, continued heat loss is prevented by sheltering the patient from the cold, replacing wet clothing, covering the head and insulating him or her from the ground. Once in hospital, even in the presence of profound hypothermia, if there is an effective cardiac output then forced-air rewarming, heat packs placed in axilla, groin and around the abdomen, inhaled warmed air and correction of fluid and electrolyte disturbances are usually sufficient. Rewarming rates of 1–2°C per hour are effective in leading to a gradual and safe return to physiological normality. Underlying conditions should be treated promptly (e.g. hypothyroidism with triiodothyronine 10 µg IV 3 times daily; p. 743).

Severe hypothermia

In the case of severe hypothermia with cardiopulmonary arrest (non-perfusing rhythm), the aim is to restore perfusion, and rapid rewarming at a rate greater than 2°C per hour is required. This is best achieved by cardiopulmonary bypass or extracorporeal membrane oxygenation. If these are unavailable, then veno–veno haemofiltration, and pleural, peritoneal, thoracic or bladder lavage with warmed fluids are alternatives. Monitoring of cardiac rhythm and arterial blood gases, including H⁺ (pH) is essential. Significant acidosis may require correction (p. 445).

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.

Non-freezing cold injury (trench or immersion foot)

This results from prolonged exposure to cold, damp conditions. The limb (usually the foot) appears cold, ischaemic and numb, but there is no freezing of the tissue. On rewarming, the limb appears mottled and thereafter becomes hyperaemic, swollen and painful. Recovery may take many months, during which there may be chronic pain and sensitivity to cold. The pathology remains uncertain but probably involves endothelial injury. Gradual rewarming is associated with less pain than rapid rewarming. The pain and associated paraesthesia are difficult to control with conventional analgesia and may require amitriptyline (50 mg nocte), best instituted early. The patient is at risk of further damage on subsequent exposure to the cold.

Chilblains

Chilblains are tender, red or purplish skin lesions that occur in the cold and wet. They are often seen in horse riders, cyclists and swimmers, and are more common in women than men. They are short-lived, and although painful, not usually serious.

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.

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.

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.

 5.12   Physics of breathing compressed air while diving in sea water

Depth	Lung volume	Barometric pressure	PiO2	PiN2
Surface	100%	101 kPa (1 atmos)	21 kPa	79 kPa
10 m	50%	202 kPa (2 atmos)	42 kPa	159 kPa
20 m	33%	303 kPa (3 atmos)	63 kPa	239 kPa
30 m	25%	404 kPa (4 atmos)	84 kPa	319 kPa

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.

 5.13   Assessment of a patient with decompression illness*

Evolution

• Progressive • Static Only gold members can continue reading. Log In or Register to continue Share this: Click to share on Twitter (Opens in new window) Click to share on Facebook (Opens in new window) Like this: Like Loading... Related Related posts: Laboratory reference ranges Stroke disease Kidney and urinary tract disease Liver and biliary tract disease Stay updated, free articles. Join our Telegram channel Join Tags: Davidsons Principles and Practice of Medicine Apr 9, 2017 | Posted by admin in GENERAL SURGERY | Comments Off on Environmental and nutritional factors in disease Full access? Get Clinical Tree Get Clinical Tree app for offline access Get Clinical Tree app for offline access %d