Chapter 18 Environmental medicine

Disease and the environment

The incidence and prevalence of disease and causes of death within a community are a reflection of interrelated factors:

Genetic predisposition

Nutrition, poverty and affluence

Purity of water sources, sanitation and atmospheric pollution

Environmental disasters and accidents

Background ionizing radiation and man-made radiation exposure, deliberate or accidental

Environmental temperature

Patterns of infective disease

Political forces determining levels of healthcare, preventative strategies and effects of war on civilian populations.

Some of these environmental effects have been clearly documented within the last decade, e.g. the massive civilian mortality and morbidity during the current Afghan and previous Iraq wars, and loss of life and disease prevalence following the 2006 tsunami, the earthquakes in Sechuan (2008) and Haiti (2010) and cyclone Nargris in the Irawaddy delta. Flooding caused by El Niño in East Africa not only resulted in an increase in breeding sites for mosquito vectors but a major outbreak of Rift Valley fever due to the enforced close proximity of cattle with humans.

Smoking (active and passive), obesity and excess alcohol consumption also play a significant role in disease. Worldwide health programmes have been established in most countries to reduce their effects.

Environmental temperature

The effect of environmental temperature (T_Env) is paramount in infective diseases; changes as small as 1°C cause major changes in disease vectors. Climate change is an unquestionable phenomenon. Patterns of infective disease are likely to change radically within the next 20 years. There are suggestions that climate effects are already becoming apparent, e.g.:

Patterns of malaria in South-east Asia

The occurrence of dengue fever in southern Italy

Outbreaks of cholera, and seasonal variation in diarrhoea and vomiting.

Research into the effect of climate change on the changing patterns of infective diseases will point to potential ways in which national and international efforts can be targeted.

Heat

Body core temperature (T_Core) is maintained at 37°C by the thermoregulator centre in the hypothalamus.

Heat is produced by cellular metabolism and is dissipated through the skin by both vasodilatation and sweating and in expired air via the alveoli. When the environmental temperature (T_Env) is >32.5°C, profuse sweating occurs. Sweat evaporation is the principal mechanism for controlling T_Core following exercise or in response to an increase in T_Env.

Heat acclimatization. Acclimatization to heat takes place over several weeks. The sweat volume increases and the sweat salt content falls. Increased evaporation of sweat reduces T_Core.

Heat cramps. Painful muscle cramps, usually in the legs, often occur in fit people when they exercise excessively, especially in hot weather. Cramps are probably due to low extracellular sodium caused by excess intake of water over salt. Cramps can be prevented by increasing dietary salt. They respond to combined salt and water replacement, and in the acute stage to stretching and muscle massage. T_Core remains normal.

Heat illness. At any environmental temperature (especially with T_Env of >25°C), and with a high humidity, strenuous exercise in clothing that inhibits sweating such as a wetsuit can cause an elevation in T_Core in <15 minutes. Weakness/exhaustion, cramps, dizziness and syncope, with T_Core >37°C, define heat illness (heat exhaustion). Elevation of T_Core is more critical than water and sodium loss. Heat illness may progress to heat injury, a serious emergency.

Management of heat illness

Reduce (T_Env) if possible. Cool with sponging and fans. Give O₂ by mask. Other causes of high T_Core, e.g. malaria, should be ruled out if appropriate.

Oral rehydration with both salt and water (25 g of salt per 5 L of water/day) is given in the first instance, with adequate replacement thereafter. In severe heat illness, i.v. fluids are needed; 0.9% saline is given; monitor serum sodium and correct secondary potassium loss.

Heat injury

Heat injury (heat stroke) is an acute life-threatening situation when T_Core rises above 41°C. There is headache, nausea, vomiting and weakness, progressing to confusion, coma and death. The skin feels intensely hot to the touch. Sweating is often absent, but not invariably.

Heat injury can develop in unacclimatized people in hot, humid windless conditions, even without exercise. Sweating may be limited by prickly heat (plugging or rupture of the sweat ducts, leading to a pruritic papular erythematous rash). Excessive exercise in inappropriate clothing, e.g. exercising on land in a wetsuit, can lead to heat injury in temperate climates. Diabetes, alcohol and drugs, e.g., antimuscarinics, diuretics and phenothiazines, can contribute. Heat injury can lead to a fall in cardiac output, lactic acidosis and intravascular coagulation.

Prevention

Acclimatization, fluids, avoiding inappropriate clothing and common sense.

Management

Reduce T_Env if possible

Cool: sponging, icepacks, fanning. Give O₂ by mask

Manage in intensive care: monitor cardiac output, respiration, biochemistry, clotting and muscle enzymes

Give fluids intravenously so the intravascular volume can remain normal.

Prompt treatment is essential and can be curative even with T_Core of >41°C. Delay can be fatal. Complications are hypovolaemia, intravascular coagulation, cerebral oedema, rhabdomyolysis, and renal and hepatic failure.

Malignant hyperpyrexia

See page 1153.

Cold

Hypothermia is defined as a core temperature of <32°C. It is frequently lethal when T_Core falls below 30°C. Survival, with full recovery has however been recorded with T_Core of <16°C. Cold injury includes:

Frostbite: the local cold injury that follows freezing of tissue

Non-freezing cold injury: the damage – usually to feet – following prolonged exposure to T_Env between 0 and 5°C, usually in damp conditions.

Hypothermia

Hypothermia occurs in many settings.

At home. Hypothermia can occur when T_Env is below 8°C, when there is poor heating, inadequate clothing and poor nutrition. Depressant drugs, e.g. hypnotics, as well as alcohol, hypothyroidism or intercurrent illness also contribute. Hypothermia is commonly seen in the poor, frail and elderly. The elderly have diminished ability to sense cold and also have little insulating fat. Neonates and infants become hypothermic rapidly because of a relatively large surface area in proportion to subcutaneous fat.

Outdoors on land. Hypothermia is a prominent cause of death in climbers, skiers, polar travellers and in wartime. Wet, cold conditions with wind chill, physical exhaustion, injuries and inadequate clothing are contributory. Babies and children are at risk because they cannot take action to warm them themselves.

Cold water immersion. Dangerous hypothermia can develop following immersion for more than 30 min to 1 hour in water temperatures of 15–20°C. In T_Water below 12°C limbs rapidly become numb and weak. Recovery takes place gradually, over several hours following rescue.

Clinical features

Mild hypothermia (T_Core <32°C) causes shivering and initially intense discomfort. However, the hypothermic subject, though alert, may not act appropriately to rewarming, e.g. by huddling, wearing extra clothing or exercising. As the T_Core falls below 32°C, severe hypothermia causes impaired judgement – including lack of awareness of cold – drowsiness and coma. Death follows, usually from ventricular fibrillation.

Diagnosis

Diagnosis is straightforward, if a low-reading thermometer is available. If not, rapid clinical assessment is reliable. Someone who feels icy to touch – abdomen, groin, axillae – is probably substantially hypothermic. If they are clammy, uncooperative or sleepy, T_Core is almost certainly <32°C.

Sequelae

Pulse rate and systemic BP fall. Cardiac output and cerebral blood flow are low in hypothermia and can fall further if the upright position is maintained, the thorax restrained by a harness or by hauling during evacuation. This is why helicopter and lifeboat winch rescues are often carried out with a stretcher, rather than a chest harness.

Respiration becomes shallow and slow. Muscle stiffness develops; tendon reflexes become sluggish, then absent. As coma ensues, pupillary and other brainstem reflexes are lost; pupils are fixed and may be dilated in severe hypothermia. Metabolic changes are variable, with either metabolic acidosis or alkalosis. Arterial PO₂ may appear normal, i.e. falsely high.

There is shift of the oxygen dissociation curve to the left because of the reduction in temperature of haemoglobin. Thus, if an arterial blood sample from a hypothermic patient is analysed at 37°C, the PO₂ will be falsely high. Within the range 37–33°C this factor is around 7% per °C. Many blood gas machines also calculate the arterial saturation; this too will be falsely high. When a patient is monitored using a pulse oximeter, the level of arterial oxygen saturation (S_aO₂) will however be correct – but if S_aO₂ is then converted by calculation to P_aO₂, a downwards correction must be applied – simply due to hypothermia.

Bradycardia with ‘J’ waves (rounded waves above the isoelectric line at the junction of the QRS complex and ST segment) are pathognomonic of hypothermia. Prolongation of PR and QT intervals and QRS complex also occur. Ventricular dysrhythmias (tachycardia/fibrillation) or asystole are the usual causes of death.

ECG showing J waves in hypothermia.

Principles of hypothermia management

Maintain the patient horizontal, or slightly head down.

Rewarm gradually.

Correct metabolic abnormalities.

Anticipate and treat dysrhythmias.

Check for hypothyroidism (see p. 962).

If the patient is awake, with a core temperature of >32°C, place them in a warm room, use a foil wrap and give warm fluids orally. Outdoors, add extra dry clothing, huddle together and use a warmed sleeping bag. Rewarming may take several hours. Avoid alcohol: this adds to confusion, boosts confidence factitiously, causes peripheral vasodilatation and further heat loss, and can precipitate hypoglycaemia.

Severe hypothermia

In severe hypothermia, people look dead. Always exclude hypothermia before diagnosing brainstem death (see p. 897). Warm gradually, aiming at a 1°C/hour increase in T_Core. Direct mild surface heat from an electric blanket can be helpful. Treat any underlying condition promptly, e.g. sepsis. Monitor all vital functions. Correct dysrhythmias. Check for sedative drugs.

Give warm i.v. fluids slowly. Correct metabolic abnormalities. Hypothyroidism, if present, should be treated with liothyronine. Various methods of artificial rewarming exist – inhaled warm humidified air, gastric or peritoneal lavage, and haemodialysis. These are rarely used.

Prevention

Hypothermia in the field can often be prevented by forethought and action. For the elderly, improved home heating and insulation, central heating in bedrooms and electric blankets are helpful in cold spells. This can be expensive and unaffordable for some people, so supplemental finance is required.

Cold injury

Frostbite

Ice crystals form within skin and superficial tissues when the temperature of the tissue (T_Tissue) falls to −3°C: T_Env generally must be below −6°C. Wind chill is frequently a factor. Typically, fingers, toes, nose and ears become frostbitten.

Frostbitten tissue is pale, greyish and initially doughy to touch. Later, tissue freezes hard, looking like meat from a freezer. Frostbite can easily occur when working or exercising in low temperatures and typically develops without the patient’s knowledge. Below T_Env 5°C, hands or feet that have lost their feeling are at risk of cold injury.

Management

Transport the patient – or if this is impossible, make them walk, even on frostbitten feet – to a place of safety before commencing warming. Warm the frozen part by immersion in hand hot water at 39–42°C, if feasible. Assess hypothermia. Continue warming until obvious thawing occurs; this can be painful. Vasodilator drugs have no part in management. Blisters form within several days and, depending on the depth of frostbite, a blackened shell – the carapace – develops as blisters regress or burst. Dry, non-adherent dressings and aseptic precautions are essential, though hard to achieve. Frostbitten tissues are anaesthetic and at risk from further trauma and infection. Recovery takes place over many weeks, and may be incomplete. Surgery may be needed, but should be avoided in the early stages.

Chilblains

These are small, purplish itchy inflammatory lesions, occurring on toes and fingers. They occur in cold, wet conditions. They are more common in women and heal in 7–14 days. Prevention is by keeping warm and wearing gloves and warm footwear.

Only gold members can continue reading. Log In or Register to continue

You may also need

Tags: Kumar and Clarks Clinical Medicine

Mar 31, 2017 | Posted by admin in GENERAL & FAMILY MEDICINE | Comments Off

Basicmedical Key

Fastest Basicmedical Insight Engine

Environmental medicine

Disease and the environment

Environmental temperature

Heat

Management of heat illness

Heat injury

Prevention

Management

Malignant hyperpyrexia

Cold

Hypothermia

Clinical features

Diagnosis

Sequelae

Principles of hypothermia management

Severe hypothermia

Prevention

Cold injury

Frostbite

Management

Chilblains

You may also need

Like this:

Related

Full access? Get Clinical Tree

Fastest Basicmedical Insight Engine

Environmental medicine

You may also need

Share this:

Like this:

Related

Full access? Get Clinical Tree