Environmental medicine

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19 Environmental medicine

Chapter Contents

Heat 697
Cold 698
Drowning and near-drowning 699
Ionizing radiation 700
Electric shock 701
Bioterrorism/biowarfare 701

Heat

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

• Heat acclimatization. This occurs over several weeks. The sweat volume increases and the sweat salt content falls. Increased evaporation of sweat results in a reduced TCore.
• Heat cramps. Painful muscle cramps, usually in the legs, occur in fit people during exercise in hot weather. They respond to combined salt and water replacement, and in the acute stage to stretching and muscle massage. TCore remains normal.
• Heat illness (heat exhaustion). At any environmental temperature (especially with TEnv of > 25°C), and with a high humidity, exercise in clothes that inhibit sweating can cause an elevation in TCore in less than 15 mins. Heat illness with a TCore > 37°C causes weakness, cramps and syncope, and may progress to heat injury.

Management

Reduce (TEnv) and cool the patient with sponging and fans. Give O2 by mask.

Oral rehydration with both salt and water (25 g of salt per 5 L of water/day) is given initially, followed by normal daily fluids. In severe heat illness, IV 0.9% saline is given. Monitoring of serum sodium with correction of secondary potassium loss is required.

Heat injury (heat stroke)

Heat injury (heat stroke) is an acute life-threatening condition when TCore rises above 41°C. Headache, nausea, vomiting and weakness, progressing to confusion, coma and death occur. The skin feels intensely hot to the touch, usually with absence of sweating.

Heat injury develops in unacclimatized people in hot, humid windless climates, often without exercise. Drugs and alcohol, e.g. antimuscarinics, diuretics and phenothiazines, contribute.

Prevention

• Acclimatization, fluids and appropriate clothing.

Management

Management is as above. Intensive care may be necessary for severe cases. Intravascular volume can remain normal and the use of IV fluids must be monitored with a CVP line.

Prompt treatment is essential, as complications of hypovolaemia, intravascular coagulation, cerebral oedema, rhabdomyolysis, and renal and hepatic failure can occur rapidly.

Cold

Hypothermia is defined as a core temperature of less than 32°C and is often lethal when TCore falls below 30°C.

Hypothermia

• Hypothermia can occur when TEnv is below 8°C with inadequate heating and clothing. Drugs, e.g. hypnotics, alcohol, hypothyroidism or intercurrent illness also contribute. 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.
• Hypothermia often occurs in climbers, skiers and polar travellers, and in wartime. Wet, cold conditions with wind chill, physical exhaustion, injuries and inadequate clothing are contributory.
• Serious hypothermia can develop following immersion for more than 1 hour in water temperatures of 15–20°C. In water temperatures below 12°C limbs rapidly become numb and weak. Recovery takes place gradually, often taking several hours.

Clinical features

Mild hypothermia (TCore < 32°C) causes shivering and initially intense discomfort. As the TCore falls below 32°C, severe hypothermia causes impaired judgement — including lack of awareness of cold. Drowsiness and coma, followed by death, occur.

Diagnosis

Someone who feels icy to the touch — abdomen, groin, axillae — is probably hypothermic. If the patent is clammy, uncooperative or sleepy, TCore is almost certainly ≤ 32°C.

Pulse rate and systemic BP can fall. Cardiac output and cerebral blood flow are greatly affected by change in posture in hypothermia, and can fall further if the upright position is maintained or the thorax is restrained by a harness. Respiration becomes shallow and slow. Muscle stiffness develops; tendon reflexes become sluggish and/or lost.

In coma, pupillary and other brainstem reflexes are lost; pupils are fixed and may be dilated in severe hypothermia.

Reduction in the temperature of haemoglobin causes a falsely high arterial PO2 and oxygen saturation. Using a pulse oximeter, the level of arterial oxygen saturation (SaO2) will, however, be correct.

Bradycardia with ‘J’ waves (rounded waves above the isoelectric line at the junction of the QRS complex and ST segment (Fig. 19.1)) is pathognomonic of hypothermia. Prolongation of PR and QT intervals and of the QRS complex also occurs. Ventricular dysrhythmia (tachycardia/fibrillation) or asystole is the usual cause of death.

image

Fig. 19.1 ECG showing J waves.

Management

Maintain the patient in a horizontal position or slightly head-down, rewarm gradually, correct metabolic abnormalities, anticipate and treat dysrhythmias, and check for hypothyroidism (p. 570).

If the patient is awake, with a core temperature of more than 32°C (with a low-reading thermometer), place him/her 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.

In severe hypothermia, people look dead. Always exclude hypothermia before diagnosing brainstem death (p. 561). Warm gradually, aiming at an increase in TCore of 1°C per hour. Direct mild surface heat can be helpful. Monitor all vital functions.

Give warm IV fluids slowly and correct metabolic abnormalities. Hypothyroidism, if present, should be treated with liothyronine.

Drowning and near-drowning

Drowning caused over 500 000 deaths worldwide in 2007. Exhaustion, alcohol, drugs and hypothermia all contribute to deaths following immersion. People can also drown after an epileptic seizure or a myocardial infarct whilst in water.

Dry drowning

Between 10 and 15% of drownings occur without water aspiration into the lungs. Laryngeal spasm develops acutely, followed by apnoea and cardiac arrest.

Wet drowning

Fresh- or sea-water aspiration destroys pulmonary surfactant, leading to alveolar collapse, ventilation/perfusion mismatch and hypoxaemia. Aspiration of hypertonic seawater (5% NaCl) pulls additional fluid into the alveoli with further ventilation/perfusion mismatch. In practice, there is little difference between salt-water and fresh-water aspiration. In both, severe hypoxaemia develops rapidly. Severe metabolic acidosis develops in the majority of survivors.

Emergency treatment

CPR should be started immediately (p. 704). Patients have survived for up to 30 mins under water without suffering brain damage — and sometimes for longer periods if the temperature of the water (TWater) is near 10°C.

Resuscitation should always be attempted, even with an absent pulse and fixed dilated pupils. All survivors should be admitted to hospital for intensive monitoring, as they are liable to develop acute lung injury during the subsequent 48 hours.

Ionizing radiation

• Ionizing radiation is either penetrating (X-rays, γ-rays or neutrons) or non-penetrating (α- or β-particles). Penetrating radiation affects the skin and deeper tissues, while non-penetrating radiation affects the skin alone.
• All radiation effects depend on the type of radiation, the distribution of dose and the dose rate.
• Dosage is measured in joules per kilogram (J/kg); 1 J/kg = 1 gray (1 Gy) = 100 rads.
• Radioactivity is measured in becquerels (Bq). 1 Bq is defined as the activity of a quantity of radioactive material in which one nucleus decays per second; 3.7 × 1010 Bq = 1 curie (Ci), the older, non-SI unit.
• Radiation differs in the density of ionization it causes. Therefore a dose-equivalent called a sievert (Sv) is used. This is the absorbed dose weighted for the damaging effect of the radiation. The annual background radiation is approximately 2.5 mSv. A CXR delivers 0.02 mSv, and CT of the abdomen/pelvis about 8–10 mSv.

Acute radiation sickness

Nausea, vomiting and malaise follow doses of approximately 1 Gy. Lymphopenia occurs within several days, followed 2–3 weeks later by a fall in all white cells and platelets. Higher doses cause:

• Haematopoietic syndrome. Absorption of 2–10 Gy is followed by transient vomiting in some individuals, while severe lymphopenia develops over several days. A decrease in granulocytes and platelets follows 14–21 weeks later, as no new cells are formed in the marrow. Bleeding and frequent overwhelming infections develop, with a high mortality.
• Gastrointestinal syndrome. Doses ≥ 6 Gy cause acute vomiting several hours after exposure. The vomiting usually then stops, only to recur some 4 days later accompanied by diarrhoea. The villous lining of the intestine becomes denuded. Intractable bloody diarrhoea follows, with dehydration, secondary infection and sometimes death.
• CNS syndrome. Exposures of ≥ 30 Gy are followed rapidly by nausea, vomiting, disorientation and coma. Death due to cerebral oedema can follow, usually within 36 hours.
• Radiation dermatitis. Skin erythema, purpura, blistering and secondary infection occur. Total loss of body hair is a bad prognostic sign and usually follows an exposure ≥ 5 Gy.

Late effects of radiation exposure

Risks of acute myeloid leukaemia and cancer, particularly of skin, thyroid and salivary glands, increase. Infertility, teratogenesis and cataract are also late sequelae, developing years after exposure.

For the sequelae of therapeutic radiation — early, early-delayed and late-delayed radiation — see p. 256).

Treatment

Prevention and treatment of infection, haemorrhage and fluid loss are the mainstays of treatment.

Accidental ingestion of, or exposure to, bone-seeking radioisotopes (e.g. 90strontium and 137caesium) is treated with chelating agents, e.g. EDTA and massive doses of oral calcium. Radio-iodine contamination should be treated immediately with potassium iodide to block radio-iodine absorption by the thyroid.

Electric shock

• The common domestic electric shock is typically painful, and is rarely fatal or followed by serious sequelae. More serious effects are rare following accidents in the home or in industry.
• Ventricular fibrillation, muscular contraction and spinal cord damage can follow a major shock. These are typically seen following lightning strikes with exceedingly high voltage and amperage.
• Non-fatal lightning strikes can cause fern-shaped burns. Deeper injuries can also occur, with muscle and spinal cord damage.

Bioterrorism/biowarfare

The potential of bacteria as weapons is illustrated by a suggestion that several kilograms of anthrax spores might kill as many people as a Hiroshima-sized nuclear weapon.

Potential pathogens

The US Centers for Disease Control in Atlanta, Georgia, have developed a classification of potential biological agents (Table 19.1).

Table 19.1 Critical biological agents

Category Pathogens
A — Very infectious and/or readily disseminated organisms: high mortality with a major impact on public health Smallpox, anthrax, botulism, plague
B — Moderately easy to disseminate organisms causing moderate morbidity and mortality Q fever, brucellosis, glanders, food-/water-borne pathogens, influenza
C — Emerging and possible genetically engineered pathogens Viral haemorrhagic fevers, encephalitis viruses, drug-resistant TB

(From Khan AS, et al 2000, with permission)

Smallpox

Smallpox is a highly infectious disease with a mortality ≥ 30%. There is no proven therapy but there is an effective vaccine. Universal vaccination was stopped in the early 1970s, with the result that most of the world’s population is now unprotected.

Smallpox has an incubation period of around 12 days; the rash develops on the second or third day of the illness. Infection is transmitted by the airborne route; the patient becomes infectious to others 12–24 hours before the rash appears, thus allowing a potential infected volunteer to pass infection to others before being recognized as suffering from smallpox.

Anthrax

In late 2001, 22 individuals who were sent anthrax organisms through the US mail were infected; 11 developed pulmonary anthrax; 5 died despite ciprofloxacin therapy. The other 11 suffered from cutaneous anthrax.

Botulism

As a bioweapon, botulinum toxin could be transmitted in food or by air, e.g. from a crop-spraying light aircraft. The toxin is inactivated by chlorine in domestic water supplies. There is no vaccine available.

Plague

Plague (p. 38) could be transmitted as a bioweapon, either by airborne dissemination or by infected rats. Immunization is of limited value.

Further reading

Buchler JW, Berkelman RL, Hartley DM. Syndromic surveillance and bioterrorism-related epidemics. Emerg Infect Dis. 2003;10:1197-1204.

Khan AS, Morse S, Lillibridge S. Public-health preparedness for biological terrorism in the USA. Lancet. 2000;356:1179-1182.

Lazar HL. Editorial: The treatment of hypothermia. New Engl J Med. 1997;337:1545-1547.

Modell JH. Drowning. New Engl J Med. 1993;328:253-256.

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