Guidance

Health effects of explosions

Published 8 July 2005

If people involved in explosions start to develop symptoms they should contact NHS 111 or their GP for medical advice.

The immediate health effects of explosions include:

• Smoke inhalation
• Trauma and burns due to the force and heat of the blast
• Flying debris
• Worsening of pre-existing medical conditions as a result of acute physiological or psychological stress

1. Delayed health effects that can arise following exposure to chemicals in smoke

General guidance can be provided on the possibility of persistent or delayed health effects from exposure via inhalation to chemicals which are anticipated to be produced by explosions in underground tunnels ( ie through breathing in chemicals or burning of the respiratory tract or eyes by hot smoke).

It is very unlikely that any long term effects will occur if the individual had no significant acute respiratory tract, eye or other symptoms or signs at the time of probable exposure.

There is a possibility that longer-term effects on the eyes and lungs could occur as a consequence of the severe irritant effects of some of the compounds produced by combustion.

The likelihood of this happening is minimized if prompt treatment is given to the casualty, but those who have serious lung damage at the time of exposure may develop respiratory tract problems that require longer-term medical management.

For a single acute exposure the increase in risk of developing such long-term effects is assessed as being very small relative to the other risks experienced in normal life.

These chemicals pose no inherently greater risk of long term effects for children or older people. In pregnancy it is extremely unlikely that these chemicals would affect an unborn child in a mother who has few symptoms. This does not discount the possibility of effects due to stress, direct trauma or other physical injuries to the mother, arising from the incident.

It is natural and normal that individuals involved in a serious, life-threatening event experience psychological reactions to the incident. Most of these will resolve with time as the individual recovers and returns to their normal life routine. Those whose symptoms persist should be assessed and advised on treatment by their GP.

If you develop symptoms then

• contact NHS 111 or your GP
• inform your occupational health unit if you were involved in an incident through their work (including emergency services, transport services, health professionals, recovery workers etc)

2. Acute effects of smoke inhalation

Exposure to dense smoke causes irritation of the eyes, mouth and air passages because of its physical, chemical and thermal properties. However the majority of symptoms disappear soon after removal from the smoky environment.

Very dense smoke reduces the oxygen supply to the brain and may cause drowsiness or unconsciousness. Individuals who have been exposed to smoke and who subsequently develop symptoms, particularly breathlessness within a few hours, should seek medical advice. In the majority of cases the normal clinical course will be recovery without complications.

The most usual chemicals in smoke are carbon monoxide, oxides of nitrogen and sulphur. There was no evidence that the smoke associated with the London bombings contained any unusual chemicals.

2.1 Toxicity

Toxicity may occur as a result of thermal injury, direct bronchopulmonary toxins or systemic toxins.

2.2 Thermal injury

Thermal injury is more common in the upper airways causing mucosal damage with erythema, ulceration and oedema. Clinical features include blistering or oedema of the oropharynx and soot deposits in the nose or mouth. Stridor, dyspnoea and respiratory distress are late features, often developing several hours after thermal injury. Upper airway oedema usually becomes apparent within 24 hours of injury and resolves within 3 to 5 days.

Prognostic markers for patients at risk of thermal airway injury include

• fires occurring in enclosed spaces
• death of another person involved in the same fire
• loss of consciousness on scene
• presence of facial burns and soot deposits in the mouth or nose

An initial chest X-ray is often normal but the presence of pulmonary infiltrates is associated with a poor prognosis.

2.3 Lung toxins

Some of the toxins present in smoke may form free radicals, which are directly toxic to the bronchial mucosa causing airway inflammation. Clinical features include cough, breathlessness, wheeze and excess bronchial secretions. These features typically occur 12 to 36 hours after exposure. Adult respiratory distress syndrome may occur in severe cases.

2.4 Systemic toxins

Smoke inhalation may lead to absorption of systemic toxins, the commonest of which are carbon monoxide and hydrogen cyanide.

Carbon monoxide affects the oxygen carrying capacity of haemoglobin and cyanide inhibits aerobic metabolism. Hydrogen cyanide is released during combustion of materials such as polyurethane, nylon and acrylonitrile. Cyanide poisoning is often difficult to diagnose, particularly if carbon monoxide poisoning is also present.

Although generally there is a good correlation between cyanide and carboxyhaemoglobin concentrations, victims of smoke inhalation may develop significant cyanide poisoning without a significantly elevated carboxyhaemoglobin concentration.

Plasma lactate measured at the time of admission has been shown to correlate more closely with cyanide toxicity than carboxyhaemoglobin concentration. A highplasmalactate(>10.0 mmol per L) in the absence of severe burns or hypotension appears to be a good indicator of cyanide toxicity (Baud and others, 1991).

2.5 Management

1. Give high flow humidified oxygen to all patients. If the patient has chronic obstructive pulmonary disease with CO 2 retention or if hypercapnia is secondary to coma and respiratory insufficiency, immediate intubation and ventilation is necessary.
2. Immediate intubation should be carried out if there is stridor or respiratory distress. Also consider immediate or early intubation if there are facial or neck burns, erythema, blistering or oedema of the oropharynx. It is often better to electively intubate at this stage than try and perform an emergency intubation several hours later when the upper airway may be extremely oedematous.
3. If there are any signs of thermal injury to the face/oropharynx, patients must be monitored closely for 24 hours in a facility where emergency airway care can be provided if required.
4. Perform arterial blood gases and check carboxyhaemoglobin concentration and lactate concentrations.
5. Perform chest X-ray
6. Nebulised bronchodilators may be of benefit if bronchospasm present.
7. Corticosteroids are not of proven benefit.
8. If lactate concentration > 10 mmol/L in absence of significant burns and after correct of hypotension consider the possibility of cyanide poisoning.

3. Carbon monoxide (CO): features and management

Carbon monoxide causes problems in the delivery of oxygen to the brain, but unless individuals are unconscious, or suffer significant drowsiness while exposed to smoke containing this gas, long-term effects are unlikely. Early symptoms may include dizziness, headache and nausea with drowsiness. In most cases, these symptoms will disappear soon after exposure ceases. Patients who have had significant symptoms should be assessed by a GP.

3.1 Immediate features

Headache, nausea, irritability, weakness and tachypnoea followed by dizziness, ataxia, agitation, impairment of consciousness and respiratory failure. Cerebral oedema and metabolic acidosis may develop in serious cases.

Less common features include skin blisters, rhabdomyolysis, acute renal failure, pulmonary oedema, myocardial infarction, retinal haemorrhages, cortical blindness, choreoathetosis, and mutism.

3.2 Late features

The majority of people exposed to carbon monoxide recover uneventfully but others develop neuropsychiatric features after periods of several weeks free of symptoms.

These delayed features are more common in those over the age of 40 years and include memory impairment, disorientation, apathy, mutism, irritability, inability to concentrate, personality change, Parkinsonism and parietal lobe lesions. Urinary and/or faecal incontinence and gait disturbance are common.

Fortunately, the great majority recover completely or to a considerable extent within a year.

3.3 Chronic CO poisoning

Chronic carbon monoxide poisoning is frequently undiagnosed since the features are non specific. It is often associated with the use of faulty gas heaters in unventilated areas and therefore occurs more commonly in the winter months.

Features include headache, nausea and flu-like symptoms. The diagnosis should be considered particularly if there are other members of the same house experiencing similar symptoms.

3.4 Indication of severity

One or more of the following:

• any new objective acute neurological signs eg increased tone, upgoing plantars
• coma
• need for ventilation
• ECG indication of infarction or ischaemia
• clinically significant acidosis
• initial carboxyhaemoglobin > 30%

Note that the link between carboxyhaemoglobin level and outcome is weak

3.5 Management

1. Remove from exposure.
2. Maintain a clear airway and adequate ventilation.
3. Give oxygen in as high concentrations as possible.
4. Metabolic acidosis should be corrected by increasing oxygen delivery to the tissues. The use of intravenous sodium bicarbonate may make this more difficult and is, therefore, best avoided.
5. Give mannitol 1g per kg intravenously over 20 minutes if cerebral oedema is suspected.
6. Monitor the heart rhythm.
7. Measure the carboxyhaemoglobin concentration as an emergency. A carboxyhaemoglobin percentage of 30% indicates severe exposure. However, concentrations less than this do not exclude significant poisoning and the relationship between carboxyhaemoglobin and severity of poisoning and/or clinical outcome is poor.
8. In patients who have been unconscious look for extrapyramidal features and retinal haemorrhages to assess the severity of CNS toxicity.
9. The role of hyperbaric oxygen therapy has been controversial. However, a recent large double blind trial has shown benefit in patients with loss of consciousness, CNS features of poisoning, cardiac ischaemia or metabolic acidosis (Weaver, 2002). These patients were treated with hyperbaric oxygen on 3 occasions in 24 hours, the first treatment being given on average within 5.8 hours of exposure. Patients were not entered beyond 24 hours of exposure. It is uncertain how quickly hyperbaric oxygen needs to be given in light of another study which shows lack of benefit when hyperbaric oxygen was started later than in this series (a mean of 7.3 hours after exposure). In the latter series, patients received treatment daily for 3 days (Scheinkestel, 1999).

Hyperbaric oxygen therapy should only be considered if there is easy and rapid access to a suitable hyperbaric chamber. The NPIS directors do not support transfer over long distances for small clinical benefit.

You should discuss the possibility of using hyperbaric oxygen with your local poisons service: in the UK NPIS 0870 600 6266, in Ireland NPIC (01) 809 2566, if your patient is severely poisoned (as described).

4. Corrosives: inhalation

4.1 Features

Irritation of eyes and nose with sore throat, cough, chest tightness, headache, ataxia and confusion. Dyspnoea and stridor due to laryngeal oedema may follow. Pulmonary oedema with increasing breathlessness, wheeze, hypoxia and cyanosis may take up to 36h to develop.

4.2 Management:

1. Remove from exposure and give oxygen.
2. Maintain a clear airway and adequate ventilation.
3. Perform a chest X-ray if symptomatic.
4. If the patient has clinical features of bronchospasm treat conventionally with nebulised bronchodilators and steroids.
5. Treat pulmonary oedema with continuous positive airway pressure (CPAP) or in severe cases with IPPV and PEEP.
6. The role of prophylactic corticosteroids (inhaled or systemic) and antibiotics is controversial.
7. Antibiotics will be required if pneumonia develops.
8. Endotracheal intubation, or rarely, tracheostomy may be required for life-threatening laryngeal oedema.
9. Other measures as indicated by the patient’s clinical condition.

5. Oxides of nitrogen

5.1 Features

Symptoms may be delayed for 1 to 5 hours after inhalation.

Brief exposure to low concentrations causes only slight coughing, nausea and fatigue. In more severe cases vomiting, tachycardia, coughing with bloody sputum, dyspnoea, chest pain, bronchospasm, lasryngospasm and respiratory arrest may occur.

Cyanosis, methaemoglobinaemia and pulmonary oedema may occur in symptomatic patients and may be delayed up to 24 to 36 hours.

2 to 3 weeks later there may be delayed bronchiolitis.

Skin contact with compressed gas may cause frostbite.

Eye contact with vapour may cause conjunctival irritation, lacrimation and burns. Eye contact with the liquid may cause severe burns.

5.2 Management

1. Remove from exposure and give oxygen.
2. Maintain a clear airway and adequate ventilation.
3. Patients with significant exposure should be observed in hospital for 24 to 36 hours.
4. Perform a chest x-ray if symptomatic.
5. If the patient has clinical features of bronchospasm treat conventionally with nebulised bronchodilators and steroids.
6. Treat pulmonary oedema with continuous positive airway pressure (CPAP) or in severe cases with IPPV and PEEP.
7. There is no good evidence that prophylactic corticosteroids (inhaled or systemic) and antibiotics are of benefit.
8. Antibiotics will be required if pneumonia develops.
9. Ventilation may be necessary if respiratory depression occurs.
10. Check for methaemoglobinaemia if cyanosis is present and give methylene blue if indicated.
11. Other measures as indicated by the patient’s clinical condition.
12. Patients who have shown early respiratory features should be reviewed 2 to 3 weeks after exposure to check for bronchiolitis obliterans.