Q J Med 2004; 97: 75-80
© Association of Physicians 2004; all rights reserved.
Secondary contamination in organophosphate poisoning: analysis of an incident
From Southampton General Hospital, Tremona Road, Southampton, UK, and 1Ealing Hospital, Uxbridge Road, Southall, Middlesex, UK
Received 24 July 2003 and in revised form 21 November 2003
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Summary |
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Background: Acute organophosphate poisoning is rare in the UK, and the risks to attending staff are seldom appreciated.
Study design: Report of an incident.
Results: In May 2001, a 45-year-old man attempted suicide by drinking organophosphate insecticide, and was brought to an urban general hospital in a collapsed state. Twenty-five hospital workers and paramedics sought medical advice after coming into contact with the poisoned patient, of whom ten complained of symptoms related to toxin exposure. Provision of emergency services by the hospital was compromised, and the emergency department was closed until the area was decontaminated and staffing levels could be restored.
Discussion: Ingestion of OP compounds can present a significant risk to health professionals as well as patients. Problems with the management of this patient included late recognition of the need for decontamination, large numbers of non-essential staff coming into contact with the patient, and the difficulty of carrying out medical procedures while wearing protective equipment. Decontamination should always be considered early, and the possibility of an ingested poison being vomited and causing a chemical spill should not be overlooked.
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Introduction |
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Organophosphate (OP) compounds are used principally as pesticides (in agriculture, horticulture, veterinary medicine and human medicine), and have also been developed as chemical warfare agents. There are over 50 000 OP compounds, formulations being tailored to their intended use.1 Their toxic effects, whether from occupational exposure, accidental poisoning, intentional ingestion, or acts of terrorism or warfare, are associated with significant morbidity and mortality.2–5
The incidence of deliberate ingestion of OP is considerably higher in the developing world than in the West and appears to be rising, with ease of access and socio-cultural factors both playing important roles in the choice of OP as a poison.3,6 The incidence of deliberate ingestion appears to be higher in young people and those with lower socio-economic status.3,6–8 Deliberate ingestion commonly leads to severe poisoning and poor outcomes, placing a heavy burden on intensive care resources, particularly where such resources are scarce.3
We report an incident where failure to recognize OP ingestion as a chemical incident with potential for widespread contamination led to delayed decontamination, risk to hospital workers, morbidity amongst medical staff and severe disruption of hospital services.
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The incident |
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In May 2001, a 45-year-old man ingested an unknown quantity of an insecticide, while on his allotment. Family members who were present called an ambulance.
Paramedics arrived on the scene 11 min after the call; by this time, the patient was hypersalivating, his heart rate was 60 bpm, blood pressure was 110/67, pupils were constricted and Glasgow Coma score was 3/15. He was intubated and ventilated by the paramedic team.
No decontamination was undertaken at the scene. Paramedics wore no special protective clothing other than latex gloves. Retrieval was prolonged by the awkward terrain. Total transfer time from scene to hospital was 60 min. The patient vomited in the ambulance, and was given intravenous fluid and naloxone. A priority call was put through to the hospital from the ambulance service to warn that a patient who had been ‘drinking red wine and plant poison’ was arriving. Although the bottle containing the insecticide was available, its labelling was in a foreign language, and was unintelligible.
The National Poisons Information Service (NPIS) was contacted in advance of the patient's arrival. A presumption that the insecticide could be an OP was made, and advice was given regarding bowel decontamination and the use of atropine, pralidoxime and diazepam. However hospital staff were not warned of the potential for secondary contamination.
On arrival in the Emergency Department (ED), the patient's airway required a great deal of suction, and the endotracheal tube was repositioned. A foul smell was noted from the time of the patient's arrival and there was vomitus on his clothing.
The patient was treated with intravenous atropine (boluses of 1–3 mg) and sodium bicarbonate; a nasogastric tube was passed, and gastric lavage was followed by activated charcoal. Pralidoxime was requested, but was not available for several hours. The patient had a brief loss of cardiac output, which responded to further doses of atropine. Intravenous fluids were continued, and noradrenaline was commenced approximately 4 h after arrival. Although no seizure activity was noted, 4 mg midazolam was required 2 h after arrival to settle a period of restlessness.
Approximately an hour after the patient's arrival, further advice was received from the NPIS to limit staff contact with the patient, for staff to wear protective clothing, and for fresh air ventilation to be increased (windows were opened). From this point, theatre gowns, face-masks with visors, and gloves were donned by staff, and access to the resuscitation room was limited.
The patient was then fully decontaminated by removing all his clothes and washing him with soap and water. In the course of resuscitation, full protective suits with self-contained ventilation were used by the attending medical doctors, but proved too cumbersome to allow medical procedures to be carried out. Those who had been in contact with the patient were restricted from moving around the hospital freely, because of increasing fears of further spreading the effects of the organophosphate. Several staff members started complaining of symptoms of chest tightness and light-headedness.
Approximately 2 h after the arrival of the patient, the ED was closed because of concerns of secondary contamination, and because the concentration of hospital medical staff in the ED left other services under-resourced. The ED remained closed until the next morning.
The Chemical Incident Response Service attended the hospital, to coordinate a review of the affected staff and to ensure adequate decontamination of the environment. The clothing of staff that had been in direct contact with the patient was removed and destroyed.
Hospital staff and paramedics who had come into contact with the patient were examined for evidence of toxicity by senior doctors. Seven of the ten staff who reported symptoms related to the incident complained of chest tightness or discomfort. Twenty-five staff members presented for examination. Of these, two were observed for up to 4 h (anaesthetic registrar and SHO), eight complained of symptoms and were discharged without any monitoring or intervention, and one had an incidentally abnormal ECG but no clinical signs of poisoning. None was judged to have been poisoned and none required pharmacological treatment (Tables 2 and 3).
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The patient was transferred to the intensive care unit. His plasma cholinesterase level reached a low of 0.1 kU/l (N > 1.4), and erythrocyte cholinesterase level dropped to 3.3 kU/l (N > 14). He survived with normal neurological status, having spent 24 days on the ICU.
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Discussion |
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Organophosphates act by inhibiting cholinesterase enzymes. Clinical effects of acute poisoning are due to over-stimulation by accumulated acetylcholine, followed by disruption of transmission at cholinergic synapses both centrally and peripherally. Effects can therefore be considered to be muscarinic, nicotinic or direct central nervous system effects (Table 1).2
OPs are generally highly lipid-soluble and are well absorbed from the skin, oral mucous membranes and conjunctiva, and by gastrointestinal and respiratory routes. The onset, severity and duration of poisoning is determined by the degree and route of exposure, the lipid solubility and rate of metabolism of that particular compound, and whether metabolism in the liver is required before the compound is active. The onset of clinical effects may be from 5 min to 24 h post exposure.2
The principles of treatment are: protection of the rescuer by protective clothing, eye shields and breathing apparatus, termination of exposure, decontamination, support of vital functions, and the administration of antidotes. The muscarinic antagonist atropine may be needed in high doses. Diazepam is used for controlling muscle twitching and convulsions. The antidote pralidoxime acts by splitting the phosphate–acetylcholinesterase bond and regenerating active acetylcholinesterase.
Following recovery from the acute phase of poisoning, some patients develop the intermediate syndrome of muscle weakness, which is refractory to atropine and pralidoxime, and is reversible over days or weeks.2,6 A variety of chronic neurological effects due to acute or chronic exposure have been described. These may last months or even years.2,6,9,10
Secondary contamination
The phenomenon of health workers and rescuers who care for patients with OP poisoning developing signs of toxicity themselves has been described in case reports of intentional ingestion of OP pesticides11 and in reports of terrorist attacks using gaseous OP agents.5,12 Secondary exposure of 15 doctors in Tokyo treating two victims of the 1995 sarin attack led to symptoms of dim vision, rhinorrhoea, chest tightness and cough in 13. Six of these required atropine treatment, one also required pralidoxime. After limited decontamination by room ventilation and sealing patients’ clothes, symptoms did not progress.13
In Georgia a case of intentional ingestion of OP resulted in one carer requiring ventilation and another requiring pralidoxime: in this incident, no decontamination was performed.11 Other incidents of chemical exposure where decontamination was not carried out have also resulted in secondary contamination of ED staff.14 This risk should therefore be of prime consideration when treating these patients.
The response to this case highlights the difficulty that health professionals have in dealing with an unfamiliar situation when the risks they face are not well understood, while the patient is seriously unwell and in need of urgent attention.
Recognition of OP as a likely cause of the poisoning was made before the patient arrived at the ED, following a phone call from the ED to the NPIS. Definitive airway management was provided rapidly in the pre-hospital setting, and on arrival in the ED treatment with atropine and supportive measures was immediately available. However in the hour it took to get the patient from the scene to the hospital, and for at least one hour after arriving in the ED, hospital staff and paramedics failed to appreciate the need for decontamination and the potential danger of secondary contamination. It is worth noting therefore that had decontamination been considered early, there would probably have been time to do so without compromising the patient‘s eventual outcome.
Decontamination
The OP contamination was internal until the patient vomited, and from then on can be regarded as a chemical spill. With hindsight this could have been anticipated, to prevent further dermal or inhalational contact. Recommendations include removal of clothing and placement, along with secretions and gastric contents, in sealed containers, thorough washing of the patient's skin, and isolation of the ED ventilation system from the main hospital ventilation system. Early decontamination, by washing the patient vigorously and repeatedly with soap containing 30% ethanol (high pH hydrolyses OPs in aqueous solution) and plenty of warm water is an essential part of patient management to prevent further patient contamination and secondary contamination of staff.15 Eyes should be irrigated for 15 min with water or saline. This should be carried out in a dedicated decontamination room or outside the hospital with staff wearing level C protection suits (i.e. full face mask and canister or cartridge filtration respirator) or level B (self-contained breathing apparatus), depending on the extent of contamination.11 Rescuers, such as ambulance and medical staff, should not enter a contaminated area without full personal protective equipment (PPE) and self-contained breathing apparatus.2
This particular OP compound was demeton-s-methyl which smells of rotten cabbage (V. Murray, personal communication). This is a poorly volatile compound, but exposure may occur via inhalation of the aerosol.
Gut decontamination with gastric lavage is most effective in the first 30 min of ingestion. Oral charcoal may also limit further absorption.15
Spills of organophosphate should be dealt with while wearing PPE by absorbing the spilled liquid with a mixture of 1:3 sodium carbonate crystals and damp sawdust (or lime, sand or earth). This mixture is then swept up and placed in a sealed container pending safe disposal.2
Once effective dermal and gut decontamination are achieved and adequate ventilation has been established, the patient may be considered safe from causing secondary contamination.
The use of PPE raises questions as to the extent to which resuscitation can accompany decontamination. Given the cumbersome nature of the protective suits, it was not possible to carry out practical procedures while wearing them. In this case the airway had been secured at the scene of the incident, and hospital resuscitation was underway before any consideration was given to PPE.
While awareness of the need for decontamination is prerequisite in such cases, availability of decontamination facilities varies across the UK. In a recent survey of decontamination facilities in A&E departments in the UK, 26% had no decontamination facilities. Only 24% had ‘satisfactory’ facilities (with separate dirty and clean entrance and exit, separate air circulation, and the possibility to seal the area).16 There has been little change since a similar survey 2 years previously of six English health regions, which found that 23% had no decontamination facilities and only 10% had both decontamination facilities and adequate PPE.17 However, there has probably been dramatic improvement to these figures in the light of recent efforts to increase preparedness for terrorist attacks.
Conclusions
While uncommon in the UK, ingestion of OP compounds can present a significant risk to health professionals as well as patients. Early airway management, gut decontamination and supportive treatment resulted in the survival of this patient. Acute morbidity amongst staff was mild, and none was considered poisoned, despite delays in attending to decontamination and personal protection. Symptomatic staff were not followed-up, and their cholinesterase levels were not measured. Problems with the management of this patient included late recognition of the need for decontamination, large numbers of non-essential staff coming into contact with the patient, and the difficulty of carrying out medical procedures wearing PPE. Decontamination should always be considered early, and the possibility of an ingested poison being vomited and causing a chemical spill should not be overlooked. In this case emergency services throughout the hospital were disrupted and the closing of the emergency department had a considerable knock-on effect on neighbouring hospitals. Earlier recognition of potential problems, greater familiarity with chemical incident procedures and focussed deployment of staff would have attenuated the secondary effects on staff and the logistical consequences for the hospital as a whole.
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Acknowledgments |
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The authors would like to acknowledge the advice and assistance of Dr Virginia Murray, Director of the Chemical Incident Response Service at Guy's and St Thomas's Hospital Medical Toxicology Unit.
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Footnotes |
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Address correspondence to Dr D. Morfey, Ealing Hospital, Uxbridge Road, Southall, Middlesex UB1 3HW, UK. e-mail: DMorfey{at}aol.com
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References |
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17. Horby P, Murray V, Cummins A, Mackway-Jones K, Euripidou R. The capability of accident and emergency departments to safely decontaminate victims of chemical incidents. J Accid Emerg Med 2000; 17:344–7.
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