https://orcid.org/0000-0003-3608-144X
Abstract
Introduction
Controversy exists with regard to risk of secondary exposure of health care workers caring for patients who have ingested an organophosphate insecticide. We aim to report clinical effects of staff members caring for an organophosphate poisoned patient.
Incident
A 76-year-old male presented to the Emergency Department exhibiting a cholinergic toxidrome requiring atropine, intubation and mechanical ventilation.
Methods
We undertook a retrospective chart review of any Emergency Department presentations for medical assessment in relation to the incident and conducted telephone interviews of any healthcare workers who did not present but were deemed to be closely involved with patient care. We collected data including age, gender, symptoms reported and plasma cholinesterase activity measurement.
Results
We collected data from 13 individuals, of whom nine presented for medical assessment, including the patient’s spouse. Five additional staff members were interviewed, having been identified via Emergency Department rostering documentation. The 13 healthcare workers comprised five nurses, four paramedics and four doctors. Dizziness and nausea were reported in two and the patient’s spouse reported one episode of vomiting. Of the nine patients who had plasma cholinesterase activity measured, none were below the laboratory reference range, including those who experienced symptoms.
Conclusions
We found no clinical nor biochemical evidence of toxicity in healthcare workers caring for a critically ill patient with organophosphate ingestion. These findings are consistent with previously published guidelines advocating standard/Level D personal protective equipment. We believe that emergency departments should not be closed as a safety measure.
Introduction
Poisoning with organophosphate (OP) insecticides is an uncommon presentation to Emergency Departments (ED) in Australia, in contrast with low, middle-income countries [Citation1,Citation2]. Organophosphates inhibit cholinesterase enzymes at nicotinic and muscarinic neuromuscular junctions [Citation3] resulting in a number of clinical features including miosis, bradycardia, respiratory failure, excessive salivation and sweating [Citation4].
Treating ED and prehospital staff often perceive OP ingestion as posing a significant risk of secondary exposure potentially leading to toxic effects in treating health care workers [Citation5]. As a result, overly cautious approaches are utilised such as aggressive external decontamination and ED closure/diversion of patients elsewhere. Evidence for this approach is lacking and could lead to delayed patient assessment and management with subsequent negative effects on patient care. Additionally, ED closure and diversion may potentially lead to similar consequences for other patients [Citation6].
A review of secondary effects of chemical exposure on health care workers concluded from the amount of data available currently, that OP ingestion does not appear to represent significant secondary exposure risk [Citation7]. We aim to report the effect on an ED of a confirmed OP ingestion presentation and health care worker experiences of secondary exposure effects including measurement of plasma cholinesterase activity.
Incident
A 76-year-old male with dementia was transported to an urban ED following ingestion of a fig from a group he had previously injected with pesticide to prevent consumption by birds. The pesticide was in an unlabelled container, thus unable to be identified.
He initially complained of abdominal pain and was incontinent of urine and faeces. Respiratory rate (RR) was 24 breaths per minute, heart rate (HR) 118 beats per minute, blood pressure (BP) 140/45, SpO2 96% with no supplemental oxygen, and lungs clear to auscultation. He rapidly deteriorated prior to ED arrival with HR 46 beats per minute, RR 36 breaths per minute, audible crepitations, and SpO2 94%. At this point, the four attending paramedics, two transporting and two following as back up, initiated bag valve-mask ventilation with 15 L oxygen.
Staff involved noted a pungent odour from the patient as personal protective equipment (PPE) including eyewear, facemasks, gowns and gloves was donned. He received 1.2 mg atropine to control respiratory secretions before intubation for respiratory distress followed by activated charcoal administration via nasogastric tube.
He was transferred to the intensive care unit but required no further atropine overnight. The following day he was extubated and transferred to a general ward. He was discharged three days post presentation.
Plasma cholinesterase (butyrylcholinesterase) activity on presentation was 0.54 U/mL (reference range 4.39–10.90). A urine specimen analysed for OP metabolites quantified a dimethyl phosphate concentration of 219 μmol/L.
Due to concerns in regard to secondary exposure, several other measures were implemented following discussion with hospital administration. These included the relocation of patients from a group of six beds adjacent to the resuscitation room to a more physically distant location within the ED. Provision was made to keep these beds free whilst resuscitative efforts were ongoing via an arrangement for ambulance presentations to be re-directed to other hospitals within the local area health service. This arrangement was discontinued after a 2 h period.
Any health care workers concerned regarding possible secondary chemical exposure were encouraged to undergo a medical assessment, including measurement of plasma cholinesterase activity.
Methods
We subsequently undertook a quality assurance project to ascertain the occurrence of any secondary exposure effects. The electronic ED information system was used to identify any staff member, or other who presented for a medical assessment in relation to the incident. Review of the “shift report”, an internal document completed at the end of shift as part of hospital process, was used to identify staff closely involved with patient care but not presenting for medical assessment.
We contacted all staff members identified by phone and invited them to participate. Written consent was obtained to discuss the incident and clarify demographic details such as age and gender. Further questioning documented healthcare role (paramedic, doctor, nurse), any symptoms experienced deemed temporally related to the exposure, decontamination (showering), use of PPE (facemask, gown, gloves, protective eyewear) and subsequent absence from work. We extracted plasma cholinesterase activity details, if measured, from the medical record of those undergoing a medical assessment.
We reviewed the record of the patient ingesting the OP and one other non-staff member, his spouse, who also underwent a medical assessment, for demographic and clinical information.Footnote1
We entered all information into an Excel® (Microsoft, Redmond, WA) spreadsheet. The project was approved by the local health research ethics committee (AU202302-03).
Results
Nine individuals, eight health care workers and the spouse, presented to ED for assessment. Five individuals were identified from review of the shift report making a total of 14.
The 13 health care workers included five registered nurses, four doctors and four paramedics. Seven were male and median age was 35 years (range 23–63 years). One nurse experienced nausea and dull headache, whilst one of the paramedics, who treated the patient directly on scene, reported dizziness. No other symptoms were reported. The spouse vomited on one occasion after the incident. Reported PPE use included wearing gloves (13), eye protection (nine), face-masks (eight), and protective gowns (seven). Nine individuals reported showering and change of clothing following the incident. No health care workers were absent from duties as a result of their involvement beyond time involved in completing administrative tasks generated by the incident. Plasma cholinesterase activity was measured in all nine cases who had an ED assessment. None were below the laboratory reference range, including those who experienced symptoms ().
Table 1. Demographics and cholinesterase testing.
Discussion
Our observations support a 2004 consensus statement, on behalf of Australian poison centres medical consultants, recommending appropriate precautions whilst preventing over-zealous interventions that interfere with patient care [Citation6]. A review by De Groot et al. [Citation7] concluded that most cases of chemical poisoning pose minimal risk of secondary exposure to health care workers and rarely require higher than standard level PPE.
Geller et al. [Citation8] reported three health care workers who developed symptoms following involvement in the care of a critically ill ED patient secondary to OP ingestion. Of these, all three received atropine and two pralidoxime. One individual, who had contact with the patient’s skin, respiratory secretions and emesis, required intubation for 24 h. Criticisms of this incident were lack of PPE use by staff, no recorded external decontamination of the patient, and no measure of cholinesterase activity to substantiate significant exposure [Citation2,Citation7].
Stacey et al. [Citation5] reported a case of a patient presenting to ED following OP ingestion. Health care workers did not don PPE and did not undertake external decontamination until 1 h post-presentation on the advice of the poison centre. An additional decision was made that physicians don PPE including a self-contained ventilation apparatus, which makes medical procedures cumbersome, impacting on the ability to deliver care. The ED was closed overnight due to concern regarding secondary exposure. Following the incident, the authors followed up 25 health care workers of whom 10 complained of symptoms such as chest tightness and light headedness, with 15 cases asymptomatic. The authors concluded that no health care workers were considered poisoned, however, if a similar scenario recurred level C or possibly level B PPE should be used. Criticisms of the article included the over-zealous response, lack of cholinesterase testing and the dearth of evidence of secondary exposure occurring in developing countries where OP poisoning is much more common [Citation2].
Butera et al. described 14 of 15 health care workers reporting symptoms after caring for a critically ill patient who ingested malathion. The patient died 45 min after arrival to the ED. Staff did not don PPE during the resuscitation. Cholinesterase activity measured immediately after termination of resuscitation and again 4 h later found no abnormally low values [Citation6,Citation9].
Three of our cases reported symptoms similar to those reported by Stacey et al. [Citation5]. These were not consistent with a cholinergic toxidrome and could potentially be attributed to anxiety. Another plausible cause of non-specific symptoms is the unpleasant odour associated with the hydrocarbon solvent, a substantive component of OP formulations [Citation6].
In our case, as with that of Stacey et al., [Citation5] the ED was closed for a period of time. This unnecessarily denies access to appropriate and timely care to other patients [Citation7]. Such measures do not seem justified based on the evidence that risk of secondary exposure is low.
There are limitations relevant to our case including our findings being based on voluntary ED presentation and a presumption of accurate records of staff involved. We undertook a single measurement of cholinesterase activity and were also unable to identify the specific OP involved.
Conclusions
We found no clinical nor biochemical evidence of toxicity in health care workers caring for a critically ill patient with OP ingestion. These findings are consistent with previously published guidelines advocating standard/Level D personal protective equipment. We believe that emergency departments should not be closed as a safety measure.
Disclosure statement
No potential conflict of interest was reported by the authors.
Additional information
Funding
Notes
1 The patient’s wife gave consent on behalf of herself and the patient, due to his lack of capacity resulting from dementia.
References
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