We present the clinical case of a 67-year-old male, with a history of moderate-severe enolism, arterial hypertension and ischaemic heart disease, who was transferred to the Emergency Department from another centre where he had come 4 hours after ingestion of an OP (Metasystox®: oxydemeton-methyl) in an attempt at autolysis. At the centre of origin, he underwent gastric lavage and was given a dose of activated charcoal.
On arrival at the ED, the patient was conscious and oriented, hypotensive and bradycardic, with clear muscarinic manifestations: profuse sweating, sialorrhoea, abundant tear secretion, and diffuse colicky pain with nausea and vomiting. At the nicotinic level, there were no motor deficits but there was some perceptible fasciculation in both thighs. During his stay in the Emergency Department, the patient presented generalised myoclonus, miosis and desaturation with peripheral cyanosis, probably secondary to the fasciculations of the peripheral muscles and the diaphragm.
In view of the symptoms, joint treatment with atropine and pralidoxime (1 g over 30 minutes) was started, achieving an improvement in the peripheral symptoms, with a decrease in the number of fasciculations and disappearance of the abdominal cramps. A second dose of 25 g of activated charcoal and a bolus of intravenous diazepam were administered to control the convulsions.
Given the refractory nature of the seizures, orotracheal intubation was performed to protect the airway and treatment was started with pralidoxime (12 g/day) and atropine (20 mg/day), both in continuous infusion. Under these conditions he was admitted to the Intensive Care Unit (ICU), where he remained for 12 days. During the first 10 days post-intoxication, he continued with the treatment given in the emergency department, according to the doses specified in table I.
Until day 6 post-intoxication, the patient presented miosis and high peristalsis, and from this day onwards he manifested mydriasis and impaired tolerance to enteral nutrition as a consequence of the absence of peristalsis. This improves as the dose of atropine is reduced. However, reactive mydriasis persisted until discharge to the ward. Another symptomatology of the patient, characteristic of OP poisoning, is generalised myoclonus and thoracic muscle weakness. This weakness could also be a consequence of the sedation to which he is subjected due to his agitated state. By day 5 post-intoxication, isolated facial myoclonus is noticeable, still in the context of neurological symptoms.
Progressive recovery of limb strength begins on day 6 post-intoxication, and is complete by day 9. However, between these days, even under treatment with pralidoxime in continuous perfusion, the patient develops an IS with proximal and facial muscle weakness. This led to hypoventilation due to muscle fatigue.
As for the respiratory symptoms, which are critical in patients with OP poisoning, there is an episode of initial respiratory failure, which is subsequently corrected by keeping the patient on mechanical ventilation (MV) until 5 days after the poisoning. From this day on, gradual disconnections from MV begin, with the patient tending towards hypoventilation due to muscle fatigue. Improvement in respiratory function, although hampered by nosocomial tracheobronchiolitis due to H. influenzae, became apparent around day 8 post-intoxication. Despite psychomotor agitation, he tolerates MV disconnections allowing extubation one day after initiation. However, a tendency to hypoventilation persists throughout his stay in the ICU.
As a biomarker of exposure to the toxicant, plasma cholinesterase levels were assessed. The first measurement, carried out at 16 hours post-ingestion, showed a level of 13 ukat/L (reference range: 89-215 ukat/L). Its evolution can be seen in figure 1.