We report the case of a 67-year-old man with a history of moderate-severe enolism, ischemic heart disease and self-harm in an OP-Emergency Department from another center where he came 4 hours later.
A gastric lavage has been performed in the centre of provenance and an activated charcoal dose has been administered.
Upon arrival to the emergency department, the patient is conscious and oriented, hypotensive and oriented, with clear muscarinic manifestations: profuse nausea and vomiting sialorrhea, abundant tear secretion, and diffuse pain
At the nicotinic level, there is no motor deficit but some perceptible fasciculation in both thighs.
During his passage to the Emergency Department, the patient presents with generalized myoclonus, miosis and desaturation with peripheral tapering, probably secondary to fasciculations of the peripheral muscles and diaphragm.
Associated symptomatology was initiated with atropine and pralidoxima (1 g in 30 minutes), showing improvement of peripheral symptoms with decreased number of fasciculations and disappearance of abdominal cramping.
In addition, a second 25 g bolus of intravenous diazepam is administered to control seizures.
If these are refractory, orotracheal intubation is performed to protect the airway and treatment with pralidoxima (12 g/day) and atropine (20 mg/day) is initiated both in continuous infusion.
Under these conditions he is admitted to the Intensive Surveillance Unit (ICU), where he stays 12 days.
During the first 10 days post-intoxication, emergency treatment is maintained according to the doses specified in Table I.
Up to day 6 post-intoxication, the patient presents high miosis and peristalsis, and from this day manifests mydriasis and difficult tolerance to enteral nutrition due to the absence of peristalsis.
This improves by decreasing the dose of atropine.
However, reactive mydriasis persists until discharge.
Another patient's symptoms, characteristic of poisoning by OP, are generalized myoclonus and thoracic muscle weakness.
This weakness could also be a consequence of the sedation to which she is subjected by her agitation state.
Towards day 5 post-intoxication isolated facial myoclonus is noticeable, still in a context of neurological clinic.
Progressive recovery of limb strength starts on day 6 post-intoxication and is complete on day 9.
However, between these days, even under continuous infusion of pralidoxima, the patient develops SI with proximal and facial muscle weakness.
This conditions hypoventilation due to muscle fatigue.
As for the respiratory symptoms, critical in the poisoned by OP, she presents an episode of initial respiratory failure, corrected later to keep the patient under mechanical ventilation (MV) up to 5 days after intoxication.
From this day onwards, gradual discontinuation of MV is initiated, in which the patient tends to hypoventilate due to muscle fatigue.
The improvement of the respiratory function, although hampered by nosocomial bronchiolitis due to H. influenzae, manifests towards day 8 post-intoxication.
Despite psychomotor agitation, the patient tolerated withdrawal of MV that allowed extubation one day after starting it.
However, a tendency to hypoventilation persists throughout the ICU stay.
Plasma cholinesterase levels were evaluated as a biomarker of exposure to the toxic substance, whose first determination, performed 16 hours after ingestion, showed a level of 13 ukat/L (reference range: 89-215).
Its evolution can be seen in Figure 1.
