Late-onset intermediate syndrome due to organophosphate poisoning

Late-onset intermediate syndrome due to organophosphate poisoning

To the Editor:

The intermediate syndrome (IS) is characterized clinically by weakness in the proximal limb muscles, the flexor muscles of the neck, and/or respiratory muscles (1). It has been reported that IS can develop within first 96 hours of acute organophosphate poisoning (OP) (1,2). To the best of our knowledge, there is no reported case of IS developing over 96 hours after OP exposure.

A 46-year-old male patient was admitted to our emergency service with respiratory failure eight hours after ingesting methamidophos. The patient had no history of any significant illness. On admission, the patient had a blood pressure 90/70 mmHg, heart rate 96 beats/minute, and respiratory rate 5 breaths/minute. His initial Glasgow Coma Score was 3/15. There were rales and ronchi. Initial pseudocholinesterase concentration (PCC) was 172 U/L (3600 to 12900 U/L); other laboratory findings were normal.

The patient was transferred to the emergency intensive care unit for observation. He was intubated and received atropine and pralidoxime (400 mg/hour IV for eight days) in addition to general supportive measures. Nine hours after admission (17 hours post-ingestion), the patient was alert and hemodynamically stable, had adequate spontaneous respiration, and was extubated. While under observation, he developed weakness in the muscles of the neck, face and extremities, and diarrhea 114 hours post-ingestion. He then developed dyspnea with intercostals retractions but without rales or rhonchi. The PCC at that time was 2444 U/L. The clinical picture was consistent with IS and lasted six days. With additional supportive care, our patient recovered completely and was discharged from hospital on day 11 with a PCC of 4868 U/L.

The IS probably results from post-synaptic neuromuscular junction dysfunction (3), manifests with prolonged depression of cholinesterase (4,5), and occurs at 24 to 96 hours post-ingestion (1,2). The most important initial sign of IS is respiratory failure (1–5). The muscle weakness begins at first in the extremities, the neck, the eyes, and the respiratory system (6). In our case, there was weakness in the muscles of the neck, face, extremities and respiratory system.

There are numerous theories of the etiology of IS, such as inadequate or initiated late oxime therapy, and the persistence of organophosphate in the body (3–5). In the present case, we believe that the patient received adequate oxime therapy according to typical dosing guidelines. On the other hand, it has been reported that IS is related to the severity of poisoning and some varieties of organophosphates (methamidophos, dimethoate) (1,7). Our patient was exposed to methamidophos and exhibited a severe poisoning. Methamidophos is highly lipophilic and persists in the fat stores, which may lead to re-inhibition of cholinesterase (1). When IS developed in our case, PCC was 67% of normal minimum value (2444 U/L).

Both the clinical and electromyography features of the IS suggest dysfunction of neuromuscular transmission (7). In our case, electromyography was not available.

We think that IS may develop more than 96 hours after OP. Therefore, patients, particularly those with severe poisonings, should be observed closely over 96 hours after OP for probable IS.

Notes

*Presented at the 3rd Mediterranean Emergency Medicine Congress, September 1–5, 2005, Nice, France.