Major component causing neurological toxicity in acute glufosinate ammonium poisoning: determination of glufosinate, 1-methoxy-2-propanol, and ammonia in serum and cerebrospinal fluid.

OBJECTIVE

To determine the primary contributor to neurotoxicity in patients with glufosinate ammonium (GLA) poisoning, by quantifying glufosinate, 1-methoxy-2-propanol, and ammonia in serum and the cerebrospinal fluid (CSF).

MATERIALS AND

METHODS

We collected and analysed data from confirmed cases of GLA poisoning between May 2018 and August 2020. Based on the occurrence of neurological complications (mental change, seizure, and central apnoea), patients were assigned to one of two groups: those with complications (NCx) and without (non-NCx) complications. Concentrations of glufosinate, 1-methoxy-2-propanol (1M2P), and ammonia were measured in the serum upon admission and during hospital stay. The concentrations of all these substances were again measured in the CSF following a decline in the mental status or seizure (NCx group) or on the day after hospitalisation (non-NCx group).

RESULTS

Of the 20 patients included, ammonia levels in the serum and CSF at onset of altered sensorium in the NCx group (n = 16) were significantly higher than those at one day after hospitalisation in the non-NCx group (n = 4) (p = 0.011 in serum, p = 0.047 in CSF), with its concentration in the CSF being higher than that in the serum in 15/16 cases. The concentration of 1M2P was similar in the serum and CSF (8/16), but the concentrations of glufosinate (7/16) was lower in the CSF than in the serum. In the non-NCx group (n = 4), only ammonia was detectable.

CONCLUSIONS

Among patients with GLA poisoning, increased CSF ammonia was significantly correlated with neurological complications.