“Hyperammonemia following glufosinate-containing herbicide poisoning: A potential marker of severe neurotoxicity” by Yan-Chido Mao et al., Clin Toxicol (Phila) 2011; 49:48–52

To the Editor:

We read the article by Mao et al. on hyperammonemia following glufosinate-containing herbicide poisoning with interest.¹ We wish to report a further 13 cases of poisoning with the ammonium salt of glufosinate (Basta^® 18.5%) and comment on the predictive value of hyperammonemia (Table 1). Among our 13 patients, 7 had severe neurotoxicity, including coma (GCS of under 8), respiratory failure requiring intubation, and seizures, which lasted from 9.5 to 18 h post-ingestion. Of these seven patients, four had generalized tonic-clonic seizures preceded or followed by coma or respiratory failure. All patients with glufosinate-related severe neurotoxicity had amnesia during the recovery phase (Table 1).

Table 1. Characteristics of 13 patients with glufosinate-containing herbicide poisoning.

					Glufosinate-related severe neurotoxicity			Ammonia levels (20–80 ug/dL)
No.	Sex/age	Ingested amounts (mL)	Time to hospital arrival	GCS	Symptoms	Onset	Amnesia	1	Sampling time	2	Sampling time	Predictive value of hyperammonemia
1	M/43	150	17 h 57 min	7	8 <GCS and respiratory failure	17 h 57 min	Yes	76	17 h 57 min	60	30 h 23 min	Unfavorable
					Diabetes inspidus	70 h 30 min
2	F/50	250	1 h 23 min	15	No severe neurotoxicity		No	–		–		–
3	F/41	150	2 h 56 min	15	No severe neurotoxicity		No	151	13 h 11 min	94	22 h 23 min	Unfavorable
4	F/78	150	3 h 11 min	15	8 <GCS and respiratory failure	13 h 00 min	Yes	–		–		–
5	F/84	200	0 h 36 min	15	8 <GCS	12 h 10 min	Yes
					Seizure and respiratory failure	18 h 50 min
6	F/27	100	2 h 26 min	15	8 <GCS and respiratory failure	14 h 10 min	Yes	–		–		–
					Seizure	45 h 00 min
7	M/55	100	16 h 01 min	15	Seizure	10 h 00 min	Yes	–		–		–
					8 < GCS and respiratory failure	23 h 30 min
8	M/47	150	4 h 13 min	15	No severe neurotoxicity		No	116	5 h 42 min	96	17 h 44 min	Unfavorable
9	M/72	200	1 h 20 min	15	Seizure and 8 <GCS	9 h 45 min	Yes	194	2 h 23 min	261	16 h 31 min	Favorable
10	M/43	100	2 h 16 min	15	No severe neurotoxicity		No	87	3 h 08 min	54	15 h 40 min	Favorable
11	F/44	500	4 h 43 min	15	8 <GCS and respiratory failure	9 h 30 min	Yes	188	22 h 56 min	154	46 h 17 min	Favorable
					Seizure	52 h 36 min
12	F/48	30	4 h 35 min	15	No severe neurotoxicity		No	88	6 h 19 min			Not confirmed
13	F/67	30	3 h 00 min	15	No severe neurotoxicity		No	25	3 h 29 min			Not confirmed

Neurotoxicity following glufosinate poisoning was delayed and abrupt, usually occurring 10–24 h post-ingestion.^2–4 Clinicians must therefore be alert for these complications, which may be related to poor prognosis. Therefore, early prediction of neurotoxicity may be clinically important, but no clinical markers have been shown to be useful for this purpose. Suggestion of hyperammonemia as a potential marker of neurotoxicity by Yan-Chido Mao et al. is therefore very interesting.

However, we wish to point out the limitation of their study, which is a lack of time relationship between hyperammonemia and onset of neurotoxicity. Hyperammonemia as a predictor may be more valuable when it precedes neurotoxicity and is measured within the risk period. Table 1 shows the time relationships between hyperammonemia and onset of severe neurotoxicity in our eight patients with the results of serum ammonia. Three patients (Nos. 9–11) suggested the predictive value of hyperammonemia, whereas in other patients (Nos. 1, 3, and 8) this was not the case. The results of two patients (Nos. 12 and 13) could not be confirmed because appropriate ammonia levels were not measured. We suggest that rising or maintained patterns of hyperammonemia within 24 h post-ingestion may be more predictable rather than absolute value of hyperammonemia. Further studies will be needed to confirm the predictive values of hyperammonemia following glufosinate-containing herbicide poisoning.