Acute glufosinate-ammonium poisoning complicated with respiratory depression: a case report

Glufosinate-ammonium (GLA) is a widely used herbicide. GLA poisoning frequently manifests with neurological symptoms, including impaired consciousness and seizures.^[1] At present, there are no treatment guidelines for GLA poisoning, and its management relies primarily on clinical experience. Therapeutic strategies emphasize toxin elimination like gastrointestinal decontamination and blood purification.^[1] In severe cases complicated by respiratory depression, mechanical ventilation is often required.^[1,2] Herein, we report a case of acute GLA poisoning complicated by respiratory depression admitted to the Emergency Department of the Affiliated Hospital of Yunnan University.

A 55-year-old woman without significant past medical history or trauma during consultation was admitted to the hospital after ingesting approximately 100 mL of a GLA pesticide and experiencing impaired consciousness for 8 h. According to her family, she developed nausea, vomiting, and abdominal pain shortly after intentional ingestion of the pesticide but did not disclose the exposure or seek medical attention in a timely manner. Approximately 4 h prior to admission, the family reported the onset of impaired consciousness accompanied by recurrent convulsions and immediately transported the patient to a local health center. She underwent gastric lavage and received anti-inflammatory therapy and cholinesterase reactivators. However, her clinical condition did not improve significantly. Therefore, the patient was transferred to a tertiary hospital for further management.

On admission to the Emergency Department, she was in a deep coma (Glasgow Coma Scale [GCS] 3). Physical examination revealed temperature (T) 36.5 °C, respiratory rate (RR) 3 breaths/min, pulse (P) 70 beats/min, blood pressure (BP) 179/105 mmHg (1 mmHg=0.133 kPa), and saturation of peripheral oxygen (SpO₂) 62%. Her bilateral pupils were equal and round (3.0 mm) with sluggish light reflexes. She presented with cyanotic lips, irregular breathing, cold upper extremities, and cyanotic skin. Chest examination revealed bilateral decreased breath sounds with scattered rales. The abdominal examination was unremarkable. Routine blood examination revealed white blood cell (WBC) count 18.67×10⁹/L, neutrophil (NEUT) 87.0%, blood glucose 13.55 mmol/L, and blood ammonia 219 μmol/L. After cerebral lesions and hypoglycemic coma were ruled out, the preliminary diagnosis was GLA poisoning complicated by acute respiratory failure.

Given severe consciousness disturbance, convulsions, and respiratory depression, emergency tracheal intubation and mechanical ventilation were performed (pressure assist/control [P-A/C] mode: fraction of inspired oxygen [FiO₂] 40%, peak inspiratory pressure [Pinsp] 12 cmH₂O [1 cmH₂O=0.098 kPa], RR 15 breaths/min, inspiratory time (Ti) 1.1 s, positive end-expiratory pressure [PEEP] 5 cmH₂O). She received mannitol for dehydration and intracranial pressure reduction, levetiracetam for seizure control, and bedside continuous venovenous hemodiafiltration (CVVHDF)+hemoperfusion (HP), with an HA230 perfusion device, 150 mL/min blood flow, citrate anticoagulation. The ventilator parameters were adjusted daily, and supportive care was provided. After 5 d of stable vital signs, the ventilation was switched to pressure-support ventilation (PSV) mode (FiO₂ 50%, pressure support [Psupp] 10 cmH₂O, PEEP 5 cmH₂O), and the tracheal tube was removed following a successful spontaneous breathing trial (SBT).

On day 6, respiratory depression recurred (RR 8 breaths/min, SpO₂ 56%), requiring re-intubation and mechanical ventilation (P-A/C mode: FiO₂ 25%, Pinsp 14 cmH₂O, RR 16/min, Ti 1.1 s, PEEP 6 cmH₂O). Active fluid replacement was administered to promote residual toxin excretion. On day 8, she fully regained consciousness, and the tracheal tube was removed after a successful SBT. Mild dizziness persisted, so symptomatic and organ-supportive treatments were continued until day 16. She was discharged with no obvious discomfort and normal blood gas analysis results. The dynamic changes in blood gas parameters during hospitalization are presented in Table 1.

Table 1.

Blood gas analysis results of the patient during hospitalization

Time	pH	SO2 (%)	PO2 (mmHg)	PCO2 (mmHg)	Lac (mmol/L)	BE (mmol/L)
Day 1	6.955	86.2	74.2	74.4	1.9	-15.5
Day 2	7.251	95.9	130	39.2	7.0	-10.0
Day 3	7.528	98.6	109	27.8	1.7	0.4
Day 4	7.467	98.5	110	33.4	2.2	0.4
Day 5	7.428	97.5	103	38.2	1.7	1.5
Day 6	7.343	98.8	163	39.6	2.6	-4.3
Day 7	7.485	98.2	109	29.0	0.9	-1.5
Day 8	7.347	97.5	105	41.7	0.9	-0.9
Day 9	7.433	97.1	91	41.1	0.7	3.2
Day 10	7.476	98.7	110	38.7	0.7	3.5
Day 13	7.452	99.3	132	38.6	0.9	3.0

Normal reference values: pH 7.35-7.45, SO₂ 95%-98%, PO₂ 8-100 mmHg, PCO₂ 35-45 mmHg, Lac 1-1.7 mmol/L, BE -2 to +2 mmol/L. SO₂: oxygen saturation; PO₂: oxygen tension; PCO₂: pressure of carbon dioxide; Lac: lactate; BE: base excess.

After discharge, no further medication was administered. Follow-up every 2 weeks for 3 months revealed no discomfort or sequelae.

In this case, the patient developed severe respiratory depression shortly after ingestion of GLA, which subsequently worsened repeatedly on day 6. The favorable outcome was mainly attributed to continuous respiratory monitoring and rapid initiation of mechanical ventilation.

GLA can enter the human body through inhalation, dermal exposure, and ingestion, with ingestion being the most common route. GLA poisoning may involve multiple organ systems. Early manifestations are mainly gastrointestinal, nausea, vomiting, and abdominal pain, followed by respiratory and neurologic involvement. Neurologic involvement is clinically significant and includes dizziness, headache, bradycardia, seizures, and loss of consciousness. With respect to symptom onset, respiratory depression typically occurs 6.5 to 48.0 h after ingestion, convulsions occur 6.0 to 45.0 h after ingestion, and bradycardia occurs 12.5 to 46.3 h after ingestion.^[3] Because GLA-induced neurologic injury is often delayed, early neurologic symptoms may be absent, leading to misdiagnosis or delayed treatment and increasing the risk of disease progression and mortality. Therefore, during the management of GLA poisoning, clinicians should remain highly vigilant for delayed neurologic injury, prioritize respiratory function monitoring, and initiate early respiratory support to improve patient outcomes.^[3]

In this case, the patient was admitted 8 h after poisoning. On admission, blood ammonia was markedly elevated at 219 μmol/L, a characteristic laboratory finding in patients with GLA poisoning. With continuous treatment, blood ammonia levels gradually decreased and normalized by day 4 of hospitalization. GLA, a structural analog of glutamate, irreversibly inhibits glutamine synthetase (GS) and glutamate decarboxylase (GAD), thereby blocking glutamine (Gln) synthesis, disrupting nitrogen metabolism, and causing hyperammonemia.^[4] Excess intracellular ammonia disrupts mitochondrial function and energy metabolism, leading to cellular injury and death. Moreover, elevated blood ammonia can cross the blood-brain barrier, enter the central nervous system, and exert neurotoxic effects that cause neurologic damage.^[5] This process is considered a key mechanism of GLA-induced central neurotoxicity.

In addition, the patient developed recurrent respiratory depression on day 6 after admission, representing a rare manifestation of delayed respiratory dysfunction. Similar cases have been reported, suggesting that GLA poisoning may present with delayed neurotoxicity under certain conditions.^[6] Based on previous case reports and this patient’s clinical course, delayed respiratory depression may be related to excessive accumulation of GLA and inadequate toxin clearance.

GLA poisoning progresses rapidly and is associated with a high risk of respiratory failure and multiple organ dysfunction. No specific antidote or standardized guidelines are available; management relies mainly on clinical experience and general principles of acute poisoning care.^[7,8] Evidence suggests that early gastrointestinal decontamination, close respiratory monitoring, and timely respiratory support are important, and early blood purification may enhance toxin removal in patients with large ingestions or rapid deterioration.^[9]

In conclusion, GLA poisoning is associated with a significant risk of neurotoxicity. As respiratory depression is a key clinical manifestation, it is recommended to continuously monitor arterial blood gas and blood ammonia levels during treatment, and respiratory support should be initiated immediately as needed.

Funding: None.

Ethical approval: This study was approved by the Local Ethical Committee. Written informed consent for publication of their clinical details and clinical images was obtained from our patient.

Conflicts of interest: The authors declare that they have no conflicts of interest.

Contributors: SP, LX, LZ, and TCZ contributed equally to this work and are co-first authors. All authors made significant contributions to the work reported.