Research Article - (2022) Volume 9, Issue 4

A Rare Case of Glufosinate Ammonium Poisoning

Shankar D1, Murali Thangaraj2*, Gopinathan T3 and Varun S4
1DNB Registrar, Department of Critical Care Medicine,, Kovai Medical Centre and Hospital, Coimbatore, India
2MD., IDCCM., FIECMO., Consultant Intensivist, Department of Critical Care Medicine,
Kovai Medical Centre and Hospital, Coimbatore, India
3Consultant Intensivist, Department of Critical Care Medicine, Kovai Medical Centre and Hospital, Coimbatore, India
4Consultant Infectious Diseases, Department of Critical Care Medicine, Kovai Medical Centre and Hospital, Coimbatore, India
*Correspondence: Murali Thangaraj, MD., IDCCM., FIECMO., Consultant Intensivist, Department of Critical Care Medicine,
Kovai Medical Centre and Hospital, Coimbatore, India, Email:

Received: Apr 22, 2022, Manuscript No. JEBMH-22-61609; Editor assigned: Apr 25, 2022, Pre QC No. JEBMH-22-61609 (PQ); Reviewed: Apr 28, 2022, QC No. JEBMH-22-61609; Revised: May 02, 2022, Manuscript No. JEBMH-22-61609; Published: May 16, 2022

Citation: Shankar D, Murali T, Gopinathan T, Varun S. A rare case of glufosinate ammonium poisoning. J Evid Based Med Healthc 2022; 9(08):1-6.


Glufosinate ammonium, a Herbicide is toxic if consumed in undiluted form and acts by unknown mechanisms. A 61 years old Male presented to our hospital after consumption of 350 – 400 cc of 13.5 %w/v of Glufosiante ammonium compound presenting with low GCS, which was attributed to Hyperammonemia due to the toxic compound. He underwent 2 cycles of 4 hours Charcoal Hemoperfusion session with 2 hours time interval in between and showed serial decline in serum ammonia levels and improvement in sensorium and eventually got weaned off from ventilator within 5 days of ICU stay, as we know that Hyperammonemia is independently associated with overall poor outcome .This case report also emphasizes role of Charcoal Hemoperfusion in adsorbing and clearing lipophilic toxins like glufosinate ammonium ,which eventually gets reflected in clinical outcome. Also this case report briefly describes the overall management principles of glufosiante ammonium toxicity.


Glufosinate, a glutamic acid analogue structurally, though primarily affects the excitatory neurons, its mechanism of action at molecular and cellular level is largely unknown. Toxic effect is generally less for humans and considered safer in agronomy as far as handling is according to manufacturer's instructions.1,2

Overall outcome is grave if consumed in undiluted form.3 Complications such as toxin reactions 3, hypotension, respiratory failure with apnea, loss of memory and consciousness, seizures 4 including death occurs in severe cases. This case report is about glufosinate ammonium poisoning which is very rare in our subset of population and seldom reported. This case throws light on effect of hemoperfusion on significant neurological recovery along with resolution of hyperammonemia and briefly discusses other options available for glufosinate poisoning management among critically ill.

Case Description

61 years old male, a garment business owner with no prior comorbid illness, 20 days after the demise of his wife presented to hospital with consumption of 350 – 400 cc of

13.5 % Glufosinate ammonium compound along with ethanol. Initially had multiple episodes of vomiting and hence taken to,and underwent gastric lavage within 30 minutes from local clinic.5

He was admitted initially in a nearby hospital and for observation over next 24 hours during which he developed hypoxia and drop in sensorium. Eventually he got intubated and referred to our hospital. During admission to our hospital, his GCS was E3VTM2. Vitals were stable and patient was euthermic and euglycemic. CT brain showed no neuroparenchymal abnormality.

On Day 1 of ICU stay, patient had Hyperammonemia with preserved renal functions and acid base parameters. Since Hyperammonemia is considered as potential risk factor for neurotoxicity,6 Nephro consultation was taken and initiated on 2 subsequent sessions of 4 hours of Charcoal Hemoperfusion with 2 hours gap in between. Concomitantly, Syrup lactihep 10 ml 6th hourly has been started for ammonia clearance.

Ammonia levels started decreasing from day 3 and by day 4 patients GCS improved and started obeying commands. By Day 5 of ICU stay, Patient got extubated once he has successfully tolerated a SBT trial with PSV/CPAP with 0.4 FiO2, PEEP of 5 and Psupport of 10 cm H2O.Post extubation, monitored serum ammonia levels have come down and Patient was able to protect his airway, cough out and clear his oropharyngeal secretions well, was ambulent, getting mobilized and started taking oral feeds. Hence got shifted to ward and eventually with good neurological recovery got discharged from the hospital over the next 3 days (Table 1) (Figure 1).7

Table 1: Serial Ammonia Levels after Hemoperfusion

Days of stay in ICU D1(Hemoperfusion 2 cycles given) D2 D3 D4 D5
Serum Ammonia levels(micromol/L) 187.9 166.8 128 126.9 102.2

Figure 1.Glufosinate ammonium 13.5%W/V Containing Herbicide Compound Consumed by Our Patient


Glufosinate ammonium produces varied systemic toxic manifestations.8 In cases of severe toxicity, median toxic dose is 30.4 gm unlike 6.8gms in non- fatal group as reported in literature.9 In few studies, the amount ingested if equal to or greater than 13.9 grams which roughly equates to 100 cc of 13.5 % w/v consumption or 75 cc of 18.5 % w/v consumption is found to produce severe glufosinate toxicity.10 Neurological effects is due to toxin exposure and its metabolites which leads to imbalance between glutamate, ammonium and glutamine.7 The inhibition of glutamine decarboxylase and glutamine synthetase down regulates glutamic acid levels and leads to drowsiness, amnesia and seizure.11 Hemodynamically, changes in vascular resistance and cardiac output is caused due to sodium polyoxylethylene sulfur ethyl sulfate.12 Cardiovascular depression and Vasodilatation in Glufosinate poisoning occurs predominantly due to surfactant, which is anionic in nature, which is sodium polyoxyethylene alkyl ether sulfate and also its concentration varies from 30 % to 70 %.12 Possibility of cardiovascular toxicity has also been attributed to presence of some solvents like Propylene glycol in glufosinate herbicide compounds. Late onset memory loss, most distinctive feature occurs due to toxin -induced hippocampal damage.13 Even in our case, patient had late onset amnesia by 6th day of illness which correlates with findings in literature. Though it is believed that cholinesterase inhibition and cholinergic manifestations occur due to phosphorus in glufosinate, the electronegativity along with electron withdrawing capacity of phosphorus in glufosinate is much weaker and in turn there is very low likelihood of cholinesterase inhibition due to glufosinate toxicity. Proposed mechanism of Hyperammonemia secondary to glufosiante exposure is inhibition of Glutamine Synthetase in human cells. In a retrospective observational study, out of 11 cases 6 patients with severe toxicity were found to have hyperammonemia which indicates poor prognosis, and also literature of reported cases of hyperammonemia is scarce. Though efficacy is unclear, Hemodialysis and Hemoperfusion have been attempted for toxin clearance and in our case Charcoal hemoperfusion is used primarily with the idea that lipophilic compounds like glufosinate will get adsorbed much often than hydrophilic compounds. Ethanol consumption is inversely correlated with sevreity of toxicity. Possible mechanisms proposed in the literature are Induced vomiting, N- methyl D-Aspartate receptor Inhibition, and diuretic effect since major route of excretion of glufosinate toxin is through the kidney.

Treatment for Glufosinate toxicity is largely supportive. Activated Charcoal administration and Early Decontamination of GI tract is found useful if administered in patients whose oral consumption is quite significant. Adequate resuscitation of IV fluids, and monitoring of Central nervous system, Cardiovascular system and Respiratory system repeatedly and in particular among patients at risk for severe toxicity is needed. Need for Intensive care management comes into play if patient develops life threatening manifestations. Due to lipophilic nature of the surfactant in composition with Glufosinate compounds,Intravenous lipid Emulsion is found to be promising treatment modality. After an initial bolus of 20 % ILE with 1.5 ml/Kg of lean body mass, a maintanence infusion of 0.25 - 0.5 ml / kg / min is recommended.


Hemoperfusion is proposed to have therapeutic benefit as it adsorbs the surfactant and other lipophilic substances and in turn improves Glufosinate ammonium clearance. Clinicians must be watchful for episodes of apnea with respiratory failure, altered mental status, Seizures and other systemic manifestation of glufosinate ammonium toxicity and respective supportive measures should be addressed.