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Case Report | Volume 14 Issue 5 (Sept - Oct, 2024) | Pages 18 - 20
Glyphosate Surfactant Herbicide poisoning manifestations and management: A case series
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1
Associate Professor, Department of Anaesthesiology, Pandit Bhagwat Dayal Sharma Post Graduate Institute of Medical Sciences, Rohtak, Haryana, India
2
Senior Resident, Department of Anaesthesiology, Pandit Bhagwat Dayal Sharma Post Graduate Institute of Medical Sciences, Rohtak, Haryana, India
Under a Creative Commons license
Open Access
Received
July 10, 2024
Revised
July 28, 2024
Accepted
Aug. 5, 2024
Published
Sept. 5, 2024
Abstract

Roundup (41% glyphosate and 15% poly oxy ethylene amine, POEA surfactant) is a common herbicide used by famers in India. Its cause of poisoning is mostly suicidal, consumed by oral route. Acute poisoning involves gastro intestinal system, respiratory system, renal and cardiovascular system. Glyphosate and its surfactant (POEA) cause hyperkalaemia, metabolic acidosis and cardiac arrest which is the main cause of mortality associated with poisoning. Treatment involves supportive care in high dependency units as there is no specific antidote available.1,2. We report three cases of herbicide poisoning managed in critical care unit.

Keywords
INTRODUCTION

Roundup (41% glyphosate and 15% poly oxy ethylene amine, POEA surfactant) is a common herbicide used by famers in India. Its cause of poisoning is mostly suicidal, consumed by oral route. Acute poisoning involves gastro intestinal system, respiratory system, renal and cardiovascular system. Glyphosate and its surfactant (POEA) cause hyperkalaemia, metabolic acidosis and cardiac arrest which is the main cause of mortality associated with poisoning. Treatment involves supportive care in high dependency units as there is no specific antidote available.1,2

 

We report three cases of herbicide poisoning managed in critical care unit.

CASE 1

A female patient 28 years of age presented in emergency with 100 ml of roundup herbicide ingestion 1 hour before the time of admission. The intent of consumption was suicidal. The poison was identified by the bottle brought by attendants. On presentation she was conscious, oriented with Glassgow coma scale of 15/15. Her vitals were stable with mild tachycardia (heart rate 120-130 beats per minute). Blood pressure was 110/70 mm of Hg, respiratory rate was 20 breaths per minute with room air oxygen saturation of 99% and patient was afebrile. Blood investigations were sent. Ryles tube was inserted for gastric lavage and intravenous normal saline was started at 100ml per hour. Patient was shifted to intensive care unit for further management. Her investigations revealed Hb%: 10gm/dl, leucocyte count was 12000, platelet count 2 lakh/cu mm, serum creatinine was 1.5mg/dl, blood urea 57mg/dl, serum sodium 132mEq/L, serum potassium 5.8mEq/L (managed with 10 units insulin in 100 ml 25% dextrose), liver function tests were normal. Arterial blood gas analysis showed metabolic acidosis pH:7.28, PaO2: 157, PCO2: 28, bicarbonate: 22, base excess: -4.0. Acute Physiology and Chronic Health Evaluation (APACHE-II) score was 7. Treatment was started as per ICU protocol. Patient was started empirically on ceftriaxone and kept nil per oral.

 

After 8 of hours ICU admission, patient had 4 episodes of loose stools and started having respiratory distress with a respiratory rate of 32 breaths per minute, fall in oxygen saturation to 82% on 4litres of oxygen by face mask. On examination bilateral crepts were present and lung ultrasound score of 2. Patient was put on non-invasive ventilation with face mask. There was a fall in mean arterial pressure to 55 mm Hg for which nor adrenaline infusion was started. Repeat arterial blood gases showed pH: 7.20, PaO2: 68, bicarbonate 16, serum potassium 6.3 mEq/L. Urine output decreased to 25 ml/hour, serum creatinine was raised to 5 mg/dl. Potassium correction was started and continuous renal replacement therapy was initiated. Patient’s condition improved after 48 hours, non-invasive ventilation was gradually taken off. Urine output improved on 5th day of ICU admission. Patient was treated successfully and discharged on 11th day. 

CASE 2

A 46 years male, farmer by occupation, known case of hypertension ingested 400 ml of Glyphosate surfactant herbicide. He presented in the emergency after 6 hours of ingestion with respiratory distress (oxygen saturation of 78%) and hypotension (systolic blood pressure:80 mm Hg) and GCS of 7/15. Patient was immediately intubated, put on mechanical ventilation and nor adrenaline infusion was started. Patient was transferred to ICU for further management. Investigations were sent, arterial blood gases showed pH 7.15, PaO2: 77, bicarbonate: 9 mEq/L, serum potassium: 7.00. ECG showed ventricular tachycardia with heart rate of 180 beats per minute, systolic blood pressure of 66 mmHg and oxygen saturation of 85% on FiO2 of 1. APACHE-II score was 39. Corrective measures for serum potassium were started, bicarbonate infusion was started according to deficit, salbutamol nebulisation and insulin-glucose drip was started, intravenous Calcium was given. Intravenous infusion of adrenaline was started due to persistent hypotension. Despite of all treatment patient succumbed within 1 hour of admission to ICU due to cardiac arrest for which 12 cycles of CPR(cardio pulmonary resuscitation) were given but patient could not be revived.

CASE 3

A 36 years old female patient presented with ingestion of around 350 ml of roundup with suicidal intent. She presented to emergency after 2 hours of ingestion with palpitations, restlessness, agitation and breathing difficulty.  GCS was 12/15, respiratory rate was 32 per minute and bilateral basal crepts were present on auscultation. She had tachycardia with heart rate 154 beats per minute and blood pressure of 90/56 mm Hg. Her oxygen saturation was 88% on room air.  Immediate gastric lavage was done and oxygen was supplemented by face mask. Investigations were sent and patient was shifted to ICU for management. Hb%: 11gm/dl, leucocyte count was 20000, platelet count 1.8 lakh/cu mm, serum creatinine was 2.8 mg/dl, blood urea 84 mg/dl, serum sodium 136mEq/L, serum potassium 6.2mEq/L, liver function tests were normal. Arterial blood gas analysis showed metabolic acidosis pH:7.28, PaO2: 92, PCO2: 36, bicarbonate: 14, base excess: -6.0. Acute Physiology and Chronic Health Evaluation (APACHE-II) score was 20. Treatment was started as per ICU protocol. Condition of patient deteriorated after 12 hours, patient was intubated and mechanical ventilation was instituted. Continuous renal replacement was started because of decreasing urine output, persistent metabolic acidosis and raised creatinine levels (6.4mg/dl). Lung condition and PaO2 levels deteriorated further by day 3 and patient developed ground glass opacities. Hypotension worsened despite of nor adrenaline and adrenalin infusions. Patient succumbed on day 4 of ICU admission despite all resuscitative measures.

DISCUSSION

Glyphosate (isopropyl amine salt) is widely used as herbicide in different formulations. Alone it only results corrosive effects like gastrointestinal and skin irritation, but when combined with surfactant (POEA) it forms a lethal combination.3 Toxicity results from damage to mitochondrial cell walls, uncoupling of oxidative phosphorylation and direct myocardial toxicity. This results in metabolic acidosis, cardiogenic shock and respiratory failure. Hepatic dysfunction results from secondary damage. Mortality associated with Roundup ingestion ranges from 7% to 30%.4 It depends on several factors like amount of herbicide ingested, delay in presentation to hospital and associated comorbidities of the patient.5 Amongst these cases the patient who presented within 1 hour of ingestion survived. Peak plasma concentration is reached in 6-8 hours after ingestion. Only about 36% ingested Glyphosate is absorbed and rest is excreted unchanged mainly in faeces and some amount in urine.6,7 Currently there is no anti dote available for roundup poisoning. All the cases should be managed in high dependency unit as they require vigilant monitoring and prompt treatment due to fulminant course of poisoning related illness. Gastric lavage is useful only within 1 hour of ingestion.8 Haemodialysis has proved to be effective in some patients but not all. There is some evidence that renal replacement therapies can remove the toxins from the body in patients with large volume ingestion.9 Intravenous fat emulsion has also been used for managing roundup toxicity as lipid combines with lipophilic POEA and removes it from the circulation.10 Early institution of supportive measures can improve the survival.

CONCLUSION

Glyphosate surfactant combination causes potentially lethal toxicity. There is no specific antidote, however supportive treatment if started early results in a better prognosis. Renal replacement therapies and Intralipid has shown promising results in some cases and can be further explored for treatment.

REFERENCES
  1. Mahendrakar K, Venkategowda PM, Rao SM, Mutkule DP. Glyphosate surfactant herbicide poisoning and management. Indian J Crit Care Med. 2014 May;18(5):328-30. doi: 10.4103/0972-5229.132508. PMID: 24914265; PMCID: PMC4047698.
  2. Sawada Y, Nagai Y, Ueyama M, Yamamoto I. Probable toxicity of surface-active agent in commercial herbicide containing glyphosate. Lancet. 1988 Feb 6;1(8580):299. doi: 10.1016/s0140-6736(88)90379-0. PMID: 2893109
  3. Stella J, Ryan M. Glyphosate herbicide formulation: a potentially lethal ingestion. Emerg Med Australas. 2004 Jun;16(3):235-9. doi: 10.1111/j.1742-6723.2004.00593.x. PMID: 15228468
  4. Venugopal, K.; Suresh, C.; Vishwanath, Huggi; Lingaraja, Mudegoudara; Bharath Raj, M. Y.. Glyphosate: Surfactant herbicide poisoning - Is it mild?. Medical Journal of Dr. D.Y. Patil University 8(6):p 816-818, Nov–Dec 2015. | DOI: 10.4103/0975-2870.169945
  5. Lee CH, Shih CP, Hsu KH, Hung DZ, Lin CC. The early prognostic factors of glyphosate-surfactant intoxication. Am J Emerg Med. 2008 Mar;26(3):275-81. doi: 10.1016/j.ajem.2007.05.011. PMID: 18358936.
  6. Cheng JC, Cheng MC. Glyphosate intoxication in 28 patients. Ann Emerg Med. 1995;26(6):721.
  7. Bradberry SM, Proudfoot AT, Vale JA. Glyphosate poisoning. Toxicol Rev. 2004;23(3):159-67. doi: 10.2165/00139709-200423030-00003. PMID: 15862083.
  8. Talbot AR, Shiaw M-H, Huang J-S, et al. Acute Poisoning with a Glyphosate-Surfactant Herbicide ('Roundup’): A Review of 93 Cases. Human & Experimental Toxicology. 1991;10(1):1-8. doi:10.1177/096032719101000101
  9. Moon JM, Min YI, Chun BJ. Can early hemodialysis affect the outcome of the ingestion of glyphosate herbicide? Clin Toxicol (Phila). 2006;44:329-332
  10. Han SK, Jeong J, Yeom S, Ryu J, Park S. Use of a lipid emulsion in a patient with refractory hypotension caused by glyphosate-surfactant herbicide. Clin Toxicol (Phila). 2010 Jul;48(6):566-8. doi: 10.3109/15563650.2010.496730. PMID: 20569074.
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