With an increasing emphasis on organic farming and a greener environment, markets today have a number of organic or bio-pesticides and herbicides, some with questionable safety profiles. We report a patient with methaemoglobinaemia due to intentional consumption of a locally manufactured bioherbicide called ‘Shooter’.

A 26-year-old man presented to the Emergency Department of our institute with an alleged history of intentional consumption of an unknown quantity of a herbicide named ‘Shooter’. Twenty minutes after consumption of the poison, the patient induced an episode of vomiting, which was followed by 5 episodes of spontaneous vomiting. The vomitus was white in color and contained gastric contents. There was no blood or bile in the vomitus. He developed altered sensorium in the next hour, and was then taken to a local district hospital, where he received a therapeutic gastric lavage, and injectable atropine and pralidoxime, before being referred to our centre.

At presentation to our institute, he had no abdominal pain, fever, frothing at the mouth, lacrimation, salivation, loose stools, sweating, shortness of breath or rhinorrhea. His Glasgow coma scale was E4V1M5, he had a pulse rate of 110/minute, blood pressure of 106/50 mmHg, respiratory rate of 16/minute, and oxygen saturation of 82% on room air. Profound central cyanosis was noted. Arterial blood gas showed partial pressure of oxygen to be 432 mmHg with a lactate of 5.61 mmol/L. His methaemoglobin level was 61%, and glucose-6-phosphate dehydrogenase levels were >18 units/g of haemoglobin. Complete blood count, liver function tests, renal function tests and a coagulation profile were within reference range. He received methylene blue 50 mg i.v. over 30 minutes, non-invasive ventilation with 100% O2, and an exchange transfusion with 2 units of packed red blood cells, 4 units of random donor platelets, and 4 units of fresh frozen plasma.

He was intubated in view of an unstable airway and non-compliance to non-invasive ventilation. With these interventions, the patient’s methaemoglobin levels reduced to <10%, but the clinical condition continued to deteriorate, possibly due to hypoxic ischaemic encephalopathy. The patient developed ventilator associated pneumonia on day 5 of his hospital stay. On day 10, the patient died due to sepsis.

Methaemoglobin is an oxidised form of haemoglobin in which the ferrous (+2) haeme iron in red blood cells is oxidised to a ferric (+3) state. Methaemoglobin cannot bind oxygen, and thus fails to deliver oxygen to tissues.1

Locally manufactured bioherbicides and possibly other bioagricultural products have questionable safety profiles and lead to severe and time-sensitive complications such as methaemoglobinaemia.2,3 Agents generally implicated in the development of acute toxic methaemoglobinaemia are aniline dyes, nitrates, nitrosohydrocarbons and a number of drugs––dapsone, topical local anaesthetics (benzocaine), nitrates and sulphonamides.4

The diagnosis of methaemoglobinaemia was missed on initial evaluation and he received treatment for presumed organophosphate poisoning before presentation to us. This may have led to toxicities associated with treatment agents.5 Thus in patients in whom organophosphates as the causative agent for poisoning cannot be ascertained, alternative diagnoses must be considered and investigations done accordingly.

‘Natural’ and ‘bio-derived’ agents are now more prevalent than ever in industry, and mechanisms through which these interact with human physiology needs to be studied as their use becomes more common. Appropriate compositions and initial management must be made available as standardized hazard labels on containers for these products. As in our patient, treatment of unknown toxins can be tricky and may lead to incorrect management. This delay, coupled with the severity of methaemoglobinaemia led to precipitation of irreversible hypoxic damage, and despite aggressive management efforts, eventually resulted in the death of the patient.

There should be a high index of suspicion for methaemoglobinaemia in patients with a history of consumption of unknown agents followed by unexplained cyanosis, normal-appearing pulse oximetry and respiratory distress.