Journal of Emergencies, Trauma, and Shock
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Year : 2011  |  Volume : 4  |  Issue : 3  |  Page : 435-437
DORMEX® -hydrogen cyanamide poisoning

Department of Medicine, M S Ramaiah Medical Teaching Hospital, MSRIT Post, Bangalore, India

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Date of Submission13-Aug-2010
Date of Acceptance18-Feb-2011
Date of Web Publication16-Aug-2011


Case reports of acute and chronic exposure to hydrogen cyanamide (DORMEX; ) have been reported but mainly as a result of occupational or accidental exposure and without any mortality. We report a case of acute hydrogen cyanamide poisoning in a young male due to suicidal intent. The patient was managed under intensive care with all the standard protocols for detoxification. However, in spite of aggressive management, patient could not be rescued. An extensive literature search did not yield any similar case reports. Hence, we report this case to the medical community to be aware of the entity.

Keywords: Disulfiram-like syndrome, hydrogen cyanamide, poisoning

How to cite this article:
Sheshadri SH, Sudhir U, Kumar S, Kempegowda P. DORMEX® -hydrogen cyanamide poisoning. J Emerg Trauma Shock 2011;4:435-7

How to cite this URL:
Sheshadri SH, Sudhir U, Kumar S, Kempegowda P. DORMEX® -hydrogen cyanamide poisoning. J Emerg Trauma Shock [serial online] 2011 [cited 2021 May 13];4:435-7. Available from:

   Introduction Top

Self-poisoning with pesticide accounts for nearly one-third of the world's suicides. [1] Over the last few decades, agricultural pesticides have become major cause of self-poisoning in rural areas of the developing world due to their easy availability. [2] While organophosphorus compounds cause most self-poisoning deaths in southern and central India, aluminium phosphide causes most deaths in northern India. [3],[4] Although accidental poisoning with hydrogen cyanamide is known, reports of self-poisoning with the same are limited. [5],[6] We present a case of 22-year-old male who succumbed to hydrogen cyanamide following self-poisoning. Awareness of the incident is necessary to provide an early and aggressive management as there is no specific antidote for the same.

   Case Report Top

A 22-year-old male was brought in with alleged history of consuming approximately 150 ml of hydrogen cyanamide (DORMEX; -active ingredient: 520 g/L of cyanamide) about 2 hours prior to hospitalization. Patient was stuporous and responding to painful stimuli. Initial assessment revealed Glasgow Coma Scale (GCS) score of 7/15 (E2, M4, V1), pulse of 110 beats/min, blood pressure of 90/60 mmHg, respiratory rate of 30/min, and oxygen concentration of 88% (98% with 6L oxygen inhalation by mask) in supine position. He had occasional spontaneous jerky movements and weak cough reflex. Pupils were 5 mm and bilaterally reactive. The remaining physical examination did not reveal any significant findings. His central venous pressure (CVP) was 7 cm H 2 O.

His laboratory parameters [Table 1] were essentially within normal limits. Blood gas analysis revealed metabolic acidosis [Table 2]. Chest X-ray showed minimal pleural effusion, otherwise normal, and the electrocardiograph showed sinus tachycardia [Figure 1]. Computerised tomography (CT) brain and echocardiography were done as a part of initial assessment and were normal. Ultrasonography of abdomen revealed bilateral grade I nephropathy, mild ascitis, and minimal right pleural effusion. Comprehensive toxicology profile including serum pseudocholinesterase was normal and benzodiazepines and barbiturates were not detected on urine examination.
Table 1: Baseline and follow - up investigation reports of the patient

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Table 2: Arterial blood gas analysis and the correction given for the metabolic acidosis at different timeline during patient's hospitalization

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Figure 1: Electrocardiograph of the patient showing sinus tachycardia

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Patient was given gastric lavage and fluid management was done according to CVP. As the patient was drowsy and responding only to painful stimulus, he was electively intubated and mechanically ventilated (SIMV Mode; FiO 2 -60%; PEEP-5 cm H 2 O). Sodium bicarbonate (25 mEq/h intravenously) was given to correct the metabolic acidosis and the dosage was adjusted by repeated blood gas analysis [Table 2].

Twenty-two hours after admission, the patient deteriorated into cardiogenic shock. CVP dropped to 2 cm of H 2 O. Dopamine was started at 5 mg/kg/min, followed by noradrenaline 5 mg/kg/min and dobutamine at 2mg/kg/min, which were gradually stepped up to their maximum dose (Dopamine 15 mg/kg/min, noradrenaline 20 mg/kg/min, dobutamine 10 mg/kg/min). Patient had persistent metabolic acidosis with lactic acidosis despite corrective measures. After 25 hours of admission, patient went into asystolic cardiac arrest. Cardio pulmonary resuscitation was started and atropine (1.2 mg IV) and adrenaline (1 mg IV) were given. This was followed by intravenous sodium bicarbonate (50 mEq). Atropine (0.6 mg IV) and adrenaline (1 mg IV) were repeated every 5 minutes over next one hour. In spite of all these measures, the patient could not be revived and was declared dead.

   Discussion Top

Although insecticide poisoning has been reported worldwide time and again, there are limited reports of poisoning with a plant growth regulator-hydrogen cyanamide. [5],[6] Hydrogen cyanamide is an active ingredient of Dormex; (Degussa AG, Trostberg, Germany), which is used as a plant growth regulator designed to stimulate more uniform bud-break following dormancy, resulting in more uniform flowering and maturity at harvest. [6] Reports of the toxic effects of hydrogen cyanamide is limited.

The department of pesticide regulation of the california environmental protection agency have studied the toxic effects of hydrogen cyanamide and concluded that hydrogen cyanamide causes adverse effects in the liver, thyroid, kidney, ovaries, and testes of laboratory animals. It further stated that in the absence of additional data to the contrary, hydrogen cyanamide has the potential to cause similar effects in humans. In their study, approximately 40% of oral dose was recovered in the urine in the first 24 hours. The remainder of oral doses was excreted in the feces or exhaled as carbon dioxide. [7] There was no indication of hydrogen cyanamide being converted to cyanide in vivo. [8] The principal metabolite excreted in the urine was N-acetylcyanamide.

The adverse health effects from contact of hydrogen cyanamide include severe irritation and ulceration of the eyes, skin, and respiratory tract. The exact mechanism of action of this compound has not been established. Animal studies have indicated that at cellular level, cyanamide is activated by catalase, which in turn causes catalase inhibition resulting in uncoupling of oxidation and phosphorylation and inhibition of adenosine nucleotide synthesis. [9] The substance also inhibits aldehyde dehydrogenase and can produce Disulfiram-like syndrome (e.g., vomiting, parasympathetic hyperactivity, dyspnoea, hypotension, and confusion) when exposure coincides with alcohol use. [10],[11]

Cederbaum and Dicker [12] showed that ethanol prevented inhibition of catalase if given before or at the same time as cyanamide, suggesting that ethanol may protect against the activation of cyanamide by catalase. Also, the catalase mediated activation of cyanamide is inhibited by 3-amino-1, 2, 4-triazole in vivo. [13] The application of these principles in treating acute cyanamide toxicity is an option although there are no supporting studies for the same.

There are reports of cutaneous reaction to exposure to hydrogen cyanamide in India and worldwide. [5],[6] Ingestion of hydrogen cyanamide has been reported in a 44-year-old male from Ragusa, Italy when he unintentionally ingested the product that had been placed in a plastic water bottle in refrigerator. Following consumption, he became seriously ill with third degree shock, coma, miosis, and hepatic necrosis and required care in an intensive care unit. [6] In our patient, we found similar manifestation of toxicity due to hydrogen cyanamide. Also, persistent metabolic acidosis and hypotension with lactic acidosis was noted. Since there is no known antidote for this compound, patient was managed symptomatically. The cause of death was inhibition of respiration at cellular level.

   Conclusion Top

Poisoning with plant growth regulator has been described from Italy, USA, and India. Majority of these reports were incidents of adverse effects following the occupational or accidental exposure to the chemical. The present case is probably the first reporting hydrogen cyanamide ingestion with a suicidal intent, leading on to persistent metabolic acidosis, encephalopathy, and refractory shock with a fatal outcome.

   References Top

1.Gunnell D, Eddleston M, Phillips MR, Konradsen F. The global distribution of fatal pesticide self-poisoning: Systematic review. BMC Public Health 2007;7:357.  Back to cited text no. 1
2.Srinivas Rao Ch, Venkateswarlu V, Surender T, Eddleston M, Buckley NA. Pesticide poisoning in south India: Opportunities for prevention and improved medical management. Trop Med Int Health 2005;10:581-8.  Back to cited text no. 2
3.Batra AK, Keoliya AN, Jadhav GU. Poisoning: An unnatural cause of morbidity and mortality in rural India. J Assoc Physicians India 2003; 51:955-9.  Back to cited text no. 3
4.Atul M, Sharma GK. A comparative study of poisoning cases autopsied in LHMC, New Delhi, and JIPMER, Pondicherry. Journal of Forensic medicine and Toxicology 2002;19:18-20.  Back to cited text no. 4
5.Inamadar AC, Palit A. Cutaneous reactions simulating erythema multiforme and Stevens Johnson syndrome due to occupational exposure to a plant-growth regulator. Indian J Dermatol Venereol Leprol 2007;73:330-2.  Back to cited text no. 5
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6.Centers for Disease Control and Prevention (CDC). Pesticide-related illnesses associated with the use of a plant growth regulator-Italy, 2001. MMWR Morb Mortal Wkly Rep 2001;50:845-7.  Back to cited text no. 6
7.Available from: Cochran RC, Leung P, Moore TB, Miller CD, Patterson GT, Formoli TA, et al. Hydrogen Cyanamide Risk Characterization Document. Department of Pesticide Regulation California Environmental Protection Agency. 1993. Available from: [Last Retrieved on 2010 Jul 29]  Back to cited text no. 7
8.Mertschenk B, Bornemann W, Filser JG, von Meyer L, Rust U, Schneider JC, et al. Urinary excretion of acetylcyanamide in rat and human after oral and dermal application of hydrogen cyanamide (H2NCN). Arch Toxicol 1991;65:268-72.  Back to cited text no. 8
9.Manoilov S, Sedykh N, Firsova V, Vennikas O, Chelyadina L. Effect of the catalase inhibitor 3-amino-1,2,4-triazole on oxidation-phosphorylation coupling and the state of the mitochondrial adenosine system in the liver of albino rats. Bull Exp Biol Med 1996;121:576-8.  Back to cited text no. 9 Haro L. Disulfiram-like syndrome after hydrogen cyanamide professional skin exposure: Two case reports in France. J Agromedicine 2009;14:382-4.  Back to cited text no. 10
11.Lorenzo de la Peña L, Montero Santos JM, Benito Lozano M, Martín Cabrera F. Acetaldehyde syndrome after laboral exposition to hydrogen Cyanamide. Med Clin (Barc) 2006;127:717-8.  Back to cited text no. 11
12.Cederbaum AI, Dicker E. Inhibition of the peroxidatic activity of catalase towards alcohols by the aldehyde dehydrogenase inhibitor cyanamide. Toxicol Lett 1985;29:107-14.  Back to cited text no. 12
13.DeMaster EG, Shirota FN, Nagasawa HT. Catalase mediated conversion of cyanamide to an inhibitor of aldehyde dehydrogenase. Alcohol 1985;2:117-21.  Back to cited text no. 13

Correspondence Address:
Punith Kempegowda
Department of Medicine, M S Ramaiah Medical Teaching Hospital, MSRIT Post, Bangalore
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0974-2700.83894

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