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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2012  |  Volume : 23  |  Issue : 6  |  Page : 1300-1303
Imidacloprid poisoning presenting as leukoclastic vasculitis with renal and hepatic dysfunction

1 Department of Internal Medicine, Armed Forces Hospital Southern Region, Khamis Mushayt, Saudi Arabia
2 Emergency Medicine, Emory University School of Medicine, Georgia Poison Center, USA
3 Department of Medicine, King Khalid University, Abha, Saudi Arabia

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Date of Web Publication17-Nov-2012

How to cite this article:
Agha A, Bella A, Aldosary B, Kazzi ZN, AlHumaidi MA. Imidacloprid poisoning presenting as leukoclastic vasculitis with renal and hepatic dysfunction. Saudi J Kidney Dis Transpl 2012;23:1300-3

How to cite this URL:
Agha A, Bella A, Aldosary B, Kazzi ZN, AlHumaidi MA. Imidacloprid poisoning presenting as leukoclastic vasculitis with renal and hepatic dysfunction. Saudi J Kidney Dis Transpl [serial online] 2012 [cited 2023 Feb 2];23:1300-3. Available from: https://www.sjkdt.org/text.asp?2012/23/6/1300/103584
To the Editor,

Imidacloprid, a nicotinic acetylcholine receptor agonist, is considered to be a moderately toxic and relatively safe insecticide that is being increasingly used around the world. However, recent case reports of imdicloprid poisoning and fatalities indicate that its toxicity may be underestimated. We report the case of a 62-year-old Saudi male who presented to the emergency department with a history of fever, disorientation, passing red-colored urine, lower abdominal pain and vomiting of four days duration prior to admission. He showed no improvement after two days of treatment with intravenous antibiotics and fluids. Detailed evaluation and observation revealed that the patient had high-grade intermittent fever up to 38.5°C relieved only by antipyretics, mild irritability and was not fully oriented to person; there was no focal neurological deficit. He was a known diabetic on oral hypoglycemic agents and suffered from hypertension that was well controlled on medications. There was no recent modification in his medications. He also gave a past history of having undergone surgery for stone in the left kidney. He was a cultivator by profession and was actively involved in all chores related to his farm.

During the present visit, he was seen by the emergency physician and referred to the urologist for evaluation of hematuria. On examination, the patient was febrile (38.7°C), blood pressure was 138/76 mmHg, pulse was 108/min, oxygen saturation of 91% on room air and he was alert and oriented, but ill appearing. The remainder of his examination was normal except for mild irritability and presence of mild coarse rales in the right lower chest. There was no abdominal or loin tenderness or organomegaly. The laboratory data was significant for metabolic acidosis with serum bicarbonate (HCO 3 ) of 17.0 meq/L. Urinanalysis showed hematuria with greater than 200 red blood cells (RBC) and five to six white blood cells (WBC). The serum creatinine was 276 umol/L. A chest X-ray showed patchy pneumonitis in the right lung base [Figure 1]A. A provisional diagnosis of obstructive uropathy with infection was made and the patient was admitted to urology and the pulmonary team was consulted to comment on the abnormal chest X-ray. The ultrasound and computerized tomography (CT) scan of the abdomen showed only a small right renal cyst.
Figure 1A: Chest X-ray on admission showing right basal pnemonitis (supine AP view).
Figure 1B: Chest X-ray on discharge showing resolution of the pneumonitis (PA view).

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The laboratory work-up revealed that the alanine amino transferase (ALT) was raised four times the normal limit along with raised urea and creatinine [Table 1]. The patient was aggressively managed by urology, pulmonary as well as nephrology and gastroenterology teams as a case of sepsis with urinary tract infection as a likely source. The patient had already been started on ceftriaxone (1 gram every 12 hours) and intravenous (IV) hydration, but there was no response. The patient then developed a diffuse maculopapular erythematous rash over the trunk and extremities [Figure 2]A. The dermatologist was consulted and a clinical diagnosis of leukoclastic vasculitis was considered and a skin biopsy was planned. The patient was found to have an erythematous posterior pharynx and mildly inflamed tonsils. On the third post-admission day, the patient admitted to spraying insecticide on his farm trees for 30 min almost one week prior to presentation without wearing any mask or gloves. As the liver and renal functions started to deteriorate further with ALT in range of 270s IU/L and creatinine in the range of 350s umol/L, and the patient became more irritable, the attendant was asked to bring the bottle of the insecticide that the patient was exposed to. This was found to contain 30% imidacloprid, branded as SUREKILL by Riyadh Chemicals Limited. Serum and urine samples of the patient along with the insecticide material were sent to toxicology and subjected to gas chromatography and mass spectrometry electron impact (GC-MS EI) via GCMS machine #6890/5973 from AGILENT to detect the presence of parent compound imidacloprid in the serum as well as in urine. Imidacloprid levels were detectable in these samples even eight days after exposure to the drug, although, as per the manufacturer's information, the compound gets metabolized within 72 h and is excreted in urine. The patient continued to deteriorate with increasing confusion and drowsiness along with further derangement in hepatic and renal function tests [Table 1]. Based on the presence of imidacloprid levels detectable in serum, continued downhill course of the patient and good water solubility of the compound, a suggestion was made to hemodialyze the patient. However, both the patients' family and the nephrologist were skeptical about the advantage of simple hemodialysis in removing imidacloprid as it has never been attempted before. Hence, the decision to perform hemodialysis was temporarily postponed.
Figure 2A: Generalized multiple maculopapular erythematous rash typical of leukoclastic vasculitis.
Figure 2B: Skin biopsy showing hyperkeratosis with damage to vessel wall with neutrophils, indicative of neutrophilic vasculitis.

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Table 1: Summary of laboratory investigations of the study patient.

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On the fourth post-admission day, punch biopsy of one of the skin lesions from the thigh was taken and was reported as hyperkeratosis with damage to the vessel wall, with neutrophils indicative of neutrophilic vasculitis [Figure 2]B. Prednisone, in a dose of 1 mg/kg body weight, was started for leukoclastic vasculitis. The antibiotic was changed to pipercillin/tazobactam adjusted according to creatinine clearance of about 17 mL/min. The patient's condition remained unchanged, with drowsiness, decreased appetite and deranged liver and renal profile, microscopic hematuria and itchy erythematous papular eruptions for about four days on supportive therapy. It was decided to recheck imidacloprid levels in the serum and urine and, if detectable, to proceed with hemodialysis. On the ninth post-admission day, the patient started to show improvement. The imidacloprid level was re-checked and was not detectable. The patient was maintained on supportive therapy, the antibiotics were discontinued and the dose of steroids was decreased. The patient had almost complete resolution of his clinical symptoms, including the skin rash as well as the chest findings, and, by the 14 th post-admission day, the laboratory results returned to near-baseline levels. He was discharged the next day on a tapering dose of steroids.

Imidacloprid is increasingly used worldwide as an insecticide that acts as a nicotinic acetylcholine receptor agonist. The inherent structural differences between insect and mammalian nicotinic receptors make this insecticide selective to insects and relatively non-toxic to humans. [1],[2] The World Health Organization rates imidacloprid as moderately toxic while the United Sates Environmental Agency considers it of unlikely carcinogenic potential; therefore, it is not banned, restricted, or illegal to import in any country. [2]

This safety profile and apparent non-irritability to skin and eyes makes it a good and commonly used pesticide, but fatality and morbidity due to exposure to this pesticide might be underestimated. [3] There have been many case reports of imidacloprid toxicity and even fatalities. [4] Severe cardiac toxicity after massive ingestion of imidacloprid has been reported, with ventricular arrhythmia being one of the fatal complications in a patient with known coronary artery disease. [5] Rhabdomyolysis, which might be related to direct nicotinic end-plate stimulation or fever, may lead to renal failure and ensuing fatality. [6] Central nervous system effects including neuropsychiatric manifestations are common reported in imidacloprid poisoning cases, although it is reported by the manufacturer to have poor penetration of the blood-brain barrier in mammals. [7] Other toxic effects include cough, hemorrhagic gastritis, fever and elevated white blood cell count. [8] Post-mortem levels of imidacloprid and its metabolite 6-chloronicotinic acid have been detected in some fatalities from large ingestions, confirming the cause of death. [9],[10] When compared with other available organophosphorus compounds, imidacloprid is generally less toxic to humans, with serious complications being respiratory failure and reduced level of consciousness. Thus, it has been advocated to replace organophosphorus compounds with imidacloprid in agruiculture. [11] However, based on the experience from our case and several other similar reports, we would like to emphasize that self-poisoning from imidacloprid still carries a significant morbidity and there is a need for exercising caution while using this product and using appropriate personal protective equipment.

Accidental imidacloprid toxicity can be life-threatening and should be considered in the differential diagnosis in patients presenting with multi-organ dysfunction after exposure to it. To the best of the authors' knowledge, this is possibly the first reported case of leukoclastic vasculitis due to imidacloprid skin contact and inhalation exposure. Patients with significant exposure to this compound with renal and liver impairment should be managed in the critical care unit. Although dialysis was not used in our patient, it was felt that it would expedite recovery, and future research may further study this question.

   References Top

1.Cox C. Imidacloprid insecticide factsheet. J Pestic Reform 2001;21:15-21.  Back to cited text no. 1
2.Tomizawa M, Maltby D, Talley TT, et al. Atypical nicotinic agonist bound conformations conferring subtype selectivity. Proc Natl Acad Sci U S A 2008; 105:1728-32.  Back to cited text no. 2
3.U.S. Environmental Protection Agency. 1995. Imidacloprid; pesticide tolerance and raw agricultural commodities. 40 CFR Part 180 Section 472.  Back to cited text no. 3
4.Costa C, Silvari V, Melchini A, et al. Geno-toxicity of imidacloprid in relation to metabolic activation and composition of the commercial product. Mutat Res 2009;672:40-4.  Back to cited text no. 4
5.Wu IW, Lin JL, Cheng ET. Acute poisoning with the neonicotinoid insecticide imidacloprid in N-methyl pyrrolidone. J Toxicol Clin Toxicol 2001;39:617-21.  Back to cited text no. 5
6.Huang NC, Lin SL, Chou CH, Hung YM, Chung HM, Huang ST. Fatal ventricular fibrillation in a patient with acute imidacloprid poisoning. Am J Emerg Med 2006;24:883-5.  Back to cited text no. 6
7.Agarwal R, Srinivas R. Severe neuropsychiatric manifestations and rhabdomyolysis in a patient with imidacloprid poisoning. Am J Emerg Med 2007;25: 844-5.  Back to cited text no. 7
8.Shadnia S, Moghaddam HH. Fatal intoxication with imidacloprid insecticide. Am J Emerg Med 2008;26: 630-4.  Back to cited text no. 8
9.David, D, George IA, Peter JV. Toxicology of the newer neonicotinoid insecticides: Imidacloprid poisoning in a human. Clin Toxicol 2007;45: 485-6.  Back to cited text no. 9
10.Proenca, P, Teixeira H, Castanheira F, et al. Two fatal intoxication cases with imidacloprid: LC/MS analysis. Forensic Sci Int 2005;153:75-80.  Back to cited text no. 10
11.Mohamed F, Gawarammana I, Robertson TA, et al. Acute human self-poisoning with imidacloprid compound: A neonicotinoid insecticide, PLoS ONE 2009;4:4. e5127.  Back to cited text no. 11

Correspondence Address:
Adnan Agha
Department of Internal Medicine, Armed Forces Hospital Southern Region, Khamis Mushayt
Saudi Arabia
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-2442.103584

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