Archives of Medicine and Health Sciences

CASE REPORT
Year
: 2015  |  Volume : 3  |  Issue : 1  |  Page : 97--100

Plant growth nutrient (nitrobenzene) poisoning with multiple complications


Yatendra Singh, Makrand Singh, Sandeep Raj Saxena, Khalil Mohammad 
 Department of Medicine, Government Medical College, Haldwani, Uttarakhand, India

Correspondence Address:
Dr. Yatendra Singh
Department of Medicine, Government Medical College, Haldwani - 263 139, Uttarakhand
India

Abstract

Nitrobenzene, a pale yellow oily liquid with an odor of bitter almonds, is used in the synthesis of Aniline dyes, flavoring agent, and also in rubber industry. Recently it is also used as a plant growth nutrient. It causes methemoglobinemia with symptoms including headache, nausea, dizziness, fatigue, shortness of breath, cyanosis, and convulsions. Severe acute exposure to nitrobenzene can cause jaundice, renal failure, and coma, and it may be fatal. We report a case of Plant growth nutrient (nitrobenzene) poisoning with multiple complications like hemolytic anemia, renal failure, seizures, and pneumonia. Patient was managed with intravenous methylene blue along with other supportive therapy and survived. So, early aggressive management and a watch on complications might be helpful in saving patient«SQ»s life from this poisoning.



How to cite this article:
Singh Y, Singh M, Saxena SR, Mohammad K. Plant growth nutrient (nitrobenzene) poisoning with multiple complications.Arch Med Health Sci 2015;3:97-100


How to cite this URL:
Singh Y, Singh M, Saxena SR, Mohammad K. Plant growth nutrient (nitrobenzene) poisoning with multiple complications. Arch Med Health Sci [serial online] 2015 [cited 2020 Oct 22 ];3:97-100
Available from: https://www.amhsjournal.org/text.asp?2015/3/1/97/154956


Full Text

 Introduction



Nitrobenzene also known as nitrobenzol or oil of mirbane is used in dyes, paints, printing, lubricating oil, and synthetic rubber. Acute oral ingestion of nitrobenzene results in gastric irritation, including nausea and vomiting, the onset of which may be delayed for up to 12 hours post-exposure. [1] Methemoglobinemia will develop 1-4 hours post-exposure, indicated by cyanosis, the symptoms of which may be similar to those following inhalation. [2] Severe exposure to nitrobenzene by ingestion can also give rise to progressive drowsiness, seizures, and coma, which may prove fatal due to respiratory failure. [1] There is increasing use of this compound as plant growth nutrient in recent era because it promotes flowering in plants and also prevent flower shedding. [3] Nitrobenzene is a combination of nitrogen and plant growth regulators that act as plant energizer, flowering stimulant, and yield booster. [4] Here, we report a case with multiple complications due to ingestion of plant growth nutrient, which contains 20 % nitrobenzene. Poisoning with nitrobenzene as a plant growth nutrient is uncommon, and a very few cases reported till now with best of my knowledge. Life-threatening complications require immediate definitive management, which may change the patient's outcome.

 Case Report



A 30-year-old healthy married man presented to our hospital emergency department with history of consumption of around 100 ml of plant growth stimulant for suicidal intention. He was pale, conscious, disoriented, irritable, tachypneic, cyanotic, had 2-3 episodes of vomiting and 2 episodes of tonic-clonic seizures, and there was a bitter almond like pungent smell from patient's body.

On examination, BP was 110/60 with pulse of 120/min and respiratory rate 24/min, febrile. His body weight and height was 56 kg, 160 cm, respectively. His body mass index (BMI) was 21.8 kg/m 2 . Other systemic examination was normal. Treatment started with oxygen, intravenous (IV) fluids, and gastric lavage was done with normal saline. Patient was shifted to intensive care unit after brain imaging. Arterial blood gas (ABG) blood samples had a dark brown color. [Figure 1]a] Electrocardiogram (ECG) showed sinus tachycardia. X-ray chest and non-contrast computerized tomography (NCCT) head were normal. [Figure 1]b] His oxygen saturation decreased gradually, up to 60% on oxygen mask. Immediate intubation and ventilation with 100% oxygen and 5 cm positive end expiratory pressure (PEEP) improved the SpO 2 to 86% only. Arterial blood gas analysis shows metabolic acidosis (pH-7.20 and bicarbonate level 12 meq/l). Blood sugar was 106 mg/dl. Total leukocyte count was slightly raised, i.e 11,000/mm 3 with polymorphonuclear leukocytosis. Platelet count was 180,000/mm 3 . Liver enzymes (AST-42U/L,ALT-44U/L, Bilirubin-0.8), serum creatinine (1.4 mg/dl), and electrolytes (serum sodium- 145 meq/l, serum potassium-4.6 meq/l) were within normal range. Methemoglobin level was 42%. [Table 1] So diagnosis of nitrobenzene-induced methemoglobinemia was made, which was again supported when the patient's attendant brought empty bottle, which contain 20% nitrobenzene compound. [Figure 1]d] Ten milliliters (100 mg) of methylene blue and ascorbic acid 500 mg were given intravenously. This improved his SpO 2 to 94%, which dropped after about 6 hours, and then 100 mg IV methylene blue was repeated. Intravenous vitamin K, dextrose containing intravenous fluids and an antibiotic (piperaciilin + tazobactum) were also given. Inially patient was managed symptomatically, and methylene blue was available after 8 hours. He started to follow command after 2 days, but he was having SpO 2 between 85% and 90%. He was extubated on fourth day oxygen saturation, which was around 90%.{Figure 1}{Table 1}

Fourth day onward, the patient developed jaundice, progressive decrease in urine output, and renal failure. Investigation shows rising creatinine, bilirubin, aminotransferase levels, and deranged prothrombin time with a significant reduction in his hemoglobin and hematocrit values [Table 1] with increase in serum lactic dehydrogenase level and an uncorrected reticulocyte count of 8.0%. Peripheral blood smear showed normocytic, normochromic red blood cells that demonstrated polychromasia, anisocytosis, tear drop cells, and bite cells consistent with hemolysis. Coombs tests direct and indirect were negative, and a glucose-6-phosphate dehydrogenase (G6PD) screening test was normal. Urine was cola colored, and dipstick test was positive for heme protein. [Figure 1]c] Over next four days, the patient was given five units of blood transfusion and had two session of hemodialysis on day 6 and 8. Chest X-ray was repeated on sixth day, which shows right lower lobe pneumonitis. [Figure 2] On 10 th day, patients hematological and biochemical parameters improved significantly. He was discharged after 2 weeks of antibiotic therapy. Patient followed after 2 weeks. His chest X-ray was normal, and hemoglobin was 12.0 gm%.{Figure 2}

 Discussion



Nitrobenzene is readily absorbed following inhalation, ingestion, and dermal contact. There are few studies investigating the metabolism of nitrobenzene in humans. Following accidental nitrobenzene poisoning in humans, the highest concentration was found in the liver, brain, blood, and stomach. In a human volunteer study following the oral administration of 30 mg nitrobenzene, the urinary excretion of P-nitrophenol was slow, with an initial elimination half-life of approximately 5 hours, followed by a secondary slow phase with an elimination half-life of over 20 hours. [1] The principal characteristic health effect following acute exposure to nitrobenzene is the development of methemoglobinemia, which can give rise to symptoms including headache, nausea, dizziness, drowsiness, shortness of breath, fatigue, cyanosis, and convulsions. [1],[2],[5] In some cases of acute nitrobenzene ingestion, hemolytic anemia may develop approximately 5 days post-exposure. [1] Serious acute exposure to nitrobenzene may result in jaundice, liver failure, renal failure, coma, and can potentially be fatal. [1],[5],[6] Our patient had progressive involvement all these system and also had severe hemolytic anemia after 5 days of illness. Severe hemolytic anemia might be due to oxidative stress seen in nitrobenzene poisoning.

The lethal dose ranges from 1 to 10 g, but there are no consistent reports regarding fatalities and the dose of ingestion. [7],[8] Acute exposure to nitrobenzene leads to the development of methemoglobinemia, a condition in which the iron within the hemoglobin is oxidized from ferrous (Fe 2+ ) to ferric (Fe 3+ ) state, resulting in the inability to transport oxygen and thus causing a brownish discoloration of the blood. [8] Systemic manifestations of methemoglobinemia at different blood levels are as follows, at 10-15%, cyanosis alone is obvious, though asymptomatic. Beyond 20%, headache, dyspnea, chest pain, tachypnea, and tachycardia develop. At 40-50%, confusion, lethargy and metabolic acidosis occur, and fractions around 70% are fatal. [9],[10] Anemic patients and those with G6PD enzyme deficiency suffer more severe symptoms. [11] Systemic redistribution of nitrobenzene from tissue stores is likely. As in our patients methemoglobin was 42% and was having most of complications. Recurrent methemoglobinemia suggested by persistence of significant methemoglobin levels up to 72-96 hours after exposure. It is rare but was present in our patient, might be due to large amount intake. In these situations, metabolism of parent compound and active metabolites is saturated because of slow hepatic microsomal nitroreductase rates leading to prolonged exposure to the active metabolite and a prolonged zero-order production of a toxic metabolite of nitrobenzene causing persistent oxidative stress. [12] Treatment is based on the principles of decontamination and symptomatic and supportive management. Methylene blue is the antidote of choice for the acquired (toxic) methemoglobinemia. It is an exogenous cofactor, which greatly accelerates the NADPH-dependant methemoglobin reductase system and is indicated if the methemoglobin levels, which are more than 30%. [13] It is administered intravenously at 1-2 mg/kg (up to 50 mg dose in adults,) as a 1% solution over 5 minutes; with a repeat in 1 hour, if necessary. Methylene blue is an oxidant at levels of more than 7 mg/kg, and therefore, may cause methemoglobinemia in susceptible patients. It is contraindicated in patients with G6PD deficiency, because it can lead to severe hemolysis. Ascorbic acid is an antioxidant that may also be administered in patients with methemoglobin levels of more than 30%. [14]

Our patient had clinical manifestation of methemoglobinemia like characteristic smell of bitter almonds, persisting cyanosis on oxygen therapy without severe cardiopulmonary disease, low arterial oxygen saturation, which later confirmed due to nitrobenzene when patient's attendant brought empty bottle. Our patients had four unusual features. First, patient had intake of plant growth nutrient/stimulant, which is not a very common source of nitrobenzene poisoning seen in clinical practice. Second, our patient had severe renal insufficiency, which required hemodialysis. Third, our patient was having severe hemolytic anemia, which indicates that only persistent methemoglobinemia is not only cause of low saturation. Fourth, patient presented with seizures. Besides this, the patient also developed ventilator-associated pneumonia, but our patient survived despite all these complication.

In this case, early recognition of poisoning, availability of methylene blue, blood transfusion, hemodialysis, and adequate antibiotics lead to good outcome.

 Conclusion



Acute methemoglobinemia is a life-threatening condition, which requires immediate and definitive management. Nitrobenzene poisoning is one of the important causes of methemoglobinemia. Poisoning with dyes, paints, printing, lubricating oil, and synthetic rubber, which have nitrobenzene as main constituent, is well known. But one should also know that plant growth stimulant that widely used now, also have nitrobenzene compound. Physicians must be aware of common substance containing nitrobenzene compound, pathophysiology of these compound, and its complications and treatment modalities.

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