2,4,6-TRINITROTOLUENE (TNT) is used extensively in the manufacturing of explosives. Methemoglobinemia induced by TNT has been previously reported after occupational exposure to TNT in mining and chemical industries. 1,2However, this is the first report describing the occurrence of methemoglobinemia in a man who was exposed to a blast injury while manipulating a TNT bomb.

A 17-yr-old man, previously healthy, sustained a blast injury while manipulating a bomb. Based on information from the patient, the bomb was identified as containing TNT. In the emergency room, the patient was conscious and anxious and reported severe headache. He presented with partial-thickness and full-thickness burns with tattooing on his trunk, upper extremities, and face. Also, he had swollen lips and bilateral severe corneal burns and lacerations. The electrocardiogram, chest radiograph, blood count, coagulation profile, and serum biochemistry results were normal. A fiberoptic bronchoscopy performed under sedation with 2 mg intravenous midazolam revealed normal airways. The patient was scheduled for bilateral corneal suturing and was premedicated with 0.5 mg intramuscular atropine. In the operating room, the patient’s heart rate was 90 beats/min, and his blood pressure was 100/70 mmHg. Pulse oximetry (Spo2) on room air was 89%. The patient was preoxygenated with 100% oxygen using a tight-fitting facemask; however, preoxygenation failed to increase the Spo2. It was difficult to notice whether the patient’s fingers or lips were blue because of the burns and soot due to the explosion. Checking the Spo2on the toe revealed cyanosis associated with the same Spo2value of 89%. An arterial blood gas analysis (Stat profile 1; Nova Biomedical, Waltham, MA) after the patient had breathed room air for 10 min revealed chocolate-colored blood associated with an arterial partial pressure of oxygen (Pao2) of 90 mmHg, a partial pressure of carbon dioxide (Pco2) of 44 mmHg, a pH of 7.35, and an arterial oxygen saturation (Sao2) of 97%. Arterial blood sampling, repeated after the patient breathed 100% oxygen, showed a significant increase in Pao2up to 480 mmHg associated with an Sao2of 100%, without any increase in Spo2(90%). Methemoglobinemia was suspected because of the low pulse oximetry value associated with a normal Pao2. However, methemoglobinemia could not be confirmed immediately because of the unavailability of cooximetry. Because it was urgent to repair the corneal lacerations, it was decided to proceed with the surgery as planned. Anesthesia was induced intravenously with 2 mg/kg propofol, 6 mg vecuronium, and 100 μg fentanyl. After tracheal intubation, anesthesia was maintained with 1–2% sevoflurane in 100% oxygen. At the end of surgery, the patient was kept intubated and was ventilated postoperatively with an inspired oxygen fraction (Fio2) of 40%. The next day, the Spo2was 91%, and the diagnosis of methemoglobinemia was confirmed by an arterial blood gas analysis, measured by cooximetry (ABL 700 series; Radiometer, Copenhagen, Denmark), which revealed the following results: Pao2, 160 mmHg; oxyhemoglobin (O2Hb) saturation, 98%; reduced hemoglobin (RHb) saturation, 2.2%; carboxyhemoglobin (COHb) saturation, 0.2%; methemoglobin (MetHb) saturation, 18%; functional oxygen saturation, 98%[Sao2= (O2Hb/O2Hb + RHb) × 100%)]; fractional oxygen saturation, 80%[SfO2= (O2Hb/O2Hb + RHb + COHb + MetHb) × 100%]. No treatment was instituted, and the trachea was extubated uneventfully. On day 3, the Spo2during spontaneous breathing of room air increased up to 98%, and analysis of arterial blood gas by cooximetry revealed an Sao2of 98%, a Pao2of 100 mmHg, an oxyhemoglobin concentration of 96%, and a methemoglobin concentration of 1.8%. The patient was discharged from the hospital on day 4.

Acute methemoglobinemia can be hereditary, 3,4but most often, it is acquired after exposure to a variety of chemicals and drugs, 5among which nitrites and aniline derivatives have been reported to be the most common agents. 6,7There were no hereditary factors that might have predisposed our patient to greater methemoglobin formation from TNT exposure.

2,4,6-Trinitrotoluene  is a nitroaromatic compound that is used as an explosive in military armaments and as a chemical intermediate in the manufacture of dyestuffs and photographic chemicals. 1TNT produces methemoglobinemia by a direct oxidizing effect on the hemoglobin. 8The rate constants of oxyhemoglobin oxidation by nitroaromatic explosives are related to their structure; the rate constant is increased with an increase in a single-electron reduction potential or with a decrease of the enthalpies of single-electron reduction of nitroaromatics. 8When comparing the structure–activity relations in methemoglobin formation in human erythrocytes by high explosives, 2,4,6-TNT, 2,4,6-tetryl, and 2,4,6-pentryl, 2,4,6-TNT is found to be a more efficient methemoglobin-forming agent than the other explosives. 8TNT is absorbed through the gastrointestinal tract, the skin, and the lungs. 1In our patient, inhalation and/or cutaneous absorption are assumed to be the primary pathways for exposure. However, the absence of airway involvement, as evidenced by fiberoptic bronchoscopy, suggests that cutaneous absorption is more likely.

The toxicity of TNT occurs predominantly after occupational exposure in mine workers and chemical industrial workers. 1,2,9Also, TNT has been found in the soil, surface water, and groundwater due to the release of waste water from TNT-manufacturing facilities and from buried ammunition wastes. 10,11Thus, TNT toxicity may occur in individuals drinking contaminated water or ingesting contaminated foods from contaminated soils. 12In addition to methemoglobinemia, short-term exposure to TNT may result in contact burns to the skin and eyes, headache, weakness, dizziness, nausea, shortness of breath, and tachycardia. 1 

In our patient, who had a methemoglobin concentration of 18%, the oxygen saturation on room air as measured by pulse oximetry was 91%. The absorbance characteristics of methemoglobin are such that the pulse oximetry shows an Spo2around 85%, regardless of the Pao2. 13The diagnostic test of choice for methemoglobinemia is cooximetry, which provides a spectrophotometric analysis of different hemoglobin types. 14 

In patients with methemoglobinemia, cyanosis is usually observed at concentrations that are greater than 1.5 g/dl and is often one of the earliest clinically evident features of methemoglobinemia. 15Our patient presented only with cyanosis, with no other symptoms of methemoglobinemia. However, the classic slate-gray cyanosis of the hands and face was masked by burns until further examination revealed cyanosed toes.

In patients with consequences of increased methemoglobin, the decision to treat is based on the methemoglobin concentration as well as on the clinical presentation. Typically, methylene blue is the treatment of choice; it is initiated at methemoglobin concentrations between 10 and 30% in symptomatic patients and in patients with concomitant disease states. In acquired methemoglobinemia, after exposure to the offending agent ends, methemoglobin concentrations usually return to normal within 36 h. 15Our patient was previously healthy and presented only with cyanosis; hence, no treatment was instituted. His methemoglobin concentration was 18% at 12 h after the exposure and decreased to a concentration of 1.8% after 48 h.

In conclusion, the current report directs our attention to the possibility of developing methemoglobinemia as one of the consequences of TNT explosion.

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