members and brought to the ED without any prehospital treatment. At the time of presentation, he was restless and irritable with features of facial flushing, profuse sweating, stridor, and drooling of saliva. Because the offending agent was a powder, it was spilled over his face.

Physical examination revealed cold and clammy periph- eries, and injected conjunctiva. His blood pressure was 90/60 mm Hg; and pulse and respiratory rate per minute were 110 and 28, respectively, and regular. There was no cyanosis, icterus, itching, or swollen lips or tongue. His pupils were normal and reacting to light. Systemic examination revealed bilateral end-expiratory wheeze and positive Trousseau and Chvostek response. There were no abnormal movements. Clinical examination of other systems was unremarkable.

The white powder seen over his face and eye was collected and sent for chemical analysis, and then thoroughly rinsed with tepid tap water as a part of decontamination procedure [2]. Analysis of gastric lavage did not reveal any evidence for oral ingestion of MAP or other Toxic substances. Direct visualization of the oropharynx revealed chalk-like white powder deposited over the swollen erythematous vocal cord. In view of Obstructed airway, endotracheal intubation was performed immediately and ventilated mechanically. Bron- choalveolar lavage was performed. His cardiac activities were monitored continuously from the time of admission.

Analysis of arterial blood gases revealed a pH of 7.24 with PCO₂ of 38, PO₂ of 220 mm Hg, and HCO₃ of 15.7 mEq/L with normal anion gap. His blood glucose, urea nitrogen, creatinine, sodium, Creatine phosphokinase, myoglobin, potassium, albumin, Liver enzymes, bilirubin, lipase, and amylase were within normal levels. He had hyperphosphate- mia (11.0 mg/dL [normal 3-4.5]), hypocalcemia (ionized calcium,

1.18 mg/dL [normal 4.4-5.1]; total calcium, 3.6 mg/dL

[normal 8.4-10.2]), and hypomagnesemia (1.2 mg/dL [normal 1.8-2.4]). He had prolonged QT interval of 340 with a calculated QTc of 498 milliseconds. Result of initial chest film was normal. His hematological features did not reveal any abnormalities on admission and during in-hospital follow-up. Chemical analysis of the powder confirmed it to be MAP.

The patient received 20 mL of 10% Calcium gluconate (approximately 200 mg of elemental calcium) intravenously

0735-6757/$ - see front matter (C) 2012

515.e4 Case Report

over a period of 10 minutes. magnesium sulfate was infused at a dose of 2 g over a period of 1 hour intravenously to correct his hypomagnesemia. He was shifted to the intensive care where continuous infusion of calcium gluconate was started (1 mg/[kg h]). Two hours after presentation, the patient developed Generalized seizure unresponsive to 2 + 2 mg of intravenous lorazepam. However, intravenous calcium gluconate 100 mg resulted in resolution of Seizure activity. He subsequently manifested 4 episodes of pulseless Polymorphic ventricular tachycardia (PVT) requiring defi- brillation. He was managed with infusion of vasopressors, amiodarone, and calcium gluconate in addition to calcium carbonate 500 mg through nasogastric tube every 4 hours, along with maintenance fluids that included 5% dextrose, lactated Ringer, and 0.45% sodium chloride.

The admission chest radiograph was clear; but the picture taken on the second day revealed infiltrative changes, which cleared after 7 days. He was on ventilator, although alert and oriented. Bronchoscopy was performed 24 hours after injury and revealed a gradual resolution of an edematous tracheobronchial mucosa. Even after intensive management over a period of 36 hours, the patient was found to have hypernatremia, hypocalcemia, hyperphosphatemia, and acid- emia. Hence, he was subjected to 2 cycles of hemodialysis to rapidly lower the phosphate concentration and correct acidosis. Over the next 36 hours, the patient was successfully weaned off the ventilator.

To avoid postextubation stridor, the patient was started on 40 mg of methylprednisolone at 6-hour interval 24 hours before extubation. As he experienced a postextubation stridor, he required tracheotomy. Over the next 48 hours, the patient was successfully decannulated and became symptom-free. Results of repeated estimation of Serum electrolytes including calcium, magnesium, and phosphorus were within normal limits. He did not develop chronic pulmonary or kidney manifestations during follow-up.

The occupational hazards associated with industrial chemicals in the workplace are known. Similarly, the general public has an access to a plethora of chemical products available at home or in the workplace. Knowing the offending agent is the key in the management of this environmental toxicological exposure [2]. Monoammonium phosphate, a dry chemical (lyophobic colloid) present in fire extinguishers, is the culprit in the present case; and it is corrosive.

Respiratory complications caused by inhalation and their treatment epitomize the challenges that confront clinicians caring for these cases. In this case, upper airway injury has resulted in obstruction, which commonly occurs in approx- imately one fifth to one third of hospitalized victims with inhalation injury and is a major hazard because of the possibility of Rapid progression from mild pharyngeal edema to complete upper airway obstruction with asphyxia. [3]

Delayed recognition resulting in lung injury following inhalation of fire extinguisher powder was observed by Beitland et al [4]. In inhalational poisoning, the admission chest radiograph may be clear and serve as baseline, but is

seldom diagnostic. In the present case, infiltrative changes appeared in the chest radiograph on the second day and cleared after 7 days. Hence, the current standard for diagnosis of inhalation injury is fiberoptic bronchoscopy. Two thirds of the patients with inhalational injury develop diffuse or focal infiltrates or pulmonary edema within 5 to 10 days of injury, although the admission film may not be contributory.

Many texts and reviews [5,6] indicate that occurrence of QTc prolongation without alterations in T-wave morphology is associated with PVT, which is also observed frequently in pharmacologically induced or inherited types of long QT syndrome. Concurrent magnesium levels were not reported in those patients. The present case exhibited abnormally low calcium and magnesium levels, as well as high phosphate. Hypomagnesemia generating clinically relevant electrocardio- graphic abnormalities [7] or arrhythmias was attributed to its effect on transmembrane ion channels for sodium, potassium, and calcium. Although no clear consensus is apparent, most electrocardiographic abnormalities in the clinical setting of hypocalcemia and hypomagnesemia are attributed to the former. However, hypomagnesemia as a cause of QTc prolongation and/or PVT has been discussed earlier [7].

Phosphate is a major component of intermediary metabolism. Orally, it is absorbed in duodenum and jejunum. However, in the present case, absorption might occur through the upper respiratory tract in a significant manner in view of the high concentration of MAP in the spray, due to a linear relationship between phosphate absorption and mucosal phosphate concentration. [8] Thus, the patient had hyperphosphatemia, which resulted in hypocalcemia. Altera- tions in serum phosphorus and calcium levels were shown to occur within 40 minutes in a case in which phosphate- containing retention enema was administered [9]. Further- more, acute hyperphosphatemia causing acute phosphate nephropathy and acute renal failure was observed in patients who received sodium phosphate solution via the oral [10-12] or rectal route [13] as laxative. The risk factors for acute phosphate nephropathy are advanced age, female sex, Volume depletion, preexisting illnesses, and use of thera- peutic agents such as angiotensin-converting enzyme inhibitors, diuretics, or nonsteroidal Anti-inflammatory agents. In this case, early management of hyperphosphate- mia and acidosis by hemodialysis [13] and absence of risk factors might have prevented him from developing acute phosphate nephropathy.

Treatment of phosphate-induced hypocalcemia is directed toward normalization of calcium so as to prevent and treat potential severe adverse effects including cardioVascular abnormalities, seizures, or tetany as observed in this case. rapid correction of hypocalcemia in this case might have reverted the QTc prolongation and controlled the seizures, too. The importance of rapid correction in a similar situation was documented earlier. Although Torsades de pointes was documented, the combination of seizure activity, pulseless- ness, and QTc prolongation further suggested dangerous ventricular arrhythmia that occurred on 4 occasions in the

Case Report 515.e5

present case. Calcium chloride is generally used because it contains the highest concentration of ionized calcium compared with other calcium salts.

Because there is an easy access to these types of fire extinguishers and in view of systemic toxicity including cardiac arrest [14], emergency physicians have to know this entity. However, awareness of MAP poisoning, early recognition of the metabolic abnormalities, and appropriate intervention have helped in the recovery of this case.

Intentional inhalation of MAP had resulted in metabolic derangement, respiratory manifestations, seizures, cardiac arrhythmias, acidosis, hyperphosphatemia, hypocalcemia, and hypomagnesemia. Hemodialysis was found to be a valid therapeutic option to correct life-threatening hyperphosphate- mia and acidosis even in the presence of normal renal function.

The case was evaluated in detail, the chemical constituent of the powder was analyzed, and appropriate measures were provided to the patient. Early recognition and management of hyperphosphatemia and acidosis by hemodialysis pro- tected the individual from acute phosphate nephropathy. The limitation was lack of histopathological studies of lung and renal tissues, as the patient refused such procedures.

Subramanian Senthilkumaran MD

Sri Gokulam Hospitals & Research Institute

Salem Tamil Nadu, India E-mail address: [email protected]

Ramachandran Meenakshisundaram MD

Madras Medical College, Chennai, India

Namasivayam Balamurgan DM

Sri Gokulam Hospitals & Research Institute

Salem Tamil Nadu, India

Krishnanswamy SathyaPrabhu MD

Vinayaga Mission university hospitals, Salem, India

V Karthikeyan DM

Sri Gokulam Hospitals & Research Institute

Salem Tamil Nadu, India

Ponniah Thirumalaikolundusubramanian MD

Chennai Medical College Hospital & Research Center

Irungalur, Trichy, India

doi:10.1016/j.ajem.2011.01.018

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