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Hydrogen Fluoride Inhalation Injury from a Fire Suppression System

Capt Matt Chauviere and Lt Col Dustin Zierold60th Medical Group, Dept of Surgery, David Grant Medical Center

101 Bodin CircleTravis AFB, CA 94535

USA

[email protected]

ABSTRACT

Automatic fire suppression systems use hydrofluorocarbons (HFC) to chemically extinguish fires. At high temperatures, HFC can release hydrogen fluoride, a toxic and potentially lethal gas. We report the deaths of three US military personnel at Bagram Air Base from acute respiratory failure after the fire suppression system in their vehicle received a direct hit from a rocket propelled grenade. Despite presenting with little to no additional signs of trauma, these individuals all died within 24 hours from hydrogen fluoride induced respiratory failure. When two patients later presented with similar symptoms after damage to their vehicle's fire suppression system, they were aggressively treated with nebulized calcium and positive pressure ventilation. Both survived. The presence of HFC-containing fire suppression systems in military vehicles may lead to future cases of this quaternary blast injury, and further research must be done to help rapidly diagnose and effectively treat this injury.

1.0 INTRODUCTION

Automatic fire suppression systems (FSS) have been used in US military ships, aircraft, and vehicles since World War II. FSS typically feature a chemical extinguishing agent such as a hydrofluorocarbon (HFC). One commonly used HFC is 1,1,1,2,3,3,3-hepatofluoropropane (also known as HFC-227 or FM 200®). While HFC-227 itself is nontoxic, at high temperatures it decomposes, producing hydrogen fluoride (HF).1-3 HF inhalation causes devastating pulmonary injuries that can rapidly result in death.4-7 We report two events involving HF inhalation injury due to FSS.

2.0 CASE REPORT

2.1 Case #1Three US soldiers presented to a Forward Operating Base in Afghanistan after a rocket propelled grenade (RPG) struck their Mine Resistant Ambush Protected vehicle (MRAP). All three had dyspnea, but only one had evidence of trauma (rib fractures and a unilateral pneumothorax). Their respiratory distress worsened, and two patients were intubated. They were then transferred to Bagram Air Base at four hours post-injury.

At Bagram, reexamination revealed no additional injuries. The unintubated patient was severely dyspneic and intubated soon after arrival. All three patients were admitted to the Intensive Care Unit (ICU). Subsequent radiographs showed bilateral pulmonary infiltrates in each patient (see Fig. 1). All patients were ventilated with a lung-protective ventilation strategy using a pressure control mode to achieve low tidal volumes (6-8 mL/kg). High positive end-expiratory pressures (PEEP) in excess of 15 cm H2O and FiO2 settings over 80%

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were required to maintain adequate oxygenation. Central venous pressures were initially in normal ranges but soon rose to above normal limits with low mean arterial pressures despite aggressive fluid resuscitation.

Figure 1: Appearance of chest CT at 12 hours and chest radiograph at 18 hours after injury.

Due to the severe refractory hypoxemia present in these patients, the Acute Lung Rescue Team (ALRT) based at Landstuhl Regional Medical Center (LRMC) was activated. The ALRT, composed of experienced critical care physicians, critical care nurses, and respiratory technicians, specializes in transporting patients with severe lung injuries.8 The ALRT facilitates transport of critically ill patients outside of Critical Care Air Transport criteria and even offers salvage therapy with extracorporeal support.8

The ALRT arrived at Bagram 18 hours after the patients were injured. By then, two patients were dead. Despite maximal supportive care, one patient developed severe hypotension and died 8 hours post-injury from cardiovascular collapse. The patient with rib fractures died of hypoxemic respiratory failure at 18 hours post-injury. The ALRT evaluated the remaining patient for transport and extracorporeal support. This patient, however, was unstable throughout his course and also died from hypoxemic respiratory failure at 24 hours post-injury.

The dramatic and rapid demise of these patients prompted further investigation. While the patients could have suffered from primary blast injuries and/or pulmonary contusions from blunt trauma, the patients would have likely survived if these were the only mechanisms of lung injury.9-11 Due to the relative lack of associated injuries, the acute mortality, and the profound respiratory failure experienced by each patient, a quaternary blast injury from toxic inhalation was suspected.

Upon investigation, evidence from the scene provided a likely scenario for such an inhalation injury from HF. The RPG had struck the rear of the MRAP and directly hit the FSS, rupturing its HFC-227 containing cylinders. The explosion caused by the RPG would have generated enough heat to produce HF from HFC-227. Extricating the soldiers from the MRAP took several minutes, and rescuers noted a sharp, pungent odor present inside the MRAP. Such a smell is characteristic of HF, and the MRAP’s interior would have created a closed space with a high concentration of HF fumes.12 Taking these details into account, the most likely cause of these patients' death was HF inhalation injury.

This incident generated a heightened awareness of HF inhalation injury. Treatment providers at Bagram were educated on the presentation of HF injury and its treatment. Medics were instructed to give nebulized calcium in the field if HF exposure was suspected.

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2.2 Case #2This incident generated a heightened awareness of HF inhalation injury. Treatment providers at Bagram were educated on the presentation of HF injury and its treatment. Medics were instructed to give nebulized calcium in the field if HF exposure was suspected. Several weeks later, four US soldiers presented to Bagram an hour after their MRAP was struck by a RPG. As with the first case, the RPG directly struck the FSS. Two soldiers were thrown from the vehicle and excluded from further review for this report. The two other soldiers, a young man and woman, were trapped in the MRAP and had prolonged exposure to HF fumes. Both complained of dyspnea, but due to the rapidity of transport, neither received nebulized calcium during transfer.

At Bagram, both patients rapidly developed pulmonary failure and were intubated. Neither patient had signs of traumatic injuries. Treatment providers were informed that the patients’ MRAP had received damage to its FSS. The patients were monitored in the ICU and empirically given nebulized calcium chloride every 4 hours along with IV calcium boluses. Imaging once again showed global pulmonary infiltrates (see Fig. 2).

Figure 2: Chest radiograph 24 hours post-injury.

The ALRT was activated immediately and arrived within 8 hours to provide support. The man worsened, and the ALRT placed him on a high frequency percussive ventilator and gave him IV epoprostenol sodium (Flolan®). The woman improved with a lung-protective ventilation strategy using pressure control mode ventilation alone. Due to the high ventilatory pressures required, both patients received prophylactic bilateral chest tubes. Both patients were eligible for air transport with ALRT support 30 hours post-injury, and they were transferred at that time to LRMC.

The woman's condition deteriorated soon after arriving at LRMC; she was quickly transferred to a nearby German hospital for extracorporeal support. Her respiratory status improved just prior to cannulation, however, and she went back to LRMC the next day. Her condition continued to improve, and she was extubated a week later. The young man, however, had a prolonged ICU course complicated by pneumonia. He was transferred to the National Naval Medical Center at Bethesda, Maryland where he was breathing without ventilator support 3 weeks after injury.

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3.0 DISCUSSION

To our knowledge, this is the first report of a HF inhalation injury secondary to a damaged FSS containing HFC-227. Almost all US military vehicles are equipped with FSS containing HFC-227.13 Industry literature warns of the decomposition of HFC-227 to HF at high temperatures, but the medical literature does not contain any reports of such cases.14 While it took a specific mechanism for these injuries to occur, the ubiquity of FSS in US military vehicles could result in future HF inhalation injuries. Diagnosing a HF inhalation injury may be difficult, though, due to HF’s biochemical properties.

3.1 HF- Biochemical PropertiesHydrofluoric acid, the aqueous form of HF, is a weak acid and thus highly water soluble.12 Unlike strong acids that immediately cause pain and coagulative necrosis, hydrofluoric acid may initially cause no symptoms on exposure. Similarly, HF exposure may be initially asymptomatic while the fluoride ion diffuses through lipid membranes and penetrates into deeper tissues. Over time, however, the fluoride ion binds intracellular calcium and magnesium, leading to liquefactive tissue necrosis and systemic electrolyte disturbances resulting in death. Several reports document patients dying from pulmonary injuries and cardiac arrhythmias within hours of HF exposure.

3.2 Diagnosing HF Inhalation InjuryDue to the sometimes benign presentation of such a rapidly fatal injury, providers must rely on the context of the HF exposure rather than the patient’s symptoms. Though confirmatory tests such as serum or urine fluoride levels are available, practitioners should not wait for these test results to begin treatment for HF inhalation injury. In the cases above, neither confirmatory test was available, but the rapid deterioration of all these patients demonstrates that early and aggressive treatment is sometimes the only option. A significant inhalation injury should be assumed with:

1. Exposure to any hydrofluoric acid solution with over 50% concentration

2. Cutaneous exposures involving over 5% total body surface area or with head and neck

3. HF exposure in a confined space.

HF inhalation injury should thus be assumed in anyone exposed to a damaged FSS or trapped in a vehicle where the FSS is triggered.

3.2 Treating HF Inhalation InjuryTreatment for HF inhalation injury is based on typical respiratory supportive measures and calcium, a proven treatment for cutaneous hydrofluoric acid injuries. The first step in treating HF inhalation injury is to limit exposure. Rescuers should don protective gear if possible prior to extricating the vehicles crew.12

Contaminated clothing should be removed from all involved to prevent further exposure. Patients should then be transferred to a facility capable of intensive monitoring, and patients should be admitted and monitored closely regardless of their initial presentation as symptoms may take hours to develop. Providers should have a low threshold for placing these patients on positive pressure ventilation if respiratory distress develops. Though unproven, treatment with nebulized calcium should be administered as soon as possible. An example regimen would employ a 2.5% calcium gluconate solution (add 1.5 mL of 10% calcium gluconate to 4.5 mL water or 2.5 g calcium gluconate in 100 mL of water) given at least every 4 hours.23 The appropriate treatment duration of is unknown, but normalization of serum calcium and fluoride levels seems a reasonable endpoint.24

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IV calcium should also be administered due to the risk of systemic hypocalcemia precipitating cardiac arrhythmias.5 Electrolyte disturbances such as hypocalcemia, hypomagnesia, and hyperkalemia should be expected and treated appropriately. Finally, for refractory hypoxemia, extracorporeal support may be used which requires activation of the ALRT or equivalent and transfer to a facility with extracorporeal support capabilities.15 Even with these measures, patients with significant HF exposures will likely suffer extensive pulmonary injuries requiring prolonged hospitalizations. Chronic respiratory issues may develop requiring further rehabilitation and treatment.

4.0 CONCLUSION

While this report specifically discusses HF injury in ground vehicles, the presence of FSS containing HFC (e.g. HFC-125) in NATO ships and aircraft should make all military practitioners aware of the presentation and treatment of HF inhalation injuries. Future efforts should focus on preventing HF inhalation injuries with improvements in vehicle design, FSS protection, and development of alternative chemical extinguishing agents. Rapid detection indicators for HF placed in military vehicles could also aid in diagnosing HF exposure. Experimental evidence verifying the efficacy of nebulized calcium and sodium bicarbonate for HF inhalation injuries should also be pursued.

The opinions and/or assertions expressed in this article are solely those of the authors and do not reflect the official policy of the U.S. Air Force, the Department of Defense, or U.S. government.

5.0 REFERENCES

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[4] Blodgett DW, Suruda AJ, Crouch BI. Fatal unintentional occupational poisonings by hydrofluoric acid in the U.S. Am J Ind Med. Aug 2001;40(2):215-220.

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[8] Dorlac GR, Fang R, Pruitt VM, et al. Air transport of patients with severe lung injury: development and utilization of the Acute Lung Rescue Team. J Trauma. Apr 2009;66(4 Suppl):S164-171.

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[9] Avidan V, Hersch M, Armon Y, et al. Blast lung injury: clinical manifestations, treatment, and outcome. Am J Surg. Dec 2005;190(6):927-931.

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[14] Soldier and vehicle survivability and safety. In: Spectrex, ed. Spectrex Inc.

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[16] Skolnik S. Acute inhalation exposure to hydrogen fluoride. J Occup Environ Hyg. Jun 2010;7(6):D31-33.

[17] Tsonis L, Hantsch-Bardsley C, Gamelli RL. Hydrofluoric acid inhalation injury. J Burn Care Res. Sep-Oct 2008;29(5):852-855.

[18] Kirkpatrick JJ, Enion DS, Burd DA. Hydrofluoric acid burns: a review. Burns. Nov 1995;21(7):483-493.

[19] Wing JS, Brender JD, Sanderson LM, Perrotta DM, Beauchamp RA. Acute health effects in a community after a release of hydrofluoric acid. Arch Environ Health. May-Jun 1991;46(3):155-160.

[20] Kirkpatrick JJ, Burd DA. An algorithmic approach to the treatment of hydrofluoric acid burns. Burns. Nov 1995;21(7):495-499.

[21] Stuke LE, Arnoldo BD, Hunt JL, Purdue GF. Hydrofluoric acid burns: a 15-year experience. J Burn Care Res. Nov-Dec 2008;29(6):893-896.

[22] Lee DC, Wiley JF, 2nd, Synder JW, 2nd. Treatment of inhalational exposure to hydrofluoric acid with nebulized calcium gluconate. J Occup Med. May 1993;35(5):470.

[23] Upfal M, Doyle C. Medical management of hydrofluoric acid exposure. J Occup Med. Aug 1990;32(8):726-731.

[24] Kono K, Watanabe T, Dote T, et al. Successful treatments of lung injury and skin burn due to hydrofluoric acid exposure. Int Arch Occup Environ Health. Jun 2000;73 Suppl:S93-97.

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