MILITARY MEDICINE, 177, 1:108, 2012

Hydrogen Fluoride Inhalation Injury Because of a Fire

Suppression System
Lt Col Dustin Zierold, USAF MC; Capt Matthew Chauviere, USAF MC

ABSTRACT Automatic fire suppression systems (FSSs) use hydrofluorocarbons (HFCs) to chemically extinguish
fires. At high temperatures, HFC can release hydrogen fluoride (HF), a toxic and potentially lethal gas. We report the
deaths of three U.S. military personnel at Bagram Air Base from acute respiratory failure after the FSS 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 HF-induced respiratory failure. When two patients later presented with simi-

Downloaded from https://academic.oup.com/milmed/article/177/1/108/4345530 by guest on 20 March 2021

lar symptoms after damage to their vehicle’s FSS, they were aggressively treated with nebulized calcium and positive
pressure ventilation. Both survived. The presence of HFC-containing FSSs in military vehicles may lead to future cases
of HF inhalation injury, and further research must be done to help rapidly diagnose and effectively treat this injury.

INTRODUCTION (6–8 mL/kg). High positive end-expiratory pressures in excess

Automatic fire suppression systems (FSSs) have been used in
U.S. 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).1,2 Although 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 2 events involving
HF inhalation injury because of FSS.
CASE REPORT
Case 1
Three U.S. soldiers presented to a Forward Operating Base
(FOB) in Afghanistan after a rocket-propelled grenade
(RPG) struck their Mine Resistant Ambush Protected vehi-
cle (MRAP) (Table I). All three had dyspnea, but only one
had evidence of trauma (rib fractures and a unilateral pneu-
mothorax). Their respiratory distress worsened, and two
were intubated. The patients were transferred to the Craig
Joint Theater Hospital (CJTH) at Bagram Air Base 4 hours
postinjury.
At CJTH, re-examination revealed no additional injuries.
The unintubated patient was tachypneic on 10-L facemask
oxygen after transfer and was intubated soon after arrival
(Fig. 1). All three patients were admitted to the intensive care
unit (ICU). Subsequent radiographs showed bilateral pulmo-
nary infiltrates in each patient (Figs. 2 and 3). All patients
were ventilated with a lung protective ventilation strategy
using a pressure control mode to achieve low tidal volumes
David Grant USAF Medical Center, 101 Bodin Circle, 60 MSGS/SGCQ,
Travis Air Force Base, CA 94535-1800.
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.
of 15 cm H2O and FiO2 settings over 80% were required to
maintain adequate oxygenation. Central venous pressures
were initially in normal ranges, but soon rose to above nor-
mal limits with low mean arterial pressures despite aggressive
fluid resuscitation.
Because of the severe refractory hypoxemia present in
these patients, the Acute Lung Rescue Team (ALRT) based
at Landstuhl Regional Medical Center (LRMC) was acti-
vated. The ALRT, composed of experienced critical care
physicians, critical care nurses, and respiratory technicians,
specializes in transporting patients with severe lung inju-
ries.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 postinjury from cardiovascular collapse.
The patient with rib fractures died of hypoxemic respira-
tory failure at 18 hours postinjury. The ALRT evaluated
the remaining patient for transport and extracorporeal sup-
port. This patient, however, was unstable throughout his
course and also died from hypoxemic respiratory failure at
24 hours postinjury.
The dramatic and rapid demise of these patients prompted
further investigation. Although the patients could have suf-
fered 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 Because of
the relative lack of associated injuries, the acute mortality, and
the profound respiratory failure experienced by each patient, a
toxic inhalation injury was suspected.
Upon investigation, evidence from the scene provided
a likely scenario for such an inhalation injury from HF. A
RPG had struck the rear of the MRAP and directly hit the
FSS, rupturing its HFC-227 containing cylinders. The explo-
sion caused by the RPG would have generated enough heat to

108 MILITARY MEDICINE, Vol. 177, January 2012


TABLE I.
Patient Presentation
1 FSS in MRAP damaged. Seen Initially
at FOB. Dyspnea, no other injuries
2 FSS in MRAP damaged. Seen initially
at FOB. Fractures and pneumothorax
3 FSS in MRAP damaged. Seen initially
at FOB. Dyspnea, no other injuries
4 FSS in MRAP damaged. Dyspnea,
no other injuries. Seen at Bagram
<1 hour after injury
5 FSS in MRAP damaged. Dyspnea,
no other injuries. Seen at Bagram
<1 hour after injury
Laboratory values and autopsy results are unavailable. Patients 1 to 3 are described in case 1, and patients 4 and 5 are described in case 2.
FIGURE 1. One of the patients soon after admission to Bagram. Note the
lack of external trauma. This patient would die 18 hours after injury.
FIGURE 2. Appearance of chest computed tomography scan at 12 hours
postinjury.
MILITARY MEDICINE, Vol. 177, January 2012
Case Report
Description of Patients Included in Case Reports
Initial Treatment Course
Intubated at FOB. Transferred to Bagram 4 hours later Died 8 hours postinjury of
cardiovascular collapse
Tube thoracostomy and intubated at FOB. Transferred to Died 18 hours postinjury of
Bagram 4 hours later hypoxemic respiratory failure
Transferred to Bagram and intubated there Died 24 hours postinjury of
hypoxemic respiratory failure
Given 1 ampule of nebulized sodium bicarbonate before Transferred to LRMC at 30
presentation. Intubated at Bagram for respiratory failure. hours. Extubated a week after
Received nebulized calcium chloride injury
Given 1 ampule of nebulized sodium bicarbonate before Transferred to LRMC at
presentation. Intubated at Bagram respiratory failure. 30 hours. Developed hospital
Downloaded from https://academic.oup.com/milmed/article/177/1/108/4345530 by guest on 20 March 2021
Received nebulized calcium chloride. Given IV acquired pneumonia, received
epoprostenol sodium and high frequency percussive tracheostomy. Off mechanical
ventilation by ALRT at 8 hours ventilation 3 weeks postinjury
FIGURE 3. Chest radiograph of the same patient taken at 18 hours
postinjury.
produce HF from HFC-227. Extricating the soldiers from the
MRAP took several minutes, and rescuers noted a sharp, pun-
gent odor present inside the MRAP. Such a smell is charac-
teristic 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 CJTH were edu-
cated on the presentation of HF injury and its treatment.
Medics were instructed to give nebulized sodium bicarbon-
ate and calcium in the field if HF exposure was suspected.
No specific guidelines were given to rescuing personnel other
than to monitor themselves for dyspnea since their expo-
sure to HF would be presumptively brief and dilute once
the MRAP was opened.
109
 Case Report
FIGURE 4. Chest radiograph taken at 24 hours postinjury. This patient
survived.
Case 2
Several weeks later, four U.S. soldiers presented to CJTH an
hour after their MRAP was struck by a RPG (Table I). As
with the first case, the RPG directly struck the FSS. Two sol-
diers 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 and
received an ampule of nebulized sodium bicarbonate before
presentation.
At CJTH, both patients rapidly developed pulmonary fail-
ure and were intubated. Neither patient had signs of trau-
matic 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 intravenous
(IV) calcium boluses. Imaging once again showed global pul-
monary infiltrates (Fig. 4). The ALRT was activated imme-
diately 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 venti-
lation strategy using pressure control mode ventilation alone.
Because of the high ventilatory pressures required, both patients
received prophylactic bilateral chest tubes. Both patients were
eligible for air transport with ALRT support 30 hours postin-
jury, 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 hospi-
tal for extracorporeal support. Her respiratory status improved
just before cannulation, however, and she went back to LRMC
the next day. Her condition continued to improve, and she was
110
extubated a week later. The young man, however, had a pro-
longed ICU course complicated by pneumonia. A tracheos-
tomy was performed, and he was transferred to the National
Naval Medical Center where he was breathing without venti-
lator support 3 weeks after injury.
DISCUSSION
To our knowledge, this is the first report of a HF inhala-
tion injury secondary to a damaged FSS containing HFC-
227. Almost all U.S. 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
Downloaded from https://academic.oup.com/milmed/article/177/1/108/4345530 by guest on 20 March 2021
the medical literature does not contain any reports of such
cases.14 Although it took a specific mechanism for these inju-
ries to occur, the ubiquity of FSS in U.S. military vehicles
could result in future HF inhalation injuries. Diagnosing an
HF inhalation injury may be difficult, though, due to HF’s bio-
chemical properties.
Hydrofluoric acid, the aqueous form of HF, is a weak acid
and thus highly water soluble.12 Unlike strong acids that imme-
diately cause pain and coagulative necrosis, hydrofluoric acid
may initially cause no symptoms on exposure.4,5,15–17 HF expo-
sure may also be initially asymptomatic or only cause coughing
and mild airway irritation while the fluoride ion diffuses through
lipid membranes and penetrates into deeper tissues.12,18,19 Over
time, however, the fluoride ion binds intracellular calcium and
magnesium, leading to liquefactive tissue necrosis and sys-
temic electrolyte disturbances resulting in death.5,12 Several
reports document patients dying from pulmonary injuries and
cardiac arrhythmias within hours of HF exposure.4–7,15
As a result of the possibly benign presentation of such a
rapidly fatal injury, providers must rely on the context of the
HF exposure rather than the patient’s symptoms. A signifi-
cant inhalation injury should be assumed with exposure to any
hydrofluoric acid solution with over 50% concentration, cuta-
neous exposures involving over 5% total body surface area or
with head and neck involvement, clothing soaked with hydro-
fluoric acid, and most relevant to these cases, HF exposure
in a confined space.12,19,20 HF inhalation injury should thus be
assumed in anyone exposed to a damaged FSS or trapped in a
vehicle where the FSS is triggered. Though confirmatory tests
such as serum or urine fluoride levels are available, practitio-
ners should not wait for these test results to begin treatment
for HF inhalation injury. In the cases above, neither confirma-
tory test was available, but the rapid deterioration of all these
patients demonstrates that early and aggressive treatment is
sometimes the only option.
Treatment guidelines for HF inhalation injury are based
on typical respiratory supportive measures and calcium,
a proven treatment for cutaneous hydrofluoric acid inju-
ries. Cutaneous hydrofluoric acid injuries occur frequently,
and successful treatment with topical calcium gluconate is
well supported by clinical and experimental data.4,5,12,18,21,22
Significant hydrofluoric acid exposures (>1% body surface
area) are life threatening and treated aggressively with IV
MILITARY MEDICINE, Vol. 177, January 2012
 Case Report

TABLE II. Case Reports Documenting Use of Nebulized Calcium for HF Inhalation Injury

Reference Presentation Treatment Course

Lee et al22 13 oil refinery workers 1 hour after
exposure to highly concentrated HF mist
Kono et al24 52-year-old welder who rapidly
developed dyspnea after exposure
to HF and was quickly hospitalized
Tsonis et al17 40-year-old metal worker who developed
hemoptysis 3 hours and presented with
hypoxia 9 hours after HF exposure
Single treatment of 4-mL 2.5% calcium
gluconate mixed in normal saline
Intubated at presentation. 5% calcium
gluconate delivered by intermittent
positive pressure breathing over 4 days
Intubated at presentation. Continuous
2.5% calcium gluconate for 3 hours
with additional doses every 4 hours
for 48 hours
No side effects noted. All discharged
by 24 hours
Extubated after 10 days. Discharged
at 22 days with normal pulmonary
function tests
Course complicated by pulmonary
embolus and pneumonia. Off ventilator
at 10 weeks and discharged to rehab
facility at 12 weeks. Mild pulmonary
function abnormalities with few
symptoms at 5 month follow-up

Downloaded from https://academic.oup.com/milmed/article/177/1/108/4345530 by guest on 20 March 2021

Wing et al19 also mentioned nebulized calcium in their report of an HF release by a petrochemical plant in a U.S. community but did not give any further
details.

calcium and even intra-arterial calcium infusions with surgi-
cal debridement.21
Treatment for HF inhalation injury is not as well established
like those for other toxic exposures. The first step in treat-
ing HF inhalation injury is to limit exposure. Rescuers should
don protective gear if possible before extricating the vehicles
crew.12 Contaminated clothing should be removed from all
involved to prevent further exposure.5,12,18 Patients should then
be transferred to a facility capable of intensive monitoring,
and patients should be admitted and monitored closely regard-
less of their initial presentation as symptoms may take hours
to develop. Providers should have a low threshold for plac-
ing these patients on positive pressure ventilation if respiratory
distress develops. Though anecdotal and unproven, treat-
ment with nebulized calcium should be administered as soon
as possible (Table II). 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 appropri-
ate treatment duration is unknown, but reasonable endpoints
would be normalization of serum calcium and fluoride lev-
els.24 IV calcium should also be administered because of the
risk of systemic hypocalcemia precipitating cardiac arrhyth-
mias.5 Other electrolyte disturbances such as hypomagnesia
and hyperkalemia should be expected and treated appropri-
ately.5,12 Nebulized sodium bicarbonate is generally advised
for other inhaled acid exposures, though its use for HF injury
has not been recorded.25,26 This treatment was given in the
second case, but its usefulness is debatable. The low disso-
ciation of HF may render sodium bicarbonate ineffective, yet
given bicarbonate’s low side effect profile and the gravity of
HF inhalation injury, its use could be considered. A single
ampule of 8.5% sodium bicarbonate diluted in 2 mL of normal
saline would be a recommended dose.26 Finally, for refrac-
tory 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.16,17,24 Chronic respiratory issues may develop
requiring further rehabilitation and treatment.5,16,17
CONCLUSION
Although this report specifically discusses HF injury in
ground vehicles, the presence of FSS containing HFC (e.g.
HFC-125) in U.S. ships and aircraft should make all mili-
tary practitioners aware of the presentation and treatment
of HF inhalation injuries. A Joint Theater System Clinical
Practice Guideline for Inhalation Injury is currently undergo-
ing revision to include information regarding potential inju-
ries from FSSs. Future efforts should focus on preventing HF
inhalation injuries with improvements in vehicle design, FSS
protection, and development of alternative chemical extin-
guishing 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.
REFERENCES
1. Auwarter V, Proquitte H, Schmalisch G, Wauer R, Pragst F: Determi-
nation of 1,1,1,2,3,3,3-heptafluoropropane (HFP) in blood by headspace
gas chromatography-mass spectrometry. J Anal Toxicol 2005; 29(6):
574–6.
2. Copeland G, Lee EP, Dyke JM, Chow WK, Mok DK, Chau FT: Study of
2-H-heptafluoropropane and its thermal decomposition using UV photo-
electron spectroscopy and ab initio molecular orbital calculations. J Phys
Chem A 2010; 114(10): 3540–50.
3. Emmen HH, Hoogendijk EM, Klopping-Ketelaars WA, et al: Hu-
man safety and pharmacokinetics of the CFC alternative propellants
HFC 134a (1,1,1,2-tetrafluoroethane) and HFC 227 (1,1,1,2,3,3, 3-
heptafluoropropane) following whole-body exposure. Regul Toxicol
Pharmacol 2000; 32(1): 22–35.
4. Blodgett DW, Suruda AJ, Crouch BI: Fatal unintentional occupational
poisonings by hydrofluoric acid in the U.S. Am J Ind Med 2001; 40(2):
215–20.
5. Caravati EM: Acute hydrofluoric acid exposure. Am J Emerg Med 1988;
6(2): 143–50.
6. Chela A, Reig R, Sanz P, Huguet E, Corbella J: Death due to hydrofluoric
acid. Am J Forensic Med Pathol 1989; 10(1): 47–8.

MILITARY MEDICINE, Vol. 177, January 2012 111

 Case Report
7. Dote T, Kono K, Usuda K, Shimizu H, Kawasaki T, Dote E: Lethal inha-
lation exposure during maintenance operation of a hydrogen fluoride liq-
uefying tank. Toxicol Ind Health 2003; 19(2–6): 51–4.
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 2009; 66(Suppl 4): S164–71.
9. Avidan V, Hersch M, Armon Y, et al: Blast lung injury: clinical manifes-
tations, treatment, and outcome. Am J Surg 2005; 190(6): 927–31.
10. Champion HR, Holcomb JB, Young LA: Injuries from explosions: phys-
ics, biophysics, pathology, and required research focus. J Trauma 2009;
66(5): 1468–77; discussion 1477.
11. Ritenour AE, Blackbourne LH, Kelly JF, et al: Incidence of primary blast
injury in US military overseas contingency operations: a retrospective
study. Ann Surg 2010; 251(6): 1140–4.
12. Makarovsky I, Markel G, Dushnitsky T, Eisenkraft A: Hydrogen
fluoride—the protoplasmic poison. Isr Med Assoc J 2008; 10(5):
381–5.
13. Defense Technical Information Center 2010. Fire extinguishing agents
for protection of occupied spaces in military ground vehicles. Available
at http://www.dtic.mil/dtic/tr/fulltext/u2/a517470.pdf; accessed April 12,
2011.
14. Spectrex (editor): Soldier and Vehicle Survivability and Safety. Cedar
Grove, NJ, Spectrex Inc, 2008. Available at http://spectrex-inc.com/files/
military/presentations/survivabilitysafety_aug2008.pdf; accessed October
11, 2011.
15. Shin JS, Lee SW, Kim NH, et al: Successful extracorporeal life support
after potentially fatal pulmonary oedema caused by inhalation of nitric
and hydrofluoric acid fumes. Resuscitation 2007; 75(1): 184–8.
112
16. Skolnik S: Acute inhalation exposure to hydrogen fluoride. J Occup
Environ Hyg 2010; 7(6): D31–3.
17. Tsonis L, Hantsch-Bardsley C, Gamelli RL: Hydrofluoric acid inhalation
injury. J Burn Care Res 2008; 29(5): 852–5.
18. Kirkpatrick JJ, Enion DS, Burd DA: Hydrofluoric acid burns: a review.
Burns 1995; 21(7): 483–93.
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 1991; 46(3): 155–60.
20. Kirkpatrick JJ, Burd DA: An algorithmic approach to the treatment of
hydrofluoric acid burns. Burns 1995; 21(7): 495–9.
21. Stuke LE, Arnoldo BD, Hunt JL, Purdue GF: Hydrofluoric acid burns:
a 15-year experience. J Burn Care Res 2008; 29(6): 893–6.
22. Lee DC, Wiley JF II, Synder JW II: Treatment of inhalational exposure to
Downloaded from https://academic.oup.com/milmed/article/177/1/108/4345530 by guest on 20 March 2021
hydrofluoric acid with nebulized calcium gluconate. J Occup Med 1993;
35(5): 470.
23. Upfal M, Doyle C: Medical management of hydrofluoric acid exposure.
J Occup Med 1990; 32(8): 726–31.
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 2000; 73(Suppl): S93–7.
25. Cevik Y, Onay M, Akmaz I, Sezigen S: Mass casualties from acute
inhalation of chlorine gas. South Med J 2009; 102(12): 1209–13.
26. Joint Theater Trauma System Clinical Practice Guideline. Inhalation
Injury and Toxic Industrial Chemical Exposure. Fort Sam Houston, TX,
U.S. Army Institute of Surgical Research, 2008. Available at http://www.
usaisr.amedd.army.mil/cpgs/Inhalation_Injury_and_Toxic_Chemical_
Exposure_7_Nov_08.pdf; accessed August 16, 2011.
MILITARY MEDICINE, Vol. 177, January 2012