The Journal of Emergency Medicine, Vol 16, No 3, pp 409 412, 1998 Copyright 1998 Elsevier Science Inc.

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Clinical Communications

COLD INJURY FROM PRESSURIZED LIQUID AMMONIA: A REPORT OF TWO CASES

Georgia Sotiropoulos,
MD,*

Taline Kilaghbian,

BA,

William Dougherty,

MD,

and Sean O. Henderson,

MD

Departments of Emergency Medicine and Surgery, University of Southern California School of Medicine, Los Angeles, California, and *Los Angeles County and University of Southern California Medical Center, Los Angeles, California Reprint Address: Georgia Sotiropoulos, MD, Department of Emergency Medicine, Los Angeles County and University of Southern California Medical Center, Unit #1, Room 1011, 1200 N. State St., Los Angeles, CA 90033

e AbstractPatients exposed to pressurized liquids or gases present unique diagnostic and treatment challenges to the Emergency Physician. The potential for injury depends upon the properties of the chemical in addition to the thermodynamic effects from exposure to a pressurized substance. We present two cases of exposure to pressurized ammonia during an industrial accident. One patients symptoms were consistent with an ammonia alkali burn, whereas the other patients symptoms were more characteristic of a signicant thermal injury caused by the rapid expansion and evaporation of a pressurized liquid. 1998 Elsevier Science Inc. e Keywordsammonia; burn; industrial-exposure; human; hypothermia

alkali effects of the ammonia. Neither worker was wearing specically designed protective clothing.

CASE REPORTS A 51-year-old maintenance man was assisting in the inspection and repair of a leaky refrigerator coolant storage vessel when pressurized liquid ammonia exploded onto him and his partner. He was immediately placed under a shower for several minutes and both layers of his tight tting clothing were removed. At the time of the shower, the patient thought that he had exposure to his face and mouth. When paramedics arrived, the patient was placed on a dry sheet and transported to the nearest trauma center. The patients only complaints were of pain to all four extremities at the areas of exposure. There were no complaints of visual changes, chest pain, or difculty breathing, and no other apparent signs of trauma. Physical examination revealed a shivering, 51-yearold male, alert and oriented. The patient was in no apparent respiratory distress. Initial vital signs were blood pressure 154/75 mmHg, a pulse rate of 89 beats/ min, and a respiratory rate of 24 breaths/min. A rectal temperature of 37.3C (99.1F) was taken after the patient had received warmed saline. Pulse oximetry on room air was 94%. There were no facial burns, erythema, mucosal swelling, or signs of inhalation injury. No stridor or hoarse voice was noted. The lung sounds were clear without any wheezing, and heart tones were regular. The abdomen was soft without tenderness or distention, and bowel sounds were present. Skin examination revealed 28% total body surface area burns to all four
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INTRODUCTION The widespread use of ammonia in agriculture and industry has resulted in signicant exposures and burns, yet the incidence of reported cases remains low. Of these cases, injury has been attributed to the strong alkali effects of ammonia, which cause a chemical burn. The contribution of a cold (frostbite) injury that results from the evaporation of pressurized liquid anhydrous ammonia has been minimized or overlooked by other authors (1). We present two cases of patients exposed to pressurized anhydrous ammonia. One patient sustained signicant injury from the thermodynamic effects of evaporative freezing, with a total body surface area burn of 28% (71% of which was full thickness). The second case, involved in the same exposure, developed delayed symptoms with 1% total body surface area burns from the

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Physical examination showed normal vital signs, no injury to his chest, face, or extremities, and a genitourinary examination signicant for blistering of the scrotum and distal penis. The patient refused admission to the hospital and treated himself at home. Telephone follow-up revealed that he healed without incident or sequelae.

DISCUSSION Ammonia (NH3) is a colorless, extremely pungent, and irritating gas. It is widely used in industry for the manufacture of plastics, petroleum, explosives, textiles, and, in very dilute concentrations, household cleaners (3). Due to its high nitrogen content (82%), it is extensively used in agriculture as a fertilizer and has a very high solubility in water (1300 U volumes of anhydrous ammonia dissolvable in 1 U volume of water) (4). Its boiling point at atmospheric pressure (760 torr or mmHg) is 33C. After World War I, the incidence of ammonia burns increased proportionally to its use in refrigeration (1), and, although it was largely replaced by freon in the 1970s, the occurrence of ammonia burns continues today primarily because of its increased use in agriculture as a fertilizer. Anhydrous ammonia is also widely used in chemical, petroleum, and water treatment industries as well as in refrigeration. As of 1993, anhydrous ammonia was the third largest chemical produced by volume in the United States, and 30% of this volume was used in agriculture. There are no known national databases that record deaths or injuries caused by this chemical (5). A case series from Iowa State University describes 55 workers injured by exposure to anhydrous ammonia between 1990 and 1992. Of these, 19 required hospitalization for burns, respiratory problems, and loss of eyesight (6). Exposure to anhydrous ammonia is usually accidental during transfer of material from one tank to another or as a result of faulty equipment. Injuries from exposure can be multifactorial. Like other alkalis, it can produce a rapidly penetrating liquefactive necrosis. Anhydrous ammonia vapor has a pH of 13, is highly soluble, and is reactive with water. Therefore, it has a predilection for moisture-rich areas such as the eyes, mucous membranes of the respiratory tract, and skin (1,7). When ammonia reacts with water, it yields ammonium hydroxide, which in turn dissociates into free hydroxyl ions. The concentration of these ions dictates the severity of the burns (4,8). Furthermore, the reaction is exothermic and liberates heat energy, thereby causing thermal burns and cellular dehydration. Ultimately, the reaction initiated by

Figure 1. Burn diagram for patient 1 showing 28% total body surface area burned.

extremities with partial involvement of the torso (Figure 1). The patient was uid resuscitated with warmed normal saline, followed by lactated Ringers solution, according to the Parkland-Brooke formulae (24 cc/kg/% total body surface area burned/24 h) (2). He received 16 mg of morphine for pain. Initial and delayed chest radiographs were normal. The patient did well and, on hospital day 3, he underwent tangential excision and split thickness skin graft of full thickness burns to 20% of total body surface area, with removal of necrotic tissue. The pathology report of the burn showed eschar tissue with full thickness skin necrosis. Special stains for microorganisms were negative. The patient had a 90% take on the graft. The rest of the hospital course was uneventful. After receiving physical and occupational therapy, he was discharged on operative day 10.

Case 2 A 57-year-old white male supervisor, and work partner to case 1, was exposed on the chest and groin areas. He reported that his thin, loose-tting short sleeve shirt was white with frost, frozen solid. Both men were in the shower within 10 20 s after the explosion, the supervisor being rst. In contrast to his partner, who complained of immediate pain, this patient rst noted pain conned to the genital area 1 h after the accident.

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ammonia denatures proteins and saponies lipids in the cell membrane, causing a liquefactive necrosis, allowing further migration of the chemical deeper into the moisture-rich areas of the dermis and submucosa. Tissue destruction continues until the ammonia is neutralized (4). The extent of injury from the alkali effects of ammonia depends on the concentration, amount, condition, and time of contact with the skin, tissue permeability, and sensitivity of the injured area (8). The epidermis normally provides a protective barrier to the more moisturerich areas below. Frosch et al. demonstrated, using human volunteers, that the minimal blistering time from exposure to ammonium hydroxide is positively correlated to the number of cell layers in the stratum corneum and ranges from 3 to 57 min in different regions and persons (9). The areas most susceptible to ammonias chemical injury are moisture-rich areas such as the eyes, oropharynx, lungs, and the skin, where protective clothing is not worn. In addition to the chemicals alkali effects, ammonia has the potential to cause signicant injury due to evaporative freezing. Ammonia is usually stored as a liquid under pressure (120 lb/in2) at room temperature. When it is released through a small aperture it expands, resulting in vaporization and a large endothermic reaction. As the ammonia is released, everything with which it comes in contact exceeds its boiling point (33C), and heat is literally sucked out of the immediate environment. This resulting temperature drop may be as much as 80C, with tissue temperatures dropping as low as 60C (10). Critical damage to mammalian tissue occurs at approximately 4C, with irreversible damage occurring below 20C (10). This pathophysiology has been studied by Hicks, who developed an animal model using rats exposed to pressurized propane. Propane is stored at 200 lb/in2 and has a boiling point of 44.5C (11). Eight rats sprayed with liquid propane had their skin temperatures reduced from a baseline of 35C to 60C within 5 s of exposure. The depth of the injury varied depending on the length of time of exposure (12). Although this model used rats and pressurized propane, it demonstrated how frostbite injury can result from the vaporization of a pressurized liquid exposed to atmospheric pressure. When pressurized ammonia contacts the skin, it vaporizes rapidly, producing evaporative freezing with cell damage and vascular thrombosis. The wetness of the skin is a contributing factor to the frostbite injury from the added heat transfer through evaporation. This resulting frostbite injury is different from one occurring as a result of prolonged exposure to cold temperatures. The amount of damage that a cell sustains depends on the rate of freezing and thawing (7,10). Also, the sizes of the ice

crystals formed are inversely proportional to the rate at which the cooling occurs. Therefore, tissues subjected to a slow rate of cooling develop large ice crystals in the cellular interspaces. In contrast, rapid cooling, within seconds or minutes, induces the same process uniformly throughout the tissue, producing smaller intracellular ice crystals. Although smaller, these crystals are more lethal, as they are larger than the cells that contain them. Moreover, the microvasculature in the vicinity of the exposure undergoes thrombosis with subsequent ischemia and necrosis. Injury prevention efforts with regards to anhydrous ammonia focus primarily on education of the proper use of transfer equipment as well as prevention of equipment failure. Personal injury may be lessened by the use of ventless goggles or a full face shield. Rubber gloves with long cuffs and long sleeved shirts are recommended by the industry (6). Contact lens use should be avoided because lenses collect the chemical and intensify the caustic effects (6). We believe that Patient 1 sustained full thickness burns primarily from frostbite injury. He was wearing double layer, tight-tting clothes because he had been working inside the freezer before assisting his supervisor outside with what turned out to be faulty equipment. His exposure to the ammonia was instantaneous, and within 15 s, he was placed in the shower. If the alkali effects of the ammonia vapor caused his injuries, then ocular or respiratory injury would have been expected because protective facewear was not worn. Furthermore, the patients clothing was removed immediately in the shower. If these were chemical burns from the strong alkali effects of ammonia, then prolonged exposure times would be needed to penetrate both layers of clothing to produce full thickness burns. It could be argued that the patients skin was not irrigated long enough, yet the patient complained of pain immediately at the subsequent sites of the burns, suggesting that the thermal mechanism of injury occurred at that time. Patient 2 was working outside, where the ambient temperature was approximately 26.7C (80F). He was wearing a loose-tting shirt that turned white with frost and was frozen solid away from his body, which he removed immediately before entering the shower. The loose-tting shirt was probably protective from the evaporative cooling. He did not develop any pain until 1 h after exposure, when he noted pain conned to the groin area only. His injuries to that area subsequently healed, suggesting that they were supercial rst- or seconddegree burns. Most likely, his burn resulted from the delayed effects of prolonged exposure to an improperly irrigated alkali substance.

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Most authors attribute the burns sustained from exposure to pressurized anhydrous ammonia to the strong alkali effects of the ammonia gas, and the severity of these injuries is directly related to the concentration of the ammonia and the duration of the exposure. It has been thought that the contribution of the cold injury is minimal compared to these alkali effects. In fact, most of the case reports in the literature emphasize the similarities of the cutaneous injuries to other alkali burns (3,4,8). However, alkali burns, although similar in appearance to frostbite injuries, tend to be more supercial. The clinician should therefore be aware of the potential of deeper full thickness injury caused by cold injury from exposure to pressurized ammonia.

For treatment purposes, it is important to differentiate the two injury patterns. History of frost formation and the time sequence of the onset of pain may be valuable clues. In addition, litmus paper may be utilized to check the wound pH, which will be greater than 7 in alkali wounds. Copious irrigation is the recommended initial treatment for the alkali burns, with the endpoint being a neutral pH (4). The use of warm uids (40C) to irrigate an ammonia injury can serve as an initial treatment until the exact nature of the injury is determined. Both chemical and cold injuries should be referred to a regional Burn Center for denitive care, surgery, and follow-up to maximize the patients chances for survival and functional outcome.

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