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Background: Although the incidence of caustic ingestion is declining, the management of caustic esophageal strictures remains a challenge. Although many agents have been tried experimentally to treat strictures, few have gained clinical application. The aim of this study was to investigate the influence of mitomycin C (MMC), which inhibits fibroblastic proliferation in treating delayed caustic esophageal strictures., Methods: Forty-two rats were allocated into 3 groups. Caustic esophageal burns were created as described by Gehanno. Group A was instilled only with saline. Group B was injured with 10% NaOH and left untreated. Group C was injured and received topical MMC at 0.04% concentration in the fourth week. At 56 days, stenosis index (SI), collagen deposition, and hydroxyproline content (HP) were determined in distal esophageal segments. Statistical analyses were performed., Results: The mean SI in group B was significantly higher than others (SI: 1.15 +/- 0.37 d/lum, P < .05). Collagen accumulation was highest in group B, followed by groups C and A, respectively. Collagen deposition in group C was statistically lower than group B (P < .018). The mean HP in group B was statistically higher than others (5.07 +/- 1.30 microg/mg tissue, P < .05), and similar between groups A and C (1.20 +/- 0.20, 1.91+/- 0.79, respectively, P = .73)., Conclusion: In the current study, MMC treatment ameliorated caustic esophageal stricture as reflected in the significantly lower SI. We conclude that MMC application is effective in the treatment of caustic esophageal strictures.

Bullous pemphigoid is a blistering disorder characterized by antibody deposition in the lamina lucida of the basement membrane zone. In addition to the idiopathic form, there are many agents that have been implicated in inducing bullous pemphigoid or bullous pemphigoid-like lesions. We describe a patient who developed a bullous pemphigoid-like eruption after a chemical burn.

Study Background: Alkali ingestions cause progressive and devastating injury to the esophagus by liquefaction necrosis. However, the therapeutic efficacy of water or milk dilution for alkali-induced esophageal injury has not been determined. This study used our previously reported model of alkali-induced esophageal injury to evaluate the effectiveness of water and milk dilution., Hypothesis: Early dilution with water or milk is efficacious in decreasing esophageal damage from alkali exposure., Methods: The esopgagi of 75 Sprague-Dawley rats were harvested, and each end was cannulated with a 20-gauge catheter. Specimens were maintained in an oxygenated saline solution (at 37 degrees C) during a 60-minute experimental period and then fixed immediately in 10% Formalin solution for histologic examination. Esophagi from six experimental groups (total of 60) were perfused with 50% NaOH solution at time 0. Water or milk dilution was performed immediately at 0 minutes, 5 minutes after injury, and 30 minutes after injury. Blinded pathologic examination was performed using a score of 0 (no injury), 1 (minimal), 2 (moderate), or 3 (severe) for the following six histologic categories: epithelial viability, cornified epithelial cell differentiation, granular cell differentiation, epithelial cell nuclei, muscle cells, and muscle cell nuclei., Results: Positive and negative controls showed expected outcomes. Significant progressions of injury over time were seen for every histologic category for both water and milk dilution. The injury scores for the milk-treated group at 0 minutes were less than or equal to the injury score for the water-treated group for all categories. However, these differences were significant only for the cornified epithelial cells., Conclusion: Early dilution therapy with water or milk reduces acute alkali injury of the esophagus and supports use of these forms of emergency treatment.

Study Objective: To gather preliminary data on the safety and efficacy of IV magnesium in a rat model of hydrofluoric acid burns., Model: Forty-seven anesthetized male rats (200 to 300 g) received a standardized burn with 52% hydrofluoric acid., Interventions: Animals were anesthetized with 30 to 50 mg/kg ketamine IM and 1 to 3 mg/kg xylazine IM. A standardized chemical burn was created by topical application of 52% hydrofluoric acid. The rats were divided into four treatment groups: group 1 received no treatment; group 2 received intradermal injection of 10% calcium gluconate; group 3 received 80 mg/kg MgSO4 IV; and group 4 received 160 mg/kg MgSO4 IV. After the rats were killed, the burn lesions were excised and examined by a pathologist to determine the grade of burn (which was equal to the clinical degree of burn)., Measurements and Main Results: Microscopic examination of the burns revealed differences among the four groups. Five of 13 group 1 rats (37%) died within 24 hours of burn initiation. Of group 1 survivors, 50% had grade 2 burns, and the other 50% had grade 3 burns. In group 2, eight of 11 rats (73%) had grade 3 burns. Twenty-five percent of group 3 rats (three of 12) had grade 3 burns, and only 9% of group 4 rats (one of 11) had grade 3 burns. Only the difference in the rates of grade 3 burns for groups 2 and 4 was statistically significant. Although not statistically significant, burns in groups 3 and 4 tended to be smaller in diameter than burns in groups 1 and 2., Conclusion: High-dose IV magnesium sulfate reduces the severity of hydrofluoric acid burn compared with conventional intradermal calcium gluconate therapy. Early deaths appeared to be prevented by both calcium and magnesium therapies.

Hydrofluoric acid is used for different purposes in industry and in the home as a rust remover. Most exposures are accidental and may result in severe superficial and deep tissue injury as well as systemic toxicity. There is uncertainty regarding the optimal treatment of hydrofluoric acid eye injury. A patient in whom a solution of 49% hydrofluoric acid induced a large corneal erosion is described. Repeated instillation of 1% calcium gluconate eye drops combined with the conventional treatment of acid eye burns resulted in a complete and quick recovery.

Study Objective: To compare the effects of water rinse with those of isopropyl alcohol, polyethylene glycol with industrial methylated spirits, or ethanol on cutaneous phenol burns., Design: Controlled trial with all animals receiving all treatments applied to different cutaneous phenol burn sites., Type of Participants: Swine weighing 9 to 18 kg., Interventions: In phase 1, each burn site was treated with water rinse for zero, one, or five minutes combined with either isopropyl alcohol, polyethylene glycol with industrial methylated spirits, ethanol, or no other treatment. Biopsies of treatment sites were done at 30 minutes and at 48 hours. In phase 2, a pilot study, the effect of isopropyl alcohol, polyethylene glycol with industrial methylated spirits, or water treatment on serum phenol levels was noted in animals with 5%, 10%, and 15% body surface area burns., Measurements and Main Results: In phase 1, on histological examination of biopsy specimens, significant differences in tissue damage occurred among the groups (P < .05). Isopropyl alcohol and polyethylene glycol with industrial methylated spirits were the most efficacious treatments; the duration of water rinse had no significant effect. In phase 2, the systemic absorption of phenol may be greater with water treatment than with isopropyl alcohol treatment., Conclusion: Isopropyl alcohol and polyethylene glycol with industrial methylated spirits are equally effective in the amelioration of phenol burns of less than 5% total surface area. The wider availability of isopropyl alcohol makes it potentially the most useful treatment for these small burns. Further studies of its risks are needed.

Between 1968 and 1988, 679 patients were hospitalized for ingestion of caustic substances, and 87 had severe caustic burns of the entire esophagus, together with panparietal necrosis. Twenty-one of them had tracheobronchial necrosis with perforation. Fifteen have not been operated on; six have had operations, with success in four. We describe an original technique for repairing these tracheobronchial perforations with a pulmonary patch.

Sulfur mustard is a chemical warfare agent of historical and current interest. Favored militarily because of its ability to incapacitate rather than its ability to kill, its use results in large numbers of casualties requiring prolonged, intensive care. In light of recent threats of chemical warfare and the possibilities of chemical acts of terrorism, North American physicians should be knowledgeable of its effects and the care of its victims.

During the past 8 1/2 years, we have treated 34 adult patients admitted for ingestion of caustic materials. In 19 patients the injury was accidental, and in 15 patients ingestion was a suicide attempt. Ingested agents included hydrochloric acid in four patients, sulfuric acid in one patient, a strong alkali such as sodium hydroxide or Drano in 15 patients, liquid bleach in eight patients, detergents in four patients, and ammonia in two patients. Each patient underwent early fiberoptic endoscopic evaluation. The extent and severity of the injury varied according to the ingested agent. Seven patients who had second- or third-degree injury had surgery. One patient who ingested sulfuric acid required hemigastrectomy for pyloric stenosis. Two patients with Drano ingestion had necrosis of the stomach and required total gastrectomy. Five patients with strong alkali ingestion had esophageal strictures, and colonic interposition was performed on four of these patients. No patient who had ingested bleach, ammonia, or detergent required surgery. Panendoscopy after caustic ingestion can be performed safely and provides an accurate guide for therapy. The ingestion of strong acid or alkali may produce profound pathologic changes, which may require surgery for perforation or stricture. Bleach, detergent, and ammonia usually cause mild injuries that will respond with medical treatment.

Eight cases of an acquired perforating disease are reported in oil field workers who were exposed to drilling fluid. Analysis of the drilling fluid showed it to contain many components, including calcium chloride. Histopathologic study of patient lesions demonstrated transepidermal elimination of calcium. An in vivo mouse model was developed to study this phenomenon, which may represent a calcium-mediated perforating disorder.

Hydrofluoric acid (HF) produces a unique chemical burn due to tissue penetration by fluoride ion. Fluoride ion interferes with calcium activity in a variety of cell membranes and calcium-dependent processes, resulting in severe pain and deep tissue destruction. The currently accepted methods of treating HF burns include application of topical soaks or ointments with calcium or magnesium salts for minor burns and local injection of calcium gluconate for more severe burns. Digital burns also may require nail removal and direct injection into the nail bed. We present the cases of a series of patients with moderate to severe HF burns involving one or more fingers who were treated with selective intraarterial calcium infusion of dilute (1.66%) calcium salts. All patients had excellent relief of symptoms and marked improvement of the burn lesions following one to three four-hour infusions of calcium chloride or calcium gluconate. One patient required subsequent surgical intervention for grafting of a full-thickness burn, and one patient developed transient spasm at the site of percutaneous arterial line insertion. Intraarterial calcium infusion for the treatment of HF burns of the fingers provides many therapeutic advantages, including elimination of painful calcium injection directly into fingertips, avoidance of debilitating procedures such as fingernail removal, and assurance that all affected cells are receiving adequate amounts of calcium to replenish depleted stores and to complex with remaining free fluoride ion.

A patient with a 70% hydrofluoric acid burn developed systemic dissemination of fluoride ion from a 9% to 10% body surface area exposure on the lower extremities. Severe hypocalcemia and intractable ventricular arrhythmias resulted. This case is the second documented occurrence of hypocalcemia from hydrofluoric acid burns. It is the first case to document myocardial injury and systemic fluorosis from a skin burn.

A case of a patient with an alkaline chemical burn to the face from the misuse of the aerosol form of an oven cleaner is presented. The low concentration of sodium hydroxide and lack of early pain delayed the patient's presentation to the emergency department for two hours. After this delay in seeking treatment, continuous irrigation in the ED did little to modify the pH of the patient's injured skin. Thus, she developed a full-thickness alkaline burn that eventually required skin grafting.