SUMMARY

The Authors examined caustic ingestions

INTRODUCTION

Accidental and intentional exposure to caustic agents represents a significant source of morbidity and mortality. Strong acids and bases can be found in both household and industrial settings. In the home, caustics represent a particularly serious danger for children who may sustain serious perioral, gastrointestinal, or cutaneous burns as a result of an accidental exposure. When ingested or spilled on the skin, caustic acids or bases may produce extensive tissue destruction and possibly death. Effective management requires aggressive but careful diagnostic and therapeutic intervention to minimize morbidity and maximize the probability of survival.

PATHOPHYSIOLOGY OF ALKALINE BURNS

When ingested, alkaline agents, such as sodium hydroxide and potassium hydroxide, may result in severe injury to the gastrointestinal tract. With a pH of 12.5 or greater, they produce an injury described histologically as liquefaction necrosis. Solid alkali, when swallowed, tends to adhere to the mucous membranes of the oropharynx and esophagus, producing severe proximal burns. In contrast, liquid lye, a strong alkali found in household drain cleaners such as Drano, Liquid Plumr and Plunge is easier to swallow, tasteless, and odorless. It causes less damage to the oropharynx and greater damage to the esophagus. In addition, liquids, because of their high specific gravity, can pass rapidly through the esophagus and reach the stomach, injuring tissue on contact.

Acutely, direct cellular destruction results from the saponification of fats and proteins. Blood vessels thrombose, resulting in further tissue necrosis and cellular death. This is followed in 2 to 3 days by the sloughing of a thin layer of necrotic tissue. If the acute injury is survived, a healing phase occurs between days 5 and 14 in which granulation tissue develops and collagen is deposited. During this period there is maximal softening of the injured tissue and, therefore, an increased risk of perforation. By day 21 following severe injuries, stricture formation begins, when the collagen contracts circumferentially and longitudinally.

Esophageal injury may result in a nonulcerative, mild or severe ulcerative esophagitis. Nonulcerative esophagitis is characterized by erythema, edema, and an intact mucous membrane. Mild ulcerative esophagitis is characterized by the presence of isolated areas of superficial ulceration with areas of vesiculation. Injuries that result in severe ulcerative esophagitis are characterized by total denudation of the esophageal epithelium and necrosis that may involve the entire esophageal wall and extend into underlying structures. Alkaline products do not directly produce systemic effects, apart from the systemic consequences of extensive tissue destruction.

Household bleaches are probably the most common caustic ingestant. Although perceived as moderately dangerous, household bleach (5% sodium hypochlorite) is not a strong caustic. When ingested, it may produce emesis, a burning sensation, and superficial mucosal erythema. Occasionally, following the ingestion of very large quantities of household bleach or following the ingestion of more highly concentrated industrial bleach, significant injury with strictures has resulted. In general, nothing more than symptomatic treatment is required, and most result in a favorable outcome. Ammonia or ammonium hydroxide and nonphosphate detergents, on the other hand, may produce serious injury with mucosal burns, ulceration, and sometimes full-thickness burns.

PATHOPHYSIOLOGY OF ACID BURNS

Strong or corrosive acids are characterized by a pH of less than 2. Commonly ingested acids include sulfuric and hydrochloric acid, which may be found in household products such as toilet bowl cleaners and drain openers. The ingestion of acids occurs less frequently but results in a higher rate of complications and mortality. Acids produce coagulation necrosis and eschar formation, which allegedly protects underlying tissue from further caustic damage. On ingestion, acids have their major effect on the columnar epithelium of the stomach. The esophagus tends to be spared. This effect has been attributed to a rapid transit time through the esophagus and to the resistance of esophageal squamous epithelium to acid injury. Once the acid reaches the gastroesophageal junction it tends to follow the lesser curvature of the stomach, pooling in the antrum and eventually inducing pylorospasm and extensive antral damage. Destruction of the gastric mucosa and musculature results in edema, inflammation, the loss of glandular tissue and sometimes immediate or delayed hemorrhage. Eventually, if the initial injury is survived, fibrosis develops and may result in gastric outlet obstruction. Serious ingestions may result in complete gastric necrosis, hemorrhage, early perforation, and the destruction of adjacent structures. In addition, acids are well absorbed and may produce a profound systemic acidemia as well as massive hemolysis.

Clinical Presentation

Acutely, patients who have ingested a strong acid or base may present with burns of the face, oropharyngeal pain, dysphagia, drooling, dyspnea, retching, or emesis. Hoarseness, stridor, and dyspnea are strong indicators of laryngeal and epiglottic edema. Esophageal injury is suggested by complaints of dysphagia and odynophagia. Intravascular volume depletion, resulting from the third spacing of fluids, vomiting or hemorrhage may result in hypotension or shock.

Acids cause immediate, severe pain in the oropharynx and are usually expelled rapidly following an accidental ingestion. Epigastric pain and retching develop initially, followed by intractable ulcer-type pain that is associated with vomiting. Hematemesis and melena are common sequelae. Acidemia and hemolysis are frequent accompaniments of large acid ingestions. Gastric perforation and the subsequent development of peritoneal involvement may become evident and must be watched for vigilantly.

The ingestion of solid alkaline agents will result in severe oropharyngeal pain. The mouth and pharynx may have a soapy white film over the mucosa that eventually becomes brown and edematous. Perforation of the esophagus can produce severe chest pain from subsequent chemical and later bacterial mediastinitis.

It is important to note that no constellation of signs and symptoms will accurately predict the presence or severity of esophageal injury. Recently, it has been demonstrated that the occurrence of two or more of the symptoms of stridor, drooling, or vomiting accurately predicts the presence of significant esophageal injury 50 percent of the time. The absence of visible lesions in the oropharynx cannot exclude visceral burns. The ingestion of strong acids has resulted in complete gastric necrosis and death in the absence of any demonstrable proximal injury. Although patients with significant injuries are very likely to be symptomatic, children and patients who are suicidal may inaccurately report the presence or absence of symptoms.

Stabilization

Following a caustic ingestion, the initial management of the patient begins with stabilization. Health care workers must take precautions to ensure their own protection from exposure to the caustic agents on the patient's skin or in emesis or gastric aspirate. Airway obstruction secondary to oropharyngeal or laryngeal edema is the most life-threatening immediate sequela. Endotracheal intubation may be necessary for airway protection or for the prevention or treatment of upper airway obstruction. Ideally, intubation should be done under direct visualization, with the patient sedated or paralyzed to prevent additional soft tissue damage that inevitably results from the intubation of an agitated, uncooperative patient. If the treating physician is skilled in the use of fiberoptic laryngoscopy, intubation may be most safely accomplished over the laryngoscope. When the extent of soft tissue edema prevents the passage of an endotracheal tube, the patient may require a cricothyrotomy. Blind nasotracheal intubation is contraindicated because the tube may be passed through an area of necrotic tissue.

Following (or simultaneously with) airway management, two large-bore intravenous catheters need to be placed and an infusion of crystalloid begun. Blood specimens should be sent to the laboratory for an analysis of serum electrolytes and a complete blood count, type, and crossmatching. Profound hypovolemia may develop (as in the setting of a significant thermal burn) and should be treated with crystalloid, colloid, or blood products when indicated. Acid-base disorders, when clinically significant, need to be corrected. Most often, metabolic acidosis results from the ingestion of a strong acid. Following the ingestion of sulfuric, phosphoric, or acetic acid, the disorder will be an anion gap metabolic acidosis due to the absorption of hydrogen and the respective anions. Following the ingestion of hydrochloric acid, and in the absence of a significant lactic acidosis, a nonanion gap metabolioc acidosis will result from the systemic absorption of hydrogen and chloride ions. Difference of opinion exists regarding the indication for the treatment of a metabolic acidosis. Although some practitioners would treat a pH of 7.2, most physicians would agree that a pH of less than 7.1 is an indication for the judicious intravenous administration of sodium bicarbonate. An in-depth discussion of this issue may be found elsewhere.

Gastric Decontamination

Dilution with water or milk is controversial. The administration of a diluent may cause vomiting, leading to repeated exposure of esophageal and oropharyngeal tissues to the caustic, thus exacerbating damage. Dilution is contraindicated prior to airway interventions in patients with acute or impending airway obstruction. In addition, dilution should not be attempted in patients with clinical signs of esophageal or gastric perforation. Dilution with milk will make it impossible to visualize tissues by endoscopy. Neutralization of an acid or a base is not recommended because the heat of neutralization may result in additional thermal injury to already damaged tissues. Ipecac is absolutely contraindicated because emesis will expose the oropharyngeal and esophageal tissues to a repeated caustic insult. The blind passage of a nasogastric tube is not recommended and in the setting of an alkaline injury is contraindicated. The risk of perforating an area of compromised and fragile tissue is great. Because alkaline ingestions are not associated with systemic effects (in contrast to acid ingestions), the benefits of gastric evacuation do not clearly outweigh this risk. Some authors advocate the blind passage of a small soft feeding tube for gastric aspiration in patients who have ingested large amounts of acid. These authors argue that the eschar formation that accompanies acid ingestions protects the underlying tissues so the risk of iatrogenic perforation is small. In addition, the elimination of the acid from the stomach may prevent or ameliorate the systemic consequences of acid ingestion and minimize tissue damage. This recommendation is controversial, however, and no good clinical data exist to support this practice. Under direct visualization, however, insertion of a nasogastric tube may serve several purposes such as the removal of caustic materials, the measurement of gastric pH and maintenance of esophageal lumen patency. Patients with clinical evidence of perforation (peritoneal findings on physical examination) are best managed by surgical intervention. Caustics will not be bound by activated charcoal, and it, therefore, has no utility in this setting.

An upright chest radiograph is essential because it may provide evidence of the presence of a gastric or esophageal perforation. In addition, a chest radiograph may provide the findings of an aspiration pneumonitis. Ocular, cutaneous, and oral burns must not be overlooked. All require irrigation with copious amounts of normal saline until a physiologic pH is achieved.

Prior to further evaluation or diagnostic testing, a directed history and physical examination should be completed. Product identification, when possible, is extremely helpful and allows health care workers to form judgments about the likely quality and extent of damage and will help in the anticipation of potential complications.

DIAGNOSTICS

Endoscopy

It is well recognized that the presence or absence of oropharyngeal lesions cannot be used to accurately predict the pattern or extent of esophageal pathology. Ten to 30 percent of patients with esophageal burns have no identifiable oropharyngeal lesions. Endoscopy is the most reliable and accurate method for the evaluation of esophageal injury. It has value in the identification of injuries that require pharmacologic intervention (such as the administration of steroids and antibiotics), as well as esophageal or gastric perforations that require immediate surgical intervention. The procedure should be performed on all patients with a history of caustic ingestion. Endoscopy should be accomplished as early as possible following stabilization, and certainly within the first 12 to 24 h. Caustic burns may be classified by their gross endoscopic appearance in terms of depth and extent. First-degree burns are characterized by superficial hyperemia, mucosal edema, and areas of superficial mucosal epithelial sloughing. Second-degree burns involve damage to deeper layers. Typically, transmucosal injury with white exudative ulcerations is evident. Third-degree burns involve the entire esophageal wall and possibly penetrate to involve adjacent structures. The pattern of caustic burns may be linear and streaky or patchy and circumferential. Gross perforation may be apparent.

The standard recommendation has been to advance the endoscope only as far as the first circumferential second-degree burn or any third-degree burn because the risk of iatrogenic perforation is felt to be high. Some authors advocate the complete evaluation of the esophagus and stomach using a flexible endoscope until an area of obvious necrosis is identified. If frank necrosis is identified, many authors advocate surgical intervention to evaluate the extent of injury and to remove dead tissue. The presence of esophageal or gastric burns is an indication for hospitalization. Patients should have nothing by mouth. Repeated endoscopy during the first 2 to 3 days is helpful in the identification of progressive injury requiring surgical intervention. In addition, it also allows for the insertion of stents, strings, and feeding tubes that may help maintain esophageal lumen patency while healing occurs. Endoscopy should be avoided from the fifth day until one and one half weeks following ingestion. At this time the risk of perforation increases due to wound softening that occurs as healing progresses. Endoscopy is contraindicated in patients with necrosis of the pharynx or in patients in respiratory distress who have not undergone airway management.

Radiographic Contrast Imaging

Imaging Contrast-enhanced visualization of the esophagus is not recommended in the initial evaluation of esophageal or gastric burns. Most authors agree that these studies are rarely sensitive enough for the detection of mucosal injuries. Some features of injury evident from esophagrams are the intramucosal retention of contrast material and gaseous dilatation of esophagus due to air trapping. The blurring of mucosal margins, linear streaking of contrast material and abnormal displacement of the pleural reflection may be seen. Following the third week postingestion, serial barium swallows will identify the development of strictures.

MANAGEMENT

Steroids and Antibiotics

Evidence in support of the use of steroids for the prevention of stricture formation following significant caustic ingestions is somewhat controversial. Steroids are believed to prevent stricture formation by inhibiting the degree of fibroplasia. Adequately controlled clinical trials to prove the efficacy of steroids have not been performed. However, animal studies support their use. In general, first-degree burns of the esophagus will heal completely without stricture formation and, therefore, steroid use is not indicated. Third-degree burns are felt to consistently result in stricture formation. However, the additional risk of immune supression, wound softening with perforation, and bacterial invasion that occurs secondary to steroid use is very significant and probably not justified. Steroid use is recommended by many authors for patients with circumferential second-degree burns because it is felt that the risk of perforation is lower in these patients but the benefits of reduced scar formation are greater. The use of steroids may increase the risk of bacterial invasion and mask infection, so antibiotics are always recommended in conjunction with steroids. Contraindications for the use of steroids include signs of infection, perforation, or gastrointestinal bleeding. Treatment will only have benefit when initiated within 48 h of ingestion. The dosage of methyl prednisolone is 40 mg q8h for 2 to 3 weeks followed by a 6-week taper. The antibiotics of choice include penicillin 12 million units or ampicillin 8 to 12 g intravenously over 24 h in divided doses. Other antibiotics may include clindamycin, vanomycin, or tetracycline. If steroids are not used, antibiotics are recommended only if signs of infection develop.

Additional treatment for esophageal strictures is undergoing further study. Substances with lathyrogenic properties have been reported to prevent stricture formation in animals. ß-Aminopropionitrile inhibits intermolecular covalent cross-linking in newly formed collagen and decreases the tensile strength of scar tissue. Penicillamine has also been used experimentally in animal studies. It inhibits lysine-derived aldehyde groups and prevents the cross-bonding of collagen. Currently, these treatments are not available or recommended for human use.

Delayed Complications

The most common delayed complication secondary to lye ingestions is stricture formation. Strictures are usually the result of second- and third-degree burns. Patients may become symptomatic with signs of gradual esophageal obstruction between 3 weeks and 1 year postingestion. Acid burns may result in gastric outlet obstruction. Symptoms of early satiety and weight loss occur and may develop any time after the first 6 weeks or several years following ingestion. Esophageal carcinoma has been reported to be a late complication of lye ingestion with an average latency period of 40 years. The incidence of esophageal carcinoma is reported to be 1,000 times that of the general population.

Dilatation

The use of bougienage to treat stricture formation in the esophagus following caustic ingestion is controversial. Prophylactic bougienage has been started as early as the week following ingestion. However, many authors believe that dilatation prior to the third week following ingestion is contraindicated because the risk of trauma and perforation is high. If stricture formation is apparent, steroid administration may be reduced and dilitation begun cautiously. Strictures of moderate degree may be dilated successfully by antegrade bougienage. In patients with more severe stricture formation, retrograde dilitation using an indwelling string is considered by some the safest and most successful method, but it requires a gastrostomy. Strictures that do not respond to dilatation may require surgical reconstruction and colonic interposition. Surgical management at this point is controversial. Many authors advocate esophagectomy and colonic interposition as prophylaxis against the later development of esophageal carcinoma. Some believe that the risk of thoracotomy and resection of the esophagus is greater than that of the development of esophageal carcinoma.

OTHER CAUSTIC AGENTS

Clinitest Tablets

Clinitest tablets, which are used by some diabetic patients to test urine for ketones, contain caustic chemicals including copper sulfate 20 mg, citric acid 300 mg, sodium hydroxide 232.5 mg, and sodium bicarbonate 80 mg. The sodium hydroxide in each tablet provides the strongly basic pH required for its reducing action. The tablets are approximately the same size and shape as a tablet of acetaminophen or salicylate. Patients often keep bottles of Clinitest tablets in the medicine cabinet alongside other over-the-counter products. Occasionally an error results in the accidental ingestion of Clinitest tablets, most frequently by children, but adults have also made this error. Full-thickness burns of the esophagus and esophageal strictures have resulted. The preferred treatment is dilution with cold milk or water to decrease the causticity and to absorb the heats of solution and neutralization. Management recommendations include stabilization as described above, esophagoscopy, with further management decisions based on the results.

Button Batteries

Button batteries are an occasional source of foreign body ingestion, most frequently by children, but occasionally by adults. The chemical composition of the batteries is variable, but they may contain potassium or sodium hydroxide, and salts of mercury, zinc, or other metals. A knowledge of the diameter of the battery and the identification of the chemical system is helpful in patient management. Batteries with a diameter of greater than 15 mm usually contain mercuric oxide. Following ingestion, most batteries pass uneventfully through the gastrointestinal (GI) tract. However, if the battery becomes impacted in the esophagus, at some other site, or aspirated into a bronchus, it must be removed. The impacted battery can produce a local pressure necrosis. Furthermore, if the battery opens, the leakage of alkali can result in an area of liquefaction necrosis with subsequent perforation. In addition, the systemic absorption of heavy metal salts can occur and is of concern.

On presentation, radiographs should be done to identify the position of the ingested battery. Batteries that have passed beyond the esophagus need not be removed unless the patient develops signs of necrosis, obstruction, or hemorrhage. Patients with batteries lodged in the esophagus may develop dysphagia, vomiting, anorexia, or fever. Batteries lodged in the GI tract, and batteries that have split open, need to be removed emergently, either surgically or endoscopically. Recently, the use of endoscopes with magnetized probes and drugs that decrease esophageal tone have been used to dislodge these batteries. Syrup of ipecac has not been shown to be effective and may encourage aspiration of the battery. Follow-up radiographs are necessary only to confirm passage of the button battery. Confirmation by inspection of the stools is preferred, however, because it eliminates the need to perform additional abdominal radiography. Mercury levels in blood and urine need only be followed if the battery splits open. Although elevated blood mercury levels have been found in this setting, no case has been reported in which chelation has been necessary.

Hydrofluoric Acid

Hydrofluoric (HF) acid is an inorganic compound used widely in industry and in some household products. Fluorine compounds are found in plastics, germicides, dyes, fire-proofing materials, and resins. In addition, HF acid is used in the pickling of stainless steel; the polishing of metal; the polishing, etching, and frosting of glass; in making rust removers; and in manufacturing semiconductors. It is found in solutions of various concentrations ranging from 20% to 70%. It is highly toxic, producing severe injury to exposed tissues as well as significant and potentially lethal systemic effects. Exposure to the skin, eyes, or respiratory system may result in extensive burns and death from tissue destruction or the systemic effects of hypocalcemia, hypomagnesemia, and other electrolyte abnormalities.

Pathophysiology

Hydrofluoric acid is a weak acid when compared with other mineral acids. It is poorly dissociated in solution and produces less free hydrogen ion than other acids of equimolar solutions. HF acid exposure results in the dessication of skin and severe local tissue injury. Because it is relatively nonpolar, it is highly lipophilic. It therefore readily crosses cell membranes and penetrates deeply. The fluoride ion dissociates slowly and is responsible for much of the tissue destruction. It has a strong affinity for positively charged ions and is not neutralized until contact with calcium or other cations occurs. Insoluble calcium fluoride and magnesium fluoride salts are formed. The removal of these essential ions from biologic systems interferes with the electrical activity of cellular membranes and disrupts cellular metabolism. As fluoride ion penetrates more deeply, bony destruction occurs through the interaction of fluoride ion with the calcium of bone. In addition, the absorption of fluoride ion can have significant systemic effects. Death from profound hypocalcemia has been reported following the exposure of a relatively small skin area (< 2.5 percent total body surface area) to a highly concentrated solution.

Because HF exposure most frequently occurs in an occupational setting, patients frequently present with complaints of burns to the hand and nail bed. HF acid will penetrate pin holes in rubber gloves. Exposure of the nail plate will result in the penetration of subungual tissue. The patient may complain of excruciating pain, throbbing and burning in character. Early following exposure to relatively dilute solutions, there may be pain but no gross evidence of injury to the tissues. Pallor of the exposed skin or sometimes mild erythema may be evident on presentation. Typically, the physical findings are so unimpressive that the significance of the injury is missed initially. Unless the physician is careful to elicit the source of the exposure, the patient may be discharged without appropriate treatment only to return with necrosis of the involved tissue. The intensity and rapidity of onset of the signs and symptoms varies with the concentration of the acid and the duration of contact. Solutions of 50% to 70% concentration will produce immediate signs and symptoms, whereas solutions with concentrations of 20% or less will produce signs and symptoms up to 12 h later.

Burns secondary to exposure to highly concentrated HF acid will progress to complete necrosis of the involved area unless treated correctly. The affected skin will become firmly edematous and pasty white with vesiculation. The vesicles may appear cloudy and usually contain caseous material which is necrotic tissue. The burns may progress to ulceration with full thickness tissue loss.

Management

Prior to arrival in the emergency department, initial management of a cutaneous exposure involves the removal of saturated clothing and copious irrigation of the affected area with water. This should be followed by immersion of the affected part in an iced solution of magnesium sulfate, calcium salts, or a high molecular weight quarternary ammonium compound (benzethonium chloride). The cold constricts lymph and blood vessels, retarding the diffusion of fluoride ions. The cations bind with fluoride to produce a nonionized complex preventing further tissue penetration. Care must be taken not to produce a superimposed thermal injury.

Initial emergency department management includes stabilization as described previously. Cardiac monitoring and routine laboratory studies and are essential. A 12-lead electrocardiogram (ECG) will be valuable initially. In particular, the QT interval should be inspected for evidence of the lengthening that occurs with various electrolyte disturbances. In addition, the physician should look carefully for ECG evidence of hyperkalemia. Systemic acidosis, hypocalcemia, hypomagnesemia, and hyperkalemia are common potentially lethal complications of exposure to highly concentrated HF.

Successful therapy for mild HF acid burns may be accomplished with the topical application of a 2.5% calcium gluconate gel. The gel can be made by mixing 3.5 g calcium gluconate with 5 oz of water-soluble lubricant. The gel may be placed in a surgical glove and used to cover the affected part. If the patient experiences relief from pain, remains pain free, and the burn does not appear to progress, no more aggressive treatment is required. If involvement of the nail bed is suspected, the nail must be removed and the nail bed treated as the rest of the skin. Burns not responding to topical treatment and severe burns may require intradermal injection with 10% calcium gluconate. A 30-gauge needle should be used for intrademal injections. No more than 5 mL of 10% calcium gluconate per square centimeter of tissue should be injected into the affected area. Pain relief is the end point of treatment. Recurrence of pain is an indication for additional treatment. Intradermal injections of the hand and fingers requires the infiltration of limited amounts of volume as vascular compromise may occur and result in further necrosis. Calcium chloride should never be used intradermally because it causes tissue necrosis.

An alternative to intradermal calcium gluconate or magnesium sulfate injection is the intra-arterial perfusion of calcium gluconate. This type of therapy is effective if the area of exposure is an area with a discreet vascular supply, such as a digit. Placement of an intra-arterial catheter proximal to the site of injury (radial, ulnar, or brachial arteries) is performed. Proper placement of the catheter is confirmed by blood flow and pressure tracing or by angiography. An infusion of 10 mL of 10% calcium gluconate diluted in 40 to 50 mL of 5% dextrose is given over 4 h. Calcium chloride solutions have also been used effectively; however, they are not recommended by most authors because extravasation of solution will result in tissue necrosis at the site. Patients may require multiple treatments. This mode of treatment has significant advantages over intradermal injections. Selective arterial perfusion avoids the need to remove the fingernail and avoids the pressure necrosis that may result from the injection of liquid into a closed space. In addition, it provides a greater concentration of calcium to the affected area. The disadvantages of intra-arterial infusion include the requirement for hospitalization and the risk of arterial spasm or thrombosis. Following either mode of treatment, the serum calcium must be carefully monitored.

Ocular exposure to HF acid results in the rapid onset of pain, tearing, conjunctival inflammation, corneal opacification, and erosion. An immediate single irrigation with normal saline or water for 15 min is thought to be appropriate intervention. Injections of calcium gluconate or magnesium sulfate are very toxic to the eye and increase the risk for corneal ulceration. There is now evidence that repeated instillation of 1% calcium gluconate drops may be efficacious in the treatment of ocular burns. All patients with an ocular exposure to HF acid require a consultation with an ophthalmologist.

Patients who ingest HF acid will develop gastrointestinal symptoms, nausea, vomiting, and sometimes hemorrhage. Oral ingestions of HF acid require the administration of calcium or magnesium salts. Ideally, the magnesium or calcium should be given on a milliequivalent-for-milliequivalent basis. Although it is usually impossible to know the amount of ingested HF acid, an attempt must be made to get a reasonable estimate from the historical data. Otherwise, 300 mL magnesium citrate or calcium salts can be given empirically. Ipecac is contraindicated in this setting. Therapy should be initiated quickly because the ingestion of HF acid often results in death.

Inhalation burns with very concentrated or anhydrous fluoride may result in a compromised airway, systemic fluorosis, delayed pulmonary edema, electrolyte abnormalities, and arrhythmias. Following the inhalation of HF acid, the patient must be moved to an uncontaminated area, the airway must be protected, 100% oxygen administered, and treatment begun with bronchodilators and systemic steroids as indicated. Nebulized 2.5% calcium gluconate has been recommended; however, insufficient studies exist in support of its use. The prognosis following fluoride inhalation is poor.

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