Injury from ammonia most commonly is caused by inhalation, but it also may follow ingestion or direct contact with eyes or skin. Relevant thresholds of exposure to toxic gases are defined as follows:
The TWA is defined as the concentration for an 8-hour workday of a 40-hour workweek that nearly all workers can be exposed to without adverse effects. The STEL is the concentration at which an exposure of longer than 15 minutes is potentially dangerous and may produce immediate or chronic compromise to health. Anhydrous ammonia has a TWA of 25 parts per million (ppm), a STEL of 35 ppm, and an IDLH of 300 ppm.[1]
The clinical presentations of these injuries and their evaluation and treatment are discussed in this article. Chloramine gas inhalation injury also is discussed.
Symptoms of exposure to gaseous ammonia include the following:
Symptoms usually subside within 24-48 hours. Because ammonia vapor is highly water soluble, onset of symptoms occurs very rapidly after inhalational exposure. Absence of symptoms following inhalational exposure to ammonia essentially rules out significant injury.
Ingestion of ammonia can produce the following symptoms:
On physical examination, inhalation injury from ammonia is marked by the following findings:
Alkali burns to the skin from ammonia are yellow, soapy, and soft in texture; with severe burns, skin turns black and leathery.
Manifestations of ocular toxicity from ammonia include the following:
See Clinical Presentation for more detail.
Serum ammonia concentrations are of little value in patients with ammonia exposure because they do not correlate well with toxicity. Laboratory studies in patients with ammonia exposure include the following:
Patients with eye injury should have a slit-lamp examination with fluorescein staining. Perform tonometry to determine if intraocular pressure is elevated. Measure conjunctival pH.
Depending on the clinical presentation, other tests and procedures may include the following:
See Workup for more detail.
As with all toxic gases, removal from exposure is the most important first step. Subsequent management of toxic exposure to ammonia is largely supportive, as follows:
Indications for tracheal intubation include the following:
Treat ingestions using the following steps:
Corticosteroids are controversial therapies for ammonia toxicity, and should be used only after appropriate expert consultation. Accepted indications include the following:
See Treatment and Medication for more detail.
For patient education resources, see the First Aid and Injuries Center, as well as Thermal (Heat or Fire) Burns.
At room temperature, ammonia (NH3) is a highly water-soluble, colorless, irritant gas with a unique pungent odor. Ammonia has a boiling point of -33°C and an ignition temperature of 650°C.
Anhydrous ammonia is one of the most widely produced chemicals in the United States, one third of which is used by the farming industry as a component of fertilizer and animal feed. Anhydrous ammonia is widely used as refrigerant in industrial facilities such as meat, poultry, and fish processing facilities, seafood processing facilities aboard ships, dairy and ice cream plants, wineries and breweries, juice and soft drink processing facilities, cold storage warehouses, and petrochemical facilities.[3]
Ammonia also is used in the production of explosives, pharmaceuticals, pesticides, textiles, leather, flame-retardants, plastics, pulp and paper, rubber, petroleum products, and cyanide. Furthermore, ammonia is a major component of many common household cleaning and bleaching products (eg, glass cleaners, toilet bowel cleaners, metal polishes, floor strippers, wax removers, smelling salts).
Ammonia most commonly causes damage when anhydrous ammonia (liquid or gas) reacts with tissue water to form the strongly alkaline solution, ammonium hydroxide. The formula for this is as follows:
NH3 + H2 O ⇒ NH4 OH
This reaction is exothermic and capable of causing significant thermal injury.
Ammonium hydroxide can cause severe alkaline chemical burns to skin, eyes, and especially the respiratory system. Mild exposures primarily affect the upper respiratory tract, while more severe exposures tend to affect the entire respiratory system (see Presentation). The gastrointestinal tract also may be affected if ammonia is ingested.
Tissue damage from alkali is caused by liquefaction necrosis and theoretically can penetrate deeper than that caused by an equipotent acid. In the case of ammonium hydroxide, the tissue breakdown liberates water, thus perpetuating the conversion of ammonia to ammonium hydroxide. In the respiratory tract, this results in the destruction of cilia and the mucosa, eliminating the barrier to infection. Furthermore, secretions, sloughed epithelium, cellular debris, edema, and reactive smooth muscle contraction cause significant airway obstruction.[15]
Airway epithelium can regain barrier integrity within 6 hours after exposure if the basal cell layer remains intact.[16] However, damaged epithelium often is replaced by granular tissue, which may be one of the causes of chronic lung disease following ammonia inhalation injury.
Liquid anhydrous ammonia (-33°C) freezes tissue on contact. To put this in perspective, critical skin damage begins at -4°C and becomes irreversible at -20°C. The degree of tissue injury, however, is proportional to the duration and concentration of exposure. Similarly, damage to the respiratory system is proportional to depth of inhalation, duration of exposure, concentration, and pH of the gas or liquid.
Chloramines (NH2 Cl, NHCl2) are highly water-soluble irritant gases formed when household bleach (5.25% sodium hypochlorite [NaOCl]) is mixed with 5-10% ammonia solutions (usually cleaning products). When inhaled, the gases react with the water in airway mucous membranes to produce free ammonia gas, hypochloric acid, and hypochlorous acid. In turn, hypochlorous acid reacts with water to form hydrochloric acid and nascent oxygen, a strong oxidizing agent with corrosive effects.
Ammonia is a product of protein catabolism and is metabolized by the liver. Normal blood ammonia levels range from 10-40 µmol/L. This increases 10% with exposure to 25 ppm but is not considered harmful. Theoretically, patients with liver dysfunction are at increased risk for ammonia toxicity; however, currently no sufficient clinical evidence can confirm this.
Chloramines (NH2 Cl, NHCl2) are highly water-soluble irritant gases formed when household bleach (5.25% sodium hypochlorite [NaOCl]) is mixed with 5-10% ammonia solutions (usually cleaning products). When inhaled, the gases react with the water in airway mucous membranes to produce free ammonia gas, hypochloric acid, and hypochlorous acid. In turn, hypochlorous acid reacts with water to form hydrochloric acid and nascent oxygen, a strong oxidizing agent with corrosive effects.[17]
Agriculture-related ammonia injury most often results from either ammonia leaks in fertilizer tanks and hoses or toxic ammonia levels in animal confinement buildings, where ammonia is adsorbed by dust particles that transport it more directly to small airways. Because of this synergistic effect, symptoms have reportedly developed within minutes of entering animal confinement buildings.
Firefighters are at risk for exposure this irritant gas.[4] Anhydrous ammonia may be released in industrial fires (eg, at fertilizer plants). In addition, ammonia is liberated during combustion of nylon, silk, wood, and melamine.
Household exposure may occur because ammonia is a major component of many common household cleaning and bleaching products, including the following:
Smelling salts are a less common source of household ammonia ingestion. Often in capsule form, smelling salts, which contain approximately 20% ammonia, release a pungent odor when broken. Smelling salts are found in many first-aid kits as a treatment for syncope; unfortunately, children sometimes bite into them, resulting in minor esophageal burns and mild respiratory symptoms.
The 2017 Annual Report of the American Association of Poison Control Centers' National Poison Data System (AAPCC-NPDS) reported 1846 single exposures of ammonia, but no deaths. In addition, 1513 single exposures to ammonia-containing glass cleaners, 489 single exposures to all-purpose ammonia cleaners, and 2115 single exposures to chloramine gas were reported, with no deaths.[5]
Of note, ingestion of household solutions usually is unintentional and occurs in young children; adult ingestions, however, most often are suicide attempts. In contrast, inhalation injury is almost always unintentional and generally occurs in an industrial setting; therefore, it is far more common in adults than children.
Ammonia exposure may be one factor in an elevated risk for chronic bronchitis and chronic obstructive pulmonary disease (COPD) seen in livestock farmers. Susceptibility to farming-related COPD appears to be heightened in farmers with underlying atopy.[6]
Large-scale exposure due to industrial accidents have occurred. In August 2010, a cloud of anhydrous ammonia was released from the roof-mounted pipe of a warehouse and distribution center 15 miles south of Mobile, Alabama. The cloud traveled a quarter mile across the river adjacent to the plant, exposing 9 crew members on docked ships and 143 contractors working outdoors at a clean-up site. One employee onsite sustained injuries after briefly losing consciousness from ammonia inhalation. Of those exposed, 130 sought medical care, 32 required hospitalization, and 4 were placed in intensive care.[7]
In March 2011, equipment and operator error in a poultry plant in Alabama released 32,000 pounds of anhydrous ammonia, resulting in the hospitalization of 150 people.[3]
Most individuals with ammonia inhalation who survive the first 24 hours will recover. Patients begin showing improvement within 48-72 hours and may recover fully during this time if exposure was mild. For patients with more significant respiratory symptoms, recovery can be expected within several weeks to months.
Interestingly, Arwood et al found that initial chest radiography findings and oxygenation level correlate poorly with outcome and that physical examination on arrival provides more sensitive prognostic information.[8] Montague and MacNeil, however, note that patients who do not develop chest radiograph abnormalities are less likely to have chronic respiratory sequelae.[9]
In a study of 12 patients exposed to anhydrous ammonia as a result of the same accident, Close and colleagues found that patients exposed to high concentrations of ammonia over a short period of time manifested upper airway obstruction and required early intubation or tracheostomy but recovered with few pulmonary sequelae. In contrast, patients exposed to lower concentrations of gas over a prolonged period did not manifest upper airway obstruction, but suffered significant long-term pulmonary sequelae.[10]
Patients in this case series who developed long-term pulmonary sequelae experienced gradual deterioration of pulmonary function during the first 2-6 months after exposure.[10] A period of slight improvement was then observed, followed by stabilization of symptoms.[10]
Long-term effects of ammonia inhalation injury include the following:
Chronic obstructive disease from ammonia toxicity is often only minimally improved by bronchodilators. The reason is thought to be that this sequela results from airway lesions more than from hyperreactivity.
The effects of gaseous ammonia effects at various concentrations are as follows:
Symptoms of inhalational ammonia toxicity include rhinorrhea, scratchy throat, chest tightness, cough, and dyspnea; eye irritation from the ammonia gas may also be present. Symptoms usually subside within 24-48 hours. Absence of symptoms following inhalational exposure to ammonia essentially rules out significant injury. Individuals with reactive airway disease, such as asthmatics, are particularly sensitive to ammonia inhalation.
The first classification of injury from unintentional ammonia exposure, published in 1941 by Caplin, categorized cases as mild, moderate, or severe. Patients in the mild group presented with conjunctival and upper respiratory inflammation and pain but showed no signs of respiratory distress.[11] The moderate group presented similarly but with more exaggerated symptoms. The severe group presented in frank respiratory distress with productive cough, acute lung injury (ALI), and dysphagia.
With brief ammonia exposure, damage generally is limited to the upper airway mucosa. Brief exposures at very high concentrations, however, can be overwhelming and affect the entire respiratory system. People who are capable of escaping their environment usually are not subject to severe exposures, because they flee upon detection of ammonia's pungent odor. Infants, the elderly, and others with limited mobility are at greatest risk because of their inability to remove themselves from exposure.
Gaseous ammonia combines with water of the skin, eyes, and airways to form ammonium hydroxide. This exothermic reaction results in both heat and chemical burns. Liquid ammonia freezes tissue on contact and may cause full-thickness tissue injury that penetrates deeper than the more conspicuous superficial chemical burns.
Concentrations greater than 10,000 ppm are required to cause skin damage. The eyes begin to feel irritated at concentrations of 50-100 ppm; at 700 ppm, immediate eye damage occurs.
Typical household ammonia products (3-10% ammonium hydroxide) have a pH of less than 12.5, although the pH of industrial solutions (up to 30% ammonium hydroxide) is often greater than 13. Because caustic alkali burns generally are thought to occur at a pH greater than 12.5, ammonia ingestions in the home usually do not lead to significant injury. However, Klein et al reported 3 cases of oropharyngeal and esophageal injury following intentional ingestion of household solutions with a pH less than 12.[12]
Patients present with oropharyngeal, epigastric, and retrosternal pain. Abdominal pain and other gastroenterologic symptoms may occur if ingestion causes perforation of a viscus (perforation may occur up to 24-72 hours post ingestion). Respiratory symptoms may be present if aspiration pneumonia or pneumonitis complicates ingestion.
At low concentration, symptoms of chloramine gas toxicity include tearing, rhinorrhea, oropharyngeal burning, and cough. Although chloramine gases produce rapid onset of symptoms, these symptoms are mild enough that patients often do not remove themselves promptly from the toxic environment; thus, patients often present after a prolonged exposure time.
The physical examination following mild exposure reveals only mild wheezing and decreased air entry or may be entirely unremarkable. Patients with more significant exposure may present with dyspnea, pulmonary edema with secondary hypoxia, nausea, tracheobronchitis, toxic pneumonitis, intrapulmonary shunt, and/or pneumomediastinum. Note that pulmonary edema may ensue within minutes or be delayed for up to 24 hours following exposure.
Pulmonary function tests may reveal obstructive, restrictive, or combined patterns. The pulmonary artery occlusive pressure may be less than 17 mm Hg.[17]
For more information, see Chlorine Toxicity.
Inhalation injury from ammonia is marked by the following findings:
Skin or eye contact with ammonia can result in burns or cold injury. Alkali burns to the skin are yellow, soapy, and soft in texture; with severe burns, skin turns black and leathery.
Burns to the eye penetrate particularly deeply and rapidly, leading to destruction of the inner structures within 2-3 minutes; this may progress to globe perforation. Ammonia typically causes more corneal epithelium and lens damage than other alkalis. Intraocular pressure and pH of the anterior chamber rise, resulting in a syndrome similar to acute narrow-angle glaucoma.
Other ophthalmic symptoms include the following:
With intentional ingestion of ammonia, hypovolemic shock may occur because of vomiting and third-spacing of intravascular fluid. HEENT findings may include edema of the lips, oropharynx, and upper airway.
On abdominal examination, patients may exhibit epigastric tenderness. Mediastinitis and peritoneal signs may be present with viscus perforation, which can occur as late as 24-72 hours post ingestion. Respiratory manifestations include aspiration pneumonitis and pulmonary edema.
Serum ammonia lconcentrations are of little value in patients with ammonia exposure because they do not correlate with clinical toxicity. However, patients with compromised hepatic function may show increased serum ammonia concentrations because of less efficient metabolism.
Laboratory studies and procedures in patients with ammonia exposure include the following:
Depending on the clinical presentation, other tests and procedures may include the following:
Once the acute emergency is controlled, PFTs are useful to gauge the severity of injury and to monitor progress and recovery. PFTs may show obstructive lung disease (in both acute and chronic cases) or restrictive lung disease (in chronic cases).
A V/Q scan may be useful to gauge the severity or progression of disease, but the results are unlikely to change acute management. Ventilation deficits generally are more pronounced in the larger airways. The ventilation scan also may show abnormal air trapping in the setting of lower airway obstruction.
Perform bronchoscopy to assess respiratory tract damage following acute inhalation injury (in severe cases), or in cases of ingestion with aspiration. Bronchoscopic findings may include the following:
Consider endoscopy for significant ingestion exposures (large volume and/or industrial concentrations). Indications are somewhat controversial; obtain toxicology and GI consultations if needed. Perform endoscopy on symptomatic patients and patients with intentional exposure within 24-48 hours following ingestion. The risk of perforation increases if endoscopy is performed more than 72 hours post ingestion.
Findings on endoscopy may include the following:
Management of toxic exposure to ammonia is largely supportive. Decontaminate the patient (if that was not done at the site of exposure) and support airway, breathing, and circulation (ABCs) as necessary. Provide warmed humidified oxygen.
Patients with facial or oral lesions from ammonia, like all patients with burns in these areas, are at high risk for developing laryngeal edema. Airway intervention should be aggressive. Indications for tracheal intubation include the following:
If intubation is necessary, use a large-size tube to prevent plugging by sloughed mucosa. Some experts consider procedural sedation preferable to rapid sequence intubation (RSI) because paralysis is risky in patients with a difficult and edematous airway. Furthermore, ventilation cannot be predicted to be successful if intubation fails in this context.[18] Positive end respiratory pressure (PEEP) generally is useful (5 cm water minimum).
Beware of fluid over-resuscitation. Patients may have or may be developing acute lung injury (ALI).
Follow standard initial burn management; see Thermal Burns. Once the patient is adequately stable, irrigate the involved skin with tepid water for at least 15 minutes. Continue frequent regular irrigation for the first 24 hours, in addition to conventional burn management. No salves, creams, ointments, or jellies should be applied to the skin during a 24-hour period following the injury since this will prevent natural elimination of the ammonia from the skin.[13] Administer tetanus prophylaxis.
Irrigate eye injuries with copious amounts of tepid water for at least 30 minutes or until the conjunctival pH is 6.8-7.4; use pH indicator paper to monitor. Consult ophthalmology promptly because of risk of perforation and/or permanent eye damage.
Treat ingestions using the following steps:
Corticosteroids are controversial therapies for ammonia inhalation injury. Many experts believe that corticosteroids may actually increase morbidity in these cases. However, corticosteroids are recommended to treat acute bronchospasm in patients with underlying reactive airways disease, and to treat chronic respiratory complications from acute inhalation injury.
Use of steroids for the treatment of caustic injuries after caustic ingestion is also controversial. However, patients exhibiting signs of airway edema after caustic exposure may benefit from intravenous (IV) dexamethasone (adults, 10 mg; children, 0.6 mg/kg up to a maximum of 10 mg). In addition, use of IV corticosteroids can be considered in symptomatic patients with grade IIb (near-circumferential) caustic injuries, to reduce the formation of esophageal strictures.
Prehospital care for patients exposed to ammonia begins with immediate removal of the patient from the contaminated environment and removal of all clothing. In the case of industrial accidents, clothes that have been saturated by liquid ammonia may freeze to the skin. The patient, still clothed, should get immediately under a shower, if available, or jump into a stock tank, pond, or into any other source of water. Remove clothes only after they are thawed and they can be freely removed from frozen areas. If the clothing is removed incorrectly, whole sections of skin can be torn off. A physician should view any second- or third-degree freeze burns of the skin.[13]
If the patient is sufficiently stable, begin copious skin and eye irrigation immediately. Continue irrigation for at least 20 minutes. Patients then can be covered with a dry, clean dressing and sheet.
If ammonia is ingested, do not induce vomiting. If vomiting begins, place the patient face down with head lower than hips to prevent vomitus from entering the lungs.[13]
Support ABCs as per advanced cardiac life support (ACLS) and advanced trauma life support (ATLS) guidelines (ACLS and ATLS guidelines may vary by region, according to training and legal responsibilities of prehospital care providers). In severe inhalation exposure to higher concentrations, administer oxygen. Patients should be kept warm (but not hot) and rested until transported to the hospital.[13]
The majority of patients with unintentional household ammonia exposure will have very mild symptoms and can be discharged safely if asymptomatic and able to tolerate oral intake. Admit patients to observation for at least 24 hours if they show significant and persistent signs, symptoms, or abnormalities in laboratory findings attributable to ammonia exposure. Admit unstable or potentially unstable patients to the intensive care unit.
Patients with ammonia ingestion may be discharged if endoscopy results are normal and oral intake is tolerated. Intentional ingestions require psychiatric evaluation.
The rationale for corticosteroid use after ammonia ingestion is that these agents may decrease the incidence and severity of esophageal strictures that occur during healing from significant alkaline injuries.
The use of corticosteroids remains controversial, but the best recent evidence suggests that they are helpful for grade IIB (circumferential partial thickness) esophageal injuries.[19] Steroid therapy will not alter the risk of stricture formation in patients with severe transmural burns. If steroids are given, the recommended dose is 1-2 mg/kg/d of methylprednisolone for 3 weeks followed by gradual tapering.
The decision to continue or stop corticosteroid therapy is based on endoscopic findings. Discontinue steroids for patients with no injury or mild mucosal inflammation or ulceration, as they are not at risk for stricture formation.
Antibiotic use is also controversial. They may be considered because of the increased risk of mediastinitis associated with steroid use in patients with full-thickness esophageal alkaline corrosive burns, but no well-controlled human trials have been performed. Consequently, prophylactic antibiotics should not be administered unless recommended after consultation with a toxicologist, gastroenterologist, and surgeon. If antibiotics are given, a broad-spectrum antibiotic (eg, a second-generation cephalosporin) is appropriate.
According to the U.S. Environmental Protection Agency (EPA), 72% of all reported chemical accidents from 2004-2014 in Iowa, Kansas, Missouri, and Nebraska involved anhydrous ammonia and up to 96% were preventable through increased operator training, improved procedures, and better communication of lessons learned. All commercial facilities with anhydrous ammonia refrigeration systems are required by the EPA to develop and implement recognized and generally accepted good engineering practices which includes adherence to a program like the International Institute of Ammonia Refrigeration (IIAR) Ammonia Refrigeration Management (ARM).[3]
Pharmacologic therapy for ammonia toxicity is directed at hypoxia, bronchospasm, acute lung injury (ALI), hypovolemia, and burns of the skin and eyes. Corticosteroids and antibiotics have limited indications; broader use of these agents in ammonia toxicity is common but controversial.
Clinical Context: Albuterol (known as salbutamol in Canada and the United Kingdom) is a beta 2-agonist used for the treatment of bronchospasm. This agent relaxes bronchial smooth muscle by its action on beta 2-receptors. It has little effect on cardiac muscle contractility.
These agents produce selective stimulation of beta 2-adrenergic receptors in the bronchial tree and lungs. The resulting relaxation of bronchial smooth muscle relieves bronchospasm and reduces airway resistance.
Clinical Context: Furosemide inhibits sodium chloride reabsorption in the ascending loop of Henle. It should be administered intravenously in patients with ammonia toxicity because this route allows for superior potency and a higher peak concentration, despite an increased incidence of adverse effects, particularly ototoxicity (rare).
A trial of diuretics can be considered in patients with ammonia toxicity who have evidence of concomitant fluid overload. Diuretics are sometimes considered for the treatment of acute lung injury (ALI), but ventilation with positive end-expiratory pressure (PEEP) may be much more useful than diuretics for optimizing oxygenation because ALI is secondary to alveolar capillary injury, not excess fluid.
Clinical Context: Ciprofloxacin is a fluoroquinolone with activity against pseudomonads, streptococci, methicillin-resistant Staphylococcus aureus (MRSA), Streptococcus epidermidis, and most gram-negative organisms, but no activity against anaerobes. It inhibits bacterial DNA synthesis and growth.
Clinical Context: This agent is indicated for infections caused by susceptible strains of microorganisms and for prevention of corneal and conjunctival infections.
Clinical Context: Neomycin has been an option through the years. However, it is used less frequently, because of the high incidence of sensitivity. Patients with burns to the skin (eg, eyelids) are rarely given prophylactic antibiotics. Neomycin binds to 30S ribosomal subunits, which, in turn, interferes with bacterial protein synthesis.
For patients with eye exposure to ammonia, ophthalmic antibiotic preparations reduce the risk of infection secondary to tissue injury.
Clinical Context: Cyclopentolate blocks the response of the muscle of the ciliary body and the sphincter muscle of the iris to cholinergic stimulation, thus causing pupillary dilation (mydriasis) and cycloplegia mydriasis and cycloplegia. It induces mydriasis in 30-60 minutes and cycloplegia in 25-75 minutes; these effects last up to 24 hours.
Clinical Context: Homatropine blocks the response of the sphincter muscle of the iris and the muscle of ciliary body to cholinergic stimulation, producing mydriasis and cycloplegia. It induces mydriasis in 10-30 min and cycloplegia in 30-90 minutes; these effects last up to 48 hours.
Clinical Context: Tropicamide blocks the response of the sphincter muscle of the iris and the muscle of the ciliary body to cholinergic stimulation.
These agents induce paralysis of accommodation (cycloplegia) by blocking parasympathetic (cholinergic) effects in the eye. This effect is beneficial to prevent ciliary spasm. These agents should be used in consultation with the ophthalmology service.
Clinical Context: Prednisolone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability. Note that ophthalmologic steroids are controversial; consult with the ophthalmology service before prescribing.
Clinical Context: Fluorometholone suppresses migration of polymorphonuclear leukocytes and reverses capillary permeability.
Clinical Context: Rimexolone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.
Corticosteroids decrease the formation of fibroblasts on the cornea and may limit intraocular inflammation. However, these agents may potentiate infection. Ophthalmic corticosteroids should be used in patients with ammonia exposure only in consultation with the ophthalmology service. Also, steroid-antibiotic combinations may be useful.
Clinical Context: Proparacaine prevents the initiation and transmission of impulses at the nerve cell membrane by stabilizing and decreasing ion permeability. This agent provides rapid onset of anesthesia, beginning 13-30 seconds after instillation. However, it has a short duration of action (about 15-20 minutes). It is the least irritating of all topical anesthetics.
Ophthalmic anesthetics are used primarily for pain relief. Their duration of action is relatively short-lived, limiting their usefulness outside of the hospital or clinic setting.
Clinical Context: Controls or prevents inflammation by controlling rate of protein synthesis, suppressing migration of polymorphonuclear leukocytes (PMNs) and fibroblasts, reversing capillary permeability, and stabilizing lysosomes at cellular level
In patients with grade IIb caustic esophageal burns, high doses of methylprednisolone (1 g/1.73 m2/day for 3 days) may reduce stricture development.[19]