a) Alkaline corrosive ingestion may produce burns to the oropharynx, upper airway, esophagus and occasionally stomach. Spontaneous vomiting may occur. The absence of visible oral burns does NOT reliably exclude the presence of esophageal burns. The presence of stridor, vomiting, drooling, and abdominal pain are associated with serious esophageal injury in most cases.
b) PREDICTIVE: The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and GI complications and mortality.

a) Remove contaminated clothes and any particulate matter adherent to skin. Irrigate exposed skin with copious amounts of water for at least 15 minutes or longer, depending on concentration, amount and duration of exposure to the chemical. A physician may need to examine the area if irritation or pain persist.

a) In more severe cases chemosis, conjunctival epithelial defects or limbal ischemia may develop (Morgan, 1987).

a) Severity of corneal injury is dependent on the concentration of the alkali, the duration of exposure, and the pH of the solution. With a solution containing sodium as the principal cation, a pH greater than 11.5 is associated with a sharper increase in severity of injury to the corneal stroma (Grant & Schuman, 1993).
b) Ammonium hydroxide penetrates the cornea the fastest due to its fat solubility; it causes the deepest injury, with edema and wrinkling of the posterior corneal surface and damage to the iris and possibly cataract. Calcium hydroxide may cause superficial opacification of the cornea, and sodium hydroxide may commonly induce pearly opacification of deeper layers of the stroma (Grant & Schuman, 1993).
c) In severe cases the cornea may be overgrown by conjunctival epithelium, permanent corneal opacification may develop or corneal perforation and blindness may ensue (Mattax & Mcculley, 1988; Sawhney & Kaushish, 1989; Saini & Sharma, 1993).

a) GRADE 1 INJURY: Corneal epithelium damage, no conjunctival ischemia; good prognosis (Roper-Hall, 1965; Saini & Sharma, 1993).
b) GRADE 2 INJURY: Hazy cornea; visible iris details, ischemia less than 1/3 of limbus; good prognosis (Roper-Hall, 1965; Saini & Sharma, 1993).
c) GRADE 3 INJURY: Total epithelial loss, stromal haze, obscured iris details, ischemia 1/2 to 1/3 limbus; guarded prognosis (Roper-Hall, 1965; Saini & Sharma, 1993).
d) GRADE 4 INJURY: Opaque cornea, ischemia more than 1/2 limbus; poor prognosis (Roper-Hall, 1965; Saini & Sharma, 1993).

a) Negative effects include possible replacement of ciliary and iris tissue with granulation tissue (producing fibrosis) (Pfister et al, 1971), and corneal ulceration.

a) The ability to produce the water and/or mucin portion of the tear film may be affected (Lemp, 1974).
b) In severe cases visual loss may be permanent (McLaughlin, 1946; Sawhney & Kaushish, 1989). Corneal perforation may rarely develop (Sawhney & Kaushish, 1989).

a) A 2-year-old boy developed bilateral photophobia, tearing, redness, and a tear pH of 8.5 to 9 approximately 4 hours following an accident in which he was thrown from the rear seat, landing face up under the dashboard in an automobile with a driver's air bag that burst (Ingraham et al, 1991).
b) A 22-year-old woman developed chemical conjunctivitis after being exposed to the white powder in her airbag when it deployed during a motor vehicle accident (Swanson-Biearman et al, 1991a). Another woman experienced alkali keratitis as a result of activation of an automobile air bag, with diffuse corneal opacification in one eye. Following aggressive medical management, her eye slowly re-epithelialized over 5 weeks (White et al, 1995).
c) Sodium hydroxide released from automotive air bags has been suspected as a cause of the ocular injuries (Ingraham et al, 1991) Swanson-Bierman et al, 1993).

a) SEQUELAE: Permanent sequelae were reported in 2 of 27 patients; one patient had a corneal scar and permanently decreased visual acuity, and one patient had dry eye syndrome. Both patients were presumed to have had no immediate irrigation, since lime fragments were found imbedded in the conjunctiva (Rozenbaum et al, 1991).

a) The presence or absence of burns in the mouth does not indicate burns of the esophagus. Severe esophageal burns have been reported in cases where burns of the mouth or oropharynx were not seen (Uhde, 1946; Alford & Harris, 1959; Viscomi et al, 1961; Yarington et al, 1964; Feldman et al, 1973; Gaudreault et al, 1983; Previtera et al, 1990; Rauch, 2000). Of 389 pediatric patients who were hospitalized following ingestion of corrosive substances but did not have oral cavity burns, endoscopy revealed that 240 of the patients (61%) had esophageal lesions (Dogan et al, 2006).
b) CASE SERIES: In a series of 95 patients with suspected or obvious corrosive burns, 91 had involvement of the oral mucosa, 39 of the hypopharynx or esophagus, and 31 of the epiglottis, epiglottic folds, or larynx (Sellars & Spence, 1987).
c) Sign and symptoms associated with oral burns include pain, crying, sialorrhea, lip swelling and dysphagia (Vergauwen et al, 1991; Rauch, 2000).

a) Hypotension and tachycardia are not common acutely but may develop in patients with severe gastrointestinal bleeding or extensive gastrointestinal necrosis after corrosive ingestion (Palmer et al, 2007; Hawkins et al, 1980; McCabe et al, 1969; Singh et al, 1976; Sarfati et al, 1987).

a) Burns and edema of the epiglottis and larynx may develop after caustic ingestion and may cause severe respiratory distress, particularly in children. Massive necrosis of the laryngeal and pharyngeal wall may necessitate tracheostomy (Jaillard et al, 2002).
b) INCIDENCE: In a series of 95 patients with suspected or obvious corrosive burns, 31 (33%) had involvement of the epiglottis, epiglottic folds, or larynx (Sellars & Spence, 1987).
c) Tracheostomy may be required in severe cases (Oakes et al, 1982; Schild, 1985; Estrera et al, 1986; Previtera et al, 1990).
d) DELAYED-ONSET of upper airway compromise, in the absence of significant esophageal injury, has been reported in an infant following ingestion of a hair relaxer cream. On initial emergency department (ED) examination no respiratory problems were noted and the infant was sent home.

a) Pulmonary burns may occur following inhalation of vaporized caustics. Destruction or damage may occur to alveoli with subsequent pulmonary edema and pneumonitis.
b) CASE REPORT: Hypoxia, stridor, upper airway burns and pulmonary infiltrates developed in a 20-year-old man who sustained an inhalation injury from calcium hydroxide and heat produced when he added crystals of calcium oxide to an acid solution of industrial waste (Bonatucci et al, 1984).
c) Pulmonary infiltrates have been reported in a few patients after ingestion of caustics (Burrington, 1975; Symbas et al, 1983).
d) Recurrent atelectases and pneumonia developed in two adults who sustained bronchial burns after ingesting concentrated sodium hydroxide (Meredith et al, 1988).

a) PERSISTENT PULMONARY DISEASE: Obstructive airway disease developed in a 63-year-old man with chronic occupational exposure to sodium hydroxide mist (Bentur & Rubin, 1991). It was postulated that the alkaline mist induced a bronchial inflammatory reaction and fibrous tissue formation leading to irreversible obstructive airway disease (Rubin et al, 1992).
b) Reactive airways dysfunction syndrome (exertional dyspnea, wheezing, productive cough, reduced FEV1, positive methacholine challenge test) developed in 3 men who were exposed at the scene of an accident involving a truck carrying sodium hydroxide, silicon tetrachloride, and trichlorosilane (Promisloff et al, 1990).
c) CASE REPORT: An 88-year-old non-smoking woman without a prior history of lung disease was exposed to an oven cleaner containing sodium hydroxide with isobutane propellant sprayed into a heated oven of 200 degrees Fahrenheit, and developed bronchiolitis obliterans organizing pneumonia (BOOP). Clinical effects including cough, fever, and flu-like symptoms developed within minutes of exposure. Three days after exposure she developed worsening dyspnea and was treated with inhaled beta agonists, steroids and antibiotics and was discharged to home.

a) Severe tracheal stricture developed in a 2-year-old girl who ingested an oven cleaner paste (Leape et al, 1972). Her clinical course was complicated by esophageal stricture which required repeated dilation and then perforated, causing mediastinal abscess formation.

a) Tracheoesophageal fistulae have been reported as delayed sequelae of alkaline corrosive ingestion (Borja et al, 1969; McCabe et al, 1969; Singh et al, 1976; Sarfati et al, 1987).
b) Tracheobronchial injuries following a severe caustic alkali ingestion are considered a poor prognostic factor. In a case of ingestion of 200 mL of potassium hydroxide, a 26-year-old man developed tracheobronchial involvement caused by necrotic extension from his burned esophagus. Lesions affected the posterior wall of the trachea and both main bronchi. Operation through a right thoracotomy was necessary for esophagectomy, with a long left bronchial tube placed distally in the left main bronchus to prevent air leak. In this case, healing of the tracheobronchial perforation occurred (Jaillard et al, 2002).

a) The esophagus is the most common site of gastrointestinal burns after alkaline corrosive ingestion (Poley et al, 2004; Kirsh & Ritter, 1976; Moazam et al, 1987; Chen et al, 1988). Risk of stricture formation may be clinically determined by the initial depth of injury noted on endoscopic visualization or of the esophagus (Rao & Hoffman, 1998).

a) Gastric burns may also occur after alkaline corrosive ingestion (Previtera et al, 1990; Davis et al, 1972; Allen et al, 1970; Warren et al, 1984; Lowe et al, 1979; Carroll et al, 1994) (Bernardino & Lawson, 1977) (Welsh & Welsh, 1978).
b) CAUSTIC INJURY SCALES
c) OTHER

a) Intestinal burns, mostly duodenal, have been reported (Allen et al, 1970; Cello et al, 1980), but are much less frequent, occurring in about 2% to 6% of patients with caustic (acids, basic, acid/basic) ingestions (Poley et al, 2004; Previtera et al, 1990) and in 20% of alkaline ingestion cases in another series (Sugawa & Lucas, 1989).
b) Severe duodenal injury may be more common with suicidal ingestions (Allen et al, 1970; Cello et al, 1980).
c) A 38-year-old man who had previously undergone vagotomy and antrectomy with gastroduodenostomy reconstruction developed necrosis of the small and large intestines with perforations to the level of the sigmoid colon after swallowing lye (Sperling & Wheeler, 1974).
d) Following the ingestion of 200 mL of potassium hydroxide, a 26-year-old man developed severe injuries to the gastrointestinal tract necessitating extensive resection of necrotic organs (total gastrectomy, cephalic duodenopancreatectomy, and cholecystectomy). All layers of the esophagus were found to be necrotic, including the periesophageal tissues (Jaillard et al, 2002).
e) Duodenal ulcers have been reported after ingestion of Clinitest tablets (Warren et al, 1984).
f) A 30-year-old man developed necrosis of the duodenum and transverse colon after ingesting liquid drain cleaner (Guth et al, 1994).

a) Multiple studies have demonstrated that the absence of oral lesions can not be reliably used to exclude the possibility of significant esophageal or gastric burns (Dogan et al, 2006; Muhlendahl et al, 1978; Cello et al, 1980; Crain et al, 1984; Dabadie et al, 1989; Previtera et al, 1990; Gorman et al, 1992; Nuutinen et al, 1994).

a) OVERDOSE EFFECTS

a) Esophageal strictures are common sequelae of caustic burns (Afzal et al, 2002; Chen et al, 1988) (Edmondson, 1987) (Patrick et al, 1986; Mackenzie, 1982; Leape et al, 1972; Leape et al, 1971). Risk of stricture formation may be clinically determined by the initial depth of injury noted on endoscopic visualization of the esophagus (Rao & Hoffman, 1998). Strictures are more likely to develop after second or third degree or circumferential burns (Zargar et al, 1991) (Meredith et al, 1988; Estrera et al, 1986). Grade III burns result in deep ulcers and necrosis into the periesophageal tissues, which almost invariably progress to stricture formation with a high risk of perforation (Rao & Hoffman, 1998).
b) INCIDENCE: The incidence of strictures varies widely, from 1% to 56% in several large series (Hardin, 1956; Borja et al, 1969; Moazam et al, 1987; Symbas et al, 1983; Waldron & Fitzgerald, 1987; Ferguson et al, 1989; Sellars & Spence, 1987; Clausen et al, 1994; Nuutinen et al, 1994; Poley et al, 2004).
c) According to a retrospective review of cases, from 1957 to 1994 and involving 215 patients who ingested commercial sodium hydroxide, esophageal lesions occurred in 88.4% of patients, with stenosis occurring in 73% of patients. The incidence and severity of the stenosis directly correlated with the amount of sodium hydroxide ingested (Mamede & De Mello Filho, 2002).
d) PREDICTIVE: One study of children and adults found stridor to be 100% specific for marked esophageal injury on endoscopy (Gorman et al, 1992). Another prospective study of 79 children with caustic ingestion found a combination of two or more signs of vomiting, drooling, or stridor was predictive of esophageal injury (Crain et al, 1995).
e) CLINITEST: Strictures developing after ingestion of Clinitest tablets tend to form at the level of the carina and aortic arch (Burrington, 1975; Genieser & Becker, 1969).
f) INCREASED OROCECAL TRANSIT TIME: A prospective study was conducted to evaluate the orocecal transit time in patients who are in the chronic phase of a corrosive injury, The study involved 30 patients who underwent successful endoscopy for esophageal strictures induced by ingestion of caustic agents and 30 subjects in the control group with normal endoscopic findings and no history of corrosive ingestion. The orocecal transit time was measured via lactulose hydrogen breath test. The results of the test showed that the orocecal transit time was significantly prolonged in the study group as compared to the control group (135.4 +/-15.8 min vs 90.6 +/-10.36 min; p <0.05) and that, within the study group, there was significant delay in orocecal transit time in patients with strictures involving the lower one third of the esophagus as compared to those patients with strictures involving the upper or mid third of the esophagus (170.6 +/-11.9 min vs 94.5 +/-11.2 min; p <0.001) (Rana et al, 2008).
g) CASE REPORT: An 11-month-old boy was brought to the emergency department (ED) approximately 1 hour after a suspected ingestion of a callous remover containing potassium hydroxide (concentration unknown). Other than white plaque at the base of his tongue, his physical examination was normal. An endoscopy was not performed. Following a 1-hour observation period, he was discharged home. Eighteen days later, he returned to the ED due to intolerance of liquids for 24 hours and several days of gagging and vomiting with intake of solid foods. An esophagram revealed severe esophageal stricture, involving almost the entire length of the esophagus. Immediate gastrostomy tube placement was performed for enteral access. Over the next several months, several esophageal dilatations were performed with limited success. In addition, gastric and esophageal perforations occurred requiring gastric repair and esophageal stent placement. However, he remained dependent on gastrostomy tube feedings, would likely require periodic serial dilatations and possible esophageal replacement (Plumb et al, 2015).

a) Severe gastrointestinal bleeding may develop in patients with significant burns (Symbas et al, 1983) (Zargar et al, 1991) (Schild, 1985; Welsh & Welsh, 1978; Oakes et al, 1982; Hawkins et al, 1980; Guth et al, 1994).

a) Gastric or esophageal perforation is a life threatening complication that may develop in patients with severe burns (Oakes et al, 1982) (Edmondson, 1987) (Allen et al, 1970; Welsh & Welsh, 1978; Schild, 1985) (Alford & Harris, 1958) (Hawkins et al, 1980; Sugawa & Lucas, 1989) (Zargar et al, 1991).

a) Tracheoesophageal and aortoesophageal fistulae may develop as delayed sequelae of severe burns (Makela et al, 1998; Borja et al, 1969; Sarfati et al, 1987; McCabe et al, 1969; Singh et al, 1976; Rabinovitz et al, 1990).
b) Fistulae may not develop until 1 to 4 weeks after the ingestion; aortic fistulae may result in massive hemorrhage (Singh et al, 1976; McCabe et al, 1969; Rabinovitz et al, 1990).
c) The delay between exposure and development of esophagorespiratory fistulas are the most important predictors of death. Anastomotic strictures after reconstruction may require repeated esophageal dilatations (Makela et al, 1998).

a) Pyloric stenosis and gastric outlet obstruction may develop in patients with severe gastric burns (Wright & Hennessey, 1972) (Hawkins et al, 1980; Oakes et al, 1982) (Term et al, 1987).

a) Esophageal diverticula have been reported as an unusual delayed complication of alkaline corrosive ingestion in two patients (Chen et al, 1988).

a) Following the use of enemas containing caustic alkalies, ulcerative proctocolitis has been reported. da Fonsecaea et al (1998) reported 2 cases of acute proctocolitis resulting from rectal application of caustic products, ammonia solution enema and lye enema, respectively. Sigmoidoscopy and biopsy revealed erythematous colon with ulcerations (da Fonseca et al, 1998).

a) CASE REPORT: A 5-year-old girl presented with a 2-day history of pelvic pain and brownish vaginal discharge. Microscopic examination of the urine revealed the presence of erythrocytes and inflammatory cells and examination of the outer labia demonstrated severe reddening with brown appositions. A vaginoscopy done under general anesthesia showed the presence of an alkaline battery (size AAA). After removal of the battery, circular necrotic lesions of the vaginal wall were observed; however, there was no evidence of fistulas or other abnormalities. Following antibiotic therapy and insertion of a urinary catheter for 5 days, the patient's condition improved. The brownish vaginal discharge persisted for several weeks. A repeat vaginoscopy, performed 3 weeks post-presentation revealed coverage of the burns with a fibrinous layer, and a third vaginoscopy 3 months post-presentation demonstrated complete resolution. No long term issues were reported at one year follow-up (Semaan et al, 2015).

a) A lactic acidosis may develop after severe alkali ingestion, due to severe tissue burns and shock (Okonek et al, 1981).
b) CASE REPORT: Metabolic acidosis (pH 7.27, pCO2 38 mmHg) was reported in a 50-year-old man following ingestion of approximately 4 ounces of liquid drain opener containing 10% sodium hydroxide (Palmer et al, 2007).

a) Dermal contact with alkaline corrosives may cause significant injury, ranging from mild pain and erythema to full thickness burns requiring grafting (Singer et al, 1992; Mozingo et al, 1988; Lorette & Wilkinson, 1988; Harper & Dickson, 1994) (Sawhney & Kaushih, 1989) (Winder, 1997) (Winek et al, 1999). Skin contact with strong alkalies (greater that pH 12.5) results in irritation, progressing to desquamation and cell necrosis. Once this occurs, the alkali is able to penetrate further and cause deep burns. Because of its ability to penetrate tissue and produce vascular thrombosis and necrosis, continuing alkali damage occurs (Winder, 1997). Scarring may result.
b) The delay in the onset of pain after dermal contact with alkaline corrosives may delay decontamination and encourage the development of deeper burns (Lorette & Wilkinson, 1988).
c) Complications may include cellulitis, contractures and recurrent skin breakdown (O'Donoghue et al, 1994) (Mozigo et al, 1988) (Singer et al, 1992).
d) AUTOMOTIVE AIR BAG SYSTEMS: Four cases of dermal burns were associated with the white powdery residue (talc and sodium hydroxide) from air bags found in the driver compartment after a motor vehicle accident (Swanson-Biearman et al, 1991).
e) HOUSEHOLD OVEN CLEANER: A 20-year-old woman developed a full-thickness alkaline burn that required skin grafting after she accidentally sprayed the right side of her face and neck with an aerosol oven cleaner. She removed the foam with a moist cloth but did not irrigate the exposed area (Lorette & Wilkinson, 1988).
f) CEMENT: Severe burns and skin necrosis may result from prolonged contact with wet cement (Flowers, 1978; Hannuksela et al, 1976). The delay in onset of pain and prolonged contact from cement trapped in boots and clothing may contribute to the severity of the injury.
g) ALKALINE BATTERIES: A case of accidental third-degree burns occurred in a 2-year-old boy after he sat in a seat where alkaline batteries had leaked. The chemical had penetrated through his pants resulting in full thickness burns on his rear right thigh, requiring skin grafting (Winek et al, 1999).
h) HAIR RELAXERS: Hair relaxer cream was inadvertently smeared on the face of a 27-month-old girl and resulted in first-degree burns (Rauch, 2000).
i) TETRAMETHYLAMMONIUM HYDROXIDE: A 39-year-old man was found dead approximately 1 hour following occupational dermal exposure to a pallet cleaning solution containing 35% of a 25% tetramethylammonium hydroxide (TMAH) solution. An autopsy revealed second degree burns on 12% of his skin. There were no other apparent complications that were attributed to his death. Because it is rare that burns on 12% of skin without complications would cause death, it is believed that TMAH may have caused ganglion blockage via dermal absorption, resulting in respiratory failure (Park et al, 2013).

a) Scarring ALOPECIA has been reported in black patients using hair relaxers or straighteners which are either sodium hydroxide-or ammonium thioglycollate-based. The hair loss occurred as soon as 2 weeks after a single application and up to 5 years after regular use (Nicholson et al, 1993).

a) Eight patients developed dermatitis (superficial burns with marked edema, erythema and severe pruritus) following contact with a complex amine used in the potash industry (Sagi et al, 1988). In three patients partial thickness burns developed 5 days later.

a) INCIDENCE - A history of alkaline corrosive ingestion is found in 1 to 4% of patients treated for esophageal carcinoma (Isolauri & Markkula, 1989). Compared to age-matched nonexposed individuals, the risk of esophageal carcinomas was 1000 times greater in a series of 381 cases of lye corrosive injury (Kiviranta, 1950).
b) TYPE - In a series of 15 cases of lye-induced esophageal carcinoma, all were squamous cell tumors. The site was the region of tracheal bifurcation in 11 of the 15 cases (Isolauri & Markkula, 1989).
c) LATENCY - The mean latent time between lye corrosion and esophageal carcinoma was 41 years in one study; the later in life the lye was ingested, the earlier the carcinoma appeared (Appelqvist & Salmo, 1980). The range in another study of 15 cases was 22 to 81 years, with a mean of 58 years in men and 47 years in women (Isolauri & Markkula, 1989). A latency as short as 12 years has been reported (Kinnman et al, 1968).
d) PROGNOSIS - One and 5-year survival rates in patients with resectable tumors were 50% and 20%, respectively, in a series of 10 cases. Five patients with nonresectable tumors had 1 and 5-year survival rates of 20% and 0%, respectively (Isolauri & Markkula, 1989).
e) CASE REPORT - A 14-year-old boy developed an esophageal stricture within a few months after unintentionally ingesting caustic soda. He did well with periodic dilatation over the next 24 years. He then felt that his response to dilatation became poor, and developed anorexia and weight loss. Endoscopy of the esophagus revealed a papillary growth, with features of squamous cell carcinoma on biopsy and local spread to contiguous organs on CT. Despite treatment with chemotherapy and radiation, the patient died within months of diagnosis (Kochhar et al, 2006).

a) Monitor pulse oximetry or arterial blood gases in patients with signs and symptoms suggestive of upper airway burns.

a) Endoscopic ultrasound has been used to determine the depth of lesions in alkaline esophagitis, although there is much less experience with this technique than with endoscopy (Kamijo et al, 2001).
b) ESOPHAGEAL SCINTIGRAPHY

a) Immediate dilution with milk or water decreased the extent of tissue injury induced by 50% sodium hydroxide in isolated rat esophagi (Homan et al, 1994).
b) In an in vitro model, the dissolution time of clinitest tablets was not affected by the amount or type of fluid added, but heat generation was less then large fluid volumes were used, and pH change was less with orange juice than with water or milk but was independent of the fluid volume (Lacoulture et al, 1986).

a) REFERENCES: (Dogan et al, 2006; Symbas et al, 1983; Crain et al, 1984b; Gaudreault et al, 1983b; Schild, 1985; Moazam et al, 1987a; Sugawa & Lucas, 1989; Previtera et al, 1990a; Zargar et al, 1991; Vergauwen et al, 1991a; Gorman et al, 1992a)

a) Advancing across the cricopharynx under direct vision
b) Gently advancing with minimal air insufflation
c) Never retroverting or retroflexing the endoscope
d) Using a pediatric flexible endoscope
e) Using extreme caution in advancing beyond burn lesion areas
f) Most authors recommend endoscopy within the first 24 hours of injury, not advancing the endoscope beyond areas of severe esophageal burns, and avoiding endoscopy during the subacute phase of healing when tissue slough increases the risk of perforation (5 to 15 days after ingestion) (Zargar et al, 1991).

a) Several scales for grading caustic injury exist. The likelihood of complications such as strictures, obstruction, bleeding, and perforation is related to the severity of the initial burn (Zargar et al, 1991):
b) Grade 0 - Normal examination
c) Grade 1 - Edema and hyperemia of the mucosa; strictures unlikely.
d) Grade 2A - Friability, hemorrhages, erosions, blisters, whitish membranes, exudates and superficial ulcerations; strictures unlikely.
e) Grade 2B - Grade 2A plus deep discreet or circumferential ulceration; strictures may develop.
f) Grade 3A - Multiple ulcerations and small scattered areas of necrosis; strictures are common, complications such as perforation, fistula formation or gastrointestinal bleeding may occur.
g) Grade 3B - Extensive necrosis through visceral wall; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding are more likely than with 3A.

a) ANIMAL
b) HUMAN

a) A systematic pooled analysis was conducted over a 50-year-period and involving only those studies with patients diagnosed with endoscopically documented caustic-induced grade II burns that were either treated with a minimum 10-day course of steroid therapy or with no steroid therapy. A total of 328 patients with grade II esophageal burns were included in the analysis: 244 patients (from 3 prospective and 8 retrospective studies) given a minimum 10-day course of steroid therapy and 84 patients (from 4 prospective and 1 retrospective study) with no steroid therapy. Thirty patients (12.3%) in the steroid group developed strictures and 16 patients (19%) in the non-steroid group developed strictures, which was not statistically significant, indicating that there appears to be no proven benefit for the use of steroid therapy in patients with grade II esophageal burns (Fulton & Hoffman, 2007).
b) In a study of 154 children with grade IIb and 3 corrosive burns (mostly alkali) who received antibiotics, steroids, and H2 receptor blockers, esophageal stricture developed in 11 patients, 2 had gastric outlet obstruction and 1 developed perforation following exposure (Dogan et al, 2006).
c) A retrospective review of cases over a 37-year-period (from 1957 to 1994), involving 239 patients who had ingested commercial sodium hydroxide, revealed that the mean incidence of stenosis present in patients following the use of prednisone, in doses ranging from 0.75 to 2 mg/kg/day, was 48.1% (n=79) as compared with 69% (n=29) in patients who were not treated with a corticosteroid. During the period from 1957 to 1987, the incidence of stenosis in the prednisone-treated group was 61% (n=46) as compared with 100% (n=14) in the patients not treated with a corticosteroid. A contributing factor to the incidence of stenosis was the amount of sodium hydroxide ingested. The review showed that patients who had ingested from a trace to one tablespoon were less likely to develop stenosis, and were given lower doses of prednisone, resulting in fewer corticosteroid-induced complications. Other therapies given following sodium hydroxide ingestion included dilution with water or milk, the use of a nasogastric tube, and antibiotics combined with prednisone (Mamede & De Mello Filho, 2002).

a) STUDY - In a study of 11 children with deep circumferential esophageal burns after caustic ingestion, insertion of a silicone rubber nasogastric tube for 5 to 6 weeks without steroids or antibiotics was associated with stricture formation in only one case (Wijburg et al, 1989).

a) STUDY - In a retrospective study of patients with extensive transmural esophageal necrosis after caustic ingestion, all 4 patients treated in the conventional manner (esophagoscopy, steroids, antibiotics, and repeated evaluation for the occurrence of esophagogastric necrosis and perforation) died while all 3 patients treated with early laparotomy and immediate esophagogastric resection survived (Estrera et al, 1986a).

a) Among 15 pediatric patients with esophageal strictures who received endoscope-associated dilatation, 9 patients had functionally subnormal recovery and 6 had poor recovery, requiring either frequent feeding or having growth retardation (Huang et al, 2004).
b) Anastomotic esophagorespiratory strictures may require repeated esophageal dilatations after reconstruction (Makela et al, 1998).
c) A retrospective study, involving 11 children (ages ranging from 1 to 14 years) who developed esophageal strictures following ingestion of a corrosive substance and subsequently underwent balloon dilatation, showed that the dilatation procedure was technically successful in 10 patients (91%) and in 35 dilatation sessions (97%), with improvement of the luminal diameter as seen with an esophagram performed immediately after dilatation. However, clinical success, defined as improved food intake and reduced dysphagia within one month of the first dilatation procedure, only occurred in 7 patients (64%). During the 35-month follow-up period, 10 of the 11 patients experienced recurrence of the esophageal strictures following the initial balloon dilatation. Seven patients underwent additional dilatations and 3 patients underwent either stent placement or surgery or both (Doo et al, 2009).

a) In a retrospective study of 53 patients with clinical and/or endoscopic signs of caustic agent injury, 8 patients (6 with acid ingestion; 7 as intentional ingestions) underwent urgent surgery. Four had esophageal necrosis and gastric perforation, 2 had esophageal, gastric, duodenal and jejunal necrosis, 1 had necrosis of the gastric fundus and 1 had normal findings at laparotomy. The mortality rate was 11% and the authors concluded that endoscopic evaluation and early surgery may reduce morbidity and mortality (Ertekin et al, 2004).
b) In a retrospective review of 9 patients with intentional alkali ingestions of greater than 100 mL, early, aggressive surgical intervention to identify and resect necrotic tissue allowed for successful later reconstruction and improved outcomes. The development of an esophagorespiratory fistula required immediate surgical intervention. First- and second-degree injuries can be treated after the patient has been stabilized (Makela et al, 1998).
c) Esophageal reconstruction, involving colon interposition, has been performed in patients with esophageal strictures due to ingested caustic substances. According to a retrospective review, conducted in Belgrade, Serbia, over a 40-year-period, 336 patients with caustic-induced esophageal strictures underwent colon interposition, with 12.5% of patients also undergoing an esophagectomy concurrently. Left colon transplants were used in 258 (76.7%) patients. Early postoperative complications occurred in 89 patients and included pneumothorax/hemopneumothorax (13.09%), cervical anastomotic leakage (9.23%), transplant necrosis (2.38%), and abdominal anastomotic leakage (0.89%). Late postoperative complications occurred in 47 patients and included cervical anastomotic strictures (4.46%), thoracic outlet compression (2.08%), bowel obstruction (1.49%), and peptic colon ulceration (1.19%). Long-term follow up (1 to 30 years post-transplant, median 14.3 years) in 285 patients (84.82%) indicated good functional results in 233 patients (81.75%) (Knezevic et al, 2007).
d) POST-CAUSTIC INJURY STENOSIS SURGICAL MANAGEMENT - Almost 50% of patients with post-caustic injury stenosis will require surgical treatment. Laryngeal, pharyngeal, esophageal and/or gastric dilations, resections and/or plastic reconstruction with colon or ileum may be required. In a 10-year Romanian experience, the hospital mortality rate was 3.4% with postoperative morbidity in 20.6% including cervical anastomosis leakages and pleural effusions (Dascalescu et al, 2005).

a) Administer beta2 adrenergic agonists. Consider use of inhaled ipratropium and systemic corticosteroids. Monitor peak expiratory flow rate, monitor for hypoxia and respiratory failure, and administer oxygen as necessary.

a) 2.5 to 5 milligrams diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response, administer 2.5 to 10 milligrams every 1 to 4 hours as needed OR administer 10 to 15 milligrams every hour by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.5 milligram by nebulizer every 30 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).

a) 0.15 milligram/kilogram (minimum 2.5 milligrams) diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response administer 0.15 to 0.3 milligram/kilogram (maximum 10 milligrams) every 1 to 4 hours as needed OR administer 0.5 mg/kg/hr by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.25 to 0.5 milligram by nebulizer every 20 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).

a) The incidence of adverse effects of beta2-agonists may be increased in older patients, particularly those with pre-existing ischemic heart disease (National Asthma Education and Prevention Program, 2007). Monitor for tachycardia, tremors.

a) Consider systemic corticosteroids in patients with significant bronchospasm. PREDNISONE: ADULT: 40 to 80 milligrams/day in 1 or 2 divided doses. CHILD: 1 to 2 milligrams/kilogram/day (maximum 60 mg) in 1 or 2 divided doses (National Heart,Lung,and Blood Institute, 2007).

a) ASSESSMENT CAUSTIC EYE BURNS: It may take 48 to 72 hours after the burn to assess correctly the degree of ocular damage (Brodovsky et al, 2000).
b) The 1965 Roper-Hall classification uses the size of the corneal epithelial defect, the degree of corneal opacification and extent of limbal ischemia to evaluate the extent of the chemical ocular injury (Brodovsky et al, 2000; Singh et al, 2013):
c) A newer classification (Dua) is based on clock hour limbal involvement as well as a percentage of bulbar conjunctival involvement (Singh et al, 2013):

a) Begin irrigation immediately with copious amounts of water or sterile 0.9% saline, which ever is more rapidly available. Lactated Ringer's solution may also be effective. Once irrigation has begun, instill a drop of local anesthetic (eg, 0.5% proparacaine) for comfort; switching from water to slightly warmed sterile saline may also improve patient comfort (Singh et al, 2013; Spector & Fernandez, 2008; Ernst et al, 1998; Grant & Schuman, 1993a). In one study, isotonic saline, lactated Ringer's solution, normal saline with bicarbonate, and balanced saline plus (BSS Plus) were compared and no difference in normalization of pH were found; however, BSS Plus was better tolerated and more comfortable (Fish & Davidson, 2010).

a) SUMMARY
b) ARTIFICIAL TEARS
c) TOPICAL CYCLOPLEGIC
d) TOPICAL ANTIBIOTICS
e) PAIN CONTROL

a) SUMMARY
b) ARTIFICIAL TEARS
c) PAIN CONTROL
d) CARBONIC ANHYDRASE INHIBITOR
e) TOPICAL STEROIDS
f) ASCORBATE
g) CITRATE
h) COLLAGENASE INHIBITORS
i) ANTIBIOTICS
j) TOPICAL CYCLOPLEGIC
k) SOFT CONTACT LENSES

a) SURGICAL THERAPY CAUSTIC EYE INJURY

a) Topical human amniotic fluid (HAF) was evaluated in the treatment of ocular acute alkali burns in mice. Median epithelial defect at day 4 and overall change in ocular burn score between days 2 and 14 were significantly improved with both pre-term and term HAF versus saline. On histologic examination saline solution-treated corneas had more inflammatory cells and blood vessels than HAF-treated cornea (Herretes et al, 2006).