ACIDS

Classification | Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

1) Ability to make litmus dye turn red
2) Ability to react with and dissolve certain metals to form salts
3) Ability to react with bases or alkalies to form salts
4) Ability to cause other indicator dyes to change to characteristic colors
5) Sour taste

1) LEMON JUICE: Citric acid (2 to 8%)
2) TOILET BOWL CLEANER: Sulfuric acid (80%), hydrochloric acid (10 to 25%), oxalic acid (2%), sodium bisulfate (70 to 100%)
3) DRAIN CLEANERS: Sulfuric acid (95 to 99%)
4) METAL CLEANERS AND ANTI-RUST COMPOUNDS: Phosphoric acid (5 to 80%), oxalic acid (1%), hydrochloric acid (5 to 25%), sulfuric acid (10 to 20%), chromic acid (5 to 20%)
5) AUTOMOBILE BATTERY FLUID: Sulfuric acid (25 to 30%)
6) POOL SANITIZERS: Calcium or sodium hypochloride (70%)

1) CHROMIC ANHYDRIDE (99.8%): Used in plating, photography, cement manufacturing, leather tanning
2) HYDROCHLORIC ACID (MURIATIC ACID) (10 to 36%): Bleaching agents, metal refining, plumbing
3) NITRIC ACID: Engraver's acid is 63% nitric acid
4) PHOSPHORIC ACID: Disinfectant (10%), metal cleaning, rust proofing (85 to 90%)
5) HYDROFLUORIC ACID: See hydrofluoric management
6) SULFURIC ACID (95 to 98%): Chemical, munitions and fertilizer manufacturers
7) ACETIC ACID: 60% solution for hat makers, printing, dyeing, and rayon manufacturing. Disinfectants and hair wave neutralizers are 6 to 40% solutions.
8) OXALIC ACID: Tanning, blueprint paper
9) CITRIC ACID: Anhydrous, used as a diluent and preservative in food stuffs

Specific Substances

1) Acetic acid 5% to 10%
2) Alum, Aluminum sulfate 5% to 20%
3) Ammonium nitrate
4) Calcium chloride, anhydrous
5) Hydrochloric acid <5%
6) Phosphoric acid 15% to 35%

1) Acetic acid 10% to 50%
2) Alum, Aluminum sulfate 20%
3) Boric acid
4) Glycolic acid 0.5% to 10%
5) Hydrochloric acid 5% to 10%
6) Nickel ammonium sulfate
7) Oxalic acid <10%
8) Phosphoric acid 35% to 60%
9) Sulfuric acid <10%
10) Zinc chloride 1% to 10%
11) Zinc sulfate 5% to 50%

1) Acetic acid >/= 50%
2) Acid, liquid,N.O.S.
3) Bichloride of mercury
4) Glycolic acid >10%
5) Hydrochloric acid >10%
6) Oxalic acid >10%
7) Phosphoric acid >60%
8) Sodium bisulfate granules
9) Sulfamic acid >10%
10) Sulfuric acid >10%
11) Zinc chloride >10%
12) Zinc sulfate >50%

1) HYDROBROMIC ACID SOLUTION, GREATER THAN 49% HYDROBROMIC ACID
2) BENZOYLCHLORID
3) BUTTERSAEURE (GERMAN)
4) CHROMIC TRIOXIDE (CAS 7738-94-5)
5) CHROMIUM, DICHLORODIOXO-
6) ACETIC ACID SOLUTION (MORE THAN 10% BUT NOT MORE THAN 80% ACID)
7) CHROMYCHLORID (GERMAN)
8) CLORURO DE ACETILO
9) ACID, LIQUID, N.O.S.
10) HYDROBROMIC ACID SOLUTION
11) TRICHLORACETIC ACID
12) SULFUR TRIOXIDE, UNINHIBITED
13) PROPYLFORMIC ACID
14) COLLO-DIDAZ
15) ACID
16) HYDROBROMIC ACID SOLUTION, NOT GREATER THAN 49% HYDROBROMIC ACID

Available Forms Sources

1) The most common acids involved in accidents are hydrochloric (muriatic), sulfuric, and Aqua Regia (mix of hydrochloric and nitric) acids. Other acids involved are nitric, trichloroacetic, carbolic (phenol), acetic (glacial), phosphoric and various mixed acids.
2) Vinegar (acetic acid 4 to 6%) is not generally toxic. Gaseous oxides may be formed when acid comes in contact with certain metal or organic materials, creating a severe aspiration hazard.
3) SODIUM BISULFATE, a constituent of many toilet bowl cleaners, becomes sulfuric acid in solution or on hydration after ingestion.
4) Dilute hydrochloric acid (10%) prescribed for achlorhydra may produce burns in overdose.
5) Compound W, an over the counter wart remover, containing 17% w/w salicylic acid, has been described as causing mucosal injury after ingestion (Sacchetti & Ramoska, 1986).
6) ADIPIC ACID: Found in beet juice (Budavari, 1996).
7) BUTYRIC ACID: It is present in butter as an ester (Budavari, 1996). It occurs as glyceride in animal milk fats (Lewis, 1997).
8) MALIC ACID: The L-form of malic acid is the naturally occurring isomer which has been found in apples and in many other fruits and plants (Budavari, 1996).
9) METHACRYLIC ACID is used as a primer to prepare fingernails prior to the application of artificial nails (Woolf & Shaw, 1998).

1) Clandestine methamphetamine laboratories are possible sources of exposure to acids, including hydrochloric acid and sulfuric acid, which are commonly used during methamphetamine production (Farst et al, 2007).

Overview

Life Support

Clinical Effects

0.2.1)

A) USES: Household uses include toilet, metal and drain cleaners, rust remover, in batteries, and as a primer for artificial nails. Used in clandestine methamphetamine labs (ie, hydrochloric and sulfuric acid). Industrial uses include: metal refining, plumbing, bleaching, engraving, plating, photography, disinfection, munitions, fertilizer manufacture, metal cleaning, and rust removal.
B) TOXICOLOGY: Acids cause coagulation necrosis. Hydrogen ions desiccate epithelial cells, causing edema, erythema, tissue sloughing and necrosis, with formation of ulcers and eschars.
C) EPIDEMIOLOGY: Inadvertent ingestions occur with moderate frequency in children, and are less common than alkaline exposures. Serious exposures are rare in the developed world (generally only seen with deliberate ingestions), largely because only low concentration acids are available in the home. Serious effects are more common in developing countries.
D) WITH POISONING/EXPOSURE

1) MILD TO MODERATE ORAL TOXICITY: Patients with mild ingestions may only develop irritation or Grade I (superficial hyperemia and edema) burns of the oropharynx, esophagus or stomach; acute or chronic complications are unlikely. Patients with moderate toxicity may develop Grade II burns (superficial blisters, erosions and ulcerations) are at risk for subsequent stricture formation, particularly gastric outlet and esophageal. Some patients (particularly young children) may develop upper airway edema.
2) SEVERE ORAL TOXICITY: May develop deep burns and necrosis of the gastrointestinal mucosa. Complications often include perforation (esophageal, gastric, rarely duodenal), fistula formation (tracheoesophageal, aortoesophageal), and gastrointestinal bleeding. Upper airway edema is common and often life threatening. Hypotension, tachycardia, tachypnea and, rarely, fever may develop. Other rare complications include metabolic acidosis, hemolysis, renal failure, disseminated intravascular coagulation, elevated liver enzymes, and cardiovascular collapse. Stricture formation (primarily gastric outlet and esophageal, less often oral) is likely to develop long term. Esophageal carcinoma is another long term complication. Severe toxicity is generally limited to deliberate ingestions in adults in the US, because acidic products available in the home are generally of low concentration.

a) PREDICTIVE: The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and GI complications and mortality. Initial signs and symptoms may not reliably predict the extent of GI burns.

3) INHALATION EXPOSURE: Mild exposure may cause dyspnea, pleuritic chest pain, cough and bronchospasm. Severe inhalation may cause upper airway edema and burns, hypoxia, stridor, pneumonitis, tracheobronchitis, and rarely acute lung injury or persistent pulmonary function abnormalities. Pulmonary dysfunction similar to asthma has been reported.
4) OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal ischemia, permanent vision loss and in severe cases perforation.
5) DERMAL EXPOSURE: A minor exposure can cause irritation and partial thickness burns. More prolonged or a high concentration exposure can cause full thickness burns. Complications may include cellulitis, sepsis, contractures, osteomyelitis, and systemic toxicity.

0.2.20)

A) Single doses of dibromoacetic acid has resulted in reductions of sperm and serum testosterone in experimental animals. Repeated or single oral administration of monobromoacetic acid did not produce effects on male rat reproductive organs or sperm.

Laboratory Monitoring

Treatment Overview

0.4.2)

A) MANAGEMENT OF MILD TO MODERATE ORAL TOXICITY

1) Within the first 12 hours of exposure, if burns are absent or grade I severity, patient may be discharged when able to tolerate liquids and soft foods by mouth. If mild grade II burns, admit for intravenous fluids, slowly advance diet as tolerated. Perform barium swallow or repeat endoscopy several weeks after ingestion (sooner if difficulty swallowing) to evaluate for stricture formation.

B) MANAGEMENT OF SEVERE ORAL TOXICITY

1) Resuscitate with 0.9% saline; blood products may be necessary. Early airway management in patients with upper airway edema or respiratory distress. Early (within 12 hours) gastrointestinal endoscopy to evaluate for burns. Early bronchoscopy in patients with respiratory distress or upper airway edema. Early surgical consultation for patients with severe grade II or grade III burns, large deliberate ingestions, or signs, symptoms or laboratory findings concerning for tissue necrosis or perforation.

C) DECONTAMINATION

1) INGESTION: In patients without vomiting or respiratory distress who are able to swallow, dilute with 4-8 ounces milk/water if possible shortly after ingestion; then NPO until after endoscopy. Neutralization, gastric lavage, and activated charcoal are all contraindicated. OCULAR: Copious irrigation until pH neutral. DERMAL: Remove contaminated clothes, brush off particulate corrosives, follow with copious irrigation. INHALATION: Humidified oxygen.

D) AIRWAY MANAGEMENT

1) Aggressive airway management in patients with deliberate ingestions or any indication of upper airway injury. Severe edema may make intubation difficult; be prepared for surgical airway management (cricothyroidotomy) in patients with severe upper airway edema.

E) ENDOSCOPY

1) Should be performed as soon as possible (preferably within 12 hours, not more than 24 hours) in any patient with acid ingestion. The grade of mucosal injury at endoscopy is the strongest predictive factor for the occurrence of systemic and GI complications and mortality. The absence of visible oral burns does NOT reliably exclude the presence of esophageal or gastric burns.

F) BRONCHOSPASM

1) Treat with oxygen, inhaled beta agonists and consider systemic corticosteroids.

G) CORTICOSTEROIDS

1) The use of corticosteroids to prevent stricture formation is controversial. Corticosteroids should not be used in patients with grade I or grade III injury, as there is no evidence that it is effective. Evidence for grade II burns is conflicting, and the risk of perforation and infection is increased with steroid use, so routine use is not recommended.

H) STRICTURE

1) A barium swallow or repeat endoscopy should be performed several weeks after ingestion in any patient with grade II or III burns or with difficulty swallowing to evaluate for stricture formation. Recurrent dilation may be required. Some authors advocate early stent placement in these patients to prevent stricture formation.

I) SURGICAL MANAGEMENT

1) Immediate surgical consultation should be obtained on any patient with grade III or severe grade II burns on endoscopy, significant abdominal pain, metabolic acidosis, hypotension, coagulopathy, or a history of large ingestion. Early laparotomy can identify tissue necrosis and impending or unrecognized perforation, early resection and repair in these patients is associated with improved outcome.

J) EYE INJURY

1) Copious irrigation until pH neutral; perform slit lamp exam. Ophthalmology consult. Antibiotics and mydriatics may be indicated.

K) PATIENT DISPOSITION

1) OBSERVATION CRITERIA: Patients with an acid ingestion should be sent to a health care facility for evaluation. Patients with an endoscopic evaluation that demonstrates no burns or only minor grade I burns and who can tolerate oral intake can be discharged to home.
2) ADMISSION CRITERIA: Symptomatic patients, and those with endoscopically demonstrated grade II or higher burns should be admitted. Patients with respiratory distress, grade III burns, or extensive grade II burns, acidosis, hemodynamic instability, gastrointestinal bleeding, or large ingestions should be admitted to an intensive care setting.

L) PITFALLS

1) The absence of oral burns does NOT reliably exclude the possibility of significant esophageal burns.
2) Patients may have severe tissue necrosis and impending perforation requiring early surgical intervention without having severe hypotension, rigid abdomen, or radiographic evidence of intraperitoneal air.
3) Patients with any evidence of upper airway involvement require early airway management before airway edema progresses.
4) The extent of eye injury (degree of corneal opacification and perilimbal whitening) may not be apparent for 48 to 72 hours after the burn. All patients with acidic eye injury should be evaluated by an ophthalmologist.

M) DIFFERENTIAL DIAGNOSIS

1) Alkaline corrosive ingestion, gastrointestinal hemorrhage, or perforated viscus.

0.4.3)

A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
B) INHALATION: Administer oxygen. If respiratory symptoms develop obtain chest x-ray, monitor pulse oximetry and/or blood gases. Treat bronchospasm with inhaled beta2-adrenergic agonists. If acute lung injury develops, consider PEEP. Evaluate for esophageal, dermal and eye burns as indicated.

0.4.4)

A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
B) CAUSTIC EYE DECONTAMINATION: Immediately irrigate each affected eye with copious amounts of water or sterile 0.9% saline for about 30 minutes. Irrigating volumes up to 20 L or more have been used to neutralize the pH. After this initial period of irrigation, the corneal pH may be checked with litmus paper and a brief external eye exam performed. Continue direct copious irrigation with sterile 0.9% saline until the conjunctival fornices are free of particulate matter and returned to pH neutrality (pH 7.4). Once irrigation is complete, a full eye exam should be performed with careful attention to the possibility of perforation.
C) EYE ASSESSMENT: The extent of eye injury (degree of corneal opacification and perilimbal whitening) may not be apparent for 48 to 72 hours after the burn.

0.4.5)

A) OVERVIEW

1) DECONTAMINATION: Remove contaminated clothing and jewelry and irrigate exposed areas with copious amounts of water. A physician may need to examine the area if irritation or pain persists.

Range Of Toxicity

Clinical Effects

Musculoskeletal

3.15.2)

A) NECROSIS

1) WITH POISONING/EXPOSURE

a) CASE REPORT: A 63-year-old man intentionally injected heroin and 3 mL of hydrochloric acid into the right inguinal area. He presented to the emergency department with right leg pain, and ischemia and ecchymosis of the right abdomen and thigh and extending to the right lower leg, ankle, and foot. Angiography of the lower extremities showed complete occlusion of the right external iliac artery. Surgery revealed severe necrosis of the sartorius, rectus femoris, adductor, gracillis, piriformis, short rotator, and hamstring muscles, requiring amputation at the hip and extensive muscle debridement (Hsieh & Lin, 2005).

Immunologic

3.19.2)

A) ACUTE ALLERGIC REACTION

1) WITH POISONING/EXPOSURE

a) A 27-year-old woman was reported to have immediate hypersensitivity reactions (hives, itching, dyspnea, tachycardia) to ingestion or topical application of acetic acid or vinegar (Przybilla & Ring, 1983).

Reproductive

3.20.1)

Carcinogenicity

3.21.3)

A) SUMMARY

1) Severe caustic esophageal injury from lye ingestion is associated with an increased incidence of esophageal cancer. Occupational exposure to acid mists has been associated with an increased incidence of laryngeal cancer.

B) ESOPHAGEAL CARCINOMA

1) Increased incidence of esophageal cancer has been associated with severe caustic injury of the esophagus from lye ingestion, although an association with acid-induced burns has not been proven. Development of carcinoma may require 20 to 40 years or more.

a) Some authors advocate prophylactic esophagectomy in young patients with stenosed grade III lesions to avoid this complication (Sugawa & Lucas, 1989).

2) Two patients developed esophageal strictures requiring intermittent dilatation, involving the mid to upper third of the esophagus, after ingesting acids. Both patients presented with progressive dysphagia 17 and 24 years, respectively, after the initial event. Endoscopy showed a growth on the esophagus and biopsy of the mass revealed characteristic features of squamous cell carcinoma. Despite external radiation therapy and chemotherapy, both patients died approximately 1 month after completing therapy (Kochhar et al, 2006).

C) LARYNX CARCINOMA

1) Several studies have found an increased incidence of laryngeal cancer in workers chronically exposed to acid mists (Soskolne et al, 1992; Soskolne et al, 1984; Steenland et al, 1988) Ahlborg et al, 1981; Forastiere et al, 1988 . Two of these studies did not control for smoking (Forastiere et al, 1988; Ahlborg et al, 1981).

Summary Of Exposure

Vital Signs

3.3.2)

A) WITH POISONING/EXPOSURE

1) Shortness of breath may develop following inhalation of acid vapors, mists or aerosols.

Heent

3.4.3)

A) WITH POISONING/EXPOSURE

1) SUMMARY: Pain, swelling, corneal erosions, limbal ischemia, chemosis, intraconjunctival/subconjunctival hemorrhage, increased intraocular pressure, and loss of vision may result from splash exposures. Concentration dependent eye irritation or severe eye injury may develop after exposure to mists, aerosols or vapors.

a) Normally, brief exposures to acidic solutions with pH greater than 2 produce no injury to the corneal epithelium (Grant & Schuman, 1993).

2) CORNEAL OPACIFICATION AND EPITHELIAL INJURY may occur with acid burns to the eye (Saini & Sharma, 1993). Permanent corneal opacification has been associated with exposure to 100% glacial acetic acid (US DHHS, 1981).
3) LIMBAL ISCHEMIA occurs with more severe acid injuries (Saini & Sharma, 1993).
4) CHEMOSIS and INTRACONJUNCTIVAL/SUBCONJUNCTIVAL HEMORRHAGE may make limbal ischemia difficult to assess (Beare, 1990)
5) INCREASED INTRAOCULAR PRESSURE may be seen with severe injuries (Beare, 1990).
6) BLINDNESS AND DEFORMITY OF THE GLOBE occurs with the most severe burns (Saini & Sharma, 1993).
7) EYE IRRITATION can occur with exposure to vapors (Stueven, 1992).

3.4.5)

A) WITH POISONING/EXPOSURE

1) SUMMARY: Nasal irritation, congestion and discharge may occur. Severe exposure to some acids may produce nasal ulceration.
2) IRRITATION: Exposure of a hospital technician to glacial acetic acid vapors resulted in nasal irritation shortly after exposure and the development of nasal stuffiness and discharge 4 hours later. The odor of vinegar was reported. Other exposed hospital employees also reported nasal irritation and the detection of a vinegar odor (Kern, 1991).
3) ULCERATION: Exposure to chromic acid mist can result in nasal ulceration (US DHHS, 1981).

3.4.6)

A) WITH POISONING/EXPOSURE

1) SUMMARY: Oral, oropharynx, and esophageal burns with mucosal necrosis may develop. Erosion of tooth enamel may occur with excessive citric acid ingestion.
2) BURNS and necrosis of the oral mucosa (Caravati, 1987; Zargar et al, 1989; Zamir et al, 1985; Munoz et al, 2001) and esophagus (Wu & Lai, 1993) can occur with acid ingestions. Ingestion of 1.0 ml of glacial acetic acid has resulted in esophageal perforation (US DHHS, 1981). The presence or absence of peri-oral and pharyngeal burn does not predict the severity of esophageal or gastric injury (Gaudreault et al, 1983; Crain et al, 1984a).
3) DENTAL ENAMEL EROSION occurs with chronic excessive ingestion of citric acid (Fuller & Johnson, 1977).
4) ULCERATION: Chronic occupational exposure to acid mists and gases has been associated with an increased incidence of ulcerative lesions of the oral mucosa in workers who do not lip seal (eg those who mouth breathe or have shortened upper lips)(Pereira Vianna et al, 2004).

B) ANIMAL STUDIES

1) ESOPHAGEAL BURNS: Severe burns developed in cat esophageal tissues left in situ within 30 seconds of exposure to 9% sulfuric acid (Ashcraft & Padula, 1974).

Cardiovascular

3.5.2)

A) HYPOTENSIVE EPISODE

1) WITH POISONING/EXPOSURE

a) Shock with clammy skin, weak and rapid pulse, and shallow respiration can occur with exposure to strong mineral acids (Finkel, 1983). Circulatory collapse is one of the most common immediate causes of death from acute exposure to hydrochloric acid (Gosselin et al, 1984).

B) ACUTE ISCHEMIC HEART DISEASE

1) WITH POISONING/EXPOSURE

a) Ischemic lesions in the heart may occur after several hours of uncorrected circulatory collapse (Gosselin et al, 1984).

C) MYOCARDIAL INFARCTION

1) WITH POISONING/EXPOSURE

a) CASE REPORT: A 63-year-old woman, with a history of myocardial infarction, presented to the emergency department with epigastric pain approximately 1 hour after ingesting 250 mL of a cleaning solution containing hydrochloric acid (concentration unknown). An initial ECG showed no evidence of ST segment elevation or T wave abnormality and the cardiac markers (troponin T, creatine kinase, and CK-MB) were all within normal limits. One hour post presentation, the patient developed severe chest pain. A repeat ECG showed ST segment elevation at the inferolateral leads; and angiography revealed 80% luminal narrowing of the right coronary artery and left anterior descending artery. After the angiography, the ST segment elevation decreased; however, the patient's clinical condition continued to deteriorate, with the development of hypotension, hyperkalemia (potassium 6.5 mmol/L), anemia, and worsening metabolic acidosis. The patient's level of consciousness also decreased, necessitating intubation. One hour post-intubation, the patient developed bradycardia progressing to asystole. Despite resuscitation attempts, she died 5 hours post presentation (Yanturali et al, 2005).

Respiratory

3.6.2)

A) DYSPNEA

1) WITH POISONING/EXPOSURE

a) Inhalation may produce dyspnea and pleuritic chest pain.

B) HYPOXEMIA

1) WITH POISONING/EXPOSURE

a) Severe irritation results in hypoxemia. The onset of symptoms following inhalation of vapors may be delayed for several hours.

C) BRONCHOSPASM

1) WITH POISONING/EXPOSURE

a) Bronchospasm, occupational asthma and reversible airway obstruction may develop after inhalation of acid vapor (Hamel & Ford-Hutchinson, 1985; Rajan & Davies, 1989; Stueven, 1992; Goldstein, 1994; Parra et al, 1992).

D) REACTIVE AIRWAYS DYSFUNCTION SYNDROME

1) WITH POISONING/EXPOSURE

a) An asthma-like pulmonary dysfunction (RADS) has been associated with exposure to glacial acetic acid vapors after a hospital spill (Kern, 1991).
b) The following criteria were used for the diagnosis of RADS:

1) Symptoms developed after a single exposure to high concentrations of an irritating substance.
2) Symptoms developed within 24 hours of exposure and persisted for at least 3 months.
3) Symptoms were similar to asthma (cough, wheezing, dyspnea).
4) Pulmonary function test results indicated airflow obstruction.
5) Methacholine challenge test was positive.
6) Preexisting pulmonary diseases and complaints were ruled out.

c) CASE SERIES: In one study of 33 children who had ingested caustic substances and were referred to a health care facility within 24 hours, 14 (42.5%) had evidence of upper airway lesions on direct laryngoscopy (Moulin et al, 1985).

E) PNEUMONIA

1) WITH POISONING/EXPOSURE

a) Interstitial pneumonitis and airway obstruction reversible by bronchodilators and corticosteroids were reported in a 37-year-old man after exposure to glacial acetic acid, resulting in burns of the face and arms. In the process, he inhaled a large cloud of vaporized acid. Symptoms progressed over 3 months until he was seen and treated (Rajan & Davies, 1989).
b) Chemical pneumonitis was reported in 19% of patients (n=187) after acute ingestion of concentrated acetic acid, and was present in 57% of patients who died after exposure (n=28) (Borisovsky & Birtanov, 1998).
c) According to a retrospective study, involving 370 patients who were treated for a corrosive acid ingestion, aspiration pneumonia was a rare occurrence, developing in only 15 patients (4.2%) within 24 hours post-ingestion. However, there was a significant increase in the mortality rate in the patients with aspiration pneumonia who underwent emergency surgery (n=8) as compared with the non-aspiration group (n=53) (87.5% vs 32%, p=0.000). For those patients who did not undergo emergency surgery, there was also a significant increase in the mortality rate in the aspiration group (n=7) as compared with the non-aspiration group (n=215) (28.5% vs 5.1%, p=0.050). For those patients in the aspiration group who did survive, laryngeal or tracheobronchial sequelae appeared to be prevalent on long-term follow-up (Tseng et al, 2002).

F) RESPIRATORY FINDING

1) WITH POISONING/EXPOSURE

a) PULMONARY FUNCTION ABNORMALITIES: PFT abnormalities have been reported after inhalation of hydrochloric acid, sulfur trioxide, and glacial acetic acid vapors (Stueven, 1992; Kern, 1991).
b) CASE REPORT: Tachypnea and mild respiratory acidosis (initial ABG: pH 7.35, pCO2 60, pO2 67, O2 sat 92%) were reported in a 10-month-old infant with RSV pneumonia following administration of nebulized albuterol inadvertently diluted with 5% acetic acid, in a 1:1 ratio. The patient recovered 36 hours later, without sequelae, following treatment with oxygen and bronchodilators (Sigg et al, 2001).

G) ACUTE LUNG INJURY

1) WITH POISONING/EXPOSURE

a) Pulmonary edema may complicate severe poisonings (Soni et al, 1985).
b) CASE REPORT: A 21-month-old boy developed respiratory distress, requiring mechanical ventilation, immediately after ingesting an unknown amount of methacrylic acid. Bronchoscopy revealed marked edema of the epiglottis, aryepiglottic folds, and both main stem bronchi (Dowsett & Woolf, 1994).
c) CASE REPORT: A 25-year-old man developed noncardiogenic pulmonary edema and died approximately 24 hours after inhalational exposure to fumes of acryloyl chloride (96%) and methacrylic anhydride (94%). Post-mortem examination showed congested and edematous lungs with microscopic features consistent with adult respiratory distress syndrome. Lab analysis revealed an acrylic acid level of 1.15 mcg/mL and a methacrylic acid level of 1.11 mcg/mL (Lau et al, 1998). Acrylic acid and methacrylic acid are the hydrolyzed products of acryloyl chloride and methacrylic anhydride, respectively.

H) AIRWAY EDEMA

1) WITH POISONING/EXPOSURE

a) Life threatening upper airway edema may develop after ingestion, particularly in children.

1) An 18-month-old child ingested an unknown quantity of 80% acetic acid. He rapidly developed respiratory distress and presented to the emergency department with stridor and severe upper airway obstruction. He developed severe hypoxia when endotracheal intubation was attempted unsuccessfully due to swelling in the pharynx; therefore, transtracheal jet ventilation was necessary and ultimately tracheostomy. He recovered (Tibballs et al, 2006).

3.6.3)

A) ANIMAL STUDIES

1) PULMONARY EDEMA

a) Pulmonary edema and increased pulmonary vascular permeability develops in rabbits after intratracheal installation of hydrochloric acid (Mizus et al, 1985).

Neurologic

3.7.2)

A) NEUROPATHY

1) WITH POISONING/EXPOSURE

a) A case-control study following an environmental hydrochloric acid exposure detected impaired balance, visual reaction time, digit symbol testing and timed placement of pegs in a pegboard in exposed patients (Kilburn, 1996)

Gastrointestinal

3.8.2)

A) CHEMICAL BURN

1) WITH POISONING/EXPOSURE

a) Burns of the oropharynx, esophagus, stomach, and duodenum may occur. Complications such as stricture, perforation, gastrointestinal bleeding and gastric outlet obstruction are related to the depth of burn. The presence or absence of peri-oral and pharyngeal burn does not predict the severity of esophageal or gastric injury (Gaudreault et al, 1983; Crain et al, 1984a).

1) ESOPHAGEAL burns are commonly found after significant acid ingestions (Farst et al, 2007; Wu & Lai, 1993; Linden et al, 1998). Maximum involvement is usually in the middle and lower thirds (Showkat et al, 1989).

a) INCIDENCE: Burns were noted in 15 of 16 patients (94%) in one study, 36 of 41 patients (88%) in another study, 10 of 11 patients (91%) in a third study and 9 of 23 patients (39%) in a fourth study (Dilawari et al, 1984; Zargar et al, 1989; Muhletaler et al, 1980a; Nuutinen et al, 1994). Esophageal burns developed in 11 of 18 patients (61%) who ingested 30% sulfuric acid (Wormald & Wilson, 1993). A retrospective analysis of 279 patients with acute 70% acetic acid poisoning revealed that chemical burns of the GI tract occurred in 89% of the patients (Sarmanaev & Yamanaeva, 2001). The mean dose ingested was 53.6 +/- 3.2 mL.
b) Severe acute complications such as perforation and death are associated with Grade III burns (Sittig, 1985; Zargar et al, 1989).
c) Chronic complications such as dysphagia and esophageal stricture formation are associated with Grade II and III burns (Zargar et al, 1989; Dilawari et al, 1984) .

1) ESOPHAGEAL STRICTURES were reported in 8 patients following deliberate acid ingestions (Jovic-Stosic et al, 2001).
2) 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).

d) CASE REPORT: A 21-month-old boy developed first and second degree burns to the entire oropharynx and esophagus and second degree burns to the stomach after ingesting an unknown quantity of methacrylic acid. The patient gradually recovered with no residual swallowing problems (Dowsett & Woolf, 1994).

2) STOMACH: Gastric burns are commonly found after significant acid ingestions (Wu & Lai, 1993; Dowsett & Woolf, 1994; Borisovsky & Birtanov, 1998).

a) INCIDENCE: Gastric burns were noted in 12 of 16 patients (75%) in one study and 35 of 41 patients (85%) in another study (Dilawari et al, 1984a; Zargar et al, 1989). Maximum involvement of the stomach is usually along the lesser curvature and the antrum (Dilawari et al, 1984a).
b) Severe acute complications such as perforation and massive gastrointestinal bleeding are associated with Grade III burns (Dilawari et al, 1984a; Zargar et al, 1989; Jeng et al, 1994; Christesen, 1995). Perforation primarily occurs at the fundus in the acute stage of injury (Wu & Lai, 1993).
c) Delayed complications such as gastric stricture and gastric outlet obstruction are associated with Grade II and III burns (Dilawari et al, 1984a; Zargar et al, 1989).

3) DUODENUM/JEJUNUM: Duodenal and jejunal burns may occur with acid ingestion (Wu & Lai, 1993).

a) INCIDENCE: Duodenal and jejunal burns are much less frequent (6 of 16 patients in one study and 0 of 41 in another) and are usually less severe (Dilawari et al, 1984; Zargar et al, 1989). Duodenal burns developed in 11 of 18 patients (61%) who ingested 30% sulfuric acid (Wormald & Wilson, 1993).
b) Grade III duodenal burns are associated with a high mortality and have been reported in patients ingesting sulfuric acid (Aitken, 1985; Dilawari et al, 1984a).

b) CAUSTIC INJURY SCALES

1) Several scales for grading caustic injury exist. The likelihood of complications such as strictures, obstruction, bleeding and perforation are related to the severity of the initial burn.

a) GRADING SCALES

1) GRADE 0: Normal examination
2) GRADE 1: Edema and hyperemia of the mucosa; strictures unlikely
3) GRADE 2A: Friability, hemorrhages, erosions, blisters, whitish membranes, exudates and superficial ulcerations; strictures unlikely
4) GRADE 2B: Grade 2A plus deep discreet or circumferential ulceration; strictures may develop.
5) GRADE 3A: Multiple ulcerations and small scattered areas of necrosis; strictures common, complications such as perforation, fistula formation or gastrointestinal bleeding may occur.
6) GRADE 3B: Extensive necrosis through visceral wall; strictures common, complications such as perforation, fistula formation or gastrointestinal bleeding may occur.
7) REFERENCE: (Zargar et al, 1991a)

1) According to a retrospective chart review of 273 patients, admitted to a Taiwanese hospital from 1999 to 2006 for caustic ingestion, the Zargar grading classification of mucosal injury was a strong and useful predictor in determining patient outcome. In this study, patients with grade 3B mucosal injuries were at an increased risk for prolonged hospital stay (odds ratio (OR) 2.44; 95%CI: 1.25 to 4.80; p<0.05), ICU admission (OR 10.82; 95%CI: 2.05 to 200.39; p<0.05), and gastrointestinal (OR 4:07; 95%CI: 1.81 to 9.69; p<0.05) and systemic complications (OR 4.15; 95% CI: 1.55 to 13.29; p<0.05) as compared with patients who had grade 3A mucosal injuries (Cheng et al, 2008).

2) The severity of burns found on endoscopy is a better predictor of complications, such as stricture formation, systemic complications or death, than is the type of substance ingested (Poley et al, 2004).

B) GASTROINTESTINAL HEMORRHAGE

1) WITH POISONING/EXPOSURE

a) GI hemorrhage with hematemesis, melena or hematochezia may develop after acid ingestions with injury to the gastrointestinal mucosa (Zargar et al, 1989; Dilawari et al, 1984a; Wu & Lai, 1993; Borisovsky & Birtanov, 1998).
b) INCIDENCE: GI bleeding and perforation occurred in 12% and 0.6%, respectively, of patients (n=279) following acute ingestions of 70% acetic acid. The mean dose ingested was 53.6 +/- 3.2 mL (Sarmanaev & Yamanaeva, 2001).
c) CASE REPORT: Hemorrhagic gastric necrosis occurred in a 57-year-old man who intentionally ingested 20 mL of a non-diluted solution containing hydrochloric acid. A gastroscopy revealed ulcerated gastric mucosa at the esophago-gastric junction with severe hemorrhagic necrosis. According to the Zargar's classification for grading caustic injury, it was identified as a grade-3 caustic gastritis. A partial esophagectomy and total gastrectomy were emergently performed to minimize the risk of future complications. An esophago-gastrectomy specimen showed extensive hemorrhagic gastric necrosis with damage to the gastric wall (Diaz-Sanchez et al, 2009).

C) GASTRITIS

1) WITH POISONING/EXPOSURE

a) Hydrochloric acid may cause gastritis (HSDB , 2000).

D) GASTRIC ULCER WITH PERFORATION

1) WITH POISONING/EXPOSURE

a) Perforations with peritonitis, though uncommon, may occur (Jeng et al, 1994; Christesen, 1995). The degree of damage in the stomach depends on the concentration and acidity of the solution and the amount of material already in the stomach (Fisher et al, 1985).

E) STENOSIS

1) WITH POISONING/EXPOSURE

a) A retrospective review of records, collected from hospitalized adult patients in Macedonia from 2002 to 2011, showed that of 932 patients with reported exposure to corrosive agents, 84 (9%) had ingested acetic acid, of which 80 patients had ingested with intent. The amount ingested varied from 5 to 100 mL. Gastric stenosis was reported in 22 patients, esophageal stenosis was reported in 5 patients, and combined gastric and esophageal stenosis was reported in 11 patients. Death occurred in 11 of the 84 patients, including 4 who died due to gastrointestinal complications (ie, perforation, acute peritonitis) within the first 96 hours post-exposure and 7 who died due to organ failure more than 96 hours post-exposure (Chibishev et al, 2013).

F) ESOPHAGITIS

1) WITH POISONING/EXPOSURE

a) Esophageal dilation, atony, and mucosal/submucosal edema have been reported following ingestion of muriatic acid (Muhletaler et al, 1980a).

G) VOMITING

1) WITH POISONING/EXPOSURE

a) Severe irritation may produce spontaneous vomiting. Viscid white or blood-stained foamy mucous and threads of tissue appear in the mouth. The vomit often has a characteristic coffee grounds appearance.

H) PYLORIC STENOSIS

1) WITH POISONING/EXPOSURE

a) Severe burns usually involve the pylorus. Delayed stricture with gastric outlet obstruction may develop several weeks after ingestion (Christesen, 1995; Keh et al, 2006).
b) Antro-pyloric strictures are the most common cause of pyloric stenosis, but the gastric body may also be involved or in severe cases the entire stomach may be scarred (Agarwal et al, 2004). Associated symptoms include post prandial vomiting, early satiety, dysphagia and weight loss.
c) A 38-year-old woman required laparoscopic distal gastrectomy and Billroth 1 end-to-end gastroduodenostomy 3 months after a caustic ingestion causing circumferential thickening of the distal antral wall with outlet obstruction (Kanyama et al, 2003).
d) An 8-year-old child developed pyloric obstruction and proximal duodenal wall involvement following ingestion of sulfuric acid. He required gastrojejunal transmesocholic isoperistaltic anastomosis 50 days post-ingestion and had a good post-operative result (Tamisani et al, 1992).
e) Three patients who ingested large amounts of hydrochloric acid developed gastric outlet obstruction and cicatrical antral stenosis over a 1 to 2 month period after the ingestion; all three required gastric resection (Chong et al, 1974).

I) TRACHEOESOPHAGEAL FISTULA

1) WITH POISONING/EXPOSURE

a) Tracheoesophageal fistula developed 65 days postingestion in a 60-year-old woman following ingestion of an unknown amount of muriatic acid, with a fatal outcome. Pressure necrosis from the endotracheal tube probably contributed (Pense et al, 1988).

J) DIVERTICULUM

1) WITH POISONING/EXPOSURE

a) Esophageal intramural pseudodiverticulosis (multiple, flask- shaped diverticuli in the esophageal wall) associated with esophageal stricture developed in 14 of 59 patients after acid ingestion. Esophageal dilatation relieved dysphagia with associated reduction in the number or disappearance of the diverticuli (Kochhar et al, 1991).
b) An intraluminal esophageal diverticulum developed in a 36-year-old woman one week after ingestion of sulfuric acid (Plavsic & Robinson, 1992).

K) VASCULAR INSUFFICIENCY OF INTESTINE

1) WITH POISONING/EXPOSURE

a) Massive gastric necrosis with extravasation of acid into the peritoneum and necrosis of the duodenum was reported in several patients following ingestion of 100 mL of 24% to 32% hydrochloric acid solutions (Munoz et al, 2001).

Hepatic

3.9.2)

A) LIVER DAMAGE

1) WITH POISONING/EXPOSURE

a) ISCHEMIC LESIONS may rarely occur in the liver after several hours of uncorrected circulatory collapse (Gosselin et al, 1984).
b) SYSTEMIC TOXICITY FROM BURNS: Chromic acid burns can result in systemic toxicity, with resulting acute hepatic injury (US DHHS, 1981; Ellenhorn & Barceloux, 1988).

B) LIVER ENZYMES ABNORMAL

1) WITH POISONING/EXPOSURE

a) CASE REPORT: A 3-year-old child presented to the emergency department after ingesting a small amount (believed to be a few drops) of 60% acetic acid. There were no signs of circumoral burns or erosions, and there was no drooling or signs of dysphagia. Approximately 12 hours post-ingestion, the patient developed hematuria, and laboratory data indicated hemolysis with an LDH of 2478 units/L and a bilirubin level of 4.06 mg/dL. Twenty-four hours post-ingestion, the patient's liver enzyme levels were also elevated (AST 444 units/L, ALT 349 units/L). With supportive care, the hematuria resolved after 24 hours and the laboratory values normalized after 3 days (Yonatan & Dan, 2007).
b) CASE SERIES: Five patients, who ingested glacial acetic acid, underwent abdominal CT scans to determine the extent of injury to the liver. In 3 patients, wedge-shaped hypodensities were found (segments 2,3, and 4 in 2 patients and segments 5 and 6 in 1 patient). Four of the 5 patients also had elevated transaminase levels. Two patients developed hepatic failure, as well as metabolic acidosis, hemolysis, and disseminated intravascular coagulation, and died within 1 to 2 days of ingestion (Kim et al, 2007). Although liver biopsies were not performed, the authors suggest that the wedge-shaped hypodensities may have been due to hepatic necrosis resulting from direct action of the glacial acetic acid following absorption through the damaged mucosal barrier into the portal circulation.

C) HEPATIC FAILURE

1) WITH POISONING/EXPOSURE

a) A retrospective review of records, collected from hospitalized adult patients in Macedonia from 2002 to 2011, showed that of 932 patients with reported exposure to corrosive agents, 84 (9%) had ingested acetic acid, of which 80 patients had ingested with intent. The amount ingested varied from 5 to 100 mL. Combined acute renal failure and liver failure was reported in 23 patients and combined acute renal failure, liver failure, and disseminated intravascular coagulation was reported in 17 patients. Eleven patients died, including 4 who died due to gastrointestinal complications within the first 96 hours post-exposure and 7 who died due to organ failure more than 96 hours post-exposure (Chibishev et al, 2013).

Genitourinary

3.10.2)

A) RENAL FAILURE SYNDROME

1) WITH POISONING/EXPOSURE

a) Renal failure may occur following chromic acid burns (US DHHS, 1981; Ellenhorn & Barceloux, 1988) and ingestions of 70% acetic acid (Chibishev et al, 2013; Sarmanaev & Yamanaeva, 2001).
b) Hydrochloric acid ingestion has been associated with kidney failure and decreased urine output (Gosselin et al, 1984). The kidney failure can occur after several hours of uncorrected circulatory collapse.
c) Acute renal failure has been reported in several patients who developed metabolic acidosis and perforated viscus after acid ingestion (Jeng et al, 1994).
d) CASE REPORT: A 69-year-old man developed acute renal failure after receiving 2 injections of 50% acetic acid solution (10 and 15 mL, respectively, administered 2 weeks apart) for treatment of hepatocellular carcinoma. Biochemical analyses showed elevated serum urea and creatinine levels. The patient gradually recovered after receiving several hemodialysis sessions (Van Hoof et al, 1999).
e) Acute renal failure was reported in 3.7% of patients (n=187) after acute ingestion of concentrated acetic acid, and was found in 78.6% of patient fatalities (n=28) (Borisovsky & Birtanov, 1998).
f) A retrospective review of records, collected from hospitalized adult patients in Macedonia from 2002 to 2011, showed that of 932 patients with reported exposure to corrosive agents, 84 (9%) had ingested acetic acid, of which 80 patients had ingested with intent. The amount ingested varied from 5 to 100 mL. Acute renal failure was reported in 28 patients, combined acute renal failure and liver failure was reported in 23 patients, and combined acute renal failure, liver failure, and disseminated intravascular coagulation was reported in 17 patients. Eleven patients died, including 4 who died due to gastrointestinal complications within the first 96 hours post-exposure and 7 who died due to organ failure more than 96 hours post-exposure (Chibishev et al, 2013).

B) HEMOGLOBINURIA

1) WITH POISONING/EXPOSURE

a) Hemoglobinuria has developed secondary to hemolysis after acetic acid ingestion (Yonatan & Dan, 2007; Greif & Kaplan, 1986; Teixeira et al, 1992) and after extensive dermal sulfuric acid burns (Husain et al, 1989).

C) NEPHRITIS

1) WITH POISONING/EXPOSURE

a) Ingestion of hydrochloric acid may cause nephritis (HSDB , 1992).

Acid-Base

3.11.2)

A) ACIDOSIS

1) WITH POISONING/EXPOSURE

a) Metabolic acidosis has been reported following ingestions of 100 to 200 milliliters of 24% to 32% hydrochloric acid, 90 to 120 milliliters of 20% hydrogen phosphate, and unspecified amounts of other acids (Farst et al, 2007; Yanturali et al, 2005; Caravati, 1987a; Linden et al, 1983; Jeng et al, 1994; Munoz et al, 2001).
b) Large doses of citric acid may cause metabolic acidosis and hypocalcemia (Gosselin et al, 1984).
c) CASE REPORT: Metabolic acidosis was also reported in a 4.5 year-old boy after 60% body surface area burns from concentrated sulfuric acid (Husain et al, 1989).
d) CASE REPORT: HYPERCHLOREMIC METABOLIC ACIDOSIS developed in a patient following accidental chlorine gas exposure. It was postulated that the mechanism for production of the acidosis was the absorption of hydrochloric acid following the reaction of chlorine gas with tissue water (Szerlip & Singer, 1984).
e) CASE REPORT: Severe metabolic acidosis (pH 6.9, base deficit -24 mEq/L) was reported in a 50-year-old pool worker who had was overcome by fumes and developed burns over 40% of his total body surface area after soaking in a mixture of muriatic acid and blue chlorinated rubber-based paint for at least 3 hours while cleaning and resurfacing a pool (O'Cleireachain et al, 2014).

Hematologic

3.13.2)

A) HEMOLYSIS

1) WITH POISONING/EXPOSURE

a) Hemolysis may occur following significant acid ingestion (Verstraete et al, 1989; Teixeira et al, 1992; Sarmanaev & Yamanaeva, 2001).
b) Hemolysis was reported in 65.2% of patients (n=187) after concentrated acetic acid ingestion and was found in all patient fatalities (n=28) (Borisovsky & Birtanov, 1998).
c) CASE REPORT: A 3-year-old child presented to the emergency department after ingesting a small amount (believed to be a few drops) of 60% acetic acid. There were no signs of circumoral burns or erosions, and there was no drooling or signs of dysphagia. Approximately 12 hours post-ingestion, the patient developed hematuria, and laboratory data indicated hemolysis with an LDH of 2478 units/L and a bilirubin level of 4.06 mg/dL. Twenty-four hours post-ingestion, the patient's liver enzyme levels were also elevated (AST 444 units/L, ALT 349 units/L). With supportive care, the hematuria resolved after 24 hours and the laboratory values normalized after 3 days (Yonatan & Dan, 2007).

B) DISSEMINATED INTRAVASCULAR COAGULATION

1) WITH POISONING/EXPOSURE

a) Disseminated intravascular coagulation may occur following significant acid ingestion. It has been reported with ingestion of 200 mL of 27% hydrochloric acid (Soni et al, 1985) and one cup of 96% acetic acid (Greif & Kaplan, 1986).
b) Disseminated intravascular coagulation was reported as a complication in the death of 10.7% of patients (n=28) following acute ingestion of concentrated acetic acid (Borisovsky & Birtanov, 1998).
c) INCIDENCE: Coagulopathy has been reported in 39% of patients (n=279) following acute ingestions of 70% acetic acid. The mean dose ingested was 53.6 +/- 3.2 mL (Sarmanaev & Yamanaeva, 2001).
d) A retrospective review of records, collected from hospitalized adult patients in Macedonia from 2002 to 2011, showed that of 932 patients with reported exposure to corrosive agents, 84 (9%) had ingested acetic acid, of which 80 patients had ingested with intent. The amount ingested varied from 5 to 100 mL. Combined acute renal failure, liver failure, and disseminated intravascular coagulation was reported in 17 patients. Eleven patients died, including 4 who died due to gastrointestinal complications within the first 96 hours post-exposure and 7 who died due to organ failure more than 96 hours post-exposure (Chibishev et al, 2013).

3.13.3)

A) ANIMAL STUDIES

1) HEMOLYSIS

a) In vitro hemolytic activity of four acids in phosphate buffered saline are reported below (Verstraete et al, 1989):

ACID	PARTIAL HEMOLYSIS		COMPLETE HEMOLYSIS
ACID	Conc (mcg/mL)	pH	Conc (mcg/mL)	pH
Acetic Acid	375	4.77	3,000	3.38
Hydrochloric Acid	---	---	228	2.58
Orthophosphoric Acid	306	3.4	612	2.42

Dermatologic

3.14.2)

A) CHEMICAL BURN

1) WITH POISONING/EXPOSURE

a) Severe dermal burns may occur and are often associated with chemical burns, particularly in a military setting (Mozingo et al, 1988; Husain et al, 1989).
b) GRAFTS: Skin grafts are often required for severe burns (Mozingo et al, 1988; Sawada & Doi, 1984) (Domonic et al, 1987)(Husain et al, 1989).

1) Dermal burns from concentrated sulfuric acid drain cleaner required grafting in 14 of 21 patients admitted to a burn unit (Bond et al, 1998).

c) CASE REPORT/CHILD: A 2.5-year-old child accidentally spilled 5 to 7 mL of 98.5% methacrylic acid onto his face, right arm, and chest, and 20 minutes later, developed patchy erythema and blistering. The patient recovered, without scarring, following supportive care (Linden et al, 1998).
d) CASE REPORT/ADULT: A 50-year-old pool worker developed burns on his flanks, back, and upper extremity (40% of total body surface area) after he was overcome by fumes and was found soaking in a mixture of muriatic acid and blue chlorinated rubber-based paint for at least 3 hours, while cleaning and resurfacing a pool. Initial arterial blood gas results indicated severe metabolic acidosis (pH 6.9, base deficit of -24 mEq/L). Removal of the acid was hindered by the adherence of the paint to the skin. Bacitracin ointment was the most effective agent for removal of the rubber-based paint. Initial debridement was also hampered by the odor coming from the patient limiting contact and attempts to remove the paint by hospital staff. Following removal of the paint, surgical debridement and a mid-humeral amputation were performed. Post-operatively, the patient continued to deteriorate clinically with severe hypothermia, coagulopathy, and persistent acidosis. Despite aggressive supportive measures, the patient died after a second cardiac arrest (O'Cleireachain et al, 2014).

B) ALOPECIA

1) WITH POISONING/EXPOSURE

a) A nationwide outbreak of alopecia was reported following application of a commercial hair-straightening product, known as Rio Hair Naturalizer System (World Rio Corporation), which included a neutral formula and a color enhancer formula. Product labeling indicated that the pH of the products was 3.4, however FDA chemists determined that the pH of the neutral hair product and the color enhancer product were 1.39 (range 1.1 to 3.15) and 2.82 (range 2.29 to 3.08), respectively (Swee et al, 2000).

Laboratory Monitoring

Monitoring Parameters Levels

4.1.1)

A) Obtain a complete blood count and electrolytes in all patients with significant burns after acid ingestion.
B) In patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions), obtain renal function tests, liver enzymes, serial CBC, INR, PT, PTT, fibrinogen, fibrin degradation products, type and crossmatch for blood, and monitor urine output and urinalysis. Serum lactate and base deficit may also be useful in these patients.
C) Monitor pulse oximetry or arterial blood gases in patients with signs and symptoms suggestive of upper airway edema or burns.
D) Obtain an upright chest x-ray in patients with signs and symptoms suggesting severe burns, perforation, or bleeding (or adults with deliberate, high volume or high concentration ingestions) to evaluate for pneumomediastinum or free air under the diaphragm. The absence of these findings DOES NOT rule out the possibility of necrosis or perforation of the esophagus or stomach. Obtain a chest radiograph in patients with pulmonary signs or symptoms.
E) Several weeks after ingestion, barium contrast radiographs of the upper GI tract are useful in patients who sustained grade 2 or 3 burns, to evaluate for strictures.

Radiographic Studies

1) Esophagrams in the acute and subacute phase demonstrate edema, hemorrhage, ulcerations, atony, and dilation. Strictures of the esophagus may be present in the chronic phase. These radiographic findings are not different from those found in alkaline corrosive esophagitis (Muhletaler et al, 1980).
2) Krypton esophageal transit studies and manometric measurements correlated better with residual clinical symptoms and functional outcomes than did morphological findings of stenosis late (3 months to 7 years) after caustic ingestions (Cadranel et al, 1990).

1) Obtain an upright chest x-ray to evaluate for perforation, mediastinitis and aspiration in severely symptomatic patients.

1) Abdominal CT scans were performed on 5 patients who ingested glacial acetic acid. Diffuse edematous thickening of the walls of the esophagus and stomach were found in all patients. Wedge-shaped low density areas in the liver were found in 3 patients; clinically these 3 developed hepatic failure, hemolysis, metabolic acidosis and coagulopathy, and 2 of these patients died. The authors postulated that wedge-shaped low densities in the liver after acid ingestion may represent areas of hepatic necrosis secondary to toxin absorption into the portal circulation (Kim et al, 2007).

Methods

1) For acids of unknown content, analytical chemistry laboratories could be used to identify content; however, this is rarely, if ever, necessary. The pH of the acid will give some idea about its relative corrosiveness.

Treatment

Life Support

Patient Disposition

6.3.1)

6.3.1.1) ADMISSION CRITERIA/ORAL

A) Symptomatic patients, and those with endoscopically demonstrated grade II or higher burns should be admitted. Patients with respiratory distress, grade III burns, or extensive grade II burns, acidosis, hemodynamic instability, gastrointestinal bleeding, or large ingestions should be admitted to an intensive care setting.

6.3.1.5) OBSERVATION CRITERIA/ORAL

A) Patients with an acid ingestion should be sent to a health care facility for evaluation. Patients with an endoscopic evaluation that demonstrates no burns or only minor grade I burns and who can tolerate oral intake can be discharged to home.

Monitoring

Oral Exposure

6.5.1)

A) DILUTION

1) If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
2) USE OF DILUENTS IS CONTROVERSIAL: While experimental models have suggested that immediate dilution may lessen caustic injury (Homan et al, 1993; Homan et al, 1994; Homan et al, 1995a), this has not been adequately studied in humans.
3) DILUENT TYPE: Use any readily available nontoxic, cool liquid. Both milk and water have been shown to be effective in experimental studies of caustic ingestion (Maull et al, 1985a; Rumack & Burrington, 1977; Homan et al, 1995a; Homan et al, 1994; Homan et al, 1993).
4) ADVERSE EFFECTS: Potential adverse effects include vomiting and airway compromise (Caravati, 2004).
5) CONTRAINDICATIONS: Do NOT attempt dilution in patients with respiratory distress, altered mental status, severe abdominal pain, nausea or vomiting, or patients who are unable to swallow or protect their airway. Diluents should not be force fed to any patient who refuses to swallow (Rao & Hoffman, 2002).

B) ACTIVATED CHARCOAL

1) Activated charcoal is of no value, may induce vomiting and may obscure endoscopy findings. It is NOT recommended.

6.5.2)

A) In patients without vomiting or respiratory distress who are able to swallow, dilute with 4-8 ounces milk/water if possible shortly after ingestion; then NPO until after endoscopy. Neutralization, gastric lavage, and activated charcoal are all contraindicated.

6.5.3)

A) MONITORING OF PATIENT

1) Monitor vital signs, CBC and electrolytes after significant ingestion.
2) Monitor renal function tests, liver enzymes, serial CBC, INR, PTT, type and crossmatch for blood, serum lactate and base deficit, monitor urine output and urinalysis in patients with severe burns or deliberate ingestion.
3) Monitor for occult GI hemorrhage, respiratory distress and increasing pain.
4) Obtain chest radiograph and pulse oximetry in any patient with respiratory signs or symptoms.

B) CONTRAINDICATED TREATMENT

1) Do not induce vomiting or give bicarbonate to neutralize. Addition of buffer to strong acid causes an exothermic reaction and an immediate rise in solution temperature (Maull et al, 1985; Penner, 1980).
2) A report concerning emergency surgical resection of the alimentary tract following caustic ingestions has indicated that 5 out of 6 patients sustained injuries beyond the pylorus as a result of gastric lavage (Wu & Lai, 1993).

C) IRRIGATION

1) Irrigate the mouth with copious amounts of water. Immediate dilution with small amounts of milk or water may help decontaminate the oral mucosa or dislodge particles of granular acids from the esophageal mucosa.
2) The amount of diluent recommended by the POISINDEX editorial board for caustic alkali ingestion varied, and may be useful in establishing guidelines for acid ingestion. Suggestions ranged from 2 to 12 ounces in adults and 1 to 8 ounces in children. The majority recommended a maximum amount of 8 ounces in adults and 4 ounces in children (Consensus, 1988).
3) Dilution of acid with water has been shown to be ineffective in altering the pH. The dilution of 50 mL of 9.5% hydrochloric acid with 800 mL of water resulted in a pH change of 0.99 to 1.73 (Maull et al, 1985).
4) Dilution with milk or water immediately or after 5 minutes reduced the extent of tissue injury induced by 0.5 N hydrochloric acid in isolated rat esophagi (Homan et al, 1995).
5) Follow dilution with appropriate demulcents - milk, cornstarch, and water.

D) SUCRALFATE

1) Sucralfate may be useful in relieving symptomatology from acid induced injury. Efficacy in accelerating healing or preventing complications has not been proven.
2) CASE REPORT: Administration of sucralfate, 1 gram dissolved in 30 mL of water, four times a day, was used in a 25-year-old man with moderately severe gastric injury after ingestion of hydrochloric acid. No other therapy was given other than antibiotic. Within 48 hours, improvement in symptoms was noted, enabling progression to a liquid diet on the 3rd day. Strictures were not prevented, although nearly complete gastric mucosal healing occurred after 2 weeks. The patient received a gastrojejunostomy for pyloric stricture 6 weeks postingestion (Mittal et al, 1989).

E) LEUCOVORIN CALCIUM

1) In a case where the individual had ingested 250 mL of a 44% solution of formic acid, intravenously infused leucovorin (ie, folinic acid) was used to enhance hepatic degradation of formate and furosemide was administered to prevent the renal absorption of formate (Moore et al, 1993). Hemofiltration was also instituted. The patient survived.

F) INSERTION OF NASOGASTRIC TUBE

1) Its been suggested that following a large ingestion of strong acids, a nasogastric tube should be passed and suction performed in an attempt to remove as much acid as possible prior to cold water dilution which may result in an exothermic reaction and worsen the burn (Penner, 1980).
2) Many authorities oppose this procedure fearing esophageal or gastric perforation. Soft nasogastric or orogastric tube should only be passed within 90 minutes following the large ingestion of a strong acid.

G) HYPOTENSIVE EPISODE

1) SUMMARY

a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.

2) DOPAMINE

a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).

3) NOREPINEPHRINE

a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
b) DOSE

1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).

4) If hypotension is secondary to gastrointestinal bleeding, blood or blood products replacement therapy is the treatment of choice.

H) BURN

1) SUMMARY - Burns of the oropharynx, esophagus, stomach, and duodenum may occur. Complications such as stricture, perforation, gastrointestinal bleeding and gastric outlet obstruction are related to the depth of burn. Early (within 24 hours) endoscopy should be performed to assess the severity of injury and guide future management.

I) ENDOSCOPIC PROCEDURE

1) SUMMARY: Obtain consultation concerning endoscopy as soon as possible and perform endoscopy within the first 24 hours when indicated.
2) INDICATIONS: Most studies associating the presence or absence of gastrointestinal burns with signs and symptoms after caustic ingestion have involved primarily alkaline ingestions. Because acid ingestion may cause severe gastric injury with fewer associated initial signs and symptoms, endoscopic evaluation is recommended in any patient with a definite history of ingestion of a strong acid, even if asymptomatic.
3) RISKS: Numerous large case series attest to the relative safety and utility of early endoscopy in the management of caustic ingestion.

a) REFERENCES: Gaudreault et al, 1983; Symbas et al, 1983; Crain et al, 1984; (Schild, 1985; Moazam et al, 1987; Sugawa & Lucas, 1989a; Previtera et al, 1990a; Zargar et al, 1991; Vergauwen et al, 1991a; Gorman et al, 1992a; Nuutinen et al, 1994a)

4) The risk of perforation during endoscopy is minimized by (Zargar et al, 1991):

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).

5) GRADING

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.

6) FOLLOW UP - If burns are found, follow 10 to 20 days later with barium swallow or esophagram.

J) ULTRASONOGRAPHY

1) A small study suggests that esophageal ultrasonography may be useful in predicting the likelihood of strictures after corrosive ingestion (Kamijo et al, 2004).

a) Miniprobe ultrasonography was performed endoscopically at the site of the most severe lesion in 11 patients with corrosive esophageal injury. Grading was as follows: grade 0 distinct muscular layers without thickening (5 patients); grade I distinct muscular layers with thickening (4 patients): grade II obscured muscular layers with indistinct margins 1 patient); and grade III muscular layers that could not be differentiated (1 patient). Lesions were also classified as to whether the area of worst damage involved part of the circumference (type a) or the entire circumference (type b).
b) Strictures did not develop in patients with grade 0 or 1 lesions. A transient stricture developed in the patient with a grade IIa lesion. A stricture that required repeated dilatation developed in the patient with a grade IIIb lesion.

K) CORTICOSTEROID

1) CORROSIVE INGESTION/SUMMARY: The use of corticosteroids for the treatment of caustic ingestion is controversial. Most animal studies have involved alkali-induced injury (Haller & Bachman, 1964; Saedi et al, 1973). Most human studies have been retrospective and generally involve more alkali than acid-induced injury and small numbers of patients with documented second or third degree mucosal injury.
2) FIRST DEGREE BURNS: These burns generally heal well and rarely result in stricture formation (Zargar et al, 1989; Howell et al, 1992). Corticosteroids are generally not beneficial in these patients (Howell et al, 1992).
3) SECOND DEGREE BURNS: Some authors recommend corticosteroid treatment to prevent stricture formation in patients with a second degree, deep-partial thickness burn (Howell et al, 1992). However, no well controlled human study has documented efficacy. Corticosteroids are generally not beneficial in patients with a second degree, superficial-partial thickness burn (Caravati, 2004; Howell et al, 1992).
4) THIRD DEGREE BURNS: Some authors have recommended steroids in this group as well (Howell et al, 1992). A high percentage of patients with third degree burns go on to develop strictures with or without corticosteroid therapy and the risk of infection and perforation may be increased by corticosteroid use. Most authors feel that the risk outweighs any potential benefit and routine use is not recommended (Boukthir et al, 2004; Oakes et al, 1982; Pelclova & Navratil, 2005).
5) CONTRAINDICATIONS: Include active gastrointestinal bleeding and evidence of gastric or esophageal perforation. Corticosteroids are thought to be ineffective if initiated more than 48 hours after a burn (Howell, 1987).
6) DOSE: Administer daily oral doses of 0.1 milligram/kilogram of dexamethasone or 1 to 2 milligrams/kilogram of prednisone. Continue therapy for a total of 3 weeks and then taper (Haller et al, 1971; Marshall, 1979). An alternative regimen in children is intravenous prednisolone 2 milligrams/kilogram/day followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks then tapered (Anderson et al, 1990).
7) ANTIBIOTICS: Animal studies suggest that the addition of antibiotics can prevent the infectious complications associated with corticosteroid use in the setting of caustic burns. Antibiotics are recommended if corticosteroids are used or if perforation or infection is suspected. Agents that cover anaerobes and oral flora such as penicillin, ampicillin, or clindamycin are appropriate (Rosenberg et al, 1953).
8) STUDIES

a) ANIMAL

1) Some animal studies have suggested that corticosteroid therapy may reduce the incidence of stricture formation after severe alkaline corrosive injury (Haller & Bachman, 1964; Saedi et al, 1973a).
2) Animals treated with steroids and antibiotics appear to do better than animals treated with steroids alone (Haller & Bachman, 1964).
3) Other studies have shown no evidence of reduced stricture formation in steroid treated animals (Reyes et al, 1974). An increased rate of esophageal perforation related to steroid treatment has been found in animal studies (Knox et al, 1967).

b) HUMAN

1) Most human studies have been retrospective and/or uncontrolled and generally involve small numbers of patients with documented second or third degree mucosal injury. No study has proven a reduced incidence of stricture formation from steroid use in human caustic ingestions (Haller et al, 1971; Hawkins et al, 1980; Yarington & Heatly, 1963; Adam & Brick, 1982).
2) META ANALYSIS

a) Howell et al (1992), analyzed reports concerning 361 patients with corrosive esophageal injury published in the English language literature since 1956 (10 retrospective and 3 prospective studies). No patients with first degree burns developed strictures. Of 228 patients with second or third degree burns treated with corticosteroids and antibiotics, 54 (24%) developed strictures. Of 25 patients with similar burn severity treated without steroids or antibiotics, 13 (52%) developed strictures (Howell et al, 1992).
b) Another meta-analysis of 10 studies found that in patients with second degree esophageal burns from caustics, the overall rate of stricture formation was 14.8% in patients who received corticosteroids compared with 36% in patients who did not receive corticosteroids (LoVecchio et al, 1996).
c) Another study combined results of 10 papers evaluating therapy for corrosive esophageal injury in humans published between January 1991 and June 2004. There were a total of 572 patients, all patients received corticosteroids in 6 studies, in 2 studies no patients received steroids, and in 2 studies, treatment with and without corticosteroids was compared. Of 109 patients with grade 2 esophageal burns who were treated with corticosteroids, 15 (13.8%) developed strictures, compared with 2 of 32 (6.3%) patients with second degree burns who did not receive steroids (Pelclova & Navratil, 2005).

3) Smaller studies have questioned the value of steroids (Ferguson et al, 1989; Anderson et al, 1990), thus they should be used with caution.
4) Ferguson et al (1989) retrospectively compared 10 patients who did not receive antibiotics or steroids with 31 patients who received both antibiotics and steroids in a study of caustic ingestion and found no difference in the incidence of esophageal stricture between the two groups (Ferguson et al, 1989).
5) A randomized, controlled, prospective clinical trial involving 60 children with lye or acid induced esophageal injury did not find an effect of corticosteroids on the incidence of stricture formation (Anderson et al, 1990).

a) These 60 children were among 131 patients who were managed and followed-up for ingestion of caustic material from 1971 through 1988; 88% of them were between 1 and 3 years old (Anderson et al, 1990).
b) All patients underwent rigid esophagoscopy after being randomized to receive either no steroids or a course consisting initially of intravenous prednisolone (2 milligrams/kilogram per day) followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks prior to tapering and discontinuation (Anderson et al, 1990).
c) Six (19%), 15 (48%), and 10 (32%) of those in the treatment group had first, second and third degree esophageal burns, respectively. In contrast, 13 (45%), 5 (17%), and 11 (38%) of the control group had the same levels of injury (Anderson et al, 1990).
d) Ten (32%) of those receiving steroids and 11 (38%) of the control group developed strictures. Four (13%) of those receiving steroids and 7 (24%) of the control group required esophageal replacement. All but 1 of the 21 children who developed strictures had severe circumferential burns on initial esophagoscopy (Anderson et al, 1990).
e) Because of the small numbers of patients in this study, it lacked the power to reliably detect meaningful differences in outcome between the treatment groups (Anderson et al, 1990).

6) ADVERSE EFFECTS

a) The use of corticosteroids in the treatment of caustic ingestion in humans has been associated with gastric perforation (Cleveland et al, 1963) and fatal pulmonary embolism (Aceto et al, 1970).

9) 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).

L) STRICTURE OF ESOPHAGUS

1) Seven patients who developed esophageal strictures 3 weeks to 3 months after intentional acid ingestions were treated by endoscopic balloon dilatation upon diagnosis. The diameter of the initial balloon was 8 to 12 millimeters. Following the first successful dilatation, the interval between successive dilatations was 1 to 4 weeks. The progressive widening of the esophageal lumen to 15 millimeters was achieved after 3 to 7 dilatations. Endoscopic balloon dilatation was successful in 5 of the 7 patients with annular or short tubular strictures, and they currently are able to eat regular diets (Jovic-Stosic et al, 2001).
2) 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 oesophagram 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).
3) Early intraluminal esophageal stenting with a special nasogastric tube was recommended after caustic ingestion to prevent later esophageal stricture formation (Wijburg et al, 1989).
4) 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/hematopneumothorax (13.09%), cervical anastomotic leakage (9.2%), 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).

M) DIETARY FINDING

1) Depends on degree of damage as assessed by early endoscopy (Dilawari et al, 1984a).

1) mild (grade I): may have oral feedings first day
2) moderate (grade II): may have liquids after 48 to 72 hours
3) severe (grade III): jejunostomy tube feedings after 48 to 72 hours

2) Observe for symptoms of gastric outlet obstruction, at which time parenteral fluids and/or hyperalimentation should be considered. Classically, this occurs at 3 weeks after ingestions.

N) FOLLOW-UP VISIT

1) Obtain a follow-up esophagram and upper GI series to evaluate presence or absence of secondary scarring and/or stricture formation about 2 to 4 weeks following ingestion.
2) One 3-year-old child developed esophageal stricture 2 years after the acid ingestion in a prospective study of 41 patients. This child had a normal barium study at one year after ingestion (Zargar et al, 1989).

O) SURGICAL PROCEDURE

1) In severe cases of gastrointestinal necrosis or perforation, emergent surgical consultation should be obtained. The need for gastric resection or laparotomy in the stable patient is controversial (Chodak & Passaro, 1978; Dilawari et al, 1984).
2) LAPAROTOMY/LAPAROSCOPY - Early laparotomy or laparoscopy should be considered in patients with endoscopic evidence of severe esophageal or gastric burns after acid ingestion to evaluate for the presence of transmural gastric or esophageal necrosis (Estrera et al, 1986; Meredith et al, 1988; Wu & Lai, 1993a). Emergent laparotomy should be strongly considered in any patient with hypotension, altered mental status, or acidemia (Hovarth et al, 1991).

a) STUDY - In a retrospective study of patients with extensive transmural gastroesophageal necrosis after caustic ingestion, all 4 patients treated in the conventional manner (endoscopy, 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, 1986).
b) Wu & Lai (1993) reported the results of emergency surgical resection of the alimentary tract in 28 patients who had extensive corrosive injuries due to the ingestion of acids or other caustics. Operative mortality was most frequently associated with sepsis. Non-fatal bleeding, infections, biliary or bronchial fistulas were other noted complications. Morbidity and mortality were related to the severity of the damage and the extent of surgery required.

1) Immediate postoperative management included antibiotics, extensive respiratory care, tracheobronchial toilet, maintenance of fluid, electrolyte and acid-base balance, and jejunostomy feeding or total parenteral nutrition.

Inhalation Exposure

6.7.1)

A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

6.7.2)

A) OXYGEN

1) With severe dyspnea or hypoxemia, administer humidified oxygen until symptoms subside.

B) GENERAL TREATMENT

1) Evaluate for nasopharyngeal burns.
2) ANIMAL STUDIES - In rabbits, isoproterenol and aminophylline significantly reduced the increased pulmonary artery pressure, vascular permeability, and fluid-flux associated with hydrochloric acid lung injury (Mizus et al, 1985).

C) BRONCHOSPASM

1) If bronchospasm or wheezing occur, consider treatment with inhaled sympathomimetic agents.

D) ACUTE LUNG INJURY

1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).

a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)

3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).

E) EXPERIMENTAL THERAPY

1) INTRATRACHEAL SURFACTANT - A study, conducted with rats, showed that surfactant, given intratracheally 1 minute and 10 minutes following aspiration of hydrochloric acid, prevented deterioration of gas exchange within the lungs. Groups of rats that were either given ventilation alone, received only saline intratracheally, or were given surfactant intratracheally 60 min and 90 min after hydrochloric acid aspiration, developed significant deterioration in gas exchange (Eijking et al, 1993). The surfactant given within 10 minutes of hydrochloric acid aspiration prevented respiratory failure, but did not prevent accumulation of plasma-derived proteins into the alveolar space, which may progressively lead to inhibition of the surfactant.

F) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

6.8.1)

A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
B) The pH of the conjunctival sac should be tested after irrigation and irrigation continued until it is no longer acidic.

6.8.2)

A) INJURY OF GLOBE OF EYE

1) EVALUATION

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, 2000a).
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, 2000a; Singh et al, 2013):

1) GRADE 1 (prognosis good): Corneal epithelial damage; no limbal ischemia.
2) GRADE 2 (prognosis good): Cornea hazy; iris details visible, ischemia less than one-third of limbus.
3) GRADE 3 (prognosis guarded): Total loss of corneal epithelium; stromal haze obscures iris details; ischemia of one-third to one-half of limbus.
4) GRADE 4 (prognosis poor): Cornea opaque; iris and pupil obscured, ischemia affects more than one-half of limbus.

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):

1) GRADE 1 (prognosis very good): 0 clock hour of limbal involvement and 0% conjunctival involvement.
2) GRADE 2 (prognosis good): Less than 3 clock hour of limbal involvement and less than 30% conjunctival involvement.
3) GRADE 3 (prognosis good): Greater than 3 and up to 6 clock hour of limbal involvement and greater than 30% to 50% conjunctival involvement.
4) GRADE 4 (prognosis good to guarded): Greater than 6 and up to 9 clock hour of limbal involvement and greater than 50% to 75% conjunctival involvement.
5) GRADE 5 (prognosis guarded to poor): Greater than 9 and less than 12 clock hour of limbal involvement and greater than 75% and less than 100% conjunctival involvement.
6) GRADE 6 (very poor): Total limbus (12 clock hour) involved and 100% conjunctival involvement.

2) MEDICAL FACILITY IRRIGATION

a) IRRIGATION: In a medical facility: Begin irrigation with copious amounts of water or sterile 0.9% saline, which ever is more rapidly available, immediately. Once irrigation has begun, instill a drop of local anesthetic for comfort; switching from water to slightly warmed sterile saline may also improve patient comfort (Ernst et al, 1998; Grant & Schuman, 1993a).
b) Continue irrigation for at least an hour or until the superior and inferior cul-de-sacs have returned to neutrality, pH of 7.0 to 8.0, and remain so for 30 minutes after irrigation is discontinued (Brodovsky et al, 2000).
c) Search the conjunctival sac for solid particles and remove them while continuing irrigation (Grant & Schuman, 1993a). Emergent ophthalmologic consultation is needed in these cases.

3) MINOR INJURY

a) SUMMARY

1) If ocular damage is minor, artificial tears/lubricants, topical cycloplegics, and antibiotics may be all that are needed.

b) ARTIFICIAL TEARS

1) To promote re-epithelization, preservative-free artificial tears/lubricants (eg, hyaluronic acid hourly) may be used (Fish & Davidson, 2010; Tuft & Shortt, 2009).

c) TOPICAL CYCLOPLEGIC

1) Use to guard against development of posterior synechiae and ciliary spasm (Brodovsky et al, 2000b; Grant & Schuman, 1993a). Cyclopentolate 0.5% or 1% eye drops may be administered 4 times daily to control pain (Tuft & Shortt, 2009; Spector & Fernandez, 2008).

d) TOPICAL ANTIBIOTICS

e) PAIN CONTROL

1) If pain control is required, oral or parenteral NSAIDs or narcotics are preferred to topical ocular anesthetics, which may cause local corneal epithelial damage if used repeatedly (Spector & Fernandez, 2008; Grant & Schuman, 1993a). However, topical 0.5% proparacaine has been recommended (Spector & Fernandez, 2008).

4) SEVERE INJURY

a) SUMMARY

1) If the damage is minor, the above may be all that is needed. For grade 3 or 4 injuries, one or more of the following may be used, only with ophthalmologic consultation: acetazolamide, topical timolol, topical steroids, citrate, ascorbate, EDTA, cysteine, NAC, penicillamine, tetracycline, or soft contact lenses.

b) ARTIFICIAL TEARS

1) To promote re-epithelization, preservative-free artificial tears/lubricants (eg, hyaluronic acid hourly) may be used (Fish & Davidson, 2010; Tuft & Shortt, 2009).

c) PAIN CONTROL

d) CARBONIC ANHYDRASE INHIBITOR

1) Acetazolamide (250 mg orally 4 times daily) may be given to control increased intraocular pressure (Singh et al, 2013; Tuft & Shortt, 2009; Spector & Fernandez, 2008).

e) TOPICAL STEROIDS

1) DOSE: Dexamethasone 0.1% ointment 4 times daily to reduce inflammation. If persistent epithelial defect is present, discontinue dexamethasone by day 14 to reduce the risk of stromal melt (Tuft & Shortt, 2009). Other sources suggest that corticosteroids should be stopped if the epithelium has not covered surface defects by 5 to 7 days (Grant & Schuman, 1993b).
2) Topical prednisolone 0.5% has also been used. A further increase in corneoscleral melt may occur if topical steroids are used alone. In one study, topical prednisolone 0.5% was used in combination with topical ascorbate 10%; no increase in corneoscleral melt was observed when topical steroids were used until re-epithelization (Singh et al, 2013; Fish & Davidson, 2010).
3) In one retrospective study, fluorometholone 1% drops were administered every 2 hours initially, then decreased to four times daily when there was evidence of progressive corneal reepithelialization and lessened inflammation, and discontinued when corneal reepithelialization was complete (Brodovsky et al, 2000).

a) STUDY: The combination of intensive topical corticosteroids, topical citrate and ascorbate, and oral citrate and ascorbate was associated with improved best corrected visual acuity and a trend towards more rapid corneal reepithelialization in Grade 3 alkali burns in one retrospective study (Brodovsky et al, 2000).

f) ASCORBATE

1) Oral or topical ascorbate may be used to promote epithelial healing and reduce the risk of stromal necrosis (Fish & Davidson, 2010).
2) DOSE: Ascorbate 10% 4 times daily topically or 1 g orally (2 g/day) (Singh et al, 2013; Tuft & Shortt, 2009).
3) Ascorbate is needed for the formation of collagen and the concentration of ascorbate in the anterior chamber is decreased when the ciliary body is damaged by alkali burns (Tuft & Shortt, 2009; Grant & Schuman, 1993b). In one retrospective study, ascorbate drops (10%) were administered every 2 hours, then decreased to 4 times a day when there was evidence of progressive corneal reepithelialization and lessened inflammation, and discontinued when corneal reepithelialization was complete. These patients also received 500 mg of oral ascorbate 4 times daily, until discharge from the hospital (Brodovsky et al, 2000).

g) CITRATE

1) Topical citrate may be used to promote epithelial healing and reduce the risk of stromal necrosis (Fish & Davidson, 2010).
2) DOSE: Potassium citrate 10% 4 times daily topically (Tuft & Shortt, 2009).
3) Citrate chelates calcium, and thereby interferes with the harmful effects of neutrophil accumulation, such as release of proteolytic enzymes and superoxide free radicals, phagocytosis and ulceration (Grant & Schuman, 1993b). In one retrospective study, 10% citrate drops were administered every 2 hours, then decreased to 4 times a day when there was evidence of progressive corneal reepithelialization and lessened inflammation, and discontinued when corneal reepithelialization was complete. These patients also received a urinary alkalinizer containing 720 mg of citric acid anhydrous and 630 mg of sodium citrate anhydrous 3 times daily, until discharge from the hospital (Brodovsky et al, 2000).

h) COLLAGENASE INHIBITORS

1) Inhibitors of collagenase can inhibit collagenolytic activity, prevent stromal ulceration, and promote wound healing. Several effective agents, such as cysteine, n-acetylcysteine, sodium ethylenediamine tetra acetic acid (EDTA), calcium EDTA, penicillamine, and citrate, have been recommended (Singh et al, 2013; Tuft & Shortt, 2009; Perry et al, 1993; Seedor et al, 1987).
2) TETRACYCLINE: Has been found to have an anticollagenolytic effect. Systemic tetracycline 50 mg/kg/day reduced the incidence of alkali-induced corneal ulcerations in rabbits (Seedor et al, 1987).
3) DOXYCYCLINE: Decreased epithelial defects and collagenase activity in a rabbit model of alkali burns to the eye (Perry et al, 1993). DOSE: 100 mg twice daily (Tuft & Shortt, 2009).

i) ANTIBIOTICS

1) An antibiotic ophthalmic ointment or drops should be used for as long as epithelial defects persist (Brodovsky et al, 2000b; Grant & Schuman, 1993a). Topical erythromycin or tetracycline ointment may be used (Spector & Fernandez, 2008). In patients with severe burns, a topical fluoroquinolone antibiotic drop 4 times daily may also be used (Tuft & Shortt, 2009). A topical fourth generation fluoroquinolone has been recommended as an antimicrobial prophylaxis in patients with large epithelial defect (Fish & Davidson, 2010).

j) TOPICAL CYCLOPLEGIC

1) Cyclopentolate 0.5% or 1% eye drops may be administered 4 times daily to control pain (Tuft & Shortt, 2009; Spector & Fernandez, 2008).

k) SOFT CONTACT LENSES

1) A bandage contact lens (eg, silicone hydrogel) may make the patient more comfortable and protect the surface (Fish & Davidson, 2010; Tuft & Shortt, 2009). Hydrophilic high oxygen permeability lenses are preferred (Singh et al, 2013). Soft lenses with intermediate water content and inherent rigidity may facilitate reepithelialization. The use of 0.5 normal sodium chloride drops hourly and artificial tears or lubricant eyedrops instilled 4 times a day may help maintain adequate hydration and lens mobility.

5) SURGICAL THERAPY

a) SURGICAL THERAPY CAUSTIC EYE INJURY

1) Early insertion of methylmethacrylate ring or suturing saran wrap over palpebral and cul-de-sac conjunctiva may prevent fibrinosis adhesions and reduce fibrotic contracture of conjunctiva, but the advantage of such treatments is not clear.
2) Limbal stem cell transplantation has been used successfully in both the acute stage of injury and the chronically scarred healing phase in patients with persistent epithelial defects after chemical burns (Azuara-Blanco et al, 1999; Morgan & Murray, 1996; Ronk et al, 1994).
3) In some patients, amniotic membrane transplantation (AMT) has been successful in improving corneal healing and visual acuity in patients with persistent epithelial defects after chemical burns. It can restore the conjunctival surface and decrease limbal stromal inflammation (Fish & Davidson, 2010; Sridhar et al, 2000; Su & Lin, 2000; Meller et al, 2000; Azuara-Blanco et al, 1999).
4) Control glaucoma. Remove any cataracts formed (Fish & Davidson, 2010; Tuft & Shortt, 2009).
5) In patients with severe injury, tenonplasty can be performed to promote epithelialization and prevent melting (Tuft & Shortt, 2009).
6) A keratoprosthesis placement has also been indicated in severe cases (Fish & Davidson, 2010). Penetrating keratoplasty is usually delayed as long as possible as results appear to be better with a greater lag time between injury and keratoplasty (Grant & Schuman, 1993a).

B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

6.9.1)

A) Remove contaminated clothing and jewelry and irrigate exposed areas with copious amounts of water. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

6.9.2)

A) BURN INJURY

1) Treat burns prophylactically for infection.
2) Once irrigation is completed standard burn therapy should be instituted including tetanus prophylaxis, dressings and careful follow up to observe for complications and infection.
3) GRAFTS - Skin grafts are often required for severe burns (Sawada & Doi, 1984; Husain et al, 1989)(Mozigo et al, 1988; Domonic et al, 1987).

B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Abstracts

Range Of Toxicity

Summary

Minimum Lethal Exposure

1) A retrospective review of records, collected from hospitalized adult patients in Macedonia from 2002 to 2011, showed that of 932 patients with reported exposure to corrosive agents, 84 (9%) had ingested acetic acid, of which 80 patients had ingested with intent. The amount ingested varied from 5 to 100 mL. Acute renal failure was reported in 28 patients, combined acute renal failure and liver failure was reported in 23 patients, and combined acute renal failure, liver failure, and disseminated intravascular coagulation was reported in 17 patients. Gastric stenosis was reported in 22 patients, esophageal stenosis was reported in 5 patients, and combined gastric and esophageal stenosis was reported in 11 patients. Death occurred in 11 of the 84 patients, including 4 who died due to gastrointestinal complications (ie, perforation, acute peritonitis) within the first 96 hours post-exposure and 7 who died due to organ failure more than 96 hours post-exposure (Chibishev et al, 2013).

Maximum Tolerated Exposure

1) Any of the listed acids may cause injury. In undiluted form they are almost invariably damaging. Dilute solutions are less likely to be so. Mixed acids with high concentrations of nitric acid are highly corrosive (eg, aqua regia).

a) Esophageal burns were noted in 15 of 16 patients (94%) in one study, 36 of 41 patients (88%) in another study, 10 of 11 patients (91%) in a third study and 9 of 23 patients (39%) in a fourth study (Dilawari et al, 1984; Zargar et al, 1989; Muhletaler et al, 1980a; Nuutinen et al, 1994). Esophageal burns developed in 11 of 18 patients (61%) who ingested 30% sulfuric acid (Wormald & Wilson, 1993). A retrospective analysis of 279 patients with acute 70% acetic acid poisoning revealed that chemical burns of the GI tract occurred in 89% of the patients (Sarmanaev & Yamanaeva, 2001). The mean dose ingested was 53.6 +/- 3.2 mL.
b) Gastric burns were noted in 12 of 16 patients (75%) in one study and 35 of 41 patients (85%) in another study (Dilawari et al, 1984a; Zargar et al, 1989). Maximum involvement of the stomach is usually along the lesser curvature and the antrum (Dilawari et al, 1984a).
c) Formulations of household cleaning products now contain lower concentrations of acids and alkaline corrosives. Series of caustic ingestions (mixed liquid and solid, alkaline and acids) in children report incidences of significant esophageal burns from 5% to 35% (Crain et al, 1984; Gorman et al, 1992; Previtera et al, 1990; Vergauwen et al, 1991).

2) INHALATION EXPOSURE: Inhalation danger is not present with those acids that have low vapor pressure, such as phosphoric acid. With nitric acid, breathing an atmosphere containing 25 parts per million for an 8 hour period may cause pulmonary signs and symptoms.

a) Pulmonary edema will follow exposure to 100 to 150 parts per million for 30 minutes to 1 hour.
b) A few breaths of the gaseous oxides in concentrations of 200 to 700 parts per million will cause severe pulmonary damage and may be fatal in as little as 5 to 10 hours.

1) ACID STRENGTH: The pKa is an index of acid strength. The higher the pKa of an organic acid, the less potential there is to produce irritation.

a) In an in vitro study, corrosive potential of methacrylic acid in artificial nail primers was predicted by the concentration of acid and its corresponding pH in each individual product (Woolf & Shaw, 1999).

2) HOUSEHOLD ACID SOLIDS: Potentially caustic household acid solids did not result in a detectable erosion in an in vitro model using recently sacrificed canine esophagus (Hoffman et al, 1989).
3) TITRATABLE ALKALINE RESERVE: The titratable alkaline reserve (TAR) of potentially caustic household acid liquids was found to correlate better than pH in an in vitro model using recently sacrificed canine esophagus (Hoffman et al, 1989).
4) ACETIC ACID

a) CASE REPORT/CHILD: A 3-year-old child ingested a small amount (believed to be a few drops) of 60% acetic acid and subsequently developed hematuria, hemolysis and hepatitis. There were no apparent circumoral burns or erosions, no drooling, and no signs of dysphagia. With supportive care, the patient recovered without apparent sequelae (Yonatan & Dan, 2007).
b) A retrospective review of records, collected from hospitalized adult patients in Macedonia from 2002 to 2011, showed that of 932 patients with reported exposure to corrosive agents, 84 (9%) had ingested acetic acid, of which 80 patients had ingested with intent. The amount ingested varied from 5 to 100 mL. Acute renal failure was reported in 28 patients, combined acute renal failure and liver failure was reported in 23 patients, and combined acute renal failure, liver failure, and disseminated intravascular coagulation was reported in 17 patients. Gastric stenosis was reported in 22 patients, esophageal stenosis was reported in 5 patients, and combined gastric and esophageal stenosis was reported in 11 patients. Death occurred in 11 of the 84 patients, including 4 who died due to gastrointestinal complications (ie, perforation, acute peritonitis) within the first 96 hours post-exposure and 7 who died due to organ failure more than 96 hours post-exposure (Chibishev et al, 2013).

1) DOGS: In an experimental dog model, weak acids (less than 10N) produced reversible mucosal injury in the distal esophagus and stomach. Stronger acids (>20N) were associated with irreversible injury to the stomach and esophagus (Fisher et al, 1985).

a) Fundic perforation was consistently observed with exposures to 20N and 36N sulfuric acid, whereas no perforations were noted with exposure to 10N solutions.
b) Fed dogs tended to have less mucosal injury of the stomach than fasting dogs.

Serum Plasma Blood Concentrations

7.5.2)

A) TOXIC CONCENTRATION LEVELS

1) ADULT

a) Post-mortem lab analysis of a 25-year-old male, who died following inhalational exposure to fumes of acryloyl chloride (96%) and methacrylic anhydride (94%), revealed an acrylic acid level of 1.15 mcg/mL and a methacrylic acid level of 1.11 mcg/mL (Lau et al, 1998). Acrylic acid and methacrylic acid are the hydrolysed products of acryloyl chloride and methacrylic anhydride, respectively.

Pharmacology Toxicology

Toxicologic Mechanism

1) Categories of potentially caustic household agents include alkaline solids, alkaline liquids, acid solids, and acid liquids.
2) Depth of erosion was compared with titratable acid/alkaline reserve (TAR) and pH to evaluate which factor is more closely associated with production of esophageal injury in this model.

a) TAR DEFINITION - The number of mL (mean of 3 determinations) of a 0.1 M solution of hydrochloric acid or NaOH required to titrate 100 mL of a 1% solution of test product to pH 8.00.

3) ALKALINE SOLIDS RESULTS - Depth of erosion correlated well with TAR (p=0.015, r=0.947) and pH (p=0.015, r=0.945).
4) ALKALINE LIQUIDS RESULTS - Depth of erosion correlated better with TAR (p=0.024, r=0.925) than with pH (p=0.240, r=0.645).
5) ACID SOLIDS RESULTS - Were not evaluated because these products failed to produce injury.
6) ACID LIQUIDS - Depth of erosion correlated better with TAR (p=0.056, r=0.868) than with pH (p=0.497, r= -0.407).

Physicochemical

Physical Characteristics

Ph

Molecular Weight

Animal Toxicology

References

General Bibliography

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ACIDS

Classification | Detailed evidence-based information

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Ph

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General Bibliography