Substances Included Synonyms

Therapeutic Toxic Class

A)

Specific Substances

1) BURNT LIME
2) CALCIUM OXIDE
3) CALCIA
4) CALX
5) CALXYL
6) Oxyde de calcium (French)
7) DESICAL P
8) RHENOSORB C
9) RHENOSORB F
10) WAPNIOWY TLENEK (Polish)
11) LIME
12) LIME, BURNED
13) LIME, UNSLACKED
14) QUICKLIME
15) CALOXOL CP2
16) CALOXOL W3
17) CAS 1305-78-8
18) BURNED LIME
19) CALCIUM MONOXIDE
20) FLUXING LIME
21) GEBRANNTER KALK
22) LIME, UNSLAKED
23) PEBBLE LIME
24) UNSLAKED LIME

1.2.1) MOLECULAR FORMULA
1) Ca-O

Available Forms Sources

A)

1) White or grayish white lumps or crystals which may be crushed or ground to a powder. Commercial calcium oxide may have a yellow or brown tint (Budavari, 1996).
2) BY-PRODUCT - Calcium reacts with water to form calcium hydroxide (Budavari, 1996).

B)

1) INDUSTRIAL USES -

a) Commonly found in food additives, fungicides and insecticides, sewage treatments, glass, lubricants, building materials (plaster, mortar, bricks, cement and stucco), paper groups, and non-ferrous smelting and refining techniques (OHM/TADS , 1994).
b) It is also used in the manufacture of steel, magnesium, and aluminum (Wands, 1981), as a laboratory agent to absorb calcium dioxide, and as a dehydrating agent (Sittig, 1991).
c) Additionally, it is used in dehairing hides and in the clarification of cane and beet sugar juice (Sittig, 1991).

2) MEDICAL USES -

a) Calcium oxide has been used experimentally in root canal dental procedures as an antibacterial medication (Cavalleri et al, 1990).
b) A paste, containing calcium oxide and sodium hydroxide and known as London paste, has been used as an escharotic (S Sweetman , 2002).

Overview

Life Support

A)

Clinical Effects

0.2.1)

A) USES: Calcium oxide is an alkaline irritant that becomes an alkaline corrosive material (calcium hydroxide) after reacting with water. It is commonly found in food additives, fungicides and insecticides, sewage treatments, glass, lubricants, building materials (plaster, mortar, bricks, cement and stucco), paper groups, and non-ferrous smelting and refining techniques.
B) TOXICOLOGY: As an alkaline corrosive, calcium oxide may cause liquefaction necrosis. It can saponify the fats in the cell membrane, destroying the cell and allowing deep penetration into mucosal tissue. In gastrointestinal tissue, an initial inflammatory phase may be followed by tissue necrosis (sometimes resulting in perforation), then granulation and finally stricture formation.
C) EPIDEMIOLOGY: Exposure is unusual; calcium oxide is generally available for industrial use only.
D) WITH POISONING/EXPOSURE

1) Limited data regarding specific human toxicity following calcium oxide exposure is available. The following effects could be expected to occur, based on exposure data of other alkaline corrosives.
2) 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) and are at risk for subsequent stricture formation, particularly esophageal. Some patients (particularly young children) may develop upper airway edema.

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

3) 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. Hypotension, tachycardia, tachypnea and, rarely, fever may develop. Stricture formation (esophageal, less often oral or gastric) is likely to develop long term. Esophageal carcinoma is another long term complication. Upper airway edema is common and often life threatening. Severe toxicity is generally limited to deliberate ingestions in adults in the US, because alkaline products available in the home are generally of low concentration.
4) INHALATION EXPOSURE: Mild exposure may cause cough and bronchospasm. Severe inhalation may cause upper airway edema and burns, stridor, and rarely acute lung injury.
5) OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal ischemia, permanent visual loss and in severe cases perforation.
6) DERMAL EXPOSURE: Mild exposure causes irritation and partial thickness burns. Prolonged exposure or high concentration products can cause full thickness burns.

0.2.3)

A) WITH POISONING/EXPOSURE

1) Increased respiratory rate and/or dyspnea may be present.
2) Hypotension may result.
3) Increased temperature may occur in severe cases if infection is present.
4) Pulse rate may be increased.

0.2.4)

A) WITH POISONING/EXPOSURE

1) May cause severe irritation or thermal burns of the eyes, resulting in lacrimation, spasmodic blinking, ulceration, and ocular perforation.
2) Significant nasal irritation, ulceration and perforation of the nasal septum have been attributed to inhalation of calcium oxide dust.
3) Inflammation of the throat, buccal mucosa, and respiratory tract may result from exposure to calcium oxide dust.
4) Ingestion of calcium oxide may result in esophageal burns and ulcerations. Dysphagia and drooling may be present.

0.2.5)

A) WITH POISONING/EXPOSURE

1) Marked reductions in systemic vascular resistance, cardiac output and circulatory shock are possible following ingestion of calcium oxide, based on information about other alkaline ingestions.

0.2.6)

A) WITH POISONING/EXPOSURE

1) Calcium oxide dust is irritating and may be caustic to the mucous membranes of the upper respiratory tract, causing inflammation and possibly pneumonia, pulmonary edema, and/or bronchitis. Airway burns resulted from severe exposure in an industrial accident.

0.2.8)

A) WITH POISONING/EXPOSURE

1) Spontaneous emesis, abdominal pain and dysphagia with drooling may be present.
2) In severe ingestions, burns, bleeding and perforation can occur.

0.2.10)

A) WITH POISONING/EXPOSURE

1) Oliguria may result following ingestion if massive blood loss occurs due to gastroesophageal burns, ulceration and/or perforation.

0.2.13)

A) WITH POISONING/EXPOSURE

1) Hematocrit may fall in cases of ingestions with blood loss.

0.2.14)

A) WITH POISONING/EXPOSURE

1) Calcium oxide produces skin burns, nasal ulceration and septum perforation. Dermatitis, skin thickening, cracking of the skin and brittleness of the nails have been reported.

0.2.20)

A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

0.2.21)

A) No information regarding possible carcinogenic effects of calcium oxide as a single exposure were found at the time of this review.
B) Oral squamous cell carcinoma was detected in 77 percent of 169 New Guinea persons who chewed powdered slaked lime applied to Areca nuts.

Laboratory Monitoring

A)

B)

C)

D)

E)

Treatment Overview

0.4.2)

A) As there is little data on exposure to calcium oxide, the following treatment information is based on experience with other alkaline corrosive agents.
B) MANAGEMENT OF MILD TO MODERATE ORAL TOXICITY

1) Perform early (within 12 hours) endoscopy in patients with stridor, drooling, vomiting, significant oral burns, difficulty swallowing or abdominal pain, and in all patients with deliberate ingestion. 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.

C) 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.

D) DILUTION

1) Dilute with 4 to 8 ounces of water may be useful if it can be performed shortly after ingestion in patients who are able to swallow, with no vomiting or respiratory distress; then the patient should be NPO until assessed for the need for endoscopy. Neutralization, activated charcoal, and gastric lavage are all contraindicated.

E) AIRWAY MANAGEMENT

1) Aggressive airway management in patients with deliberate ingestions or any indication of upper airway injury.

F) ANTIDOTE

1) None

G) ENDOSCOPY

1) Should be performed as soon as possible (preferably within 12 hours, not more than 24 hours) in any patient with deliberate ingestion, adults with any signs or symptoms attributable to inadvertent ingestion, and in children with stridor, vomiting, or drooling after inadvertent ingestion. Endoscopy should also be considered in children with dysphagia or refusal to swallow, significant oral burns, or abdominal pain after unintentional ingestion. Children and adults who are asymptomatic after inadvertent ingestion do not require endoscopy. 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 burns.

H) 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.

I) 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.

J) 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.

K) PATIENT DISPOSITION

1) OBSERVATION CRITERIA: Patients with alkaline corrosive ingestion should be sent to a health care facility for evaluation. Patients who remain asymptomatic over 4 to 6 hours of observation, and those with endoscopic evaluation that demonstrates no burns or only minor grade I burns and who can tolerate oral intake can be discharged 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, 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 corrosive eye injury should be evaluated by an ophthalmologist.

M) DIFFERENTIAL DIAGNOSIS

1) Acid ingestion, gastrointestinal hemorrhage, or perforated viscus.

0.4.3)

A) DECONTAMINATION

1) Administer oxygen as necessary. Monitor for respiratory distress.

B) AIRWAY MANAGEMENT

1) Manage airway aggressively in patients with significant respiratory distress, stridor or any evidence of upper airway edema. Monitor for hypoxia or respiratory distress.

C) BRONCHOSPASM

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

0.4.4)

A) DECONTAMINATION

1) Exposed eyes should be irrigated with copious amounts of 0.9% saline for at least 30 minutes, until pH is neutral and the cul de sacs are free of particulate material.
2) An eye examination should always be performed, including slit lamp examination. Ophthalmologic consultation should be obtained. Antibiotics and mydriatics may be indicated.

0.4.5)

A) OVERVIEW

1) DECONTAMINATION

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

Range Of Toxicity

A)

B)

C)

Clinical Effects

Summary Of Exposure

A)

B)

C)

D)

1) Limited data regarding specific human toxicity following calcium oxide exposure is available. The following effects could be expected to occur, based on exposure data of other alkaline corrosives.
2) 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) and are at risk for subsequent stricture formation, particularly esophageal. Some patients (particularly young children) may develop upper airway edema.

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

3) 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. Hypotension, tachycardia, tachypnea and, rarely, fever may develop. Stricture formation (esophageal, less often oral or gastric) is likely to develop long term. Esophageal carcinoma is another long term complication. Upper airway edema is common and often life threatening. Severe toxicity is generally limited to deliberate ingestions in adults in the US, because alkaline products available in the home are generally of low concentration.
4) INHALATION EXPOSURE: Mild exposure may cause cough and bronchospasm. Severe inhalation may cause upper airway edema and burns, stridor, and rarely acute lung injury.
5) OCULAR EXPOSURE: Ocular exposure can produce severe conjunctival irritation and chemosis, corneal epithelial defects, limbal ischemia, permanent visual loss and in severe cases perforation.
6) DERMAL EXPOSURE: Mild exposure causes irritation and partial thickness burns. Prolonged exposure or high concentration products can cause full thickness burns.

Vital Signs

3.3.1)

A) WITH POISONING/EXPOSURE

1) Increased respiratory rate and/or dyspnea may be present.
2) Hypotension may result.
3) Increased temperature may occur in severe cases if infection is present.
4) Pulse rate may be increased.

3.3.2)

A) WITH POISONING/EXPOSURE

1) Increased respiratory rate, depth of inspirations and minute volume have been reported in exposed workers (Lemyasev, 1964). Dyspnea may be present (OSHA, 1990).

3.3.3)

A) WITH POISONING/EXPOSURE

1) Elevated temperature should be anticipated if infection and/or ulcerative esophagitis are present.

3.3.4)

A) WITH POISONING/EXPOSURE

1) Ingestion of other alkalies has resulted in hypotension or shock when significant esophageal or gastric ulcerations, perforations and blood loss were present (Dreisbach & Robertson, 1987; Previtera et al, 1990).

3.3.5)

A) WITH POISONING/EXPOSURE

1) Increased pulse rate may occur in severe cases due to shock syndrome.

Heent

3.4.1)

A) WITH POISONING/EXPOSURE

1) May cause severe irritation or thermal burns of the eyes, resulting in lacrimation, spasmodic blinking, ulceration, and ocular perforation.
2) Significant nasal irritation, ulceration and perforation of the nasal septum have been attributed to inhalation of calcium oxide dust.
3) Inflammation of the throat, buccal mucosa, and respiratory tract may result from exposure to calcium oxide dust.
4) Ingestion of calcium oxide may result in esophageal burns and ulcerations. Dysphagia and drooling may be present.

3.4.3)

A) WITH POISONING/EXPOSURE

1) ULCERATION AND PERFORATION: Ulceration and perforation can occur and may be delayed about a week after an initial burn from alkalies (Bernardino & Lawson, 1977; Potts, 1996).
2) BURNS: Severe burns can result from ocular exposure to calcium oxide. The effects are similar to those caused by calcium hydroxide, with sequelae possibly including corneal opacification, ulceration, perforation, and glaucoma (Grant & Schuman, 1993).

a) CASE SERIES: Twenty-seven cases of ocular burns resulting from calcium oxide have been reviewed by Rozenbaum et al (1991). Reported effects included (Rozenbaum et al, 1991):

1) Corneal erosion in 25 out of 27 cases
2) Conjunctival erosion in 16 out of 27 cases
3) Conjunctival congestion in all cases
4) Conjunctival chemosis in 6 out of 27 cases

b) CASE SERIES: Among 57 cases of ocular burns due to calcium oxide, 51 cases healed within 48 hours, 3 healed in 3 to 10 days, and 3 experienced residual impairment of vision. Two cases with impaired vision did not have first aid or other medical treatment shortly after exposure (McLaughlin, 1946).

3) CORNEAL OPACIFICATION: Effects similar to calcium hydroxide including (Grant & Schuman, 1993):

a) MILD LIME BURNS: Immediate, superficial opacification of the cornea, with a frosted or groundglass appearance and appreciable loss of epithelium. A layer of epithelium may regenerate over the cornea, appearing like calcific band keratopathy.
b) MODERATE TO SEVERE LIME BURNS generally result from prolonged exposure. Stromal opacification occurs. Severely burned corneas may have sensation loss for several days after the injury.

4) IRRITATION: Severe irritation of the eyes may occur from calcium oxide dust or particles (OSHA, 1990; Rozenbaum et al, 1991; HSDB , 2002).

a) CASE REPORT: Bilateral conjunctivitis, corneal abrasions and injection of the sclera were reported in a 20-year-old man who was involved in an explosion resulting from the addition of calcium oxide to acidic industrial wastes. The man was exposed to calcium oxide powder and by-products generated from the chemical reactions (Bonatucci et al, 1984).
b) CASE REPORTS: Pain, impaired vision, tearing and photophobia developed in two cases exposed to calcium oxide dust from construction sites (Rozenbaum et al, 1991).

5) LACRIMATION may result from contact (Sittig, 1991; Rozenbaum et al, 1991).
6) BLINKING: Spasmodic blinking may occur from contact (Sittig, 1991).

3.4.5)

A) WITH POISONING/EXPOSURE

1) IRRITATION: Severe nasal irritation can result from dust inhalation (OSHA, 1990; Sittig, 1991; Hathaway et al, 1996).
2) ULCERATION AND PERFORATION: Exposure to the dust may result in nasal ulceration and perforation of the septum (OSHA, 1990; Hathaway et al, 1996).

3.4.6)

A) WITH POISONING/EXPOSURE

1) CIRCUMORAL BURNS: Burns to the lips, mouth and laryngopharynx may be present.

a) A study of pediatric cases of caustic ingestions found that burns of the cheeks, lips and/or oropharynx suggest the presence of serious visceral burns, but the absence of circumoral lesions cannot be used to exclude the likelihood of visceral burns (Previtera et al, 1990). Calcium oxide was not specifically mentioned in this study.

2) ESOPHAGEAL BURNS and ULCERATION may follow ingestion of calcium oxide or other alkaline corrosives (Crain et al, 1984; Gorman et al, 1989).
3) ESOPHAGEAL STENOSIS can occur after ingestion of caustic chemicals (Alford & Harris, 1959; Previtera et al, 1990).
4) DYSPHAGIA, STRIDOR and DROOLING may result from injury to the epiglottis, vocal cords, trachea and esophagus following ingestion of caustic chemicals (Crain et al, 1984; Gorman et al, 1989).

a) Children who ingest caustic chemicals can appear asymptomatic despite the presence of visceral lesions (Previtera et al, 1990). The cases reviewed principally involved sodium hypochloride, sodium hydroxide or ammonia ingestions.

5) INFLAMMATION of throat and buccal mucosa can result from exposure to the dust (Hathaway et al, 1991) or from ingestion.

a) CASE REPORT: A 46-year-old woman developed erythema and swelling of the lips and buccal mucosa after ingesting a few mouthfuls of cement powder containing 22% CaO, 7% silica and 66% granite (Shibata et al, 1995).

Cardiovascular

3.5.1)

A) WITH POISONING/EXPOSURE

1) Marked reductions in systemic vascular resistance, cardiac output and circulatory shock are possible following ingestion of calcium oxide, based on information about other alkaline ingestions.

3.5.2)

A) HYPOTENSIVE EPISODE

1) WITH POISONING/EXPOSURE

a) Marked reductions in systemic vascular resistance may occur following ingestion due to blood loss from gastroesophageal ulcerations, based on information about other alkaline ingestions.

B) HYPOVOLEMIA

1) WITH POISONING/EXPOSURE

a) Severe poisoning is associated with hypovolemia accompanied by a 65% to 70% increase in hematocrit. Reduced mass of circulating blood is reported at 50% of normal in extremely severe cases. An increase in overall peripheral resistance is also reported.
b) Stroke and minute cardiac volumes reduced to 30% of normal are associated with impaired nonperipheral circulation and microcirculation resulting in shock (Luzhnikov & Kostomarova, 1976; Luzhnikov & Kostomarova, 1978).

Respiratory

3.6.1)

A) WITH POISONING/EXPOSURE

1) Calcium oxide dust is irritating and may be caustic to the mucous membranes of the upper respiratory tract, causing inflammation and possibly pneumonia, pulmonary edema, and/or bronchitis. Airway burns resulted from severe exposure in an industrial accident.

3.6.2)

A) BURN OF RESPIRATORY TRACT

1) WITH POISONING/EXPOSURE

a) CASE REPORT: Hypoxia, stridor, upper airway burns and pulmonary infiltrates developed in a 20-year-old man who sustained an inhalation injury after adding crystals of calcium oxide to an acidic solution of industrial waste which resulted in explosion of the slurry (Bonatucci et al, 1984).

1) Chest radiograph and xenon lung scans did not demonstrate pulmonary injury until 4 days after the event despite persistent hypoxemia.

B) ACUTE LUNG INJURY

1) WITH POISONING/EXPOSURE

a) Although not frequently reported from calcium oxide exposure, alkaline chemicals may produce pulmonary edema if they reach the lower respiratory tract (Hoffman, 1994).
b) Inhalation of dry cement dust (contains calcium oxide and other chemicals) was associated with acute respiratory irritation, progressing to respiratory insufficiency in one case. Cough, dyspnea, sore throat and wheezing were present (Turchen et al, 1993).

C) INJURY OF UPPER RESPIRATORY TRACT

1) WITH POISONING/EXPOSURE

a) Inflammation of the mucous membranes of the upper respiratory tract is not uncommon after exposure to the dust (Sittig, 1991; OSHA, 1990). Inflammation of the supraglottis and tracheobronchial regions occurred in a case exposed during an explosion of an acidic industrial waste slurry to which calcium oxide crystals had been added (Bonatucci et al, 1984).

D) PNEUMONITIS

1) WITH POISONING/EXPOSURE

a) Pneumonia may result from exposure (S Sweetman , 2002; Sittig, 1991; OSHA, 1990).
b) Dry cement may contain 60% to 67% calcium oxide in addition to other chemicals (Finkel, 1983; Sax & Lewis, 1989). In a series of 6 patients evaluated after swallowing cement, 1 adult developed bronchopneumonia and a child developed aspiration pneumonitis (Visvanathan, 1986).
c) Pneumonia developed in one case as a complication of pulmonary injury incurred during an industrial explosion involving calcium oxide crystals and acidic industrial wastes (Bonatucci et al, 1984).

E) IRRITATION SYMPTOM

1) WITH POISONING/EXPOSURE

a) Inhalation of calcium oxide dust can result in upper respiratory and pulmonary irritation, with a sensation of chest tightness and pain, dyspnea and coughing (OSHA, 1990).

Gastrointestinal

3.8.1)

A) WITH POISONING/EXPOSURE

1) Spontaneous emesis, abdominal pain and dysphagia with drooling may be present.
2) In severe ingestions, burns, bleeding and perforation can occur.

3.8.2)

A) CHEMICAL BURN

1) WITH POISONING/EXPOSURE

a) Gastric burns can occur from ingestion of caustics (Gorman et al, 1989; Previtera et al, 1990).

B) GASTRIC ULCER WITH PERFORATION

1) WITH POISONING/EXPOSURE

a) Little information is available concerning calcium oxide ingestions. Ingestion of other caustic chemicals has resulted in gastric ulceration and perforation (Gorman et al, 1989; Previtera et al, 1990).

C) VOMITING

1) WITH POISONING/EXPOSURE

a) Spontaneous vomiting may occur after ingestion of caustic chemicals (Crain et al, 1984; Gorman et al, 1989).

D) ABDOMINAL PAIN

1) WITH POISONING/EXPOSURE

a) Extreme abdominal pain or cramps can occur after ingestion of caustic chemicals (Gorman et al, 1989; Previtera et al, 1990).

Genitourinary

3.10.1)

A) WITH POISONING/EXPOSURE

1) Oliguria may result following ingestion if massive blood loss occurs due to gastroesophageal burns, ulceration and/or perforation.

3.10.2)

A) OLIGURIA

1) WITH POISONING/EXPOSURE

a) Oliguria may result if massive blood loss (> 15%) occurs following ingestion resulting in significant gastroesophageal burns, ulceration and/or perforation.

Hematologic

3.13.1)

A) WITH POISONING/EXPOSURE

1) Hematocrit may fall in cases of ingestions with blood loss.

3.13.2)

A) ANEMIA

1) WITH POISONING/EXPOSURE

a) Hematocrit may decrease in cases of ingestion where blood loss is significant.

Dermatologic

3.14.1)

A) WITH POISONING/EXPOSURE

1) Calcium oxide produces skin burns, nasal ulceration and septum perforation. Dermatitis, skin thickening, cracking of the skin and brittleness of the nails have been reported.

3.14.2)

A) CHEMICAL BURN

1) WITH POISONING/EXPOSURE

a) Skin burns can result (Herbert & Lawrence, 1989; Hathaway et al, 1996).
b) Calcium oxide reacts with perspiration, skin moisture, or water to produce calcium hydroxide, pH 12.4 to 12.5. Immediate discomfort may not be noticed; severe burns are frequently the result of prolonged exposure (Stewart, 1985).
c) Cement can contain up to 67% calcium oxide (Flowers, 1978). Partial- to full-thickness burns and necrosis of the toes, soles of the feet, knees, or hands have been reported from exposure to cement water or wet cement (Rowe, 1963; Fisher, 1979; Vickers & Edwards, 1976; Skiendzielewski, 1980; Koo et al, 1992) or lime dust, which is similar to cement in that it also contains calcium oxide and calcium hydroxide (Farkas, 1981). Immediate symptoms often were absent. The skin developed a green discoloration, pain, erythema, edema or blisters, generally 3 to 24 hours after initial exposure.

B) ULCER OF NOSE

1) WITH POISONING/EXPOSURE

a) Nasal ulceration and perforation of the nasal septum have been attributed to inhalation of calcium oxide dust (OSHA, 1990).

C) NAIL FINDING

1) WITH POISONING/EXPOSURE

a) Fissuring and brittleness of the nails can result from topical exposure (Hathaway et al, 1996).

D) DERMATITIS

1) WITH POISONING/EXPOSURE

a) Extreme dryness and cracking of the skin may occur with topical exposure. Dermatitis with desquamation and vesicular rash is common (Sittig, 1991).

Reproductive

3.20.1)

A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

3.20.2)

A) LACK OF INFORMATION

1) At the time of this review, no data were available to assess the teratogenic potential of this agent.

3.20.3)

A) LACK OF INFORMATION

1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

3.21.1)

A) IARC Carcinogenicity Ratings for CAS1305-78-8 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):

1) Not Listed

3.21.2)

A) No information regarding possible carcinogenic effects of calcium oxide as a single exposure were found at the time of this review.
B) Oral squamous cell carcinoma was detected in 77 percent of 169 New Guinea persons who chewed powdered slaked lime applied to Areca nuts.

3.21.3)

A) LACK OF INFORMATION

1) No information regarding possible carcinogenic effects of calcium oxide as a single exposure were found at the time of this review (IARC, 1987; OSHA, 1990) NIOSH, 1994; (US DHHS, 1994; HSDB , 1996; REPROTEXT(R) , 1996) RTECS, 1996).

B) MOUTH CARCINOMA

1) The use of calcium oxide with betel nut (Thomas & MacLennan, 1992; Jeng et al, 1994), as a component of pan masala, a mixture of areca nut, calcium oxide, catechu and flavoring agents (Patel et al, 1994) 1994a) or as a component of nas, a mixture of tobacco, calcium oxide, ash and cotton oil (Zaridze et al, 1986) have been associated with oral cancer, precarcinogenic effects and/or genotoxic effects.
2) The direct contribution of calcium oxide has not been established. Chemicals other than calcium oxide in these preparations are highly carcinogenic and/or cytotoxic.

C) ESOPHAGEAL CARCINOMA

1) Esophageal carcinoma has been reported in patients at the site of corrosive-induced strictures or injury (Benedict, 1941) Bigelow, 1953; Appelqvist & Salmo, 1980; Isolauri & Markkula, 1989). Lye was associated with cancer in these studies.

Genotoxicity

A)

Laboratory Monitoring

Monitoring Parameters Levels

4.1.1)

A) Obtain a complete blood count in symptomatic patients following calcium oxide 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, serum electrolytes, INR, PTT, type and crossmatch for blood, and monitor urine output. 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 II or III burns, to evaluate for strictures.

4.1.2)

A) HEMATOLOGIC

1) Obtain a complete blood count in patients with symptomatic calcium oxide ingestion.

B) COAGULATION STUDIES

1) In patients with signs and symptoms suggesting severe burns, perforation, or bleeding, obtain renal function tests, PT or INR, PTT, and type and crossmatch for blood.

4.1.3)

A) OTHER

1) Monitor urine output in patients with significant gastrointestinal burns, perforation, or bleeding.

4.1.4)

A) OTHER

1) MONITORING

a) Monitor pulse oximetry or arterial blood gases in patients with signs and symptoms suggestive of upper airway burns.
b) Eso-gastro-duodenoscopy within 24 hours of exposure has been recommended for obvious or suspected caustic ingestions (Previtera et al, 1990).
c) The pH of the exposed eye or skin may be determined with the use of pH paper or dipstick in order to check the adequacy of irrigation. Ideally the pH should be neutral (Pfister & Koski, 1982; Stewart, 1985) Driesbach & Robertson, 1987).

Radiographic Studies

A)

1) Obtain an upright chest x-ray in patients with significant signs and symptoms to evaluate for pneumomediastinum or free air under the diaphragm.
2) The absence of these findings does not rule out the possibility of necrosis or perforation of the esophagus or stomach (Davis et al, 1972; Allen et al, 1970).
3) Obtain a chest x-ray in patients with significant pulmonary signs or symptoms.
4) A water-soluble contrast material should be used initially to exclude esophageal perforation in patients with GI burns associated with alkaline ingestions, as water soluble contrast causes less injury than barium if it extravasates into tissue (Kirsh & Ritter, 1976; Chen et al, 1988).
5) Barium esophagogram performed once perforation has been excluded may be useful to evaluate extent of injury or presence of strictures (Leape et al, 1971; Lowe et al, 1979; Chen et al, 1988).

Treatment

Life Support

A)

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, 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 alkaline corrosive ingestion should be sent to a health care facility for evaluation. Patients who remain asymptomatic over 4 to 6 hours of observation, and those with endoscopic evaluation that demonstrates no burns or only minor grade I burns and who can tolerate oral intake can be discharged home.

Monitoring

A)

B)

C)

D)

E)

Oral Exposure

6.5.1)

A) SUMMARY

1) Activated charcoal, lavage, and neutralization are contraindicated.
2) Residual perioral alkali should be rinsed with milk or water.

B) GASTRIC/MUCOSAL DECONTAMINATION

1) MUCOSAL DECONTAMINATION: 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. Patients should not be forced to drink after ingestion of an acid, nor should they be allowed to drink larger volumes since this may induce vomiting, and thereby re-exposure of the injured tissues to the corrosive acid. Dilution may only be helpful if performed in the first seconds to minutes after ingestion.
2) GASTRIC DECONTAMINATION: Ipecac contraindicated. Activated charcoal is not recommended as it may interfere with endoscopy and will not reduce injury to GI mucosa. Consider insertion of a small, flexible nasogastric or orogastric tube to suction gastric contents after recent large ingestion of a strong acid; the risk of further mucosal injury or iatrogenic esophageal perforation must be weighed against potential benefits of removing any remaining acid from the stomach.

6.5.2)

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, 1994a; Homan et al, 1995), 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, 1985; Rumack & Burrington, 1977; Homan et al, 1995; Homan et al, 1994a; 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) NEUTRALIZATION

1) The use of neutralizing agents after caustic ingestion is NOT recommended. Neutralization has the potential to generate gas and cause exothermic reactions which might worsen injury.
2) Experimental studies suggest that neutralization generates heat, does not limit injury unless performed immediately and that very large volumes of fluid are required to reach neutral pH (Homan et al, 1995a) Maull et al, 1985; (Rumack & Burrington, 1977a).
3) In an in vitro model, 5% acetic acid was more effective than water at neutralizing 1.8% sodium hydroxide, but caused a greater increase in temperature (Maull et al, 1985).

C) GASTRIC EMPTYING

1) Should be avoided to prevent reexposure of the esophagus to the corrosive agent.

D) NASOGASTRIC SUCTION

1) Some clinicians may choose to insert a small, flexible nasogastric tube through the mouth, if the patient is alert and cooperative, in an attempt to remove the corrosive substance following a recent ingestion.

a) The decision should be based on the amount of the ingestion, the concentration of the alkaline material, the type of product ingested, and the risk and potential benefit to the patient.
b) In the typical pediatric ingestion involving small volumes of corrosive materials, nasogastric suction is unlikely to be of benefit. In suicidal ingestions involving large quantities of material and an increased likelihood of severe mucosal burns, the risk of causing perforation may outweigh the potential benefit of removing caustic material.

E) ACTIVATED CHARCOAL

1) Since the hazard of alkaline corrosive ingestion stems from local tissue injury and not from systemic absorption of toxicant, activated charcoal is not of benefit. Charcoal administration may worsen injury by causing vomiting and may interfere with the ability to visualize burns at endoscopy.

6.5.3)

A) DILUTION

1) Do not exceed 8 ounces in adults and 4 ounces in children (Consensus, 1988), as vomiting may occur with excessive fluid. Contraindications include perforations and patients at risk of vomiting. Keep patient NPO following initial dilution until after medical/surgical evaluation.

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

B) ENDOSCOPIC PROCEDURE

1) SUMMARY: Obtain consultation concerning endoscopy as soon as possible, and perform endoscopy within the first 24 hours when indicated.
2) INDICATIONS: Endoscopy should be performed in adults with a history of deliberate ingestion, adults with any signs or symptoms attributable to inadvertent ingestion, and in children with stridor, vomiting, or drooling after unintentional ingestion (Crain et al, 1984a). Endoscopy should also be performed in children with dysphagia or refusal to swallow, significant oral burns, or abdominal pain after unintentional ingestion (Gaudreault et al, 1983; Nuutinen et al, 1994). Children and adults who are asymptomatic after accidental ingestion do not require endoscopy (Gupta et al, 2001; Lamireau et al, 2001; Gorman et al, 1992).
3) RISKS: Numerous large case series attest to the relative safety and utility of early endoscopy in the management of caustic ingestion.

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

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.
7) SCINTIGRAPHY - Scans utilizing radioisotope labelled sucralfate (technetium 99m) were performed in 22 patients with caustic ingestion and compared with endoscopy for the detection of esophageal burns. Two patients had minimal residual isotope activity on scanning but normal endoscopy and two patients had normal activity on scan but very mild erythema on endoscopy. Overall the radiolabeled sucralfate scan had a sensitivity of 100%, specificity of 81%, positive predictive value of 84% and negative predictive value of 100% for detecting clinically significant burns in this population (Millar et al, 2001). This may represent an alternative to endoscopy, particularly in young children, as no sedation is required for this procedure. Further study is required.
8) MINIPROBE ULTRASONOGRAPHY - was performed in 11 patients with corrosive ingestion . Findings were categorized as grade 0 (distinct muscular layers without thickening, grade I (distinct muscular layers with thickening), grade II (obscured muscular layers with indistinct margins) and grade III (muscular layers that could not be differentiated). Findings were further categorized as to whether the worst appearing image involved part of the circumference (type a) or the whole circumference (type b). Strictures did not develop in patients with grade 0 (5 patients) or grade I (4 patients) lesions. Transient stricture formation developed in the only patient with grade IIa lesions, and stricture requiring repeated dilatation developed in the only patient with grade IIIb lesions (Kamijo et al, 2004).

C) 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).

D) SURGICAL PROCEDURE

1) SUMMARY: Initially if severe esophageal burns are found a string may be placed in the stomach to facilitate later dilation. Insertion of a specialized nasogastric tube after confirmation of a circumferential burn may prevent strictures. Dilation is indicated after 2 to 4 weeks if strictures are confirmed. If dilation is unsuccessful colonic intraposition or gastric tube placement may be needed. Early laparotomy should be considered in patients with evidence of severe esophageal or gastric burns on endoscopy.
2) STRING - If a second degree or circumferential burn of the esophagus is found a string may be placed in the stomach to avoid false channel and to provide a guide for later dilation procedures (Gandhi et al, 1989).
3) STENT - The insertion of a specialized nasogastric tube or stent immediately after endoscopically proven deep circumferential burns is preferred by some surgeons to prevent stricture formation (Mills et al, 1978; (Wijburg et al, 1985; Coln & Chang, 1986).

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

4) DILATION - Dilation should be performed at 1 to 4 week intervals when stricture is present(Gundogdu et al, 1992). Repeated dilation may be required over many months to years in some patients. Successful dilation of gastric antral strictures has also been reported (Hogan & Polter, 1986; Treem et al, 1987).
5) COLONIC REPLACEMENT - Intraposition of colon may be necessary if dilation fails to provide an adequate sized esophagus (Chiene et al, 1974; Little et al, 1988; Huy & Celerier, 1988).
6) LAPAROTOMY/LAPAROSCOPY - Several authors advocate laparotomy or laparoscopy in patients with endoscopic evidence of severe esophageal or gastric burns to evaluate for the presence of transmural gastric or esophageal necrosis (Cattan et al, 2000; Estrera et al, 1986; Meredith et al, 1988; Wu & Lai, 1993).

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

E) FLUID/ELECTROLYTE BALANCE REGULATION

1) Fluid and electrolyte replacement may be necessary in cases of hypovolemia or lactic acidosis due to severe tissue burns and shock.

F) ANTIBIOTIC

1) Antibiotics may be indicated for specific infections.

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) GENERAL TREATMENT

1) Manage airway aggressively. Intubate any patient with significant stridor, respiratory distress or upper airway edema. Be prepared to perform cricothyroidotomy as intubation may be difficult secondary to edema.
2) CAUSTIC INHALATION: Administer humidified oxygen, and remove from exposure. Monitor patient for respiratory distress; if a cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, and pneumonitis.
3) Patients with upper airway burns may develop significant edema abruptly; early intubation is advised.
4) Determine pulse oximetry and/or blood gases, obtain chest x-ray, perform endotracheal intubation and provide mechanical ventilation as clinically indicated.
5) Administer inhaled beta2-adrenergic agonists in patients with bronchospasm (National Heart,Lung,and Blood Institute, 2007). If acute lung injury develops, consider PEEP (Haas, 2011; Leaver & Evans, 2007; Stolbach & Hoffman, 2011).
6) Evaluate for esophageal, dermal and eye burns as indicated.

B) 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).

C) BRONCHOSPASM

1) BRONCHOSPASM SUMMARY

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

2) ALBUTEROL/ADULT DOSE

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

3) ALBUTEROL/PEDIATRIC DOSE

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

4) ALBUTEROL/CAUTIONS

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

5) CORTICOSTEROIDS

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

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

Eye Exposure

6.8.1)

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

1) Continue irrigation for at least an hour or until the superior and inferior cul-de-sacs have returned to neutrality (check pH every 30 minutes), pH of 7.0 to 8.0, and remain so for 30 minutes after irrigation is discontinued (Spector & Fernandez, 2008; Brodovsky et al, 2000). After severe alkaline burns, the pH of the conjunctival sac may only return to a pH of 8 or 8.5 even after extensive irrigation (Grant & Schuman, 1993a). Irrigating volumes up to 20 L or more have been used to neutralize the pH (Singh et al, 2013; Fish & Davidson, 2010). Immediate and prolonged irrigation is associated with improved visual acuity, shorter hospital stay and fewer surgical interventions (Kuckelkorn et al, 1995; Saari et al, 1984).
2) Search the conjunctival sac for solid particles and remove them while continuing irrigation (Grant & Schuman, 1993a).
3) For significant alkaline or concentrated acid burns with evidence of eye injury irrigation should be continued for at least 2 to 3 hours, potentially as long as 24 to 48 hours if pH not normalized, in an attempt to normalize the pH of the anterior chamber (Smilkstein & Fraunfelder, 2002). Emergent ophthalmologic consultation is needed in these cases (Spector & Fernandez, 2008).

B) DEPOSITS

1) Remove deposits immediately via vigorous irrigation with water or saline to dislodge particles mechanically. A pulsatile jet stream irrigation (Grant, 1986) or other devices which provide continuous irrigation (Burns et al, 1989) may be useful.
2) Swab or brush material from the fornices after double everting the lids. This procedure may be facilitated by application of a local anesthetic and use of a 0.01 to 0.05 M disodium edetate (EDTA) at pH 4.6 to 7 (Grant & Schuman, 1993) Burns et al, 1989).

6.8.2)

A) EDETATE CALCIUM DISODIUM

1) Immediate irrigation with water or saline followed by an irrigation with 0.01 to 0.05 M EDTA solution is recommended. Irrigate with EDTA for at least 15 minutes to remove any finely granular ground-glass film of opacity at the level of Bowman's membrane (Grant & Schuman, 1993).

B) BURN

1) 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.

C) ANALGESIC

1) Topical analgesics may be necessary (Rozenbaum et al, 1991).

D) 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) 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

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).

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).

3) 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

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).

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).

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).

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).

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).

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.

4) 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).

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

Dermal Exposure

6.9.1)

A) PERSONNEL PROTECTION

1) Rescuers and other health care personnel should use appropriate protective equipment to prevent exposure.

B) CLOTHING

1) Immediately remove contaminated clothing, including footwear.

C) DERMAL DECONTAMINATION

1) Brush off particles of calcium oxide from intact skin and debride particulates from any wounds either before or during irrigation.
2) Irrigate immediately with normal saline or water under low pressure, taking care to avoid splashing contaminated fluid into the patient's eyes.

D) MULTIPLE WASHES

1) Two hours of shower alternating with a rest period for up to 24 hours of irrigation has been recommended in severe cases (Stewart, 1985). Disappearance of the "soapy" feeling to the skin and the use of pH paper or dipstick to measure pH (should be neutral) have been recommended as methods to indirectly assess adequacy of irrigation (Stewart, 1985; Dreisbach & Robertson, 1987).

6.9.2)

A) BURN

1) APPLICATION

a) These recommendations apply to patients with MINOR chemical burns (FIRST DEGREE; SECOND DEGREE: less than 15% body surface area in adults; less than 10% body surface area in children; THIRD DEGREE: less than 2% body surface area). Consultation with a clinician experienced in burn therapy or a burn unit should be obtained if larger area or more severe burns are present. Neutralizing agents should NOT be used.

2) DEBRIDEMENT

a) After initial flushing with large volumes of water to remove any residual chemical material, clean wounds with a mild disinfectant soap and water.
b) DEVITALIZED SKIN: Loose, nonviable tissue should be removed by gentle cleansing with surgical soap or formal skin debridement (Moylan, 1980; Haynes, 1981). Intravenous analgesia may be required (Roberts, 1988).
c) BLISTERS: Removal and debridement of closed blisters is controversial. Current consensus is that intact blisters prevent pain and dehydration, promote healing, and allow motion; therefore, blisters should be left intact until they rupture spontaneously or healing is well underway, unless they are extremely large or inhibit motion (Roberts, 1988; Carvajal & Stewart, 1987).

3) TREATMENT

a) TOPICAL ANTIBIOTICS: Prophylactic topical antibiotic therapy with silver sulfadiazine is recommended for all burns except superficial partial thickness (first-degree) burns (Roberts, 1988). For first-degree burns bacitracin may be used, but effectiveness is not documented (Roberts, 1988).
b) SYSTEMIC ANTIBIOTICS: Systemic antibiotics are generally not indicated unless infection is present or the burn involves the hands, feet, or perineum.
c) WOUND DRESSING:

1) Depending on the site and area, the burn may be treated open (face, ears, or perineum) or covered with sterile nonstick porous gauze. The gauze dressing should be fluffy and thick enough to absorb all drainage.
2) Alternatively, a petrolatum fine-mesh gauze dressing may be used alone on partial-thickness burns.

d) DRESSING CHANGES:

1) Daily dressing changes are indicated if a burn cream is used; changes every 3 to 4 days are adequate with a dry dressing.
2) If dressing changes are to be done at home, the patient or caregiver should be instructed in proper techniques and given sufficient dressings and other necessary supplies.

e) Analgesics such as acetaminophen with codeine may be used for pain relief if needed.

4) TETANUS PROPHYLAXIS

a) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.

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

Abstracts

Case Reports

A)

1) A 42-year-old woman developed a caustic ulcer on her feet and ankles as a result of direct contact with lime dust she was using to fertilize an acid soil. The patient wore rubber boots and the lime dust inadvertently seeped into them where perspiration dissolved the lime.

a) Within 6 hours, a burning erythema developed. Within 24 hours, a brown-black necrotic crust developed over the affected area. Shedding of the crust and scar formation ensued (Farkas, 1981).

2) Seventy-five workers exposed to quicklime dust were compared to controls for study of lung function. Measurements of vital capacity (VC), FEV, Tiffeneau, residual volume, and diffusion capacity were carried out.

a) The workers exposed to calcium oxide dust consistently were reported to exhibit abnormal pulmonary function tests as compared to controls. Smokers exhibited poorer test results than non-smokers (Lahaye et al, 1987).

Range Of Toxicity

Summary

A)

B)

C)

Minimum Lethal Exposure

A)

1) The minimum lethal human dose to this agent has not been delineated.
2) INHALATION - Dust concentrations in air of 25 mg/m(3) are considered immediately dangerous to life or health (NIOSH, 1994).

Maximum Tolerated Exposure

A)

1) Strong nasal irritation resulted from exposure to a mixture of dusts containing calcium oxide in the range of 25 mg/m(3), but levels of 9 to 10 mg/m(3) produced no observable irritation (Hathaway et al, 1996).

Workplace Standards

A)

1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.

a) Adopted Value

1) Calcium oxide

a) TLV:

1) TLV-TWA: 2 mg/m(3)
2) TLV-STEL:
3) TLV-Ceiling:

b) Notations and Endnotes:

1) Carcinogenicity Category: Not Listed
2) Codes: Not Listed
3) Definitions: Not Listed

c) TLV Basis - Critical Effect(s): URT irr
d) Molecular Weight: 56.08

1) For gases and vapors, to convert the TLV from ppm to mg/m(3):

a) [(TLV in ppm)(gram molecular weight of substance)]/24.45

2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:

a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

e) Additional information:

B) NIOSH REL and IDLH Values for CAS1305-78-8 (National Institute for Occupational Safety and Health, 2007):

1) Listed as: Calcium oxide
2) REL:

a) TWA: 2 mg/m(3)
b) STEL:
c) Ceiling:
d) Carcinogen Listing: (Not Listed) Not Listed
e) Skin Designation: Not Listed
f) Note(s):

3) IDLH:

a) IDLH: 25 mg/m3
b) Note(s): Not Listed

C) Carcinogenicity Ratings for CAS1305-78-8 :

1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Calcium oxide
2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Calcium oxide
5) MAK (DFG, 2002): Not Listed
6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

D) OSHA PEL Values for CAS1305-78-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

1) Listed as: Calcium oxide
2) Table Z-1 for Calcium oxide:

a) 8-hour TWA:

1) ppm:

a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.

2) mg/m3: 5

a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.

3) Ceiling Value:
4) Skin Designation: No
5) Notation(s): Not Listed

Pharmacology Toxicology

Pharmacologic Mechanism

A)

1) Calcium oxide has been used experimentally in root canal dental procedures as an antibacterial medication (Cavalleri et al, 1990).
2) Bacterial cell walls are destroyed by the thermal and alkalinity effects of calcium oxide.

Toxicologic Mechanism

A)

1) Chemical and thermal burns can result from calcium oxide exposure in the presence of moisture, including perspiration or water. Calcium oxide reacts with water to form calcium hydroxide, which is a strong alkali which can produce chemical burns (Koo et al, 1992). The reaction of calcium oxide and water is extremely exothermic (Budavari, 1996; Rice & Cohen, 1996).
2) The initial reaction following exposure to an alkali is saponification, followed by liquefactive necrosis which can destroy the epithelium and underlying tissues (Stewart, 1985).

B)

1) Injury is due primarily to alkalinity, but dehydrating and thermal effects are also contributing factors.
2) Burns of the esophagus from alkaline agents, in general, classically follow four distinct phases (Wolpowitz, 1974; Endicott, 1971):

a) INFLAMMATORY PHASE lasts one or two days and demonstrates marked fibroblastic proliferation. Perforations may occur at this stage with resultant mediastinitis.
b) NECROTIC PHASE occurs one to four days after injury. Cells die from coagulation of intracellular protein and inflammation of surrounding tissue develops. Vascular thrombosis and bacterial invasion worsen injury. Esophagoscopy is contraindicated as the esophagus is especially vulnerable to perforation.
c) GRANULATION PHASE begins 3 to 5 days post injury when necrotic tissue sloughs. Granulation tissue begins to fill in tissue defects and connective tissue begins to form in 10 to 12 days.
d) CONSTRICTION PHASE occurs 2 1/2 to 3 weeks following injury. Marked narrowing of the esophageal lumen may occur as the collagen fibers begin to contract.

C)

1) Calcium oxide reacts with the protein and moisture in the eye, forming clumps that lodge deep in the cul-de-sacs and are very difficult to remove. These clumps are a source of gradual generation of heat and alkaline injury, since as the calcium oxide absorbs water, an exothermic (heat generating) reaction occurs and calcium hydroxide (pH 11 to 12) is produced (Grant & Schuman, 1993; Potts, 1996).
2) Mechanisms of ocular effects of alkaline chemicals, in general, include (Grant & Schuman, 1993; Rozenbaum et al, 1991; Potts, 1991) Hoffman, 1994; (Potts, 1996):

a) Saponification of the plasma membrane
b) Impairment of epithelial repair
c) Increased intraocular pressure as a result of prostaglandin release
d) Stimulation of inflammatory processes which cause the production of collagenase and other lytic enzymes from polymorphonuclear leukocytes, leading to denaturing of collagen, additional damage to the corneal stroma and delayed healing. Delayed injury has been attributed to lytic enzymes.
e) Damage by free radicals has also been proposed

D)

Physicochemical

Physical Characteristics

A)

1) Commercial material sometimes has a yellowish or brownish tint, due to iron (Budavari, 1996).
2) Properly stored lime of commerce contains 90% to 95% free calcium oxide (Budavari, 1996).

Ph

A)

Molecular Weight

A)

Animal Toxicology

References

General Bibliography

1)

2)

3)

4)

5)

6)

7)

8)

9)

10)

11)

12)

13)

14)

15)

16)

17)

18)

19)

20)

21)

22)

23)

24)

25)

26)

27)

28)

29)

30)

31)

32)

33)

34)

35)

36)

37)

38)

39)

40)

41)

42)

43)

44)

45)

46)

47)

48)

49)

50)

51)

52)

53)

54)

55)

56)

57)

58)

59)

60)

61)

62)

63)

64)

65)

66)

67)

68)

69)

70)

71)

72)

73)

74)

75)

76)

77)

78)

79)

80)

81)

82)

83)

84)

85)

86)

87)

88)

89)

90)

91)

92)

93)

94)

95)

96)

97)

98)

99)

100)

101)

102)

103)

104)

105)

106)

107)

108)

109)

110)

111)

112)

113)

114)

115)

116)

117)

118)

119)

120)

121)

122)

123)

124)

125)

126)

127)

128)

129)

130)

131)

132)

133)

134)

135)

136)

137)

138)

139)

140)

141)

142)

143)

144)

145)

146)

147)

148)

149)

150)

151)

152)

153)

154)

155)

156)

157)

158)

159)

160)

161)

162)

163)

164)

165)

166)

167)

168)

169)

170)

171)

172)

173)

174)

175)

176)

177)

178)

179)

180)

181)

182)

183)

184)

185)

186)

187)

188)

189)

190)

191)

192)

193)

194)

195)

196)

197)

198)

199)

200)

201)

202)

203)

204)

205)

206)

207)

208)

209)

210)

211)

212)

213)

214)

215)

216)

217)

218)

219)

220)

221)

222)

223)

224)

225)

226)

227)

228)

229)

230)

231)

232)

233)

234)

235)

236)

237)

238)

239)

240)

241)

242)

243)

244)

245)

246)

247)

248)

249)

250)

251)

252)

253)

254)

255)

256)

257)

258)

259)

260)

261)

262)

263)

264)

265)

266)

267)

268)

269)

270)

271)

272)

273)

274)

275)

276)

277)

278)

279)

280)

281)

282)

283)

284)

285)

286)

287)

288)

289)

290)

291)

292)

293)

294)

295)

296)

297)

298)

299)

300)

301)

302)

303)

FeedBack

CALCIUM OXIDE

Classification | Detailed evidence-based information

Therapeutic Toxic Class

Specific Substances

Available Forms Sources

Life Support

Clinical Effects

Laboratory Monitoring

Treatment Overview

Range Of Toxicity

Summary Of Exposure

Vital Signs

Heent

Cardiovascular

Respiratory

Gastrointestinal

Genitourinary

Hematologic

Dermatologic

Reproductive

Carcinogenicity

Genotoxicity

Monitoring Parameters Levels

Radiographic Studies

Life Support

Patient Disposition

Monitoring

Oral Exposure

Inhalation Exposure

Eye Exposure

Dermal Exposure

Case Reports

Summary

Minimum Lethal Exposure

Maximum Tolerated Exposure

Workplace Standards

Pharmacologic Mechanism

Toxicologic Mechanism

Physical Characteristics

Ph

Molecular Weight

General Bibliography