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KETONE PEROXIDES

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Ketones are organic compounds containing a carbonyl group attached to two carbon atoms. Peroxides of ketones are powerful oxidizers, and are used as catalysts in hardening of fiberglass resins and curing unsaturated polyester resins.

Specific Substances

    A) CYCLOHEXANONE PEROXIDE
    1) CAS 78-18-2
    METHYL ETHYL KETONE PEROXIDE
    1) 2-Butanone peroxide
    2) Ethyl methyl ketone peroxide
    3) MEKP
    4) MEK Peroxide
    5) CAS 1338-23-4
    METHYL ISOBUTYL KETONE PEROXIDE
    1) CAS 37206-20-5

Available Forms Sources

    A) SOURCES
    1) MEKP is a mixture of peroxides and hydroperoxides, usually available as a 40% to 60% solution combined with a plasticizer, such as dimethyl phthalate.
    B) USES
    1) Ketone peroxides are used as catalysts for hardening of fiberglass resins and curing unsaturated polyester resins.

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Ketone peroxides are used as catalysts for hardening of fiberglass resins and curing unsaturated polyester resins.
    B) TOXICOLOGY: Ketones are organic compounds containing a carbonyl group attached to two carbon atoms. Peroxides of ketones are powerful oxidizers. Methyl ethyl ketone peroxide (MEKP) is a mixture of peroxides and hydroperoxides, usually available as a 40% to 60% solution combined with a plasticizer, such as dimethyl phthalate. MEKP is a model for experimental lipid peroxidation, and generates free oxygen radicals, which may be responsible for tissue damage. In one case, elevated oxygen concentrations during mechanical ventilation in the setting of coagulopathy was thought to contribute to hemorrhagic alveolar damage.
    C) EPIDEMIOLOGY: Exposure is rare.
    D) WITH POISONING/EXPOSURE
    1) ORAL EXPOSURE: Ketone peroxides are extremely corrosive; exposure usually results in pharyngitis, esophagitis or esophageal necrosis, and gastritis. Complications in fatal cases have included gastric perforation, gastric or pulmonary hemorrhage, coagulopathy, severe metabolic acidosis, rhabdomyolysis, acute renal failure, interstitial pneumonia/ARDS, cardiac arrest, and hepatic coma. Other effects included leukocytosis, myocarditis, hypertension, and hypotension. OCULAR EXPOSURE results in moderate to severe injury (chemosis, conjunctival necrosis, corneal opacity). MEKP is moderately irritating at concentrations of 3% and severely irritating in concentrations of 40% after ocular instillation.

Laboratory Monitoring

    A) Monitor vital signs, serum electrolytes, renal function and liver enzymes in symptomatic patients.
    B) Monitor for gastrointestinal burns and respiratory distress.
    C) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests, and obtain a chest x-ray in any patient with respiratory symptoms.
    D) Obtain an ECG, and institute continuous cardiac monitoring.
    E) Monitor prothrombin time or INR after significant ingestion.
    F) Test stools for occult blood in patients with gastrointestinal symptoms.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive. There is little information regarding the use of endoscopy, corticosteroids or surgery in the setting of ketone peroxides ingestion. The following information is derived from experience with other corrosives. Perform endoscopy early (within 12 hours) in patients with stridor, drooling, vomiting, significant oral burns, and difficulty swallowing or abdominal pain, or large deliberate ingestions. 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.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Early airway management in patients with acute respiratory distress. Early (within 12 hours), perform a gastrointestinal endoscopy to evaluate for burns. Treat hypotension with fluids, vasopressors if needed. In one case report, IV n-acetylcysteine and 4 hours of hemodialysis followed by continuous veno-venous hemofiltration (CVVH) were used successfully in a man with gastrointestinal injury and metabolic acidosis after ingesting approximately 120 mL solution of 33% methyl ethyl ketone peroxide in dimethyl phthalate.
    C) DECONTAMINATION
    1) INGESTION: In patients who have ingested high concentration solutions without vomiting or respiratory distress who are able to swallow, dilute with 4 to 8 oz milk/water if possible shortly after ingestion; then NPO until after endoscopy. Neutralization, gastric lavage, and activated charcoal are not indicated. OCULAR: Irrigate exposed eyes with water. DERMAL: Remove contaminated clothes, follow with copious irrigation. INHALATION: Humidified oxygen.
    D) AIRWAY MANAGEMENT
    1) Ensure adequate ventilation and perform endotracheal intubation early in patients with significant CNS and respiratory depression, pulmonary toxicity, severe bleeding, hemodynamic instability, or severe upper GI bleeding.
    E) ANTIDOTE
    1) None.
    F) ENDOSCOPY
    1) Should be performed as soon as possible (preferably within 12 hours, not more than 24 hours) in any patient with large, deliberate ingestions, 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.
    G) CORTICOSTEROID
    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 they are 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) ENHANCED ELIMINATION
    1) In one case report, IV n-acetylcysteine and 4 hours of hemodialysis followed by continuous veno-venous hemofiltration (CVVH) were used successfully in a man with gastrointestinal injury and metabolic acidosis after ingesting approximately 120 mL solution of 33% methyl ethyl ketone peroxide in dimethyl phthalate.
    I) EYE IRRITATION
    1) Copious irrigation until pH neutral; perform slit lamp exam. Ophthalmology consult. Antibiotics may be indicated.
    J) PATIENT DISPOSITION
    1) OBSERVATION CRITERIA: Patients with caustic 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.
    3) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear. Consult a gastroenterologist for endoscopic evaluation of any patient with concern for corrosive GI injury.
    K) PITFALLS
    1) Missing an ingestion of another chemical or other possible etiologies for a patient’s symptoms. History of exposure may be difficult to obtain in some settings.
    2) The absence of oral burns does NOT reliably exclude the possibility of significant esophageal burns.
    3) 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.
    4) Patients with any evidence of upper airway involvement require early airway management before airway edema progresses.
    5) The extent of eye injury may not be apparent for 48 to 72 hours after the burn. All patients with corrosive eye injury should be evaluated by an ophthalmologist.
    L) DIFFERENTIAL DIAGNOSIS
    1) Ingestion of another irritant, or an acid or base, gastrointestinal hemorrhage, or perforated viscus.
    0.4.4) EYE EXPOSURE
    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.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) TOXICITY: The minimum toxic or lethal dose is variable and not well defined in the literature. Severe effects have been reported after ingestion of 50 to 100 mL. Methyl ethyl ketone peroxide is moderately irritating at concentrations of 3% and severely irritating in concentrations of 40% after ocular instillation.

Clinical Effects

Summary Of Exposure

    A) USES: Ketone peroxides are used as catalysts for hardening of fiberglass resins and curing unsaturated polyester resins.
    B) TOXICOLOGY: Ketones are organic compounds containing a carbonyl group attached to two carbon atoms. Peroxides of ketones are powerful oxidizers. Methyl ethyl ketone peroxide (MEKP) is a mixture of peroxides and hydroperoxides, usually available as a 40% to 60% solution combined with a plasticizer, such as dimethyl phthalate. MEKP is a model for experimental lipid peroxidation, and generates free oxygen radicals, which may be responsible for tissue damage. In one case, elevated oxygen concentrations during mechanical ventilation in the setting of coagulopathy was thought to contribute to hemorrhagic alveolar damage.
    C) EPIDEMIOLOGY: Exposure is rare.
    D) WITH POISONING/EXPOSURE
    1) ORAL EXPOSURE: Ketone peroxides are extremely corrosive; exposure usually results in pharyngitis, esophagitis or esophageal necrosis, and gastritis. Complications in fatal cases have included gastric perforation, gastric or pulmonary hemorrhage, coagulopathy, severe metabolic acidosis, rhabdomyolysis, acute renal failure, interstitial pneumonia/ARDS, cardiac arrest, and hepatic coma. Other effects included leukocytosis, myocarditis, hypertension, and hypotension. OCULAR EXPOSURE results in moderate to severe injury (chemosis, conjunctival necrosis, corneal opacity). MEKP is moderately irritating at concentrations of 3% and severely irritating in concentrations of 40% after ocular instillation.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) IRRITATION
    a) METHYL ETHYL KETONE PEROXIDE is moderately irritating at concentrations of 3% and severely irritating (chemosis, corneal opacity, conjunctival necrosis) in concentrations of 40% after ocular instillation (Grant & Schuman, 1993).
    b) CYCLOHIXANONE PEROXIDE can produce moderately severe corneal injury (Grant & Schuman, 1993).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) CARDIAC ARREST
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: An adult inebriated male developed cardiac arrest following an accidental ingestion of 50 to 100 mL of methyl ethyl ketone peroxide in dimethyl phthalate (Karhunen et al, 1990).
    B) MYOCARDITIS
    1) WITH POISONING/EXPOSURE
    a) Myocarditis was reported in one case of MEKP ingestion (Dines & Shipman, 1962).
    b) CASE REPORT: An adult developed signs/symptoms of myocarditis (gallop rhythm, sinus tachycardia, inverted T waves, congestive heart failure) 5 days after ingesting an unknown amount of MEKP; cardiac symptoms resolved within 6 weeks (Dines & Shipman, 1962).
    C) HYPERTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Several episodes of hypertension developed in a 6-year-old boy who ingested an unknown quantity of 36% solution of methyl ethyl ketone peroxide in 52% dimethyl phthalate. His hospital course was complicated by respiratory distress, metabolic acidosis, esophageal and gastric burns, hematuria, myoglobinuria, and coagulopathy. Following approximately 3 months of hospitalization, he was discharged on a program of endoscopy and esophageal dilation (Bates et al, 2001).
    D) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypotension has been reported in patients after ingesting methyl ethyl ketone peroxide (Moon et al, 2010; Bates et al, 2001).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) PNEUMONITIS
    1) WITH POISONING/EXPOSURE
    a) Aspiration pneumonitis has been reported in patients after ingesting methyl ethyl ketone peroxide (Bates et al, 2001).
    b) CASE REPORT: An adult vomited spontaneously after ingestion of MEKP. He developed aspiration pneumonitis with progressive dyspnea over the next 48 hours (Dines & Shipman, 1962).
    B) RESPIRATORY DISTRESS
    1) WITH POISONING/EXPOSURE
    a) Respiratory distress, requiring intubation, was reported in one case of MEKP ingestion in an adult (Mittleman et al, 1986).
    b) CASE REPORT: Respiratory distress developed in a 6-year-old boy who ingested an unknown quantity of 36% solution of methyl ethyl ketone peroxide in 52% dimethyl phthalate. His hospital course was complicated by metabolic acidosis, esophageal and gastric burns, hypertension, hematuria, myoglobinuria, and coagulopathy. Following approximately 3 months of hospitalization, he was discharged on a program of endoscopy and esophageal dilation (Bates et al, 2001).
    c) CASE REPORT: An adult presented with moderate respiratory distress, requiring intubation hours after ingestion of an unknown amount of MEKP (Mittleman et al, 1986).
    C) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) One case of interstitial pneumonia/ARDS, with hemorrhage, was reported after ingestion of MEKP (Karhunen et al, 1990).
    b) MECHANISM: MEKP is a model for experimental lipid peroxidation, and generates free oxygen radicals, which may be responsible for tissue damage. Elevated oxygen concentrations during mechanical ventilation in the setting of coagulopathy was thought to contribute to hemorrhagic alveolar damage in this case (Karhunen et al, 1990).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) COMA
    1) WITH POISONING/EXPOSURE
    a) Coma has been reported in patients after ingesting methyl ethyl ketone peroxide (Moon et al, 2010; Bates et al, 2001).
    b) CASE REPORT: Ingestion of 50 to 100 mL methyl ethyl ketone peroxide in dimethyl phthalate resulted in loss of consciousness approximately 30 minutes later in an inebriated 47-year-old man (Karhunen et al, 1990).
    B) DROWSY
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 3-year-old boy presented hypotonic and mildly drowsy (GCS 11) after ingesting an unknown quantity of methyl ethyl ketone peroxide. He developed esophageal stenosis one month later, necessitating esophageal dilatation (Prez-Martnez et al, 1997).
    C) TOXIC ENCEPHALOPATHY
    1) WITH POISONING/EXPOSURE
    a) OCCUPATIONAL EXPOSURE
    1) CASE REPORT: A 38-year-old laborer experienced solvent intoxication during each of two spray paintings in an enclosed, unventilated garage. The paint consisted primarily of toluene and methyl ethyl ketone. Nausea, headaches, dizziness, respiratory difficulty, and other symptoms began after exposures. Over the next several days the patient developed impaired concentration, memory loss, and cerebellar signs including an intention tremor, gait ataxia, and dysarthria. Examination by a toxicologist and neurologist revealed likely toxic encephalopathy with dementia and cerebellar ataxia (Welch et al, 1991).
    D) CHRONIC POISONING
    1) WITH POISONING/EXPOSURE
    a) OCCUPATIONAL EXPOSURE
    1) CASE REPORTS: The occurrence of major neurological disease following occupational exposure to organic solvents has been observed. In long-term exposure to methyl-ethyl ketone (MEK) daily neurological effects in 2 patients included: slurred speech, cerebellar ataxia, lightheadedness, vertigo, disorientation, and memory loss and subsequent dementia in one patient (Seaton et al, 1992).
    a) The authors speculated that neurological disease secondary to solvent exposure may force some workers into early retirement. Further epidemiological research was suggested.

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) INJURY OF GASTROINTESTINAL TRACT
    1) WITH POISONING/EXPOSURE
    a) Spontaneous vomiting and hematemesis, with moderate to severe gastroesophageal injury (gastritis, hemorrhagic esophagitis) occurred in most cases (Prez-Martnez et al, 1997; Karhunen et al, 1990; Deisher, 1958); one case of gastric perforation and one case of esophageal strictures were reported (Karhunen et al, 1990; Deisher, 1958).
    b) CASE REPORT: A 70-year-old man presented with sore throat, shortness of breath, nausea and vomiting within 1 hour of ingesting about 10 mL of 50% methyl ethyl ketone peroxide in dimethyl phthalate solution. Superficial mucosal injury with edema of the oropharynx, uvula, posterior pharynx, epiglottis, arytenoids and vocal cords were observed during a laryngoscope examination. Lateral cervical radiography showed a narrowing of airway due to a thickened epiglottis. His symptoms resolved following supportive care (Bozdemir et al, 2011).
    c) CASE REPORT: Severe esophageal and gastric burns developed in a 6-year-old boy who ingested an unknown quantity of 36% solution of methyl ethyl ketone peroxide in 52% dimethyl phthalate. Although he was discharged 19 days after admission, esophagoscopy on day 35 showed a tight stricture at the gastroesophageal junction and complete fibrosis of the middle third of the stomach, requiring gastric resection and reconstruction. He was discharged on day 93 with a scheduled program of endoscopy and esophageal dilation. At age 11, he experiences swallowing difficulty once or twice a year, necessitating esophageal dilation (Bates et al, 2001).
    d) CASE REPORT: Esophageal stenosis developed in a 3-year-old boy who ingested an unknown quantity of methyl ethyl ketone peroxide. He presented with hypotonia, drowsiness, ketone odor, sialorrhea, hematemesis, erythema of lips, throat and palate, and tonsillar edema. Following supportive care, he became asymptomatic and was discharged on day 8. An esophagogram one month post-ingestion revealed esophageal stenosis, necessitating esophageal dilatation (Prez-Martnez et al, 1997).
    e) CASE REPORT: A 53-year-old man presented with nausea and sore throat after ingesting approximately 120 mL solution of 33% methyl ethyl ketone peroxide in dimethyl phthalate. He also vomited after drinking milk shortly after arrival. An esophagogastroduodenoscopy showed severe inflammation and necrotic lesions of the mucosal surfaces of the distal esophagus, the stomach and the duodenum with ulceration of the antral region of the stomach. Following supportive care and treatment with n-acetylcysteine and hemodialysis (to treat metabolic acidosis), he recovered completely. A second endoscopy 3 weeks post-presentation did not show any residual abnormalities (vanEnckevort et al, 2008).
    f) CASE REPORT: Severe burning of the mouth and vomiting along with superficial esophageal burns occurred after accidental ingestion of MEKP by a 47-year-old male (Karhunen et al, 1990).
    g) CASE REPORT: A 57-year-old man vomited spontaneously after ingestion of MEKP. On arrival to the ED, he had dysphagia and was coughing up blood (Dines & Shipman, 1962).
    h) CASE REPORT (STRICTURE): A 34-year-old man presented 15 minutes after ingestion of 2 ounces of a 60% MEKP solution with vomiting, dysphagia, and abdominal pain. He had chemical burns of the mouth and throat, which healed within 11 days. Dysphagia persisted, and he was found to have a stricture in both lower and upper esophagus (Deisher, 1958).
    B) VASCULAR INSUFFICIENCY OF INTESTINE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 41-year-old man presented after ingestion of an unknown amount of MEKP with oral mucosal burns. Over several hours, he developed epigastric tenderness and heme positive stools. Laparotomy showed a necrotic perforated stomach, with diffuse necrosis of the small intestine, colon, and liver (Mittleman et al, 1986).
    C) EMPHYSEMATOUS GASTRITIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 53-year-old man was found at home with an altered mental status after ingesting an unknown amount of a chemical. He presented 2 hours later unconscious and hypotensive (BP 80/45 mmHg). Physical examination revealed redness in the oropharynx but no ulceration. After performing bag-valve-mask ventilation, an orotracheal intubation was performed. At this time, it was discovered that the patient had ingested an unknown amount of methyl ethyl ketone peroxide in dimethyl phthalate from a 200-mL paper cup. Radiography revealed diffused gastric emphysema. Laboratory results also revealed metabolic acidosis (pH 7.025, PaCO2 50.3 mmHg, PaO2 109.5 mmHg, HCO3 12.8 mmol/L). Despite supportive care, his condition worsened and he died 6 hours after presentation. It was suggested that the radiographic findings were derived from the increased upper gastrointestinal tract pressure during bag-valve-mask ventilation in a patient with severely damaged esophagogastric mucosa from the ingestion of methyl ethyl ketone peroxide, a corrosive chemical (Moon et al, 2010).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) HEPATIC FAILURE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 47-year-old man died from hepatic coma associated with blood coagulation disorders 4 days following an accidental ingestion of 50 to 100 mL methyl ethyl ketone peroxide in dimethyl phthalate. Autopsy showed massive peripheral zonal hepatic necrosis (Karhunen et al, 1990).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ACUTE RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT (ADULT): Anuria developed on the second day after ingestion of 50 to 100 mL of 40% MEKP by an adult male; acute renal failure was secondary to rhabdomyolysis (CPK peak 68,600 U/L) (Karhunen et al, 1990).
    B) ABNORMAL RENAL FUNCTION
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Elevated serum urea and creatinine (peaked 2 days after ingestion), hematuria, and myoglobinuria developed in a 6-year-old boy who ingested an unknown quantity of 36% solution of methyl ethyl ketone peroxide in 52% dimethyl phthalate. His hospital course was complicated by respiratory distress, metabolic acidosis, esophageal and gastric burns, hypertension, and coagulopathy. Following approximately 3 months of hospitalization, he was discharged on a program of endoscopy and esophageal dilation (Bates et al, 2001).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Metabolic acidosis (pH 6.86, base deficit 28 mmol/L) was reported in a 47-year-old inebriated man following an accidental ingestion of 50 to 100 mL of methyl ethyl ketone peroxide in dimethyl phthalate (Karhunen et al, 1990).
    b) CASE REPORT: Metabolic acidosis (pH 7.025, PaCO2 50.3 mmHg, PaO2 109.5 mmHg, HCO3 12.8 mmol/L) developed in a 53-year-old man who presented unconscious and hypotensive after ingesting an unknown amount of methyl ethyl ketone peroxide in dimethyl phthalate from a 200-mL paper cup (Moon et al, 2010).
    c) CASE REPORT: A 6-year-old boy ingested an unknown quantity of 36% solution of methyl ethyl ketone peroxide in 52% dimethyl phthalate. On admission, he was tachycardic, pale, agitated with peripheral cyanosis. He experienced increasing stridor and hypoxemia requiring endotracheal intubation. Arterial blood gas estimation revealed mixed metabolic and respiratory acidosis (pH, 7.03; PaCO2, 9.2 kPa; PO2, 35.6 kPa; base deficit, 13 mmol/L; bicarbonate, 21). Following intubation, he experienced metabolic acidemia (pH, 7.30; PaCO2, 4.8 kPa; PO2, 38.5 kPa; base deficit, 7 mmol/L; bicarbonate, 19) which subsequently became a mild metabolic acidosis 3 days later. His hospital course was complicated by respiratory distress, esophageal and gastric burns, hematuria, myoglobinuria, and coagulopathy. Following approximately 3 months of hospitalization, he was discharged on a program of endoscopy and esophageal dilation (Bates et al, 2001).
    d) CASE REPORT: Metabolic acidosis with an elevated anion gap and osmolal gap developed in a 53-year-old man after ingesting approximately 120 mL solution of 33% methyl ethyl ketone peroxide in dimethyl phthalate. Following treatment with n-acetylcysteine, 4 hours of hemodialysis followed by continuous veno-venous hemofiltration, he recovered completely with no further sequelae (vanEnckevort et al, 2008).
    e) CASE REPORT: A 41-year-old man presented several hours after ingestion of MEKP with severe metabolic acidosis (pH 6.7, serum bicarbonate 10 meq/L, base deficit 30) (Mittleman et al, 1986).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) BLOOD COAGULATION PATHWAY FINDING
    1) WITH POISONING/EXPOSURE
    a) Coagulopathy, with decreased hematocrit, increased PT and PTT, and hematuria, was present in two fatal cases of MEKP ingestion (Karhunen et al, 1990; Mittleman et al, 1986).
    b) CASE REPORT: Coagulopathy developed in a 6-year-old boy who ingested an unknown quantity of 36% solution of methyl ethyl ketone peroxide in 52% dimethyl phthalate. A coagulation screen revealed increased prothrombin time, activated partial thromboplastin time, and decreased fibrinogen, as well as markedly abnormal D-dimers (greater than 1000 International Units/L; normal, less than 500 IU/L). His hospital course was complicated by respiratory distress, metabolic acidosis, esophageal and gastric burns, hypertension, hematuria, and myoglobinuria. Following approximately 3 months of hospitalization, he was discharged on a program of endoscopy and esophageal dilation (Bates et al, 2001).
    c) Prolonged prothrombin time (65%) developed in a 3-year-old boy who experienced esophageal stenosis after ingesting an unknown quantity of methyl ethyl ketone peroxide (Prez-Martnez et al, 1997).
    B) LEUKOCYTOSIS
    1) WITH POISONING/EXPOSURE
    a) Leukocytosis has been reported in patients after ingesting methyl ethyl ketone peroxide (Bates et al, 2001).
    b) Leukocytosis (32.360 WBC x 10(9)/L) developed in a 3-year-old boy who experienced esophageal stenosis after ingesting an unknown quantity of methyl ethyl ketone peroxide (Prez-Martnez et al, 1997).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) ALLERGIC CONTACT DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: After working for 6 years at a fiberglass-reinforced plastics factory producing gutter covers, a 64-year-old man, who refused to use skin protection, developed severe acute hand dermatitis. Patch tests revealed positive results to methyl ethyl ketone peroxide, cobalt naphthenate, 2-hydroxyethyl methacrylate, and methyl methacrylate. Following supportive therapy for 2 months, his symptoms resolved (Minamoto et al, 2002).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) RHABDOMYOLYSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Acute renal failure secondary to rhabdomyolysis (CPK peak 68,600 U/L) was reported after the ingestion of 50 to 100 mL of 40% MEKP by an adult (Karhunen et al, 1990).
    b) CASE REPORT: Elevated creatine kinase (584 International Units; normal, 24 to 195 IU) developed in a 6-year-old boy who ingested an unknown quantity of 36% solution of methyl ethyl ketone peroxide in 52% dimethyl phthalate. His hospital course was complicated by respiratory distress, metabolic acidosis, esophageal and gastric burns, hypertension, hematuria, and coagulopathy. Following approximately 3 months of hospitalization, he was discharged on a program of endoscopy and esophageal dilation (Bates et al, 2001).

Immunologic

    3.19.2) CLINICAL EFFECTS
    A) ALLERGIC CONTACT DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: After working for 6 years at a fiberglass-reinforced plastics factory producing gutter covers, a 64-year-old man, who refused to use skin protection, developed severe acute hand dermatitis. Patch tests revealed positive results to methyl ethyl ketone peroxide, cobalt naphthenate, 2-hydroxyethyl methacrylate, and methyl methacrylate. Following supportive therapy for 2 months, his symptoms resolved (Minamoto et al, 2002).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS1338-23-4 (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
    B) IARC Carcinogenicity Ratings for CAS78-18-2 (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
    C) IARC Carcinogenicity Ratings for CAS37206-20-5 (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

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs, serum electrolytes, renal function and liver enzymes in symptomatic patients.
    B) Monitor for gastrointestinal burns and respiratory distress.
    C) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests, and obtain a chest x-ray in any patient with respiratory symptoms.
    D) Obtain an ECG, and institute continuous cardiac monitoring.
    E) Monitor prothrombin time or INR after significant ingestion.
    F) Test stools for occult blood in patients with gastrointestinal symptoms.
    4.1.2) SERUM/BLOOD
    A) ACID/BASE
    1) Monitor arterial blood gases in patients with respiratory symptoms.
    B) BLOOD/SERUM CHEMISTRY
    1) Monitor liver function tests after significant ingestion.
    C) COAGULATION STUDIES
    1) Monitor prothrombin time or International Normalized Ratio (INR) after significant ingestion.
    4.1.4) OTHER
    A) OTHER
    1) FECAL
    a) Test stools for occult blood in patients with gastrointestinal symptoms.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Obtain chest x-ray in patients with respiratory signs or symptoms.

Methods

    A) GAS CHROMATOGRAPHY: Gas chromatography was used in one case report to confirm the presence of methyl ethyl ketone and acetic acid in the patient's serum (vanEnckevort et al, 2008).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    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.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear. Consult a gastroenterologist for endoscopic evaluation of any patient with concern for corrosive GI injury.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with caustic 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) Monitor vital signs, serum electrolytes, renal function and liver enzymes in symptomatic patients.
    B) Monitor for gastrointestinal burns and respiratory distress.
    C) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests, and obtain a chest x-ray in any patient with respiratory symptoms.
    D) Obtain an ECG, and institute continuous cardiac monitoring.
    E) Monitor prothrombin time or INR after significant ingestion.
    F) Test stools for occult blood in patients with gastrointestinal symptoms.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) ORAL
    1) Activated charcoal is of no value, may induce vomiting, and may obscure endoscopy findings. It is NOT recommended.
    2) DILUTION
    a) 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).
    b) 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, 1995), this has not been adequately studied in humans.
    c) 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, 1977a; Homan et al, 1995; Homan et al, 1994; Homan et al, 1993).
    d) ADVERSE EFFECTS: Potential adverse effects include vomiting and airway compromise (Caravati, 2004).
    e) 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) OCULAR
    1) Irrigate exposed eyes with water.
    C) DERMAL
    1) Remove contaminated clothes, follow with copious irrigation.
    D) INHALATION
    1) Humidified oxygen.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) INGESTION: In patients who have ingested high concentration solutions without vomiting or respiratory distress who are able to swallow, dilute with 4 to 8 oz milk/water if possible shortly after ingestion; then NPO until after endoscopy. Neutralization, gastric lavage, and activated charcoal are not indicated.
    B) DILUTION
    1) USE OF DILUENTS IS CONTROVERSIAL: In a survey of the POISINDEX(R) Editorial Board, the majority routinely recommend dilution with SMALL amounts of milk or water to decontaminate the oral mucosa in patients without respiratory compromise. Several had experience with precipitation of emesis from dilution.
    2) ADVERSE EFFECTS: In 4 of 7 corrosive ingestions treated with dilution, vomiting occurred, compared to none of 15 who were not given diluents. Two patients died after vomiting following 6 ounces and a full glass of milk, respectively (Honcharak & Marcus, 1989).
    3) DILUENT TYPE: Swallowed milk may obscure endoscopy, but is not a problem with equipment containing water irrigation attachments. Both milk and water have been shown to be effective in vitro for caustic ingestion (Rumack & Burrington, 1977).
    4) DILUENT AMOUNT: The amount of diluent recommended varies widely, from 2 to 12 ounces in adults and 1 to 8 ounces in children. The majority recommended a maximum of 8 ounces in adults and 4 ounces in children (Consensus, 1988).
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment is symptomatic and supportive. There is little information regarding the use of endoscopy, corticosteroids or surgery in the setting of ketone peroxides ingestion. The following information is derived from experience with other corrosives. Perform endoscopy early (within 12 hours) in patients with stridor, drooling, vomiting, significant oral burns, and difficulty swallowing or abdominal pain, or large deliberate ingestions. 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.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Early airway management in patients with acute respiratory distress. Early (within 12 hours), perform a gastrointestinal endoscopy to evaluate for burns. Treat hypotension with fluids, vasopressors if needed. In one case report, IV n-acetylcysteine and 4 hours of hemodialysis followed by continuous veno-venous hemofiltration (CVVH) were used successfully in a man with gastrointestinal injury and metabolic acidosis after ingesting approximately 120 mL solution of 33% methyl ethyl ketone peroxide in dimethyl phthalate.
    3) N-ACETYLCYSTEINE AND HEMODIALYSIS: Intravenous n-acetylcysteine and 4 hours of hemodialysis followed by continuous veno-venous hemofiltration (CVVH) were used successfully in a man with gastrointestinal injury and metabolic acidosis after ingesting 33% solution of methyl ethyl ketone peroxide in dimethyl phthalate (vanEnckevort et al, 2008).
    B) MONITORING OF PATIENT
    1) Monitor vital signs, serum electrolytes, renal function and liver enzymes in symptomatic patients.
    2) Monitor for gastrointestinal burns and respiratory distress.
    3) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests, and obtain a chest x-ray in any patient with respiratory symptoms.
    4) Obtain an ECG, and institute continuous cardiac monitoring.
    5) Monitor prothrombin time or INR after significant ingestion.
    6) Test stools for occult blood in patients with gastrointestinal symptoms.
    C) 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, 1984). 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, 1984a; Gaudreault et al, 1983a; Schild, 1985; Moazam et al, 1987; Sugawa & Lucas, 1989; Previtera et al, 1990; 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).
    D) 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).
    E) 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).
    F) 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).
    G) EXPERIMENTAL THERAPY
    1) SUMMARY: Sucralfate and cimetidine were used in one case of lye ingestion to decrease odynophagia; strictures were not prevented. Animal studies have shown some benefit from beta-aminopropionitrile, N-acetylcysteine, and sodium polyacrylate in caustic ingestion, but results are preliminary.
    2) N-ACETYLCYSTEINE: CASE REPORT - Intravenous n-acetylcysteine (NAC) and hemodialysis were used successfully in a man with gastrointestinal injury and metabolic acidosis after ingesting approximately 120 mL solution of 33% methyl ethyl ketone peroxide in dimethyl phthalate. He recovered completely without experiencing any acute liver damage. In this case, the following acetaminophen-poisoning NAC dosing was used for 48 hours: Bolus IV - 150 mg/kg n-acetylcysteine in a 5% glucose solution in 15 minutes; Continuous IV - 50 mg/kg n-acetylcysteine in a 5% glucose solution in 8 hours (vanEnckevort et al, 2008).

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Eye Exposure

    6.8.1) DECONTAMINATION
    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) METHYL ETHYL KETONE PEROXIDE is moderately irritating at concentrations of 3% and severely irritating (chemosis, corneal opacity, conjunctival necrosis) in concentrations of 40% after ocular instillation. Prompt irrigation (4 to 30 seconds postexposure) is effective in preventing severe injury (Grant & Schuman, 1993).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Enhanced Elimination

    A) HEMODIALYSIS
    1) CASE REPORT: Intravenous n-acetylcysteine and 4 hours of hemodialysis followed by continuous veno-venous hemofiltration (CVVH) were used successfully in a man with gastrointestinal injury and metabolic acidosis after ingesting approximately 120 mL solution of 33% methyl ethyl ketone peroxide in dimethyl phthalate. He recovered completely without experiencing any acute liver damage (vanEnckevort et al, 2008).

Abstracts

Case Reports

    A) ADVERSE EFFECTS
    1) A 34-year-old man vomited immediately following accidental ingestion of 2 ounces of 60% MEKP in dimethyl phthalate. On examination, he had mouth and throat redness, epigastric tenderness, and pain on swallowing. After 24 hours, he could not swallow liquids, which persisted for 2 days. He returned 3 weeks after discharge with complaints of continued dysphagia and was found to have strictures in both upper and lower esophagus; dilation resulted in amelioration of symptoms (Deisher, 1958).
    B) SPECIFIC AGENT
    1) ORAL
    a) MEKP: A 41-year-old man ingested an unknown amount of MEKP and presented after hours with mild to moderate respiratory distress, copious brown, foamy secretions, and severe metabolic acidosis. Within several hours, he developed upper quadrant and epigastric tenderness, heme positive stools, and hypotension. Hematocrit dropped to 24% and PT and PTT were elevated. Endoscopy revealed oral burns and pharyngeal edema, beyond which the scope could not be passed. Peritoneal lavage produced coffee ground material. Laparotomy revealed gastric perforation. The patient died shortly thereafter (Mittleman et al, 1986).
    C) ADULT
    1) A 47-year-old inebriated male ingested 50 to 100 mL of 35 to 40% MEKP in dimethyl phthalate. He developed severe burning of the mouth, vomited after ingesting sea water, and was comatose within 30 minutes. Shortly after presentation to the hospital, he developed cardiac arrest, and was resuscitated. The hospital course included metabolic acidosis (pH 6.86, base excess 28 mmol/L), acute renal failure due to rhabdomyolysis, respiratory failure, severe hepatic failure, hypoglycemia, paralytic ileus, sepsis, and bleeding disorder. He died 4 days following ingestion (Karhunen et al, 1990).
    2) A 57-year-old man ingested an unknown amount of plastic catalyst containing 60% methyl ethyl ketone peroxide and 40% dimethyl phthalate in a suicide attempt. He vomited spontaneously en route to the hospital. Over 48 hours, he developed progressive dyspnea, dysphagia, vomiting, and coughing bright red blood. He was treated for aspiration pneumonitis and gastritis. Three days later, myocarditis developed, with gallop rhythm, cyanosis, dyspnea, orthopnea, JVD, and EKG changes (T wave inversion, sinus tachycardia). Cardiac symptoms resolved after treatment with prednisone, theophylline, digoxin, and a mercurial diuretic (Dines & Shipman, 1962).

Range Of Toxicity

Summary

    A) TOXICITY: The minimum toxic or lethal dose is variable and not well defined in the literature. Severe effects have been reported after ingestion of 50 to 100 mL. Methyl ethyl ketone peroxide is moderately irritating at concentrations of 3% and severely irritating in concentrations of 40% after ocular instillation.

Minimum Lethal Exposure

    A) CASE REPORTS
    1) ADULT
    a) A 47-year-old man died from hepatic coma associated with blood coagulation disorders 4 days following an accidental ingestion of 50 to 100 mL of 35% to 40% methyl ethyl ketone peroxide in dimethyl phthalate. This corresponds to about 300 to 600 mg/kg of MEKP (Karhunen et al, 1990).
    b) A 46-year-old man collapsed immediately after ingesting 50 mL of a plastic catalyst containing 60% methyl ethyl ketone and cyclohexanone peroxides in dimethyl phthalate. Despite intensive supportive care a pseudomonas respiratory infection developed and the patient died on hospital day 27 of massive gastrointestinal bleeding and septicemia (Burger & Chandor, 1971).

Maximum Tolerated Exposure

    A) CASE REPORTS
    1) ADULT: A 34-year-old man recovered, with residual esophageal strictures following accidental ingestion of 2 ounces (about 60 mL) of 60% MEKP in dimethyl phthalate (Deisher, 1958).
    2) ADULT: A 53-year-old man developed gastrointestinal edema and ulceration, as well as metabolic acidosis after ingesting approximately 120 mL solution of 33% methyl ethyl ketone peroxide solution in dimethyl phthalate. Following treatment with n-acetylcysteine, hemodialysis followed by continuous veno-venous hemofiltration, he recovered completely with no further sequelae (vanEnckevort et al, 2008).
    B) Methyl ethyl ketone peroxide is moderately irritating at concentrations of 3% and severely irritating (chemosis, corneal opacity, conjunctival necrosis) in concentrations of 40% after ocular instillation (Grant & Schuman, 1993).

Workplace Standards

    A) ACGIH TLV Values for CAS1338-23-4 (American Conference of Governmental Industrial Hygienists, 2010):
    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) Methyl ethyl ketone peroxide
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL:
    3) TLV-Ceiling: 0.2 ppm
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): Eye and skin irr; liver and kidney dam
    d) Molecular Weight: 176.24
    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) ACGIH TLV Values for CAS78-18-2 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    C) ACGIH TLV Values for CAS37206-20-5 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    D) NIOSH REL and IDLH Values for CAS1338-23-4 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Methyl ethyl ketone peroxide
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling: 0.2 ppm (1.5 mg/m(3))
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH: Not Listed

    E) NIOSH REL and IDLH Values for CAS78-18-2 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    F) NIOSH REL and IDLH Values for CAS37206-20-5 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    G) Carcinogenicity Ratings for CAS1338-23-4 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Methyl ethyl ketone peroxide
    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: Methyl ethyl ketone peroxide
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    H) Carcinogenicity Ratings for CAS78-18-2 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    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
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    I) Carcinogenicity Ratings for CAS37206-20-5 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    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
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    J) OSHA PEL Values for CAS1338-23-4 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

    K) OSHA PEL Values for CAS78-18-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

    L) OSHA PEL Values for CAS37206-20-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (ORAL)RAT:
    1) 484 mg/kg ((RTECS, 2000))
    B) LD50- (INTRAPERITONEAL)RAT:
    1) 65 mg/kg ((RTECS, 2000))
    C) LD50- (ORAL)MOUSE:
    1) 470 mg/kg ((RTECS, 2000))

Pharmacology Toxicology

Toxicologic Mechanism

    A) MEKP is a model for experimental lipid peroxidation, and generates free oxygen radicals, which may be responsible for tissue damage. Elevated oxygen concentrations during mechanical ventilation in the setting of coagulopathy was thought to contribute to hemorrhagic alveolar damage in this case (Karhunen et al, 1990).

Physicochemical

Physical Characteristics

    A) CYCLOHEXANONE PEROXIDE: Off-white thick paste, often combined with dibutyl or dimethyl phthalate.
    B) METHYL ETHYL KETONE PEROXIDE: is a colorless liquid with an acetone like odor (Budavari, 1996).

Molecular Weight

    A) Varies

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