a) Explosion of a 25 mL ampule of amyl nitrite into the eyes caused hyperemia and corneal corrosion of the right eye, and linear turbidity of the left eye (Stasnik, 1935).
b) The vapors may produce transient lacrimation and a stinging sensation. Splash contact usually only produces mild irritation, but there are two reports of corneal damage (Grant & Schuman, 1993).

a) Prolonged exposure to isobutyl nitrite can produce eye irritation (Bradberry, 2000; Covalla et al, 1981).

a) Duration was about a week; recovery occurred.
b) Loss was thought to be due to hypoxia of the middle ear.

a) Peripheral vasodilatation presents as headache, nausea, vomiting, postural lightheadedness, warm flushed sweaty skin that later becomes cold and cyanotic, syncope, and tachycardia (Gosselin et al, 1984; Ellenhorn et al, 1997; HSDB , 1999). Initial vasodilatation is followed by reflex vasoconstriction with sinus tachycardia (Modarai et al, 2002; Bradberry, 2000; Stambach et al, 1997).
b) Nitrite-induced vasodilation produces hypotension, decreased peripheral vascular resistance, cardiovascular collapse, seizures, and coma in severe toxicity (HSDB , 1999; Ellenhorn et al, 1997; Shesser et al, 1980).

a) Transient ECG changes (T wave inversion and ST segment depression) have been reported following inhalant abuse (Bradberry, 2000; Edwards & Ujma, 1995).

a) Paradoxical profound bradycardia and syncope were reported in 2 adult patients following inhalation of amyl nitrite for evaluation of cardiac murmurs (Rosoff & Cohen, 1986).

a) Hypotension is common and may develop within minutes of exposure (Wilkerson, 2010; Hosek et al, 1998; Stambach et al, 1997; Osterloh & Olson, 1986; Hewlett, 1906; Hewlett, 1906). Hypotensive effects are worse in arteriosclerotic blood vessels (von Rzentkowski, 1909). Hypotension may be followed by a reflex tachycardia (Modarai et al, 2002; Bradberry, 2000).

a) Sinus tachycardia is common and may result from vasodilation or from hypoxia secondary to methemoglobinemia (Wilkerson, 2010; Modarai et al, 2002; Bradberry, 2000; Stambach et al, 1997). Tachycardia was noted in 12 of 14 cases reviewed (Osterloh & Olson, 1986). Sinus tachycardia was noted on ECG in a hypotensive patient following inhalational abuse of butyl nitrite (Hosek et al, 1998).

a) Orthostatic hypotension has been reported after butyl and isobutyl nitrite ingestion (Wason et al, 1980). Inhalant abuse results in postural hypotension and syncope due to vasodilation (Bradberry, 2000).

a) Methemoglobinemia may produce profound cyanosis and hypoxia (Modarai et al, 2002; Bradberry et al, 1994; Shesser et al, 1980). Cyanosis is disproportionately greater than the degree of respiratory distress in these patients. Suspect methemoglobinemia in all cyanotic patients who do not improve with supplemental oxygen (Bradberry, 2000).
b) CASE REPORT: A 2-year-old girl was deeply cyanotic approximately one hour after ingestion of 5 mL of amyl nitrite (Liquid Gold (R)) (Forsyth & Moulden, 1991).
c) Cyanosis was a reported effect in all of 14 cases reviewed in one study (Osterloh & Olson, 1986).

a) Shortness of breath and tachypnea are common, both after inhalation and ingestion (Wason et al, 1980; Osterloh & Olson, 1986). Tachypnea has been reported in animal experiments as well (Macefield & Nail, 1985).

a) Cough, dyspnea, and hemoptysis may also be seen due to the irritant effects of these compounds (Wood & Cox, 1981).

a) Tracheobronchitis has resulted from inhalational abuse of isobutyl nitrite (Covalla et al, 1981).

a) Seizures have been reported following severe intoxication (Modarai et al, 2002); seizures are seen in experimental animals (Haley, 1980).

a) CNS depression resulting in coma may occur in patients with severe methemoglobinemia (Stambach et al, 1997; Edwards & Ujma, 1995). CNS depression was seen in 5 of 14 patients (Osterloh & Olson, 1986).

a) Ataxia has been reported in humans; decreased motor performance was noted in experimental animals (Rees et al, 1986).

a) Vertigo and fainting may develop (Bradberry, 2000; von Oettingen, 1945).

a) Throbbing headache may occur (Bradberry, 2000).

a) Euphoria may result from a vasodilatation of cerebral vessels and increased intracranial pressure (Bradberry, 2000; Haverkos & Dougherty, 1988).

a) Lethargy may be seen (Osterloh & Olson, 1986; Shesser et al, 1980).

a) Speech may be incoherent (Shesser et al, 1980).

a) Nausea and vomiting may be seen in exposed humans; nausea and vomiting were reported in experimental animals (Cohen, 1979).

a) Anion gap acidosis may occur in patients with severe poisoning exhibiting tissue hypoxia and methemoglobinemia (Modarai et al, 2002; Stambach et al, 1997; Edwards & Ujma, 1995). Acidosis is generally seen at methemoglobin levels greater than 50% (Modarai et al, 2002). An anion gap acidosis was reported in one patient abusing butyl nitrite (Shesser et al, 1980).

a) Methemoglobinemia may be noted and is associated with cyanosis that does not respond to oxygen therapy. If nitrite-induced, methemoglobinemia may be delayed in onset and circulating methemoglobin levels may be prolonged (Bradberry, 2000; Smith et al, 1967; Nee & Fitzgerald, 1950).
b) Patients with methemoglobin concentrations less than 20% are usually asymptomatic (Bradberry, 2000). Patients with 15% to 30% methemoglobin may be symptomatic (dizziness, headache, cyanosis); those with 30% to 50% may have weakness, tachycardia, tachypnea, and mild dyspnea; patients with levels of 50% or more may have lethargy, stupor, coma, seizures, respiratory depression, cardiac dysrhythmias and acidosis; and levels above 70% are potentially lethal (Modarai et al, 2002; Wason et al, 1980). Patients with pre-existing cardiopulmonary disease or anemia are at increased risk of symptomatic methemoglobinemia at lower methemoglobin concentrations (Bradberry, 2000).
c) Nitrite-generated methemoglobinemia presents as cyanosis of the lips and the mucous membranes at methemoglobin levels as low as 1.5 grams/dL (10% saturation in a patient with normal hemoglobin levels) (Ellenhorn et al, 1997). Arterial blood samples appear as a chocolate brown color (Modarai et al, 2002).
d) Ethyl nitrite, butyl nitrite, isobutyl nitrite, and amyl nitrite are weak methemoglobin generating agents when inhaled (Gosselin et al, 1984). Acute ingestion of 15 mL of amyl nitrite resulted in a methemoglobin level of 83% in an adult woman (Stambach et al, 1997). In another case, a young man developed a methemoglobin level of 68% after ingesting an unknown amount of oral nitrites ('poppers') and an excessive amount of alcohol (blood alcohol level was 2.48% upon admission). He had profound cyanosis of the lips and fingers and was successfully treated with IV toluidine blue (100 mg) and hyperbaric oxygen therapy (3 sessions) (Lindenmann et al, 2015).
e) AMYL NITRITE
f) BUTYL NITRITE
g) ISOBUTYL NITRITE
h) ORAL: It appears that oral ingestion of these agents produces a more rapid and malignant methemoglobinemia than does inhalation exposure (Horne et al, 1979).

a) Massive Heinz body hemolytic anemia was described in a 33-year-old man following repeated inhalations of isobutyl nitrite. No G-6-PD deficiency was demonstrated (Bogart et al, 1986).
b) Mild hemolysis was noted in two patients following inhalation of volatile nitrites (Romeril & Concannon, 1981), and following inhalation of isobutyl nitrite in a patient with G6PD deficiency (Little & Schacter, 1979).
c) Two episodes of Heinz body hemolysis associated with amyl nitrite were seen in a 28-year-old. Subsequent testing showed his G6PD level was 40 percent of normal.
d) CASE REPORT: Hemolytic anemia was noted in a 23-year-old black man who had inhaled an unknown amount of butyl nitrite over 2 days (Owens & Davis, 1978).
e) CASE SERIES: Three patients (2 patients with G6PD deficiency) developed acute hemolysis after inhaling "poppers" (glass ampules containing alkyl nitrites) used as an aphrodisiac (Stalnikowicz et al, 2004).

a) MICE: Following exposure to 900 ppm of cyclohexyl nitrite for 45 minutes, blood was drawn from mice. Anemia was noted with 7% decreased erythrocyte counts and hemoglobin and hematocrit counts reduced by 10% and 8%, respectively (Soderberg & Flick, 1997).

a) MICE: Peripheral blood leukocytes decreased by an average of 40% following a 45 minute inhalation exposure to 300 ppm of cyclohexyl nitrite in mice (Soderberg & Flick, 1997).

a) Spilled isobutyl nitrite during intentional inhalation abuse has produced nasal and upper lip dermatitis, referred to as the popper's dermatitis (Bradberry, 2000; Bos et al, 1985; Fisher et al, 1981).

a) CASE REPORT: Allergic contact dermatitis was described in a 37-year-old man who had abused amyl nitrite for 4 years (Bos et al, 1985).
b) CASE REPORTS: Dax et al (1989) reported a palmar blotchy rash in one subject and facial erythema and rash in another who had abused amyl nitrite. Both had considerable pruritus (Dax et al, 1989). Both had positive skin tests to amyl nitrite.

a) Telangiectasia has been hypothesized to result from continued abuse of amyl and butyl nitrites due to continued vasodilatation (Lycka, 1987).

a) Flushing (vasodilation) and increased skin perception occurs with abuse (Bradberry, 2000; Haley, 1980).

a) A deep blue-grey discoloration of the skin, especially over the lips, nose and ears, and fingers may occur in cyanosed patients as a result of volatile nitrite abuse (Nee & Fitzgerald, 1950; Modarai et al, 2002; Lindenmann et al, 2015).

a) These substance are flammable and explosive. Burns may occur when these agents are used while smoking or near candles (Haverkos & Dougherty, 1988).

a) Nitrous acid burns of the skin and tracheobronchial tree may occur if an alkyl nitrite is hydrolyzed upon contact with skin or epithelial surfaces (Osterloh & Olson, 1986).

a) Smooth muscle relaxation occurs when high concentrations of volatile nitrites are inhaled (Haverkos & Dougherty, 1988).

a) Allergic reactions which include wheezing and itching may occur (Haverkos & Dougherty, 1988).

a) Volatile nitrites have been implicated as a factor in the development of AIDS beyond the association of high-transmission risk behavior sometimes observed with abuse of these agents (Schwarcz et al, 2007). In vitro studies have shown impaired lymphocyte and monocyte function which was irreversible after exposure to nitrites for 24 hours (Hersh et al, 1983)
b) It has been postulated that inhaled nitrites react with endogenous nitrogen, forming nitrosamine (Newell et al, 1984).
c) Various studies done with mice have shown contradictory results (McFadden et al, 1981; Lynch et al, 1985; Lewis et al, 1985).

a) Animal studies have shown various N-nitroso amine and amide compounds to be carcinogenic (Magee & Barnes, 1956; Bogovski & Bogovski, 1981; Preussman, 1983).

a) Positive (Haverkos et al, 1985; Mathur-Wagh et al, 1985; Osmond et al, 1985) and negative studies (Stevens et al, 1986; Goedert et al, 1986; Polk et al, 1987; Darrow et al, 1987) have been done concerning this linkage. More investigation needs to be done to confirm or deny this possible relationship.

a) In the presence of methemoglobinemia, it is important to remember that pulse oximetry is unreliable. Methemoglobin and oxyhemoglobin have similar maximal light absorption wavelengths, with oximeters mistaking methemoglobin for oxyhemoglobin and overestimating oxygen saturation. Arterial blood gases reveal normal partial pressures of oxygen and carbon dioxide and a normal calculated hemoglobin oxygen saturation (Bradberry, 2000; Edwards & Ujma, 1995). Use co-oximetry, which utilizes spectrophotometric techniques, to estimate the oxyhemoglobin concentration in the blood sample and calculate methemoglobin levels (Modarai et al, 2002).

a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).

a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
b) ADVERSE EFFECTS/CONTRAINDICATIONS

a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.

a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
b) ADVERSE EFFECTS/CONTRAINDICATIONS

a) In general, the vasodilatory effects of volatile nitrite abuse can usually be managed with symptomatic and supportive care. HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid for mild to moderate hypotension. SEIZURES: Evaluate for and correct methemoglobinemia. Administer benzodiazepines, barbiturates as necessary. METHEMOGLOBINEMIA: Monitor methemoglobin levels; levels above 20% to 30% may produce symptoms. Symptomatic patients should be treated with methylene blue. Administer oxygen therapy while preparing methylene blue.

a) Treatment is symptomatic and supportive. HYPOTENSION: If hypotension persists, administer dopamine or norepinephrine. SEIZURES: Monitor airway and continue to treat with benzodiazepines, barbiturates. METHEMOGLOBINEMIA: Correct any underlying methemoglobinemia as necessary.

a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).

a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .

a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).

a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).

a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).

a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):

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.

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).

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

a) Determine the methemoglobin concentration and evaluate the patient for clinical effects of methemoglobinemia (ie, dyspnea, headache, fatigue, CNS depression, tachycardia, metabolic acidosis). Treat patients with symptomatic methemoglobinemia with methylene blue (this usually occurs at methemoglobin concentrations above 20% to 30%, but may occur at lower methemoglobin concentrations in patients with anemia, or underlying pulmonary or cardiovascular disorders). Administer oxygen while preparing for methylene blue therapy.

a) INITIAL DOSE/ADULT OR CHILD: 1 mg/kg IV over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be given 1 hour after the first dose if methemoglobin levels remain greater than 30% or if signs and symptoms persist. NOTE: Methylene blue is available as follows: 50 mg/10 mL (5 mg/mL or 0.5% solution) single-dose ampules (Prod Info PROVAYBLUE(TM) intravenous injection, 2016) and 10 mg/1 mL (1% solution) vials (Prod Info methylene blue 1% intravenous injection, 2011). REPEAT DOSES: Additional doses may be required, especially for substances with prolonged absorption, slow elimination, or those that form metabolites that produce methemoglobin. NOTE: Large doses of methylene blue may cause methemoglobinemia or hemolysis (Howland, 2006). Improvement is usually noted shortly after administration if diagnosis is correct. Consider other diagnoses or treatment options if no improvement has been observed after several doses. If intravenous access cannot be established, methylene blue may also be given by intraosseous infusion. Methylene blue should not be given by subcutaneous or intrathecal injection (Prod Info methylene blue 1% intravenous injection, 2011; Herman et al, 1999). NEONATES: DOSE: 0.3 to 1 mg/kg (Hjelt et al, 1995).
b) CONTRAINDICATIONS: G-6-PD deficiency (methylene blue may cause hemolysis), known hypersensitivity to methylene blue, methemoglobin reductase deficiency (Shepherd & Keyes, 2004)
c) FAILURE: Failure of methylene blue therapy suggests: inadequate dose of methylene blue, inadequate decontamination, NADPH dependent methemoglobin reductase deficiency, hemoglobin M disease, sulfhemoglobinemia, or G-6-PD deficiency. Methylene blue is reduced by methemoglobin reductase and nicotinamide adenosine dinucleotide phosphate (NADPH) to leukomethylene blue. This in turn reduces methemoglobin. Red blood cells of patients with G-6-PD deficiency do not produce enough NADPH to convert methylene blue to leukomethylene blue (do Nascimento et al, 2008).
d) DRUG INTERACTION: Concomitant use of methylene blue with serotonergic drugs, including serotonin reuptake inhibitors (SRIs), selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), norepinephrine-dopamine reuptake inhibitors (NDRIs), triptans, and ergot alkaloids may increase the risk of potentially fatal serotonin syndrome (U.S. Food and Drug Administration, 2011; Stanford et al, 2010; Prod Info methylene blue 1% IV injection, 2011).

a) DOSE: 2 to 4 mg/kg intravenously over 5 minutes. Dose may be repeated in 30 minutes (Nemec, 2011; Lindenmann et al, 2006; Kiese et al, 1972).
b) SIDE EFFECTS: Hypotension with rapid intravenous administration. Vomiting, diarrhea, excessive sweating, hypotension, dysrhythmias, hemolysis, agranulocytosis and acute renal insufficiency after overdose (Dunipace et al, 1992; Hix & Wilson, 1987; Winek et al, 1969; Teunis et al, 1970; Marquez & Todd, 1959).
c) CONTRAINDICATIONS: G-6-PD deficiency; may cause hemolysis.

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.

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).

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

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.

1) Inhaled doses of 5 to 10 drops of amyl nitrite may cause violent flushing of the face and severe palpitations associated with feelings of severe cardiac distress. Inhalation of large amounts may also produce feelings of suffocation and muscular weakness (Prod Info amyl nitrite inhalant, 2004).
2) A death was reported in an adult following ingestion of an unknown amount of amyl nitrite. A methemoglobin level of 38% and 2 mg nitrite were noted in the blood. Stomach contents contained 77 mg nitrate (Sarvesvaran et al, 1992).
3) A fatality was reported in an adult following inhalation of amyl nitrite from a cloth tied around the nose. The brain was noted to be swollen and congested upon postmortem exam (Sarvesvaran et al, 1992).

1) Death was reported in an adult following ingestion of a small bottle of room odorizer containing approximately 9.5 mL of butyl nitrite (Wood & Cox, 1981).

1) Ingestion of less than 10 to 15 mL of an isobutyl nitrite containing room deodorizer was fatal in a 15-month-old child (Dixon et al, 1981).

1) Ingestion of a bottle of RUSH(R) (containing 10 to 15 mL of isobutyl nitrite) was fatal in a 23-year-old man (O'Toole et al, 1987).
2) A similar ingestion in a young adult man resulted in a fatality (Dixon et al, 1981).

1) Ingestion of 10 mL resulted in a methemoglobin concentration of 33%, agitation, and cyanosis in a 29-year-old man (Laaban et al, 1985).
2) An adult woman ingested 15 mL of amyl nitrite and became unconscious a short time later. She was profoundly cyanosed with tachycardia (pulse, 130 bpm) and hypotension (BP 80/30 mmHg) when admitted to the ED. Glasgow coma score of 5 was reported. Arterial blood gases revealed acidosis (pH 7.1). Methemoglobin level measured on co-oximetry was 83%. She made a full recovery following 2 doses of methylene blue (Stambach et al, 1997).

a) Roughly equivalent oral doses have produced serum nitrite concentrations that vary widely between individuals (Gowans, 1990).

a) A death was reported in an adult following ingestion of an unknown amount of amyl nitrite. A methemoglobin level of 38% and 2 milligrams nitrite were noted in the blood. Stomach contents contained 77 milligrams nitrate (Sarvesvaran et al, 1991).
b) A fatality was reported in an adult following inhalation of amyl nitrite from a cloth tied around the nose. The brain was noted to be swollen and congested upon postmortem exam (Sarvesvaran et al, 1992).

a) 158 mg/kg after 30M (McFadden et al, 1981)

a) 83 mg/kg (Wood & Cox, 1981)