Contact Us    Contact Us     |     Feedback
MOBILE VIEW  | 

DETTOL

Export To Excel

Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Dettol is a mixture of approximately 4.8% chloroxylenol, pine oil, isopropyl alcohol, and possibly castor oil, soap, and burned sugar.

Specific Substances

    1) Dettol

Available Forms Sources

    A) FORMS
    1) Dettol is a mixture of approximately 4.8% chloroxylenol, pine oil, isopropyl alcohol, and possibly castor oil, soap, and burned sugar (Meek et al, 1977; Chan et al, 1993).
    B) USES
    1) Dettol is widely used as an antiseptic and disinfectant (Countselinis & Boukis, 1976; (Joubert et al, 1978; JEF Reynolds , 1996).
    2) It has also been used as a substance of abuse (Khan et al, 1979), an abortifacient when instilled vaginally (Joubert et al, 1978), and ingested in suicide attempts (Chan et al, 1993; Chan, 1994).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) WITH POISONING/EXPOSURE
    1) Principal effects from ingestion include CNS depression ranging from drowsiness to coma, irritation or corrosive injury to the larynx which can result in airway obstruction, aspiration with secondary respiratory distress syndrome or pneumonia, and hypotension. Less common effects include renal failure and hepatotoxicity.
    2) Irritation or corrosion of the oral and gastrointestinal mucosa can occur. Irritation may result from dermal or eye contact.
    0.2.3) VITAL SIGNS
    A) WITH POISONING/EXPOSURE
    1) Tachypnea, respiratory distress, bradycardia, tachycardia, hypotension, and fever or hypothermia can occur.
    0.2.6) RESPIRATORY
    A) WITH POISONING/EXPOSURE
    1) Laryngeal obstruction, upper airway edema, aspiration pneumonia, and mild to severe respiratory distress can occur following ingestion and may be delayed hours or days.
    0.2.7) NEUROLOGIC
    A) WITH POISONING/EXPOSURE
    1) CNS depression is common and can range from drowsiness to coma.
    0.2.8) GASTROINTESTINAL
    A) WITH POISONING/EXPOSURE
    1) Nausea, vomiting, and abdominal pain are common following ingestion. Diarrhea and minor gastrointestinal hemorrhage are less common.
    0.2.9) HEPATIC
    A) WITH POISONING/EXPOSURE
    1) Mild hepatomegaly and elevated liver enzyme activities have been infrequently reported.
    0.2.10) GENITOURINARY
    A) WITH POISONING/EXPOSURE
    1) Acute renal failure in one fatal case, and renal impairment in 3 patients, have been reported. Renal effects are believed unlikely unless very high volumes (200 to 500mL) of Dettol are ingested.
    0.2.13) HEMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Leukocytosis can occur following Dettol ingestion.
    0.2.14) DERMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Corrosion or irritation of the skin and mucosa can occur. Irritation is more commonly reported. Sensitization and allergic contact dermatitis from exposure to chloroxylenol has been reported.
    0.2.20) REPRODUCTIVE
    A) DETTOL - There is insufficient information concerning the potential reproductive effects of Dettol in humans or animals.
    B) INGREDIENTS and toxicity of dettol include the following:
    1) CHLOROXYLENOL - Embryotoxicity or fetotoxicity has been reported in animals following oral administration of high concentrations of chloroxylenol during pregnancy.
    2) ISOPROPYL ALCOHOL - Skeletal malformations have been produced in rat offspring following inhalational exposure of the dams to isopropyl alcohol at levels which produced maternal toxicity. The majority of animal studies have failed to demonstrate conclusive evidence of adverse reproductive effects as a result of isopropyl alcohol exposure in the absence of maternal toxicity.
    3) PINE OIL - There is insufficient information concerning the potential reproductive effects of Pine oil in humans or animals.

Laboratory Monitoring

    A) Chloroxylenol, an ingredient of Dettol, has been measured in the blood and liver tissue post-mortem. Monitoring of blood levels of Dettol ingredients has not yet been proven to be of clinical value. A toxicology screen to rule out other drugs and for co-ingestants may be useful.
    B) Monitor electrolytes, liver function tests, BUN, creatinine and CPK.
    C) Monitor pulse oximetry and/or blood gases in patients with evidence of aspiration pneumonitis or ARDS.
    D) Monitor urine output and urinalysis.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Position the patient in the left lateral decubitus position with suction available to reduce the possibility of aspiration of vomitus. Most life threatening effects after Dettol ingestion are the result of aspiration.
    B) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression.
    C) Dilution is controversial as it may increase the risk of vomiting and aspiration, particularly in a patient with altered level of consciousness. Consider dilution only if the patient is conscious and fully alert.
    D) Activated charcoal and gastric lavage are generally not recommended. Most life-threatening effects after dettol ingestion result from aspiration, and the risk or aspiration may be increased by charcoal-induced emesis or gastric lavage. Aspiration and pulmonary complications have occurred following lavage after Dettol ingestion. If gastric lavage is chosen, airway protection using a cuffed endotracheal tube is mandatory.
    E) Monitor the respiratory status carefully and frequently for the development of laryngeal edema, airway constriction and respiratory distress. Supplemental oxygen, intubation, and/or assisted ventilation may be needed. Avoid a net positive fluid balance. Only administer antibiotics if an infection is present.
    F) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    G) HYPOTENSION
    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.
    0.4.3) INHALATION EXPOSURE
    A) The toxic effects of Dettol vapor inhalation have not been reported. Aspiration of dettol may cause life-threatening upper airway edema.
    B) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    C) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    D) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    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) Dettol ingestions of 200 and 300 milliliters were fatal in two adults. Many other reported fatalities lack information about the ingested dose. Cases of severe toxicity have survived with medical treatment usually provided within 2 hours of ingestion. Death or severe morbidity have been attributed to aspiration following Dettol ingestion and emesis or gastric lavage.
    B) Toxicity has resulted from ingestion of 20 milliliters to 600 milliliters in adults and in one pediatric case involving an estimated ingestion of 120 milliliters.

Clinical Effects

Summary Of Exposure

    A) WITH POISONING/EXPOSURE
    1) Principal effects from ingestion include CNS depression ranging from drowsiness to coma, irritation or corrosive injury to the larynx which can result in airway obstruction, aspiration with secondary respiratory distress syndrome or pneumonia, and hypotension. Less common effects include renal failure and hepatotoxicity.
    2) Irritation or corrosion of the oral and gastrointestinal mucosa can occur. Irritation may result from dermal or eye contact.

Vital Signs

    3.3.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Tachypnea, respiratory distress, bradycardia, tachycardia, hypotension, and fever or hypothermia can occur.
    3.3.2) RESPIRATIONS
    A) WITH POISONING/EXPOSURE
    1) Mild to severe respiratory distress have been reported following ingestion (Joynt et al, 1997; Chan & Critchley, 1996; Archer, 1979; Chan et al, 1993). Tachypnea may be present (Meek et al, 1977).
    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) A study of 67 cases of Dettol ingestion reported fever in 13 out of 67 (20%) patients (Chan et al, 1993). Subnormal temperature has also been reported (Joubert et al, 1978; Archer, 1979).
    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) HYPOTENSION - Mild to severe hypotension has been reported following ingestion (Meek et al, 1977; Chan et al, 1993).
    3.3.5) PULSE
    A) WITH POISONING/EXPOSURE
    1) BRADYCARDIA - Irregular bradycardia (50 beats/minute) developed approximately 9 hours after ingestion of about 300 mL of Dettol in a fatal case. The heart rate prior to this time had been normal (Meek et al, 1977).
    2) TACHYCARDIA - Sinus tachycardia was present in 4 out of 67 patients (6%) who had ingested 20mL to 600 mL Dettol (Chan et al, 1993). Tachycardia developed approximately 4 hours after ingestion of 350 mL of Dettol in another case (Joubert et al, 1978).

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) MIOSIS - Constricted pupils with decreased responsiveness to light are findings in comatose persons following Dettol ingestion (Meek et al, 1977; Joubert et al, 1978).
    2) IRRITATION - A Draize score indicating severe eye irritation, with disturbances of the cornea and iris persisting for 7 days, was produced in rabbit eyes exposed to 0.1mL of Dettol (reviewed in Grant & Schuman, 1993). If the eyes were washed with water within 2 to 4 seconds, a less severe reaction occurred and the eyes fully recovered by 14 days.
    3) CORNEAL OPACITY developed in animal eyes exposed to a Dettol ingredient, isopropyl alcohol (Rowe & McCollister, 1982).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) LARYNGEAL EDEMA - Significant laryngeal edema resulting in respiratory distress or respiratory obstruction can develop, may be delayed hours or days following ingestion, and can reoccur after periods of apparent improvement (Joynt et al, 1997; Archer, 1979; Chan et al, 1993).
    2) CORROSIVE INJURY can occur as a result of Dettol ingestion (Meek et al, 1977) but is not a consistent finding (Joubert et al, 1978). Ulceration of the vocal cords in a non-fatal case (Archer, 1979) and diffuse corrosive lesions of the esophagus found at post-mortem examination in another case (Coutselinis & Boukis, 1976) have been reported.
    3) IRRITATION - Hoarseness, dysphagia, soreness and erythema of the mouth and throat occur frequently after Dettol ingestion (Archer, 1979; Chan et al, 1993; Chan, 1994).

Respiratory

    3.6.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Laryngeal obstruction, upper airway edema, aspiration pneumonia, and mild to severe respiratory distress can occur following ingestion and may be delayed hours or days.
    3.6.2) CLINICAL EFFECTS
    A) INJURY OF UPPER RESPIRATORY TRACT
    1) WITH POISONING/EXPOSURE
    a) Severe laryngeal edema leading to upper airway obstruction can occur and may be delayed hours to days after ingestion and despite supportive treatment. Intubation and respiratory assistance may be required (Joynt et al, 1997; Archer, 1979; Chan et al, 1993; Chan, 1994; Chan & Critchley, 1995).
    b) CASE REPORT - A 69-year-old female with a history of bipolar disorder, diabetes mellitus, essential hypertension, and chronic renal impairment, was found in respiratory distress and had stridor after ingesting Dettol and Domestos (1-5% sodium hypochlorite); exact amounts were unknown for either agent. Laryngoscope revealed a red, swollen epiglottis and posterior pharyngeal wall, along with swollen and reddened vocal cords. The patient received a tracheostomy on day 2 because of continuing upper airway swelling, and was treated with methylprednisolone (500 mg daily) for a week. The tracheostomy was successfully removed 18 days after admission, and the patient received ongoing psychiatric care (Graham, 2004).
    c) CASE REPORT - A 65-year-old developed right lower lobe infiltrates and respiratory distress after ingesting Dettol (300 ml). Erythema of the pharynx and epiglottis was noted on laryngoscopy. Eighteen hours after ingestion she was extubated. Forty eight hours after admission she developed hoarseness rapidly followed by stridor and respiratory distress requiring endotracheal intubation. Vocal cord swelling and supraglottic ulcers were noted on fiberoptic laryngoscopy. She was extubated 72 hours after admission (Joynt et al, 1997).
    B) PULMONARY ASPIRATION
    1) WITH POISONING/EXPOSURE
    a) Dettol is a potential aspiration hazard. Aspiration and respiratory complications such as pneumonia and respiratory distress syndrome have been associated with spontaneous vomiting or gastric lavage following ingestion of Dettol alone or as a co-ingestant (Chan & Critchley, 1996; Chan et al, 1993; Chan, 1994; Chan, 1994; Chan & Critchley, 1995; Chan et al, 1995a). Evidence of aspiration was present in one fatal case (Chan et al, 1995a).
    b) The development of pneumonia and respiratory distress is often delayed hours to days (Chan, 1994).
    C) DISORDER OF RESPIRATORY SYSTEM
    1) WITH POISONING/EXPOSURE
    a) Chronic obstructive pulmonary disease was exacerbated in a 79-year-old female who ingested 500 milliliters of Dettol (Chan et al, 1993).
    b) Exacerbation of chronic obstructive pulmonary disease and asthma has been reported after dettol ingestion. Adult respiratory distress syndrome may develop in severe cases (Chan & Critchley, 1996).
    D) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Signs of pulmonary edema occurred 21 hours post-ingestion in a patient whose neurological status had largely returned to normal by that time; the patient died 16 hours later. At autopsy, non-cardiogenic pulmonary edema and bronchopneumonia were evident (Meek et al, 1977).

Neurologic

    3.7.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) CNS depression is common and can range from drowsiness to coma.
    3.7.2) CLINICAL EFFECTS
    A) COMA
    1) WITH POISONING/EXPOSURE
    a) Coma has resulted in 2 cases following estimated Dettol ingestions of 300 to 350 mL (Meek et al, 1977; Joubert et al, 1978), and in one case estimated to have ingested 500 mL Dettol and 500 mL of Savlon, a product containing centrimide and chlorhexidine gluconate (Chan, 1994).
    B) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) A study of 67 patients with Dettol ingestion of 20mL to 600mL reported the following (Chan et al, 1993):
    1) Drowsiness/confusion in 19 patients (28%); 6 of these patients co-ingested ethanol or hypnotics.
    2) Headache in 3 patients (5%).
    3) Dizziness in 2 patients (3%).
    b) CASE REPORT - A 69-year-old female with a history of bipolar affective disorder ingested an unknown quantity of Dettol and Domestos (a 1-5% sodium hypochlorite) and developed a decreased level of consciousness which slowly resolved over 4 days. A computed tomography (CT) scan of the brain showed cerebral atrophy; no baseline CT was available. Her neurological status had returned to baseline by the time of discharge (Graham, 2004).

Gastrointestinal

    3.8.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Nausea, vomiting, and abdominal pain are common following ingestion. Diarrhea and minor gastrointestinal hemorrhage are less common.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting occurred in 50 out of 67 (75%) of patients who ingested Dettol (Chan et al, 1993). Minor hematemesis was reported in 2 of these patients.
    B) ABDOMINAL PAIN
    1) WITH POISONING/EXPOSURE
    a) Epigastric or abdominal pain was reported in 16 out of 67 cases (24%) of Dettol ingestion (Chan et al, 1993).
    C) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea occurred in 1% of 67 cases of Dettol ingestion (Chan et al, 1993). Severe, watery diarrhea of 48 hours duration was reported in another case (Joubert et al, 1978).
    D) GASTRIC ULCER WITH HEMORRHAGE
    1) WITH POISONING/EXPOSURE
    a) Minor gastrointestinal hemorrhage occurred in up to 6% of patients with a history of Dettol ingestion; mild esophagitis and stomach erosions were detected in one patient upon gastroscopy (Chan & Critchley, 1995). No esophageal strictures were found. Gastroscopy was not recommended as a routine measure.
    b) Diffuse corrosive lesions involving the esophagus and stomach were found upon post-mortem examination in one case (Coutselinis & Boukis, 1976).

Hepatic

    3.9.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Mild hepatomegaly and elevated liver enzyme activities have been infrequently reported.
    3.9.2) CLINICAL EFFECTS
    A) LARGE LIVER
    1) WITH POISONING/EXPOSURE
    a) Mild hepatomegaly and ascites possibly attributable to ingestion of Dettol for at least 10 years was reported in one case (Khan et al, 1979).
    B) LIVER ENZYMES ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT - Elevated gamma glutamyltransferase activity (84 IU/L) was present in a woman who had a 10 year history of Dettol abuse (Khan et al, 1979). Alkaline phosphatase activity was also elevated.
    b) CASE REPORT - Elevated AST/SGOT was measured approximately 2 hours after ingestion of 300 mL (Meek et al, 1977). The patient died 38 hours after ingestion.

Genitourinary

    3.10.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Acute renal failure in one fatal case, and renal impairment in 3 patients, have been reported. Renal effects are believed unlikely unless very high volumes (200 to 500mL) of Dettol are ingested.
    3.10.2) CLINICAL EFFECTS
    A) ACUTE RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) Hematuria, glycosuria, ketonuria, elevated BUN, and oliguria unresponsive to furosemide developed approximately 21 hours after ingestion of about 300 mL of Dettol (Meek et al, 1977). The patient died 38 hours after Dettol ingestion, despite peritoneal dialysis and supportive treatment.
    B) ABNORMAL RENAL FUNCTION
    1) WITH POISONING/EXPOSURE
    a) Elevated plasma urea and creatinine occurred in three patients who ingested 200 to 500 mL of Dettol, with Savlon or Clonazepam co-ingested by two of the patients (Chan & Critchley, 1994). Coma, aspiration pneumonia, respiratory arrest, hypotension and, in one case, cardiac arrest also occurred.
    1) Renal effects were attributed by the authors to direct nephrotoxicity of chloroxylenol and the contributing factors of hypotension, vomiting and dehydration (Chan & Critchley, 1994).
    2) In another case, a 69-year-old female with a history of bipolar disorder along with renal insufficiency ingested an unknown quantity of Dettol and Domestos (1-5% sodium hypochlorite), and developed an increased BUN to a peak of 31.9 mmol/L (baseline 14 mmol/L) and creatinine to a peak of 270 micromoles/L (baseline 160 micromoles/L). Levels returned to baseline within 25 days with no intervention (Graham, 2004).

Hematologic

    3.13.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Leukocytosis can occur following Dettol ingestion.
    3.13.2) CLINICAL EFFECTS
    A) LEUKOCYTOSIS
    1) WITH POISONING/EXPOSURE
    a) Leucocytosis was reported in 37 out of 67 (55%) patients with a history of Dettol ingestion alone or with other substances (Chan et al, 1993).

Dermatologic

    3.14.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Corrosion or irritation of the skin and mucosa can occur. Irritation is more commonly reported. Sensitization and allergic contact dermatitis from exposure to chloroxylenol has been reported.
    3.14.2) CLINICAL EFFECTS
    A) CHEMICAL BURN
    1) WITH POISONING/EXPOSURE
    a) MUCOSA - Corrosive injury to the mouth, throat and vocal cords has been reported in non-fatal cases (Joynt et al, 1997; Archer, 1979) or upon autopsy (Coutselinis & Boukis, 1976; Meek et al, 1977), but is not a consistent finding (Joubert et al, 1978). Mucosal irritation is more common.
    b) SKIN - Post-mortem evidence of corrosive injury to the lips and chin was reported in one case (Meek et al, 1977). No corrosive injury was reported in another case (Joubert et al, 1978).
    B) SKIN IRRITATION
    1) WITH POISONING/EXPOSURE
    a) Significant mucosal irritation can occur (Archer, 1979; Chan et al, 1993; Chan, 1994; Chan & Critchley, 1995). Dermal irritation has been reported in an infant (Archer, 1979).
    b) INGREDIENTS - Isopropyl alcohol (Rowe & McCollister, 1982) and dilutions of chloroxylenol which are typically in use (JEF Reynolds , 1996) are not significantly irritating.
    C) CONTACT DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Sensitization and allergic contact dermatitis from chloroxylenol exposure have been reported (Storrs, 1975) Myat & Beck, 1985; (JEF Reynolds , 1996).

Reproductive

    3.20.1) SUMMARY
    A) DETTOL - There is insufficient information concerning the potential reproductive effects of Dettol in humans or animals.
    B) INGREDIENTS and toxicity of dettol include the following:
    1) CHLOROXYLENOL - Embryotoxicity or fetotoxicity has been reported in animals following oral administration of high concentrations of chloroxylenol during pregnancy.
    2) ISOPROPYL ALCOHOL - Skeletal malformations have been produced in rat offspring following inhalational exposure of the dams to isopropyl alcohol at levels which produced maternal toxicity. The majority of animal studies have failed to demonstrate conclusive evidence of adverse reproductive effects as a result of isopropyl alcohol exposure in the absence of maternal toxicity.
    3) PINE OIL - There is insufficient information concerning the potential reproductive effects of Pine oil in humans or animals.
    3.20.2) TERATOGENICITY
    A) HUMANS
    1) No information concerning teratogenic effects of Dettol in humans was found in TERIS (1996) or through a MEDLINE search.
    B) SPECIFIC AGENT
    1) CHLOROXYLENOL - The potential teratogenic risk to humans is not known due to the unavailability of data, but is considered unlikely (TERIS , 1996).
    a) Embryotoxicity and fetotoxic effects involving the musculoskeletal system occurred in rats orally administered 17100 mg/kg of chloroxylenol during days 1 to 19 of pregnancy (RTECS , 1996).
    2) ISOPROPYL ALCOHOL - The teratogenic potential of isopropanol in humans is unknown.
    a) No teratogenic effects were observed in rats inhaling 3500 ppm for 7 hours/day during organogenesis. Exposure to higher concentrations (7000 and 10,000 ppm) produced maternal toxicity and resulted in dose-related decreased fetal weight and increased skeletal malformations. The blood isopropanol levels in non-pregnant rats were shown to be undetectable after exposure to 3500 ppm, 680 mg/dL after exposure to 7000 ppm, and 790 mg/dL after exposure to 10,000 ppm (Nelson et al, 1988).

Carcinogenicity

    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) No information concerning carcinogenic effects of Dettol in humans was found at the time of this review (IARC, 1987) US DHHS, 1994; (RTECS , 1996; HSDB , 1996).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Chloroxylenol, an ingredient of Dettol, has been measured in the blood and liver tissue post-mortem. Monitoring of blood levels of Dettol ingredients has not yet been proven to be of clinical value. A toxicology screen to rule out other drugs and for co-ingestants may be useful.
    B) Monitor electrolytes, liver function tests, BUN, creatinine and CPK.
    C) Monitor pulse oximetry and/or blood gases in patients with evidence of aspiration pneumonitis or ARDS.
    D) Monitor urine output and urinalysis.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Monitor electrolytes, liver function tests, BUN, creatinine and CPK.
    2) Chloroxylenol, an ingredient of Dettol, has been measured in the blood and liver tissue post-mortem (Coutselinis & Boukis, 1976). Monitoring of blood levels of Dettol ingredients has not yet been proven to be of clinical value. A toxicology screen to rule out other drugs and for co-ingestants may be useful.
    B) ACID/BASE
    1) Monitor pulse oximetry and/or blood gases in patients with evidence of aspiration pneumonitis or ARDS.
    4.1.3) URINE
    A) URINALYSIS
    1) Monitor urine output and urinalysis.
    4.1.4) OTHER
    A) OTHER
    1) OTHER
    a) Routine endoscopy is not recommended except to investigate other causes of gastric bleeding, such as peptic ulcers, or if oral chemical burns are present and the need to evaluate if the extent of esophageal damage outweighs the risks of endoscopy (Chan & Critchley, 1995). In the later case, the endoscopy should be performed early and only in the clinically stable and conscious patient (Chan & Critchley, 1995).
    2) MONITORING
    a) Frequently assess patient for the development of signs of respiratory obstruction and respiratory distress, which may be delayed and reoccur despite apparent clinical stability (Archer, 1979).

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Chest x-ray may be required to evaluate possible pulmonary aspiration and secondary effects.

Methods

    A) SPECTROSCOPY/SPECTROMETRY
    1) Chloroxylenol, an ingredient of Dettol, has been spectrophotometrically determined in the blood and liver tissue post-mortem (Coutselinis & Boukis, 1976).

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) Persons with evidence of lip or oral mucosa injury, respiratory distress, and persons with a history of nausea, vomiting and/or impaired level of consciousness following Dettol ingestion should be admitted for a period of observation. Significant airway edema and respiratory effects may be delayed in onset, especially if vomiting or gastric lavage has occurred (Joynt et al, 1997; Archer, 1979; Chan et al, 1993; Chan, 1994).
    1) Airway edema or respiratory distress developed within 2 to 3 hours of ingestion and vomiting in 2 cases (Archer, 1979; Chan, 1994). Pulmonary edema occurred 21 hours post-ingestion in a patient whose neurological status had largely returned to normal at that time; the patient died 16 hours later (Meek et al, 1977).
    2) Delayed upper airway edema requiring reinsertion of an endotracheal tube was reported 48 hours after ingestion (30 hours after being extubated the first time) in one case (Joynt et al, 1997).

Monitoring

    A) Chloroxylenol, an ingredient of Dettol, has been measured in the blood and liver tissue post-mortem. Monitoring of blood levels of Dettol ingredients has not yet been proven to be of clinical value. A toxicology screen to rule out other drugs and for co-ingestants may be useful.
    B) Monitor electrolytes, liver function tests, BUN, creatinine and CPK.
    C) Monitor pulse oximetry and/or blood gases in patients with evidence of aspiration pneumonitis or ARDS.
    D) Monitor urine output and urinalysis.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) GENERAL -
    1) Position the patient in the left lateral decubitus position with suction available to reduce the possibility of aspiration of vomitus. Most life threatening effects after Dettol ingestion are the result of aspiration.
    B) EMESIS/ NOT RECOMMENDED -
    1) Ipecac-induced emesis is NOT recommended.
    C) DILUTION -
    1) Dilution is controversial as it may increase the risk of vomiting and aspiration, particularly in a patient with altered level of consciousness. Consider dilution only if the patient is conscious and fully alert.
    D) ACTIVATED CHARCOAL/NOT RECOMMENDED -
    1) Use of activated charcoal is controversial as it may precipitate vomiting and may obscure visualization of the mucosa in the event that endoscopy is required. Routine prehospital use is NOT recommended.
    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression.
    2) Ipecac-induced emesis was associated with severe airway edema, airway constriction, and respiratory distress in a toddler who drank Dettol (Archer, 1979). Vomiting following Dettol ingestion has been associated with aspiration pneumonia and Adult Respiratory Distress Syndrome (Chan, 1994). Most life threatening effects after Dettol ingestion are the result of aspiration (Chan et al, 1993).
    B) DILUTION
    1) Dilution is controversial as it may increase the risk of vomiting and aspiration, particularly in a patient with altered level of consciousness. Consider dilution only if the patient is conscious and fully alert. Since significant caustic injury is not common after Dettol ingestion, routine dilution is not recommended.
    C) GASTRIC LAVAGE
    1) Gastric lavage following ingestion of Dettol has been associated with aspiration and respiratory complications (Chan et al, 1993; Chan et al, 1995a), and therefore is generally NOT recommended. If gastric lavage is performed, it should be done with a wide bore tube only after airway protection with a cuffed endotracheal tube (Chan, 1994).
    D) ACTIVATED CHARCOAL
    1) Activated charcoal is generally not recommended. Most life-threatening effects after dettol ingestion result from aspiration, and the risk or aspiration may be increased by charcoal-induced emesis.
    6.5.3) TREATMENT
    A) AIRWAY MANAGEMENT
    1) Monitor the respiratory status carefully and frequently for the development of laryngeal edema, airway constriction and respiratory distress. Supplemental oxygen, intubation, and/or assisted ventilation with positive-end-expiratory pressure (PEEP) or continuous-positive-airway pressure (CPAP) may be needed. Avoid a net positive fluid balance.
    B) 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).
    C) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).

Inhalation Exposure

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

Eye Exposure

    6.8.1) DECONTAMINATION
    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.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    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

Summary

    A) Dettol ingestions of 200 and 300 milliliters were fatal in two adults. Many other reported fatalities lack information about the ingested dose. Cases of severe toxicity have survived with medical treatment usually provided within 2 hours of ingestion. Death or severe morbidity have been attributed to aspiration following Dettol ingestion and emesis or gastric lavage.
    B) Toxicity has resulted from ingestion of 20 milliliters to 600 milliliters in adults and in one pediatric case involving an estimated ingestion of 120 milliliters.

Minimum Lethal Exposure

    A) CASE REPORTS
    1) Two adult fatalities have resulted from estimated Dettol ingestions of 200 milliliters and 300 milliliters. Hospital admission occurred one and one-half hour after ingestion in both cases (Meek et al, 1977; Chan et al, 1993).
    a) Hypotension, aspiration, respiratory failure and cardiac arrest occurred in the adult who ingested 200 milliliters (Chan et al, 1993). The person who ingested 300 milliliters developed coma, hypotension, pulmonary edema and renal failure (Meek et al, 1977).
    2) Reports of two adult fatalities from Dettol ingestion did not specify the amount ingested (Coutselinis & Boukis, 1976; Chan, 1994).
    3) Aspiration as a result of emesis or unprotected gastric lavage can cause death or life-threatening effects (Chan, 1994; Chan & Critchley, 1995).
    4) A toddler was in danger of complete upper airway obstruction following induction of emesis after ingestion of a maximum of 125 milliliters of Dettol (Archer, 1979). The toddler survived with intubation and other medical support.
    5) An adult developed severe laryngeal edema and respiratory distress following unprotected gastric lavage while comatose after ingesting 500 milliliters of Dettol and an unspecified amount of Savlon liquid which contained 0.3% chlorhexidine gluconate and 3% centrimide (Chan et al, 1993). The patient was intubated and survived with medical support.

Maximum Tolerated Exposure

    A) CASE REPORTS
    1) A 24-year-old survived Dettol ingestion of 600 milliliters with only supportive medical care administered within 5 hours (Chan et al, 1993). The patient had impaired level of consciousness and developed aspiration pneumonia. No gastric lavage, charcoal or cathartics had been administered.

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) CASE REPORTS
    a) ADULT FATALITY - The blood chloroxylenol level was 2.3 milligrams per 100 milliliters (Coutselinis & Boukis, 1976). The dose and time of Dettol ingestion relative to the blood analysis were not indicated.

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Dettol is widely used as an antiseptic. Chloroxylenol is principally effective against Gram-positive bacteria, is less active against staphylococci and Gram-negative bacteria, and is ineffective againist Pseudomonas. It is also ineffective against bacterial spores (JEF Reynolds , 1996).

Toxicologic Mechanism

    A) Dettol has corrosive or irritant activities on the mucosa and gastrointestinal tract. Local tissue damage, airway obstruction, vomiting and hematemesis are examples of effects.
    B) Dettol is a central nervous system depressant.
    C) Ingested Dettol is a pulmonary aspiration hazard which can cause significant pulmonary irritation and inflammatory responses, such as, Adult Respiratory Distress Syndrome and pneumonia. In addition to low viscosity, it has been suggested that aspiration may be due to impairment of the gag reflex by Dettol.
    D) Dettol may have a direct emetic action.
    E) Ingredients of dettol may produce the following:
    1) PINE OIL - gastrointestinal irritation, hypotension, CNS and respiratory depression, aspiration and sequelae (Adult Respiratory Distress Syndrome, chemical pneumonitis, pneumonia)
    2) ISOPROPYL ALCOHOL - CNS depression, respiratory failure, hypotension
    3) CHLOROXYLENOL-RELATED CHEMICALS - CNS depression, respiratory failure, convulsions, arrhythmias
    4) References: Meek et al, 1977; Joubert et al, 1978; Chan et al, 1993; Chan and Critchley, 1995; Chan et al, 1995a.

References

General Bibliography

    1) Archer LNJ: Upper airways obstruction after Dettol ingestion. Br Med J 1979; 2(6181):19-20.
    2) Artigas A, Bernard GR, Carlet J, et al: The American-European consensus conference on ARDS, part 2: ventilatory, pharmacologic, supportive therapy, study design strategies, and issues related to recovery and remodeling.. Am J Respir Crit Care Med 1998; 157:1332-1347.
    3) Brower RG, Matthay AM, & Morris A: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Eng J Med 2000; 342:1301-1308.
    4) Burgess JL, Kirk M, Borron SW, et al: Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 1999; 34(2):205-212.
    5) Cataletto M: Respiratory Distress Syndrome, Acute(ARDS). In: Domino FJ, ed. The 5-Minute Clinical Consult 2012, 20th ed. Lippincott Williams & Wilkins, Philadelphia, PA, 2012.
    6) Chan TY & Critchley JA: Is chloroxylenol nephrotoxic like phenol? A study of patients with Dettol poisoning. Vet Human Toxicol 1994; 36:250-251.
    7) Chan TY & Critchley JA: Pulmonary and other complications with Dettol poisoning (abstract 19). Ann Emerg Med 1995; 26:718.
    8) Chan TY, Lau MS, & Critchley JA: Serious complications associated with Dettol poisoning. Q J Med 1993; 86:735-738.
    9) Chan TYK & Critchley AJH: Pulmonary aspiration following Dettol poisoning: the scope for prevention. Human Exp Toxicol 1996; 15:843-846.
    10) Chan TYK, Critchley AJH, & Lau JTF: The risk of aspiration in Dettol poisoning: a retrospective cohort study. Hum Exp Toxicol 1995a; 14:190-191.
    11) Chan TYK: Poisoning due to Savlon (cetrimide) liquid. Hum Exp Toxicol 1994; 13:681-682.
    12) Coutselinis A & Boukis D: Suicidal intoxication with Dettol (chloroxylenol) (a case report). Med Sci Law 1976; 16:180.
    13) Graham CA: Stridor after ingestion of dettol and domestos. Eur J Emerg Med 2004; 11:52-54.
    14) HSDB : Hazardous Substances Data Bank. National Library of Medicine. Bethesda, MD (Internet Version). Edition expires 1996; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    15) Haas CF: Mechanical ventilation with lung protective strategies: what works?. Crit Care Clin 2011; 27(3):469-486.
    16) IARC: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Overall Evaluations of carcinogenicity: An Updating of IARC Monographs Volumes 1 to 42, Supplement 7, International Agency for Research on Cancer, World Health Organization, Geneva, Switzerland, 1987.
    17) JEF Reynolds : Martindale: The Extra Pharmacopoeia. The Pharmaceutical Press. London, UK (Internet Version). Edition expires 1996; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    18) Joubert P, Hundt H, & Du Toit P: Severe Dettol (chloroxylenol and terpineol) poisoning. Br Med J 1978; 1(6117):890.
    19) Joynt GM, Ho KM, & Gomersall CD: Delayed upper airway obstruction: a life-threatening complication of Dettol poisoning. Anaesthesia 1997; 52:261-263.
    20) Khan JS, Wilson MC, & Taylor TV: A case of Dettol addiction. Br Med J 1979; 1(6166):791-2.
    21) Kleinman ME, Chameides L, Schexnayder SM, et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 14: pediatric advanced life support. Circulation 2010; 122(18 Suppl.3):S876-S908.
    22) Kollef MH & Schuster DP: The acute respiratory distress syndrome. N Engl J Med 1995; 332:27-37.
    23) Lau MS, Chan TY, & Critchley JA: Serious complications in Dettol poisoning (abstract P-23), XVI International Congress of the European Association of Poison Centers and Clinical Toxicologists, Vienna, Austria, 1994.
    24) Meek D, Piercy DM, & Gabriel R: Fatal self-poisoning with Dettol. Post grad Med J 1977; 53:229-231.
    25) NHLBI ARDS Network: Mechanical ventilation protocol summary. Massachusetts General Hospital. Boston, MA. 2008. Available from URL: http://www.ardsnet.org/system/files/6mlcardsmall_2008update_final_JULY2008.pdf. As accessed 2013-08-07.
    26) National Heart,Lung,and Blood Institute: Expert panel report 3: guidelines for the diagnosis and management of asthma. National Heart,Lung,and Blood Institute. Bethesda, MD. 2007. Available from URL: http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf.
    27) Nelson BK, Brightwell WS, & MacKenzie-Taylor DR: Teratogenicity of n-propanol and isopropanol administered at high inhalation concentrations to rats. Fd Chem Toxic 1988; 26:247-254.
    28) Peberdy MA , Callaway CW , Neumar RW , et al: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care science. Part 9: post–cardiac arrest care. Circulation 2010; 122(18 Suppl 3):S768-S786.
    29) Product Information: dopamine hcl, 5% dextrose IV injection, dopamine hcl, 5% dextrose IV injection. Hospira,Inc, Lake Forest, IL, 2004.
    30) Product Information: norepinephrine bitartrate injection, norepinephrine bitartrate injection. Sicor Pharmaceuticals,Inc, Irvine, CA, 2005.
    31) RTECS : Registry of Toxic Effects of Chemical Substances. National Institute for Occupational Safety and Health. Cincinnati, OH (Internet Version). Edition expires 1996; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    32) Rowe VK & McCollister SB: Alcohols. In: Clayton GD & Clayton FE (Eds): Patty's Industrial Hygiene and Toxicology, Vol 2C, John Wiley & Sons, New York, NY, 1982.
    33) Stolbach A & Hoffman RS: Respiratory Principles. In: Nelson LS, Hoffman RS, Lewin NA, et al, eds. Goldfrank's Toxicologic Emergencies, 9th ed. McGraw Hill Medical, New York, NY, 2011.
    34) Storrs FJ: Para-chloro-meta-xylenol allergic contact dermatitis in seven individuals. Contact Dermatitis 1975; 1:211-213.
    35) TERIS : Teratogen Information System - Teratogenic Risk Assessment of Drugs and Related Agents (CD-ROM Version). University of Washington. Seattle, WA (Internet Version). Edition expires 1996; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    36) Willson DF, Truwit JD, Conaway MR, et al: The adult calfactant in acute respiratory distress syndrome (CARDS) trial. Chest 2015; 148(2):356-364.
    37) Wilson DF, Thomas NJ, Markovitz BP, et al: Effect of exogenous surfactant (calfactant) in pediatric acute lung injury. A randomized controlled trial. JAMA 2005; 293:470-476.