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Indian Journal of Forensic Medicine & Toxicology

Dettol poisoning: Clinical features and management

Author(s): Sharath Kumar

Vol. 2, No. 2 (2008-07 - 2008-12)

Sharath Kumar

Assistant Professor, Department of Pediatrics, Amrita Institute of Medical Sciences, Edappally, Cochin 682 026 Kerala, India

Abstract

Dettol is a common household disinfectant and is freely available in certain countries such as UK, India and Hong Kong. It is common cause of suicidal poisoning in Hong Kong. However literature regarding incidence and case profile in other parts of the world is lacking. It has a corrosive action on the gastrointestinal tract and a depressant action on the central nervous system. Almost all the mortality in patients with Dettol poisoning is related to aspiration. Patients with Dettol poisoning have been observed to develop sudden upper airway obstruction which can require emergent endotracheal intubation. It has been observed predominantly in patients who are at high risk of aspiration in spite of the fact that other clinical signs of aspiration may be absent. This complication can be of delayed onset and should be anticipated. Treatment otherwise is mainly supportive. Prognosis is very good in patients who have not aspirated.

Key words: Dettol, Chlorxylenol, Poisoning, Stridor

Introduction

Dettol is a commonly available disinfectant. It contains Chlorxylenol (4.8%), Pine oil (9%) and Isopropyl alcohol (12%). Chlorxylenol is a phenol and is chemically related to the other phenolic disinfectants such as carbolic acid and cresols. Pine oil is made of secondary and tertiary terpene alcohols which cause central nervous system depression. The action is probably additive to the depressant action of Chlorxylenol. Similar to Chlorxyleonol it can cause renal failure and hepatitis. Iso-propyl alcohol can also cause central nervous system depression2.

The risk of serious complications and mortality following ingestion of Dettol has been reported to be around 8% and 1.8% respectively1.

The poisonous nature of phenols is common knowledge amongst lay persons. However, most are unaware that Dettol is a phenolic compound and has a similar toxicity profile. This probably contributes to the very low incidence of consumption with sucidal intent. The immediate emetic action of Dettol as suggested by Meek et al also probably contributes to the paucity of reported cases2. The medical fraternity is unaware of the toxic potential of Dettol. This general ignorance may contribute to the low incidence of reported poisoning due to Dettol. The literature regarding clinical features and case profile is deficient with respect to adults and is absent with respect to children.

Epidemiology

Self poisoning with Dettol, is a common occurrence in Hong Kong contributing to upto 10% of all the self poisonings2 and most of the known toxicities of Dettol is from studies published by Chan et al in a cohort of Dettol poisoning patients in Hong Kong. It is interesting to know that in this retrospectively studied cohort of patients in Hong Kong, nearly 88% of the patients received a gastric lavage in the ED3. This was despite the fact that lavage is contraindicated in poisoning with phenolic compounds. This just serves to highlight the extent of the deficit in our knowledge regarding the toxicity of Dettol and the devastating effect it can have on management of individual patients.

Toxicity

Dettol affects various organs systems in the body. Toxicity profile is in many ways similar to that seen in other phenolic compounds. However not all of the effects are predictable. It causes central nervous system depression, corrosion of oral mucosa and gastrointestinal tract, laryngeal edema, upper airway obstruction, nephrotoxicity, hepatitis and cardiac arrythmias. However the main risk of poisoning is aspiration with subsequent development of ARDS, pneumonia and sudden cardiorespiratory arrest. Microaspiration has been hypothesized to be the reason for delayed upper airway obstruction that may occur in totally asymptomatic patients upto 48 hrs after admission4.

Dettol has a corrosive action on the gastrointestinal tract. A retrospective study on the gastrointestinal side effects of Dettol poisoning found that many patients had nausea/ vomiting (62- 75% of patients), some had epigastric/ abdominal pain (24%) and very few had hematemesis (5.6%) following ingestion1;5. None of the patients seem to develop melena. The gastrointestinal hemorrhage usually tends to be mild and none of the patients with gastrointestinal bleeds (n=5) went on to develop oesophgeal stricture5.

Gastroscopies only found minimal gastro-oesophagitis. Rotinue endoscopy in the acute setting is indicated in corrosive poisonings to determine the extent of esophageal and gastric involvement. However, considering the fact that most of the mortality due to Dettol poisoning has been blamed on aspiration, routine endoscopy in these patients is probably not warranted in the acute setting. The studied sample seems to be too small a number to be able to conclude whether gastroscopies need not to be done at all.

CNS depression is also a prominent feature in ingestion of large amounts. Drowsiness on presentation to the ED is seen in 24% of patients6. Central nervous system depression greater than Grade 2 is usually seen in patients who have ingested greater than 200 ml1;2;7;8. Comatose patients have flaccid areflexia with constricted pupils which respond sluggishly to light2;8. Patients who arrive comatose to the ED have an initial drastic improvement on just supportive therapy but can sometimes be followed by subsequent deterioration of sensorium1;2;8.

Cardiovascular side effects that have been reported are mainly arrhythmias. All the patients in whom arrhythmias were reported developed the same during hospital stay with none of them having any rhythm disturbance at presentation. Case reports of nodal tachycardia 4 hours after admission and symptomatic sinus bradycardia occurring 21 hours after ingestion have been reported2;8. The incidence of arrhythmias is unknown. However it might have been the cause in a patient who died due to “sudden cardiorespiratory arrest” in the retrospective study conducted by Chan et al in which 170 patients with Dettol poisoning were studied7. Hypotension and cardiac depression can also occur2. Hypotension can also possibly occur due to hypovolemia secondary either to sequestration of fluids in the gastrointestinal tract or due to upper gastrointestinal bleed.

Nephrotoxicity manifesting as oliguira, hematuria and elevated urea and creatinine has been reported 2;9. The incidence however is very uncommon being only 2.5% in a retrospective study of 121 patients9. Autopsies, reported in some patients who had succumbed to the toxicity, have shown no discernible structural renal damage2;10.

Transaminitis has been reported in two patients. Autopsy on those two patients showed a normal appearing liver2;10. The main risks associated with Dettol poisoning are pulmonary aspiration leading to pneumonia, ARDS, acute exacerbation of asthma or of COPD, sudden cardiorespiratory arrest and upper airway obstruction1;2;4;6;7;11. The risk of aspiration in Dettol poisoning is 7.6% 8% 6;7. Chan et al conducted a retrospective study to determine the risk of aspiration in Dettol poisoning. This was compared with the incidence in patients who had presented to the ED with poisonings other than Dettol (mainly central nervous system depressant medication). This second group of patients served as the controls. The risk of aspiration was 8% in the patients with Dettol poisoning. There was no statistical difference between the incidence of aspiration in cases and controls. This was in spite of the fact that there were a statistically significant lower percentage of cases who had presented with drowsiness compared to controls. One explanation offered was that the corrosive action of Dettol on the throat may impair the gag reflex1. A second and more likely explanation was that the gastric lavage that the cases received put them at increased risk of aspiration even when their sensorium was not depressed6. A retrospective study by the same authors published a year later demonstrated that amongst the patients who developed aspiration upto 15% showed signs of the same only after they received unprotected gastric lavage7. Amongst the patients who had already developed signs of aspiration, 23% seemed to deteriorate following the procedure. Thus 3% of all patients with Dettol poisoning with no signs of aspiration at presentation developed aspiration subsequent to the lavage and nearly 50% of patients with Dettol poisoning and signs of aspiration had a worsening of their course7. Gastric lavage thus should be avoided in patients with Dettol poisoning. When patients with Dettol ingestion who developed aspiration were compared with those who did not develop any signs of aspiration, the former group was found to have consumed a significantly higher amount of Dettol, had a higher incidence of vomiting and a very high incidence of central nervous system depression(77% against 19.4%)7.

A very rare and interesting complication is delayed upper airway obstruction. The upper airway obstruction can have a sudden onset and progress rapidly in an otherwise stable patient4;11. It has been seen to be delayed upto 48 hours after hospital admission4. Four cases have been reported till date1;4;11;13. Two of the cases were adults who had consumed large amounts. One was a child who was 22 month of age and had consumed 125 ml. The fourth patient had consumed both Dettol and Domestos. However all the patients had either signs of aspiration or were at risk for aspiration. Two patients in whom mucosal changes were described had erythematous vocal cords with ulcerations. Tracheal ulceration has also been noted in another case report in an autopsy conducted on another patient who did not have any stridor or upper airway obstruction2. The erythema, edema and need for intubation can improve within 36 hours or persist till 10 days after intubation. In spite of the fact that all the patients with sudden upperairway obstruction had a complete and uneventful recovery, it can be a very hazardous complication unless anticipated with equipment and manpower kept ready for emergency endotracheal intubation.

Treatment

The mainstay of Dettol poisoning is supportive management along with close observation in hospital for stidor with equipment kept ready for emergency endotracheal intubation. Emesis and gastric lavage should not normally be attempted. This is especially true in children who are unlikely to have consumed large amounts of Dettol The only indication for gastric lavage in the acute setting is a patient who has consumed other poison along with Dettol. Gastric lavage should be done only subsequent to intubation with cuffed endotracheal tube. Lavage should never be done using a nasogastric tube but a wide bore orogastric tube7;12 30ml/ kg of oral liquid paraffin can be administered to the patient per orally if the patient is conscious and cooperative or by nasogastric tube if the patient is comatose. Dettol is soluble in paraffin and it’s systemic absorption is probably prevented by this measure. Patient should be started on intravenous fluids with regular monitoring of electrolytes. Adolescents and adults who have consumed more than 200 to 300 ml and children who have consumed lesser amounts should be kept nil per oral and watched carefully for signs and symptoms of nephrotoxicity and central nervous system depression. In case of severe poisoning or any evidence of hematuria or azotemia, forced alkaline diuresis should be attempted to aid in the excretion of the poisons. Exchange transfusion , and early dialysis for isopropyl alcohol can be attempted in the rare patient who is deteriorating steadily despite adequate supportive measures2. The body seems to have an efficient renal mechanism for excretion of dettol and most patients seem to improve with just supportive measures. Even patients who arrive comatose to the emergency department frequently demonstrate a rapid and complete recovery. It is however important to remember that even patients who recover completely, should be monitored closely in hospital for stridor for a minimum of 48 hours after admission. This is especially true in patients who arrive to the casualty in coma, patients who have aspirated, patients who have undergone forced emesis or unprotected gastric lavage and patients who have consumed greater than 400ml of Dettol11.

Prognosis

Dettol poisoing seems to have a mortality of 1.8% with all the mortality occurring in patients who aspirate7. The mortality amongst patients who have aspirated was seen to be 23.1%7. Thus Dettol poisoning can be fatal especially in patients at high risk of aspiration. Most of the complications are easy to manage if they are anticipated and proper therapy instituted. Therapy is more rewarding given the fact that no significant sequlae has been reported in any of the survivors of Dettol poisoning, till date.

Conclusions

Dettol poisoning is a common occurrence in Hong Kong and is probably an under reported occurrence in other areas of the world. Dettol poisoning can be fatal. Most of the fatality is related to aspiration or micro aspiration. Gastric lavage is contraindicated in patients with Dettol poisoning. Lack of knowledge can lead to institution of harmful therapy or missing potentially hazardous complications. Mainstay of treatment is supportive. Prognosis for complete recovery is favorable for most patients who have not consumed large amounts or not undergone lavage.

Reference

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  2. Meek D, Gabriel R, Piercy DM. Fatal self-poisoning with Dettol. Postgrad Med J 1977; 53(618):229-231.
  3. Chan TY, Critchley JA. The spectrum of poisonings in Hong Kong: an overview. Vet Hum Toxicol 1994; 36(2):135-137.
  4. Joynt GM, Ho KM, Gomersall CD. Delayed upper airway obstruction. A life-threatening complication of Dettol poisoning. Anaesthesia 1997; 52(3):261-263.
  5. Chan TY, Sung JJ, Critchley JA. Chemical gastrooesophagitis, upper gastrointestinal haemorrhage and gastroscopic findings following Dettol poisoning. Hum Exp Toxicol 1995; 14(1):18-19.
  6. Chan TY, Critchley JA, Lau JT. The risk of aspiration in Dettol poisoning: a retrospective cohort study. Hum Exp Toxicol 1995; 14(2):190-191.
  7. Chan TY, Critchley JA. Pulmonary aspiration following Dettol poisoning: the scope for prevention. Hum Exp Toxicol 1996; 15(10):843-846.
  8. Joubert P, Hundt H, Du TP. Severe Dettol (chloroxylenol and terpineol) poisoning. Br Med J 1978; 1(6117):890.
  9. Chan TY, Critchley JA. Is chloroxylenol nephrotoxic like phenol? A study of patients with DETTOL poisoning. Vet Hum Toxicol 1994; 36(3):250-251.
  10. Khan JS, Wilson MC, Taylor TV. A case of Dettol addiction. Br Med J 1979; 1(6166):791-792.
  11. Archer LN. Upper airways obstruction after Dettol ingestion. Br Med J 1979; 2(6181):19-20.
  12. Singh M. Accidental poisoning. Medical emergencies in children. 3 ed. New Delhi: Sagar Publications; 2000. 501-525.
  13. Graham CA. Stridor after ingestion of dettol and domestos. Eur J Emerg Med 2004; 11(1):52-54.
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