KEROSENE POISONING

CASE: HISTORY

• 2 year old female

• Chief complaint: fever, vomiting
• 1 day PTA: kerosene was ingested
• instant coffee as “home remedy”
• vomited previously ingested food three times after drinking coffee
• fever was observed a few hours after
• went to local health station, midwife advised oral amoxicillin

• History of benign focal convulsion

CASE: PHYSICAL EXAMINATION

• patient arrived at ER in respiratory distress

• vital signs: HR - 140 beats/minute, RR - 63 breaths/minute, T - 39°C, weight 8 kg
• HEENT: (-) cyanosis, (+) nasal flaring, pinkish conjunctiva, (+) sunken eyeballs,
(+) dry mucosa, supple neck
• chest: (+) symmetrical chest expansion, (+) intercostal retraction, (-) chest
indrawing, (+) rales
• abdomen: soft, flat, (-) organomegaly
• extremities: good pulses, capillary refill less than 2s
• neurological: conscious, coherent, able to obey simple commands, eyes equally
reactive to light, intact eye movement, normal reflexes
KEROSENE

• liquid mixture of hydrocarbons (C9 to C16) produced by distillation of crude oil

• kinetics and metabolism
• poorly studied
• poor oral availability in baboon and dog
• individual components are known to undergo dermal absorption
• kerosene vapour is absorbed following pulmonary exposure
• kerosene is efficiently removed from circulation by liver in primate models

• LD50 = 20-30 g/kg (oral)

• intratracheal dosing results in substantial increase (10 to 150-fold) increase in toxicity
PATHOPHYSIOLOGY

• lung ← primary target of toxicity

• affects lungs through several mechanisms → chemical pneumonitis
• produces bronchospasm and inflammatory response
• inhibition of acetylcholinesterase activity in airways
• decrease in efficiency of calcium uptake by sarcoplasmic reticulum
• volatized hydrocarbons can displace oxygen in alveolar space → hypoxia
• direct injury to lungs → lesions
• inhibits surfactant function → alveolar instability and collapse
PATHOPHYSIOLOGY

• gastrointestinal toxicity
• hydrocarbons are irritants of the GI tract → vomiting
• hydrocarbons are generally poorly absorbed by the GI tract
PATHOPHYSIOLOGY

• central nervous system toxicity

• acute exposure to kerosene in humans has been associated with a variety of CNS
effects, including irritability, restlessness, ataxia, drowsiness, convulsions, coma and
death
• secondary to hypoxia
CLINICAL IMPRESSION

• chemical pneumonitis secondary to kerosene aspiration

• (+) tachypnea, (+) tachycardia, (+) hyperthermia
• (+) nasal flaring
• (+) intercostal retraction
• (+) rales
• history of kerosene ingestion
• history of vomiting
• differentials: asthma, bacterial pneumonia, aspiration pneumonitis, acute
respiratory distress,
PARACLINICALS

• chest x-ray
• to rule out asthma and to evaluate lung fields
• sputum culture
• to rule out bacterial pneumonia
Arterial Blood Gas Analysis
to assess ventilation and acid base status
MANAGEMENT

• ABC’s
• secure airway
• support breathing
• provide supplemental oxygen
• consider inhaled β2 agonists
• circulation
• monitor blood pressure and O2 saturation
MANAGEMENT

• IV paracetamol for fever

• IV fluids for dehydration
• observation for signs of hypoxia, CNS depression
• antibiotic therapy is controversial, but can be considered if symptoms persist 48
hours post-ingestion
• levofloxacin (500 mg/day, slow infusion over 60-minute period)
• ceftriaxone (1-2 g/day)
REFERENCES

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McGraw-Hill Medical.
• Chilcott, R.P. (2006). Compendium of Chemical Hazards: Kerosene (Fuel Oil). Retrieved from the UK Health
Protection Agency: http://www.who.int/ipcs/emergencies/kerosene.pdf
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Allergologia et immunopathologia, 16(5), 363-367.
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• Lietman, P. S., & Wolfsdorf, J. (1976). Kerosene intoxication: an experimental approach to the etiology of the CNS
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