A lethal danger in the home: turpentine poisoning.

Turpentine is an oleoresin obtained from various species of pine. In turpentine poisoning, various signs and symptoms of toxicity may develop, including hematuria, renal failure, loss of vision, chest pain, vomiting, severe coughing, gastroesophageal hemorrhage, hypotension, swelling of the throat and even death. We report a case of turpentine ingestion in a 9-year-old boy. The patient was admitted to our clinic with suspected intoxication after accidentally drinking from a glass that held a turpentine oil preparation used by his father for hair care. The patient displayed no significant signs and symptoms other than bradycardia and hypotension. Laboratory investigations revealed no abnormalities. The patient was hospitalized for close monitoring and observation. During a two-and-a-half-day observation period, hypotension was corrected with administration of dopamine and intravenous fluids. In this report, we wish to draw attention to the dangerous effects of plant-derived drugs.

Turpentine oil inhalation leading to lung necrosis and empyema in a toddler.

Household poisons can cause serious damage to the health of children. Turpentine oil, used chiefly as a solvent in paints, varnishes, and waxes; is often placed within easy reach of children during polishing or painting work. It is capable of causing serious toxicity, whether ingested or inhaled. Pulmonary aspiration can lead to lung parenchymal damage and turpentine-associated pneumonia. We report a case of exploratory ingestion and inhalation of turpentine oil in an 18-month-old boy, leading to extensive lung parenchymal damage, formation of multiple abscess cavities, and necrosis treated with decortication and segmental resection.

Turpentine-induced chemical pneumonitis with broncho-pleural fistula.

Turpentine is a volatile hydrocarbon used in polishes, solvents, paints and textile industry. When hydrocarbons are aspirated into the lung, they cause chemical pneumonitis, acute respiratory distress syndrome (ARDS), and rarely pneumatoceles and pneumothorax. We report a 20-year old boy with turpentine-induced chemical pneumonitis that evolved into a bronchopleural fistula. He was treated with oxygen, steroids and intercostal tube drainage. This is the first reported case of turpentine-associated bronchopleural fistula.

Pneumatoceles following hydrocarbon aspiration.

We report an unusual evolution of turpentine-induced pneumonia due to accidental aspiration in a 21-month-old child. Chest X-rays demonstrated patchy alveolar densities evolving into large pneumatoceles. Follow-up CT optimally depicted the number, site and extent of pneumatoceles. To our knowledge, pneumatoceles developing in turpentine-induced pneumonia have never been reported in turpentine aspiration.

Improvements are needed in the existing packaging of medicated oils containing methyl salicylate.

In view of the toxic potential of medicated oils containing methyl salicylate, we have studied the existing packaging of 10 commonly used preparations from Hong Kong and Singapore and identified areas for improvement with respect to the prevention of poisonings. They were all packed in translucent bottles without child-resistant closures. The methyl salicylate content ranged from 15 to 67%. Many preparations also contained other potentially toxic ingredients in significant amounts, such as turpentine oil and camphor. The contents of the larger bottles could generally be emptied more easily because of the greater size of their openings. The product with the highest methyl salicylate content also had the biggest opening of all. The threat from ingestion of medicated oils containing methyl salicylate can probably be 'reduced' by: (i) using child-restraint closures; (ii) restricting the size of both the openings and the bottles; and (iii) reducing the methyl salicylate content.

Acute intoxication and recovery following massive turpentine ingestion: clinical and toxicological data.

Reports of acute turpentine intoxication, particularly containing toxicological data, are poorly verified in the literature. This report regards the intentional massive ingestion of turpentine solution in an elderly woman who developed mainly central nervous system manifestations, then had an impressive and quick total recovery although the initial prognosis was very bad. Blood and urine levels of turpentine were monitored using gas chromatography and at the early toxicogenic stage were 28 micrograms/mL and 15 micrograms/mL respectively. Gastric fluid analysis on admission to the hospital revealed the presence of approximately 200 mL turpentine in the intestine. A review of earlier reports is given.

Turpentine poisoning: a case report.

The use of turpentine oil for suicidal and homicidal purposes has become quite infrequent with the increased availability of pesticides and toxic substances. Available literature exhibits few case reports of turpentine poisoning. Such a case is reported here which presented as status epilepticus, unresponsive to the usual line of treatment. Detailed clinical examination and inquiry into the case history revealed turpentine poisoning.

Toxicology of selected pesticides, drugs, and chemicals. Petroleum distillates and turpentine.

Companion animal exposures to volatile hydrocarbons and turpentine accounted for 2% of all calls received by the IAPIC in 1987. Volatile hydrocarbons are also used as vehicle solvents (e.g., pesticides), and both vehicle and active ingredients pose a significant hazard to companion animals. The most significant clinical effects of the hydrocarbons are related to aspiration pneumonia. The likelihood of aspiration is generally related to the compound's viscosity, with more volatile and most widely available compounds posing the greatest risk. Treatment generally is conservative. Gastrointestinal decontamination methods (e.g., emetics and activated charcoal administration) are used only in massive ingestions or when other toxicants are present in conjunction with the hydrocarbons. Oxygen therapy and cage rest are recommended for the dyspneic animal. Close monitoring of an exposed animal and symptomatic care as needed are also recommended for at least 12 hours after exposure.

Parenteral administration of hydrocarbons.

Two cases of subcutaneously administered hydrocarbon based products are presented and the literature reviewed. The toxicity associated with subcutaneous administration is limited to the site of injection producing cellulitis and sterile abscess formation. Management is discussed with emphasis on the importance of incision and drainage of developing abscesses. Perceived toxicity and ready availability of these products suggests that similar exposures can be expected.

[Poisoning by spirits of turpentine or turpentine oil. Review of its treatment apropos of a personal case]. / Intoxicación por esencia de trementina o aguarrás. Revisión del tratamiento a propósito de nuestra casuística.

Authors deduce from their experience during 1979 that intoxication by spirit oil of turpentine is an accident with few repercussions in infancy, because the quantity ingested does not reach toxic levels, except for children over seven who try to commit suicide. Gastric lavage must not be practiced because removing turpentine can provoke its' aspiration with a consequent pulmonary disease in the majority of occasions. Only when ingestion is more than 1 ml./Kg., or symptoms suggest important disease, can gastric lavage, be done because secondary complications can aggravate the disease. Antibiotics are used if there is an obvious infection, remembering that turpentine intoxication itself can provoke fever. In their experience, corticoids don't modify the evolution.

Prognosis in chronic toxic encephalopathy. A two-year follow-up study in 26 house painters with occupational encephalopathy.

The prognosis of chronic toxic encephalopathy in former house painters was examined in a prospective study with a two-year observation period. Twenty-six patients, who at the initial examination had cerebral atrophy and/or intellectual impairment, were selected for the follow-up study. No competitive etiological factors (including alcohol) to the encephalopathy were suspected. During the two-year follow-up interval these patients were not professionally exposed to organic solvents. At the follow-up examination neurological, biochemical, neuropsychological, and neuroradiological parameters were reassessed and compared to the original findings. Generally the condition was unchanged. Slight improvements with regard to headache and dizziness were reported by some. However, the neurological status, the neuropsychological impairment, and the cerebral atrophy, did not change significantly. In three patients further deterioration was observed. It is argued that our patients suffered from a brain disorder different from presenile dementia of the Pick-Alzheimer type. Other alternative etiological entities were also excluded. Our findings indicate that long-term exposure to organic solvents may lead to a chronic brain syndrome. Once intellectual impairment and/or cerebral atrophy had developed, reversibility is not observed. Nor is further progression to be expected if exposure is stopped. Occupational exposure to organic solvents should be maximally restricted as it represents a risk of inducing invalidating brain syndromes.

Severe organophosphate poisoning complicated by alcohol and turpentine ingestion.

A 52-year-old comatose white male was admitted to the hospital with what was later learned to be severe poisoning by a turpentine solution of dicrotophos, an organophosphorous insecticide he had ingested while drunk. The patient was treated effectively with atropine and pralidoxime chloride and required the largest doses of both agents reported to data. The case was complicated by difficulty in evaluating the response to therapy because of the effects of alcohol and turpentine. The patient was discharged from the hospital on the thirty-third day with no apparent sequelae.

Pneumatoceles as a complication of chemical pneumonia after hydrocarbon ingestion.

Of 338 children with hydrocarbon ingestion, 134 (40 percent) had pneumonia. Pneumonia was most common after kerosene, furniture polish and lighter fluid ingestion. The pneumonia was most severe, however, with furniture polish. Pneumatoceles occurred in 14 children, most commonly with charcoal lighter fluid ingestion. Pneumatoceles generally appeared late, after the consolidation had cleared. Pneumatoceles were often large, septate and irregular, and sometimes contained fluid levels.

Emergency treatment of petroleum distillate and turpentine ingestion.

A comparative study was made of pulmonary complications following the use of ipecac syrup and gastric lavage for hydrocarbon ingestion. The selected 255 patients had chest radiography when first seen and again two to five days later. Of these patients 74 or 29% had been treated with ipecac syrup, 41 or 16% by gastric lavage. On follow-up radiographs 19% of the ipecac-treated group were unchanged or worsened, compared with 39% of the lavage group, suggesting that pneumonitis was significantly less severe in the ipecac-treated patients. Use of ipecac is preferred over gastric lavage for alert patients who have ingested an excessive amount of hydrocarbon.