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Fire-eater's lung.

SUMMARY

Hydrocarbon aspiration from fire-eating can result in severe necrotising pneumonia with complex cyst formation and large pleural effusions. Despite this, there is usually minimal persistent lung injury. We report the progress of two clinical cases, one of whom is the first reported case of citronella oil aspiration.

Key Words: aspiration, hydrocarbon, fire-eater

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Fire-eating is a well-loved circus, theatre and street-performance entertainment. It has also been used in religious rituals. We describe two cases of severe pulmonary injury with complex pleural involvement following aspiration of hydrocarbon.

CASE HISTORIES

Case 1

A 30-year-old male circus artist presented with cough, shortness of breath, fevers and generalised myalgias, 24 hours after aspiration of the hydrocarbon accelerant (naphtha) used in his fire-eating act. The cough was productive of yellow, bloodstained sputum. He also complained of pleuritic chest pain and aching pains in his lower back and neck. His history was unremarkable except for childhood asthma and thalassaemia minor.

Clinical examination on presentation noted a temperature of 38.3[degrees]C, tachycardia of 110 beats per minute, a respiratory rate of 22/minute with bilateral basal crackles on chest auscultation. Arterial blood gases on room air noted a pH 7.46, [P.sub.a][O.sub.2] 55 mmHg, [P.sub.a]C[O.sub.2] 32 mmHg and HC[O.sub.3] 22 mmol/l. The full blood count noted a neutrophil leukocytosis of 27 x [10.sup.9]/l. The chest X-ray showed bilateral lower lobe consolidation and right middle lobe collapse (Figure 1). Humidified oxygen was commenced and intravenous ticarcillin-clavulinate administered for nine days. Ibuprofen, endone, paracetamol and oxycontin were used for analgesia. A computer tomography (CT) scan of the thorax noted mediastinal and hilar lymph node enlargement, bilateral small pleural effusions with ground-glass opacities in both upper lobes and apical segments of the lower lobes. Confluent consolidation of the lower lobes with pneumatocoele formation was present (Figure 2). Large volumes of green sputum were produced during the first week of hospital admission. On the 11th hospital day, a CT scan of the thorax noted a large left pleural effusion with significant collapse of the left lower lobe and a small left pneumothorax (Figure 3). A needle thoracentesis drained 1300 ml of straw-coloured fluid resulting in significant re-expansion of the left lower lobe. The fluid was an exudate and remained sterile on culture. His temperature continued in a spiking manner >38.5[degrees]C for the first six days of his admission. A reactive thrombocytosis (1200 x [10.sup.9]/l), settled after two weeks. Oxygen therapy was required for the first 11 days of the admission. Discharge was made to outpatient review on day 19. After four months, his CT scan of the thorax and lung function were normal with a FE[V.sub.1]/FVC 3.61/4.95 (3.43/4.35) and a slight reduction in carbon monoxide gas transfer.

[FIGURE 1 OMITTED]

[FIGURE 2 OMITTED]

[FIGURE 3 OMITTED]

Case 2

A 33-year-old man with no significant past medical history presented to the Accident and Emergency Department three hours following choking on citronella oil during his street performance of 'fire-eating'. Initially, he had some retrosternal pain unrelieved by antacids progressing to worsening pleuritic pain, vomiting and cough with bloodstained sputum. He had a clear sensorium, a temperature of 38.8[degrees]C and a tachycardia of 94 beats per minute. Chest examination demonstrated a right-sided pleural rub with crackles and reduced breath sounds over the right lower zone. Arterial blood gases on room air noted a pH 7.38, [P.sub.a][O.sub.2] 47 mmHg, [P.sub.a]C[O.sub.2] 45 mmHg and HC[O.sub.3] 26 mmol/l with his oxygenation improving to a [P.sub.a][O.sub.2] of 76 mmHg on 35% oxygen. A chest X-ray showed right middle and lower lobe collapse with consolidation. He was transferred to the intensive care unit and managed with humidified oxygen and indomethacin suppositories, regular paracetamol and endone orally for pain. He was discharged to the general ward the following day. His white cell count began to rise on the fifth hospital day peaking at 23.3 x [10.sup.9]/l. His sputum became purulent with continued minor haemoptyses. No pathogens were isolated on sputum culture but intravenous ticarcillin-clavulinate was commenced for seven days. His temperatures continued to spike higher than 38[degrees]C until day nine. Three days after presentation he remained on 30% oxygen with a pleural effusion requiring drainage by an intercostal catheter. Eight hundred millilitres of serous exudate was drained which remained sterile on culture. Despite five days of intercostal suction at 20 cm[H.sub.2]O, the chest X-rays continued to show a significant right lower lobe collapse. A CT scan of the thorax showed a loculated right pleural effusion but little airspace disease. The intercostal catheter was removed. Supplemental oxygen continued for six days. During his admission he developed a mild hepatitis commencing on day five of admission and settling by day 11: peak alkaline phosphatase 318 IU (35-100), gamma glutamyl transferase 207 IU (0-50), alanine transaminase 190 U/I (0-35), aspartate transaminase 128 U/I (0-40) and lactate dehydrogenase 336 U/I (100-250). Three months after the initial aspiration, the chest X-ray and spirometry were normal (FE[V.sub.1]/FVC 4.34/5.41).

DISCUSSION

The skill in fire-eating is to spray an accelerant in a similar action to a trumpeter(1). Such performances are commonly associated with mucosal burns to the oropharynx(2). Aspiration or ingestion of the fuel is rare as are lead and asbestos exposure.

The hydrocarbon fuels used for fire-eating vary around the world due to availability and costs(1,3-5). For safety reasons, accelerants with high flash points (> 50[degrees]C) and low burn temperatures are used such as paraffin. Pure paraffin is relatively safe but many formulations contain benzene and naphtha. Highly explosive fuels such as alcohol, spirits and most petrochemicals are used only to create special effects such as coloured flames(1). Naphtha as was used in our first case represents a variety of distillates from crude oil or coal tar such as petroleum ether, white spirit, ligroin, petroleum spirits and shellite(1). The citronella oil in our second case is an unusual pyrochemical for fire-eating. It is obtained from Cymbopogon grasses, geraniums and basil, and is used extensively as an insect repellent and as fragrance for the soap, perfumery, cosmetic and flavouring industries(6).

Aspiration is generally required for pulmonary toxicity. However, severe lung injury has been described with ingestion alone(7). Aspiration is more common with hydrocarbons of low viscosity, surface tension and boiling point as they irritate the pharynx and gastrointestinal tract resulting in cough, gasping and vomiting(8). Pulmonary injury generally increases with the amount aspirated but injury with volumes as small as five millilitres are described(9). The site of lung injury is determined by the patient's posture at the time of aspiration(10). Toxicity is greatest with the aromatic hydrocarbons followed by the naphthenes and least with the paraffins(11). The spectrum of neurological, cardiac and pulmonary involvement relate to the dose, hydrocarbon composition, exposure to liquid or vapour and additives such as lead(11).

Low-viscosity, volatile hydrocarbon aspiration (petroleum, gasoline, white spirit) causes an acute lung injury mimicking an infectious illness. The largest series of fire-eater's lung describes 17 patients all having aspiration of kerdan: a mixture of petroleum distillates including toluene, xylene and ethilbenzene(12). As in our cases, clinical presentations universally have pleuritic pain(12). Fevers greater than 38.5[degrees]C (93%) and haemoptysis (24%) are typical(12). Severe pulmonary involvement requiring mechanical ventilation is uncommon (6%). Lung injury includes acute bronchitis(10,13), alveolar infiltrates, cavitating lesions generally less than 2 cm in diameter (30%) and pleural effusions (25%)(14). Bronchial oedema leading to ball-valve effects may cause pneumatocoeles(14). Other reported complications are bronchopleural fistula, pulmonary abscesses, parapneumonic effusions, empyema, pyopneumothorax(15,16), bronchial reactivity(17), eosinophillic alveolitis(18), ARDS(15,19) and severe multi-organ failure(20). Complete resolution of the lung injury within two weeks is the usual outcome(21). However, fatal cases are generally associated with contaminants such as pesticides and other complex hydrocarbons leading to hepatic failure, renal failure and rhabdomyolysis(12). An association with clinically important pulmonary fibrosis has not been established(22).

Computer tomography scans of the thorax generally show features consistent with an acute pneumonitis, thick wall cysts with subpleural bullae and recurrent pneumothoraces(15). Multiple pulmonary pseudotumours are rare(23). Despite the presence of acute pneumatocoeles, CT chest scans at six months are generally normal although pneumatoceles may take up to a year to resolve(24). The lesions of chronic hydrocarbon aspiration are quite different, presenting with pseudotumours' or crazy paving alveolar infiltrates having negative CT attenuation values (Hounsfield Units <0)(25).

Inflammatory parameters including blood white cell count, C-reactive protein and bronchoalveolar lavage do not differentiate acute hydrocarbon pneumonitis from infectious aetiologies. Histological studies of fire-eater's lung describe an acute necrotising and fibrinous pneumonia with prominent involvement of the bronchiolar walls, including bronchiolitis obliterans(21) and macrophages with lipid inclusions(13,26,27). Chromatography of bronchoalveolar lavage fluid, sputum or plasma may be useful to isolate the causative hydrocarbon where the aetiology is unclear(28,29).

Gastric emptying is generally not recommended following ingestion unless the hydrocarbons fall into the CHAMP group: camphor, halogenated hydrocarbons, aromatic hydrocarbons or those associated with metals and pesticides(8). Volatile hydrocarbons may result in cardiac arrhythmias with the possibility of beta-blockers limiting the catecholamine surges(8). Although many case reports have used corticosteroids as part of the management of hydrocarbon inhalation, their routine use remains unsupported(30,31). The development of early bacterial infection in patients with aspiration cannot be readily predicted by the clinical presentation or circumstances of the aspiration(32). Routine antibiotic use remains controversia1(30). However, ampicillin and metronidazole in kerosene inhalation may result in better outcomes(33). Ventilatory strategies have been similar to any case of severe ARDS(1520,34-36).

CONCLUSIONS

Despite severe initial lung injury, hydrocarbon aspiration associated with fire-eating is generally associated with an excellent prognosis. Citronella oil, although not a petrochemical, results in a similar pattern of injury and prognosis.

Address for reprints: A/Prof R. J. Boots, Deputy Director, Department of Intensive Care Medicine, Royal Brisbane and Women's Hospitals, Herston Road, Herston, Qld. 4029.

Accepted for publication on February 21, 2008.

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(16.) Chyczewska E. Case of pneumonia complicated by empyema after accidental aspiration of gasoline. Wiad Lek 1980; 33:12351238.

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(18.) Ewert R, Lindemann I, Romberg B, Petri F, Witt C. The accidental aspiration and ingestion of petroleum in a "fire eater". Deutsche Medizinische Wochenschrift 1992; 117:1594-1598.

(19.) Segev D, Szold O, Fireman E, Kluger Y, Sorkine P. Kerosene-induced severe respiratory failure in near drowning: Reports of four cases and review of the literature. Crit Care Med 1999; 27:1437-1440.

(20.) Yu M-C, Lin J-L, Wu C-T, Hsia S-H, Lee F. Multiple organ failure following lamp oil aspiration. Clin Toxicol (Phila) 2007; 45:304-306.

(21.) Grossi E, Crisanti E, Poletti G, Poletti V. Fire-eater's pneumonitis. Monaldi Arch Chest Dis 2006; 65:59-61.

(22.) Buchanan DR, Lamb D, Seaton A. Punk rocker's lung: pulmonary fibrosis in a drug snorting fire-eater. Br Med J (Clin Res Ed) 1981; 283:1661.

(23.) Scott PP. Hydrocarbon ingestion: an unusual cause of multiple pulmonary pseudotumors. South Med J 1989; 82:1032-1033.

(24.) Stones DK, van Niekerk CH, Cilliers C. Pneumatoceles as a complication of paraffin pneumonia. S Afr Med J 1987; 72:535537.

(25.) Franquet T, Gomez-Santos D, Gimenez A, Torrubia S, Monill JM. Fire eater's pneumonia: radiographic and CT findings. J Comput Assist Tomogr 2000; 24:448-450.

(26.) Nogue S, Sanz P, Borondo JC, Picon M, de la Red G, Mestre G. Fatal lipoid pneumonia due to bronco-aspiration of isoparaffin after ingestion of an organophosphate insecticide. Acta Anaesthesiol Scand 2003; 47:777-779.

(27.) Yokohori N, Taira M, Kameyama S, Kanemura T, Kondo M, Tamaoki J et al. Acute form of exogenous lipoid pneumonia caused by inhalation of liquid paraffin in a fire-eater. Nihon Kokyuki Gakkai Zasshi 2002; 40:588-593.

(28.) Dongay G, Levade T, Caratero A, Salvayre R, Lauque D, Carles P. Alveolar paraffinosis: cytologic and biochemical study of bronchiolo-alveolar lavage fluid. Rev Mal Respir 1985; 2:231-237.

(29.) Heckers H, Melcher FW, Dittmar K, Kalinowski HO. Paraffin oil pneumonia. Analysis of saturated hydrocarbons in different human tissue. J Chromatogr 1978; 146:91-102.

(30.) Steele RW, Conklin RH, Mark HM. Corticosteroids and antibiotics for the treatment of fulminant hydrocarbon aspiration. JAMA 1972;219:1434-1437.

(31.) Marks MI, Chicoine L, Legere G, Hillman E. Adrenocorticosteroid treatment of hydrocarbon pneumonia in children--a cooperative study. J Pediatr 1972; 81:366-369.

(32.) Kennedy GA, Kanter RK, Weiner LB, Tompkins JM. Can early bacterial complications of aspiration with respiratory failure be predicted? Pediatr Emerg Care 1992; 8:123-125.

(33.) Singh H, Chugh JC, Shembesh AH, Ben-Musa AA, Mehta HC. Management of accidental kerosene ingestion. Ann Trop Paediatr 1992; 12:105-109.

(34.) David M, Heinrichs W. High-frequency oscillatory ventilation and an interventional lung assist device to treat hypoxaemia and hypercapnia. Br J Anaesth 2004; 93:582-586.

(35.) Scalzo AJ, Weber TR, Jaeger RW, Connors RH, Thompson MW Extracorporeal membrane oxygenation for hydrocarbon aspiration. Am J Dis Child 1990; 144:867-871.

(36.) Bysani GK, Rucoba RJ, Noah ZL. Treatment of hydrocarbon pneumonitis. High frequency jet ventilation as an alternative to extracorporeal membrane oxygenation. Chest 1994; 106:300303.

R. J. BOOTS *, Z. J. WEEDON ([dagger])

Department of Intensive Care Medicine Royal Brisbane Hospital, Brisbane Queensland, Australia

* M.B., B.S., F.R.A.C.P., F.J.F.I.C.M., M.Med.Sci., M.Health.Admin.I.T, Ph.D., Deputy Director, Department of Intensive Care Medicine and Thoracic Physician, Royal Brisbane Hospital.

([dagger]) M.B., B.S., B.Sc., Medical Registrar, Department of Thoracic Medicine, Royal Brisbane and Women's Hospitals.
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Title Annotation:Case Report
Author:Boots, R.J.; Weedon, Z.J.
Publication:Anaesthesia and Intensive Care
Article Type:Case study
Geographic Code:8AUST
Date:May 1, 2008
Words:2663
Previous Article:Paediatric intensive care in non-paediatric ICUs.
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