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Suicide Attempt by Intravenous Injection of Gasoline: A Case Report
The Journal of Emergency Medicine, Vol. 39, No. 5, pp. 618 – 622, 2010 Copyright © 2010 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/$–see front matter
doi:10.1016/j.jemermed.2008.08.013
Selected Topics: Toxicology
SUICIDE ATTEMPT BY INTRAVENOUS INJECTION OF GASOLINE: A CASE REPORT Katrin Fink,
Alexander Kuehnemund, MD, Tilmann Schwab, MD, Annette Geibel-Zehender, Thorsten Bley, MD, Christoph Bode, PROF, and Hans-Joerg Busch, MD
MD,
Reprint Address: Katrin Fink,
University Hospital, Freiburg im Breisgau, Germany University Hospital, Hugstetter Str. 55, Freiburg im Breisgau 79110, Germany
MD,
e Abstract—Background: There is much experience with intoxication by aspiration of volatile hydrocarbon products, whereas intravenous injection of these distillates is rare. There are only few reports that describe a wide variety of associated pathological changes, predominantly in the pulmonary system. Objectives: We report the case of an intravenous self-injection of gasoline by a young man in a suicide attempt. Case Report: Immediately after injecting gasoline, the 22-year-old man developed bradycardia, hypotension, and increasing dyspnea. Computed tomography scan of the chest showed signs consistent with diffuse alveolar-toxic damage to the lung. These symptoms and radiological findings are similar to those commonly observed after inhalation of this type of substance. This may have been due to diffusion of gasoline into the alveoli, where its presence leads to this characteristic damage. In this patient, gasoline entered the intramuscular tissue, and the patient developed a soft-tissue phlegmon at the forearm. At operation, gas emanation and superficial necrosis were noted. Nevertheless, the patient’s outcome was good, with full recovery within 3 weeks. Conclusions: The major changes in this patient after intravenous injection of gasoline were in the pulmonary system, including hypoxemia and radiological findings that could be related to an exhalation of the volatile substance. In addition, gas in the musculature of the injection area caused a soft-tissue phlegmon. © 2010 Elsevier Inc.
INTRODUCTION Patients with suicidal tendencies have been known to inject unusual substances intravenously, including insecticides, lamp oil, snake venom, and others. The selfinjection of gasoline is uncommon, but not unknown. Because gasoline is a volatile mixture of toluene, xylene, and other hydrocarbons, most gasoline intoxications occur via vapor inhalation. Volatility of these substances allows displacement of alveolar oxygen and leads to hypoxia, alveolar instability, and early distal airway closure. There are some reports of hemorrhagic pneumonitis in this setting (1– 4). Intravenous self-administration of hydrocarbons like gasoline or petroleum distillates is uncommon. We report the case of a young man who injected gasoline into his left cubital vein in a suicidal attempt.
CASE REPORT A 22-year-old man was admitted to our hospital for an attempted suicide by intravenous injection of gasoline. He injected 7 mL of gasoline into his left cubital vein. Some of the gasoline was injected subcutaneously and intramuscularly. He reported an “ascending cold” along the left arm and then a feeling of “icing” in his lung. He was admitted to the hospital within 2 h after injection. Past medical history included Asperger syndrome and
e Keywords— gasoline intoxication; intravenous injection; alveolar-toxic damage; soft-tissue phlegmon
RECEIVED: 7 March 2008; FINAL ACCEPTED: 6 August 2008
PROF,
SUBMISSION RECEIVED:
28 May 2008; 618
Intravenous Injection of Gasoline
619
Figure 1. The electrocardiogram at admission shows T-wave inversions in II, III, aVF, and V2 to V6 (arrows).
history of a suicide attempt with benzodiazepine overdose. He was currently taking no medication. On arrival, the physical examination revealed a somnolent patient, arousable and cooperative, without focal neurological deficit. Initial blood pressure was 80/60 mm Hg, heart rate was bradycardic, with a regular sinus rhythm at about 50 beats/min. Heart sounds were clear, and breath sounds normal. Oxygen saturation was 92% on room air, and temperature was 33.9°C. Abdominal examination revealed no pathological findings. The extremities were cold and cyanotic; the left forearm was reddened and painfully swollen about 10 cm around the injection area, with livid streaks on the surrounding skin. At the left upper extremity pulse, movability and sensorium were intact. The electrocardiogram showed normal sinus rhythm with 54 beats/min, T-wave inversions in II, III, aVF, and V2–V6 (Figure 1). The initial serum laboratory results are shown in Table 1. In the hours after the injection, the patient developed dyspnea. Arterial blood gas analysis revealed arterial hypoxemia with a transient decrease in Horowitz-Index (PaO2/FiO2) ⬍ 200. The initial (4 h post-injection) chest X-ray study showed multiple opacities in the basal lung segments and discrete pleural effusions on both sides (Figure 2). A computed tomography (CT) scan of the chest showed ground-glass opacities predominantly in the dorso-basal segments, consistent with diffuse alveolar toxic damage of the lung (Figure 3). During the first 24 h, the patient developed progressive pain and immobility of the left forearm, which became edematous and reddened. CT scan revealed a soft-tissue phlegmon and signs of inflammation and edema reaching from the axilla to the forearm (Figure 4). The patient was treated with clindamycin, ceftriaxone, and metronidazole as empiric antibiotic therapy. Antico-
agulant therapy was started within 2 h after admission. On the second day, the patient was sent to the surgical unit for operative intervention. Intraoperative findings revealed complete edematous modified tissue. A debridement was made to remove superficial necrosis at the bicep muscle. Laboratory values and hemodynamic and respiratory parameters returned to normal range in the postoperative days. After a psychiatric consultation the patient was transferred to a psychiatric facility. No additional complica-
Table 1. Laboratory Values at Admission Parameter Erythrocyte count White blood cells count Platelet count INR aPTT Antithrombin Fibrinogen Fibrinmonomers Myoglobin Troponin T Creatine kinase MB isoenzyme Aspartate aminotransferase Alanine aminotransferase y-glutamytranferase Bilirubin C-reactive protein Procalcitonin Lactate Lactate dehydrogenase Creatinine Urea Urine analysis
Value
Normal Range
3.77 4.2–6.3 2.100 4.3–10.000 92.000 140–400.000 1.6 0.85–1.15 46 22–36 60 70–130 279 170–450 Negative 0 497 ⬍90 0.147 ⬍0.1 410 ⬍174 27 ⬍24 96 10–50 118 10–50 81 ⬍66 1.5 ⬍0.3 79 ⬍5 ⬎2 ⬍0.5 2.8 0.5–1.6 293 135–225 0.7 0.5–1.1 59 10–47 Normal
Unit Mio/L Cells/L Cells/L s % mg/dL ng/mL ng/mL U/L U/L U/L U/L U/L mg/dL Mg/L mg/L mmol/L U/L mg/dL mg/dL
INR ⫽ international normalized ratio; aPTT ⫽ activated partial thromboplastin time.
620
K. Fink et al.
Figure 2. The chest X-ray after intravenous injection of gasoline reveals multiple opacities in both lungs with predominance in the lower lobes (arrows).
tions were noted. The wound at the left forearm was noted to be healing on the 23rd postoperative day without any further complication. DISCUSSION After exposure, gasoline is concentrated in the lung as well as in bones, skeletal muscle, and in some blood components (5). Because it is a volatile mixture, most intoxications occur via vapor inhalation. The main risk of inhalation is aspiration of this substance and the development of a severe pneumonitis. The volatility of gasoline leads to displacement of alveolar oxygen and transient hypoxemia. Recent studies have reported the occurrence of alveolar instability, early distal airway closure, and ventilation-perfusion mismatch. Our patient described an “ascending cold” along the left arm, where he had injected the gasoline. Subsequently, he felt like “icing” in the lung, which may be explained by exhalation of the volatile substance. Presumably, exhalation of such substances causes pathophysiological changes that are similar to those seen with inhalation. Therefore, the observed hypoxemia is most likely due to the displacement of alveolar oxygen and the consecutive changes in lung physiology described above. In animal studies there are reports of severe hemorrhagic pneumonitis and bronchial spasm resulting in death within minutes after intravenous injection of liquid hydrocarbon compounds (6,7). There are reports of pulmonary impairment by gasoline ranging from hemoptysis to hemorrhagic pneumonitis with severe impairment of oxygenation to circulatory breakdown and hemorrhagic
pulmonary edema within several hours (1–3,8 –10). Our patient, in particular, presented with pulmonary symptoms including dyspnea and tachypnea as a consequence of a fall in oxygen saturation and arterial hypoxemia. The conventional chest X-ray study showed multiple patchy infiltrates in both lungs, with predominance to the lower lobes (Figure 1). The chest CT scan revealed defined areas of ground-glass attenuation in both lungs, presumably as the result of alveolar-toxic damage to the lung (Figure 2). These radiological findings are in accordance with those in other reports of pneumonia after hydrocarbon aspiration (2,11,12). Vital signs, including blood pressure and heart rate, were significantly decreased in our patient, similar to the case reported by Chan and Critchley (13). According to another author, it is common for such cases to include marked T-wave inversions, and a slight increase of the cardiac marker enzymes (14). However, the rise in myoglobin and creatine kinase without significant increase of the MB isoenzyme in our patient was explained by the damage to the left forearm. There are also reports of dysrhythmia, including atrial fibrillation with a rapid ventricular response, or vagal stimulation leading to cardiac arrest after acute poisoning with organic solvents (15,16). There was no dysrhythmia found in our patient. The observed rise in liver enzymes such as aspartate and alanine aminotransferase, y-glutamytranferase, and bilirubin could be related to a direct toxic effect of injected gasoline on the liver. There are reports of elevated hepatic aminotransferase, and there is a description of liver dysfunction with intravenous self-poisoning with an aliphatic compound (17). With respect to the coagulation state, our patient showed signs of an activation of blood coagulation with
Figure 3. CT scan of the chest demonstrates defined areas of ground glass attenuation (arrows) in both lungs revealing alveolitic changes, presumably as a result of alveolar-toxic damage to the lung.
Intravenous Injection of Gasoline
621
Figure 4. CT scan of the upper limb displays emphysema in the soft tissue (arrows) of the injection area resembling a soft-tissue phlegmon. (A) soft tissue window; (B) bone tissue window.
decreased platelet count and antithrombin, and a rise in prothrombin time and international normalized ratio. In the literature, consumptive coagulopathy and hemolysis is described after massive gasoline aspiration (1). Vaziri et al. described a marked leukocytosis with a significant shift to the left and relative lymphopenia in a patient after intravenous injection of a gasoline-like substance as an expression of an infection-like status (2). Our patient immediately exhibited elevated inflammation parameters, like C-reactive protein and procalcitonin, and a moderate increase in lactate dehydrogenase, whereas there was a decrease in white blood cell count without lymphopenia. An additional problem of our patient was the process of inflammation and edema, with gas in the left upper limb subsequent to the injection. The extremity was swollen and demonstrated soft-tissue air and phlegmon. CT scan of the upper limb displayed emphysema in the soft tissue of the injection area resembling a softtissue phlegmon (Figure 3). The normal septal morphology of the musculature was eliminated. Fortunately for our patient, pulse, movability, and sensorium were intact, and the rapid surgical intervention helped to recover the extremity. There are reports of damage of several nerves, a sterile abscess, or local thrombophlebitis after injection of gasoline (8,18,19). In addition, there is a description of rhabdomyolysis with subsequent proximal myopathy and acute renal failure (17). In the literature there are several reports about fatal outcome after intravenous injection and ingestion of hydrocarbon products, particularly involving respiratory insufficiency and subsequent multi-organic failure with circulatory breakdown (3,13,20). Case et al. published a report of homicide by injection of a gasoline distillate (4). Fortunately, our patient’s outcome was good, and he recovered completely within 3 weeks, with symptomatic treatment. Although intoxication with gasoline aspiration
is not rare, there is still no specific and effective treatment known.
CONCLUSION Intoxication by intravenous injection of hydrocarbon products is rare. We report a case of intravenous selfinjection of gasoline by a young man in a suicide attempt. The major problems were in the pulmonary system, from diffuse alveolar-toxic damage. Radiological findings could be related to an exhalation of the volatile substance after intravenous injection. Further, gas in the musculature of the injection area caused soft tissuephlegmon. Nevertheless, this patient eventually made a full recovery.
REFERENCES 1. Perings SM, Hennersdorf M, Koch JA, et al. Lipoid pneumonia following attempted suicide by intravenous injection of lamp oil [German]. Med Klin (Munich) 2001;96:685– 8. 2. Vaziri ND, Jeminson-Smith P, Wilson AF. Hemorrhagic pneumonitis after intravenous injection of charcoal lighter fluid. Ann Intern Med 1979;90:794 –5. 3. Wolkart N. Death caused by intravenous benzine injection. Arch Toxikol 1954;15:40 –1. 4. Case ME, Poklis A, Mackell MA. Homicide by intravenous injection of naphtha. J Forensic Sci 1985;30:208 –12. 5. Vitarella D, Wong BA, Moss OR, Dorman DC. Pharmacokinetics of inhaled manganese phosphate in male Sprague-Dawley rats following subacute (14-day) exposure. Toxicol Appl Pharmacol 2000;163:279 – 85. 6. Haddow BL. Injection of charcoal lighter fluid. J Pediatr 1975;87: 633– 6. 7. Simay A, Szabo I, Deli L. Experimental contribution on acute changes in the airways during intravenous gasoline poisoning and their treatment. Arch Toxikol 1968;23:250 –2. 8. Beck DE, Freeman B, Moore CR. Toxicities with intravenous and subcutaneous administration of a petroleum distillate. Drug Intell Clin Pharm 1981;15:693– 4. 9. Santos JW, Marchiori RC, Schneider Filho A, et al. Pneumonitis after intravenous self-administration of solvent. Respir Care 2001;46:53–5.
622 10. Vaziri ND, Smith PJ, Wilson A. Toxicity with intravenous injection of naphtha in man. Clin Toxicol 1980;16:335– 43. 11. Facon D, Coumbaras J, Bigot E, Bahlouli F, Boissonnas A, Bellin MF. Acute hydrocarbon pneumonia after white spirit aspiration: sequential HRCT findings. Eur Radiol 2005;15:31–3. 12. Lee JS, Im JG, Song KS, Seo JB, Lim TH. Exogenous lipoid pneumonia: high-resolution CT findings. Eur Radiol 1999;9:287–91. 13. Chan TY, Critchley JA. Is chloroxylenol nephrotoxic like phenol? A study of patients with DETTOL poisoning. Vet Hum Toxicol 1994;36:250 –1. 14. Goodwin SR, Berman LS, Tabeling BB, Sundlof SF. Kerosene aspiration: immediate and early pulmonary and cardiovascular effects. Vet Hum Toxicol 1988;30:521– 4. 15. Flanagan RJ, Ruprah M, Meredith TJ, Ramsey JD. An introduction to the clinical toxicology of volatile substances. Drug Saf 1990;5:359-83.
K. Fink et al. 16. Greenberg MD, Robinson T, Birrer R. Atrial fibrillation after intravenous administration of gasoline. Am Heart J 1993;125: 1438 –9. 17. Grimmett WG, Dzendolet I, Whyte I. Intravenous thiodan (30% endosulfan in xylene). J Toxicol Clin Toxicol 1996;34: 447–52. 18. Layton TR, Grant KJ, Villella ER. Gasoline injection. J Toxicol Clin Toxicol 1983–1984;21:409 –12. 19. Aguemon AR, Diallo AT, Biaou O, Atchade D. Case report of acute intoxication from intravenous injection of petroleum. Ann Fr Anesth Reanim 2000;19:758 – 60. 20. 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;47:777–9.
doi:10.1016/j.jemermed.2008.08.013
Selected Topics: Toxicology
SUICIDE ATTEMPT BY INTRAVENOUS INJECTION OF GASOLINE: A CASE REPORT Katrin Fink,
Alexander Kuehnemund, MD, Tilmann Schwab, MD, Annette Geibel-Zehender, Thorsten Bley, MD, Christoph Bode, PROF, and Hans-Joerg Busch, MD
MD,
Reprint Address: Katrin Fink,
University Hospital, Freiburg im Breisgau, Germany University Hospital, Hugstetter Str. 55, Freiburg im Breisgau 79110, Germany
MD,
e Abstract—Background: There is much experience with intoxication by aspiration of volatile hydrocarbon products, whereas intravenous injection of these distillates is rare. There are only few reports that describe a wide variety of associated pathological changes, predominantly in the pulmonary system. Objectives: We report the case of an intravenous self-injection of gasoline by a young man in a suicide attempt. Case Report: Immediately after injecting gasoline, the 22-year-old man developed bradycardia, hypotension, and increasing dyspnea. Computed tomography scan of the chest showed signs consistent with diffuse alveolar-toxic damage to the lung. These symptoms and radiological findings are similar to those commonly observed after inhalation of this type of substance. This may have been due to diffusion of gasoline into the alveoli, where its presence leads to this characteristic damage. In this patient, gasoline entered the intramuscular tissue, and the patient developed a soft-tissue phlegmon at the forearm. At operation, gas emanation and superficial necrosis were noted. Nevertheless, the patient’s outcome was good, with full recovery within 3 weeks. Conclusions: The major changes in this patient after intravenous injection of gasoline were in the pulmonary system, including hypoxemia and radiological findings that could be related to an exhalation of the volatile substance. In addition, gas in the musculature of the injection area caused a soft-tissue phlegmon. © 2010 Elsevier Inc.
INTRODUCTION Patients with suicidal tendencies have been known to inject unusual substances intravenously, including insecticides, lamp oil, snake venom, and others. The selfinjection of gasoline is uncommon, but not unknown. Because gasoline is a volatile mixture of toluene, xylene, and other hydrocarbons, most gasoline intoxications occur via vapor inhalation. Volatility of these substances allows displacement of alveolar oxygen and leads to hypoxia, alveolar instability, and early distal airway closure. There are some reports of hemorrhagic pneumonitis in this setting (1– 4). Intravenous self-administration of hydrocarbons like gasoline or petroleum distillates is uncommon. We report the case of a young man who injected gasoline into his left cubital vein in a suicidal attempt.
CASE REPORT A 22-year-old man was admitted to our hospital for an attempted suicide by intravenous injection of gasoline. He injected 7 mL of gasoline into his left cubital vein. Some of the gasoline was injected subcutaneously and intramuscularly. He reported an “ascending cold” along the left arm and then a feeling of “icing” in his lung. He was admitted to the hospital within 2 h after injection. Past medical history included Asperger syndrome and
e Keywords— gasoline intoxication; intravenous injection; alveolar-toxic damage; soft-tissue phlegmon
RECEIVED: 7 March 2008; FINAL ACCEPTED: 6 August 2008
PROF,
SUBMISSION RECEIVED:
28 May 2008; 618
Intravenous Injection of Gasoline
619
Figure 1. The electrocardiogram at admission shows T-wave inversions in II, III, aVF, and V2 to V6 (arrows).
history of a suicide attempt with benzodiazepine overdose. He was currently taking no medication. On arrival, the physical examination revealed a somnolent patient, arousable and cooperative, without focal neurological deficit. Initial blood pressure was 80/60 mm Hg, heart rate was bradycardic, with a regular sinus rhythm at about 50 beats/min. Heart sounds were clear, and breath sounds normal. Oxygen saturation was 92% on room air, and temperature was 33.9°C. Abdominal examination revealed no pathological findings. The extremities were cold and cyanotic; the left forearm was reddened and painfully swollen about 10 cm around the injection area, with livid streaks on the surrounding skin. At the left upper extremity pulse, movability and sensorium were intact. The electrocardiogram showed normal sinus rhythm with 54 beats/min, T-wave inversions in II, III, aVF, and V2–V6 (Figure 1). The initial serum laboratory results are shown in Table 1. In the hours after the injection, the patient developed dyspnea. Arterial blood gas analysis revealed arterial hypoxemia with a transient decrease in Horowitz-Index (PaO2/FiO2) ⬍ 200. The initial (4 h post-injection) chest X-ray study showed multiple opacities in the basal lung segments and discrete pleural effusions on both sides (Figure 2). A computed tomography (CT) scan of the chest showed ground-glass opacities predominantly in the dorso-basal segments, consistent with diffuse alveolar toxic damage of the lung (Figure 3). During the first 24 h, the patient developed progressive pain and immobility of the left forearm, which became edematous and reddened. CT scan revealed a soft-tissue phlegmon and signs of inflammation and edema reaching from the axilla to the forearm (Figure 4). The patient was treated with clindamycin, ceftriaxone, and metronidazole as empiric antibiotic therapy. Antico-
agulant therapy was started within 2 h after admission. On the second day, the patient was sent to the surgical unit for operative intervention. Intraoperative findings revealed complete edematous modified tissue. A debridement was made to remove superficial necrosis at the bicep muscle. Laboratory values and hemodynamic and respiratory parameters returned to normal range in the postoperative days. After a psychiatric consultation the patient was transferred to a psychiatric facility. No additional complica-
Table 1. Laboratory Values at Admission Parameter Erythrocyte count White blood cells count Platelet count INR aPTT Antithrombin Fibrinogen Fibrinmonomers Myoglobin Troponin T Creatine kinase MB isoenzyme Aspartate aminotransferase Alanine aminotransferase y-glutamytranferase Bilirubin C-reactive protein Procalcitonin Lactate Lactate dehydrogenase Creatinine Urea Urine analysis
Value
Normal Range
3.77 4.2–6.3 2.100 4.3–10.000 92.000 140–400.000 1.6 0.85–1.15 46 22–36 60 70–130 279 170–450 Negative 0 497 ⬍90 0.147 ⬍0.1 410 ⬍174 27 ⬍24 96 10–50 118 10–50 81 ⬍66 1.5 ⬍0.3 79 ⬍5 ⬎2 ⬍0.5 2.8 0.5–1.6 293 135–225 0.7 0.5–1.1 59 10–47 Normal
Unit Mio/L Cells/L Cells/L s % mg/dL ng/mL ng/mL U/L U/L U/L U/L U/L mg/dL Mg/L mg/L mmol/L U/L mg/dL mg/dL
INR ⫽ international normalized ratio; aPTT ⫽ activated partial thromboplastin time.
620
K. Fink et al.
Figure 2. The chest X-ray after intravenous injection of gasoline reveals multiple opacities in both lungs with predominance in the lower lobes (arrows).
tions were noted. The wound at the left forearm was noted to be healing on the 23rd postoperative day without any further complication. DISCUSSION After exposure, gasoline is concentrated in the lung as well as in bones, skeletal muscle, and in some blood components (5). Because it is a volatile mixture, most intoxications occur via vapor inhalation. The main risk of inhalation is aspiration of this substance and the development of a severe pneumonitis. The volatility of gasoline leads to displacement of alveolar oxygen and transient hypoxemia. Recent studies have reported the occurrence of alveolar instability, early distal airway closure, and ventilation-perfusion mismatch. Our patient described an “ascending cold” along the left arm, where he had injected the gasoline. Subsequently, he felt like “icing” in the lung, which may be explained by exhalation of the volatile substance. Presumably, exhalation of such substances causes pathophysiological changes that are similar to those seen with inhalation. Therefore, the observed hypoxemia is most likely due to the displacement of alveolar oxygen and the consecutive changes in lung physiology described above. In animal studies there are reports of severe hemorrhagic pneumonitis and bronchial spasm resulting in death within minutes after intravenous injection of liquid hydrocarbon compounds (6,7). There are reports of pulmonary impairment by gasoline ranging from hemoptysis to hemorrhagic pneumonitis with severe impairment of oxygenation to circulatory breakdown and hemorrhagic
pulmonary edema within several hours (1–3,8 –10). Our patient, in particular, presented with pulmonary symptoms including dyspnea and tachypnea as a consequence of a fall in oxygen saturation and arterial hypoxemia. The conventional chest X-ray study showed multiple patchy infiltrates in both lungs, with predominance to the lower lobes (Figure 1). The chest CT scan revealed defined areas of ground-glass attenuation in both lungs, presumably as the result of alveolar-toxic damage to the lung (Figure 2). These radiological findings are in accordance with those in other reports of pneumonia after hydrocarbon aspiration (2,11,12). Vital signs, including blood pressure and heart rate, were significantly decreased in our patient, similar to the case reported by Chan and Critchley (13). According to another author, it is common for such cases to include marked T-wave inversions, and a slight increase of the cardiac marker enzymes (14). However, the rise in myoglobin and creatine kinase without significant increase of the MB isoenzyme in our patient was explained by the damage to the left forearm. There are also reports of dysrhythmia, including atrial fibrillation with a rapid ventricular response, or vagal stimulation leading to cardiac arrest after acute poisoning with organic solvents (15,16). There was no dysrhythmia found in our patient. The observed rise in liver enzymes such as aspartate and alanine aminotransferase, y-glutamytranferase, and bilirubin could be related to a direct toxic effect of injected gasoline on the liver. There are reports of elevated hepatic aminotransferase, and there is a description of liver dysfunction with intravenous self-poisoning with an aliphatic compound (17). With respect to the coagulation state, our patient showed signs of an activation of blood coagulation with
Figure 3. CT scan of the chest demonstrates defined areas of ground glass attenuation (arrows) in both lungs revealing alveolitic changes, presumably as a result of alveolar-toxic damage to the lung.
Intravenous Injection of Gasoline
621
Figure 4. CT scan of the upper limb displays emphysema in the soft tissue (arrows) of the injection area resembling a soft-tissue phlegmon. (A) soft tissue window; (B) bone tissue window.
decreased platelet count and antithrombin, and a rise in prothrombin time and international normalized ratio. In the literature, consumptive coagulopathy and hemolysis is described after massive gasoline aspiration (1). Vaziri et al. described a marked leukocytosis with a significant shift to the left and relative lymphopenia in a patient after intravenous injection of a gasoline-like substance as an expression of an infection-like status (2). Our patient immediately exhibited elevated inflammation parameters, like C-reactive protein and procalcitonin, and a moderate increase in lactate dehydrogenase, whereas there was a decrease in white blood cell count without lymphopenia. An additional problem of our patient was the process of inflammation and edema, with gas in the left upper limb subsequent to the injection. The extremity was swollen and demonstrated soft-tissue air and phlegmon. CT scan of the upper limb displayed emphysema in the soft tissue of the injection area resembling a softtissue phlegmon (Figure 3). The normal septal morphology of the musculature was eliminated. Fortunately for our patient, pulse, movability, and sensorium were intact, and the rapid surgical intervention helped to recover the extremity. There are reports of damage of several nerves, a sterile abscess, or local thrombophlebitis after injection of gasoline (8,18,19). In addition, there is a description of rhabdomyolysis with subsequent proximal myopathy and acute renal failure (17). In the literature there are several reports about fatal outcome after intravenous injection and ingestion of hydrocarbon products, particularly involving respiratory insufficiency and subsequent multi-organic failure with circulatory breakdown (3,13,20). Case et al. published a report of homicide by injection of a gasoline distillate (4). Fortunately, our patient’s outcome was good, and he recovered completely within 3 weeks, with symptomatic treatment. Although intoxication with gasoline aspiration
is not rare, there is still no specific and effective treatment known.
CONCLUSION Intoxication by intravenous injection of hydrocarbon products is rare. We report a case of intravenous selfinjection of gasoline by a young man in a suicide attempt. The major problems were in the pulmonary system, from diffuse alveolar-toxic damage. Radiological findings could be related to an exhalation of the volatile substance after intravenous injection. Further, gas in the musculature of the injection area caused soft tissuephlegmon. Nevertheless, this patient eventually made a full recovery.
REFERENCES 1. Perings SM, Hennersdorf M, Koch JA, et al. Lipoid pneumonia following attempted suicide by intravenous injection of lamp oil [German]. Med Klin (Munich) 2001;96:685– 8. 2. Vaziri ND, Jeminson-Smith P, Wilson AF. Hemorrhagic pneumonitis after intravenous injection of charcoal lighter fluid. Ann Intern Med 1979;90:794 –5. 3. Wolkart N. Death caused by intravenous benzine injection. Arch Toxikol 1954;15:40 –1. 4. Case ME, Poklis A, Mackell MA. Homicide by intravenous injection of naphtha. J Forensic Sci 1985;30:208 –12. 5. Vitarella D, Wong BA, Moss OR, Dorman DC. Pharmacokinetics of inhaled manganese phosphate in male Sprague-Dawley rats following subacute (14-day) exposure. Toxicol Appl Pharmacol 2000;163:279 – 85. 6. Haddow BL. Injection of charcoal lighter fluid. J Pediatr 1975;87: 633– 6. 7. Simay A, Szabo I, Deli L. Experimental contribution on acute changes in the airways during intravenous gasoline poisoning and their treatment. Arch Toxikol 1968;23:250 –2. 8. Beck DE, Freeman B, Moore CR. Toxicities with intravenous and subcutaneous administration of a petroleum distillate. Drug Intell Clin Pharm 1981;15:693– 4. 9. Santos JW, Marchiori RC, Schneider Filho A, et al. Pneumonitis after intravenous self-administration of solvent. Respir Care 2001;46:53–5.
622 10. Vaziri ND, Smith PJ, Wilson A. Toxicity with intravenous injection of naphtha in man. Clin Toxicol 1980;16:335– 43. 11. Facon D, Coumbaras J, Bigot E, Bahlouli F, Boissonnas A, Bellin MF. Acute hydrocarbon pneumonia after white spirit aspiration: sequential HRCT findings. Eur Radiol 2005;15:31–3. 12. Lee JS, Im JG, Song KS, Seo JB, Lim TH. Exogenous lipoid pneumonia: high-resolution CT findings. Eur Radiol 1999;9:287–91. 13. Chan TY, Critchley JA. Is chloroxylenol nephrotoxic like phenol? A study of patients with DETTOL poisoning. Vet Hum Toxicol 1994;36:250 –1. 14. Goodwin SR, Berman LS, Tabeling BB, Sundlof SF. Kerosene aspiration: immediate and early pulmonary and cardiovascular effects. Vet Hum Toxicol 1988;30:521– 4. 15. Flanagan RJ, Ruprah M, Meredith TJ, Ramsey JD. An introduction to the clinical toxicology of volatile substances. Drug Saf 1990;5:359-83.
K. Fink et al. 16. Greenberg MD, Robinson T, Birrer R. Atrial fibrillation after intravenous administration of gasoline. Am Heart J 1993;125: 1438 –9. 17. Grimmett WG, Dzendolet I, Whyte I. Intravenous thiodan (30% endosulfan in xylene). J Toxicol Clin Toxicol 1996;34: 447–52. 18. Layton TR, Grant KJ, Villella ER. Gasoline injection. J Toxicol Clin Toxicol 1983–1984;21:409 –12. 19. Aguemon AR, Diallo AT, Biaou O, Atchade D. Case report of acute intoxication from intravenous injection of petroleum. Ann Fr Anesth Reanim 2000;19:758 – 60. 20. 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;47:777–9.