Letters to Editor
Erden Erol Ünlüer, Arif Karagöz1 Department of Emergency, Atatürk Research and Training Hospital, Izmir Katip Çelebi University, İzmir, 1Emergency, Karşıyaka State Hospital, İzmir, Turkey. E-mail: [email protected]
REFERENCES 1.
Tamura A, Kataoka H, Mikuriya Y, Nasu M. Inferior ST segment depression as a useful marker for identifying proximal left anterior descending artery occlusion during acute anterior myocardial infarction. Eur Heart J 1995;16:1795-9.
2.
Quyyumi AA, Crake T, Rubens MB, Levy RD, Rickards AF, Fox KM. Importance of "reciprocal" electrocardiographic changes during occlusion of left anterior descending coronary artery. Studies during percutaneous transluminal coronary angioplasty. Lancet 1986;15:347-50.
3.
de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J 1982;103:730-6.
4.
Farhan HL, Hassan KS, Al-Belushi A, Sallam M, Al-Zakwani I. Diagnostic value of electrocardiographic T wave inversion in lead aVL in diagnosing coronary artery disease in patients with chronic stable angina. Oman Med J 2010;25:124-7.
5.
Kosuge M, Ebina T, Hibi K, Iwahashi N, Morita S, Endo M, et al. Implications of ST-segment elevation in leads V5 and V6 in patients with reperfused inferior wall acute myocardial infarction. Am J Cardiol 2012;109:314-9. Access this article online Quick Response Code: Website: www.onlinejets.org
DOI: 10.4103/0974-2700.155526
Suicidal poisoning with cypermethrin: A clinical dilemma in the emergency department Sir, Cypermethrin, a pyrethroid compound is widely used due to its high insecticidal potential and slow resistance in pest. It is considered less toxic for human use, because of poor dermal absorption, rapid metabolism, less tissue accumulation, and environmental persistence. [1] Cases of accidental pyrethroid poisoning at work places have been reported[2], but poisoning with suicidal intention is extremely rare. [3] Increased overJournal of Emergencies, Trauma, and Shock I 8:2 I Apr - Jun 2015
the-counter availability of these insecticides is likely to increase the prevalence of their toxicity. Furthermore, resemblance of cypermethrin toxicity to organophosphate poisoning pose a diagnostic dilemma in the emergency department. [4,5] We report a case of 30-year old male who presented to our emergency department with complaints of recurrent vomiting, epigastric and throat pain, increased salivation, drooling, lacrimation, anxiety, cough, and dyspnea. There was no history of convulsion, diarrhea, frequent urination, chest pain, or fever. He gave a history of ingestion of about 300 mL of a liquid from a container 90 minutes before hospital presentation following a family dispute. There was no history suggestive of co-ingestion of any other toxin or drug. There were no relevant past medical or mental illness, or suicidal attempt. On clinical examination, patient was conscious, oriented, but anxious and restless. He had conjuctival congestion with normal pupillary size. The lips and buccal mucosa were swollen. The patient had tremors of hands but no fasciculation. His pulse was 80/min, blood pressure was 128/84 mm of Hg, Respiratory rate 20/min with SpO2 of 96% at room air. Systemic examinations were unremarkable except bilateral chest rhonchi. A diagnosis of organophosphate poisoning was made and patient was given oxygen and one intravenous dose of 1.8 mg of atropine. Meantime, the patient’s wife brought three containers of “Danger-10”, 100 ml each, [Figure 1] containing 10% of cypermethrin (equivalent to total of 33.6 g of cypermethrin). His hemogram, liver function, renal function, serum electrolytes, arterial blood gas, blood glucose, chest radiograph and electrocardiogram were within normal limit. Although he came more than one hour of ingestion, gastric lavage was performed. Activated charcoal was not given due to delayed hospital presentation and to prevent aspiration. Atropine was stopped after one dose and the patient was given symptomatic treatment in the form of hydrocortisone, chlorpheniramine maleate, ranitidine and nebulization with albuterol for bronchospasm. He improved significantly over the next 24 hours. On the second day, he developed hoarseness of voice. His indirect laryngoscopy was unremarkable and it
Figure 1: Containers of cypermethrin 10% ingested by the patient 123
Letters to Editor
improved over the next 24 hours and was discharged from the hospital. Pyrethrins and their synthetic derivatives, pyrethroids have become the predominant insecticide class for agricultural field and residential uses. It is due to their low environmental persistence and low resistance in pest. Poisoning due to pyrethroids is emerging due to their widespread use and over the counter availability without safety norms in our country. Pyrethrins refer to extracts of the Chrysanthemum flower that have insecticidal properties, but degrade rapidly; so, longerlasting synthetic-version pyrethroids have been synthesized. Pyrethroids are divided into two types. Type I pyrethroids have a cyclopropane carboxylic acid structure, while type II pyrethroids have an alpha-cyano group attached to the benzylic carbon, which enhances the insecticidal properties e.g., allethrin and cypermethrin. Type II pyrethroids are also more toxic to mammals, most of the cases of human poisoning have been due to these substances.[6] Cypermethrin is used as insecticides, pediculocides, and scabicides. Commonly used pyrethroids are deltamethrin, fenvalerate, permethrin, resmethrin, and cypermethrin. The mechanism of action for pyrethroids is complex. The main mechanism is the delay of closure of voltage-sensitive sodium channel, at high concentration pyrethroids also act on GABA-gated chloride channel which may be responsible for seizure. Pyrethroids are 2250 times more toxic to insects than mammals because insects have smaller body size, lower body temperature, and increased sodium channel sensitivity; so, insects are highly susceptible to these substances and experience massive nervous system stimulation. Beside the main ingredient pyrethroids, these insecticides often contain a surfactant, Triton-X and an additive, Piperonylbutoxide which prolong its action by inhibiting the oxidizing enzymes. Mammals, having poor dermal absorption, larger body size, higher body temperatures and rapid conversion of these substances to nontoxic metabolites, are less susceptible.[1] Although widely used, no clinical case of acute pyrethroid poisoning had been reported in the literature until the outbreak of acute deltamethrin poisoning in spray men in China in 1982. After that, there have been a few reports of occupational and accidental pyrethroid poisoning.[2] Cases due to intentional ingestion of deltamethrin[4,7], prallethrin[5,8,9], and cypermethrin[3] are extremely rare. The toxic oral dose is 100-1000 mg/kg body weight and lethal dose is 1-10 g.[7] Our patient consumed 33.6 g much above the lethal dose. However, he survived which indicates overall less mortality in pyrethroid poisoning. Toxicity to humans due to pyrethroid can be of two types. Type I can manifest as hypersensitivity reaction, like anaphylaxis, reflex hyper excitability and fine tremors. Type II produces watery diarrhoea, coarse tremor, reflex hyper excitability, choreoathetosis, and seizure. On ingestion it produces throat and epigastric pain, nausea, vomiting, salivation, dysphagia. dizziness, headache, and fatigue. Burning or tingling sensation, numbness, paraesthesias, lacrimation, photophobia, conjuctival congestion, and bronchospasm are the other manifestations due to direct or dermal exposure. In our case, most of the 124
symptoms were present. Ingestion of large doses may produce neurotoxicity like, tremors, fasciculation, convulsion, coma, pulmonary edema, respiratory failure and cardiac conduction disturbances.[4-6,8,9] Management of pyrethroid poisoning is mainly supportive and symptomatic as there is no specific antidote. Gastric lavage and activated charcoal can be given if patient presents within 1 hour of ingestion. Atropine may be given to decrease secretions in cases of increased salivation and pulmonary oedema. [10] Pyrethroid poisoning can be easily misdiagnosed as organophosphate poisoning. Smell of pyrethroids is somewhat related to OP because of common hydrocarbon solvents and features like fasciculation, pulmonary edema, and convulsions can occur in both the conditions.[4,5] Few cases of death have been reported due to atropine toxicity given to these patients.[2] However, normal pupillary size and plasma cholinesterase level, less requirement of atropine and excellent prognosis differentiate it from other insecticides.[4] Case reports and case series in the past depict that pyrethroids are not completely safe, but worldwide less than 10 deaths have been reported.[1] According to one series, seven mortalities have been reported among 573 cases of acute pyrethroid poisoning.[2] To conclude, cypermethrin intoxication should be considered as a differential diagnosis in patients presenting to ED with classical features of organophosphorous poisoning. Emergency physician are required to be aware of this entity to avoid inadvertent administration of atropine. Overall prognosis of cypermethrin poisoning is excellent despite ingestion of heavy doses and lifethreatening presentation.
Praveen Aggarwal, Nayer Jamshed, Meera Ekka, Ali Imran Department of Emergency Medicine, All India Institute of Medical Sciences, New Delhi, India. E-mail: [email protected]
REFERENCES 1.
Das RN, Parajuli S. Cypermethrin poisoning and anti-cholinergic medication- a case report. Internet J Med Update 2006;1:42-4.
2.
Ray DE, Fry JR. An assessment of the neurotoxicity of pyrethroid insecticides. Pharmacol Ther 2006;111:174-93.
3.
Bradberry SM, Cage SA, Proudfoot AT, Vale JA. Poisoning due to pyrethroids. Toxicol Rev 2005;24:93-106.
4.
Lessenger JE. Five office workers inadvertently exposed to cypermethrin. J Toxicol Environ Health 1992;35:261-7.
5.
Walters JK, Boswell LE, Green MK, Heumann MA, Karam LE, Morrissey BF, et al. Pyrethrin and pyrethroid illnesses in the Pacific Northwest: A five-year Review. Public Health Rep 2009;124:149-59.
6.
Majumdar BB, Guha G, Ray AN, Bala B . Toxic intracerebral demyelination in a case of suicidal Cypermethrin poisoning. . Ann Trop Med Public Health 2012.5;6:615-17.
7.
Gunay N, Kekec Z, Cete Y, Eken C, Demiryurek AT. Oral deltamethrin ingestion due in a suicide attempt. Bratisl Lek Listy 2010;111:303-5. Journal of Emergencies, Trauma, and Shock I 8:2 I Apr - Jun 2015
Letters to Editor
8.
Ardhanari A, Srivastava U, Kumar A, Saxena S. Management of a case of prallethrin poisoning-An unusual agent for suicidal ingestion. Sri Lankan J Anaesthesiol 2011;19:51-2.
9.
Bhaskar EM, Moorthy S, Ganeshwala G, Abraham G. Cardiac conduction disturbance due to prallethrin (pyrethroid) poisoning. J Med Toxicol 2010;6:27-30.
10. Krug EG, Dahlberg LL, Mercy JA, Zwi BA, Lozano R. World report on violence and health. Geneva: WHO; 2002. Access this article online Quick Response Code: Website: www.onlinejets.org
DOI: 10.4103/0974-2700.145424
Successful treatment of a penetrating pulmonary artery injury caused by a Japanese sword in a patient transported by a physician-staffed helicopter Sir, We herein present a case of successful treatment of a penetrating pulmonary artery injury caused by a Japanese sword (katana) in a patient transported by a physician-staffed helicopter. A 91-year-old male stabbed his chest and abdomen and cut his head with a katana and was found in a coma by his family. His history included dementia, schizophrenia, hypertension, and diabetes mellitus. A physician transported by a helicopter checked the patient at a rendezvous point in an ambulance and found that the katana had penetrated the patient’s body from the fourth intercostal of the left anterior chest to the back [Figure 1]. The patient was in a deep coma and also a state of severe hemorrhagic shock. His venous route and airway were secured, and he was transported to our hospital. He remained in a coma with shock and demonstrated left pneumoderma in the left chest; therefore, he underwent placement of an indwelling chest tube, followed by drainage of 500 ml of hemorrhagic fluid. Permissive hypotensive therapy to maintain the systolic blood pressure from 60 to 80 mmHg was selected with transfusion of blood type O, and emergency thoracotomy was performed in the operating room. Journal of Emergencies, Trauma, and Shock I 8:2 I Apr - Jun 2015
Figure 1: A katana penetrates a patient’s body from the fourth intercostal of the left anterior chest to the back
The patient temporally exhibited pulseless electrical activity due to massive hemorrhage, and fluid resuscitation resulted in spontaneous circulation. Injuries of the lingual, left pulmonary artery, and diaphragm were found, and primary closure of the pulmonary artery with clamping of the pulmonary hilum, primary closure of the diaphragm, and lobectomy of the lingual region were performed. The abdominal stab wound did not reach the intra-abdominal cavity and was also closed. After the operation, the patient developed pyothorax and was treated with antibiotics. He achieved a full somatic recovery and was transferred to a psychiatric hospital. The patient was successfully treated, despite his advanced age and severe shock state resulting from injury of major thoracic vessels.[1-4] The key to success was a multidisciplinary approach, including early medical intervention, transportation using a physician-staffed helicopter, and the administration of permissive hypotensive treatment and emergency thoracotomy with clamping of the pulmonary hilum.
Hiromichi Ohsaka, Youichi Yanagawa, Yoshikazu Miyasaka, Ken Okamoto Department of Acute Critical Care Medicine, Shizuoka Hospital, Juntendo University, Izunokuni, Shizuoka, Japan E-mail: [email protected]
REFERENCES 1.
Fatimi SH, Hanif HM, Awais A, Shamsi G, Muzaffar M. Major thoracic vessels and cardiac trauma: Case series from a center in a developing country. Ulus Travma Acil Cerrahi Derg 2012;18:490-4.
2.
Onan B, Demirhan R, Öz K, Onan IS. Cardiac and great vessel injuries after chest trauma: Our 10-year experience. Ulus Travma Acil Cerrahi Derg 2011;17:423-9.
3.
Mandal AK, Sanusi M. Penetrating chest wounds: 24 years experience. World J Surg 2001;25:1145-9.
4.
Baillot R, Dontigny L, Verdant A, Pagé P, Pagé A, Mercier C, et al. Penetrating chest trauma: A 20-year experience. J Trauma 1987;27:994-7. 125
Copyright of Journal of Emergencies, Trauma & Shock is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
Erden Erol Ünlüer, Arif Karagöz1 Department of Emergency, Atatürk Research and Training Hospital, Izmir Katip Çelebi University, İzmir, 1Emergency, Karşıyaka State Hospital, İzmir, Turkey. E-mail: [email protected]
REFERENCES 1.
Tamura A, Kataoka H, Mikuriya Y, Nasu M. Inferior ST segment depression as a useful marker for identifying proximal left anterior descending artery occlusion during acute anterior myocardial infarction. Eur Heart J 1995;16:1795-9.
2.
Quyyumi AA, Crake T, Rubens MB, Levy RD, Rickards AF, Fox KM. Importance of "reciprocal" electrocardiographic changes during occlusion of left anterior descending coronary artery. Studies during percutaneous transluminal coronary angioplasty. Lancet 1986;15:347-50.
3.
de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J 1982;103:730-6.
4.
Farhan HL, Hassan KS, Al-Belushi A, Sallam M, Al-Zakwani I. Diagnostic value of electrocardiographic T wave inversion in lead aVL in diagnosing coronary artery disease in patients with chronic stable angina. Oman Med J 2010;25:124-7.
5.
Kosuge M, Ebina T, Hibi K, Iwahashi N, Morita S, Endo M, et al. Implications of ST-segment elevation in leads V5 and V6 in patients with reperfused inferior wall acute myocardial infarction. Am J Cardiol 2012;109:314-9. Access this article online Quick Response Code: Website: www.onlinejets.org
DOI: 10.4103/0974-2700.155526
Suicidal poisoning with cypermethrin: A clinical dilemma in the emergency department Sir, Cypermethrin, a pyrethroid compound is widely used due to its high insecticidal potential and slow resistance in pest. It is considered less toxic for human use, because of poor dermal absorption, rapid metabolism, less tissue accumulation, and environmental persistence. [1] Cases of accidental pyrethroid poisoning at work places have been reported[2], but poisoning with suicidal intention is extremely rare. [3] Increased overJournal of Emergencies, Trauma, and Shock I 8:2 I Apr - Jun 2015
the-counter availability of these insecticides is likely to increase the prevalence of their toxicity. Furthermore, resemblance of cypermethrin toxicity to organophosphate poisoning pose a diagnostic dilemma in the emergency department. [4,5] We report a case of 30-year old male who presented to our emergency department with complaints of recurrent vomiting, epigastric and throat pain, increased salivation, drooling, lacrimation, anxiety, cough, and dyspnea. There was no history of convulsion, diarrhea, frequent urination, chest pain, or fever. He gave a history of ingestion of about 300 mL of a liquid from a container 90 minutes before hospital presentation following a family dispute. There was no history suggestive of co-ingestion of any other toxin or drug. There were no relevant past medical or mental illness, or suicidal attempt. On clinical examination, patient was conscious, oriented, but anxious and restless. He had conjuctival congestion with normal pupillary size. The lips and buccal mucosa were swollen. The patient had tremors of hands but no fasciculation. His pulse was 80/min, blood pressure was 128/84 mm of Hg, Respiratory rate 20/min with SpO2 of 96% at room air. Systemic examinations were unremarkable except bilateral chest rhonchi. A diagnosis of organophosphate poisoning was made and patient was given oxygen and one intravenous dose of 1.8 mg of atropine. Meantime, the patient’s wife brought three containers of “Danger-10”, 100 ml each, [Figure 1] containing 10% of cypermethrin (equivalent to total of 33.6 g of cypermethrin). His hemogram, liver function, renal function, serum electrolytes, arterial blood gas, blood glucose, chest radiograph and electrocardiogram were within normal limit. Although he came more than one hour of ingestion, gastric lavage was performed. Activated charcoal was not given due to delayed hospital presentation and to prevent aspiration. Atropine was stopped after one dose and the patient was given symptomatic treatment in the form of hydrocortisone, chlorpheniramine maleate, ranitidine and nebulization with albuterol for bronchospasm. He improved significantly over the next 24 hours. On the second day, he developed hoarseness of voice. His indirect laryngoscopy was unremarkable and it
Figure 1: Containers of cypermethrin 10% ingested by the patient 123
Letters to Editor
improved over the next 24 hours and was discharged from the hospital. Pyrethrins and their synthetic derivatives, pyrethroids have become the predominant insecticide class for agricultural field and residential uses. It is due to their low environmental persistence and low resistance in pest. Poisoning due to pyrethroids is emerging due to their widespread use and over the counter availability without safety norms in our country. Pyrethrins refer to extracts of the Chrysanthemum flower that have insecticidal properties, but degrade rapidly; so, longerlasting synthetic-version pyrethroids have been synthesized. Pyrethroids are divided into two types. Type I pyrethroids have a cyclopropane carboxylic acid structure, while type II pyrethroids have an alpha-cyano group attached to the benzylic carbon, which enhances the insecticidal properties e.g., allethrin and cypermethrin. Type II pyrethroids are also more toxic to mammals, most of the cases of human poisoning have been due to these substances.[6] Cypermethrin is used as insecticides, pediculocides, and scabicides. Commonly used pyrethroids are deltamethrin, fenvalerate, permethrin, resmethrin, and cypermethrin. The mechanism of action for pyrethroids is complex. The main mechanism is the delay of closure of voltage-sensitive sodium channel, at high concentration pyrethroids also act on GABA-gated chloride channel which may be responsible for seizure. Pyrethroids are 2250 times more toxic to insects than mammals because insects have smaller body size, lower body temperature, and increased sodium channel sensitivity; so, insects are highly susceptible to these substances and experience massive nervous system stimulation. Beside the main ingredient pyrethroids, these insecticides often contain a surfactant, Triton-X and an additive, Piperonylbutoxide which prolong its action by inhibiting the oxidizing enzymes. Mammals, having poor dermal absorption, larger body size, higher body temperatures and rapid conversion of these substances to nontoxic metabolites, are less susceptible.[1] Although widely used, no clinical case of acute pyrethroid poisoning had been reported in the literature until the outbreak of acute deltamethrin poisoning in spray men in China in 1982. After that, there have been a few reports of occupational and accidental pyrethroid poisoning.[2] Cases due to intentional ingestion of deltamethrin[4,7], prallethrin[5,8,9], and cypermethrin[3] are extremely rare. The toxic oral dose is 100-1000 mg/kg body weight and lethal dose is 1-10 g.[7] Our patient consumed 33.6 g much above the lethal dose. However, he survived which indicates overall less mortality in pyrethroid poisoning. Toxicity to humans due to pyrethroid can be of two types. Type I can manifest as hypersensitivity reaction, like anaphylaxis, reflex hyper excitability and fine tremors. Type II produces watery diarrhoea, coarse tremor, reflex hyper excitability, choreoathetosis, and seizure. On ingestion it produces throat and epigastric pain, nausea, vomiting, salivation, dysphagia. dizziness, headache, and fatigue. Burning or tingling sensation, numbness, paraesthesias, lacrimation, photophobia, conjuctival congestion, and bronchospasm are the other manifestations due to direct or dermal exposure. In our case, most of the 124
symptoms were present. Ingestion of large doses may produce neurotoxicity like, tremors, fasciculation, convulsion, coma, pulmonary edema, respiratory failure and cardiac conduction disturbances.[4-6,8,9] Management of pyrethroid poisoning is mainly supportive and symptomatic as there is no specific antidote. Gastric lavage and activated charcoal can be given if patient presents within 1 hour of ingestion. Atropine may be given to decrease secretions in cases of increased salivation and pulmonary oedema. [10] Pyrethroid poisoning can be easily misdiagnosed as organophosphate poisoning. Smell of pyrethroids is somewhat related to OP because of common hydrocarbon solvents and features like fasciculation, pulmonary edema, and convulsions can occur in both the conditions.[4,5] Few cases of death have been reported due to atropine toxicity given to these patients.[2] However, normal pupillary size and plasma cholinesterase level, less requirement of atropine and excellent prognosis differentiate it from other insecticides.[4] Case reports and case series in the past depict that pyrethroids are not completely safe, but worldwide less than 10 deaths have been reported.[1] According to one series, seven mortalities have been reported among 573 cases of acute pyrethroid poisoning.[2] To conclude, cypermethrin intoxication should be considered as a differential diagnosis in patients presenting to ED with classical features of organophosphorous poisoning. Emergency physician are required to be aware of this entity to avoid inadvertent administration of atropine. Overall prognosis of cypermethrin poisoning is excellent despite ingestion of heavy doses and lifethreatening presentation.
Praveen Aggarwal, Nayer Jamshed, Meera Ekka, Ali Imran Department of Emergency Medicine, All India Institute of Medical Sciences, New Delhi, India. E-mail: [email protected]
REFERENCES 1.
Das RN, Parajuli S. Cypermethrin poisoning and anti-cholinergic medication- a case report. Internet J Med Update 2006;1:42-4.
2.
Ray DE, Fry JR. An assessment of the neurotoxicity of pyrethroid insecticides. Pharmacol Ther 2006;111:174-93.
3.
Bradberry SM, Cage SA, Proudfoot AT, Vale JA. Poisoning due to pyrethroids. Toxicol Rev 2005;24:93-106.
4.
Lessenger JE. Five office workers inadvertently exposed to cypermethrin. J Toxicol Environ Health 1992;35:261-7.
5.
Walters JK, Boswell LE, Green MK, Heumann MA, Karam LE, Morrissey BF, et al. Pyrethrin and pyrethroid illnesses in the Pacific Northwest: A five-year Review. Public Health Rep 2009;124:149-59.
6.
Majumdar BB, Guha G, Ray AN, Bala B . Toxic intracerebral demyelination in a case of suicidal Cypermethrin poisoning. . Ann Trop Med Public Health 2012.5;6:615-17.
7.
Gunay N, Kekec Z, Cete Y, Eken C, Demiryurek AT. Oral deltamethrin ingestion due in a suicide attempt. Bratisl Lek Listy 2010;111:303-5. Journal of Emergencies, Trauma, and Shock I 8:2 I Apr - Jun 2015
Letters to Editor
8.
Ardhanari A, Srivastava U, Kumar A, Saxena S. Management of a case of prallethrin poisoning-An unusual agent for suicidal ingestion. Sri Lankan J Anaesthesiol 2011;19:51-2.
9.
Bhaskar EM, Moorthy S, Ganeshwala G, Abraham G. Cardiac conduction disturbance due to prallethrin (pyrethroid) poisoning. J Med Toxicol 2010;6:27-30.
10. Krug EG, Dahlberg LL, Mercy JA, Zwi BA, Lozano R. World report on violence and health. Geneva: WHO; 2002. Access this article online Quick Response Code: Website: www.onlinejets.org
DOI: 10.4103/0974-2700.145424
Successful treatment of a penetrating pulmonary artery injury caused by a Japanese sword in a patient transported by a physician-staffed helicopter Sir, We herein present a case of successful treatment of a penetrating pulmonary artery injury caused by a Japanese sword (katana) in a patient transported by a physician-staffed helicopter. A 91-year-old male stabbed his chest and abdomen and cut his head with a katana and was found in a coma by his family. His history included dementia, schizophrenia, hypertension, and diabetes mellitus. A physician transported by a helicopter checked the patient at a rendezvous point in an ambulance and found that the katana had penetrated the patient’s body from the fourth intercostal of the left anterior chest to the back [Figure 1]. The patient was in a deep coma and also a state of severe hemorrhagic shock. His venous route and airway were secured, and he was transported to our hospital. He remained in a coma with shock and demonstrated left pneumoderma in the left chest; therefore, he underwent placement of an indwelling chest tube, followed by drainage of 500 ml of hemorrhagic fluid. Permissive hypotensive therapy to maintain the systolic blood pressure from 60 to 80 mmHg was selected with transfusion of blood type O, and emergency thoracotomy was performed in the operating room. Journal of Emergencies, Trauma, and Shock I 8:2 I Apr - Jun 2015
Figure 1: A katana penetrates a patient’s body from the fourth intercostal of the left anterior chest to the back
The patient temporally exhibited pulseless electrical activity due to massive hemorrhage, and fluid resuscitation resulted in spontaneous circulation. Injuries of the lingual, left pulmonary artery, and diaphragm were found, and primary closure of the pulmonary artery with clamping of the pulmonary hilum, primary closure of the diaphragm, and lobectomy of the lingual region were performed. The abdominal stab wound did not reach the intra-abdominal cavity and was also closed. After the operation, the patient developed pyothorax and was treated with antibiotics. He achieved a full somatic recovery and was transferred to a psychiatric hospital. The patient was successfully treated, despite his advanced age and severe shock state resulting from injury of major thoracic vessels.[1-4] The key to success was a multidisciplinary approach, including early medical intervention, transportation using a physician-staffed helicopter, and the administration of permissive hypotensive treatment and emergency thoracotomy with clamping of the pulmonary hilum.
Hiromichi Ohsaka, Youichi Yanagawa, Yoshikazu Miyasaka, Ken Okamoto Department of Acute Critical Care Medicine, Shizuoka Hospital, Juntendo University, Izunokuni, Shizuoka, Japan E-mail: [email protected]
REFERENCES 1.
Fatimi SH, Hanif HM, Awais A, Shamsi G, Muzaffar M. Major thoracic vessels and cardiac trauma: Case series from a center in a developing country. Ulus Travma Acil Cerrahi Derg 2012;18:490-4.
2.
Onan B, Demirhan R, Öz K, Onan IS. Cardiac and great vessel injuries after chest trauma: Our 10-year experience. Ulus Travma Acil Cerrahi Derg 2011;17:423-9.
3.
Mandal AK, Sanusi M. Penetrating chest wounds: 24 years experience. World J Surg 2001;25:1145-9.
4.
Baillot R, Dontigny L, Verdant A, Pagé P, Pagé A, Mercier C, et al. Penetrating chest trauma: A 20-year experience. J Trauma 1987;27:994-7. 125
Copyright of Journal of Emergencies, Trauma & Shock is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
