- Email: [email protected]
Screening for and prophylaxis of venous thromboembolism in severe carbon monoxide poisoning?
592
Correspondence
[10] Bentley MA, Crawford JM, Wilkins JR, Fernandez AR, Studnek JR. An assessment of depression, anxiety, and stress among nationally certified EMS professionals. Prehosp Emerg Care 2013;17:330–8. [11] Studnek JR, Crawford JM, Wilkins III JR, Pennell ML. Back problems among emergency medical services professionals: the LEADS health and wellness followup study. Am J Ind Med 2010;53:12–22. [12] Myers JB, Slovis CM, Eckstein M, Goodloe JM, Isaacs SM, Loflin JR, et al. Evidencebased performance measures for emergency medical services systems: a model for expanded EMS benchmarking. Prehosp Emerg Care 2008;12:141–51.
[3] Cheungpasitporn W, Leung N, Sethi S, Gertz MA, Fervenza FC. Refractory atypical hemolytic uremic syndrome with monoclonal gammopathy responsive to bortezomibbased therapy. Clin Nephrol 2014 [Epub ahead of print].
Importance of tube position after tube thoracostomy
To the Editor, Antibody-mediated ADAMTS13 deficiency workup is commonly missed☆,☆☆
To the Editor, We thank Strobel et al [1] for their interesting case study, “A case of thrombotic thrombocytopenic purpura presenting as refractory hypoglycemia in a patient with thromboangiitis obliterans” published in The American Journal of Emergency Medicine. The authors reported a 39-year-old woman with thrombotic thrombocytopenic purpura presenting with refractory hypoglycemia. The patient was admitted to the intensive care unit and unfortunately developed cardiac arrest with unsuccessful resuscitation. We wonder if workup for ADAMTS13 deficiency was performed. In the case of severe ADAMTS13 deficiency, early identification of an antibody-mediated ADAMTS13 deficiency may allow targeted therapies such as B lymphocyte–depleting monoclonal antibodies [2]. In addition, monoclonal protein–related thrombotic microangiopathy was reported [3]. However, we agreed that this was a difficult and severe condition, and we respected the final decision of resuscitation withdrawals. The author Replies: We thank the reader for his interest in this unfortunate case of a middle-aged woman with thromboangiitis obliterans developing thrombotic thrombocytopenic purpura presenting as severe refractory hypoglycemia. We appreciate the importance of sending for ADAMTS13 deficiency early in the workup, even in an unstable patient. Based on your recommendations, treatment varies and can be targeted based on genetic profile for patients who survive until the results analysis is completed. The results of the ADAMTS13 were less than 10% in our patient. Ashley M. Strobel, MD Charat Thongprayoon, MD Department of Internal Medicine, Mayo Clinic, Rochester, MN Vareena Laohaphan, MD Department of Emergency Medicine, Phramongkutklao College of Medicine Bangkok, Thailand Narat Srivali, MD Department of Pulmonary and Critical Care Medicine, Mayo Clinic Rochester, MN Corresponding author at: Mayo Clinic, Rochester, MN 55905 E-mail address: [email protected]
We read the article of Matsumoto et al [1] with great interest. We thank them for the topic that is generally overlooked. Tube thoracostomy can be a lifesaving procedure especially in traumas. It is applied for the treatment of pneumothorax and hemothorax. Tube thoracostomy is performed blindly. Adhesions, collapse ratio of the lung, the incision site, and the guidance of the tube by the practitioner determine the tube position. Sometimes, in a trauma patient, there is a limited time and limited patient positioning for tube thoracostomy. Because of these reasons, a posterosuperiorly guided tube may be at the hilum, above the diaphragm, or even at the anterior paracardiac area. In a trauma patient, we think that evacuation of the blood is much more important than pneumothorax – excluding tension pneumothorax – that can be managed with a large bore needle before the tube thoracostomy. The amount of blood drained determines whether to perform thoracotomy. If the tube is not positioned posteriorly, the drainage may be deceiving. This misread of the drainage may lead to a delayed thoracotomy that can later result with mortality. In addition, inadequately drained hemothorax may lead to pleural thickening or empyema [2]. We think that if persistent expansion defect after a tube thoracostomy is seen, it can be evacuated by simple aspiration or with a small 7-F catheter from second intercostal space on the midclavicular line instead of tube thoracostomy [3]. We again thank the authors of the article for pointing out the topic. Sezai Çubuk, MD⁎ Gata Medical Faculty, Department of Thoracic Surgery, Ankara, Turkey ⁎ Corresponding author. Tel.: +90 5424868489; fax: +90 3123533702 E-mail: [email protected] Orhan Yücel Gata Haydarpasa Teaching Hospital Department of Thoracic Surgery, Istanbul, Turkey http://dx.doi.org/10.1016/j.ajem.2015.01.027 References [1] Matsumoto S, Sekine K, Funabiki T, Yamazaki M, Orita T, Shimizu M, et al. Chest tube insertion direction: is it always necessary to insert a chest tube posteriorly in primary trauma care? Am J Emerg Med 2015;33(1):88–91. http://dx.doi.org/10.1016/j.ajem. 2014.10.042. [2] Cangir AK, Yüksel C, Dakak M, Ozgencil E, Genc O, Akay H. Use of intrapleural streptokinase in experimental minimal clotted hemothorax. Eur J Cardiothorac Surg 2005;27(4):667–70. [3] Choi WI. Pneumothorax. Tuberc Respir Dis (Seoul) 2014;76(3):99–104. http://dx.doi. org/10.4046/trd.2014.76.3.99.
http://dx.doi.org/10.1016/j.ajem.2015.01.022 References [1] Strobel A, Gingold DB, Calvello EJ. A case of thrombotic thrombocytopenic purpura presenting as refractory hypoglycemia in a patient with thromboangiitis obliterans. Am J Emerg Med 32(12):1554 e5–7. [2] Coppo P, Schwarzinger M, Buffet M, Wynckel A, Clabault K, Presne C, et al. Predictive features of severe acquired ADAMTS13 deficiency in idiopathic thrombotic microangiopathies: the French TMA reference center experience. PLoS One 2010;5:e10208. ☆ Conflicts of interest: The authors disclose no conflicts. ☆☆ Authors’ contributions: All authors were involved and approved the final manuscript.
Screening for and prophylaxis of venous thromboembolism in severe carbon monoxide poisoning? Carbon monoxide (CO) is a colorless, tasteless, odorless, and nonirritating gas formed when carbon in fuel is not burned completely. It enters the bloodstream through the lungs and attaches to hemoglobin (Hb) forming carboxyhemoglobin (CO-Hb). High CO-Hb combination is poisonous [1-3]. Indeed, during CO poisoning, oxygen delivery
Correspondence
to the body’s organs and tissues is decreased. The effects of CO poisoning can be seen in many systems including the cardiovascular, pulmonary, visual, auditory, neuropsychiatric, dermatologic, and hematologic. Our observations and questions originated from our clinical experience and, specifically, we report the case of a previously healthy 22-year-old man who was found in a state of stupor, at his home, with 2 other people who had died. The previous evening they had cooked grilled meat on a charcoal barbecue in a poorly ventilated environment. The patient also complained of acute weakness and pain in his lower limbs. He was referred to the emergency department of our hospital with a provisional diagnosis of CO poisoning. Physical examination revealed drowsiness, but there were no other neurologic abnormalities. Laboratory findings at admission revealed CO-Hb values equal to 32.5%. Cardiac enzymes were increased (T troponin, 0.997 ng/mL). Standard hematologic tests (electrolytes, liver enzymes, serum protein, serum bilirubin, and serum creatinine), complete blood count, and coagulation tests were normal. The electrocardiogram showed sinus tachycardia and ST-segment elevation (leads V1-V3). The chest x-ray showed signs of pulmonary edema in both lung fields. The patient was admitted to the intensive care unit, treated with 100% oxygen, and quickly transferred to the hyperbaric unit. Cardiac enzymes showed T troponin level of 1.090 ng/mL, creatinine kinase–MB of 139 IU/L, and creatinine kinase of 23219 IU/L. A transthoracic echocardiogram showed moderately reduced ejection fraction (38%). Furosemide and morphine were intravenously given, and noninvasive ventilation (NIV) was started. On the second day of hospitalization the patient improved and the noninvasive ventilation was stopped. Diuretic therapy was continued leading to the resolution of the pulmonary edema. Oxygen therapy was gradually reduced. A therapy with angiotensin-converting enzyme inhibitor and β-blocker was started. The follow-up transthoracic echocardiogram, performed after 10 days, showed improved ejection fraction (until 56%). A cardiac Magnetic Resonance Imaging (MRI) was performed revealing a reduced global systolic function of the left ventricle; it also reported some localized pleural-based parenchymal consolidations in the mantle back bilaterally. To investigate this finding, the patient underwent a pulmonary computed tomography angiography that did not show intraluminal defects in the pulmonary arteries but confirmed some areas of parenchymal consolidation localized in the posterior basal segment of the right lower lobe and in the superior segment of the left lower lobe, typical of pulmonary infarctions. A venous ultrasound scan of the lower limbs detected a right peroneal vein thrombosis. A treatment with enoxaparin (4000 IU twice a day) was started. Genetic mutations related to thrombophilia were ruled out. The patient was discharged in good clinical conditions. CO is an agent that can cause systemic damage throughout various mechanisms. The reduction in oxygen delivery to the tissues results in local tissue hypoxia and hypoxemia [4]. CO intoxication usually disturbs the normal human biochemical respiratory chain cascade and the binding to myoglobin in cardiac and skeletal muscles can interrupt muscle oxygen transport and cause hypoxia [4-6]. Furthermore, it has been reported that CO is able to cause vascular damage [7], and it has been demonstrated to induce thrombus formation by slowing the bloodstream, increasing the permeability of vessel walls, inducing platelet stickiness and polycythemia [8]. Moreover, mean platelet volume and platelet counts are significantly higher in patients with CO poisoning [9]. Thus, it is possible that, in our patient, the described changes may have contributed to realize vein thrombosis and subsequent pulmonary emboli and infarctions. Very little literature data of both arterial and venous system thrombosis in CO poisoning have been reported. Moreover, some cases of intracardiac thrombus have been reported [10]. The only case of pulmonary emboli we found [11] describes a 70year-old woman with acute CO poisoning with right pulmonary perfusion defects at perfusion lung scan and partial popliteal deep venous thrombosis.
593
Currently, the short-term and long-term management of CO poisoning does not include recommendations for venous thromboembolism prophylaxis. In addition, the international evidence-based clinical practice guidelines only suggest, in critically ill patients, using lowmolecular-weight heparin or low-dose unfractionated heparin thromboprophylaxis over no prophylaxis; furthermore, they do not suggest routine ultrasound screening for deep vein thrombosis in these patients [12]. In summary, we believe that, in a patient with a critical disease such as acute CO intoxication, an early prophylactic administration of lowmolecular-weight heparin or low-dose unfractionated heparin should be considered to prevent venous thromboembolism. We also suggest that a venous ultrasonography scan of the lower limbs could be considered in these patients to rapidly diagnose subclinical thrombosis and prevent pulmonary embolism. Giuseppe De Matteis, MD⁎ Mariella Fuorlo, MD Massimo Montalto, MD, PhD Raffaele Landolfi, MD Department of Internal Medicine, Catholic University of Sacred Heart Largo Agostino Gemelli 8, 00168 Rome, Italy ⁎Corresponding author. Department of Internal Medicine, Catholic University of Sacred Heart Largo Agostino Gemelli 8, 00168 Rome, Italy Tel.: +39 063503854; fax: +39 0635502775 E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2015.01.019 References [1] Jackson DL, Menzes MD. Accidental carbon monoxide poisoning. JAMA 1980;243:772–4. [2] Kalay N, Ozdogru I, Cetinkaya Y, Eryol NK, Dogan A, Gul I, et al. Cardiovascular effects of carbon monoxide poisoning. Am J Cardiol 2007;99:322–4. [3] Marius-Nunez AL. Myocardial infarction with normal coronary arteries after acute exposure to carbon monoxide. Chest 1990;97:491. [4] Ernst A, Zibrak JD. Carbon monoxide poisoning. N Engl J Med 1998;339:1603–8. [5] Alonso IR, Cardellach F, Lopez S, Casademont J, Mirò O. Carbon monoxide specifically inhibits cytochrome c oxidase of human mitochondrial respiratory chain. Pharmacol Toxicol 2003;93:142–6. [6] Tritapepe L, Macchiarelli G, Rocco M, Scopinaro F, Schillaci O, Martuscelli E, et al. Functional and ultrastructural evidence of myocardial stunning after acute carbon monoxide poisoning. Crit Care Med 1998;26:797–801. [7] Wanstrup J, Kjeldsen K, Astrupt P. Acceleration of spontaneous intimal-subintimal changes in rabbit aorta by prolonged moderate carbon monoxide exposure. Acta Pathol Microbiol Scand 1969;75:353. [8] Grace TW, Platt FW. Subacute carbon monoxide poisoning. Another great imitator. JAMA 1981;246:1698–700. [9] Karabacak M, Varol E, Türkdogan KA, Duman A, Akpinar O, Karabacak P. Mean platelet volume in patients with carbon monoxide poisoning. Angiology 2014;65(3): 252–6. [10] Seung JL, Ju-Hyun K, Nam-yong K, In-Woon B, Mi-Youn P, Byung-Ju S, et al. A case report of carbon monoxide poisoning induced cardiomyopathy complicated with left ventricular thrombus. J Cardiovasc Ultrasound 2011;19(2):83–6. [11] Sevinc A, Savli H, Atmaca H. An interesting cause of pulmonary emboli: acute carbon monoxide poisoning. Clin Appl Thromb Hemost 2005;11(3):353–7. [12] Guyatt GH, Akl EA, Crowther M, Gutterman DD, Schuünemann HJ. American College of Chest Physicians Antithrombotic Therapy and Prevention of Thrombosis Panel. Executive summary: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 2012;141(2 Suppl.):7S–47S.
Paravertebral block in rib fractures
To the Editor, We read the article “A modified paravertebral block (PVB) to reduce risk of mortality in a patient with multiple rib fractures” written by Yoshida et al [1] with a great interest. They disclose that retrolaminar block/costovertebral canal block can be applicable at multiple rib fractures with coagulopathy. We would like to thank the authors for their contribution. We believe that these findings will enlighten further
Correspondence
[10] Bentley MA, Crawford JM, Wilkins JR, Fernandez AR, Studnek JR. An assessment of depression, anxiety, and stress among nationally certified EMS professionals. Prehosp Emerg Care 2013;17:330–8. [11] Studnek JR, Crawford JM, Wilkins III JR, Pennell ML. Back problems among emergency medical services professionals: the LEADS health and wellness followup study. Am J Ind Med 2010;53:12–22. [12] Myers JB, Slovis CM, Eckstein M, Goodloe JM, Isaacs SM, Loflin JR, et al. Evidencebased performance measures for emergency medical services systems: a model for expanded EMS benchmarking. Prehosp Emerg Care 2008;12:141–51.
[3] Cheungpasitporn W, Leung N, Sethi S, Gertz MA, Fervenza FC. Refractory atypical hemolytic uremic syndrome with monoclonal gammopathy responsive to bortezomibbased therapy. Clin Nephrol 2014 [Epub ahead of print].
Importance of tube position after tube thoracostomy
To the Editor, Antibody-mediated ADAMTS13 deficiency workup is commonly missed☆,☆☆
To the Editor, We thank Strobel et al [1] for their interesting case study, “A case of thrombotic thrombocytopenic purpura presenting as refractory hypoglycemia in a patient with thromboangiitis obliterans” published in The American Journal of Emergency Medicine. The authors reported a 39-year-old woman with thrombotic thrombocytopenic purpura presenting with refractory hypoglycemia. The patient was admitted to the intensive care unit and unfortunately developed cardiac arrest with unsuccessful resuscitation. We wonder if workup for ADAMTS13 deficiency was performed. In the case of severe ADAMTS13 deficiency, early identification of an antibody-mediated ADAMTS13 deficiency may allow targeted therapies such as B lymphocyte–depleting monoclonal antibodies [2]. In addition, monoclonal protein–related thrombotic microangiopathy was reported [3]. However, we agreed that this was a difficult and severe condition, and we respected the final decision of resuscitation withdrawals. The author Replies: We thank the reader for his interest in this unfortunate case of a middle-aged woman with thromboangiitis obliterans developing thrombotic thrombocytopenic purpura presenting as severe refractory hypoglycemia. We appreciate the importance of sending for ADAMTS13 deficiency early in the workup, even in an unstable patient. Based on your recommendations, treatment varies and can be targeted based on genetic profile for patients who survive until the results analysis is completed. The results of the ADAMTS13 were less than 10% in our patient. Ashley M. Strobel, MD Charat Thongprayoon, MD Department of Internal Medicine, Mayo Clinic, Rochester, MN Vareena Laohaphan, MD Department of Emergency Medicine, Phramongkutklao College of Medicine Bangkok, Thailand Narat Srivali, MD Department of Pulmonary and Critical Care Medicine, Mayo Clinic Rochester, MN Corresponding author at: Mayo Clinic, Rochester, MN 55905 E-mail address: [email protected]
We read the article of Matsumoto et al [1] with great interest. We thank them for the topic that is generally overlooked. Tube thoracostomy can be a lifesaving procedure especially in traumas. It is applied for the treatment of pneumothorax and hemothorax. Tube thoracostomy is performed blindly. Adhesions, collapse ratio of the lung, the incision site, and the guidance of the tube by the practitioner determine the tube position. Sometimes, in a trauma patient, there is a limited time and limited patient positioning for tube thoracostomy. Because of these reasons, a posterosuperiorly guided tube may be at the hilum, above the diaphragm, or even at the anterior paracardiac area. In a trauma patient, we think that evacuation of the blood is much more important than pneumothorax – excluding tension pneumothorax – that can be managed with a large bore needle before the tube thoracostomy. The amount of blood drained determines whether to perform thoracotomy. If the tube is not positioned posteriorly, the drainage may be deceiving. This misread of the drainage may lead to a delayed thoracotomy that can later result with mortality. In addition, inadequately drained hemothorax may lead to pleural thickening or empyema [2]. We think that if persistent expansion defect after a tube thoracostomy is seen, it can be evacuated by simple aspiration or with a small 7-F catheter from second intercostal space on the midclavicular line instead of tube thoracostomy [3]. We again thank the authors of the article for pointing out the topic. Sezai Çubuk, MD⁎ Gata Medical Faculty, Department of Thoracic Surgery, Ankara, Turkey ⁎ Corresponding author. Tel.: +90 5424868489; fax: +90 3123533702 E-mail: [email protected] Orhan Yücel Gata Haydarpasa Teaching Hospital Department of Thoracic Surgery, Istanbul, Turkey http://dx.doi.org/10.1016/j.ajem.2015.01.027 References [1] Matsumoto S, Sekine K, Funabiki T, Yamazaki M, Orita T, Shimizu M, et al. Chest tube insertion direction: is it always necessary to insert a chest tube posteriorly in primary trauma care? Am J Emerg Med 2015;33(1):88–91. http://dx.doi.org/10.1016/j.ajem. 2014.10.042. [2] Cangir AK, Yüksel C, Dakak M, Ozgencil E, Genc O, Akay H. Use of intrapleural streptokinase in experimental minimal clotted hemothorax. Eur J Cardiothorac Surg 2005;27(4):667–70. [3] Choi WI. Pneumothorax. Tuberc Respir Dis (Seoul) 2014;76(3):99–104. http://dx.doi. org/10.4046/trd.2014.76.3.99.
http://dx.doi.org/10.1016/j.ajem.2015.01.022 References [1] Strobel A, Gingold DB, Calvello EJ. A case of thrombotic thrombocytopenic purpura presenting as refractory hypoglycemia in a patient with thromboangiitis obliterans. Am J Emerg Med 32(12):1554 e5–7. [2] Coppo P, Schwarzinger M, Buffet M, Wynckel A, Clabault K, Presne C, et al. Predictive features of severe acquired ADAMTS13 deficiency in idiopathic thrombotic microangiopathies: the French TMA reference center experience. PLoS One 2010;5:e10208. ☆ Conflicts of interest: The authors disclose no conflicts. ☆☆ Authors’ contributions: All authors were involved and approved the final manuscript.
Screening for and prophylaxis of venous thromboembolism in severe carbon monoxide poisoning? Carbon monoxide (CO) is a colorless, tasteless, odorless, and nonirritating gas formed when carbon in fuel is not burned completely. It enters the bloodstream through the lungs and attaches to hemoglobin (Hb) forming carboxyhemoglobin (CO-Hb). High CO-Hb combination is poisonous [1-3]. Indeed, during CO poisoning, oxygen delivery
Correspondence
to the body’s organs and tissues is decreased. The effects of CO poisoning can be seen in many systems including the cardiovascular, pulmonary, visual, auditory, neuropsychiatric, dermatologic, and hematologic. Our observations and questions originated from our clinical experience and, specifically, we report the case of a previously healthy 22-year-old man who was found in a state of stupor, at his home, with 2 other people who had died. The previous evening they had cooked grilled meat on a charcoal barbecue in a poorly ventilated environment. The patient also complained of acute weakness and pain in his lower limbs. He was referred to the emergency department of our hospital with a provisional diagnosis of CO poisoning. Physical examination revealed drowsiness, but there were no other neurologic abnormalities. Laboratory findings at admission revealed CO-Hb values equal to 32.5%. Cardiac enzymes were increased (T troponin, 0.997 ng/mL). Standard hematologic tests (electrolytes, liver enzymes, serum protein, serum bilirubin, and serum creatinine), complete blood count, and coagulation tests were normal. The electrocardiogram showed sinus tachycardia and ST-segment elevation (leads V1-V3). The chest x-ray showed signs of pulmonary edema in both lung fields. The patient was admitted to the intensive care unit, treated with 100% oxygen, and quickly transferred to the hyperbaric unit. Cardiac enzymes showed T troponin level of 1.090 ng/mL, creatinine kinase–MB of 139 IU/L, and creatinine kinase of 23219 IU/L. A transthoracic echocardiogram showed moderately reduced ejection fraction (38%). Furosemide and morphine were intravenously given, and noninvasive ventilation (NIV) was started. On the second day of hospitalization the patient improved and the noninvasive ventilation was stopped. Diuretic therapy was continued leading to the resolution of the pulmonary edema. Oxygen therapy was gradually reduced. A therapy with angiotensin-converting enzyme inhibitor and β-blocker was started. The follow-up transthoracic echocardiogram, performed after 10 days, showed improved ejection fraction (until 56%). A cardiac Magnetic Resonance Imaging (MRI) was performed revealing a reduced global systolic function of the left ventricle; it also reported some localized pleural-based parenchymal consolidations in the mantle back bilaterally. To investigate this finding, the patient underwent a pulmonary computed tomography angiography that did not show intraluminal defects in the pulmonary arteries but confirmed some areas of parenchymal consolidation localized in the posterior basal segment of the right lower lobe and in the superior segment of the left lower lobe, typical of pulmonary infarctions. A venous ultrasound scan of the lower limbs detected a right peroneal vein thrombosis. A treatment with enoxaparin (4000 IU twice a day) was started. Genetic mutations related to thrombophilia were ruled out. The patient was discharged in good clinical conditions. CO is an agent that can cause systemic damage throughout various mechanisms. The reduction in oxygen delivery to the tissues results in local tissue hypoxia and hypoxemia [4]. CO intoxication usually disturbs the normal human biochemical respiratory chain cascade and the binding to myoglobin in cardiac and skeletal muscles can interrupt muscle oxygen transport and cause hypoxia [4-6]. Furthermore, it has been reported that CO is able to cause vascular damage [7], and it has been demonstrated to induce thrombus formation by slowing the bloodstream, increasing the permeability of vessel walls, inducing platelet stickiness and polycythemia [8]. Moreover, mean platelet volume and platelet counts are significantly higher in patients with CO poisoning [9]. Thus, it is possible that, in our patient, the described changes may have contributed to realize vein thrombosis and subsequent pulmonary emboli and infarctions. Very little literature data of both arterial and venous system thrombosis in CO poisoning have been reported. Moreover, some cases of intracardiac thrombus have been reported [10]. The only case of pulmonary emboli we found [11] describes a 70year-old woman with acute CO poisoning with right pulmonary perfusion defects at perfusion lung scan and partial popliteal deep venous thrombosis.
593
Currently, the short-term and long-term management of CO poisoning does not include recommendations for venous thromboembolism prophylaxis. In addition, the international evidence-based clinical practice guidelines only suggest, in critically ill patients, using lowmolecular-weight heparin or low-dose unfractionated heparin thromboprophylaxis over no prophylaxis; furthermore, they do not suggest routine ultrasound screening for deep vein thrombosis in these patients [12]. In summary, we believe that, in a patient with a critical disease such as acute CO intoxication, an early prophylactic administration of lowmolecular-weight heparin or low-dose unfractionated heparin should be considered to prevent venous thromboembolism. We also suggest that a venous ultrasonography scan of the lower limbs could be considered in these patients to rapidly diagnose subclinical thrombosis and prevent pulmonary embolism. Giuseppe De Matteis, MD⁎ Mariella Fuorlo, MD Massimo Montalto, MD, PhD Raffaele Landolfi, MD Department of Internal Medicine, Catholic University of Sacred Heart Largo Agostino Gemelli 8, 00168 Rome, Italy ⁎Corresponding author. Department of Internal Medicine, Catholic University of Sacred Heart Largo Agostino Gemelli 8, 00168 Rome, Italy Tel.: +39 063503854; fax: +39 0635502775 E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2015.01.019 References [1] Jackson DL, Menzes MD. Accidental carbon monoxide poisoning. JAMA 1980;243:772–4. [2] Kalay N, Ozdogru I, Cetinkaya Y, Eryol NK, Dogan A, Gul I, et al. Cardiovascular effects of carbon monoxide poisoning. Am J Cardiol 2007;99:322–4. [3] Marius-Nunez AL. Myocardial infarction with normal coronary arteries after acute exposure to carbon monoxide. Chest 1990;97:491. [4] Ernst A, Zibrak JD. Carbon monoxide poisoning. N Engl J Med 1998;339:1603–8. [5] Alonso IR, Cardellach F, Lopez S, Casademont J, Mirò O. Carbon monoxide specifically inhibits cytochrome c oxidase of human mitochondrial respiratory chain. Pharmacol Toxicol 2003;93:142–6. [6] Tritapepe L, Macchiarelli G, Rocco M, Scopinaro F, Schillaci O, Martuscelli E, et al. Functional and ultrastructural evidence of myocardial stunning after acute carbon monoxide poisoning. Crit Care Med 1998;26:797–801. [7] Wanstrup J, Kjeldsen K, Astrupt P. Acceleration of spontaneous intimal-subintimal changes in rabbit aorta by prolonged moderate carbon monoxide exposure. Acta Pathol Microbiol Scand 1969;75:353. [8] Grace TW, Platt FW. Subacute carbon monoxide poisoning. Another great imitator. JAMA 1981;246:1698–700. [9] Karabacak M, Varol E, Türkdogan KA, Duman A, Akpinar O, Karabacak P. Mean platelet volume in patients with carbon monoxide poisoning. Angiology 2014;65(3): 252–6. [10] Seung JL, Ju-Hyun K, Nam-yong K, In-Woon B, Mi-Youn P, Byung-Ju S, et al. A case report of carbon monoxide poisoning induced cardiomyopathy complicated with left ventricular thrombus. J Cardiovasc Ultrasound 2011;19(2):83–6. [11] Sevinc A, Savli H, Atmaca H. An interesting cause of pulmonary emboli: acute carbon monoxide poisoning. Clin Appl Thromb Hemost 2005;11(3):353–7. [12] Guyatt GH, Akl EA, Crowther M, Gutterman DD, Schuünemann HJ. American College of Chest Physicians Antithrombotic Therapy and Prevention of Thrombosis Panel. Executive summary: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 2012;141(2 Suppl.):7S–47S.
Paravertebral block in rib fractures
To the Editor, We read the article “A modified paravertebral block (PVB) to reduce risk of mortality in a patient with multiple rib fractures” written by Yoshida et al [1] with a great interest. They disclose that retrolaminar block/costovertebral canal block can be applicable at multiple rib fractures with coagulopathy. We would like to thank the authors for their contribution. We believe that these findings will enlighten further