The Journal of Emergency Medicine, Vol. 47, No. 5, pp. 570–572, 2014 Copyright Ó 2014 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/$ - see front matter
Letters to the Editor , CONFRONTING BLUNT CARDIAC TRAUMA
wall bruising is present in 30% of cases” and that “sternal, clavicular, or rib fractures should raise the suspicion for cardiac injury” (1). Therefore, the emergency physician should be very careful in the physical examination and in ordering the appropriate chest imaging. Especially for sternal fractures, the coexistence of a heart contusion is remarkably frequent. Furthermore, the authors reported that “ECG value as a sensitive indicator for cardiac trauma is poor” (1). Although ECG findings often may be ambiguous, ECG abnormalities are common in patients with significant troponin elevation. I agree with the authors that “The commonest ECG abnormalities include non-specific ST-T wave changes and right bundle branch block” (1). Of course, “A normal ECG does not exclude the possibility of cardiac injury” (1). Moreover, we should keep in mind that “dysrhythmias occur in 24–73% of patients with cardiac contusion and may be delayed up to 48 hours after trauma” (1). An isolated creatine kinase-MB elevation was reported by the authors to be “accompanied by a 12% incidence of dysrhythmia,” which is quite interesting because such an elevation is common in trauma patients, whereas dysrhythmias are not (1). Moreover, they surprisingly reported a recent study where troponin I < 1.05 mg/L in asymptomatic trauma patients ruled out cardiac injury (1). Cardiac contusion can be easily present with a troponin elevation < 1.05 mg/L in these patients. I agree with the authors that, “The use of transesophageal echocardiography may be limited by the need for experienced operators and the difficulty of the procedure with associated head and neck trauma” (1). Therefore, I could not agree with the opinion that “It is still considered by many to be the test of choice for diagnosing cardiac injuries after trauma” (1). Regarding myocardial scintigraphy, I do not really believe that it has a place in the assessment of trauma patients. An excellent reminder was also provided by the authors that, “the aortic isthmus is the commonest site of aortic laceration and rupture, due to shear forces in cases of horizontal deceleration” and that “vertical deceleration injuries strain the ascending aorta and the innominate artery” (1). Great vessel injuries are rare, but potentially lethal if they are not diagnosed in time. Diagnostically, the authors mentioned that “CT [computed tomography]
, To the Editor: I read with great interest the article by El-Chami et al. on blunt cardiac trauma (1). The authors explored the diagnosis and management of several forms of blunt cardiac trauma. Given the remarkable frequency of cardiac contusion in blunt chest trauma patients, especially those involved in motor vehicle accidents, I would like to comment on some of the issues raised in this wellwritten article. The authors reported in a clinical series of blunt chest trauma, “the incidence of cardiac damage is reported to range between 8% and 76%” (1). In my opinion, the lower values of this range seem more realistic. The authors’ explanation of the pathophysiology was really informative. They interestingly reported that in abdominal trauma cases, “upward displacement of the viscera can result in cardiac injury” and that increased intracranial pressure with head injury can cause cardiac injury “because of elevated epinephrine levels causing beta receptor desensitization and coronary vasoconstriction” (1). These two mechanisms of cardiac trauma are rarely taken into consideration in clinical practice. Regarding cardiac contusion, the authors mentioned that “it is the most common injury to the heart after blunt chest trauma,” which is definitely true (1). Another interesting point they reported was that “the position of the right ventricle behind the sternum makes it vulnerable to injury” (1). This can explain why right bundle branch block is much more often found than left bundle branch block on these patients’ electrocardiograms (ECGs). Regarding cardiac concussion, they mentioned that “the main manifestation of this injury is segmental wall motion abnormality on echocardiography” (1). In practice, this means that considering only ECG and troponin might lead to this diagnosis being easily missed. According to the authors, “symptoms of cardiac contusion frequently go unnoticed by the anxious multiply injured patient” (1). Consequently, “a detailed description of the incident is vital, particularly the site and force of impact” (1). This emphasizes the importance of a carefully taken history. They also reported that “chest 570
The Journal of Emergency Medicine
use is limited by hemodynamic instability of patients and nephrotoxic effect of contrast” (1). Although these are two CT limitations, it should be underlined that mediastinum CT scan with intravenous contrast is a “gold standard” imaging method to assess such injuries in trauma patients due to its availability and easy application. To sum up, there is not really “much confusion arisen with heart contusion,” which is the commonest cardiac injury in blunt chest trauma patients. We must consider the possibility of cardiac trauma also in patients without chest trauma. History taking and a thorough physical examination are of paramount importance to guide the emergency physician to appropriately manage the blunt cardiac trauma patient. Patients with high risk of an underlying heart contusion, especially those with sternal fracture, should stay in the hospital for a few days for observation of the evolution of the troponin levels and the ECG pattern. Regarding patients with great vessel injuries, mediastinum CT scan with intravenous contrast is the imaging method of choice for the initial assessment. Ioannis N. Mavridis, MD Department of General Thoracic Surgery ‘K.A.T.’ General Hospital of Attica Athens, Greece http://dx.doi.org/10.1016/j.jemermed.2013.07.022 REFERENCE 1. El-Chami MF, Nicholson W, Helmy T. Blunt cardiac trauma. J Emerg Med 2008;35(2):127–33.
, KETAMINE FOR STATUS ASTHMATICUS WITH RESPIRATORY FAILURE , To the Editor: In regards to Shlamovitz and Hawthorne’s case report on the use of “dissociative dose” ketamine in status asthmaticus with acute respiratory failure, I am hesitant to try the authors’ prescription before exhausting conventional and well-proven treatment modalities (1). In addition, the use of ketamine in anesthetic doses in patients in extremis is not without its pitfalls. In asthmatics with respiratory failure, it is crucial for physicians, nurses, and respiratory therapists to understand that there are two, and only two, physiologic urgencies once the usual inhaled bronchodilators fail: first, the respiratory rate must be reduced, and second, the chest must be deflated. Reducing the respiratory rate increases the time available for exhalation, the latter being “mother’s milk” to asthmatics. The best way to do
571
that is with a bolus of fentanyl–it is potent, has a rapid onset and short duration of action, and it works. Concomitantly, high enough levels of continuous positive airway pressure (CPAP) should be applied to stent open the airways and allow the hyperinflated chest to deflate, thereby restoring the mechanical advantage of the expiratory respiratory muscles. CPAP is the specific antidote for all kinds of physiologic airway obstruction, especially obstructive lung disease. Although ketamine may have bronchodilatory properties that may or may not have some salutary role in the rescue of such acute asthmatic patients, decades of unequivocal clinical success with opiates and CPAP put ketamine a long way down the line in the armamentarium available to the emergency physician to treat asthmatics with respiratory failure. I do not understand the authors’ failure to utilize those methods, especially given the notation about their patient’s high respiratory rate and hyperinflated chest. Opiates and CPAP should have been employed even before epinephrine was given. As an unrelated and separate matter, equally puzzling was the decision to stick the patient for a blood gas, of all things. Blood gases have no decision-making role in the management of asthmatics with preintubation acute respiratory failureddefined clinically by failure of work of breathing (ie, fatigue). I do not know any simpler measure to clinically assess than that. For sure, blood gases have no role in the decision to intubate an asthmatic. The only possible role blood gases might have in asthmatic patients is in deciding whether or not a patient should be admitted to the floor or the intensive care unit. But even then, a much better and easier index to use for that purpose is simply the room air SpO2 (peripheral oxygen saturation). Finally, it appears that it is the authors’ purpose to suggest, specifically, an anesthetic dose of ketamine as rescue therapy. Their dissociative dose, 0.75 mg/kg (and I am assuming that is ideal body weight, not actual body weight), is most definitely an anesthetic dose in a patient with acute respiratory failure. I am a bit alarmed by that idea because as both a critical care physician and an anesthesiologist, the last thing I would do to a patient who is hypoxemic with the kind of respiratory failure described is administer an anesthetic dose of any agent (unless it was immediately before tracheal intubation). That is most certainly a paradigm that would be highly unusual in the entire realm of clinical medicine, and is not something to be undertaken lightly. And even though ketamine is known to maintain spontaneous ventilation and hemodynamics, the effect of an anesthetic dose on a patient in extremis is entirely unpredictable (speaking from large experience). On the other hand, if the authors administered ketamine as a last ditch effort to avoid intubation while they stood over
Letters to the Editor , CONFRONTING BLUNT CARDIAC TRAUMA
wall bruising is present in 30% of cases” and that “sternal, clavicular, or rib fractures should raise the suspicion for cardiac injury” (1). Therefore, the emergency physician should be very careful in the physical examination and in ordering the appropriate chest imaging. Especially for sternal fractures, the coexistence of a heart contusion is remarkably frequent. Furthermore, the authors reported that “ECG value as a sensitive indicator for cardiac trauma is poor” (1). Although ECG findings often may be ambiguous, ECG abnormalities are common in patients with significant troponin elevation. I agree with the authors that “The commonest ECG abnormalities include non-specific ST-T wave changes and right bundle branch block” (1). Of course, “A normal ECG does not exclude the possibility of cardiac injury” (1). Moreover, we should keep in mind that “dysrhythmias occur in 24–73% of patients with cardiac contusion and may be delayed up to 48 hours after trauma” (1). An isolated creatine kinase-MB elevation was reported by the authors to be “accompanied by a 12% incidence of dysrhythmia,” which is quite interesting because such an elevation is common in trauma patients, whereas dysrhythmias are not (1). Moreover, they surprisingly reported a recent study where troponin I < 1.05 mg/L in asymptomatic trauma patients ruled out cardiac injury (1). Cardiac contusion can be easily present with a troponin elevation < 1.05 mg/L in these patients. I agree with the authors that, “The use of transesophageal echocardiography may be limited by the need for experienced operators and the difficulty of the procedure with associated head and neck trauma” (1). Therefore, I could not agree with the opinion that “It is still considered by many to be the test of choice for diagnosing cardiac injuries after trauma” (1). Regarding myocardial scintigraphy, I do not really believe that it has a place in the assessment of trauma patients. An excellent reminder was also provided by the authors that, “the aortic isthmus is the commonest site of aortic laceration and rupture, due to shear forces in cases of horizontal deceleration” and that “vertical deceleration injuries strain the ascending aorta and the innominate artery” (1). Great vessel injuries are rare, but potentially lethal if they are not diagnosed in time. Diagnostically, the authors mentioned that “CT [computed tomography]
, To the Editor: I read with great interest the article by El-Chami et al. on blunt cardiac trauma (1). The authors explored the diagnosis and management of several forms of blunt cardiac trauma. Given the remarkable frequency of cardiac contusion in blunt chest trauma patients, especially those involved in motor vehicle accidents, I would like to comment on some of the issues raised in this wellwritten article. The authors reported in a clinical series of blunt chest trauma, “the incidence of cardiac damage is reported to range between 8% and 76%” (1). In my opinion, the lower values of this range seem more realistic. The authors’ explanation of the pathophysiology was really informative. They interestingly reported that in abdominal trauma cases, “upward displacement of the viscera can result in cardiac injury” and that increased intracranial pressure with head injury can cause cardiac injury “because of elevated epinephrine levels causing beta receptor desensitization and coronary vasoconstriction” (1). These two mechanisms of cardiac trauma are rarely taken into consideration in clinical practice. Regarding cardiac contusion, the authors mentioned that “it is the most common injury to the heart after blunt chest trauma,” which is definitely true (1). Another interesting point they reported was that “the position of the right ventricle behind the sternum makes it vulnerable to injury” (1). This can explain why right bundle branch block is much more often found than left bundle branch block on these patients’ electrocardiograms (ECGs). Regarding cardiac concussion, they mentioned that “the main manifestation of this injury is segmental wall motion abnormality on echocardiography” (1). In practice, this means that considering only ECG and troponin might lead to this diagnosis being easily missed. According to the authors, “symptoms of cardiac contusion frequently go unnoticed by the anxious multiply injured patient” (1). Consequently, “a detailed description of the incident is vital, particularly the site and force of impact” (1). This emphasizes the importance of a carefully taken history. They also reported that “chest 570
The Journal of Emergency Medicine
use is limited by hemodynamic instability of patients and nephrotoxic effect of contrast” (1). Although these are two CT limitations, it should be underlined that mediastinum CT scan with intravenous contrast is a “gold standard” imaging method to assess such injuries in trauma patients due to its availability and easy application. To sum up, there is not really “much confusion arisen with heart contusion,” which is the commonest cardiac injury in blunt chest trauma patients. We must consider the possibility of cardiac trauma also in patients without chest trauma. History taking and a thorough physical examination are of paramount importance to guide the emergency physician to appropriately manage the blunt cardiac trauma patient. Patients with high risk of an underlying heart contusion, especially those with sternal fracture, should stay in the hospital for a few days for observation of the evolution of the troponin levels and the ECG pattern. Regarding patients with great vessel injuries, mediastinum CT scan with intravenous contrast is the imaging method of choice for the initial assessment. Ioannis N. Mavridis, MD Department of General Thoracic Surgery ‘K.A.T.’ General Hospital of Attica Athens, Greece http://dx.doi.org/10.1016/j.jemermed.2013.07.022 REFERENCE 1. El-Chami MF, Nicholson W, Helmy T. Blunt cardiac trauma. J Emerg Med 2008;35(2):127–33.
, KETAMINE FOR STATUS ASTHMATICUS WITH RESPIRATORY FAILURE , To the Editor: In regards to Shlamovitz and Hawthorne’s case report on the use of “dissociative dose” ketamine in status asthmaticus with acute respiratory failure, I am hesitant to try the authors’ prescription before exhausting conventional and well-proven treatment modalities (1). In addition, the use of ketamine in anesthetic doses in patients in extremis is not without its pitfalls. In asthmatics with respiratory failure, it is crucial for physicians, nurses, and respiratory therapists to understand that there are two, and only two, physiologic urgencies once the usual inhaled bronchodilators fail: first, the respiratory rate must be reduced, and second, the chest must be deflated. Reducing the respiratory rate increases the time available for exhalation, the latter being “mother’s milk” to asthmatics. The best way to do
571
that is with a bolus of fentanyl–it is potent, has a rapid onset and short duration of action, and it works. Concomitantly, high enough levels of continuous positive airway pressure (CPAP) should be applied to stent open the airways and allow the hyperinflated chest to deflate, thereby restoring the mechanical advantage of the expiratory respiratory muscles. CPAP is the specific antidote for all kinds of physiologic airway obstruction, especially obstructive lung disease. Although ketamine may have bronchodilatory properties that may or may not have some salutary role in the rescue of such acute asthmatic patients, decades of unequivocal clinical success with opiates and CPAP put ketamine a long way down the line in the armamentarium available to the emergency physician to treat asthmatics with respiratory failure. I do not understand the authors’ failure to utilize those methods, especially given the notation about their patient’s high respiratory rate and hyperinflated chest. Opiates and CPAP should have been employed even before epinephrine was given. As an unrelated and separate matter, equally puzzling was the decision to stick the patient for a blood gas, of all things. Blood gases have no decision-making role in the management of asthmatics with preintubation acute respiratory failureddefined clinically by failure of work of breathing (ie, fatigue). I do not know any simpler measure to clinically assess than that. For sure, blood gases have no role in the decision to intubate an asthmatic. The only possible role blood gases might have in asthmatic patients is in deciding whether or not a patient should be admitted to the floor or the intensive care unit. But even then, a much better and easier index to use for that purpose is simply the room air SpO2 (peripheral oxygen saturation). Finally, it appears that it is the authors’ purpose to suggest, specifically, an anesthetic dose of ketamine as rescue therapy. Their dissociative dose, 0.75 mg/kg (and I am assuming that is ideal body weight, not actual body weight), is most definitely an anesthetic dose in a patient with acute respiratory failure. I am a bit alarmed by that idea because as both a critical care physician and an anesthesiologist, the last thing I would do to a patient who is hypoxemic with the kind of respiratory failure described is administer an anesthetic dose of any agent (unless it was immediately before tracheal intubation). That is most certainly a paradigm that would be highly unusual in the entire realm of clinical medicine, and is not something to be undertaken lightly. And even though ketamine is known to maintain spontaneous ventilation and hemodynamics, the effect of an anesthetic dose on a patient in extremis is entirely unpredictable (speaking from large experience). On the other hand, if the authors administered ketamine as a last ditch effort to avoid intubation while they stood over
