TRAUMA NOTEBOOK
Blunt Cardiac Trauma Following a Head-on Motor Vehicle Crash Author: Maureen Harrahill, RN, MS, ACNP-CS, Portland, Ore
Maureen Harrahill, Oregon ENA, is Trauma Coordinator/Trauma Nurse Practitioner, Oregon Health Sciences University, Portland, Ore. For reprints, write: Maureen Harrahill, 1404 SE Malden, Portland, OR 97202; E-mail:
[email protected]. J Emerg Nurs 2004;30:188-90. 0099-1767/$30.00 Copyright n 2004 by the Emergency Nurses Association. doi: 10.1016/j.jen.2003.11.016
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33-year-old man was involved in a head-on car crash at highway speed. He was the restrained driver, and there was significant intrusion to the front end of his car. On arrival at the emergency department, his blood pressure was 127/72 mm Hg, his heart rate was 115 beats per minute, and his respiratory rate was 22 breaths per minute. His oxygen saturation was 96% on 3 L of oxygen by nasal cannula. His Glasgow Coma Scale score was 15. He complained of back pain, left leg pain, and pain with deep inspiration. He was previously healthy and was taking no medications. Physical examination was significant for bruising over his sternum in a seat-belt mark pattern, an obvious leftthigh deformity, and abrasions to both legs. His workup revealed left subtrochanteric femur fracture, L1-2 transverse process fracture, multiple left rib fractures with pulmonary contusion, and a small liver laceration. His head computed tomography scan was negative for acute injury, and his heart tracing showed a sinus tachycardia without ectopy. The orthopedic team took the patient to the operating room from the emergency department to repair his femur fracture. Postoperatively, he was noted to have a new right bundle branch block on EKG and continued sinus tachycardia. Serial troponin-I (TnI) enzyme studies were performed, which peaked at 2.5 ng/mL. Blunt cardiac trauma (BCT) is also known as cardiac contusion and blunt cardiac injury. These are vague terms for a wide range of injury to the heart, from clinically insignificant EKG changes to catastrophic valve disruption, hemopericardium, or cardiac wall blowout. Following blunt trauma to the heart, the patient may be at risk for arrhythmias or hypotension. The key is to
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Going hand in hand with the vague definition of BCT are the equally vague diagnostic criteria. Unfortunately, no single gold-standard test exists. Over time, 2 diagnostic tests have been identified as helpful to the bedside clinician. These tests are the EKG and cardiac enzymes studies. The EKG is the least controversial test. It is easy to obtain, noninvasive, and provides relevant information that can be interpreted immediately at the bedside. When evaluating for BCT, the presence of an arrhythmia, any ischemic changes, or a heart block pattern is considered a positive finding.1,2 The next step, performing a serum cardiac enzyme test, is more controversial. In 1994, a group of Denver researchers who used creatine kinase as the biomarker declared cardiac enzymes to be ‘‘irrelevant’’ in BCT.3 A practice management guideline published in 1998 reported that TnI did not contribute to patient management.2 Recent studies, however, have found TnI levels to be helpful.1,2 Cardiac TnI is a regulatory protein found only in cardiac muscle tissue.4 It is a protein subunit, along with troponin-T and troponin-C, making up the troponin complex. Troponin is an essential component of the sarcomere, the contractile unit of striated muscle. Troponin, tropomyosin, and actin make up the thin filament of the sarcomere. The thick filament is primarily myosin. Muscle contraction occurs when these thick and thin filaments slide past each other, thus shortening the length of the sarcomere. Other biomarkers associated with cardiac injury include the aforementioned creatine kinase, myoglobin, lactate dehydrogenase, and cardiac troponin-T. However, only TnI is a specific marker for the cardiac cell injury. It
has never been isolated in skeletal muscle and is found uniformly throughout the atria and ventricles.4 The other markers are found in noncardiac muscle and can be elevated in the face of noncardiac trauma. For this reason, these enzymes have fallen out of favor as too nonspecific to indicate BCT. TnI is typically considered abnormal with levels greater than 1.5. ng/mL.1 TnI will elevate after injury in 4 to 6 hours, hit peak elevation in about 12 hours, and return to normal in 3 to 10 days.4 Because the blood levels are dependent on the elapsed time from traumatic insult, it is important to determine serial blood levels. If the patient has both an abnormal EKG and an elevated TnI, Salim et al1 recommend the patient be monitored closely for at least 24 hours. If both tests are normal, the patient is deemed low risk for developing significant complications. Although there is no formal consensus, the development of signs and symptoms of BCT ranges from 6 to 24 hours.1 After 24 hours, the risk decreases significantly. Who, then, should prompt suspicion for BCT? BCT can follow many different types of insult, including motor vehicle crash, pedestrian versus automobile, falls, crush, assault, and sports injury.3 Biffl et al3 considered patients at high risk for BCT if the mechanism of injury involved direct chest trauma, such as impact with a steering wheel, or if the patient complained of chest pain, had sternal ecchymosis or tenderness, or had positive findings on chest radiograph or on EKG. Velmahos et al5 evaluated 333 consecutive patients who experienced major blunt thoracic trauma to rule out concurrent BCT. Major blunt trauma was defined as ‘‘multiple rib fractures, sternal fracture, lung contusion occupying more than 20% of the lung, hemopneumothorax requiring thoracostomy tube drainage, scapular fracture, major intrathoracic vascular injury and significant anterior thoracic seat belt marks.’’5 These patients all had an EKG done on admission and at 8 hours and serum TnI drawn on admission and repeated at 4 and 8 hours. In their group of 333 patients, 44 (13%) had clinically significant cardiac injury, defined as cardiogenic shock, arrhythmias requiring treatment, and posttraumatic structural deficits.5
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rapidly identify the patient at risk of having cardiac complications develop.
He was noted to have a new right bundle branch block on EKG and continued sinus tachycardia. Serial troponin-I enzyme studies. . .peaked at 2.5 ng/mL.
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Once the diagnosis is made, EKG can be a helpful adjunct, particularly for patients with unexplained shock, significant arrhythmias, or suspected anatomic defects.1-3 An EKG images the heart based on the velocity of sound traveling through the heart. The EKG evaluates the heart for wall motion defects and for structural defects. If the patient has significant anterior rib cage trauma and/or subcutaneous emphysema, the resolution of the standard transthoracic EKG is often poor. Transesophageal echocardiography may provide a more accurate picture, but it is invasive, difficult to obtain in a nonintubated patient, and often is not available as an emergent procedure.
Our patient [was a] classic blunt cardiac trauma archetype. He had head-on impact with a seat-belt mark across his chest, the first harbinger of trouble. He had pain with breathing and multiple rib fractures. A right bundle branch block developed and he had persistent tachycardia.
R EFER ENCES 1. Salim A, Velmahos G, Jindal A, Chan L, Vassiliu P, Belzberg H,
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et al. Clinically significant blunt cardiac trauma: role of serum troponin levels combined with electrocardiographic findings. J Trauma 2001;50:237-43. Pasquale M, Fabian TC. Practice management guidelines for trauma from the Eastern Association for the Surgery of Trauma. J Trauma 1998;44:941-56;discussion956-7. Biffl W, Moore A, Moore E, Sauaia A, Read R, Burch J. Cardiac enzymes are irrelevant in the patient with suspected myocardial contusion. Am J Surg 1994;168:523-8. Abbott Diagnostics. Troponin—physician’s brochure [online]. Available from: URL: http://www.abbottdiagnostics.com/medical conditions/heartdisease/. Velmahos G, Karaiskakis M, Salim A, Toutouzas K, Murray J, Asensio J, et al. Normal electrocardiography and serum Troponin I levels preclude the presence of clinically significant blunt cardiac injury. J Trauma 2003;54:45-51.
Contributions for this column are welcomed and encouraged. Submissions should be sent to: Maureen Harrahill, RN, MS, ACNP-CS 1404 SE Malden, Portland, OR 97202 503 494-6007 .
[email protected]
This situation leads us to a still relatively confusing position. Certainly the take-home message is to be suspicious for BCT based on mechanism of injury, patient complaint, and physical findings. An EKG in the emergency department is essential. TnI levels obtained serially also can be helpful. A positive finding should alert you to the concern for BCT. These patients need to be monitored closely for at least 24 hours. Our patient appears to be a classic BCT archetype. He had head-on impact with a seat-belt mark across his chest, the first harbinger of trouble. He had pain with breathing and multiple rib fractures. A right bundle branch block developed and he had persistent tachycardia. A h-blocker was started to help control his rate. Fortunately, no complications developed as a result of his BCT and he was discharged home and has continued to do well.
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