|Year : 2015 | Volume
| Issue : 1 | Page : 29-31
Isolated acute traumatic aortic injury following cardiopulmonary resuscitation with excessively forceful chest compressions
Mark W Fegley1, Ellen A Redstone2, Amitoj Singh3, Sahil Agrawal3, Jamshid Shirani3, Sudip Nanda3
1 Department of Family Medicine, St. Luke's University Hospital Network, Bethlehem, Pennsylvania, USA
2 Department of Radiology, St. Luke's University Hospital Network, Bethlehem, Pennsylvania, USA
3 Department of Cardiology, St. Luke's University Hospital Network, Bethlehem, Pennsylvania, USA
|Date of Submission||20-Sep-2015|
|Date of Acceptance||19-Oct-2015|
|Date of Web Publication||29-Dec-2015|
Department of Cardiology, St. Luke's University Hospital Network, 801 Ostrum Street, Bethlehem, Pennsylvania
Source of Support: None, Conflict of Interest: None
We report a rare cause of isolated acute traumatic aortic injury in a 58-year-old woman with a body mass index (BMI) of 19.4, following cardiopulmonary resuscitation (CPR). Our case is unique in that CPR was performed by a single CPR provider, no significant trauma occurred with the preceding syncope, and aortic injury occurred in isolation without fractures or other traumatic injury. Healthcare providers need to be aware that although chest compression of at least 2 inches depth is needed for effective CPR, the force required to achieve this compression is much less in an individual with a BMI of around 20 as opposed to a BMI of 40. Excessive chest compression can lead to acute traumatic aortic injury. We review appropriate resuscitation and chest compression depth, CPR associated injuries including aortic injuries and mechanisms of acute traumatic aortic injury.
The following core competencies are addressed in this article: Patient care and medical knowledge.
Keywords: Acute traumatic aortic injury, cardiopulmonary resuscitation-associated injuries, cardiopulmonary resuscitation-associated aortic injuries, osseous pinch, water-hammer effect
|How to cite this article:|
Fegley MW, Redstone EA, Singh A, Agrawal S, Shirani J, Nanda S. Isolated acute traumatic aortic injury following cardiopulmonary resuscitation with excessively forceful chest compressions. Int J Acad Med 2015;1:29-31
|How to cite this URL:|
Fegley MW, Redstone EA, Singh A, Agrawal S, Shirani J, Nanda S. Isolated acute traumatic aortic injury following cardiopulmonary resuscitation with excessively forceful chest compressions. Int J Acad Med [serial online] 2015 [cited 2019 Aug 21];1:29-31. Available from: http://www.ijam-web.org/text.asp?2015/1/1/29/172701
| Introduction|| |
We report the first known case of isolated acute traumatic aortic injury following cardiopulmonary resuscitation (CPR) in a 58-year-old female. Review of literature reveals two cases of aortic injury in the setting of CPR. However, these two cases occurred in the setting of significant trauma preceding CPR, multiple CPR providers, and multiple bony injuries including fractures. We propose acute traumatic aortic injury occurred via the osseous pinch and water-hammer effect because of chest compression of excessive force. CPR providers need to be aware that chest compression of excessive force, especially in individuals with low body mass index (BMI), can cause isolated acute traumatic aortic injury.
| Case Report|| |
A 58-year-old woman had syncope at home and fell. Her husband is a police officer by profession, trained in emergency medical services, found her pulseless and started CPR. Resuscitation was successful, and patient arrived to hospital service conscious. She has a known history of pulmonary embolism and was on warfarin. Her Crohn's disease had a recent flare-up with persistent diarrhea for the preceding days. She was hypokalemic with potassium of 2.8 mEq/L and her QTc was 528 ms.
Workup included spiral computed tomography (CT) and CT angiography which demonstrated new proximal descending aortic [Figure 1]a,[Figure 1]c, and [Figure 1]e, white arrows] and aortic root [Figure 1]b and [Figure 1]d, white arrows] mural injuries compared to prior CT 2 years ago. She most likely had polymorphic ventricular tachycardia/fibrillation precipitated in the setting of an acquired long QT induced by hypokalemia. She was treated conservatively, hypokalemia corrected which normalized her QTc, and was safely discharged without surgical intervention. Follow-up CT scan 6 months later demonstrated resolution of aortic injuries [Figure 1]f.
|Figure 1: (a and b) Transverse computed tomography arteriogram images following aortic injury. (a) Mural injury highlighted by white arrow which was likely caused by aortic compression and torsion, spine highlighted by black arrow. (b) Mural injury to aortic root. (c and d) Coronal computed tomography arteriogram images following aortic injury. (c) Descending aortic injury highlighted by white arrow and proximity of spine, black arrow. (d) Aortic root injury highlighted by white arrow. (e) Axial, candy-cane, computed tomography arteriogram images following aortic injury. (e) Descending aortic injury highlighted by white arrow, likely caused by the water-hammer effect given the retrograde aortic root injury. (f) Axial, candy-cane, computed tomography arteriogram images at 6 months following aortic injury. (f) Resolution of aortic injuries. Black arrow indicates location of ligamentum arteriosum|
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| Discussion|| |
The most recent American Heart Association CPR and emergency cardiovascular care guidelines from 2010, state proper resuscitation technique on an adult is chest compression to a depth of at least 2 inches at a rate of at least 100 compressions/min. The 2010 guidelines represent a change from previous guidelines recommending a compression depth of 1.5–2 inches. The most recent guidelines do not recommend an upper limit of chest compression depth.
Chest compressions are known to cause a variety of complications including those related to the ribs, thoracic and abdominal viscera, and cardiac and vascular structures. However, aortic injuries following chest compressions are rare. Aortic injury following CPR has been described in two recent cases. The first patient wan an 86-year-old female who fell ten steps sustained hemothorax and multiple rib fractures. She needed CPR for acute cardiovascular decompensation, and a thoracic aortic dissection was seen on transesophageal echocardiogram. The other patient, a 71-year-old female, had multiple cardiac arrests, CPR multiple times, thrombolytic therapy, and use of an automated chest compression device. She developed multiple injuries that included aortic intramural hematoma, hepatic pseudoaneurysm, several rib fractures, and liver lacerations.
Our patient is distinct in that there was no significant deceleration injury, simple CPR of 3 min duration, no rib fractures, and yet she developed an isolated aortic intramural injury. Aortic injuries have an incidence of 5–10 patients/1,000,000 population in the United States, most commonly affecting male patients aged 50–70 years. Acute traumatic aortic injury occurs via a variety of mechanisms. Rapid deceleration is the most frequently described mechanism; however, the incidence of isolated deceleration mechanism appears to be rare. Alternative mechanisms include (a) compression and upward motion of the heart placing torsion and shearing stress on the aorta and (b) lateral deforming forces to the chest can cause anterior displacement of the heart and sheering forces at the isthmus. Two additional mechanisms, the first known as the osseous pinch can cause injury via compression of the aorta between the spine and anterior chest wall, and the second mechanism is known as the water-hammer effect. The water-hammer effect occurs as a result of increased intravascular pressure which can exceed 2000 mmHg following direct pressure of the aorta which has been known to cause transverse tears at the isthmus and forces can travel retrograde resulting in aortic root injuries.,
The most likely mechanisms of injury occurred via the osseous pinch and the water-hammer effect. In our patient, excessive force was transmitted in an anterior to posterior direction. The osseous pinch occurred via anterior chest wall compressing the aorta along the isthmus and ligamentum arteriosum [Figure 1]f, black arrows] and direct compression of the spine [Figure 1]a and [Figure 1]c, black arrows]. In addition, the water-hammer effect occurred likely due to the direct compression of the aorta between the chest wall and spine causing a transverse tear at the isthmus and retrograde aortic root injury [Figure 1]a and [Figure 1]b.
Our patient is 5´4˝ and 51.3 kg with a BMI of 19.4. Force required for chest compression will be very different for a patient with a BMI around 20 versus a patient with a BMI around 40. The CPR guidelines recommend 2 inches of chest compression which is a very appropriate recommendation. In a healthy, thin patient, such as ours special care needs to be taken to avoid overuse of force to prevent acute traumatic aortic injuries.
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Conflicts of interest
There are no conflicts of interest.
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