Posts filed under Trauma

Unstable Cervical Spine Fractures

Screen Shot 2019-01-02 at 5.45.38 PM.png

Written by: Sarah Sanders, MD (NUEM PGY-4) Edited by: Alison Marshall, MD (NUEM Alum ‘17) Expert commentary by: Steve Hodges, MD


Fractures of the cervical spine are injuries that must be approached with caution. Some are stable, some are unstable, and mismanagement can lead to life-altering sequelae. Remembering which fractures fit into which category is imperative for optimum emergency department care.

A quick review of cervical spine anatomy is a helpful starting point:

All the cervical spine anatomy images are credited to Netter, FH Atlas of Human Anatomy, Sixth Edition.

1.png
2.png

All the cervical spine anatomy diagrams are credited to Agur, AMR & Dalley, AF of Grant’s Atlas of Anatomy: Twelfth Edition.

The common mnemonic “Jefferson Bit Off A Hangman’s Thumb,” is used to remember the unstable fractures, which will be reviewed in this post.

Screen Shot 2019-01-05 at 10.59.28 PM.png
Screen Shot 2019-01-05 at 11.05.37 PM.png
Screen Shot 2019-01-05 at 11.09.01 PM.png
Screen Shot 2019-01-05 at 11.10.04 PM.png
Screen Shot 2019-01-05 at 11.10.49 PM.png

Ultimately, understanding the mechanism of injury is crucial in identifying and accurately managing these injuries. The below PV cards are organized by mechanism and tailored down to be an on-shift reference.

In conclusion, cervical spine injuries required a high index of suspicion and caution by the emergency medicine physician as their variability and potential for neurological impairment is high. Hopefully this review can provide you with additional insight and ease of memory when the next Level 1 trauma rolls through the door.  


Expert Commentary

Thanks for this insightful post.  You've done a really nice job in laying out the most salient points.  It is important to have an understanding of the anatomy and this is a great review.  Knowing the factors that put people a high risk for injury is also paramount.   Certain chronic disease states and anatomic variances, as you note, do put select patient populations at risk for specific injury.  The mechanism of injury is something we always talk about, but when it comes to neck trauma we need to really pay attention to all available history including paramedic reports, or even cell phone video, to get the best possible picture or the mechanism of injury.   I can not stress enough the importance of a detailed neurological exam including sensation(s) and reflexes.  Any asymmetric finding should raise your level of suspicion for severe injury.   Moving to advanced imaging is especially important if there is a complaint of a focal neurological deficit; be that transient, subjective or blatantly obvious. 

Athletes or motorcyclist who have suspected cervical spine injury, who have protective shoulder pads and/or helmets pose a unique challenge.  Eventually the protective devices are going to need to be removed.   There are many opinions on how best to do this and whether an x-ray should be done before attempting the removal of protective gear.   From personal experience; it can be difficult to remove protective gear;  I recommend getting "all hands on deck" and using an methodical slow organized approach.  More recent thought is that cervical spine imaging should incorporate procedures for removal of equipment before initial radiographic evaluation.[1]  Once the gear is removed a c-collar should then be applied and you can proceed with imaging.

Recommendations for imaging the cervical spine for trauma has changed quit a lot over the last several years.  The National Emergency X-Radiography Utilization Study (NEXUS) and the Canadian C-Spine Rule (CCR) have been validated and have allowed our practice to advance such that we can effectively practice clinical medicine.  However, a word of caution on using these criteria with patients who could be impaired.  Sometimes the mild dementia, delirium or subtle drug, alcohol intoxication can lead us astray when we rely solely on these criteria.   The cross table lateral films and specifically flexion/extension views have fallen out of favor.  Most patients without focal neurological complaint or deficit are imaged with plain CT.  If your patient has a focal neurological complaint or deficit, a suspected ligamentous or disc injury an MRI should be done.  Depending on the exam and risk factors I would consider either a CTA or and MRA to evaluate for vascular injury.  

You asked about c-collars specifically.  What is available to you will be somewhat hospital - vendor specific.  I prefer the Aspen or the Miami collar, they are very similar in function overall and superior to the pre-hospital EMS ones.  When a patient has to be transported to another facility; make sure that the patient has full immobilization with back board and head-side blocks with the collar and head secured to the side blocks.    An immobilized patient that requires intubation can make an easy air way difficult and a difficult airway terrifying.  Make sure you have all your equipment prepared, including a surgical method, before you intubate.  The person holding c spine immobilization needs to knows their role.....don't let go and don't move.  This is the time when a video assisted intubation should be used.  Use either the intubating bronchoscope or a video laryngoscope.   This article talks a bit about managing airway in cervical spine injury and is a nice reference.[2]

Closing thoughts: maintain a high level of suspicion for injury in the setting of a focal neurological deficit, immobilize early immobilize often and don't be shy about intubating before transferring. 

  1. https://doi.org/10.1067/mem.2001.116333  Annals of Emergency Medicine; Baldwin et. al., "Football protective gear and cervical spine imaging" July 2001 Volume 38, Issue 1, Pages 26–30

  2. 10.4103/2229-5151.128013    International Journal of Critical Illness and Injury Science; Austin et. al., "Airway management in cervical spine injury" Jan-Mar; 4(1): 50–56

hodges.png
 

Steven W. Hodges, MD, FACEP

Assistant Medical Director

Northwestern Lake Forest Hospital


How To Cite This Post

[Peer-Reviewed, Web Publication] Sanders S, Marshall A (2019, January 21). Unstable Cervical Spine Fractures [NUEM Blog. Expert Commentary by Hodges S]. Retrieved from http://www.nuemblog.com/blog/cervical-spine-fractures.


Other Posts You May Enjoy


References

  1. Adams, J. Lin, M. Mahadevan, SV. “Spine Trauma and Spinal Cord Injury.” Section VIII, Chapter 75. Emergency Medicine: Clinical Essentials. Second Edition. P652 - 657.  

  2. Agur, AMR; Dalley AF. Grant’s Atlas of Anatomy. Twelfth Edition. Chapter 4: Back. 2009.

  3. Bergenheim, AT, Forssell, A. “Vertical Odontoid Fracture. Case Report.” Journal of Neurosurgery. Vol 74 (4) p665-667. 1991.

  4. Netter, F. Atlas of Human Anatomy. Section Head & Neck. Sixth Edition. 2014.

  5. Wheeless, CR. “Cervical Spine.” Wheeless Textbook of Orthopedics by Duke University. April 26 2016. 2 Jan 2017. http://www.wheelessonline.com/ortho/cervical_spine 

Posted on January 21, 2019 and filed under Trauma.

REBOA

Screen Shot 2019-01-02 at 5.08.24 PM.png

Written by: Andew Cunningham, MD (NUEM PGY-4) Edited by: Bill Burns, MD (NUEM Alum ‘17) Expert commentary by: Zaffer Qasim, MBBS, FRCEM, FRCPC(EM), EDIC


REBOA: Ready for Prime Time?

 For years, the resuscitative thoracotomy has been the sole weapon in the physician’s arsenal against a loss of a perfusing pressure in the crashing trauma patient. With the advent of new endovascular technologies, novel methods to control hemorrhage are being refined, among them Resuscitative Endovascular Balloon Occlusion of the Aorta or REBOA. With this newer method getting a lot of attention in the emergency and trauma communities, it’s time to take a look at what it is, how successful it is, and where we are going with it.

 

What Is It?

  • Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a possible alternative to resuscitative thoracotomy in cases of non-compressible torso hemorrhage (NCTH) that present to the Emergency Department in extremis.1

  • REBOA works via the insertion of a catheter through the femoral artery to allow an endovascular balloon to be deployed within the aorta, allowing for bleeding control and augmentation of afterload in hemorrhagic shock.2

  • REBOA can be deployed in Zone III of the Aorta, as depicted in the image below, for pelvic hemorrhage, or in Zone I of the Aorta for abdominal hemorrhage.3

Borrowed from Reference 3

Borrowed from Reference 3

  • The primary indications for REBOA include:

    • PEA arrest secondary to abdominal or pelvic hemorrhage within 10 minutes of the onset of arrest

    • Severe hypovolemic shock secondary to abdominal or pelvic hemorrhage

    • Unstable hemodynamics refractory to volume resuscitation in patients with abdominal or pelvic hemorrhage2

  • The major contraindications include age older than 70, significant comorbidities, prolonged PEA arrest (lasting longer than 10 minutes),  or high suspicion for proximal aortic injury (REBOA may exacerbate bleeding from thoracic sources).2

Does It Work?

  •  A study at U of Arizona showed that 45% of patients who received thoracotomy may have benefited from REBOA based on autopsy results, but only 32% of the patients receiving a thoracotomy did not have a contraindication for it, and of those who did not have a contraindication, only roughly half would have potentially benefited. Compared to prior literature, this may suggest that REBOA is not as useful in patients in extremis.1

  • Although the literature does suggest that REBOA reduces the amount of overall hemorrhage, there is still no definitive evidence in humans of a decrease in mortality.4

  • There are still risks of complications in humans, including arterial injury and limb ischemia.3 In animal models, REBOA has also resulted in renal failure, liver failure, intestinal ischemia, and multiple other injuries which result from occlusion of the aorta.5

  • Given that REBOA still obstructs distal flow, just like cross-clamping the aorta in a resuscitative thoracotomy, it is still reserved as a last resort maneuver. The effects of aortic occlusion can be reviewed below6:

Borrowed from Reference 6

Borrowed from Reference 6

Where Is It Going?                      

  •  An alternative to REBOA may be Selective Aortic Arch Perfusion (SAAP); in this similar yet separate endovascular approach, a catheter that has two ports is utilized instead of the single-port REBOA catheter. This allows for both occlusion of the aorta and selective administration of blood, pressors, or other medications directly to the heart and brain. Where REBOA may be useful for exclusively shock, SAAP may have advantages in cardiac arrest secondary to trauma.7

  • A new, smaller REBOA catheter, the 7 French ER-REBOA, may cause fewer injuries and also allows for simultaneous blood pressure monitoring.8

  • Partial REBOA, or P-REBOA, allows for controlled blood flow to the body distal to the area of occlusion, in efforts to limit ischemia.5 

Is It Feasible for ER Docs to Perform?

  •  Yes! Some of the larger studies performed in Japan required placement by either a surgical or emergency medicine-trained attending.9

  • In England, there are case of REBOA being deployed in the pre-hospital setting to act as a bridging method for resuscitation during transport.7 As the relay between the hospital and Emergency Medical Services, it is an EM physician’s responsibility to be aware of this method and its utility in her area.

Take-Home Points

  • REBOA is a newer up-and-coming method of controlling hemorrhage secondary to abdominopelvic trauma that may act as an alternative to resuscitative thoracotomy.

  • Although more data still needs to be collected, REBOA has not yet shown to clearly improve mortality, and does come with certain risks and complications.

  • There are more novel methods of REBOA undergoing research and development, including SAAP, ER-REBOA, and P-REBOA, which may strengthen the utility of REBOA and reduce some of the complication risks.

  • REBOA is within an EM physician’s scope of practice, and may play a role in EMS in the future. As such, it is our duty to be aware of it and follow along with its developments.


Expert Commentary

Thanks for a great post on an evolving temporary hemorrhage control concept.  Hemorrhage, and torso hemorrhage in particular, remains the largest cause of death in trauma in the first 24 hours.  In the right patient, REBOA can be another effective procedure in the emergency physician’s toolbox.  Some additional points to consider:

1.     Access is key!  The rate limiting step is early common femoral artery (CFA) access.  It’s important to emphasize accessing the common as placing the sheath in one of the smaller branch vessels could increase the risk of iatrogenic injury.  I advocate using ultrasound to define the anatomy and routinely placing a CFA arterial line in your “big sick” patients to maintain skills.  As you state, this step is well within the wheelhouse of the Emergency Physician, and the foundation to build on to train in placing REBOA

2.     Patient selection is critical! The available data generally has the inclusion/exclusion criteria listed, but definitions on who is “unstable” vary. In my opinion, an arbitrary blood pressure cutoff of <90mmHg in someone with torso hemorrhage should not automatically trigger REBOA. I think these patients should get a CFA line, and then proceed to REBOA only if not responding to initial resuscitative measures or rapidly deteriorating to imminent arrest.

3.     Placement before arrest will likely lead to better outcomes.  The evolving data shows that the group that benefits most in terms of mortality are the nonresponders who will imminently arrest unless they have a lifesaving procedure.  In the arrested patient, as mentioned, determining the time of arrest is crucial. This can certainly be challenging with prehospital arrest.

4.     While the data does not show improved mortality compared to thoracotomy, there does seem to be a trend to improved neurologically intact survival – this is our ultimate goal and speaks to the ability to use REBOA proactively, before traumatic arrest happens

5.     It is absolutely critical that REBOA is used in a system that can rapidly deliver these patients to definitive care (OR/IR). The consequences of prolonged balloon occlusion as listed are dire.  Based on collective clinical experience and translational animal data, I would not recommend occluding beyond 45 minutes to 1 hour in Zone 1.

6.     REBOA in the US is currently used only at level 1 and 2 trauma centers. I think (as the British have shown), the biggest benefit is likely at smaller centers and ultimately prehospital.  Success here will be based on procedural considerations (like p-REBOA to prolong safe inflation times), appropriate training, and systems issues (expedited transfer to definitive care). 

zaffer.png
 

Zaffer A. Qasim, MBBS, FRCEM, FRCPC(EM), EDIC

Assistant Professor of Clinical Emergency Medicine

UPenn Medicine


How to Cite This Post

[Peer-Reviewed, Web Publication]  Cunningham A, Burns W (2019, January 7). REBOA [NUEM Blog. Expert Commentary by Qasim Z]. Retrieved from http://www.nuemblog.com/blog/REBOA


Other Posts You May Enjoy


References

  1. Joseph B, Ibraheem K, Haider AA, et al. Identifying potential utility of resuscitative endovascular balloon occlusion of the aorta: An autopsy study. J Trauma Acute Care Surg. 2016;81:S128-S132.

  2. Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA). Vol 2016. LIFTL.

  3. Napolitano LM. Resuscitative Endovascular Balloon Occlusion of the Aorta: Indications, Outcomes, and Training. Crit Care Clin. 2017;33:55-70.

  4. Morrison JJ, Galgon RE, Jansen JO, Cannon JW, Rasmussen TE, Eliason JL. A systematic review of the use of resuscitative endovascular balloon occlusion of the aorta in the management of hemorrhagic shock. J Trauma Acute Care Surg. 2016;80:324-334.

  5. Perkins ZB, Lendrum RA, Brohi K. Resuscitative endovascular balloon occlusion of the aorta: promise, practice, and progress? Curr Opin Crit Care. 2016;22:563-571.

  6. Russo RM, Neff LP, Johnson MA, Williams TK. Emerging Endovascular Therapies for Non-Compressible Torso Hemorrhage. Shock. 2016;46:12-19.

  7. Bebarta V. REBOA - Ready for Prime Time? ACEP EM Education.

  8. Weingart S. Podcast 170 - the ER REBOA Catheter with Joe DuBose. Vol 2016. EMCrit Blog.:Available at [http://emcrit.org/podcasts/er-reboa].

  9. Saito N, Matsumoto H, Yagi T, et al. Evaluation of the safety and feasibility of resuscitative endovascular balloon occlusion of the aorta. J Trauma Acute Care Surg. 2015;78:897-903; discussion 904.

 

Posted on January 7, 2019 and filed under Trauma.

Topical Hemostatics

Screen Shot 2018-10-28 at 5.33.44 PM.png

Written by: Alex Ireland, MD (NUEM PGY-3) Edited by: Andrew Moore, MD (NUEM Alum ‘18) Expert commentary by: Joseph Posluszny, MD


Ireland (1).png

Expert Commentary

The above summary of the mechanism of actions, indications for and limitations of topical hemostatic agents is comprehensive and thorough.

As with most summaries of hemostatic agents, we focus on the mechanism of action or aspect of coagulation by which the agent works.  Clinically, it may be easier to take a different approach.

Sometimes, the most difficult aspect of applying a topical hemostatic agent is determining the appropriate agent given the clinical scenario- all work in some fashion, but which will work best?

To help approach this, an initial question to help frame what to do in the trauma bay or ED would be: does this wound require just a hemostatic agent as a covering/dressing to promote hemostasis or are both assisted hemostasis and pressure needed to control the bleeding?  For superficial, low volume, but persistently bleeding wounds, topical agents like Dermabond, thrombin (with gelfoam) and Surgicel are ideal.  For deep, complex wounds that require hemostatic agents and pressure, QuikClot Gauze, Ativene and Combat Guaze are more effective.

Hospitals and EMS systems purchase a variety of topical hemostatic agents.  It is imperative to become familiar with these agents and be prepared for their indications before you are presented with bleeding uncontrolled by conventional dressings or pressure.

Joseph-posluszny.png
 

Joseph Posluszny, MD

Assistant Professor of Surgery

Trauma and Critical Care, McGaw Medical Center of Northwestern University


How to Cite this Post

[Peer-Reviewed, Web Publication]  Ireland A, Moore A (2018, December 10). Topical Hemostatics  [NUEM Blog. Expert Commentary by Posluszny J]. Retrieved from http://www.nuemblog.com/blog/topical-hemostatics



Posted on December 10, 2018 and filed under Trauma.

Bruised and broken hearts: diagnosis and management of blunt cardiac injury

Screen Shot 2018-08-08 at 11.37.33 PM.png

Written by:  Paul Trinquero, MD (NUEM PGY-4) Edited by:  Victor Gappmaier, MD (NUEM Alum '18) Expert commentary by: Emily Koeck, MD


Clinical vignette

A 39-year-old male presents as a fall from a two-story window, landing on his left side. He lost consciousness after the fall but is now back to his baseline mental status. Primary survey is intact and his GCS is 15. Secondary survey is notable for a left temporal scalp hematoma and tenderness over his left anterior chest. A CT brain and CT cervical spine are obtained and both are unremarkable. CT chest is notable for two left sided rib fractures and a small underlying pulmonary contusion, without any evidence of hemothorax or pneumothorax. Given his high-risk mechanism for blunt cardiac injury, ECG and troponin are obtained. Troponin is negative but ECG demonstrates a right bundle branch block, with no prior for comparison. The patient remains well appearing and hemodynamically stable. He is asymptomatic other than mild chest wall pain. This typical multiple blunt trauma patient raises some interesting questions:

  • What is blunt cardiac injury and how is it diagnosed?
  • What are the potential complications and how should they be addressed?
  • Do all patients with chest trauma need an ECG? Troponin?
  • What about isolated sternal fractures?
  • What findings merit an emergent echo?
  • When should an otherwise well appearing patient be admitted for observation?

 

Overview of Blunt Cardiac Injury (BCI)

Blunt Cardiac Injury (BCI) encompasses a spectrum of disease caused by significant blunt force transmitted to the heart via a deceleration injury or direct blow to the precordium. Damage is done as a result of direct compression of the heart between the sternum and spine, increased intra-thoracic pressure, deceleration forces (the heart has relatively unrestricted movement in the AP direction so abrupt deceleration can cause a significant impact with the sternum), or direct trauma from fractured ribs1

BCI is an umbrella term that includes a spectrum of potential pathology such as:

  • Comotio Cordis: sudden death due to an ill-timed force during a period of electrical vulnerability
  • Cardiac rupture: traumatic rupture of the myocardium due to compression of a full chamber during early systole or raid deceleration forces shearing the atria from the vena cava or pulmonary veins.[1] Often identified on autopsy due to roughly 90% fatality within minutes
  • Pericardial rupture and cardiac herniation: very rare. Most likely will either result in death before arrival or will not be the direct cause of death.[1]
  • Valvular injury: laceration of aortic cusps can cause aortic insufficiency. Compression of heart during systole can lead to tearing of mitral valves and/or papillary muscle rupture.
  • Septal tear: traumatic ASD or VSD are less common pathological findings identifiable by characteristic loud holosystolic murmurs and echocardiography
  • Coronary artery dissection/thrombosis: rare to occur in isolation
  • Myocardial contusion: edema and necrosis of cardiac myocytes due to blunt traumatic injury

Of the above injuries, most are relatively easy to diagnosis. Comotio cordis, by definition, is not survivable. Cardiac rupture leads to immediate death in most cases, but if a stable hematoma forms, the patient may present alive and in tamponade, which can be identified clinically and with the aid of bedside ultrasound. Isolated pericardial rupture is very rare. It can be associated with cardiac herniation and subsequent impairment in cardiac output, which will manifest with unstable vitals or could be identified on echo. Valvular or septal injuries will often present with heart failure, and most will be associated with a loud, new murmur and/or hemodynamic instability. Coronary artery dissection is exceedingly rare, but diagnosis (ECG, troponin) and treatment (cardiology consultation, PCI) are similar to regular MI and not unfamiliar to the emergency physician. That leaves myocardial contusion, which is the subject of considerable debate and will be discussed in detail below.

There is no clear-cut definition or gold standard diagnosis for myocardial contusion. Pathologically, a cardiac contusion involves edema and necrosis of myocytes as well as patchy areas of hemorrhage, similar to that seen with an MI. Hence, cardiac troponins are very specific for myocardial injury from trauma just as they are for ischemic damage.[2] Serum levels are elevated much more rapidly than after MI, however some sources recommend a 4-6 hr delta troponin depending on time of initial presentation and level of suspicion.[2,3] However, cardiac contusions can occur in the absence of troponin elevation and can be variably diagnosed via TTE, TEE, or ECG. Although frequently encountered in high-risk poly-trauma patients, the vast majority of cardiac contusions tend to improve spontaneously and will heal with scar formation. They are generally well tolerated and may produce only minimal symptoms.[2] Prognosis is excellent both in-hospital and at 3 and 12 month follow up and patients who are initially clinically stable are very unlikely to deteriorate due to cardiac contusion.[4] There are two mechanisms by which blunt cardiac injury can lead to significant morbidity and mortality: significant contractile dysfunction and arrhythmia.

  1. Significant contractile dysfunction is easy to identify by assessing the patient’s vital signs. A hemodynamically stable, asymptomatic patient is unlikely to be suffering from serious traumatic heart failure. Conversely, patients with hemodynamic instability or persistent arrhythmia should have an emergent echocardiogram to assess for a structural abnormality or hemodynamically significant contusion.[3]
  2. Arrhythmia may have a delayed presentation in an otherwise asymptomatic patient. Therefore, “at risk” patients may benefit from a telemetry admission in order to identify and treat expeditiously. Twenty four hours is an appropriate duration for monitoring because evidence suggests that arrhythmia will almost always manifest within the first 24 hours.[2,5] To screen for those at risk, the Eastern Association for the Surgery of Trauma (EAST) guidelines strongly recommend an ECG on all patients with a potential mechanism.[3] Common mechanisms include motor vehicle collisions, falls from height, and crush injuries. In terms of defining a high-risk mechanism, the EAST guidelines are not specific, but many individual institutions specify particular speeds or characteristics of MVC or particular heights of falls that merit screening for BCI.

Of note, while an isolated sternal fracture is clearly indicative of significant force transmitted to the thoracic cavity, is should be thought of as a risk factor for BCI rather than pathognomonic. Only a small percentage of patients with isolated sternal fracture wind up with a cardiac contusion.[6] Hence, patients with sternal fracture should be screened (with an ECG and troponin as discussed above), but should not be immediately labeled with a diagnosis of myocardial contusion or blunt cardiac injury.

Prior guidelines hedged on the utility of a troponin, but the new 2012 EAST guidelines acknowledge several recent studies which have shown that a normal ECG alone may not be sufficient to rule out clinically significant BCI and that the addition of a negative troponin increases negative predictive value to 100%. Patients with a normal ECG and negative troponin can be ruled out for BCI.[3] This guideline is partially based on a prospective study, which evaluated 333 patients with significant thoracic trauma and concluded that patients with a normal ECG and a negative delta troponin (at 0 and 8 hrs) could be safely discharged if they lacked other criteria for admission.[7] Patients with either an ECG abnormality (arrhythmia, ST changes or evidence of ischemia, heart block) or an elevated troponin should be admitted for telemetry monitoring for 24 hours.[3]

Case Resolution

Our patient from above was admitted for 24 hour monitoring given his abnormal initial ECG. In addition to pain control, incentive spirometry, and supportive care for his rib fractures, he was monitored on telemetry given his elevated risk of dysrhythmia from a likely cardiac contusion. Fortunately, he had an uneventful hospital stay, repeat ECG showed resolution of the prior bundle branch block, and he was discharged the following afternoon.

Summary

  • Blunt cardiac injury (BCI) is an umbrella term encompassing a wide spectrum of pathology due to blunt thoracic trauma.
  • Hemodynamically unstable patients should receive an emergent echo. This will help to identify structural abnormalities such as cardiac, septal, or pericardial rupture, valvular disruption, or hemodynamically significant cardiac contusion.
  • At-risk patients should be screened with an ECG and a troponin. If both are normal, then clinically significant BCI is unlikely.
  • Isolated sternal fracture is a risk factor for BCI and should prompt screening with ECG and troponin, but is not pathognomonic and does not mandate additional BCI workup on its own
  • Patients with an abnormal ECG or an elevated troponin should be admitted for telemetry monitoring for 24 hours to ensure timely treatment if the patient develops a dysrhythmia.

Expert Commentary

Excellent overview of a broad and complicated topic; just a few points to clarify/emphasize. As you stated, blunt cardiac injury is truly a spectrum of injuries related to the delivery of significant force to the precordium/chest wall. For the most part, these patients are either stable or nearly dead. The truly serious injuries, such as comotio cordis or free cardiac/pericardial rupture, are generally fatal prior to hospital arrival. Blunt valvular injury tends to be hemodynamically significant and should be suspected in a patient with signs of cardiogenic shock or murmur. While the overall incidence of BCI in the setting of thoracic trauma ranges from 13-76%, it is rare to have serious complications from BCI, and most patients who are alive on arrival to the hospital have minor cardiac injuries. These are usually myocardial contusions or dysrhythmias, and tend to be asymptomatic and self-resolve within 24 hours.

Given the high incidence of BCI and poor sensitivity of physical exam, all patients with an appropriate mechanism should be screened with EKG and troponin. A normal EKG and negative troponin is sufficient to rule OUT blunt cardiac injury. Patients with EKG changes and/or positive troponins should be stratified by hemodynamics and clinical stability. Stable patients should be observed with telemetry for resolution of EKG changes, with serial EKG and troponins depending on the degree of abnormality. Any unstable patient with risk factors for BCI should undergo emergent echocardiography to identify a possible serious injury that would require intervention.

As a final note, the risk factors for BCI are also risk factors for aortic injury, so make sure to evaluate the aorta in unstable or symptomatic patients.

koeck.png
 

Emily Koeck, MD
Surgical Critical Care, Trauma, and Burn Fellow, John H. Stroger, Jr. Hospital of Cook County


How To Cite This Post

[Peer-Reviewed, Web Publication]   Trinquero P, Gappmaier V (2018, September 10). Blunt Cardiac Injury.  [NUEM Blog. Expert Commentary by Koeck E]. Retrieved from http://www.nuemblog.com/blog/BCI


Posts You May Also Enjoy

References:

  1. El-Menyar A, Al Thani H, Zarour A, Latifi R. Understanding traumatic blunt cardiac injury. Ann Card Anaesth. 2012;15(4):287-295.
  2. Sybrandy KC, Cramer MJ, Burgersdijk C. Diagnosing cardiac contusion: old wisdom and new insights. Heart. 2003;89(5):485-489.
  3. Clancy K, Velopulos C, Bilaniuk JW, et al. Screening for blunt cardiac injury: an Eastern Association for the Surgery of Trauma practice management guideline. J Trauma Acute Care Surg. 2012;73(5 Suppl 4):S301-306.
  4. Lindstaedt M, Germing A, Lawo T, et al. Acute and long-term clinical significance of myocardial contusion following blunt thoracic trauma: results of a prospective study. J Trauma. 2002;52(3):479-485.
  5. Fabian TC, Cicala RS, Croce MA, et al. A prospective evaluation of myocardial contusion: correlation of significant arrhythmias and cardiac output with CPK-MB measurements. J Trauma. 1991;31(5):653-659; discussion 659-660.
  6. Athanassiadi K, Gerazounis M, Moustardas M, Metaxas E. Sternal fractures: retrospective analysis of 100 cases. World J Surg. 2002;26(10):1243-1246.
  7. Velmahos GC, Karaiskakis M, Salim A, et al. Normal electrocardiography and serum troponin I levels preclude the presence of clinically significant blunt cardiac injury. J Trauma. 2003;54(1):45-50; discussion 50-41.

 

Posted on September 10, 2018 and filed under Trauma.