Trauma Tuesday! The Cervical Collar

What is a C Collar?

 They come in a couple of different flavors, but the two extremes are hard and soft collars. The primary function of C Collars is to immobilize the C spine. Hard collars provide more immobilization and restriction of ROM compared to their soft brethren, but are generally more uncomfortable for patients.  

Why use a C Collar?

C Collars are placed to protect the spinal cord from the possibility of secondary injury in the unstable cervical spine. The theoretical risk is worsening an unstable fracture, and potentially causing devastating neurological injury.

When to use a C Collar? Who should be in a C Collar?

Following trauma, early immobilization of the cervical spine can be crucial if c-spine injury is suspected. This can be obvious in patients involved in MVA, falls, and assaults to the head or neck. On history and physical, the patient may be complaining of sensation changes, neck, and back pain. But cervical injury may not be so obvious in the patient found down and unresponsive, who cannot communicate what happened to them, and may have had signs of a recent fall and possible C spine injury.  C-collars are often placed on these patients too.

Protection of the C spine is considered so important, that a rigid C collar placement is reflexive in both the in and out of hospital environment. It's built into ATLS protocols. In many EMS protocols, if a patient is complaining of neck pain or any neurological symptom after trauma, they've bought themselves a C Collar.


This all sounds great....but then why is there debate around C-Collars?

The potential harm of C Collars:

C Collars are not benign interventions. The long term changes include muscular, bone, and tendon atrophy, but what about in the short term? Hard collars, like the C collars we place in the ED for our trauma patients, are associated with pain, breathing restriction, tissue ischemia, increase aspiration events, and adds barriers to medical care, including maintaining C spine when moving, exposing, and cleaning the patient. And that's only talking about the C collar in a vacuum: C Collars are notorious for hiding extent of trauma, such as soft tissue swelling and more commonly, bleeding of the occiput and neck. They also increase ICP- Stone et al. demonstrated that C collars increase ICP in healthy volunteers placed in C Collars, potentially worsening intracranial injury. Additional studies, like that of Kolb et al, found increased ICP measured by CSF pressure obtained through LP in a group wearing a c collar compared to a group that didn't.

What else does the literature say?

A lot of the benefits associated with C Collars are theoretical. Do they actually help and do what they're supposed to do?

Here's the problem with the existing literature: There are no prospective studies comparing an experimental C collar group with a no collar control group. And thus, a lot of research on C spine injury and c collars are done on cadavers and in analogous studies. 

Some studies looked at whether C collars are even able to immobilize the spine. One study looked at "lightly embalmed" cadavers with an induced C5-6 instability injury, and then put on different types of C collar. They tested for motion using EMG sensors, and tested all planes of cervical motion. They found no significant difference in motion between the C spine groups and the no c collar group. Another cadaver study with induced c spine instability even found increased motion in axial and cranial-caudal planes in a rigid C collar group compared to no c collar group, possibly through the creation of  "pivot points" from where the collar meets the TMJ and shoulders. 

What about the possibility of preventing secondary injury? Other studies (involving mostly cadavers, again) has shown that a considerable amount of force is required to fracture the spine, and that subsequent, low energy forces from patient's moving their neck is unlikely to cause additional spinal cord injury. Additionally, these and similar studies suggest that an unstable fracture existing without already devastating neurological injury is rare. Furthermore, it is also suggested in a retrospective study looking at neurological outcome between the USA (where we routinely immobilize with C collars) vs Malaysia (a country that does not routinely immobilize patients) and found that less neurological disability occurred in the unimmobilized group, suggesting that there may even be the potential of neurological harm. Obviously, a lot of this research is not perfect but it certainly does not favor the absolute benefit of using C collars routinely.

What should we do?

The real question at the end of the day. Placing C Collars is still the standard of care, though additional research may one day point us away from reflexively using it, and perhaps protocols detailing its use in trauma may become more sparing. In the meantime, for our trauma patients, we can decrease the time sensitive risks associated with these devices by clearing them as soon as we can, as we always have. This research at least opens my eyes to the potential of C collars causing harm, and that one day what has been drilled into my head regarding trauma management may not always be the case.

Thanks for sticking around till the end!

-SD

Sources:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5481593/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2684205/

http://www.emdocs.net/cervical-collars-for-c-spine-trauma-the-facts/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2751736/

https://pubmed.ncbi.nlm.nih.gov/511875/

https://pubmed.ncbi.nlm.nih.gov/22962052/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3949434/

https://www.uptodate.com/contents/evaluation-and-initial-management-of-cervical-spinal-column-injuries-in-adults?search=Cervical%20spine%20trauma&source=search_result&selectedTitle=1~145&usage_type=default&display_rank=1


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POTD: Trauma Tuesday! Blunt Thoracic Aortic Trauma

"Level 1 trauma...high speed car crash...GCS 6, was intubated in the field...ETA 5 minutes."

The patient arrives. You start your ABCs. The patient is intubated with BL breath sounds. You start circulation when you notice the pulses on BL lower extremities are absent with no obvious injury below the waist. You trace it up and notice decreased femoral pulses. The patient is getting exposed and you see a significant seatbelt sign on the chest. Thereโ€™s a high suspicion for aortic injury. Letโ€™s talk about blunt thoracic aortic injuries.

Background: Right off the bat: 80% of these patients do not make it to the hospital. Most of these patients die on the scene, however you may be able to do something for the 20% that make it to your ED. Up to 2 percent of patient who sustain blunt trauma to the thorax sustain a blunt thoracic aortic injury. 70% of patients are male. 

Associated with rapid deceleration events, aortic injury occurs with MVC most of the time, followed by pedestrian struck, followed by fall from significant height. Sudden deceleration causes the injury at the aortic isthmus.

Where is the isthmus? Why is the isthmus? Good questions. So I looked it up:

Why do injuries occur at this spot of the aorta? Well there are several theories. 1. The aortic isthmus is a transition zone between the unfixed aortic arch and the fixed descending aorta; sudden deceleration causes the two parts to go in different directions leading to tearing. 2. The tissue surrounding the isthmus is weaker compared to the rest of the aorta. 3. The Osseous Pinch (new band name 2021): the aorta is trapped between the bones of anterior chest and the vertebral column during deceleration force.

An initial tear in the intima then leads to more intimate pathology- that of aortic dissection. A tear in the intima in a high pressure vessel leads to bleeding which can penetrate the adventitia, worsening until the point of pseudoaneurysm and free rupture. This is one of the main reasons you're not out of the woods if they're among the lucky 20% of folks to make it to the hospital. 

Diagnosis: Gotta be on your A game. It won't always be apparent from the history and physical that you're dealing with an aortic injury. High speed injury, patient complaining of chest pain, back pain, SOB, trouble swallowing- all good places to start thinking about aortic injury in the setting of trauma. Good luck getting the patient to tell you any of these things, because a GCS <8 is present in up to 41% of patients with blunt thoracic aortic injury.

Physical exam findings that can tip you off include finding seatbelt sign across the chest, steering wheel sign, new murmur on auscultation. On the rarer side of things, you may see subclavicular hematoma or pseudocoarctation leading to increased pulses and hypertension of upper extremities, and decreased pulses and hypotension of the lower extremities.

CXR can show a widened mediastinum. One study by Bruckner et al found that the positive predictive value of a CXR with widened mediastinum is only 5%, but a cxr with the absence of widened mediastinum has a NEGATIVE predictor value of 99%.

Get a CTA of the chest if possible.

Aortagraphy is technically the gold standard for diagnosing blunt aortic injury. I'll be sure to get those right alongside my cardiac biopsies to diagnose myocarditis. Jokes aside, angiography is invasive and comes with its own complications and risks. And our wonderful CT techs and their wonderful machine is just calling to us from down the hall.

An alternative in a more unstable patient who is intubated is TEE. Like CTA, it also has a high sensitivity and specificity for detecting injury.

Grading is based on findings found on CTA. Let's breakdown the classification:

Type 1: Intimal Tear

Type 2: Intramural hematoma

Type 3: Pseudoaneurysm

Type 4: Rupture


Work up and management:

A ๐Ÿ‘T๐Ÿ‘ L ๐Ÿ‘S. This is still a trauma, through and through when this arrives to your ED. Primary survey with ABCDEFast. Two large bore IVs. Fluid and blood. Secondary and tertiary surveys, imaging performed based on patient's clinic status.

For hemodynamically unstable patients, in the setting of trauma, go to the OR.

For the (initially) hemodynamically stable patient

Type 1 injuries may be managed conservatively- this means medical management- treat it like an aortic dissection. Aggressive HR control and BP control. HR below 100 and goal SBP 100. Esmolol is drug of choice, if another drug needed, can use diltiazem, nitroglycerin, nitroprusside.

Grades 2-4 require repair. Options include open repair with thoracotomy vs endovascular repair with aortic stent graft.

Oftentimes there are associated injuries. Injuries strong enough to hurt the aorta via deceleration is usually associated with blunt head, cardiac, lung, and bone injury. In fact, up to 81% of patients have an associated injury. The reason this is important, aside from having more things to treat in the ED, is that these can be distracting injuries to the true big bad laying in hiding.

Note: Thoracic aortic injury is a contraindication for REBOA therapy.

Sources:

https://www.annalsthoracicsurgery.org/article/S0003-4975(10)65322-2/pdf

https://cardiothoracicsurgery.biomedcentral.com/articles/10.1186/s13019-020-01101-6

https://pubmed.ncbi.nlm.nih.gov/16564268/

https://wikem.org/wiki/Traumatic_aortic_transection

https://www.ncbi.nlm.nih.gov/books/NBK555980/

https://pubmed.ncbi.nlm.nih.gov/21217494/

https://www.ncbi.nlm.nih.gov/books/NBK459138/

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Trauma POTD: Blunt Cardiac Injury

Definition: Refers to any blunt trauma to the heart. Ranges from mild to severe.

Includes the following:

o   Comotio Cordis: a sudden death due to an ill-timed force during a period of electrical vulnerability

o   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

o   Cardiac Contusions: edema and necrosis of cardiac myocytes due to blunt traumatic injury

o   Dysrhythmias after trauma

o   Ventricular wall rupture

o   Coronary artery dissection/thrombosis: less common

o   Septal tear: traumatic ASD or VSD less common

o   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

o   Pericardial rupture and cardiac herniation

 

Epidemiology:

o   Incidence ranges from 9 to 71% mostly because of lack of clear definition and diagnostic criteria

o   Most commonly the right ventricle or right atrium are involved

o   Most severe BCI result in wall rupture in any of the chambers and these patients typically die in the field

o   Pediatric patients have increased thoracic cavity compliance and there may be no signs of trauma on exam which makes it even important that we consider this in our trauma patients

 

Causes:

o   Significant amount of force is normally required for a BCI to occur

o   Suspect BCI in any patient with significant thoracic trauma or direct precordial impact including all of the following

o   MVA (most common)

o   Pedestrians struck

o   Crush injuries

o   Blast injuries

o   Deceleration injuries

o   Commonly occurs in patients with sternal fracture or rib fractures

 

Presentation:

o   Symptoms: most commonly patients complain of chest pain

o   Signs:

  • Dysrhythmias (most commonly sinus tachycardia or atrial fibrillation)

  •  Chest wall deformities or ecchymosis

  • Pulse deficits

  • Hypotension

  • New murmur

  • New onset HF (rales, muffled heart sounds or JVD on exam)

  • Pericardial effusion or tamponade on FAST

Work up:

o   First and foremost follow ATLS guidelines

o   Hypotension in trauma patients should be initially approached as due to hemorrhage rather than a purely cardiac cause

o   Persistent tachycardia after volume resuscitation, adequate pain control, and exclusion of intrathoracic or intrabdominal hemorrhage should raise suspicion of possible BCI

o   Obtain an EKG and look for the following (important to trend EKG)

o   Dysrhytmias

o   New conduction delays (bundle branch blocks)

o   ST segment elevations or depressions

o   Look for signs of sternal fracture or rib fracture on CXR

o   ECHO

o   TTE look for overall cardiac contractility (EF), wall motion abnormalities, turbulent blood flow, intraventricular or intraatrial thrombi

o   TEE is most sensitive in detecting cardiac injuries that may require intervention

o   Cardiac Biomarkers

o   Significance of troponin remains unclear. Presence of single elevated troponin does little to help further management and increases the likelihood of admission and cardiology consult

o   CK-MB is not a recommended biomarker in BCI

 

EAST (Eastern Association for the Surgery of Trauma) Guidelines:

o   Level 1 Evidence

o   Obtain EKG on all patients with suspected BCI

o   Level 2 Evidence

o   If the EKG reveals a new abnormality admit the patient for telemetry monitoring

o   BCI can be ruled out in patients with a normal EKG and negative troponin (although appropriate timing of troponin remains unclear)

o   Obtain an optimal TTE or TEE on patients who are hemodynamically unstable or with persistent new arrythmias

o   Sternal fracture alone does not predict BCI

 

References:

o   https://rebelem.com/blunt-cardiac-injury-bci/

o   https://www.nuemblog.com/blog/blunt-cardiac-injury

Bruised and broken hearts: diagnosis and management of blunt cardiac injury โ€” NUEM Blog

o   https://rebelem.com/rebel-core-cast-10-0-blunt-cardiac-injury/

o   https://emcrit.org/emcrit/blunt-cardiac-injuries/


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