AC Joint Separations: Overview of diagnosis and treatment

ea90ef38fb7534ffad2f6215fb663dSeparation of the acromioclavicular (AC) joint is a common injury encountered in the emergency department. Keys to optimal outcome and return of function in these patients include knowledge of injury mechanism, diagnosis and classification, and initial treatment.


A 16-year-old male presents complaining of right shoulder pain. The patient is the quarterback for his high school football team. He was tackled, falling onto his right shoulder. He appears uncomfortable, but his vital signs are within normal limits. A focused exam of the right shoulder reveals limited range of motion due to pain and tenderness over the distal clavicle and acromion. There is no deformity or palpable fracture, however, the clavicle is slightly mobile in an anterior direction. An x-ray is obtained due to your concern for a possible AC joint separation.

What is the AC joint?

The acromioclavicular joint is a synovial articulation between the distal clavicle and the acromion. Like other joints, stability of this joint is provided by a capsule and ligaments. There are the acromioclavicular (AC) ligaments and the coracoclavicular (CC) ligaments. The AC ligaments resist anterior-posterior movement, while the CC ligaments resist movement in the superior-inferior direction. On clinical exam, directional instability of the clavicle occurs with varying degrees of ligamentous injury. It is also thought that the deltoid and trapezius muscles provide dynamic stability for this joint.



Anterior view of L shoulder

How do you diagnose an AC joint separation?

Mechanism: This is generally caused by a force through the shoulder, driving the acromion inferiorly. This can occur during contact sports, falls onto the shoulder or arm, or with multidirectional forces.

Physical Exam: The patient will have localized pain and possibly a deformity. Compression of the joint and horizontal adduction of the arm will elicit joint mobility. The joint may also be unstable without these tests.

Imaging: This aids in the diagnosis. Plain films are the most common modality, but bone scan, ultrasound, and magnetic resonance imaging may also be used. Stress films are often mentioned in the literature, but are not always worthwhile to obtain in the emergency department.

Classification of AC joint separations

This is made based on the Rockford grades:

  1. Grade I: Sprain of the AC ligaments, but the ligaments are intact. There is no instability of the clavicle on exam and the patient will have a normal x-ray.
  2. Grade II: Involves rupture of the AC ligaments, but the CC ligaments remain intact. The clavicle will have some mobility in the anterior-posterior direction. On x-ray, the lateral clavicle may be slightly elevated. Stress films, however, will show normal alignment of the AC joint.
  3. Grade III: Complete disruption of the AC and CC ligaments without significant disruption of the delto-trapezial fascia. A deformity is present on exam with the clavicle appearing elevated and unstable in both vertical and horizontal directions. This separation of the clavicle and acromion is seen on x-ray.
  4. Grade IV: The distal clavicle is posteriorly displaced into the trapezius muscle. A posterior deformity is present on exam. On plain films, the clavicle will be displaced posteriorly on axillary views.
  5. Grade V: A more severe form of grade III. Not only is there disruption of the AC and CC ligaments, but there is also disruption of the delto-trapezial fascia. There may be tenting or pseudo elevation of the lateral clavicle, due to downward displacement of the scapula. On x-ray, there will be a 2-3 times increase in the distance between the coracoid and clavicle or a 100-300% increase in the clavicle-acromion distance.
  6. Grade VI: Involves inferior displacement of the distal clavicle, either subacromial or subcoracoid. This is a result of severe trauma and there are often other significant injuries present.

AC separation


How do you treat AC joint separations?

First, it should be noted that there are no randomized controlled trials on the management of AC joint separations. It is generally accepted that the objectives of management should be to reduce the risk of complications following injury, restore function, and optimize sporting performance. The consensus in the literature is that Grade I-III injuries can be managed conservatively, while Grade IV-VI injuries need surgical intervention, usually urgently, if not emergently. However, there was one study by Lizaur et al that had 46 patients with Grade III injuries [1]. Of those patients, 94% had a concurrent injury to the delto-trapezial muscle complex, needing surgical repair. This has sparked some debate in the realm of orthopedics.

Acute phase of AC joint separations: Place the injured extremity in a sling and providing analgesia and anti-inflammatory modalities. These patients will need referral to an orthopedic surgeon for further management, including some form of a rehab program. The best practice for an optimal outcome in these patients involves providers with a working knowledge of anatomy, kinematics, kinetic chain concepts, the healing continuum, exercise physiology, and the ability to adapt treatment strategies. Gladstone et al published the most common protocol for treatment and rehabilitation in 1997, which involves progressive range of motion and strengthening exercises along with assessment for return to activity [2].

In the emergency department, we can provide the initial immobilization and pain control. It is probably just as important to provide a realistic timeframe for recovery to these patients. Time based guidelines for return to sport or activity are designed to indicate when recovery is falling out of the ideal time. Recommendations are [3]:

  • 2-4 weeks for Grade I injuries
  • 4-6 weeks for Grade II injuries
  • 6-12 weeks for Grade III injuries

Case conclusion

Due to normal appearing x-ray, you diagnose the patient with a Grade II AC joint separation (due to the clavicle mobility on exam). The patient is provided analgesia and placed in a sling for comfort. You inform the patient it will likely take at least 4 weeks for full recovery, and arrange orthopedic follow up.

Bottom line

AC joint separations are common in the ED. Use a focused physical exam and imaging to make the diagnosis. Generally, Grade I-III injuries can be managed conservatively with early range of motion exercises and orthopedic follow up. Grade IV-VI injuries need an orthopedic consultation in the emergency department. Place patients in a sling and provide pain control.



  1. Lizaur A, Marco L, Cebrian R. Acute dislocation of the acromioclavicular joint. Traumatic anatomy and the importance of deltoid and trapezius. J Bone Joint Surg Br. 1994 Jul;76(4):602-6. PubMed PMID: 8027149.
  2. Gladstone JN, Wilk KE, Andrew, JR. Nonoperative treatment ofacromioclavicular joint injuries. Operative Techniques in Sports Medicine. 1997 Apr; 5(2): 78-87. Abstract
  3. Reid D, Polson K, Johnson L. Acromioclavicular joint separations grades I-III: a review of the literature and development of best practice guidelines. Sports Med. 2012 Aug 1;42(8):681-96. PMID: 22784232.


Shoulder anatomy credit (labeled by ALiEM), Rockford grading image

Author information

Matt Astin, MD
Matt Astin, MD
ALiEM Guest Contributor
Clinical Assistant Professor of Emergency/Internal Medicine
Mercer University School of Medicine
Houston Medical Center (Warner Robins, GA)

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Critical Care Horizons

Critical Care Horizones

Please welcome a new development in critical care publishing with the launch of a new open access critical care journal: CRITICAL CARE HORIZONS!!!  This will be a fresh, new, original voice in the critical care literature, offering thought provoking, cutting-edge commentary, opinion papers, plus state-of-the art review articles.

What is Critical Care Horizons?

A journal with a focus on discussion, commentary, sharing of insight, experiences, and ideas central to the progress of the critical care specialty. This will be a free to publish and free to read journal opening authorship opportunity to all working with the critically ill.  The main objective is to improve the care offered to patients with critical care illness.

How will this journal be different from other critical care journals?

The unique aspect of this journal will be combining the rapidity, broad exposure, and dynamic discussion characteristics of social media with the academic standards of an indexed, peer-review process. Since the journal will be covering the full spectrum of clinical care, submissions from all disciplines involved in the care of the critically ill and injured will be welcome.  Submissions can be from the entire spectrum of care including: pre-hospital resuscitation, emergency department care, ICU-based management, post-discharge follow-up, as well as anything else associated with improvement in patient care.

Critical Care Horizons will be aligned with the altruistic ethos of the FOAMed movement, and affiliated with several of the leading critical care and emergency medicine blogs.  There is an energetic editorial board, consisting of a deliberate mix of clinicians active in social media and world renowned academics.

What blogs are affiliated with this journal?

Critical Care Reviews
Intensive Care Network
Life in the Fast Lane
Northern Ireland Intensive Care Society
Rage Podcast
St. Emlyn’s

How and when will this journal publish?

The journal will publish directly to the website (, as soon as it has cleared the peer-review and editorial processes.  Issues will be published quarterly, with additional special editions as required.

Is there any conflicts of interest or funding disclosures for the journal?

The journal will be run on a not-for-profit basis, with editorial staff operating on a voluntary basis without monetary reimbursement. This is a journal for the critical care community, by the critical care community, without access impediment, or financial bias.

When will the first issue of this journal be published?

The first articles will be published January 2015

Where can I get more information about this journal?


Twitter: @CCHjournal



Critical Care Horizons
c/o Dr. Andrew Ferguson
Intensive Care Unit
Craigavon area Hospital
68 Lurgan Road
Portadown BT63 5QQ
United Kingdom




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Eroğlu: Yeni nesil baş belaları Bonzai ve Jamaica

Bonzai, jamaica, Spice, K2, Dream, Black mamba, Jamaican Gold, Black magic… Son yıllarda giderek artan hızda karşılaştığımız bu maddeler, bugüne kadar bir çok insanı mağdur etmiş, ve etmeye de devam etmektedir.  İnternet yoluyla 3 gramlık paketleri, 80-90 liraya kadar çıkabilen fiyatlarla satılan “bonzai” vb. sentetik kannabinoidler, sokak aralarında 5-10 lira karşılığında kolayca elde edilebilmektedir. Aşağıdaki ...

Definition of cold: Killing a Patient to Save His Life –

For the record, I’m all for this, providing it pans out in trials…

PITTSBURGH — Trauma patients arriving at an emergency room here after sustaining a gunshot or knife wound may find themselves enrolled in a startling medical experiment.

Surgeons will drain their blood and replace it with freezing saltwater. Without heartbeat and brain activity, the patients will be clinically dead.

And then the surgeons will try to save their lives.

Researchers at the University of Pittsburgh Medical Center have begun a clinical trial that pushes the boundaries of conventional surgery — and, some say, medical ethics.

By inducing hypothermia and slowing metabolism in dying patients, doctors hope to buy valuable time in which to mend the victims’ wounds.

via Killing a Patient to Save His Life –

Conclusion to Masters Case #02

This is the conclusion to Masters Case #02: 60 Year Old Female – Chest Pain, Hx of Pericarditis. If you haven’t already done so, check out the original post there.


Your patient was a 60yo F who experienced significant 8/10 chest pain that was now down to a 1 or 2 and presented with this EKG:

Masters Case 02 - Bojana Uzelac - EMS 12-Lead


What to do?

This is a really though ECG to sort out (hence it being a “Masters Case”) and will be labelled “non-specific” by most folks who see it, even experts. Indeed, that would be my official interpretation without any further investigations or follow-up to confirm my hunches. Still, by using a deliberate and step-wise approach to read the ECG, you can start to suspect what may be going on here and even make the correct diagnosis. While I don’t have a formal method I use to approach electrocardiograms and my way surely isn’t the only way, I’m going to walk you through how I interpreted this case the first time it was presented to me. As with the last Masters Case, this is how I actually read the EKG given only the basic information contained in initial case presentation linked above.


First off, this patient is not actively experiencing a STEMI. People who tell you that they look at EKG’s in a systematic way by looking first at the rate, rhythm, axis, etc… before even glancing at the T-waves are liars. We work in emergency medicine and the #1 thing we care about when running an EKG on someone with chest pain is whether they have a STEMI. Seeing ST-elevation doesn’t mean we’re done reading the EKG or closing our differential, but it’s about setting priorities starting our search where the money is (Sutton’s law).

The patient’s chief complain is chest pain. The rhythm is sinus, neither too fast nor too slow, and there is no sign of active coronary artery occlusion; that’s all I need for right this second.

Thankfully her history tells the rest. She has a very good story for ACS, she is high risk, and ruling that out is going to be a higher priority than looking for pericarditis.

Initial treatment with 324mg ASA and 0.4mg SL nitro (since she still has at least some pain).

Repeat EKG and set up my automatic vitals.

Now I’ve got the important stuff out of the way and can really see what the EKG is telling us.

- Sinus rhythm @ 64 bpm.
- Borderline 1st degree AV-block.
- Right bundle branch block (RBBB), left anterior fascicular block (LAFB), the combination of which we call a bifascicular block. This is a somewhat “gross” looking EKG for a 60-year-old, but given her age and history of diabetes it’s probably a safe bet that she has underlying CAD. It’s also comforting to know that she had the RBBB/LAFB on her prior EKG.
“Non-specific T-wave changes”


Now at this point you could probably just transport or admit this patient for an ACS rule-out (depending on your role). But we can do more with this tracing! After all, this is an ECG blog and supposedly these are cases for masters…

While there are plenty of cases of non-specific ST/T-wave changes that we really can’t read into, this is a special situation.

The first key is that the T-waves aren’t just flattened or mildly inverted like we often see with other “non-specific” changes. These T-waves are aggressively defiant of the direction they are supposed to be facing. Almost all of the precordial T-waves are opposite how they would be directed in uncomplicated RBBB. The inferior T-waves can be more variable in how they’re directed with RBBB/LAFB, but more often you’ll see aVF upright, sometimes even III as well.

There’s also a clearly abnormal morphology to the T-waves. They aren’t just inverted in III and aVF, which could be a truly nonspecific finding, but rather they are biphasic with a slight upslope before they invert. I’ve cropped and zoomed in on aVF and III below to show off their subtle up/down morphology.

2014.06.11 - Blog Case - Masters 02 - ECG 04 - Bojana Uzelac - EMS 12-Lead

More convincing than that, however, is the precordial leads.

The right precordial leads all have symmetric, peaked, upright T-waves, especially in V2 and V3. Lots of folks with RBBB and CAD/old-MI have abnormally directed T-waves, but the peaked nature of these seems more acute than we usually see.

In fact, if you look a I and aVL, they too seem to be subtly peaked.

HyperK+ crossed my mind but I doubt that’s in play in a patient presenting with a CC of chest pain and no disclosed history of renal issues. There’s also q-waves in V1 and V2 but I’m not convinced they’re too important to what we’re seeing today.

The final piece of the puzzle is the abnormal T-wave inversions in V5 and V6 (and I’ll include V4 too). They introduce one more detour on the path to our final diagnosis…

It’s true that ST-depression does not localize, meaning that just because you see inferior ST-depression it doesn’t mean there is necessarily ischemia specific to the inferior wall. On the other hand STEMI does localize. If you see true ischemic inferior ST-elevation, then the inferior wall of the heart is experiencing acute epicardial ischemia.

T-wave inversion, however, are often lumped in with ST-depression as a sign of vague ischemia, and they also don’t localize very well when you’re dealing with run-of-the-mill NSTEMI.

There is an exception, however, and that is when the T-wave inversions are due to reperfused coronary artery occlusion, in which case they localize just like STEMI. That’s why the T-wave inversions of Wellens syndrome, associated with LAD lesions, present in the anterior (and sometimes lateral) leads; there was STEMI there before the artery opened, the ST-elevation resolved, and the T-waves inverted.

As a disclaimer, this ECG could very well be the patient’s baseline (especially given her prior pericarditis and probable CAD), but in the emergency setting we have to assume the T-wave abnormalities are new until shown otherwise. Like I said, the official interpretation of this tracings would be “non-specific T-wave abnormalities,” but we’re diving a bit beyond that here.

And reperfused occlusion certainly fits nicely with her symptomatic presentation of resolving chest pain, but is the EKG specific enough? Yes! Not only are there “ischemic looking” T-wave inversions in the inferolateral leads (meaning of abnormal morphology), most dramatically in III and V6 just like we would expect in a right coronary artery (RCA) distribution, but the T-waves in V2 and V3 are unusually peaked and tall… indicating posterior reperfusion waves! The peaked T-waves in I and aVL are similar to the posterior reperfusion waves, representing the same mechanism of reciprocal reperfusion changes.

So the T-wave abnormalities we’re seeing aren’t just just vaguely defined, they actually follow a modestly convincing coronary artery distribution that fits well with the RCA.

After all of that discussion, my initial thoughts were that this patient had ACS due to a lesion of the RCA that spontaneously reperfused until proven otherwise. She should be watched closely with nitro handy, continuous ST-segment monitoring, and repeat ECG’s, but unless her symptoms return or her T-waves pseudo-normalize (or show frank ST-elevation), she doesn’t need immediate cath. Still, being at a PCI hospital or at least having a plan to administer tPA quickly should she re-occlude would probably be a good idea.

All that talk is good, but how did the case turn out?

A repeat ECG was performed when the patient arrived at the hospital:

2014.06.11 - Blog Case - Masters 02 - ECG 02 - Bojana Uzelac - EMS 12-Lead

It’s essentially the same.

Initial troponin (uncertain assay) was normal and electrolytes were all within normal limits. Echo showed no regional wall-motion abnormalities and all chambers were of normal size and appearance. While there was some separation of the pericardial layers with fibrin deposits, this was very similar to her old echo from a year ago.

Still, the patient had a good story for ACS and was at least moderate risk, if not high-risk if you buy my ECG interpretation. The plan was to admit the patient for overnight observation and workup but she felt fine and wanted to go home, choosing instead to sign out against medical advice (AMA). Perhaps I was leading you astray with the giant walkthrough above…

Except that the patient’s symptoms recurred a couple of hours later and she called EMS yet again. This time the pain didn’t resolve before EMS arrival and she presented pale and diaphoretic with the EKG below:

Masters 02 - ECG 03 - Bojana Uzelac - EMS 12-Lead

Infero-postero-lateral STEMI, in the exact pattern we predicted! Note how all of the leads that now show ST-elevation with upright T-waves had inverted T-waves before, while the leads with previously upright T-waves now show reciprocal ST-depression. This is a perfect example of the relationship between the ST-elevation of STEMI and the T-wave inversions of reperfusion!

The patient went to cath where a culprit occlusion of the dominant mid-RCA was stented to good effect. Non-culprit stenoses of the normal-sized LAD ( 50-70% both mid and distal) and small LCx (non-significant stenosis) ended up buying the patient a spot on the waiting list for a CABG, but she ended up doing well when all was said and done!


As always, I’d like to thank Dr. Bojana Uzelac for submitting such a great case. Also, congrats to reader Eric for being the only person I saw who correctly identified the posterior reperfusion T-waves that helped to make this case. Finally, thanks to everyone who followed the case and submitted comments; I hope these cases are intriguing and educational in spite of how detailed their analyses can be.

If you want to learn more about posterior reperfusion T-waves, go right to the source from the man who introduced them to me: Dr. Stephen Smith of Dr. Smith’s ECG Blog.