There are probably too many techniques for anterior shoulder reduction and too many eponyms. We need to transition to an anatomical approach but we are not there yet. For a head start, let’s think about the two most common types of anterior shoulder dislocation we see.



Subcoracoid is the most common, found in 70% of anterior dislocations. This is where the humeral head rests just below the coracoid process. The subglenoid location, with the humeral head inferior to the glenoid, is found in 30% of anterior dislocations.



The Kocher technique, one of the oldest and most popular techniques, was developed for the subcoracoid anterior dislocation. Review Neil Cunningham’s resources at shoulderdislocation.net for insight on this, as well as his translation of the original Kocher article.



Do the eponyms confuse you? Think of Kocher’s method as the “trochanteric rim roll.” First adduct the elbow all the way to get the greater trochanter right next to the glenoid rim. Then externally rotate to roll the greater trochanter on the glenoid rim. Then forward flex the shoulder (saggital plane) to tip the humeral head back toward the socket. Finally, internally rotate to complete the reduction.


Kocher’s words:

“Pressing the arm bent at the elbow towards the body, turning outward until resistance is felt, lifting of the outwardly rotated upper arm in the sagittal plane as far as possible, and finally slowly turning it inward” (translation by Cunningham)



The subglenoid dislocation will not be resolved with the Kocher technique because the external rotation phase will not latch onto anything.



-Avoid traction, which is what creates the need for sedation(Chitgopar Injury 2005).

-Make sure you fully adduct the elbow first.


Note: I use the term “trochanteric rim roll” because it conveys the mechanism of the procedure. This is more of a teaching device and is not standard terminology.




-Kocher’s “trochanteric rim roll” was originally intended for subcoracoid dislocations, not for subglenoid.



shoulderdislocation.net (see the lectures and translation of the original Kocher article)

Chitgopkar SD, Khan M. Painless reduction of anterior shoulder dislocation by Kocher’s method. Injury. 2005;36:1182-4.


A patient presents with a scalp hematoma from a remote fall. When you press on it, it feels very soft but is not swollen. You are confused, and order a CT, which shows complete lysis of the bone,. Further workup suggests metastatic renal cell carcinoma. The patient is avoidant on history and keeps explaining away the findings and concerns. Hours later, while he is awaiting a bed upstairs, he reveals that a year ago his doctor suspected renal cell carcinoma but he refused a workup.


This patient suffered from denial. Whether that is a perfect term is debatable. In this case it was severe but so often denial seems to overlap with avoidance, perhaps even procrastination. It is at times the unwillingness to address an unpleasant reality. In medicine all too often we judge “denial” as a break with reality but we need to understand it as a human experience. Denial is the way some patients try to grasp onto hope. Go read Arthur Miller’s Death of a Salesman if you want a literary exploration of denial as a silent cry for hope.


We shouldn’t always oppose denial. Don’t argue over code status. If they want to be full code don’t gripe about them at the nurse’s station. They are dying. If knowing they will get 30 minutes of CPR in the end gives them comfort then let them have that consolation. If the patient-centered reasons aren’t enough, remember that practicing code situations only makes you better at it.


The literature is accumulating articles portraying denial as a positive thing. Denial mitigates terror and allows patients to continue to function. But in the emergency department we sometimes see patients at an earlier stage, where denial gets in the way of potentially curative treatment. So what should we do?


Accentuate the positive

Without distorting the truth, emphasize the safety, tolerability, and efficacy of the treatments.


Build a relationship of trust by genuinely connecting as people

As emergency physicians we will not get long-term rapport, so build it for your consultants, whose expertise and caring we should commend to the patient (assuming we can do so truthfully). Spend some time getting to know them as people. Share anecdotes of those who have had good experiences, which not only illustrates safety but also displays your connection to patients.


Tools of persuasion – allowing an “out” lowers the cost of an “in”

Finally, point out that they can always choose to stop treatment later. That way they can say yes without feeling stuck. By giving them an “out” you are lowering the cost of going “in.”


Ultimately, denial is their choice. We will not be able to convince everyone to face the unpleasant reality but we should use the skills and techniques that best address their frame of feeling.



Take Home Points:

-Denial is an effort to have hope

-Give such patients hope through emphasizing the positives of treatment

-Connect on a genuine, human level

-Remind them they can change their minds later



Anecdote 1:Don’t call it a seizure, start CPR

Resident: Hey, remember that patient in room 7 with the heart attack? Now he’s having a seizure!

You: That is not a seizure, let’s start CPR!

(the patient survives, and receives emergent catheterization opening a blocked vessel)


Cardiac arrest is often accompanied by jerking movements. The cartoons of the 1940s understood this. Bugs Bunny would typically do a few good jerking leg kicks prior to faking death with Elmer Fudd, Yosemite Sam, etc. Elmer Fudd can get tricked by some convulsions but let’s make sure we don’t, okay? If the setting is more appropriate for cardiac arrest, check pulses first.


This is probably not substantially different from convulsive syncope but I will describe that separately:


Anecdote 2: Don’t call it a seizure, refer to cardiology

“we never figured out why the Brugada syndrome patient had a seizure” – this is an exact quote from someone who ought to know better based on their training and specialty. It wasn’t a seizure, it was convulsive syncope.


Blood bank studies show that about 10% of syncope events are accompanied by a convulsion. These can look like epileptic generalized tonic clonic seizures. The differences are:

Pre-ictal: what were the setting, the symptoms, and the signs, before the event. An aura suggests a seizure. Standing in church suggests syncope. Alcohol withdrawal suggests seizure, etc.

Ictal: convulsive syncope is less rhythmic, less symmetrical, and less sustained

Post-ictal: Convulsive syncope patients regain normal arousal within a minute, seizure patients take 10-15 minutes


If they might have had convulsive syncope, make sure they get an appropriate syncope work-up.


Ancedote 3: Don’t call it a seizure, check the temperature

A middle aged patient is waiting to be seen for generalized weakness. The triage RN rushes them out of the waiting room because of a “seizure.” He never lost consciousness and was awake the entire time. Temp is 103 oral. You ultimately diagnose sepsis from pyelonephritis.


Rigors can cause tremendous shaking and can make us worry about seizure. Obviously a seizure can raise the temperature so judgment is required. But don’t automatically assume that a convulsion from sepsis is a seizure. Rigors happen when the temperature is rising, so recheck the temperature.


Anecdote 4: Don’t call it a seizure, educate the family

A patient is here for opioids. The doctor said no. She has a history of developing “seizures” when she does not get narcotics. Now she is screaming loudly and, wait for it…. The RN runs to you announcing a seizure and asks if you will give Ativan. Okay, I admit it, I often give Ativan if I am not sure. One time I went to the patient and said “really, you are having a seizure? Can I see the tongue biting, show me the tongue” and she proceeded to show me her teeth, biting the tongue.


This is tough. Don’t expect the family to understand the difference between seizures and psychogenic convulsions (also known as pseudoseizure). Educate them on the potential for psychogenic causes (but don’t prematurely rule out epilepsy either, unless it is abundantly obvious)



-Our terminology can box us in. Don’t call it a seizure unless you are committing to an epileptic etiology.

-Ask about circumstances before, during, and after the event to identify possible convulsive syncope


We speak of physical diagnosis as if the sign and the suggested diagnosis always match. Often they do, for example when we see acromial step off and suspect anterior shoulder dislocation.


But more often there is ambiguity. Most bedside information is non-specific. For example, tachycardia can mean a lot of different things. Later when we look at everything at once, there is the chance to “put it all together.”


But when will you do that? It is necessary at times to give uninterrupted concentrated thinking to a patient’s symptoms and signs. For example, how about the chronic headache patient who saw the chiropractor for neck pain? When you put it all together you might think of vertebral dissection.


Some call this a “cognitive pause,” others just call it medical decision-making, and others focus on the disruptive effect of interruptions.


Many ED groups routinely expect charting to be done at the end of the shift, after the patients are gone.


But charting is a chance to think critically, to put it all together. And sometimes when we do that early in the visit, it can prompt a “lightbulb” moment where we realize the need to check something else.


I advocate real time charting. The act of creating a chart requires thinking. Why not do that while the patient is still in the ED? I think at the end of the visit just before discharge is okay but even better would be right after seeing the patient. The recitation of the symptoms and signs are most accurate at that time and the “cognitive pause” of thinking through the whole presentation then can happen early, when it can change the workup.


It is simply impossible to do that on all patients on all shifts. But this is something we should try to do. The bottom line is that most historical and physical findings are ambiguous. There needs to be an explicit stage after information collection, which is information “integration.”


Take Home Points

-Complex patients require a “cognitive pause”

-It is hard to do that on a busy shift but real-time charting makes it more possible



Check out Mark Jaben EP Monthly April 2013

To Reduce Medical Errors, Take a Cognitive Pause


Several years ago I wanted to write a post on the physical diagnosis of COPD exacerbation.


First of all, most of the signs were just other ways of describing labored respiration. You know it when you see it and do not need to list 10 ways of saying the same thing.


But even more provocative, no finding was really unique to COPD exacerbation. Everything I found could be true in chronic COPD, just worse in acute COPD. (Pursed lip breathing, prolonged exhalation, recruitment of accessory muscles, etc). As an ED physician we don’t know their baseline. So how helpful is all that?


Acute COPD exacerbation in general is not a distinct disease. It is chronic COPD + something else. Usually that “something else” is a viral upper respiratory infection. The GOLD criteria emphasize a change in sputum character or quantity or dyspnea. But many things cause that, not just a chest cold.


Jogging across the parking lot? COPD + dyspnea = COPD exacerbation, if you aren’t really thinking about it. Ask an ED physician to do an examination on that patient, right after the jog, and don’t tell them about the jog. They will be getting their airway equipment ready, thinking this is a severe acute COPD exacerbation.


We need to be careful. Any condition posing a respiratory challenge is going to look the same to us as a typical acute COPD exacerbation. Metabolic acidosis, viral URI, pulmonary embolism, possibly even CHF.


This is why I recommend thinking of COPD as a diagnosis of exclusion.


Does this mean you work everyone up? Of course not. I try to subtract the COPD in my mind. If everything points to a URI then I am done, just like I would be in a regular URI patient. But if they have isolated dyspnea without any reason for it (no signs of airway inflammation, like sputum) then I might broaden my workup, treating it the same as a patient with isolated dyspnea.



-Acute copd exacerbation is usually caused by a viral URI but any respiratory challenge can create the physical signs of COPD exacerbation

-Think of COPD as a diagnosis of exclusion- consider other causes like CHF, pneumonia, pulmonary embolism


Morgagni in 1761 described a man who presented with a swelling on the upper part of the sternum (Seats and Causes of Diseases). The skin became thinner and blood began to leak out. The original case describes the patient pulling at his bandages and being “ordered to keep himself still, and to think seriously and piously of his departure from this mortal life, which was very near at hand, and inevitable.” The following day Morgagni describes the lesion bursting. “Nevertheless, he had the presence of mind, (as soon as) he felt the blood gushing forth, not only to commend himself to God, but to take up with his own hands a basin that lay at his bedside; and, as if he had been receiving the blood of another person, put it beneath the gaping tumour, while the attendants immediately ran to him as fast as possible, in whose arms he soon expired.” Post-mortem examination revealed the cause to be an aortic aneurysm.


In the 1955 movie Not as a Stranger Robert Mitchum evaluates his chief of surgery who complained of chest pain. Mitchum listens to the chest (presumably hearing a diastolic murmur), recoils in horror, then checks the bilateral pulses (presumably feeling a pulse deficit), and rushes him off to the operating room.


Before one gets the conclusion that we were better at physical diagnosis then, a contemporary article of that era described the antemortem diagnosis rate of aortic dissection as 11% (Levinson 1950). Hollywood has always exaggerated the abilities of its heroes to overcome the limitations of our real world. One of the leading experts on this disease has said “…difficulty in diagnosis, delayed diagnosis or failure to diagnose are so common as to approach the norm for this disease…” (Elefteriades Cardiology 2008).


Is there anything we can we do at the bedside to improve our history and physical examination?


Full history beats partial history:

Physicians who ask about onset, location, and quality have a better chance at diagnosis. Of patients who turned out to have aortic dissection, when all 3 of those were documented the condition was suspected in 91% of cases. When at least one of those is missing from the chart, the diagnosis was initially suspected in 49%.(Rosman Chest 1998)


Pain that is sudden, severe, or radiating to the back

Sudden and severe pain are present in up to 90% of cases (Klompas JAMA 2002). Radiation to the back occurs in 47-64% of patients (Hiratzka JACC 2010).


Chest pain + neurologic deficits

Other specific findings include migration of pain along the territories of the aorta and new neurological deficits, both present in up to about a quarter of patients (Sullivan Am J Em Med 2000).


Diastolic murmur

It turns out that Robert Mitchum’s approach is still worth doing. A diastolic murmur of aortic regurgitation is a high risk finding, occurring in 45% of patients (Hagan JAMA 2000).


Pulse deficit

A “pulse deficit”, which refers to an absent or asymmetrically weak pulse, occurs in 26%(Pape 2007. Klompas says 31%). Do not bother with blood pressure limb differentials in low risk populations, as it has poor specificity, being found in 19% of chest pain patients without aortic dissection (Singer 1998). Instead, palpate both limbs feeling for a difference.


Although it is beyond the scope of this article, many advocate using d-dimer as a screening test in those with a low (but not zero) probability of disease because it is 97% sensitive and 47% specific, at least in the first 24 hours of disease (Suzuki Circulation 2009). With time that sensitivity goes down and most experts recommend not relying on this test.



-Sudden and severe pain raises your concern for aortic dissection

-Check for pulse deficits and diastolic murmurs

Deep Space Infection of the Neck? Check Range of Motion

A young man presents with a severe sore throat. He was here yesterday and received antibiotics. Today he feels worse. You look in the throat expecting a peritonsillar abscess but the throat looks completely normal, not even erythema.


Now what?


Amidst the busy emergency department practice, sometimes we need a reason to take a second, closer look. Always trust your gut. In this case the patient had severe pain but no erythema. The concerning finding was not the severe sore throat or the normal examination, but the incongruity of both. Is there something deeper going on? What else should you check?


Check range of motion. He can do it but has severe pain, not so much with flexion but definitely with extension. You order a CT scan and it shows a retropharyngeal abscess.


I would have hoped to a review of the physical findings on this condition but they appear to be very limited (odynophagia, trismus, stridor, muffled voice)


Take Home Points:

-Incongruity/anomalous findings get your attention

-Check range of motion for suspected deep space infection of the neck