A patient presents with subacute right sided shoulder pain. Could this be rotator cuff disease?

The shoulder joint is shallow, making it the most mobile joint in the body.  Much of its stability comes from muscles that traverse the glenohumeral joint.  In addition to the rotator cuff, the long head of the biceps traverses this joint.  Both are susceptible to degeneration as they rub against bone in a narrow space.  Rotator cuff disease and bicipital tendinitis should be thought of together.

Although there are many specialized tests, the most important thing is knowing muscle function and how to test for it.

INFRASPINATUS/TERES MINOR -These serve external rotation. With the elbows at the side and flexed 90 degrees (airplane seat position), test external rotation against resistance.  The best method is to tell the patient “don’t let me move you arm.”

SUBSCAPULARIS – The function of the subscapularis is internal rotation, and this could be tested in the same position.  However, internal rotation is also supplied by the pectoralis major and the latissmus dorsi. To isolate the subscapularis, have the patient put the hand behind the small of the back and lift off against resistance (Gerber’s lift-off test).

SUPRASPINATUS – The supraspinatus serves abduction from 15-90 degrees.  This is best tested in the scapular plane (not forward flexion, not pure lateral abduction, but about in between). Put the arm in this position, say “don’t let me move your arm,” and press against resistance.  The biceps contributes to arm abduction and supination, so reduce its contribution by pronating the arm, thumb down (empty can test, aka Jobe’s test).  This test is sensitive but not specific. Minor variations of this test are used to check for biceps tendinitis and labral tears, but these tests do not reliably discriminate between these diseases.

BICEPS TENDON – The biceps tendon serves arm abduction and forearm supination.  Speed’s test is basically the empty can test but with the thumb up, in supination.  Yergason’s test basically tests for resisted supination. Both are best performed with simultaneous bicipital tendon palpation. If these tests bring out bicipital tenderness, then they are considered positive.

Traditionally, it was believed that palpation of bicipital groove tenderness was pathognomonic for bicipital tendinitis.  This has since been challenged. The hard part is finding the tendon.  Here is how to do it.  Put the patient in airplane seat position (elbows 90 degrees, at the side). Palpate just lateral to the coracoid.  The bicipital groove runs between the lesser and greater tuberosity, so externally rotate the arm just a bit to expose the area.  Drop down to the humeral head and feel the tendon roll as you move your thumb side to side.  You can actually feel the tendon pulley as the patient flexes and extends the elbow (better palpated in internal rotation).  Finally, you want to palpate the part of the tendon that is internal, getting frayed, so now extend (backward) the shoulder as much as possible as you palpate the tendon you have found. Your thumb should be as proximal as possible, right up against the acromion.


  1. Infraspinatus/teres minor – external rotation (airplane seat position)
  2. Subscapularis – internal rotation (lifting off from small of back)
  3. Supraspinatus – abduction in pronation from 15-90 degrees (nonspecific)
  4. Long head of the biceps – Arm abduction, forearm supination. The tests would be very nonspecific, but palpation of the tendon can improve specificity.


For quick reference. Note that nerve root mapping has overlap and can have variations.


Movement Muscle Nerve Nerve root Remarks
Shoulder forward flexion Deltoid




C5 Deltoid abduction 15-90.


Shoulder external rotation Infraspinatus Suprascapular C5/6  
Elbow flexion biceps brachii musculocutaneous C5/6  
Elbow extension Triceps radial nerve C6/C7  
Wrist flexion FCR




Wrist extension ECRB/ECRL (C6)

ECU (C7)

Radial C6/C7  
Wrist abduction (radial flexion) FCR Median C7  
Wrist adduction (ulnar flexion) FCU Ulnar C8  
Fingers 2-5 Flexion FDP/FDS Median nerve (ulnar for DIP 4/5) C8  
Fingers 2-5 Extension extensor digitorum Radial (posterior IO branch) C7  
Fingers 2-5 Abduction Dorsal interossei Ulnar nerve T1  
Fingers 2-5 Adduction Palmar interossei Ulnar nerve T1  
Thumb palmar abduction Abd Pollicis Brevis Median T1  
Thumb radial abduction Abd pollicis longus Radial nerve (posterior IO) C7  
Thumb opposition Opponens pollicis Median C8 T1  



Here is what a normal example might look like:


Shoulder FF 5/5

Shoulder ER 5/5

Elbow flexion 5/5

Elbow extension 5/5

Wrist flexion 5/5

Wrist extension 5/5

Finger flexion 5/5

Finger extension 5/5

Finger abduction/adduction 5/5

Thumb radial abduction 5/5

Thumb palmar abduction 5/5



Movement Muscle Nerve Nerve root Sensory role

(of nerve)

Hip flexion iliopsoas Femoral nerve L1/2/3    
Hip extension Gluteus maximus Inferior gluteal nerve L4/L5/S1    
Hip abduction Gluteus medius  and minimum Superior gluteal nerve L4/L5/S1    
Hip adduction Hip adductors (adductor longus) Obturator nerve L2/3/L4 Medial thigh (small area)  
Knee flexion Hamstrings Sciatic nerve L5/S1    
Knee extension Quadriceps femoris Femoral nerve L3/4 Medial thigh and leg Patient may walk backward (with extended knee), but not forward (patellar reflex)
Ankle dorsiflexion, inversion Tibialis anterior Deep peroneal L4/5 1st webspace Slapping gait of foot drop
Ankle plantarflexion Gastrocnemius Tibial nerve S1/S2 Posterolateral leg and foot/heel, plantar foot Can not stand on toes. (Achilles reflex)
Ankle eversion Peroneus longus and brevis Superficial peroneal nerve L5/S1 anterolateral leg, dorsal foot  
Toe extension EHL, EDLs Deep peroneal L5    
Toe flexion FHL, FDLs Tibial nerve S1    


You evaluate a patient with a rash, and as you look, you notice small patches of purple lesions that are circular in distribution.  You recognize what appears to be purpura.  The differential diagnosis is long, and includes hematologic, infectious, and immune mediated conditions.  How can we use physical diagnosis to narrow the differential diagnosis at the bedside?

Blanching: Intravascular vrs extravascular

First, apply pressure to see if it blanches.  Dermatologists use glass and call it diascopy.  In the ED we just press, let go, and we have a quick look to see if it had blanched.  Blanching indicates the color is intravascular, like erythema from a rash.  If it blanches, it is not purpura.  Nonblanching indicates the problem is extravascular.  Your patient’s lesion does not blanch.

Palpable purpura: Inflammation

Next, is it palpable? Nonpalpable purpura is caused by blood leaking out of a normal blood vessel, either because of trauma or a hematologic problem.  The most common benign cause is senile or actinic purpura in the elderly, where a thin dermis renders the capillaries vulnerable to minor trauma.  A normal bruise is not palpable, nor is the purpura from thrombocytopenia and coagulation defects.

In contrast, palpable purpura means there is inflammation around the blood vessels.  Your patient’s lesions are palpable.  You have now narrowed the differential diagnosis to a vasculitis, or an infection causing inflammation around the blood vessels.  The most common cause in children is Henoch-Schonlein purpura.  The most common in adults is leukocytoclastic vasculitis, a small vessel vasculitis with various causes.

Meningococcemia is palpable in later stages of the disease but in the early stages may not be palpable, and in very early stages may actually blanch (Riordan 1996).  Petechial lesions restricted to the area above the clavicles generally signifies a benign cause, generally precipitated by coughing or vomiting (Wells 2001).

Physical diagnosis narrows the differential diagnosis of purpura to a more manageable degree. With the use of pressure to check for blanching, one can confirm whether the purple hue is intravascular or extravascular.  If it is extravascular then this suggests purpura. One can then check for palpable purpura to decide if inflammation is present.  In this manner, one can pursue this diagnosis to the highest degree at the bedside.  Depending on the findings, a phone call to the local dermatologist, rheumatologist, or hematologist and oncologist can expedite this patient’s definitive care.


-Blanching suggests a vascular cause.  Nonblanching supports purpura.

-Palpable purpura supports an inflammatory cause such as vasculitis or a systemic infection


The S3 ventricular gallop is a transient sound, sometimes only heard in a certain position or phase of respiration.  Both experience and knowledge improve detection of the S3, making this truly part of the art of physical diagnosis (Marcus GM Arch Int Med 2006). It is not sensitive for CHF, and most patients are not going to show it.  However, in the elderly population it is specific, so when it is there, we would like to recognize it.  (In the younger population and in athletes there can be a physiologic third heart sound that is normal).


The S3 gallop represents the sound of excess blood flowing into the ventricle during early diastole.  The cadence has been described as “Kentucky” but even better is “SLOSH-ING-in.”  Notice the lack of capitalization of the last bit.  The S3 can be subtle.  Steven McGee in Evidence-Based Physical Diagnosis recommends onomatopoeia for classifying auscultatory findings and describes this as “lub    du bub, lub    du bub.”


The original description is credited to Potain in 1880: “This sound is dull, much more so than the normal sound . It is a shock, a perceptible elevation ; it is hardly a sound… In addition to the two normal sounds, this bruit completes the triple rhythm of the heart. It thus produces a rhythm of three sounds unequally distinct, and occasionally unequally distant, a rhythm which the ear seizes with extreme facility, provided that it had once perceived it distinctly. This is the bruit de galop.”


The best way to recognize the S3 gallop is to listen to examples, which are widely available online.  A recommended resource would be the accompanying sounds to W. Proctor Harvey’s final work, Clinical Heart Disease.


Maneuvers to improve detection of the S3 gallop include quieting the ED (not easy to do), turning the patient to left lateral decubitus (easier) and paying particular attention to expiration.  A left-sided S3 is accentuated during expiration.  W Proctor Harvey points out in Cardiac Pearls that it is sometimes only heard every third or fourth beat. He also points out that if you press too hard with the bell of the diaphragm, it will disappear.  It is also reportedly accentuated with exercise and hand-grip. Press the stethoscope into your ear to prevent air leak (and do the same thing with your headphones when listening to audio examples). If you have trouble with the timing, move the stethoscope to the aortic area and listen for S2, then use that as your anchor for timing as you inch back down to the apex of the heart.


The bottom line is that S3 ventricular gallops can be heard in the ED, and in certain populations they are specific for CHF. Familiarize yourself with the sound through audio recordings. If we know what we are looking for, we are more likely to find it.  The next time an S3 presents itself, you will hear it.


A young patient presents with nausea and spinning vertigo.  There are no focal neurologic deficits to suggest stroke, no stroke risk factors, no neck pain or neck trauma to suggest vertebral dissection.

And yet, the patient has severe gait instability, which can be an indicator of a stroke.  Is this alone a reason to order an MRI?

This is the exact situation where head impulse testing plays a role in the ED. The head impulse test is a test of peripheral labyrinth function.  The labyrinths sense head movement, and send a signal to the eyes to maintain visual gaze despite head movement.

Turn your head side to side while reading this text.  No problem right?  If you had vestibular neuritis you could not do it.  The head impulse test is a way of testing these vestibulo-ocular reflexes.


Face your patient, put your hand on each side of the patient’s head, have them look at your nose, and jerk the head 10 degrees to one side, very abruptly.  The normal person can maintain fixation on your nose.  The vestibular neuritis patient will break gaze, and you will see a catch-up saccade as they look back again at your nose.

An abnormal test is reassuring that this is a peripheral vertigo problem.  It is exactly in the SEVERE cases of vestibular neuritis that you are more likely to see a catch-up saccade.  It is not 100% specific, as rare patients with strokes will also have catch-up saccades.  But this is rare, and in the patient with a low prior probability of stroke, the head impulse test is probably sufficient to effectively rule out stroke.


A patient recently presented with a subcutaneous nodule that appeared to be an abscess.  It was raised, erythematous, tender, indurated, and had a central plug…wait, no, it had a central hole.  And he just got back from Belize.  We put a transparent membrane on it to see if there was a creature in there.  Sure enough, a snout pushed at the membrane, seeking air.  This established the diagnosis – myiasis, secondary to a bot fly bite.

Trying to remove that larvae was an ordeal.  These creatures don’t want to leave their cubby, and trying to pull them out is like trying to give a cat a bath.  We finally decided to leave the membrane in place.  The next morning the larva was dead, and my colleague removed it.

Other skin lesions that can be confused with an abscess include a brown recluse bite.  Reportedly a blue lesion, surrounded by concentric rings of pallor (ischemia) and then erythema (vasodilation) are classic for the brown recluse bite (Rogers 2011).