Shoulder Pain: The Latest in Diagnosis and Care, Part 1

Lindsay E. Brown, MD; Bret S. Stetka, MD; Kevin D. Deane, MD, PhD; Mary K. Jesse, MD; Jason R. Kolfenbach, MD

February 24, 2015


Shoulder Pain: Introduction
Shoulder pain is a common musculoskeletal complaint that can result from trauma, referred pain, periarticular tissues, or, less commonly, a systemic inflammatory condition. Over 90% of shoulder pain stems from periarticular structures such as the subacromial/subdeltoid (SASD) bursa or rotator cuff tendons; however, recognition of an underlying systemic process like rheumatoid arthritis (RA), septic arthritis, or crystal arthropathy is paramount to avoid joint damage and delays in therapy. Mainstay therapies include NSAIDs, rest and ice, and physical therapy but certain diagnoses require more specific therapies (eg, steroids, DMARDs, surgery). This two-part slideshow provides clinical vignettes of a variety of disorders that can affect the shoulder, with a goal of providing clinicians with tips on evaluation and management of common types of shoulder disease, as well as to present more unusual cases. Part 1 starts with the basics of approaching shoulder pain and moves on to more complex conditions that can affect the shoulder; part 2 explores additional disorders of the shoulder along with the latest news in evaluating and managing shoulder pain and disease.

Image from Thinkstock

Slide 1.

Evaluating Shoulder Pain
When approaching the patient with shoulder pain, the clinician should inquire about trauma or repetitive activity, location and duration of pain, and other associated symptoms (eg, weakness, radiculopathy). In addition, symptoms from other sites that could influence the shoulder (eg, neck, abdomen, and chest pain) should be discussed with the patient. Next, an organized exam including the six elements shown above should be performed to elicit the suspected diagnosis.

Image from Thinkstock

Slide 2.

Case 1: Rotator Cuff Disease
A 45-year-old man presented with approximately 3 weeks of right shoulder pain. It started after painting several rooms at his house, with much of the painting being done over his head. The pain was located at the lateral part of his shoulder and radiates down to the middle of his upper arm. The pain was worst when doing activities that require arm movement above his head. He denied any numbness or weakness in his arm, neck pain, or abdominal pain, and he had had no fevers.

Image courtesy of Jason R. Kolfenbach, MD, and Kevin D. Deane, MD, PhD

Slide 3.

Case 1: Rotator Cuff Disease (cont.)
On examination, the patient's musculature of the right shoulder looks normal, with no atrophy. There is tenderness with palpation under the acromion as well as at the superior lateral aspect of the shoulder with the Hawkins-Kennedy test (forced internal rotation of the shoulder from the starting position of 90º forward flexion of the shoulder, with the elbow flexed at 90º; left image). The patient is able to hold his arm up against downward resistance (Jobe's test; right image). Speed's and Yergason's tests for biceps tendon disease were negative. X-rays of the right shoulder were normal while MRI demonstrated an intact rotator cuff with edema, suggestive of supraspinatus tendinitis. The patient improved with NSAIDs and a course of physical therapy.

Image courtesy of Jason R. Kolfenbach, MD, and Kevin D. Deane, MD, PhD

Slide 4.

Case 1: Discussion
Shoulder pain is one of the most common musculoskeletal complaints, and rotator cuff disease is one of the most common causes of shoulder pain.[1] There are multiple examination techniques and provocative tests to evaluate the shoulder, including those previously mentioned. In this case, the history and examination findings, as well as the imaging studies, were all consistent with supraspinatus inflammation probably caused by repetitive use. In addition, the rotator cuff seemed intact because the patient was able to hold up his arm against resistance. In some cases severe pain makes it difficult to assess whether the rotator cuff may be completely torn. In that setting, injection of an anesthetic agent like lidocaine into the subacromial space can decrease pain and allow for testing of strength. For most patients, if the history and physical examination suggest rotator cuff pathology, radiography and MRI are not required. In the following cases, however, imaging was necessary to define the cause of shoulder pain.[1,2]

Image courtesy of Jason R. Kolfenbach, MD, and Kevin D. Deane, MD, PhD

Slide 5.

Case 2: A Bone Tumor
A 66-year-old man with no prior shoulder disease presented with 6 months of left shoulder pain. He described the pain as a deep ache, dull and worse at night. He thinks it may be worst laterally but does not report worsening of the pain when he does activities with that arm above his head. He denies recent repetitive use. His other joints feel normal, and his age-appropriate cancer screening is up-to-date. Examination showed tenderness that he described as being deep in his shoulder with any movement, and he had tenderness with palpation of the proximal humerus. Specific tests such as Hawkins-Kennedy test for rotator cuff disease and the Speed's and Yergason's tests for biceps tendon disease were normal. His neck, chest, and abdominal examinations were normal. A radiograph of his left shoulder showed an aggressive lytic lesion in the proximal humerus. The lesion was believed to be most consistent with a conventional chondrosarcoma. (Yellow arrow: zone of transition between tumor and normal bone; white arrow: suspected cortical break; red arrow: endosteal scalloping related to intramedullary tumor growth; bracket: extension of the lesion from the metadiaphysis to the physeal line)

Image courtesy of Sterling West, MD

Slide 6.

Case 2: Discussion
A variety of bone tumors may present with focal pain. Often, imaging is not required for a diagnosis in routine shoulder pathology. However, what prompted radiographs in this patient were diffuse symptoms and absence of clear focal pathology with provocative maneuvers (with the exception of focal tenderness at the proximal humerus that probably corresponded to a cortical break). Several radiographic features of bone lesions can be helpful in determining whether additional evaluation is necessary: location, pattern of bone destruction, zone of transition, presence of matrix, periosteal reaction, and presence of cortical breakthrough. In general, bone lesions that are not confidently classified as benign by radiography require additional evaluation. In this case, an MRI should be obtained to accurately determine tumor size and extent of spread within the bone and adjacent soft tissues. A bone biopsy may also be obtained to help clarify the diagnosis. Finally, a PET, CT, or bone scan should be performed to determine extent of bony involvement (staging).[2,3]

Image courtesy of Sterling West, MD

Slide 7.

Case 3: Pseudogout
A 70-year-old woman with a known history of hip and knee osteoarthritis (OA) presented with right shoulder pain and swelling over 3 days. The pain started as a "twinge" and progressed to more severe, persistent pain over several hours. She denied a history of trauma or repetitive use. On examination, the patient appeared uncomfortable and was not using her right arm. She had a temperature of 100.8º F. Shoulder exam revealed diffuse tenderness with even minimal movement of the shoulder, anterior joint swelling and warmth, and limited passive and active joint motion. Plain radiographs of the shoulder demonstrated chondrocalcinosis, but no erosions, and the bone density appeared normal.

Images courtesy of Jason R. Kolfenbach, MD, and Kevin D. Deane, MD, PhD

Slide 8.

Case 3: Pseudogout (cont.)
Arthrocentesis was performed and synovial fluid obtained was cloudy yellow, with 65,000 white blood cells that were 85% neutrophils. Gram stain and culture were negative. Polarized microscopy revealed rhomboid, intracellular crystals that were weakly positively birefringent, confirming a diagnosis of pseudogout. The patient improved with a tapering course of oral corticosteroids. (White arrow: rhomboid-shaped crystal that appears yellow when perpendicular to the long axis of the red filter; yellow arrow: an intracellular CPP crystal that is blue when aligned with the long axis of the red filter)

Image courtesy of Jason R. Kolfenbach, MD, and Kevin D. Deane, MD, PhD

Slide 9.

Case 3: Discussion
Calcium pyrophosphate dihydrate deposition (CPDD) diseases encompass chondrocalcinosis, acute CPD crystal arthritis ("pseudogout"), and chronic CPD crystal arthritis. Pseudogout occurs when CPD crystals are shed from cartilage or synovium into the joint space. Chondrocalcinosis may be seen on radiographs and is best visualized in the triangular fibrocartilage complex of the wrist, the symphysis pubis, and the knee (in this case, CPDD can be seen along the contour of the humeral head). Age is the greatest risk factor for idiopathic (sporadic) CPDD. However, in patients under 55 years of age, hereditary forms, metabolic causes (including hemachromatosis), or mechanical trauma should be considered. In monoarticular arthritis, infection should be a leading consideration. Crystalline arthropathy can be associated with fever. In addition, crystals and infection can be present in the same joint, so it is imperative to evaluate for infection with Gram stain and culture of the synovial fluid. The mainstay of diagnosis of crystalline arthropathy is arthrocentesis and crystal evaluation. However, imaging modalities such as MRI and CT can also be useful in identifying crystalline disease.[4-6]

Image courtesy of Jason R. Kolfenbach, MD, and Kevin D. Deane, MD, PhD

Slide 10.

Case 4: Calcific Tendonitis
A 75-year-old woman rapidly developed stiffness, pain, and swelling of her right shoulder without any antecedent trauma. In the past she has had multiple episodes of recurrent right shoulder pain that have responded to physical therapy and NSAIDs. An exam demonstrated a large right shoulder effusion and reduced active and passive ranges of motion with associated pain.

Arthrocentesis yielded 100 cc of hemorrhagic fluid, 750/mm3 leukocytes, negative culture, and no CPD or gout crystals under plain or polarized microscopy. Radiographs of her right shoulder from 3 years prior demonstrated calcific tendinitis within the supraspinatus tendon.

Image courtesy of Sterling West, MD

Slide 11.

Case 4: Discussion
Calcific tendinitis may result from degenerative changes with aging as well as repetitive trauma to the poorly vascularized supraspinatus tendon from chronic impingement, leading to basic calcium phosphate (BCP; also known as hydroxyapatite) crystal accumulation. While symptoms of calcific tendinitis are often self-limited and the disease is not destructive, there is a syndrome of recurrent inflammation due to shedding of BCP crystals from the tendon to the synovial space. This elicits a severe inflammatory reaction that leads to joint destruction, termed Milwaukee shoulder syndrome.[7] BCP crystals are not identified on polarized microscopy as gout and CPD crystals are; they can only be identified by using alizarin red S stain (see image). The appearance of the material in this slide is typical for BCP crystals, with amorphous-appearing clumps, some forming a characteristic stack of "shiny coins." CPD crystals would be expected to take up this stain as well, but the lack of birefringence and absence of characteristic rhomboid crystal shapes rules out that diagnosis.

Image courtesy of Jason R. Kolfenbach, MD, and Kevin D. Deane, MD, PhD

Slide 12.

More on Milwaukee Shoulder Syndrome
Milwaukee shoulder syndrome is a rare, rapidly destructive arthritis of the shoulder, first described in 1981 in four elderly women in Milwaukee. It typically presents in women (gender distribution 4:1) age 60-90 years who have a history of shoulder impingement. Imaging can demonstrate significant joint destruction. The joint effusion is often bloody and noninflammatory (usually leukocytes < 800/mm3). The plain radiograph on the left shows superior migration of the humeral head, degernation of the glenohumeral joint, and periarticular calcification. The fat-saturated T2-weighted MRI on the right shows a massive rotator cuff tear (red arrow) with a large effusion freely communicating with the SASD bursa (yellow arrow), narrowing of the glenohumeral joint space (white arrow), and reactive edema in the subchondral bone (grey arrow).

Images courtesy of Jason R. Kolfenbach, MD, and Kevin D. Deane, MD, PhD

Slide 13.

Case 5: Septic Arthritis
A 65-year-old man underwent surgery to repair a torn rotator cuff. He continued to have pain in the postoperative period that worsened dramatically over 1-2 weeks and was associated with low-grade fevers. He denied any recent sexual contacts, dental procedures, or intravenous drug use. Physical examination demonstrated a temperature of 101.1º F. He had anterior swelling of his left shoulder joint and significant tenderness with even mild movement. Other joints were normal. Plain films demonstrated osseous lytic lesions (yellow arrows). MRI demonstrated diffuse synovitis and connection of the joint space, with the subacromial space representing rotator cuff disruption. Aspiration of the joint yielded cloudy yellow synovial fluid with heavy debris and "rice bodies," with a white blood cell count of 45,000 that was 90% neutrophils. Gram stain demonstrated gram-positive rods, and culture grew Propionibacterium acnes after about 15 days.

Image courtesy of Jason R. Kolfenbach, MD, and Kevin D. Deane, MD, PhD

Slide 14.

Case 5: Discussion
This patient had septic arthritis of the shoulder caused by Propionibacterium acnes. While often thought to be a contaminant in culture, P acnes is an increasingly recognized cause of septic arthritis, typically leading to infections in joints that have undergone surgical intervention. Infections in native joints are also known to occur, especially in the setting of acne with pustulosis. The organism is anaerobic and can require prolonged culture to be identified; as such, cultures should be held for up to 3 weeks. The key clinical findings in this case were persistent pain in his postoperative shoulder in the setting of fever, osseous lytic lesions on plain film, and diffuse synovitis and joint fluid on MRI. The most important test was aspiration of the joint which demonstrated inflammatory joint fluid and the causative organism. Rice bodies (see image) probably represent portions of inflamed synovium and can be seen in several conditions, including RA, as well as indolent infections such as tuberculosis.[8-12]

Image courtesy of Jason R. Kolfenbach, MD, and Kevin D. Deane, MD, PhD

Slide 15.

More on Septic Arthritis
In a sexually active person under the age of 50, the most common bacterial cause of a nontraumatic septic joint is gonorrhea. In older adults and patients who have undergone procedures, Staphylococcus and Streptococcus species are very common.[8-12]

Image courtesy of Jason R. Kolfenbach, MD, and Kevin D. Deane, MD, PhD

Slide 16.

Case 6: Avascular Necrosis
A 32-year-old woman with longstanding lupus requiring intermittent high doses of steroids reported increasing pain in both shoulders over the past several months. The pain was worse with movement. There was no history of trauma or repetitive use. She also reported pain in her hips and knees, especially with activity. Her lupus was currently very well controlled on mycophenolate mofetil and hydroxychloroquine. On examination, she had tenderness with internal and external rotation of the shoulder, but did not have signs localizing to the rotator cuff or biceps tendon. There was no warmth or clear effusions of her shoulders. Her hips were tender with internal and external rotation, and her knees were tender with palpation of the bony prominences. Plain radiographs of both shoulders demonstrated collapse of the humeral head. A diagnosis of avascular necrosis (AVN) with collapse was made, and the patient underwent surgical replacement of both shoulder joints (see next slide).[13-16] (White arrow: extensive subcortical serpentine bony sclerosis and lucency compatible with AVN; yellow arrow: AVN in this case is more advanced with areas of subchondral collapse)

Image courtesy of Jason R. Kolfenbach, MD, and Kevin D. Deane, MD, PhD

Slide 17.

Case 6: Discussion
This is a case of AVN that is probably related to use of steroids in a patient with lupus. Antiphosphoplipid antibodies have been associated with increased risk for AVN, although in this case these autoantibodies were not present. Other risk factors for AVN include trauma, decompression during underwater diving, and alcohol abuse. The most common joints involved in AVN are the hips and knees. The key diagnostic features of this case were diffuse pain in both shoulders, history of steroid use, and radiographic findings of humeral head collapse. However, plain x-rays are relatively insensitive for early AVN; as such, noncontrast MRI is the preferred modality for early diagnosis.

Image courtesy of Jason R. Kolfenbach, MD, and Kevin D. Deane, MD, PhD

Slide 18.

More on AVN
Once collapse has occurred, the treatment for AVN is typically surgical replacement. Prior to collapse, however, there are several options, such as core decompression, bone grafting, or anticoagulation. These may help preserve the joint, although data regarding the effectiveness of these approaches in the shoulders is limited. Of note, if AVN is present in one joint, it may be present in another. In this case the patient had multiple joints with AVN, including both shoulders, knees, and hips.[13-16]

Image courtesy of Jason R. Kolfenbach, MD, and Kevin D. Deane, MD, PhD

Slide 19.

Case 7: Neuroarthropathy (Charcot Joint)
A 55-year-old patient presented with increasing shoulder pain and loss of range of motion in the setting of gait instability and sensory changes in all four extremities. Initial radiographs demonstrated a high-riding humeral head, degenerative changes, and some bony fragments (left image). Radiographs taken approximately 6 weeks later showed complete destruction of the humeral head (right image). The patient was diagnosed with Charcot neuroarthropathy of the shoulder, related to cervical spine syringomyelia.

Images courtesy of Sterling West, MD

Slide 20.

Case 7: Discussion
Charcot joint is caused by neurologic injury, leading to decreased proprioception and sensation in a joint and resulting in destruction. It is most commonly seen in the foot and ankle and is commonly related to diabetic neurologic changes, although it can be seen in other conditions such as syphilis and (as in this case) spinal cord injury due to syringomyelia. Destruction can be very rapid. If a Charcot joint is suspected, the joint should be immobilized and non-weight-bearing to reduce the chance for progression of destruction. Sepsis and osteomyelitis can lead to rapid destruction of a joint as well. Charcot joint and infection may be differentiated on plain films; Charcot joint should have normal or increased bone density whereas an infected joint should have decreased bone density. Often, however, more advanced imaging such as MRI, CT, or nucleotide imaging is required to distinguish a Charcot joint from infection.[17-19]

Images courtesy of Sterling West, MD

Slide 21.

Stay Tuned for Part 2
Part 1 of this slideshow has dealt with numerous shoulder pathologies, including rotator cuff disease, bone malignancies, and septic arthritides. Part 2 will look at additional conditions that can affect the shoulder, including RA and hyperparathyroidism, as well as the latest news about managing shoulder pathology. Stay tuned.

Image from Thinkstock

Slide 22.

Contributor Information

Lindsay E. Brown, MD
Rheumatology Fellow
Division of Rheumatology
University of Colorado School of Medicine
Denver, Colorado

Disclosure: Lindsay E. Brown, MD, has disclosed no relevant financial relationships.

Bret S. Stetka, MD
Editorial Director
Medscape Rheumatology

Kevin D. Deane, MD, PhD
Associate Professor of Medicine
Division of Rheumatology
University of Colorado School of Medicine
Denver, Colorado

Disclosure: Kevin D. Deane, MD, PhD, has disclosed the following relevant financial relationships: Receiving grant funding from: National Institutes of Health for the study of genetic and environmental factors that may influence the future development of rheumatoid arthritis therapies

Mary K. Jesse, MD
Assistant Professor of Radiology and Orthopedics
Department of Radiology
University of Colorado School of Medicine

Disclosure: Mary K. Jesse, MD, has disclosed no relevant financial relationships.

Jason R. Kolfenbach, MD
Assistant Professor of Medicine
Division of Rheumatology
University of Colorado School of Medicine
Denver, Colorado

Disclosure: Jason R. Kolfenbach, MD, has disclosed no relevant financial relationships.


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