Presentation and diagnosis of prosthetic valve endocarditis

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Presentation and diagnosis of prosthetic valve endocarditis

Author
Adolf W Karchmer, MD
Section Editor
Stephen B Calderwood, MD
Deputy Editor
Elinor L Baron, MD, DTMH


Last literature review version 16.2: May 2008 | This topic last updated: May 16, 2007 (More)


INTRODUCTION — Prosthetic valve endocarditis is a serious problem with potentially fatal consequences [1] . (See "Complications and outcome of infective endocarditis", section on Mortality).

The pathogenesis, microbiology, pathology, clinical features and diagnosis of prosthetic valve endocarditis (PVE) will be reviewed here. The antimicrobial and possible surgical treatment and prevention of PVE are discussed separately. (See "Antimicrobial therapy of prosthetic valve endocarditis" and see "Surgery for prosthetic valve endocarditis").

PATHOGENESIS — PVE can arise early or late after surgery. The timing of the infection reflects different pathogenic mechanisms that, in turn, influence the epidemiology, microbiology, pathology and clinical manifestations of the infection.

Early infection — Microorganisms can reach the valve prosthesis by direct contamination intraoperatively or via hematogenous spread during the initial days and weeks after surgery. These pathogens have direct access to the prosthesis-annulus interface and to perivalvular tissue along suture pathways because the valve sewing ring, cardiac annulus, and anchoring sutures are not endothelialized early after valve implantation. These structures are coated with host proteins, such as fibronectin and fibrinogen, to which some organisms can adhere and initiate infection.

Late infection — As the sewing ring, sutures, and adjacent tissues become endothelialized over the months after valve replacement, sites for adherence of microorganisms and access to host tissues adjacent to the prosthesis are altered. The pathogenesis of late PVE has been postulated to resemble native valve endocarditis (NVE). (See "Pathogenesis of vegetation formation in infective endocarditis").

Platelet-fibrin thrombi probably form on the prosthesis and serve as sites for the organisms to adhere and cause infection. Thus, the pathogens producing PVE tend to be bacteremic isolates with the ability to adhere to these thrombi and are similar to organisms inducing NVE. Unless the infecting organism is Staphylococcus aureus or another highly virulent or invasive pathogen, the perivalvular tissues are less likely to be affected in late PVE since endothelialization limits access to these tissues. Later onset infections tend to be less invasive, are less often complicated by perivalvular abscess formation and valve dehiscence, and are more commonly restricted to the sewing ring or the bioprosthetic leaflet.

However, the leaflets of porcine bioprosthetic valves experience age-related alterations in their surface characteristics. These aging leaflets become sites for platelet-fibrin thrombus deposition and subsequent infection. As a result, the infection rates on bioprostheses increase during this later period when compared to mechanical valves [2-4] .

EPIDEMIOLOGY — The risk of developing PVE, typically expressed as a hazard function or the likelihood of infection at a given point in time, is not uniform after valve replacement. The risk is greatest during the initial three months after surgery, remains high through the sixth month, and then falls gradually with an annual rate of approximately 0.4 percent from 12 months postoperatively onward for the life of the valve recipient [3,5-8] . The percentage of patients developing PVE during the initial year after valve replacement ranges from one to three percent in studies with active follow-up; by five years, the cumulative percentage ranges from three to six percent (show table 1).

Although conclusions vary among studies, infection generally occurs with equal frequency at aortic and mitral sites and on mechanical and bioprosthetic devices during the first postoperative year [3-6,9,10] . As noted above, bioprosthetic valves carry a greater risk for infection than mechanical after the first 18 months [2-4] . When a valve is replaced in a patient with endocarditis, whether the infection was active or healed at the time of surgery, there is an increased risk for both early (some of which is recrudescence of active endocarditis) and late PVE [2,4,6,8] .

Healthcare associated infection — Some cases of prosthetic valve endocarditis result from infection acquired in healthcare settings, both inpatient (nosocomial) and outpatient (non-nosocomial). The relative frequency of health care-associated PVE was evaluated in a prospective, observational cohort multinational study of 556 patients with PVE [1] . Non-nosocomial health care-associated infection was defined as PVE diagnosed within 48 hours of admission in an outpatient with extensive healthcare contact, as defined by:

• Intravenous therapy, wound care, or specialized nursing care at home, or intravenous chemotherapy within the prior 30 days
• Residence in a nursing home or other long-term care facility
• Hospitalization in an acute care hospital for two or more days within the prior 90 days
• Attendance at a hospital or hemodialysis clinic within the prior 30 days


Healthcare-associated infection was present in 37 percent of cases: 70 percent were labeled as nosocomial and 30 percent as outpatient acquired. Approximately 70 percent of the health care-associated infections were diagnosed within the first year after valve implantation, with the majority occurring within the first sixty days. S. aureus was the most common organism, being identified as the pathogen in 34 percent of cases.

Nosocomial bacteremia occurring in patients with prosthetic valves carries a significant risk for seeding the prosthesis. Among 115 prosthetic valve recipients experiencing nosocomial bacteremia that was judged not to be the sentinel event of endocarditis, 18 (16 percent) developed PVE with the bacteremic organism between seven and 170 days thereafter (median interval 28 days) [11] . Similarly, among 37 prosthetic valve patients with postoperative candidemia without evidence of endocarditis, fungal endocarditis developed in four (11 percent) between 26 and 690 days later [12] . The patients who developed candida PVE had persistent fungemia (8.1 mean days fungemia) without evidence of endocarditis during the month after cardiac surgery. (See "Candida endocarditis").

MICROBIOLOGY — While many different organisms have caused sporadic cases of PVE, the microbiology is relatively predictable when PVE is categorized by time after implantation. The largest reported contemporary experience comes from the multinational study of 556 patients cited above [1] :

• The most frequently encountered pathogens in early PVE (within two months of implantation) were S. aureus (36 percent) and coagulase-negative staphylococci (17 percent); next in frequency were culture-negative (17 percent) and fungal infection (9 percent) (show table 2).

• When PVE presented after two months, the culture results in decreasing order of frequency were coagulase-negative staphylococci and S. aureus (18 to 20 percent each); next in frequency were no organism identified, enterococci, and viridans streptococci (10 to 13 percent each) (show table 2).


Cases occurring more than 12 months after valve surgery are usually caused by the same pathogens that produce NVE in patients who are not injection drug users, since late PVE, like NVE, usually results from transient bacteremia occurring among ambulatory patients. (See "Infective endocarditis: Epidemiology and risk factors", section on Microbiology).

The coagulase-negative staphylococci causing PVE during the initial year after surgery are almost exclusively S. epidermidis. Between 84 and 87 percent of these organisms are methicillin-resistant and thus resistant to all of the beta-lactam antibiotics [3,13] . By contrast, almost half of the coagulase-negative staphylococci causing PVE one year or more after surgery are non-epidermidis species, and only 22 to 30 percent are methicillin-resistant. (See "Microbiology, pathogenesis, and epidemiology of coagulase-negative staphylococci").

The mechanisms leading to methicillin-resistance are the same among coagulase-negative staphylococci as for methicillin-resistant S. aureus (MRSA). (See "Coagulase-negative staphylococci: antimicrobial therapy and resistance" and see "Microbiology of methicillin-resistant Staphylococcus aureus").

However, methicillin-resistant coagulase-negative staphylococci, while uniformly possessing the resistant genotype, do not always express the phenotype, a phenomenon called heteroresistance. This makes detection of methicillin-resistance among coagulase-negative staphylococci more difficult. As a result, before embarking upon therapy with a beta-lactam antibiotic, the microbiology laboratory must be asked to thoroughly exclude possible methicillin-resistance. If this cannot be done, methicillin-resistance should be assumed. (See "Overview of antibacterial susceptibility testing", section on Heteroresistance).

PATHOLOGY — The intracardiac pathology of infection involving mechanical valves, particularly when PVE presents during the early months after surgery or when it is caused by invasive organisms, shapes the requirement for therapy. Perivalvular invasion, commonly with associated dehiscence of the prosthesis and paravalvular regurgitant flow, occurs in approximately 40 percent of patients and frank extension into tissue causing myocardial abscess is seen in 15 percent [14,15] . In one series, invasion of perivalvular tissue was noted in more than 80 percent of cases [16] .

In some patients, infection of an aortic valve prosthesis extends through the annulus to cause pericarditis or, more commonly, into the membranous portion of the interventricular septum where it disrupts the conduction system, resulting in various degrees of heart block [17-19] . Large vegetations may prevent closure of the prosthesis producing incompetence or encroach upon the valve orifice causing functional stenosis.

Bioprosthetic valve endocarditis also causes invasive infection. As an example, annular and myocardial invasion was noted in 38 of 85 patients (45 percent) in one study and was more frequent among bioprosthetic PVE occurring in the first year after valve replacement than cases presenting later (59 versus 25 percent) [20] . In another series, invasive disease was more common in patients with early compared with later bioprosthetic PVE (79 versus 31 percent) [21] .

The histologic features that characterize PVE in bioprosthetic valves are not well defined. As bioprosthetic valves degenerate, they may form noninfective, calcific, vegetative-like lesions and inflammatory infiltrates thus potentially causing a noninfectious process to be misdiagnosed as PVE. A retrospective pathologic analysis of inflamed bioprosthetic valve tissue from 88 patients who underwent surgical removal of a bioprosthetic valve (21 for suspected endocarditis and 67 for noninfective dysfunction) was conducted to better define the histologic criteria for PVE [22] . Histologically, PVE was characterized by microorganisms, vegetations, and neutrophil-rich, inflammatory infiltrates. In contrast, inflammatory infiltrates in valve tissue samples from the noninfective control group consisted mainly of macrophages and lymphocytes. A neutrophil surface area with a cutoff value of >1.5 percent of total valve tissue surface was highly specific for PVE (94 percent).

CLINICAL MANIFESTATIONS — Patients with PVE present with symptoms and signs similar to those encountered in NVE. (See "Infective endocarditis: Historical and Duke criteria").

However, when PVE develops prior to discharge from the hospital, findings related to surgery or to perioperative complications may predominate over the subtle features of endocarditis.

Signs and symptoms of invasive infection — The high frequency of invasive infection results in higher rates of new or changing murmurs, heart failure, and new electrocardiographic conduction disturbances in patients with PVE than in those with NVE. The incidence of clinically overt arterial emboli is 40 percent; central nervous system complications, primarily embolic infarcts or hemorrhages, occur in 20 to 40 percent of cases [16,23-25] . (See "Complications and outcome of infective endocarditis").

Valvular dysfunction, fever which persists for nine days or more despite appropriate antibiotic therapy, new electrocardiographic conduction disturbances, and echocardiographic evidence of abscess formation are clinical manifestations of invasive infection [26,27] . These findings were noted in 64 percent of 116 patients with PVE in one study and occurred significantly more frequently when infection involved an aortic valve prosthesis and when it arose within the first year after valve replacement [27] .

DIAGNOSIS — Laboratory findings in patients with PVE are similar to those noted in patients with NVE of comparable duration. (See "Diagnostic approach to infective endocarditis").

Blood cultures — In the absence of prior antibiotic therapy, blood cultures will be positive in 90 percent or more of patients with PVE. Because bacteremia is continuous, cultures will be positive regardless of whether or not blood cultures are obtained in proximity to the fever. When blood cultures are drawn over a period of hours to days in a patient with a prosthetic valve and all or most are positive, PVE is highly probable. The duration of documented bacteremia is particularly important when the isolate is a common contaminant, such as coagulase-negative staphylococci or diphtheroids. A high rate of blood culture positivity, or molecular evidence that a sporadically isolated organism represents a single clone, helps to distinguish infecting pathogens from contaminants [28] .

If antibiotics have not been administered prior to obtaining blood cultures, it is unusual to have persistently negative blood cultures in patients with clinically overt PVE. Nevertheless, culture-negative cases can occur when infection is caused by fastidious organisms such as Legionella species, Bartonella species, Coxiella burnetii, Mycoplasma hominis, fungi other than Candida species, and the HACEK organisms. (See "Endocarditis caused by Bartonella" and see "Q fever endocarditis").

Detection of these and other unusual fastidious pathogens causing PVE relies upon the same evaluation used to assess culture-negative NVE [29] . (See "Diagnostic approach to infective endocarditis").

Echocardiography — The availability of transesophageal echocardiography (TEE) has greatly improved the diagnosis and management of PVE and is considered the procedure of choice if only one type of echocardiogram is to be obtained. Although transthoracic (TTE) and transesophageal echocardiograms are complementary in the diagnosis of PVE, TEE has a sensitivity of 82 to 96 percent compared with 17 to 36 percent for TTE [30-32] . This increased sensitivity is achieved without regard to valve position and without loss of specificity [30-34] (show table 3). (See "Diagnostic approach to infective endocarditis").

One prospective study compared TTE and TEE in 114 episodes of infective endocarditis suspected on clinical grounds (34 PVE, 80 NVE) [35] . The results of the two tests were concordant in 55 percent of cases, but TEE led to a reclassification of the case in 34 percent of patients with prosthetic valves compared to 11 percent of patients with native valves. Twenty-two patients were reclassified as definite infective endocarditis based upon the TEE results; 10 of these patients had prosthetic valves. In two patients with PVE the diagnosis would have been rejected if the evaluation had been limited to TTE data.

Echocardiography, including both TTE and TEE, is essential for both the diagnosis and management of PVE [36] . A high resolution biplane or multiplane transducer that allows continuous-wave and pulse-wave Doppler and color-flow imaging should be employed. TTE provides superior images of the ventricular surfaces of prostheses in the mitral, tricuspid, and aortic positions, whereas the atrial surfaces of the mitral and tricuspid valves and the aortic surface and outflow track of prostheses in the aortic position are better viewed by TEE. TEE is unquestionably superior to TTE for visualizing a mitral valve prosthesis.

TEE is also superior to TTE in the detection of abscesses, fistulae, and paraprosthetic leaks [37] . In one study that correlated the results of both types of echocardiography with anatomic findings at surgery in 88 valves from patients with endocarditis, the sensitivity of TEE for the detection of valve perforation was significantly higher than that of TTE [38] . TEE detected perforation in 21 of 22 cases compared to only 10 of 22 by TTE.

In patients with failing prosthetic valves, echocardiography may define the intracardiac pathology, which can provide evidence of a need for surgical therapy. However, TEE may miss some cases of prosthetic valve dehiscence. In a study that included 26 patients with prosthetic valve endocarditis, 14 (54 percent) had surgically identified valve dehiscence [43] . Dehiscence was missed on TEE in 4 cases which all involved an aortic prosthetic valve.

The negative predictive value of a full echocardiographic evaluation of a patient with suspected PVE is 86 to 94 percent. Nevertheless, if PVE is strongly suspected in the face of a negative evaluation, repeat echocardiography one week later can provide evidence of PVE in some cases [32,39] . Echocardiography has replaced other modalities of cardiac imaging in the diagnosis of PVE, including cardiac catheterization (which is now reserved for defining coronary artery anatomy).

Summary — Identifying patients with PVE requires a high index of suspicion and an appreciation of the subtle symptoms and signs of endocarditis. Obtaining three or four blood cultures over time, without confounding their utility by antibiotic administration, and an echocardiogram are paramount in the evaluation.

When sporadic blood cultures yield coagulase-negative staphylococci or when only several cultures have been obtained and are positive for these organisms, molecular techniques, such as DNA examination by pulsed-field gel electrophoresis, should be used to compare the isolates. Establishing clonality of isolates from separate cultures argues against contamination and favors that the isolates are true pathogens [28] . However, there is a potential for polyclonal infections to arise, especially from direct contamination in the operating room.

The Duke criteria for the diagnosis of endocarditis provide a systematic approach for diagnosing both NVE and PVE [40] . Among pathologically confirmed cases of PVE, 76 percent have been categorized as definite PVE and 24 percent as possible PVE when judged by the Duke criteria [41,42] . The expanded use of TEE in the assessment of patients with possible PVE has enhanced the sensitivity of these criteria for the diagnosis of PVE [35] . The standard for assessing possible PVE should include appropriately obtained blood cultures and echocardiographic imaging, with the results interpreted according to the Duke criteria. Using this approach, few cases of PVE should be missed. (See "Infective endocarditis: Historical and Duke criteria" and see "Diagnostic approach to infective endocarditis").

Approach to the patient with a suspected spider bite: An overview

Approach to the patient with a suspected spider bite: An overview

Author
Richard S Vetter, MS
David L Swanson, MD
Section Editor
Daniel F Danzl, MD
Stephen J Traub, MD
Deputy Editor
Anna M Feldweg, MD



Last literature review version 16.2: May 2008 | This topic last updated: June 12, 2008 (More)


INTRODUCTION — Spider bites are rare medical events. Of the thousands of spider species that exist around the world, only a handful cause problems in humans [1] . There are a variety of more common disorders that can mimic a spider bite, some of which represent a far greater threat to the patient if not recognized and treated appropriately.

Thus, accurate diagnosis is the initial goal of the clinician evaluating a patient with a lesion that might represent a spider bite. Discerning among the various conditions in the differential diagnosis of a spider bite requires familiarity with these disorders, as well as a rudimentary understanding of the distribution and behavior of medically important spiders.

This topic will discuss the spiders of medical importance and the clinical manifestations and diagnosis of spider bites. The differential diagnosis of bite-like lesions will be reviewed here, although disorders that mimic systemic reactions to bites of specific spiders are discussed in detail separately. Treatment of spider bites is discussed in the topics on bites of specific spiders. (See "Bites of recluse spiders").

MEDICALLY IMPORTANT SPIDERS — Spiders are arachnids (a group of arthropods), which have four pairs of legs, similar to scorpions, mites, and ticks (show figure 1). They use sharp fangs at the end of their chelicerae to bite prey (typically insects, other arthropods, or small vertebrates) and inject paralyzing venom.

Most spiders pose no threat to humans. The venom of most spiders has little or no effect on mammalian tissues [2] . In addition, only a few species have cheliceral muscles powerful enough to penetrate human skin, and most of these spiders bite humans only in rare and extreme circumstances (eg, as they are being fatally crushed between skin and some object).

The spiders most likely to inflict medically significant bites in humans include widow and false black widow spiders, recluse spiders, Australian funnel web spiders, and Phoneutria spiders. Each of these spiders are described briefly below, and their appearance and geographical distribution are summarized in the table (show table 1).

Widow spiders — Latrodectus, or widow spiders (found worldwide), include the Eastern black widow (show picture 1) and Western black widow in the United States, and the Australian redback spider. Widow bites cause unremarkable local lesions that are sometimes accompanied by a characteristic systemic reaction with prominent, proximally-spreading pain and localized diaphoresis surrounding the site of the bite. Antivenoms are available for several species.

False black widow spiders — Steatoda, or false black widow spiders (found worldwide) are less often implicated in human bites, and cause less severe symptoms that those of widows (show picture 2).

Recluse spiders — Loxosceles, or recluse spiders are found in predominantly in North and South America (show picture 3). Their bites are notorious for becoming necrotic, although this happens in a minority of cases. Systemic reactions to bites are usually mild, and consist of non-specific systemic signs and symptoms. (See "Bites of recluse spiders").

Australian funnel web spiders — Australian funnel web spiders are found in limited areas of eastern coastal Australia. Their bites can cause dramatic systemic reactions that mimic organophosphate poisoning and include salivation, diaphoresis, muscle spasms, tachycardia, hypertension, and pulmonary edema. An antivenom is available.

South American Phoneutria — Phoneutria or armed spiders are large spiders found in South America, especially urban areas of Brazil. The bites of these spiders can lead to severe systemic reactions, with occasional fatalities in children. An antivenom is available.

TYPES OF REACTIONS — A spider bite usually presents acutely as a solitary papule, pustule, or wheal. Systemic symptoms can accompany some envenomations, particularly those of widow spiders, funnel web spiders, and less often, recluse spiders. Allergic reactions typically result from contact with spiders (rather than bites).

Local reactions — Photographs of verified spider bites are rare in the medical literature, although dramatic images of necrotic lesions attributed to spider bites are commonplace in both medical journals and on the Internet. In reality, the majority of spider bites result in unremarkable wheals, papules, or pustules (show picture 4). Local redness with a tender nodule at the site of the bite appears within minutes. The lesions are similar to those induced by a bee sting. In some cases, the markings of the fangs (one or two small puncture marks) are visible. Some bites also itch or burn.

Spider bites may or may not be painful, and some go unnoticed. Pain can develop gradually over the ensuring hours after a bite, and can range from a slight prickly sensation to severe pain. The variability among bites and patients limits the clinical utility of this information in implicating a specific type of spider.

Most local reactions to spider bites resolve spontaneously in approximately 7 to 10 days. They occasionally become secondarily infected with skin-derived bacteria.

Necrotizing local reactions — Recluse (Loxosceles) spiders inflict bites that may become necrotic, although this is an uncommon complication. Other types of spiders have been implicated in causing necrotic bites, but this is based largely upon circumstantial evidence. The management of necrotic recluse spider bites is discussed separately. (See "Bites of recluse spiders").

Systemic reactions — Systemic symptoms are reported in a minority of patients, and occur when venom enters the circulation in sufficient amounts.

The bites of certain spiders are known for distinct and potentially severe systemic reactions, including bites of the widow, Australian funnel web, and Phoneutria spiders.

Allergic reactions — Allergic reactions to spiders are rare and have been reported mostly in response to contact with spiders [3-6] . In the United States, tarantulas are increasingly popular pets (show picture 5). These nonaggressive spiders rarely bite. When threatened, they dislodge small (about 1 mm long) barbed hairs at the posterior of their abdomens and launch them at their attacker. These hairs, as well as airborne material from crushed tarantulas, may cause irritation or urticaria if they come in contact with skin, eyes, or mucous membranes [1,6] . In addition, airborne material from tarantulas can cause foreign body reactions in the eye [7] .

Contact with tarantulas has also induced rare anaphylactic reactions in sensitized individuals [8] . The acute management of anaphylaxis (from any cause) is reviewed separately. (See "Anaphylaxis: Rapid recognition and treatment").

DIAGNOSIS — A presumptive diagnosis of a spider bite is most often based on the history and clinical presentation. However, the diagnosis of a spider bite can be considered definitive ONLY if both of the criteria below are fulfilled:

• A spider was observed inflicting the bite.
• The spider was recovered, collected, and properly identified by an expert entomologist.

If these criteria are not met, then other conditions such as vasculitis, infection, vascular problems, or other relevant disorders must be ruled out. (See "Differential diagnosis" below).

Unfortunately, the criteria above are rarely met, even in published medical reports. This has resulted in a body of literature and considerable media attention falsely attributing various lesions and symptoms to spider bites [1] . The extent of this problem was illustrated in a review of 600 cases of suspected spider bites, which found that 80 percent of presumed bites could be more reasonably attributed to other causes [9] . These other causes included bites of different arthropods such as ants, fleas, bedbugs, ticks, mites, mosquitoes, and biting flies, as well as erysipelas, cellulitis, ecthyma, vasculitis, pyoderma, ophthalmic zoster, urticaria, angioedema, and burns. (See "Differential diagnosis" below).

History — Most patients' reports of spider bites are unreliable. The bite history is often speculative and retrospective and a spider was never visualized, either inflicting the bite or even present [10] . Even when a bite is witnessed by the patient, the "spider" is commonly found to be some other arthropod [9] .

The diagnosis of a spider bite is thus highly suspect unless the patient actually observed a spider inflicting the bite and can retrieve it for identification. In the absence of this history and supporting evidence, another explanation should be sought.

The setting in which the patient sustained the alleged bite should be carefully reviewed to see if it is consistent with the known habitat and behavior of the venomous spiders that live in the area. People may worry about the possibility that a venomous spider was transported into a non-indigenous area on fruit or other produce. However, it is rare for spiders to survive intact through the many steps involved in produce transportation, and then end up in a situation in which they would bite. The risk may be more significant for people working in food transport and handling, but it is minimal in the general community. (See "Bites of recluse spiders").

Clinical clues that essentially EXCLUDE the diagnosis of spider bite include the following:
• Multiple lesions or more than one lesion on widely-separated parts of the body suggest another etiology. Spider bites are typically single lesions.
• Bites are generally not simultaneously sustained by multiple residents of the same household.

Spider bites capture the imagination. Reports exist of patients both feigning spider bites as part of drug seeking behavior [11] and attempting suicide with genuine spider bites [12] .

Influence of geographic location — Each of the venomous spiders lives in specific parts of the world (show table 1). Clinicians should know which spiders are indigenous to their area.
• Widows and false black widows are found worldwide.
• Recluse spiders are found predominantly in North and South America. Within the United States, they are limited to the mid-western and southern portions of the country (show figure 2). (See "Bites of recluse spiders").
• Phoneutria spiders are limited to South America.
• Australian funnel web spiders are limited to southeastern and coastal Australia.

Laboratory data — There are no commercially available laboratory tests for identifying the presence of spider venom. Thus, the diagnosis is made clinically.

DIFFERENTIAL DIAGNOSIS — A spider bite usually presents as a local lesion (possibly with necrosis in the case of recluse bites) with or without systemic symptoms. (See "Types of reactions" above). The differential diagnoses for local and systemic symptoms are reviewed in this section. Disorders that can mimic the bites of specific spiders are discussed in appropriate topic reviews. (See "Bites of recluse spiders").

As discussed previously, many other conditions are more common than spider bites and pose a more immediate threat to the patient's health if not accurately diagnosed. A patient who did not clearly witness a spider inflicting the bite should be presumed to have some other disorder, and the presence of multiple lesions essentially excludes the diagnosis of spider bite. (See "History" above).

The clinician can usually determine whether a spider bite is possible based upon a careful history of the patient's recent activities, details of the onset and evolution of the lesion, and knowledge of biting spiders found in the area. Despite this, it is not uncommon for patients to present with nondescript lesions, suggest that it might be a spider bite because of some circumstantial detail, and have that history accepted without further questioning.

A spider bite may present as a papule, pustule, wheal, plaque (possibly ecchymotic), or ulcer. The most common disorders that are mistaken for local reactions to spider bites include infections and the bites of other insects.

Infections — Papules and pustules should be carefully unroofed and cultured to identify infectious causes. Common infections that could be mistaken for spider bites include staphylococcus and streptococcal infections, the skin lesion of early Lyme disease, and atypical presentations of herpes zoster or herpes simplex.

• Community-acquired methicillin-resistance Staphylococcus aureus (CA-MRSA) skin infections can begin with singular or papules or pustules that may evolve to necrotic lesions [13] . CA-MRSA is far more prevalent than spider bites. Infections occur both sporadically and as institutional epidemics in nursing homes, prisons, military barracks, and athletic facilities. Risk factors and epidemiology of CA-MRSA are discussed separately. (See "Epidemiology of methicillin-resistant Staphylococcus aureus infection in adults" and see "Epidemiology and clinical spectrum of methicillin-resistant Staphylococcus aureus infections in children").

• Erythema migrans, the target-like skin lesion of early Lyme disease, may be mistaken for a spider bite (show picture 6). Southern tick-associated rash illness (STARI) is a similar infection with similar skin findings, which occurs in the southern United States (below Maryland). (See "Diagnosis of Lyme disease" and (See "Southern tick-associated rash illness (STARI)").

• Herpes zoster and herpes simplex infections (especially herpetic whitlow) may occasionally present with singular lesions (show picture 7). Acute onset is associated with vesicles, vesicopustules, severe edema, erythema, or pain. Tzanck staining of vesicles will demonstrate multinucleated giant cells and viral culture will grow HSV. (See "Epidemiology and pathogenesis of varicella-zoster virus infection" and see "Paronychia, herpetic whitlow, and ingrown toenails").

Other bites and stings — A wide variety of insects sting or bite humans, including triatomid bugs, ants, fleas, bedbugs, blister beetles, ticks, mites, mosquitoes, and biting flies (show table 2) [9] . Spiders are less likely to do so than many others. With the exception of tick-borne illnesses and allergic reactions, the exact insect inflicting the bite is of little clinical importance and local care suffices.

Scorpion stings are more common than spider envenomations worldwide, and most stings have been reported in Africa, the Middle East, southern Asia, and Central and South America. In the United States, scorpion stings are most common in Arizona and nearby areas of the southwest. Stings are instantaneously painful, and so patients usually capture or at least clearly witness the scorpion inflicting the sting [14,15] . Local pain is the most common presenting symptom. Systemic symptoms include hypertension, tachycardia, diaphoresis, and salivation [14] .

Other common dermatoses — Poison ivy, poison oak, and other plants in the Anacardiaceae family may occasionally cause dermatitis that presents as a single lesion, although linear lesions are more typical (show picture 8). These lesions tend to be pruritic, rather than painful. (See "Poison ivy (Toxicodendron) dermatitis").

SUMMARY AND RECOMMENDATIONS — Spider bites are uncommon medical events, since there are limited number of spiders worldwide with fangs strong enough to pierce human skin, and most spiders bite humans only as a final defense when being crushed between skin and another object. Thus, most lesions attributed to spider bites are caused by some other etiology. (See "Introduction" above).

• The spiders that can cause medically significant bites include widow and false widow spiders (worldwide), recluse spiders (mostly North and South America), Australian funnel web spiders (eastern coastal Australia) and Phoneutria spiders (Brazil) (show table 1). (See "Medically important spiders" above).

• Acute spider bites most commonly result in a solitary papule, pustule, or wheal (show picture 4). Systemic symptoms can accompany envenomations of widow, funnel web, and Phoneutria spiders, and less often, those of recluse spiders. The bites of recluse spiders can become necrotic, although most bites do not necrose. Allergic reactions to contact with spiders (rather than bites) occur most often in response to tarantulas. (See "Types of reactions" above).

• Clinicians should know which of the biting spiders (if any) are found in the areas in which they practice, and have a basic understanding of the entomology of those species (show table 1). (See "Influence of geographic location" above).

• The working diagnosis of a spider bite is based upon suggestive history and clinical presentation. However, definitive identification of a spider bite requires all of the following: a spider was observed inflicting the bite, the spider was recovered, collected, and properly identified by an expert entomologist, and other disorders have been ruled out. (See "Diagnosis" above).

• In the majority of cases, another etiology is responsible for the lesion, other than a spider bite. The differential diagnosis includes infections, bites and stings of other arthropods, and several other more common dermatosis. Culture should be performed in most cases. (See "Differential diagnosis" above).

Evaluation of the patient with neck pain and cervical spine disorders

Evaluation of the patient with neck pain and cervical spine disorders

Author
Zacharia Isaac, MD
Bruce C Anderson, MD
Section Editor
Steven J Atlas, MD
Deputy Editor
H Nancy Sokol, MD



Last literature review version 16.2: May 2008 | This topic last updated: June 12, 2008 (More)


INTRODUCTION — Approximately 10 percent of the adult population has neck pain at any one time [1] . This prevalence is similar to low back pain, but few patients with neck pain lose time from work and less than 1 percent develop neurologic deficits.

Clinical disorders affecting the cervical spine can be categorized as those that predominantly cause neck pain, and those that most often cause extremity pain and/or neurological dysfunction. Disorders that cause neck pain include cervical strain, internal disc disruption syndrome/discogenic pain, cervical facet-mediated pain, cervical "whiplash" syndrome, and myofascial pain. Disorders that predominantly cause extremity symptoms and/or neurological dysfunction include cervical radiculopathy and cervical spondylotic myelopathy.

The evaluation of the patient with cervical spine disease is reviewed here. The management of disorders of the neck are discussed separately. (See "Treatment of neck pain"). Evaluation of a patient with acute neck trauma is also discussed separately. (See "Management of spinal column injuries in adults").

ANATOMY — The cervical spine is comprised of seven vertebrae. The articulation between the occiput and the first cervical vertebra (the atlantooccipital joint) allows for approximately one-third of flexion and extension and one-half of lateral bending of the neck [2] . The articulation between the first and second cervical vertebrae (the atlantoaxial joint) allows for 50 percent of rotational range of motion. The articulations between the second and seventh cervical vertebrae allow for approximately two-thirds of flexion and extension, 50 percent of rotation, and 50 percent of lateral bending.

The most severe injuries and greatest wear and tear occur between C4 and C7 [2] ; the nerve roots passing through the intervertebral foramena in these areas are C5, C6, and C7. Uncovertebral articulations (also known as joints of Luschka) are present in the C3-7 spinal segments, located on the posterolateral border of the intervertebral disc, and in the anteromedial portion of the intervertebral foramen. These articulations are not true synovial joints, but can hypertrophy, associated with disc degeneration, and result in narrowing of the intervertebral foramen. This foramenal narrowing is a common cause of cervical radiculopathy [3] .

The cervical and trapezius muscles have two major functions: to support and provide movement and alignment for the head and neck, and to protect the spinal cord and spinal nerves when the spinal column is under mechanical stress. The normal cervical spine has a shallow lordosis, maintained by the neck muscles.

This lordosis can be decreased, in patients with degenerative changes. Severe degenerative changes in the cervical spine can result in reversal of the lordosis. The lordosis may also become accentuated, in compensation for patients with prominent thoracic kyphosis. Alterations in spinal alignment, however, have not definitively been demonstrated to cause cervical pain.

Neuroanatomy — There are eight cervical spinal nerves. Each spinal nerve arises from the spinal cord by two roots, the ventral and dorsal spinal roots. The ventral root contains motor efferent fibers from alpha motor neurons in the ventral horn of the spinal cord. The dorsal root carries primary sensory afferent fibers from cells in the dorsal root ganglion. The dorsal and ventral spinal roots combine to form the spinal nerve.

This spinal nerve then divides into two branches, a dorsal primary ramus and a ventral primary ramus. The dorsal ramus divides and supplies innervation to muscular, cutaneous, and articular branches for posterior neck structures. The ventral rami supply the prevertebral and paravertebral muscles and form the brachial plexus which subsequently innervates the upper limb. The sensory cervical dermatomes are illustrated in the figure (show figure 1).

A myotome is the group of muscles innervated by a spinal nerve. The diaphragm is innervated by C3 to C5 spinal nerves and respiratory paralysis may result from spinal cord injuries above C5.

Cervical radiculopathy may be caused by degenerative changes in the spine that impact the ventral root and cause focal weakness. Specific findings with different levels of nerve root involvement are discussed below (see "Cervical level correlates to findings" below).

CLINICAL CLASSIFICATION — A 2007 task force on neck pain, representing multiple specialties and institutions, recommends a classification system for neck pain severe enough to cause patients to seek care [4] :

• Grade I: No signs of major pathology and little interference with daily activities.
• Grade II: No signs of major pathology but may impact daily activities.
• Grade III: Neck pain with neurological signs or symptoms (radiculopathy)
• Grade IV: Neck pain with major pathology (eg, fracture, myelopathy, neoplasm, spinal infection)


These classifications can be helpful in determining urgency of care and appropriateness of intervention. (See "Treatment of neck pain").

AXIAL NECK PAIN SYNDROMES — Neck pain can arise from a variety of causes [5] . Systemic diseases, such as rheumatoid arthritis, spondyloarthritis, polymyalgia rheumatica, or bone metastases should be considered in appropriate patients. Degenerative changes are the most common etiology for axial neck pain. An approach to diagnosis is described below, for patients in whom there is no evidence of rheumatologic, oncologic, and infectious etiologies on history and examination.

Cervical strain — Cervical strain is a nonspecific diagnosis, classically used to describe an injury to the cervical paraspinal muscles and ligaments with associated spasm of the cervical and upper back muscles. The diagnosis of cervical strain is reasonable in patients with acute axial neck and trapezius pain, where neurological dysfunction has been excluded.

Cervical strain may result from the physical stresses of everyday life, including poor posture and sleeping habits. Typically, symptoms are experienced as pain, stiffness, and tightness in the upper back or shoulder, and last for up to six weeks. Patients with chronic symptoms that extend beyond the expected time frame for resolution should not receive this nonspecific diagnosis; muscle pain alone should not be routinely considered a chronic nociceptor.

Potential mechanisms for chronic pain include cervical discogenic pain, facet mediated pain, cervical spondylotic myelopathy, cervical radicular pain, myofascial pain, and centrally mediated pain.

Cervical spondylosis — The term cervical spondylosis is variably used to include soft tissue, disc, and degenerative bony lesions [6] . Degenerative changes in the cervical spine are apparent on radiographs of many adults over the age of 30 [7] . The abnormalities include a sequential change in the intervertebral discs, with osteophyte formation along the vertebral bodies, and changes in the facet joints and laminal arches. There is a continuum from normal aging to the overtly pathologic state. (See "Clinical features and diagnosis of cervical radiculopathy", section on Pathophysiology).

Correlation between the degree of radiographic change and the presence or severity of pain is poor [7] . Given the prevalence of radiographic abnormalities in asymptomatic subjects, clear distinction of the clinical entity of cervical spondylosis is difficult [5] .

Cervical discogenic pain — Cervical degenerative disc disease is more aptly a radiologic diagnosis, rather than a clinical syndrome, as it is commonly seen on x-ray studies in both symptomatic and asymptomatic patients. For this reason, other terms have been introduced to describe patients who are symptomatic with disc-related neck pain: cervical internal disc disruption syndrome or cervical discogenic pain [8,9] . Cervical discogenic pain may be the most common cause of neck pain.

In contrast to patients with cervical disc herniations, cervical discogenic pain refers to derangement in the architecture of the disc that results in mechanical neck pain with or without features of inflammation. The degenerative process that occurs in the intervertebral disc is associated with an inability to effectively distribute pressures between the disc, vertebral endplates, and facet joints.

Axial pain is more severe than extremity pain in cervical discogenic pain. Extremity pain can occur, but is felt to result from somatic referral rather than spinal nerve root impingement. Symptoms are often exacerbated when the neck is held in one position for prolonged periods, such as occurs with driving, reading, or working at a computer. There is often associated muscle tightness and spasms.

Examination should demonstrate axial neck discomfort with range of motion, a decreased range of motion, and a benign neurological examination. MRI imaging demonstrating the degree of degeneration does not accurately implicate which discs are symptomatically painful; asymptomatic degenerative changes are common [10,11] .

Cervical facet syndrome — The zygapophyseal joint, commonly referred to as the facet joint, can cause axial pain and is probably the most common cause of whiplash-related neck pain and headaches [12,13] . Historically, patients often have a history of trauma with an abrupt flexion-extension type injury, or an occupation which leads to repeatedly positioning the neck in extension.

Pain is often midline or offset slightly to one side. Symptoms can be somatically referred to the shoulders, periscapular region, occiput, or proximal limb. As with cervical discogenic pain, axial symptoms are greater than extremity symptoms.

Unfortunately, there is no specific historical examination, or imaging finding, that provides confirmatory diagnostic information. A fluoroscopically guided intraarticular injection of a small aliquot of local anesthetic, or anesthetization of the innervation of the joint resulting in relief are considered the definitive diagnostic tests.

Whiplash injury — The cervical "whiplash" syndrome is caused by a traumatic event with an abrupt flexion/extension movement to the cervical spine. Symptoms of whiplash include severe pain, spasm, loss of range of motion in the neck, and occipital headache. Pain can be persistent with little identifiable abnormality seen on MRI, CT, x-ray, or bone scan imaging. Often multiple structures can be injured including soft tissues, spinal nerve, intervertebral disc, posterior longitudinal ligament, interspinous ligaments, alar ligaments, facet joints, or other osseous structures.

The injury is common but remains poorly understood [14] . In a case controlled study of 1843 drivers involved in a motor vehicle accident, 26 percent of whom had neck pain for more than one day, eight variables were identified as risk factors for whiplash injury: female, younger age, prior history of neck pain, rear collision, stationary vehicle, severity of collision, not being at fault, and monotonous work [15] . In a systematic review of 47 studies, approximately 50 percent of adults with whiplash injury reported neck pain symptoms at one year [16] .

The pathology of the condition is unclear. Microvascular bleeding and local release of inflammatory mediators may explain the acute symptoms, but some patients remain symptomatic for many months or even years. Soft tissue injury may be associated with the degree of impairment. A study using high resolution MRI imaging of the C spine in patients with a remote history of whiplash injury (mean 6 years), and symptoms that had persisted at least 3 months following injury, demonstrated soft tissue damage, particularly of the alar ligaments, not seen in MRI images in control patients [17] .

In a study in the United Kingdom (UK), the most important predictors of pain at one year were pain severity at the time of the rear-end collision and the presence of a compensation claim [18] . Chronic whiplash symptoms may also be associated with different cultural expectations; 50 percent of Canadian and British subjects surveyed anticipated chronic neck pain following a hypothetical whiplash injury compared to negligible numbers from respondents in Lithuania and Germany, where late neck pain prevalence is very low [19,20] . A legislative change in Australia, removing financial compensation for pain and suffering from whiplash injuries, was associated with improvement in functional status and pain indices in patients with whiplash, compared to historical controls [21] .

Cervical myofascial pain — Regional pain with associated trigger points, taut bands, and pressure sensitivity has been called myofascial pain. Myofascial pain can be a nonspecific manifestation of any pathologic condition which causes pain from the neck to the shoulder and should not be considered a defining diagnosis. Myofascial pain can also be associated with muscle sensitivity, depression, and insomnia, much akin to fibromyalgia.

Diffuse skeletal hyperostosis — Diffuse skeletal hyperostosis (DISH) is a syndrome of inappropriate bone deposition in the insertions of the ligaments and tendons. Large osteophytes connect adjacent vertebral bodies in a somewhat asymmetric fashion. The diagnosis is based on three criteria for spinal radiographs [22] :

• The presence of calcification or ossification along the anterolateral aspects of at least four contiguous vertebral levels.
• Relative preservation of intervertebral disc height in the involved vertebral segments without extensive changes of primary degenerative disc disease.
• The absence of apophyseal joint ankylosis or sacroiliac joint erosions, sclerosis, or intraarticular bony ankylosis.

DISH can be associated with stiffness, loss of mobility, and pain, but can also often be asymptomatic. The bony fusion that results from the hyperostosis may cause mechanical pain at segments adjacent to the fused segments. Prominent anterior vertebral hyperostosis associated with DISH can cause dysphagia. (See "Diffuse idiopathic skeletal hyperostosis (DISH)").

EXTREMITY PAIN AND/OR NEUROLOGIC DEFICIT

Cervical spondylotic myelopathy — Cervical spondylotic myelopathy is defined by degenerative changes narrowing the spinal canal, resulting in cervical spinal cord injury or dysfunction. Cervical spondylotic myelopathy can result from an extradural mass, as seen with endplate hyperostosis, herniated nucleus pulposus, ossification of the posterior longitudinal ligament, spondylolisthesis, congenital narrowing, or degenerative C1 to C2 (atlantoaxial) or subaxial cervical instability due to rheumatoid arthritis. (See "Cervical subluxation in rheumatoid arthritis"). Patients may present with a variety of neurological complaints: weakness, coordination impairment, gait disturbance, bowel or bladder retention or incontinence, and sexual dysfunction.

Upper extremity pain can be precipitated when spondylotic changes or a focal protrusion lead to cervical foramenal stenosis. In this setting, a concurrent radiculopathy is often present and this is termed cervical myeloradiculopathy. Inherent to this disorder is a clinical picture of mixed upper and lower motor neuron abnormalities, such as hyperreflexia and spasticity simultaneously present with depressed reflexes and weakness.

Spinal cord compression due to spondylotic change tends to occur in the lower cervical spine; degenerative changes are more severe and more common between C5 and T1 and the spinal cord is enlarged between C4 and T2 [23] .

The differential diagnosis for cervical spondylotic myelopathy includes multiple sclerosis, syringomyelia, tumor, epidural abscess, and amyotrophic lateral sclerosis. Distinguishing cervical spondylotic myelopathy from other causes of neck pain is critical because optimal neurological recovery depends on early surgical decompression. (See "Treatment of neck pain", section on cervical spondylotic myelopathy).

Cervical radiculopathy — Cervical radiculopathy refers to dysfunction of the spinal nerve root that may manifest with pain, weakness, reflex changes, or sensory changes. Multiple conditions can give rise to cervical radiculopathy, including cervical foramenal stenosis, cervical herniated disc, herpes zoster, Lyme radiculopathy, or diabetic polyradiculopathy, but degenerative changes in the spine are overwhelmingly more common than the other causes, accounting for 70 to 90 percent of cases.

Diagnosis and clinical features of cervical radiculopathy are discussed separately (see "Clinical features and diagnosis of cervical radiculopathy").

NON-SPINAL CAUSES OF NECK PAIN

Thoracic outlet syndrome — The thoracic outlet syndrome can present as neck and shoulder pain with referred pain to the upper extremities and variable neurovascular signs and symptoms. The triad of numbness, weakness, and a sensation of swelling of the upper limbs is strongly suggestive of thoracic outlet syndrome. Examination may demonstrate a positive Roos sign (repetitive and vigorous hand grip while the arms are abducted overhead) or a positive Adson's test (diminution of the radial pulse when the arm is abducted, extended backward, the head is turned ipsilaterally, and the patient inspires). (See "Brachial Plexus syndromes" section on Thoracic outlet syndrome).

Herpes zoster — Herpes zoster (shingles) may present with unilateral radicular symptoms without neurologic findings. The rash may not appear for several days after the onset of pain. (See "Epidemiology and pathogenesis of varicella-zoster virus infection").

Diabetic neuropathy — Diabetes mellitus can be associated with various neuropathic pain syndromes related to vasculitis of the vasa vasorum. Cervical and thoracic polyradiculopathy, plexopathy, and peripheral entrapments can be associated with neck, thoracic, scapular, extremity pain and/or weakness. (See "Clinical manifestations and diagnosis of diabetic polyneuropathy").

Other causes — The differential diagnosis of neck pain is broad. Although the majority of neck pain complaints are related to musculoskeletal causes, numerous other conditions can present with a constellation of symptoms that include neck pain. While the differential listed below should be kept in mind in evaluating the patient with neck pain, diagnosis of these conditions is usually evident from accompanying symptoms (ie, fever, neck stiffness, diffuse joint pain, etc.):

• Malignancy: tumors involving the cervical spinal column.
• Vascular: vertebral artery or carotid artery dissection
• Cardiovascular: angina and myocardial infarction (causing neck, chest, and arm symptoms that may mimic cervical radicular pain)
• Infection: pharyngeal abscess, meningitis, subdiaphragmatic abscess, herpes zoster, Lyme disease
• Visceral: esophageal obstruction, biliary disease, apical lung tumor
• Referred shoulder pain: impingement, adhesive capsulitis, rotator cuff tear
• Rheumatologic: polymyalgia rheumatica, fibromyalgia
• Neurologic: cervical dystonia, tension headache, Chiari malformations

PHYSICAL EXAMINATION — The approach to the patient who has suffered serious head or neck trauma differs dramatically from the typical office evaluation of neck complaints ("See "Management of spinal column injuries in adults").

Routine cervical spine evaluation includes the following:

• Observe movement and resting posture of the head and neck
• Estimate cervical range of motion
• Palpate the paraspinal and upper trapezial muscles
• Evaluate for radicular neurological symptoms: reflexes, motor and sensory testing
• Evaluate for upper motor neuron signs
• Perform provocative maneuvers for radicular pain
• Examine the shoulder for painful range of motion

General observation — The routine examination begins by noting the movement of the head and neck. Posture and general movements (rigid and guarded, general stiffness, or loose and free) should be consistent during the interview phase as well as during the actual examination. Lack of consistency may be the only clue to malingering in the case of trauma- related whiplash and cervical radiculopathy that are under litigation.

Range of motion — Neck rotation and lateral bending, when combined with palpation of the trapezius and paraspinal muscles for tenderness and spasm, are used to assess the degree of cervical spine involvement. The presence of torticollis can be consistent with acute muscle spasm or a herniated disk. Assessment of the shoulder is important since overlapping symptoms can occur.

• The cervical spine can rotate an average of 90 degrees (show picture 1). Less rotation is abnormal.
• The cervical spine can bend an average of 45 degrees laterally (show picture 2).
• The cervical spine can forward flex to 60 degrees
• The cervical spine can extend backward 75 degrees

Abnormal neck range of motion suggests an injury to the cervical spine but does not indicate a specific diagnostic etiology. Conditions such as cervical strain, pain inhibited movement, cervical discogenic pain, cervical facet syndrome, DISH, cervical radiculopathy, and cervical myeloradiculopathy can all be associated with range of motion alterations. Neck rotation may be more prominently affected by upper cervical spine abnormalities (C1 to C3) whereas lateral flexion impairment may be more prominent with lower cervical spine disease (C4 to C7).

Range of motion of the cervical spine appears to be an important predictor of outcome in patients with whiplash injury. In one prospective study of 141 patients with acute whiplash, reduction in cervical range of motion was the single best predictor of long-term handicap, with a sensitivity and specificity of 73 and 91 percent, respectively [24] .

Muscle palpation — Local muscular tenderness can result from trauma (a direct blow to the upper back or trauma to the head), or can be a nonspecific feature of a number of cervical spine syndromes. The upper trapezius and paraspinal muscles should be palpated to determine the degree of tenderness and spasm (show picture 3).

Trapezius muscle tenderness is a nonspecific finding seen in many conditions and is consistent with a diagnosis of cervical muscle strain, fibromyalgia, whiplash, or cervical radiculopathy. Severe muscular rigidity and guarding are associated with severe neck strain, occult vertebral body fracture, and fracture/dislocation. Muscle spasm is so dramatic with neck fracture that the neck is totally rigid.

The superior division of the trapezius muscle is often quite hard to palpation in the elderly. The dorsokyphotic posture (prominent C7 spinous process, drooped shoulders, and head forward) places the trapezius under constant tension. The extremes of rotation may show endpoint stiffness and mild pain.

Neurologic examination — A detailed upper extremity neurologic examination is warranted for patients with radicular symptoms. The neurological exam should involve the following components: muscle strength, reflex testing, muscle tone, gait, and testing for upper motor neuron signs. A detailed neurological examination is described separately. (See "The detailed neurologic examination in adults").

A negative neurological examination indicates a low likelihood of root compression; positive findings, however, are not specific for root compression [4] . These correlations, however, are tempered by variability in the quality of the neurological examination performed.

The majority of patients with pure sensory radiculopathy have a good prognosis and respond to a combination of rest, exercise, and occasionally medication or corticosteroid injection. In contrast, patients with sensorimotor involvement (with or without spinal cord compression) have a less predictable prognosis; they are more likely to have more dramatic degrees of disk herniation, are at higher risk for nerve damage, and are more likely to require surgical intervention.

Muscle strength — Strength should be evaluated by testing the following actions against resistance: shoulder abduction, elbow flexion and extension, wrist flexion and extension, and lower limb extension and flexion. Strength should be recorded using the Medical Research Council manual muscle testing scale as follows:

• 0 = No contraction
• 1 = Visible muscle twitch but no movement of the joint
• 2 = Weak contraction insufficient to overcome gravity
• 3 = Weak contraction able to overcome gravity but no additional resistance
• 4 = Weak contraction able to overcome some resistance but not full resistance
• 5 = Normal; able to overcome full resistance

Reflex testing — Deep tendon reflexed should be checked at the bicep, brachioradialis, and tricep muscles and compared from side to side. Grading scale is as follows:

• 0 = No observable reflex
• 1 = Trace reflex
• 2 = Normal reflex
• 3 = Brisk reflex
• 4 = Nonsustained clonus ( two or less beats of clonus)
• 5 = Greater than 3 beats of clonus or sustained clonus

Cervical level correlates to findings — There is some overlap in clinical symptoms and physical findings that suggest involvement of a specific nerve root. In general, however, assessment of strength, reflexes, and sensory examination, in combination with patient symptoms, can target a specific root lesion (show table 1).

• C4 radiculopathy may affect the levator scapular and trapezius muscles, resulting in weakness in shoulder elevation. There is no reliable associated reflex.

• C5 radiculopathy is associated with weakness of the rhomboid, deltoid, bicep, and infraspinatus muscles. Patients may have weakness of shoulder abduction and external rotation. The bicep reflex may be diminished.

• C5-C6 paracentral and/or foramenal herniation or foramenal stenosis at C5-C6 affects the C6 nerve root and produces pain at the shoulder tip and trapezius with radiation to the anterior upper arm, radial forearm, and thumb, and sensory impairment in these areas. C6 radiculopathy can easily be confused for C5 or C7 radiculopathy. Weakness can overlap with the C5 or C7 muscles. Muscles affected include: infraspinatus, bicep, brachioradialis, pronator teres, and tricep. Weakness involves flexion at the elbow, or shoulder external rotation. The bicep or brachioradialis reflex may be diminished.

• C6-C7 paracentral and/or foramenal herniation or foramenal stenosis at C6-C7 affects the C7 nerve root and produces pain at the shoulder blade, pectoral area, and medial axilla with radiation to posterolateral upper arm, dorsal elbow and forearm, index and medial digits or all of the fingers, and sensory impairment in these areas. C7 radiculopathy can result in weakness of the tricep, pronator teres, flexor carpi radialis. Weakness involves the elbow extensors, and forearm pronators. There may be a diminished tricep reflex.

• C7-T1 paracentral and/or foramenal herniation or foramenal stenosis at C7-T1 causes C8 radiculopathy. Weakness can be present in the opponens pollicis, flexor digitorum profundus, flexor pollicis longus, and hand intrinsic muscles. Clinically, patients present with symptoms similar to an ulnar or median motor neuropathy and can have weakness of finger abductors and grip strength; they may also have findings suggesting median motor neuropathy. No reliable reflex test is available.

• Central disc herniation at any cervical level — Large central disc herniation or any cause of spinal cord compression in the midline can produce a cervical myelopathy with bilateral upper motor neuron signs in the extremities. Small central herniations are common and are often not clinically associated with radicular pain or myelopathic features.

Provocative maneuvers

• Spurling's maneuver — The Spurling's and modified Spurling's maneuver can reproduce the patient's radicular pain (show picture 4). The Spurling's maneuver (also called the neck compression test) is performed by keeping the head in a forward flexed, ipsilaterally rotated, and ipsilaterally tilted position. The modified Spurling's maneuver is performed by keeping the head extended, ipsilaterally rotated, and ipsilaterally tilted. Additional axial load by applying pressure on top of the head can be applied. Reproduction of symptoms beyond the shoulder is considered positive. Reproduction of neck pain alone is nonspecific.

This maneuver is highly specific for the presence of cervical root compression, but the sensitivity is low [25] . One study, as an example, using electrodiagnostic testing as a reference, found a sensitivity of 30 percent and specificity of 93 percent for the Spurling's maneuver [26] . Thus, a positive test is helpful, but a negative test does not rule out radicular pain.

The Spurling maneuver should be performed with caution in patients with suspected rheumatoid arthritis, cervical malformations, or metastatic disease since it may cause further injury to the spine in these patients.

Upper limb tension test — The Elvey's upper limb tension sign is a root tension sign for the upper extremity, akin to the straight leg raise in the lower extremity. The head is turned contralaterally, the arm is abducted with the elbow extended. Reproduction of arm symptoms is considered positive. The sensitivity and specificity of Elvey's upper limb tension test were 0.97 and 0.22 in one study [27] . This test is most useful for ruling out radiculopathy.

A combination of tests may provide the most accurate diagnostic assessment. One study analyzed a cluster of four tests: Spurling's maneuver, Elvey's upper limb tension test, cervical rotation less than 60 degrees, and diminution in neck symptoms with distraction. The post test probability for radiculopathy in patients with two, three, or four positive tests was 21, 65, and 90 percent, respectively.

CONFIRMATORY TESTS — Radiographic studies, magnetic resonance imaging, electromyography/nerve conduction studies (EMG/NCS), and minimally invasive functional testing are useful tests for determining diagnosis in selected patients with cervical spine disorders.

Because degenerative changes can occur at multiple levels, neurologic findings must be correlated with radiographic abnormalities. As an example, symptoms and signs involving C6 should correlate with the presence of foramenal encroachment at the C5-C6 intervertebral space.

Radiography
Plain films — Plain films are indicated in patients with neck complaints who are age greater than 50 with new symptoms, or constitutional symptoms.

Patients who fail a four to six week trial of conservative care, and patients who present with symptoms and signs of radiculopathy, should have imaging studies as well. A plain film x-ray of the neck may be obtained for these patients, but is probably not necessary if a CT or MRI scan can be performed in a reasonable timeframe.

The routine cervical series of x-rays consists of seven views, including the odontoid, lateral, PA, two oblique views, lateral view in flexion, and lateral view in extension. However, in a series of 258 patients undergoing radiography for evaluation of neck-related disorders (axial cervical, upper extremity radicular, or myelopathic symptoms), flexion and extension views did not lead to findings that changed clinical management [28] . The additional expense and radiation exposure associated with dynamic views are not routinely warranted.

The lateral view demonstrates vertebral alignment; the normal cervical lordotic curve can be replaced by a straightened or even a reversed curve in moderate to severe cases of cervical strain. The lateral view is also used to screen for the degree of osteoarthritis (at the facet and paravertebral joints), disk space narrowing (osteoarthritis or radiculopathy), or bony pathology (compression fracture) (show radiograph 1).

Oblique views are primarily used to determine the role of foramenal encroachment (osteophytes reducing the overall diameter of the neuroforamena) (show radiograph 2). However, radiographic presence of foramenal stenosis can both underestimate and overestimate the degree of foramenal stenosis because of the variable angle of the cervical foramenae.

Severe torticollis may cause a lateral deviation of the cervical spine that is best appreciated on a PA view of the neck. Odontoid views are most appropriate in patients with acute trauma.

• CT scan can detect degenerative changes such as disc herniations, foramenal stenosis, central stenosis, facet osteoarthritis, tumor, and fractures. CT is a better study than MRI when facet osteoarthritis or other osseous changes are suspected. There is significant radiation exposure.

• MRI detects soft tissue processes including disc herniations, foramenal stenosis, central stenosis, and tumor. MRI can also detect spinal cord changes from myelopathy, fractures, and infection. The addition of gadolinium contrast intravenously allows better diagnosis of infection, tumor, or post surgical epidural fibrosis [29-32] . Administration of gadolinium-containing MRI contrast agents should be avoided in patients with moderately or severely impaired renal function (eg, estimated glomerular filtration rate < 15-30 mL/min).

If gadolinium-based imaging must be performed in a patient with moderate to severely impaired renal function, there may be a role for dialysis to reduce the risk of development of nephrogenic systemic fibrosis (NSF). Approaches to prevention of this disorder are discussed separately. (See "Nephrogenic systemic fibrosis/nephrogenic fibrosing dermopathy in advanced renal failure", section on If gadolinium must be given).

MRI does not expose the patient to radiation, but exposes the patient to a strong magnetic field, which precludes patients with pacemakers, intracranial vascular clips, and prior eye injury with metal fragments. Most metal placed as part of orthopedic procedures, including spine procedures, is considered permissible.

A limitation of MRI is that anatomic abnormalities such as disk protrusion or extrusion are present in up to 30 percent of asymptomatic individuals [7,10] . In one study of 100 patients referred for MRI of the larynx who had no neck symptoms, cervical disc protrusion or herniation was seen in 20 percent of patients between the ages of 45 and 54, and 57 percent of those older than age 64 [7] .

CT myelography is utilized at times as part of presurgical planning.
Other studies

Electrodiagnostic testing — EMG should be considered when peripheral nerve entrapment syndromes are a potential cause for extremity symptoms that can mimic cervical radicular pain. EMGs should be considered when there is more prominent pain and dysesthesia in the extremities than in the neck. In some patients, the pain symptoms travel retrograde to the neck. EMG studies are not indicated in patients without suspected radiculopathy [4] .

The needle portion of the EMG/NCS is the most useful test to identify cervical radiculopathy but will only identify radiculopathy and its associated radicular pain when motor axonal injury is present. It is important to recognize that cervical radicular pain can exist in the absence of axonal injury. Irritation of the dorsal root ganglion and the dorsal sensory afferent fibers can result in pain without motor injury.

The sensitivity of the needle EMG increases with the number of muscles sampled. One study demonstrated that sampling six upper limb muscles along with the paraspinal muscles was sufficient to identify cervical radiculopathy by EMG [33] .

Blood tests — Blood studies are not routinely indicated, but should be ordered, based on individual patient history and examination, when non-spinal causes of neck pain (ie, rheumatologic, infectious, or oncologic) are suspected. Serologic markers of inflammation such as erythrocyte sedimentation rate and c-reactive protein should be normal in degenerative causes of neck pain such as cervical radiculopathy, stenosis, myelopathy, discogenic pain, and facet syndrome. However, the erythrocyte sedimentation rate and c-reactive protein may be elevated in patients with polymyalgia rheumatica, rheumatoid arthritis, or infectious processes such as septic discitis. (See "Polymyalgia rheumatica").

EVALUATION OF THE TRAUMA PATIENT — Patients with significant head and neck trauma should be immobilized, stabilized, and transported by ambulance to an emergency department. A discussion of evaluation of the trauma patient is presented separately. (See "Management of spinal column injuries in adults").

INFORMATION FOR PATIENTS — Educational materials on this topic are available for patients. (See "Patient information: Neck pain"). We encourage you to print or e-mail this topic, or to refer patients to our public web site www.uptodate.com/patients, which includes this and other topics.

SUMMARY AND RECOMMENDATIONS
• Disorders of the cervical spine can cause either neck pain, or extremity pain with or without neurological dysfunction. The most severe injuries and wear and tear occur between C4 and C7, affecting the C5, 6, and 7 nerve roots. (See "Introduction" above and see "Anatomy" above).

• Cervical strain is associated with spasm of the cervical and upper back muscles, often related to posture and sleeping habits, and does not cause chronic pain. (See "Cervical strain" above).

• Cervical discogenic pain is the most common cause of neck pain, with normal neurological findings and discomfort on range of motion. (See "Cervical discogenic pain" above).

• Cervical spondylosis is a nonspecific term referring to degenerative changes in the disc and bones, causing osteophytes, and impacting facet joints. Degenerative changes in the cervical spine are age-related, commonly seen on x-ray, and do not necessarily indicate clinical symptoms. (See "Cervical spondylosis" above).

• Cervical facet syndrome is often associated with a flexion-extension type injury, such as is seen with whiplash. Whiplash symptoms may also involve soft tissues, ligaments, nerves, discs, and other bony structures; the pathology is unclear and testing is not confirmatory. (See "Whiplash injury" above).

• Cervical spondylotic myelopathy may result from central canal narrowing and causes upper motor neuron signs (weakness, coordination impairment, gait disturbance, bowel or bladder retention or incontinence, and sexual dysfunction); surgical decompression is necessary. (See "Cervical spondylotic myelopathy" above).

• Cervical radiculopathy is most commonly due to degenerative changes and is discussed in detail separately. (See "Clinical features and diagnosis of cervical radiculopathy").

• The physical examination should include observation of movement, range of motion, palpation, neurological examination for radicular and upper motor neuron signs, and provocative maneuvers. (See "Physical examination" above).

• Plain films are indicated for patients with history of neck trauma, new symptoms in patients >50 years or with constitutional symptoms. (See "Plain films" above).

• CT scan or MRI should be done for patients with objective neurological impairment, dramatic bony tenderness coupled with dramatically impaired mobility, or persistent symptoms despite conservative care for six weeks. (See "CT scan or MRI" above).

• EMG testing can distinguish peripheral nerve entrapment syndromes from cervical radiculopathy, and should be considered when pain and dysesthesia is more prominent in the extremities than in the neck. Blood testing for patients with neck symptoms is not routinely indicated. (See "Other studies" above).

• Emergency evaluation of the trauma patient requires immobilization, neurological assessment, spinal palpation, and radiographic studies. Patients with neurological deficits should be evaluated by a spinal surgeon. The need for radiographic studies in alert and stable trauma patients can be determined with the Canadian C-spine rule or NEXUS criteria. (See "Evaluation of the trauma patient" above).

Evaluation of the patient with shoulder complaints

Evaluation of the patient with shoulder complaints

Author
Bruce C Anderson, MD
Ronald J Anderson, MD
Section Editor
Karl B Fields, MD
Deputy Editor
Jonathan Grayzel, MD, FAAEM



Last literature review version 16.2: May 2008 | This topic last updated: April 22, 2008 (More)


INTRODUCTION — Shoulder pain is a common musculoskeletal complaint that may be due either to intrinsic disorders of the shoulder or referred pain. The former include injuries and acute or chronic inflammation of the shoulder joint, tendons, surrounding ligaments, or periarticular structures [1] .

This Topic will provide an overview of the evaluation of patients with shoulder pain, including discussions of musculoskeletal etiologies and examination techniques. In addition, a basic clinical approach to diagnosis is provided. In-depth discussions of the diagnosis and treatment of specific disorders of the shoulder are found separately.

ANATOMY AND BIOMECHANICS — A complex network of anatomic structures endows the human shoulder with tremendous mobility, greater than any other joint in the body. The shoulder girdle is composed of three bones (the clavicle, scapula, and proximal humerus) and four articular surfaces (sternoclavicular, acromioclavicular, glenohumeral, and scapulothoracic) (show figure 1A-1C). The glenohumeral joint, commonly referred to as the shoulder joint, is the principal articulation.

Glenohumeral structures — The glenohumeral joint is loosely constrained within a thin capsule bounded by surrounding muscles and ligaments (show figure 1A-1C). The shoulder's great mobility is due in large part to the shallow depth of the glenoid and the limited contact between the glenoid and the humeral head. Only 25 percent of the humeral head surface makes contact with the glenoid. The labrum, a fibrocartilaginous ring attached to the outer rim of the glenoid, provides some additional depth and stability. The shallowness and small surface area of the glenohumeral joint make it susceptible to instability and injury, and require that stability be provided primarily by extrinsic supports.

Surrounding muscles and ligaments provide these supports. The glenohumeral ligament serves as the primary static stabilizer. The rotator cuff serves as the primary dynamic stabilizer. The rotator cuff is composed of four muscles (supraspinatus, infraspinatus, subscapularis, and teres minor) that form a cuff around the head of the humerus, to which these muscles attach.

Shoulder pain is frequently caused by an acute or chronic injury of the rotator cuff, most often the supraspinatus muscle or tendon. The supraspinatus originates on the supraspinous fossa of the superior-posterior scapula, superior to the scapular spine, and inserts on the greater tubercle of the superior-lateral humeral head, just posterior to the biceps tendon. Proximal to its insertion it passes, along with the subacromial bursa, through the narrow space between the acromion process and the humeral head.

The acromion is a projection of the scapular spine that extends superiorly and anteriorly over the humeral head. Thus, with the shoulder in abduction, the supraspinatus is susceptible to impingement between the greater tubercle and the acromion. Activities involving repeated abduction with impingement can cause repetitive muscle and tendon trauma and ischemic compression of the tendon.

The sole, vital function of the subacromial bursa, also referred to as the subdeltoid bursa, is to lubricate and protect the rotator cuff tendons from the pressure and friction of the under side of the acromion.

Three other muscles contribute to the rotator cuff. The infraspinatus arises from the infraspinatus fossa of the posterior scapula and inserts on the lateral humeral head (greater tuberosity), just posterior to the supraspinatus where their insertions blend. The teres minor arises from the inferior-posterior scapula and blends with the infraspinatus to attach on the lateral humeral head (greater tuberosity). The subscapularis, the largest of the four cuff muscles, arises from the anterior scapula, inferior to the coracoid, and attaches to the anterior humeral head (lesser tuberosity).

The rotator cuff muscles rotate the humerus internally (subscapularis) and externally (infraspinatus primarily and teres minor), and contribute to abduction (supraspinatus), along with the deltoid muscle [2] . The deltoid is the most superficial muscle overriding the glenohumeral area, and it acts as the primary shoulder abductor. It arises from the acromion and attaches to the mid humerus.

The rotator cuff compresses the humoral head in the glenoid fossa, thereby stabilizing the glenohumoral joint, and serves to counterbalance the elevating forces of the deltoid, as well as the forces of other muscles acting on the humerus [3,4] . Weakness of the rotator cuff can lead to superior subluxation of the humeral head when the shoulder is abducted beyond 90 degrees, predisposing to impingement syndromes.

The suprascapular nerve innervates the supraspinatus and infraspinatus muscles. Suprascapular nerve injury causes a peripheral neuropathy that is estimated to account for one to two percent of pathologic shoulder conditions [5,6] . Injuries to the suprascapular nerve arise most often from mechanical compression by cysts or tumors. Suprascapular neuropathy causes pain, progressive atrophy, and weakened abduction and external rotation of the shoulder, and can be difficult to distinguish from rotator cuff tears.

Extraglenohumeral structures — Shoulder motion is also dependent upon the acromioclavicular (AC) and sternoclavicular (SC) joints and the scapulothoracic articulation (show figure 1A-1C). Together, they are capable of compensating significantly for decreased motion at the glenohumeral joint due to injury. The acromioclavicular joint is a common site of injury.

Coordination between glenohumeral and scapulothoracic motion is particularly important for shoulder function. Proper scapular motion and stability allows the humeral head to remain properly seated in the glenoid during abduction, provides a solid base from which the rotator cuff muscles can move the humerus, and enables proper elevation of the coracoacromial arch, thereby diminishing the risk of impingement syndrome. The muscles primarily responsible for scapular stability and motion are the trapezius, serratus anterior, rhomboids, and levator scapulae.

The tendon of the long head of the biceps runs in the bicipital groove between the greater and lesser tubercles of the anterior proximal humerus. Transverse tendonous structures (either a continuation of the subscapularis tendon or a distinct transverse humeral ligament [7] ) prevent subluxation of the tendon. Anterior shoulder pain can be caused by inflammation or injury to the biceps tendon.

Although the neural networks of the brachial plexus form proximally to the glenohumeral joint, the major peripheral nerves emanating from the plexus pass inferiorly to the joint. Pain from an injury to the plexus or related peripheral nerves from acute or chronic injury can present as shoulder pain. (See "Overview of upper extremity peripheral nerve syndromes").

PATIENT HISTORY AND PAIN PATTERNS

General approach — Patients with acute shoulder pain often seek treatment following an episode of trauma. Diagnosis in this case can often be made by observation, gentle palpation, and x-ray. Next, the clinician must distinguish between extrinsic and intrinsic causes of shoulder pain. (See "Stepwise clinical approach" below). Once traumatic injury and potentially dangerous extrinsic causes have been excluded (show table 1), the clinician is generally faced with one of several common patterns of shoulder pain, which are described below.

Patients experiencing a problem intrinsic to the shoulder present either with complaints of pain provoked by specific movement(s), stiffness or lack of flexibility, weakness or loss of function, instability, or a combination of these symptoms.

A standard pain history (ie, onset, duration, palliation/provocation, quality, location, and radiation) aids diagnosis. The clinician should inquire about activities that exacerbate symptoms either at work (eg, lifting overhead, painting) or leisure (eg, racquet sports, swimming). In addition, questions about previous injuries and treatment, including past surgery, and about comorbidities such as diabetes (increased risk of adhesive capsulitis) are important.

Anterolateral shoulder pain — Anterolateral shoulder pain aggravated by reaching overhead is a common pain pattern. It is often associated with impingement syndrome and the various stages of rotator cuff tendinopathy (simple strain, uncomplicated tendinopathy, chronic calcific tendinopathy, tendinopathy complicated by tear). Rotator cuff tendinopathy with tendon tear is suspected when pain is complicated by weakness and a notable loss of strength in external rotation or abduction (a loss that is not attributable to poor effort). Adhesive capsulitis (ie, frozen shoulder) is the most likely diagnosis when pain is accompanied by stiffness and a significant loss of movement in external rotation or abduction. Labral tears may present with anterolateral pain, although pain may be deep and poorly localized, and may be associated with instability and a catching sensation.

Conditions affecting the acromioclavicular (AC) joint, such as AC separation, if trauma has occurred, or osteoarthritis, are suspected when pain is well localized (the patient often uses one finger to point to the end of the clavicle). Involvement of the glenohumeral joint is suspected when pain is aggravated by movement in multiple directions. Pain originating from the tendon of the long head of the biceps can create well-localized anterior shoulder pain aggravated by lifting or carrying objects like shopping bags.

Posterior shoulder pain — Posterior shoulder pain is the least common pattern of the intrinsic conditions affecting the shoulder. Rotator cuff tendinopathy involving the external rotators (teres minor and infraspinatus) can cause focal pain, or sometimes referred pain over the scapula. More diffuse pain over the general area of the superior trapezius can be referred from the cervical spine (cervical strain or radiculopathy).

Poorly localized pain — Pain that is poorly localized or vaguely described is often extrinsic. Cervical nerve root impingement can produce sharp pain radiating from the neck into the posterior shoulder area and arm. Shoulder pain can be referred from the neck or abdomen, result from a compression neuropathy, or arise from the bone (show table 1). Poorly localized shoulder pain in the setting of a normal shoulder examination should raise concern for intraabdominal or other extrinsic pathology. Although uncommon, elbow pathology may refer to the shoulder.

Shoulder pain may also reflect psychological overtones of cases under litigation or malingering, however, such diagnoses should be entertained only after true pathology has been ruled out. Intrinsic pathology may cause poorly localized pain. Examples include large rotator cuff tears and avascular necrosis of the humoral head. A large Finnish survey found nonspecific shoulder complaints without clinical findings to correlate with depressive illness and not to correlate with rotator cuff tendinopathy [8] .

Trauma — Fractures and dislocations of the shoulder often occur as a result of blunt trauma. Falls directly onto the shoulder can cause acromioclavicular separation. (See "Acromioclavicular injuries"). Falls or direct blows can cause a clavicle fracture. Falls onto an outstretched arm are the most common cause of proximal humerus fractures. Blunt trauma and, less often, violent muscular contractions, such as those that occur with generalized seizures, can cause glenohumeral dislocations. Generally, the patient can localize pain to the site of injury, and deformity may be present. Post-traumatic shoulder pain can also be referred from intraabdominal injuries causing diaphragmatic irritation (eg, bleeding from liver or spleen).

Sometimes patients present several weeks or months following an injury. Pain may cause the patient not to use the shoulder in the interim leading to adhesive capsulitis. (See "Adhesive capsulitis" above).

ETIOLOGY — The majority of patients who present to primary care clinics with shoulder pain have an intrinsic disorder. Acute symptoms (less than two weeks duration) in patients with a history of recent shoulder trauma are typically due to an acromioclavicular (AC) separation, glenohumeral dislocation, fracture, or rotator cuff tear [9] . In addition to pain, patients may complain that the shoulder is discolored, deformed, or swollen. Significant medical problems, however, such as cardiac ischemia, hepatobiliary disease, and intraabdominal injury, can present with referred shoulder pain (show table 1).

Patient age — In addition to location (see "Patient history and pain patterns" above), several other historical factors can help to differentiate among the intrinsic causes of shoulder pain. Patient age is one such factor (show table 2):

Sports injuries due to overuse ("muscular strain") and subluxation of the glenohumeral joint are most common in adolescents and young adults [9] . "Shoulder separation," due to a sprain of the acromioclavicular ligaments, is also more common in younger patients. It is seen following a fall, with the arm adducted, directly onto the acromion, commonly referred to as the point or tip of the shoulder. (See "Acromioclavicular injuries").

Middle-aged and older individuals more often develop shoulder pain due to rotator cuff lesions, such as supraspinatus tendinopathy and partial or full-thickness tendon tears [10,11] .

Frozen shoulder syndrome and symptomatic osteoarthritis also occur predominately in older patients. Bilateral shoulder involvement, also more common among older patients, suggests an inflammatory process such as polymyalgia rheumatica or rheumatoid arthritis, or rarely hyper or hypothyroidism.

Rotator cuff injury — Rotator cuff injury is among the most common causes of shoulder pain. The rotator cuff tendons, particularly the supraspinatus tendon, are uniquely susceptible to the compressive forces of subacromial impingement (see "Anatomy and biomechanics" above) and dominate the conditions affecting the shoulder, especially in patients over the age of 30 [12] . Improper athletic technique, poor muscular conditioning, poor posture, and failure of the subacromial bursa to protect adequately the supporting tendons may result in a progression of injury from acute inflammation, to calcification, to degenerative thinning, and finally to tendon tear. (See "Rotator cuff tendinopathy" and see "Presentation and diagnosis of rotator cuff tears").

Impingement syndrome — Impingement syndrome is the term used to describe symptoms and signs that result from compression of the rotator cuff tendons and the subacromial bursa between the greater tubercle of the humeral head and the lateral edge of the acromion process [13] .

The symptoms of impingement syndrome are nearly identical to those of rotator cuff tendinopathy (see "Tendinopathy" below). Overhead reaching and positioning cause pain over the outer deltoid. Atrophy of the muscles around the top and back of the shoulder may be apparent if symptoms are longstanding. Crepitus may be felt with attempts to abduct the arm beyond 60 degrees. Patients with rounded shoulders (a down-sloping acromial angle), poor muscular development, and occupations that require repetitive work at or above the shoulder are at greatest risk. (See "Shoulder impingement syndrome").

Tendinopathy — Rotator cuff tendinopathy almost always represents chronic injury to the supraspinatus (abduction) and/or infraspinatus (external rotation) tendons. Tendinopathy usually develops as a consequence of repetitive activity, generally at or above shoulder height, which leads to tendon degeneration and microvascular insult.

Patients complain of shoulder pain aggravated by reaching, pushing, pulling, lifting, positioning the arm above the shoulder level, or lying on the affected side. Most patients do not describe an injury or fall. The patient typically places the hand over the outer deltoid, rubbing the muscle in an up-and-down direction when describing the pain. Common shoulder tendinopathy must be distinguished from frozen shoulder (loss of range of motion), rotator cuff tendon tear (persistent weakness), and biceps tendinopathy (painful arm flexion). (See "Rotator cuff tendinopathy").

Tendon tear — Rotator cuff tendon tears (ie, loss of the normal integrity of the supraspinatus tendon, the infraspinatus tendon, or both) occur as the end result of chronic subacromial impingement, progressive tendon degeneration, traumatic injury, or a combination of these factors. Tears occur primarily in the supraspinatus tendon. (See "Presentation and diagnosis of rotator cuff tears").

Patients complain of shoulder weakness, pain over the anterolateral shoulder, or sometimes the upper back, and a popping or catching sensation when the shoulder is moved. Night pain is common and often affects sleep because the patient is unable to keep the arm in a position that does not elicit pain (ie, adducted without rotation).

Injuries most commonly associated with acute rotator cuff tendon tears include falls onto the outstretched arm, falls directly onto the outer shoulder, vigorous pulling (such as on a lawn mower cable), and unusual heavy pushing and pulling. Acute, subacute, and chronic tears all occur most often in patients over the age of 40 with a history of impingement [10,11] .

Shoulder function will be preserved if the tear parallels the direction of the tendon fibers or is small in size, and the patient will complain only of shoulder pain, pain with direct pressure, and pain aggravated by active reaching, lifting, pushing, and pulling. However, if the tear is large, affecting both the supraspinatus and infraspinatus tendons, and is transverse in direction (total interruption of the tendon with muscle retraction), the patient will complain of weakness, the typical symptoms of tendinopathy, and dramatic loss of function - an inability to reach overhead, lift with an outstretched arm, and an impairment of pushing and pulling.

Labral tear — Many of the same mechanisms that produce rotator cuff injury can also produce tears of the labrum. Athletes who engage in repetitive overhead activities that load the shoulder (eg, baseball pitching, tennis serving, swimming) are at greater risk for such injuries. Symptoms include deep shoulder pain, catching sensation, instability, and crepitus.

Adhesive capsulitis — Adhesive capsulitis (commonly referred to as frozen shoulder) refers to a stiffened glenohumeral joint that has lost significant range of motion (abduction and rotation). It is a reversible contraction of the joint capsule in almost all cases. (See "Frozen shoulder"). Any shoulder pain or disability that causes the patient not to use his or her shoulder can lead to diminished joint mobility and ultimately adhesive capsulitis.

The most common cause is rotator cuff tendinopathy. Diabetes mellitus also puts patients at significantly increased risk of developing adhesive capsulitis [14-16] . Other diseases that increase the risk for frozen shoulder, most likely due to immobility, include stroke, Parkinson's disease, and chronic pulmonary disease. Low pain tolerance, poor compliance with exercise therapy, and immobilization in a sling (eg, for treatment of a shoulder or elbow injury) can also contribute to the development of a frozen shoulder.

While the symptoms and signs of adhesive capsulitis and rotator cuff tendinopathy overlap, presentation often differs. Patients with adhesive capsulitis complain primarily of stiffness, although they may have pain, and always demonstrate diminished passive range of motion. Patients with rotator cuff tendinopathy typically complain of pain with active motion, while passive motion remains normal (in the absence of guarding). The loss of motion associated with a frozen shoulder causes various degrees of impaired function, including limited reaching (eg, overhead, across the chest) and limited rotation (eg, unable to scratch the back, difficulty putting on a coat). Patients with rotator cuff tendinopathy suffer similar restrictions, but their limitations are due more to pain than an absolute loss of movement. Patients with either condition may experience increased pain at night either from direct pressure or shoulder movement.

Acromioclavicular pain — The acromioclavicular (AC) joint is another common site of pathology in patients with shoulder complaints. The joint is susceptible to arthritic change and trauma ("shoulder separation"). (See "Acromioclavicular injuries").

Patients complain of anterior shoulder pain, deformity, or both and often point to the AC joint when describing their symptoms. Patients with osteoarthritis may describe a grinding or popping sensation when reaching overhead or across the chest. The adduction part of the Apley scratch test can elicit this sign. (See "Joint rotation" below). Patients with an acute separation usually relate a history of falling directly onto the shoulder. Those with second and third-degree sprains typically have a palpable step-off deformity at the AC joint. They often hold their arm close to the chest and resist rotation and elevation.

Biceps tendinopathy/rupture — Biceps tendinopathy is an inflammation of the long head of the biceps tendon as it passes through the bicipital groove of the anterior proximal humerus. Repetitive lifting, and to a lesser extent overhead reaching, leads to inflammation, microtearing, and, if untreated, degenerative change. Unusual or vigorous lifting in the setting of a chronically inflamed tendon can lead to spontaneous rupture. (See "Biceps tendonitis and rupture").

The patient complains of anterior shoulder pain aggravated by lifting, carrying objects like shopping bags, and overhead reaching. A dramatic worsening of symptoms and description of a lump just above the antecubital fossa suggests an acute long head tendon rupture. Weakness is most often attributed to the pain of active tendinopathy. Rupture of the long head of the biceps rarely is associated with significant weakness; the brachioradialis and the short head of the biceps account for 80 to 85 percent of the strength of elbow flexion.

Multidirectional shoulder instability — Multidirectional instability of the shoulder is synonymous with "subluxation," "loose" shoulder, or partial dislocation. It is more common in young women with poor muscular development, patients with large rotator cuff tendon tears (loss of muscular support), and in athletes under the age of 40, especially swimmers and throwers. The symptoms are often vague and nonspecific ("dead arm," looseness, or crepitation) unless the condition is complicated by rotator cuff tendinopathy. Typically the patient has an excessive range of motion, particularly with internal and external rotation. (See "Multidirectional instability of the shoulder").

Glenohumeral osteoarthritis — Osteoarthritis of the glenohumeral joint represents wear-and-tear of the articular cartilage of the glenoid, labrum, and humeral head. It is an uncommon problem that is generally preceded by trauma, although the injury may have occurred years earlier. Injuries that are associated with the development of osteoarthritis include previous dislocation, humeral head or neck fracture, large rotator cuff tendon tears (loss of musculotendinous support), and rheumatoid arthritis. Patients complain of the gradual development of anterior or deep shoulder pain and stiffness over a period of months to years. Both active and passive motion, particularly abduction and external rotation, become diminished as articular degeneration grows more severe. (See "Glenohumeral osteoarthritis").

Because osteoarthritis of the shoulder is so rare, clinicians should also consider the possibility of metabolic disease (eg, hemochromatosis) as a cause.

Scapular instability — Weakness of the muscles that stabilize the scapula predisposes the patient to impingement syndrome. (See "Anatomy and biomechanics" above).

Although a difficult diagnosis to make, scapular instability may manifest with abnormal shoulder motion, shoulder weakness, or mild scapular winging in patients with symptoms suggestive of rotator cuff pathology. Improvement of abduction strength when performed while the scapula is stabilized by the examiner suggests weakness of the scapula stabilizers. Less commonly, nerve injury can cause winging of the scapula. (See "Scapulothoracic motion and strength" below and see "Nerve entrapment syndromes of the shoulder").

Scapulothoracic bursitis — Scapulothoracic (subscapular) bursitis may result from mechanical pressure and friction, most often between the superior-medial angle of the scapula and the adjacent second and third ribs. Poor muscular development in thin patients, kyphotic posture, repetitive to-and-fro motion of the scapula (ironing, assembly work, throwing sports), and direct pressure are common causes.

Affected patients complain of localized pain over the upper back or a popping sound whenever the shoulder is shrugged. A typical patient has poor muscular development, an asthenic physique, and poor posture.

Referred pain — Referred pain to the shoulder may be seen in a variety of clinical settings:

• Neural impingement at the level of the cervical spine due to disc herniation (generally at the C5 or C6 levels) or spinal stenosis. (See "Evaluation of the patient with neck pain and cervical spine disorders").

• Peripheral nerve entrapment distal to the spinal column, with involvement of either the long thoracic or suprascapular nerves. (See "Nerve entrapment syndromes of the shoulder").

• Diaphragmatic irritation (eg, from splenic laceration, perforated viscus, or ruptured ectopic pregnancy), intrathoracic tumors, and distension of the hepatic capsule can produce ipsilateral shoulder pain. (See "Cancer pain syndromes" and see "Pancoast's syndrome and superior (pulmonary) sulcus tumors").

• Myocardial ischemia with associated left shoulder pain.

A distinguishing characteristic of referred pain, in contrast to intrinsic shoulder problems, is that shoulder movement is normal and does not alter the character of the pain. A careful history can often distinguish among the causes of referred shoulder pain.

EXAMINATION — Examination of the shoulder is guided by the history. Although some components of the examination, such as inspection and a basic neurovascular evaluation are universal, other components are performed selectively based upon the diagnoses being entertained. What follows is an overview of the physical examination of the shoulder, which includes both preliminary screening tools and tests designed to evaluate for specific diagnoses. A framework for determining when to perform specific maneuvers is provided in the shoulder pain algorithm and the section on clinical evaluation below. (See "Stepwise clinical approach" below).

The sensitivity and specificity of the various diagnostic maneuvers are given when well-performed studies are available, but data are limited. Studies have found relatively poor interobserver agreement in the interpretation of clinical examinations of the shoulder, even by highly experienced physician and non physician examiners (show table 3) [17,18] .

Inspection — The clinician should inspect the shoulder looking for any obvious deformity or asymmetry, muscle atrophy, or abnormal motion. A clavicle fracture, anterior glenohumeral dislocation, or high-grade acromioclavicular (AC) sprain is often immediately recognizable on the basis of the deformity present. As an example, the patient with an anterior glenohumeral dislocation typically holds the arm in slight abduction with external rotation, and a concavity below the acromion is visible. Atrophy can develop with chronic rotator cuff tears or nerve injury, such as subscapular nerve entrapment.

If possible, the clinician can observe shoulder motion by watching the patient take off a coat or don an examining gown. Unilateral abnormalities in motion, such as an inability to lower the arm smoothly (possible supraspinatus tear) or the use of accessory muscles to raise the arm (possible impingement syndrome), may provide diagnostic clues.

Neurovascular assessment — A screening neurovascular examination should be performed on every patient to confirm peripheral nerve function and adequate perfusion. If the clinician suspects neurologic injury on the basis of history or preliminary examination findings, then a thorough examination is needed. (See "The detailed neurologic examination in adults").

Palpation — As with the shoulder examination generally, palpation is often performed selectively and is guided by the history and inspection of the shoulder. Involvement of the acromioclavicular (AC) or sternoclavicular (SC) joints, or the subscapular bursa, is determined by direct palpation. If referred pain from an intraabdominal source is suspected, the abdomen should be carefully examined.

In patients with trauma, gentle palpation may reveal focal tenderness or a step-off in the clavicle or AC joint, consistent with a fracture or ligament rupture. Glenohumeral dislocation can manifest as a palpable concavity in the subacromial space along with a bony prominence anteriorly (displaced humeral head).

For patients with nontraumatic intrinsic shoulder problems, at a minimum, systematic palpation of high-yield sites is needed. These sites include:

• The clavicle including SC and AC joints
• The acromion and the subacromial space
• The bicipital groove, and greater and lesser tubercles
• The scapular spine and adjacent musculature
• The cervical spine

Because the glenohumeral joint lies deep within the soft tissues, small or moderate sized effusions are usually not detectable. Warmth or redness may not be observed even with acute inflammation. Therefore, ultrasound imaging may be required to establish the presence of an effusion. However, demonstrating excessive synovial fluid by joint aspiration remains the definitive test.

Joint tenderness — Tenderness of the acromioclavicular (AC) and sternoclavicular (SC) joints is assessed as follows. The anterior, lateral, and posterior edges of the acromion are demarcated. The AC joint is palpated at the juncture of the acromion and distal clavicle, approximately one and one-half inches proximally from the lateral edge of the acromion (show picture 1). The SC joint is palpated at the juncture of the proximal end of the clavicle and the lateral edge of the sternum, approximately one inch from the midline of the body.

If subscapular pathology is suspected, the subscapular bursa can be palpated at the junction of the superior-medial angle of the scapula and the closest underlying rib; exposure of this bursa requires full adduction of the ipsilateral arm by asking the patient to hold his or her opposite shoulder (show picture 2).

Subacromial space tenderness — The acromial process of the scapula is covered by the deltoid muscle. The supraspinatus tendon attaches to the greater tubercle, located just under the anterior third of the acromion. The subacromial structures may be indirectly examined by palpating directly below the acromion (show picture 3). Alternatively, these structures can be moved anteriorly and better palpated by extending the shoulder [19] . This is accomplished by gently lifting the elbow of the adducted arm posteriorly (show picture 4). Tenderness is consistent with impingement syndrome, rotator cuff tendinopathy, rotator cuff tear, subacromial bursitis, muscle contusion, or a humeral lesion.

Range of motion — Motion testing is performed to help determine the site and nature of intrinsic shoulder pain. If the patient is able to perform the "NFL touchdown sign" test without difficulty, there is no need for further range of motion testing. Any problems with the test indicate a need for further evaluation. Generally, active motion is assessed before passive. Symptom reproduction with active motion testing suggests a contractile structure (ie, muscle, tendon) is injured. Symptom reproduction with passive motion testing suggests a noncontractile structure (ie, bone, cartilage) is causing pain.

Preliminary screen — The "NFL touchdown sign" (raising both arms from the sides to straight overhead) is a simple active maneuver used to assess range of motion of the shoulder joint and the basic strength of abduction (show picture 5). Full abduction requires a normal glenohumeral joint, intact rotator cuff tendons, a functional AC joint, and reasonably well developed deltoid and rotator cuff muscles. The following findings may be noted during this test:

• Full painless motion excludes glenohumeral pathology and suggests an extrinsic source of pain.

• Severe pain is consistent with acute rotator cuff tendinopathy and inflammatory or septic arthritis.

• True weakness is associated with rotator cuff tendon tear, but it can also be caused by severe atrophy of the rotator cuff and deltoid muscles, severe C5 radiculopathy, or supracapsular nerve palsy. Adhesive capsulitis will limit motion and may cause pain.

• Patients who have had trauma resulting in dislocation, AC joint separation, or fracture will rarely even attempt the maneuver.

Joint rotation — The Apley scratch tests are used to assess motion
of the shoulder joint. Full rotation requires a normal
glenohumeral joint, intact rotator cuff tendons, and reasonably well
developed rotator cuff muscles. Thus, rotation is limited with:

• Acute inflammation of rotator cuff tendinopathy
• Adhesive capsulitis (ie, frozen shoulder)
• Arthritis of the glenohumeral joint (osteoarthritis or inflammatory arthritis)
• The impairment of rotation correlates well with the severity of these conditions. Side-to-side comparison provides the most practical and objective measurement of rotation.

The Apley scratch tests are simple to perform (show picture 6).

To assess adduction more thoroughly, the patient is asked to reach across his or her chest and touch the opposite shoulder (show picture 6). A patient with acromioclavicular pathology will have difficulty with this maneuver.

To assess external rotation and abduction, the patient is asked to reach behind his or her head and touch the superior medial tip of the opposite scapula (show picture 6). A patient with normal function can reach approximately the level of the T4 spinous process.

To assess internal rotation and adduction, the patient is asked to reach behind his or her back and touch the inferior tip of the opposite scapula (show picture 6). A patient with normal function can reach approximately the level of the T8 spinous process [19] .

In addition to assessment, the Apley scratch maneuvers are used to follow objectively the response to treatment. As an example, effective conservative therapy might enable a patient who could reach only the level of the L1 spinous process to reach the T10 level.

Active range of motion can also be assessed by having the patient perform each shoulder motion (flexion, extension, abduction, adduction, internal and external rotation) in isolation and comparing sides (show table 4). The examiner can brace the superior trapezius with one hand to prevent the use of accessory muscles in abduction.

Scapulothoracic motion and strength — Coordination of motion at the glenohumeral joint and the scapulothoracic articulation is important for normal shoulder function. (See "Anatomy and biomechanics" above). Normally, once the shoulder is abducted more than 20 degrees, further abduction occurs at these articulations in a 2:1 ratio: for every two degrees of abduction at the glenohumeral joint, the scapulothoracic articulation moves one degree. Normal motion is smooth and symmetric.

Clinicians can assess scapulothoracic motion and abduction by observing the undressed patient from behind while simultaneous shoulder abduction is performed.

Another technique is to place a thumb on or to hold the inferior tip of each scapula and have the patient abduct the arm.

Patients can compensate for decreased glenohumeral motion by using scapulothoracic motion, which is capable of up to 90 degrees of abduction. Such compensation is manifest as shoulder shrugging. Abnormal motion most often occurs either to compensate for an injury that limits glenohumeral movement or because the stabilizing muscles of the scapula are weak, in which case there may be no asymmetry.

Scapular instability, whether from nerve damage or muscle weakness alone, can be evaluated by either the push-off or stabilization tests. In the former, the patient pushes against a wall, as if performing an upright push-up. Instability manifests as scapular winging. In the scapular stabilization test, the patient flexes his or her shoulder, while the examiner manually compresses the patient's scapula against the ribcage [20] . Elimination of pain and improved shoulder motion (shoulder flexion ≥150 degrees) and strength suggests scapular instability is causing the patient's symptoms. Evaluation of supraspinatus strength can also be performed with and without scapular stabilization [21] . Pain relief and improved strength with stabilization suggest that scapular instability is contributing to the patient's symptoms. (See "Assessment of abduction and the supraspinatus" below).

Passive range of motion — If active motion is limited, passive range of motion should be assessed for each major movement of the shoulder. Such testing helps the clinician to distinguish between motion limitations caused by pain and those caused by a structural constraint (eg, adhesive capsulitis or glenohumeral arthritis).

Strength and tendon integrity — Strength testing is used both to assess neurologic integrity and to identify injury. Significant focal weakness, in the setting of lancinating pain radiating from the neck along the posterior shoulder and back or into the arm, is consistent with cervical nerve root impingement or peripheral nerve entrapment. (See "Evaluation of the patient with neck pain and cervical spine disorders"). Weakness associated with nonradiating, dull or achy pain is more consistent with a rotator cuff or other muscle tear.

With intrinsic pain, the essential distinction to be made by strength tests is between pain without weakness (tendinopathy) and pain with weakness (tendon tear). Several tests exist to evaluate the strength of specific muscle groups [19,22] .

Assessment of abduction and the supraspinatus — Of the three abductors of the shoulder (deltoid, supraspinatus, and trapezius muscles), the supraspinatus is responsible for abduction in the mid arc (approximately 30 to 90 degrees). Thus, isometric testing of the supraspinatus tendon in midarc assesses the strength, integrity, and degree of inflammation of the supraspinatus tendon:

Pain with normal strength is seen in patients with rotator cuff tendinopathy (affecting the supraspinatus).

Pain and weakness are seen in patients with rotator cuff tendinopathy or rotator cuff tendon tear. It may also occur with radiculopathy.
Weakness alone may be seen in patients with rotator cuff tear, muscular atrophy, weakness of muscles stabilizing the scapula, C5 radiculopathy, or suprascapular nerve palsy.

Supraspinatus isometric strength is assessed by having the patient abduct the arm about 45 degrees with about 30 degrees of forward flexion, and then having the patient resist, while the examiner attempts to adduct the arm (show picture 7).

This isometric test of supraspinatus strength is highly sensitive but nonspecific for the diagnosis of supraspinatus tendon injury [23] . The severity of functional impairment during testing does not correlate well with the size of the tear.

The integrity of the supraspinatus tendon can also be assessed with the "drop arm" test and the active painful arc test. The drop arm test assesses the ability of the patient to lower his or her arms from a fully abducted position. A positive test occurs when the patient is unable to lower the affected arm with the same smooth coordinated motion as the unaffected arm. It is highly specific but insensitive for the diagnosis of rotator cuff tear [24] .

The active painful arc test (not to be confused with the Neer test, an impingement test performed passively) is used to assess rotator cuff tendinopathy (show picture 8). Pain with active abduction beyond 90 degrees marks a positive test.

The "empty can" (or Jobe's) test is another means of evaluating supraspinatus function (show picture 9). It is performed by having the patient place a straight arm in about 90 degrees of abduction and 30 degrees of forward flexion, and then internally rotating the shoulder completely. The patient then resists the clinician's attempts to adduct the arm. Pain without weakness is consistent with tendinopathy; pain with weakness is consistent with tendon tear.

When pain limits the ability to evaluate strength in abduction, the clinician can assess the integrity of the axillary nerve by having the patient fully adduct the shoulder and then abduct against some resistance [25] .

Assessment of external rotation and the infraspinatus — The infraspinatus muscle is responsible for external rotation with the teres minor muscle contributing to a minor degree. Isometric testing of the infraspinatus tendon in neutral position is used to assess the strength and integrity of the infraspinatus tendon, as well as pain indicative of injury (show picture 10). Testing with resistance bands can be used to further evaluate the functional strength of external shoulder rotation (show picture 11). The following findings may be noted:

-Pain and normal strength are consistent with rotator cuff tendinopathy.

-Pain and unilateral weakness are consistent with rotator cuff tendon tear, C5 radiculopathy, or supracapsular nerve palsy.

-Weakness alone is consistent with rotator cuff tear, muscular atrophy, C5 radiculopathy, or suprascapular nerve palsy.

Bilateral weakness is consistent with poor muscular development, bilateral rotator cuff tears, bilateral glenohumeral arthritis, or other chronic conditions.
Assessment of internal rotation and the subscapularis — The subscapularis is the rotator cuff muscle primarily responsible for internal rotation. Its strength can be assessed using the push-off (or Gerber's lift-off) test. This test is performed by having the patient place one hand behind his or her back and push posteriorly against resistance (show picture 12). As with other strength tests, the essential distinction is between pain with weakness (tendon tear) and pain without weakness (tendinopathy).

Assessment of biceps tendon — Injury or inflammation of the long head of the biceps tendon can cause anterior shoulder pain. In addition to direct palpation, two simple tests allow for evaluation of this tendon. To perform the "Speed's" test, the patient forward flexes the shoulder about 30 degrees against the clinician's resistance, while keeping the elbow fully extended and the arm fully supinated (show picture 13). To perform the "Yergason's" test, the patient holds his or her arm adducted with elbow flexed to 90 degrees and the arm fully pronated. The patient holds the examiner's hand and attempts to supinate it while the examiner resists (show picture 13). Either test is considered positive for bicipital tendinopathy, if it elicits pain in the bicipital groove.

Impingement — The rotator cuff tendons and subacromial bursa are located in the narrow space between the acromial process of the scapula and the top of the humeral head making them susceptible to injury. (See "Anatomy and biomechanics" above). Testing for impingement is an important part of the shoulder examination for any patient in whom the diagnosis of rotator cuff injury is being considered [22] . If impingement is present clinically, isometric strength testing of individual rotator cuff tendons follows to determine which tendons are inflamed (most commonly affected is the supraspinatus; the infraspinatus can also be involved). (See "Strength and tendon integrity" above).

Two straightforward tests for impingement are described below.

Passive painful arc (Neer) test — The "passive painful arc maneuver" (passively flexing the glenohumeral joint while simultaneously preventing shoulder shrugging) is used to assess the degree of impingement (show picture 14). The clinician should note whether the patient is guarding by shrugging as the maneuver is performed. The severity of impingement and rotator cuff tendinopathy is determined by the angle at which the arc becomes painful.

- Pain at 90 degrees is consistent with mild impingement.
- Pain at 60 to 70 degrees is consistent with moderate impingement.
- Pain at 45 degrees or below is consistent with severe impingement.


One study of 125 patients with painful shoulders found this test to be specific but not sensitive; a negative test does not rule out rotator cuff pathology [26] .

Flexion with internal rotation (Hawkins) test — In this test, the clinician stabilizes the shoulder with one hand and, with the patient's elbow flexed 90 degrees, internally rotates the shoulder using the other hand (show picture 15). Shoulder pain elicited by internal rotation represents a positive test.
Yocum's test — This test of impingement involves placing the hand of the affected side on the patient's unaffected shoulder and then raising the elbow, without elevating the shoulder. Shoulder pain elicited by raising the elbow represents a positive test.

Instability — General glenohumeral instability or looseness may be the cause of shoulder discomfort in young throwing athletes, people with weak shoulder musculature, and patients who have sustained a rotator cuff tear. Instability may be multi or unidirectional; anterior and inferior laxity are most common. Several tests are used to assess this problem [27] .

Sulcus sign — Downward movement of the humeral head is influenced by the tone and bulk of the deltoid, the tone and thickness of the supraspinatus tendon, and the redundancy of the glenohumeral capsule.
The sulcus sign maneuver evaluates the looseness of the shoulder (especially the subacromial space) and is used to assess the patient's tolerance of the Codman pendulum stretch exercise (show picture 16). The following findings may be noted:

- No movement can be seen in patients with extreme guarding or tension, fibromyalgia, or an overly developed deltoid muscle.

- One-quarter inch of movement is normal.


- One-half inch or greater movement is consistent with hypermobility (subluxation).


Apprehension, relocation, and release tests — These tests work in combination and are most easily performed with the patient supine. (show picture 17). To perform the apprehension test, the patient is asked to place the symptomatic arm in the throwing position (shoulder abducted and externally rotated). Next, the clinician braces the posterior shoulder with one hand while using the other hand to push back on the wrist with steady pressure, thereby increasing the abduction and external rotation of the shoulder (as if he or she were attempting to dislocate the shoulder anteriorly). Any sensation of impending dislocation at any time on the part of the patient constitutes a positive test.

The relocation test is begun at the end of the apprehension test and is performed by simply reversing the forces being exerted by the examiner. Forced abduction and external rotation are stopped, and the clinician moves the hand that was bracing the posterior shoulder to the anterior shoulder. The examiner then pushes the humerus posteriorly (as if he or she were attempting to relocate the shoulder). Relief of pain or of the sensation of impending dislocation on the part of the patient represents a positive test.

The release test is performed at the end of the relocation test when the clinician abruptly stops pushing the humerus posteriorly. Again, any sensation of impending dislocation on the part of the patient constitutes a positive test.

One meta-analysis of these tests found both the relocation and release tests to have reasonable sensitivity (85 percent) and specificity (87 percent) for the detection of glenohumeral instability [27] . The authors warn, however, that most of the studies reviewed involved patients in orthopedic clinics, and it remains uncertain whether their findings apply to more general populations.

STEPWISE CLINICAL APPROACH — For many primary care clinicians, determining how best to evaluate patients with shoulder pain can be difficult. The anatomy of the shoulder is complex and the differential diagnosis broad. Fortunately, patients with shoulder pathology most often present in stereotypical fashion. By following the basic approach outlined here (show algorithm 1), clinicians should be able to diagnose and either manage or refer appropriately the great majority of patients with shoulder complaints.

Step one: traumatic versus nontraumatic — The first step is to determine whether a traumatic injury is present. Most often this determination is straightforward based on the patient's history, although delayed presentations do occur, for example, with mild acromioclavicular (AC) separations. Examination may reveal deformity, and the patient is nearly always able to localize the pain. Plain x-rays make or confirm the diagnosis.

The most common shoulder injuries from minor blunt trauma include: fractures of the clavicle and proximal humerus, dislocations of the glenohumeral joint, and sprains of the AC joint.

Should x-rays fail to reveal an injury but the patient's symptoms persist, a soft tissue injury (eg, rotator cuff tear) is likely and the clinician should perform an appropriate assessment (step three below).

Step two: extrinsic versus intrinsic — Once traumatic injury has been excluded, the second step is to determine whether the patient's shoulder pain is a referred symptom caused by pathology extrinsic to the shoulder (show table 1), or intrinsic. A careful history and preliminary examination should enable the clinician to make this distinction. Often, if the cause is extrinsic, the patient has difficulty localizing the pain. The pain itself is often vague, if it is referred from a thoracic or abdominal source, or sharp with radiation if it is from a neurologic source.

The history may reveal details or associated symptoms of concern:

• Cervical nerve root impingement may be present in the patient with sharp pain radiating from the neck into the posterior shoulder area or arm.
• Splenic injury may be present in the patient with shoulder pain recently involved in an automobile accident in which the shoulder was not initially injured.
• Myocardial ischemia may be present in the patient who experiences diaphoresis or dyspnea with each episode of shoulder pain.

Examination of patients with an extrinsic cause of shoulder pain most often reveals painless range of motion and no asymmetry in appearance, motion, or strength when compared with the opposite shoulder.

Step three: glenohumeral versus extraglenohumeral — If an intrinsic problem is present, the clinician must next determine whether its focus is the glenohumeral joint or not. Generally the patient is able to localize the pain from extraglenohumeral pathology to a specific site, such as the bicipital groove for biceps tendinopathy, or the acromioclavicular (AC) joint for AC osteoarthritis. Weakness of the stabilizing muscles of the scapula is a notable exception, and this diagnosis can be difficult to make. A careful assessment of scapulothoracic motion and observation for any scapular winging can aid diagnosis.

In all cases of extraglenohumeral pathology, passive range of motion of the glenohumeral joint should be normal, although assessment may be limited by pain or guarding. With problems related directly to the glenohumeral joint and its surrounding structures, examination should reveal some abnormality, be it pain, weakness, or abnormal motion.

Step four: differentiating glenohumeral pathology — Once extraglenohumeral pathology has been ruled out, the clinician must try to determine which of several glenohumeral abnormalities is causing the patient's symptoms. Assessment of shoulder range of motion, strength, and signs of impingement will help to distinguish among such diagnoses as rotator cuff tendinopathy, rotator cuff tear, and adhesive capsulitis. A summary of the key examination findings for each common diagnosis is found immediately below. Further detail is found in the text (show table 3). (See "Examination" above).

Impingement and rotator cuff tendinopathy — Anterolateral shoulder pain that increases with overhead reaching; pain with supraspinatus testing and/or external rotation; positive impingement tests

Rotator cuff tendon tear — Older patient (age >40); pain and weakness with supraspinatus testing and/or external rotation; positive impingement tests

Adhesive capsulitis — History of diabetes or immobilizing disability (eg, stroke, injury requiring sling); diminished active and passive range of motion

Glenohumeral osteoarthritis — History of shoulder trauma; pain; diminished active and passive range of motion; x-ray shows sclerosis and diminished joint space

Multidirectional shoulder instability — Younger patient (age <40); positive sulcus sign; positive instability test

INJECTION TESTS — When the examination suggests the presence of a specific disorder, certain tests can be performed to confirm the diagnosis.

Lidocaine injection test — The lidocaine injection test is used to (show picture 18):

-Exclude glenohumeral joint involvement
-Confirm rotator cuff tendinopathy
-Exclude rotator cuff tear
-Determine the degree of frozen shoulder

Patients with a rotator cuff tear will have persistent weakness despite pain relief with injection, while those with rotator cuff tendinopathy will have normal strength in association with pain relief. Patients with a frozen shoulder will have persistent loss of range of motion. Dramatic reduction in pain and improvement in overall shoulder function after injection of the subacromial bursa effectively rules out a significant glenohumeral joint process.

The lidocaine injection test in the subacromial bursa is indicated when the history and physical examination cannot effectively exclude an underlying rotator cuff tendon tear, a developing frozen shoulder, or concurrent involvement of the acromioclavicular (AC) joint.

Local anesthetic block at the bicipital groove — Bicipital tendinopathy can be confirmed by local anesthetic block (show picture 19). This is most often indicated in the patient presenting with anterior shoulder pain with an equivocal physical examination demonstrating signs of bicipital tendinopathy and rotator cuff tendinopathy, especially involving the subscapularis tendon (an internal rotator and adductor of the shoulder).

RADIOGRAPHIC STUDIES — Diagnostic imaging of the shoulder may be valuable when directed by the history and physical examination. A variety of modalities may be employed. A complete discussion of these studies is found elsewhere. (See "Radiologic evaluation of the painful shoulder").

Plain radiographs — Plain radiographs of the shoulder generally have limited benefit in the evaluation of nontraumatic shoulder pain. This was illustrated in a study of 312 patients seen in an emergency department setting for shoulder pain: only 37 of the 185 shoulder films (20 percent) were therapeutically informative, ie, identified conditions requiring specific therapy such as a fracture or dislocation [28] . No patient without a shoulder deformity or a precipitating fall had an informative radiograph.

A subsequent study of 206 patients used the presence or absence of the following features: history of falling, swelling, rest pain, abnormalities in range of motion, and obvious deformities of the shoulder, to help identify those in whom a shoulder radiograph was unlikely to be informative [29] . Among those without obvious shoulder deformities and swelling, the following three groups had relatively insignificant radiographs:

Patients without rest pain who had fallen. No significant radiographic findings were found among 18 patients with these features.

Patients who had fallen, had rest pain, and had normal range of motion. No therapeutically informative radiographs were reported in 10 such patients.
Patients who had not fallen. Only 1 of 107 such patients had a lytic lesion discovered on radiograph; this individual was already known to have multiple myeloma.

While there are no specific guidelines for when radiography is indicated, we generally recommend obtaining plain films in patients who have lost range of motion, particularly when there is severe pain, and after trauma. Plain films can identify the following:

• Fractures of the proximal humerus, clavicle, and scapula

Glenohumeral dislocations

• Glenohumeral osteoarthritis (show radiograph 1)
• Acromioclavicular (AC) joint arthritis or injury (show radiograph 2)
• Sternoclavicular (SC) joint arthritis (apical lordotic views of the chest)

In addition, indirect evidence of rotator cuff thinning, tear, or both may be evident on plain x-ray of the shoulder (show radiograph 3). A subacromial space measurement less than 1 cm suggests thinning with or without tear, which can be confirmed by MRI.

When plain films are obtained in a patient with a history of trauma, both AP and axillary views are warranted since some conditions can be missed on the former alone.

Magnetic resonance imaging — MRI is the preferred imaging study for patients with suspected impingement and rotator cuff injury. A normal MRI suggests that the likelihood of a rotator cuff tear is less than 10 percent [30-32] . On the other hand, MRI findings for rotator cuff tears are not highly specific, particularly in older patients [33] . The sensitivity and specificity of MRI for the diagnosis of impingement are approximately 93 and 87 percent, respectively [34] . MRI is also useful in the evaluation of avascular necrosis, biceps tendinopathy and rupture, inflammatory processes, and tumors [35] .

Ultrasonography — In the hands of skilled operators, the diagnostic accuracy of ultrasound has been found to be the equivalent of MRI in identifying rotator cuff tears, labral tears, and biceps tendon tears and dislocations [36-42] . Ultrasound is less expensive than MRI and preferred by patients [42,43] .

Arthrography — Arthrography has largely been replaced by MRI for the diagnosis of rotator cuff disorders. It is specific for rotator cuff tears, but it has a low sensitivity since it cannot detect partial-thickness tears nor associated soft tissue injuries [44] . Arthrography still may be useful for evaluating frozen shoulder and may even be therapeutic. (See "Frozen shoulder").

INFORMATION FOR PATIENTS — Educational materials on this topic are available for patients. (See "Patient information: Rotator cuff tendinitis and tear" and see "Patient information: Biceps tendonitis" and see "Patient information: Bursitis"). We encourage you to print or e-mail these topics, or to refer patients to our public web site www.uptodate.com/patients, which includes these and other topics.