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MRI revealed an extensive joint effusion extending outside the joint capsule and into the surrounding shoulder bursae. There was abnormal signal intensity in the adjacent muscles, suggesting an element of associated myofasciitis. There was marrow edema seen in the epiphysis of the humerus, suggestive of early osteomyelitis or reactive hyperemia related to a septic joint.

 

Arthrocentesis fluid analysis revealed:

  • WBC=187,770; RBC=74,000; Lymphocytes=90; Monocytes=2; Eosinophils=8; Glucose=7;
  • Gram Stain=Gram Positive Cocci; Crystals=None
  • The patient was empirically treated with Vancomycin and Ceftriaxone. She was taken to the OR by orthopedics for a wash out of her septic shoulder.
  • Shoulder joint arthrocentisis cultures and intra-operative cultures yielded group A strep species. Antibiotic coverage was narrowed down to Ceftriaxone and a PICC line was placed for continued parenteral antibiotics.


Background: Septic arthritis of the shoulder alone is uncommon in adolescents and adults. There are only a few published case reports of glenohumeral subluxation secondary to septic arthritis, and these occurred after local corticosteroid injections, IV drug abuse, and in ESRD patients. Furthermore, there is only one case report in the English medical literature of a complete dislocation of the glenohumeral joint following septic arthritis, and this case occurred in an IV drug abuser. To the author’s knowledge, there are no prior adolescent case reports of shoulder subluxation associated with septic arthritis.

Epidemiology: Septic arthritis is an acute bacterial joint infection. There are an estimated 20,000 cases of septic arthritis diagnosed per year, with an annual incidence of 5.5 to 12.2 cases per 100,000 children. Half of all cases occur by 2 years of age and about 75% of cases occur by 5 years of age.

Septic arthritis is most likely to occur in the joints of the lower extremity. In infants and children, the hip and knee are most often involved. In adults, the knee is the site of infection 50% of the time, followed by the hip (20%), shoulder (8%), ankle (7%), and wrist (7%). Infections are almost always a monoarticular process, with fewer than 10% polyarticular involvement in the pediatric population and fewer than 20% in adults.

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Etiology: The majority of septic joint infections are of hematogenous origin, although spread from a contiguous focus or by direct inoculation may also occur. Septic arthritis may occur concomitantly with osteomyelitis, with infection spreading from bone to joint or vice-versa. Direct inoculation usually results from penetrating trauma or iatrogenically via procedures that invade the synovium, such as arthrocentesis, joint injection, and arthroscopy. Instrumentation of the urinary and intestinal tracts may also predispose patients to joint infection. Both sexually active adolescents and neonates are at increased risk for gonococcal septic arthritis. IV drug abusers, immunocompromised populations, and patients with rheumatologic joint disease are all at increased risk for bacterial joint infections.

Bacterial pathogens in septic arthritis vary based on the age and population of the affected individual (Table 2). S. aureus (including CA-MRSA) is the primary organism causing septic arthritis and acute hematogenous osteomyelitis in both children and adults. In children, it accounts for about 50% of all cases of septic arthritis and 70%- 90% of all cases of acute hematogenous osteomyelitis. Group A streptococcus is the second most common entity. Immunocompromised individuals are at increased risk for fungal infections, while puncture wounds pose increased risk for gram-negative species and pseudomonas.

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Differential Diagnosis Considerations for Septic Arthritis: Many disease processes may mimic bacterial septic arthritis. Other diagnoses to consider include rheumatologic disease, soft tissue inflammatory processes, trauma, and other infectious processes.

Juvenile rheumatoid arthritis (JRA) may present as a monoarticular process that can be confused with a septic joint. JRA is usually characterized by more gradual onset of symptoms and produces polyarticular arthritis in children less than 16 years of age.

Reactive arthritis is an inflammatory process within the joint secondary to a host-mediated immunologic response to microbial antigens. Pathogenesis of the syndrome includes immune complex deposition within the joint and a subsequent inflammatory response. While classically felt to be a sterile process, more recent evidence suggests that infectious antigens are present within the joint. Post-streptococcal reactive arthritis is the most recognized of these syndromes. Chlamydia, Salmonella, Shigella, and Yersinia species have been implicated, as well as Rubella virus, hepatitis B, adenovirus, parvovirus, and Epstein-Barr virus.

Polyarthropathy and a migratory pattern of symptoms help to distinguish reactive arthritis from a septic joint. The inflammatory process is often less severe than that in septic arthritis with mild erythema, effusion, pain, and swelling. WBC count in synovial fluid analysis of reactive arthritis is usually <50,000.

Transient synovitis is another inflammatory process that deserves special consideration in the pediatric population. This process usually occurs in the 3-month to 6-year age group and tends to involve the hip. It is a self-limited disease process without any long-term morbidity and tends to occur after a viral respiratory infection. Transient synovitis normally produces less pain with passive range of motion of the joint than in patients with septic arthritis. Patients are usually afebrile and non-toxic appearing. Laboratory testing will frequently reveal a normal WBC count and ESR and no radiographic abnormalities are seen on imaging studies. Arthrocentesis with synovial fluid analysis is usually performed to reliably differentiate between transient synovitis and a septic joint.

In adults, physical exam findings of gout, pseudogout, bursitis, and osteoarthritis may resemble those of septic arthritis. Seronegative sponylarthropaties, including psoriatic arthritis, Reiter’s syndrome, ankylosing spondylitis, and arthritis associated with inflammatory bowel disease should also be considered in the differential of septic arthritis.

Trauma causing hemarthrosis and synovitis may be mistaken for septic arthritis. In the hemophiliac, hemarthrosis can cause joint inflammation and destruction along with a superimposed infection.

Diagnosis: Diagnosis of bacterial septic arthritis involves initial clinical suspicion and synovial fluid analysis after joint arthrocentesis. Serum blood tests may also be obtained to aid in decision-making. Confirmation of septic arthritis is made by positive growth of bacteria on synovial fluid culture.

Clinical signs and symptoms of septic arthritis include fever, painful joint, resistance to passive and active range of motion, and joint swelling, erythema, and warmth. An acute, hot swollen, and tender joint should be considered septic until proven otherwise.

Although not diagnostic, initial studies from synovial fluid, including WBCs are helpful in clinical decision making when dealing with a suspected septic joint. Classic teaching has indicated that a WBC >50,000 is suggestive of a septic joint. However, this finding alone is only 64% sensitive. Serum ESR >30 has been found to be 96% sensitive, although this test has a low specificity.

When a septic joint cannot be reliably ruled out after exam and arthrocentesis, the patient should be admitted until synovial fluid culture results are obtained.

Treatment: All patients with suspected septic arthritis should be admitted and started on parenteral antibiotics. Empiric treatment while awaiting culture results should be based on knowledge of likely bacterial pathogens at various ages and gram stain results (Table 2). Duration of antibiotic therapy is often dependent upon clinical course and the organism isolated. Normalization of ESR and CRP and resolution of clinic exam findings may be used as indicators to stop antibiotic therapy.

Orthopedic consultation should be made for possible joint irrigation in the operating room if synovial fluid analysis is consistent with infection. Infectious disease consultation may also be considered to optimize antibacterial treatment.

Discussion: The exact mechanism of shoulder subluxation in association with septic arthritis is not yet known. It has been theorized that expansion of the glenohumeral capsule and the closely associated ligaments from accumulation of pus and fluid leads to joint instability. Some suggest that accumulation of pus must be gradual over time to allow for joint instability, as a rapid accumulation would cause intolerable pain, leading the patient to seek earlier medical treatment. Another thought is that patients who are insensitive to pain or intentionally mask pain (IV drug abusers) may be able to tolerate longer periods of pain secondary to pus accumulation, which allows for more stretching and joint instability. These theories have not been verified, and more studies are needed to determine the role of both the inflammatory response and infectious process on the integrity of joint structures. It remains unclear weather subluxation/dislocation during acute infection results in permanent joint incompetency or recurrent subluxation/ dislocation.

References:

  • Gompels BM, Darlington LG. Septic arthritis in rheumatoid disease causing bilateral shoulder dislocation: Diagnosis and treatment assisted by grey scale ultrasonography. Am Rheum Dis. 1981;40:609–611
  • Thomas E, Leroux J, Lazema MJ, Blotman F. Inferior glenohumeral sublaxation; an indirect sign of septic of the shoulder. Revue Du Rhumatisme. 1994;61:349–352
  • Resnik CS, Septic arthritis: a rare cause of drooping shoulder.  Skeletal Radiology.  1992, 21(5):307-9
  • Bagheri et al.  Pathologic dislocation of the shoulder secondary to septic arthritis: a case report.  Cases Journal.  2009, 2:9131
  • Zink BJ, Raukar NP.  Bone and Joint Infections.  In: Marx J, Hockberger R, Walls R: Rosen’s Emergency Medicine: Concepts and Clinical Practices, 7th Ed. Elsevier Mosby Health Sciences, 2009
  • Krogstad P.  Osteomyelitis and Septic Arthritis.  In: Feign RD, Cherry JD, Demmler GJ, Kaplan SL:  Textbook of Pediatric Infectious Disease 5th Ed.  WB Saunders, 2004.
  • Biviji AA, Paiement GD, Steinbach LS: Musculoskeletal manifestations of human immunodeficiency virus infection. J Am Acad Orthop Surg 2000; 10:312
  • Dikranian A, Weisman M: Principles of diagnosis and treatment of joint infections. In: Koopman W, ed. Arthritis and Allied Conditions: A Textbook of Rheumatology, Philadelphia: Lippincott Williams & Wilkins; 2001:255
  • Masuko-Hongo K, Kato T, Nishioka K: Virus-associated arthritis. Best Pract Res Clin Rheumatol 2003; 17:309
  • Li EK: Rheumatic disorders associated with streptococcal infections. Best Pract Res Clin Rheumatol 2000; 14:559
  • Taylor-Robinson D, Keat A: Septic and aseptic arthritis: A continuum?.  Best Pract Res Clin Rheumatol 1999; 13:179
  • Hopkins-Mann C, Ogunnaike-Joseph D, Moro-Sutherland D.  Musculoskeletal Disorders in Children.  In: Tintinalli, JE, Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD:  Emergency Medicine: A Comprehensive Study Guide, 7th Ed.  McGraw-Hill Companies Inc, 2011.
  • Gordon EJ, Hutchful GA. Pyarthrosis simulating ruptured rotator cuff syndrome. South Med J. 1982;75(6):759–762
  • Rankin KC, Rycken JM. Bilateral dislocation of the proximal humeral epiphysis in septic arthritis: a case report. J Bone Joint Surg. 1992;75-B:329

 

 

Comments   

# Hueydoc 2011-08-26 19:08
No response from the orthopedist ?
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# Sharon 2011-08-27 04:46
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# DRLast Laugh 2011-10-30 19:56
This just proves the need for your parasitic colleagues. This type of negligence of emergency physician could be averted if a highly trained radiologist reviewed the plain film.
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