Shoulder pain following a hornet sting in a 2-year-old

Contemporary PEDS Journal, June 2021, Volume 38, Issue 6

A 2-year-old girl with a 36-hour history of left shoulder redness and pain. She developed a fever 24 hours prior to presentation. She was stung by a hornet on multiple areas of her left upper extremity 10 days earlier. What’s the diagnosis?

The case

A 2-year-old girl presents to the emergency department (ED) with a 36-hour history of left shoulder redness and pain. She developed a fever 24 hours prior to presentation. She is restless, crying, and refusing to move her left shoulder. Mother reports that the patient was stung by a hornet on multiple areas of her left upper extremity when playing outside 10 days prior.

History and examination

Mother notes that a day prior to presentation at the ED, the day care staff reported that patient seemed more irritable. Patient has a history of recurrent ear infections. The mother was concerned about another ear infection and had gone to the pediatrician, where patient received a diagnosis of otitis media and was prescribed cefdinir. There is no history of rash, weight loss, vomiting, diarrhea, or abdominal pain. Patient is up to date on immunizations.

She is alert and crying but easily consoled. Vital signs show a temperature of 37.8 °C (100 °F), heart rate of 146 beats/min, respiratory rate of 26 breaths/min, blood pressure at 98/67 mm Hg, and oxygen saturations 100% in room air. There is an area of erythema measuring about 1 by 3 cm over the left shoulder without swelling. She cries with pain at abduction, adduction, and rotation of the left shoulder. There is no swelling over the clavicular area and no tenderness on palpation. Elbow and wrist examination findings are normal. Her tympanic membranes are erythematous and show purulence. Her physical examination findings are normal.

Laboratory testing

In the ED, initial laboratory studies reveal a white blood cell (WBC) count of 20,980 with a neutrophil predominance, C-reactive protein (CRP) level of (12 mg /L), and erythrocyte sedimentation rate (ESR) of 28 mm/hr. Her chemistry panel results are normal. Left humerus and left shoulder radiograph results are normal. Results from ultrasonography of the left shoulder are negative for joint effusion. With persistence of left shoulder pain, elevated WBC with a neutrophil predominance, and mildly increased inflammatory markers, she is admitted to the hospital and further testing reveals the diagnosis.

Differential diagnosis

The differential diagnosis for joint pain and fever includes infectious and noninfectious causes (Table 1). In the absence of trauma, considerations include cellulitis, septic arthritis (SA), osteomyelitis, and, less likely, transient synovitis.

The patient was started on clindamycin although radiographs were normal, which can be seen in early osteomyelitis. She received parenteral ketorolac for pain control. She continued to be febrile with a maximum recorded temperature of 39.4 °C (103 °F) while on admission and continued with pain and resistance to any movement of the left shoulder. An orthopedic surgeon was consulted, and magnetic resonance imaging (MRI) was obtained on the second day of admission because of persistent symptoms. MRI showed left shoulder joint effusion and mild synovitis with significant surrounding myositis (Figure). There was no evidence of osteomyelitis. Based on the imaging appearance alone, SA could not be excluded. Her blood culture did not grow any organism after 5 days.


SA is defined as infection of the joint space. In the United States, estimated incidence is approximately 3 to 4 per 100,000 children, with those aged younger than 5 years affected most frequently.1 There is a higher prevalence in boys than girls1 and it can affect any major joint, with the hip and knee joints frequently involved.


SA can be caused by bacteria, viruses, mycobacteria, and fungi, with bacterial joint infections being the most common etiology.2 It is spread via hematogenous means, direct inoculation, or extension of a contiguous focus of infection. Hematogenous spread is said to account for most cases of bacterial arthritis.3 Approximately two-thirds of infections are caused by Staphylococcus species,4 followed by gram-negative bacilli and streptococci. Kingella kingae, a gram-negative coccobacillus, has been identified in the younger age group (2 to 3 years). However, more recently, there has been an emergence of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA).5

Clinical features

Patients classically present with acute onset of fever and joint pain. Swelling may or may not be present with limited range of motion of the affected joint. Other symptoms include malaise, poor appetite, and irritability, especially younger infants. A high index of suspicion for SA should be maintained in all children with acute onset of fever and joint pain suggested by limping or limited movement, even in the absence of other associated symptoms.


Laboratory findings in SA include elevated inflammatory markers (CRP, ESR) and elevated peripheral WBC.6 Elevated inflammatory markers have more negative than positive predictive value for SA.7 Blood cultures are positive in approximately 40% of cases. Additionally, joint/synovial fluid studies (WBC count, gram stain, and culture) are important in the diagnosis of SA, where synovial fluid WBC count of greater than 50,000 cells/­L with neutrophil predominance are usually seen.8,9 Culture of a bacterial pathogen from the synovial fluid confirms the diagnosis of SA. Kocher criteria (Table 2) can help differentiate between SA and transient synovitis in a case of nontraumatic painful hip in a child. Although first introduced in 1999, more recent studies have validated its continued usefulness in the evaluation of SA.10,11 Components of the Kocher criteria are: (1) walking or weight-bearing inability, (2) fever greater than 38.5 °C (101.3 °F), (3) ESR greater than 40 mm/hr, and (4) WBC greater than 12,000 cells/­L. A point is awarded for the presence of each criterion and is associated with a likelihood of child having SA. The likelihood of a child with no Kocher criteria having SA is 0.2%. This percentage increases with each additional point, up to 99% likelihood at 4 points.

Plain radiographs usually show negative findings in SA. Ultrasonography is helpful in detecting joint fluid, but the presence/absence of fluid is not specific for joint infection12 as was the case in this patient. Using MRI is extremely sensitive for the early detection of joint fluid13; however, it is not as readily available as ultrasonography. It is important to note that a diagnosis of probable SA can be made even if blood culture or synovial fluid culture do not isolate a bacterial pathogen or if other diagnoses are excluded and if the patient has characteristic clinical, laboratory, and radiographic features.


The mainstay of treatment for SA is joint drainage and antimicrobial therapy.14 Joint drainage can be accomplished through arthrotomy, arthroscopy, or needle aspiration. Antibiotics that cover for common pathogens should be instituted promptly.15 It is recommended that initial antibiotics be given parenterally when treating SA. The antibiotic of choice will usually depend on the severity of illness, local prevalence of CA-MRSA, the susceptibility of CA-MRSA isolates to clindamycin, and suspicion for other pathogens. Antibiotic options include cefazolin, clindamycin, nafcillin/oxacillin, and vancomycin with duration of treatment usually 2 to 3 weeks. Clinical improvement as well as improved inflammatory markers is typically expected within 3 to 5 days after instituting treatment.16


Early diagnosis of SA and treatment are associated with improved outcome. Long-term complications of SA, especially with delayed treatment, include limited range of motion of the joint, limb-length discrepancy or angular deformities, especially if there is involvement of the growth plate, and avascular necrosis or pathologic fractures.17

Patient course

On receipt of MRI results, patient was taken to the operating room, where she had left shoulder aspiration, left shoulder open irrigation, and debridement. Cloudy fluid was identified at the glenohumeral joint and 2 milliliters of necessary purulent fluid was aspirated. The glenohumeral joint was then irrigated with normal saline. Joint aspirate was sent for cell count, gram stain, aerobic, anaerobic, and fungal cultures. Synovial fluid aspirate showed 79,500 cells/­L with neutrophil predominance at 96.7%. Gram stain showed moderate WBC but no organisms were seen and there was no growth on culture. She was continued on parenteral clindamycin. She was discharged on hospital day 5 with much improved range of motion of her left shoulder. She was transitioned to oral clindamycin and received a total of 3 weeks of antibiotic therapy. At her outpatient follow-up a week after discharge, she was using her left arm without any difficulty.


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