26 Septic Arthritis of the Hip

Robert Axel Sershon, Joshua Alan Bell

26 Septic Arthritis of the Hip

Native Hip

I. Background ¹ – ⁶ : Septic arthritis of the hip is a relatively rare condition in healthy adults and is more common in the pediatric setting. Due to the destructive nature of an infection on native cartilage, septic arthritis is typically treated emergently to prevent future sequelae.
1. Epidemiology:
  1. Most commonly monoarticular and in large joints:
    1. Hip is the second most common location, involved in 13% of cases.
    2. Knee is most common (~50% of cases).
  2. Low incidence of native septic hip infections in adults:
    1. Two to 10 out of 100,000.
  3. Higher incidence in the pediatric population:
    1. 0.25% of all hospitalizations
    2. Ninety-five percent single joint infections.
  4. Adult risk factors:
    1. Elderly, intravenous drug users, recent sepsis, malnutrition, prior surgery, and immunocompromised (HIV/AIDS, diabetics, rheumatoid, cirrhosis).
  5. Pediatric risk factors:
    1. Fifty percent occur in children younger than 2 years.
    2. Immunocompromised, prematurity, and cesarean section.
  6. Origins of inoculation:
    1. Pneumonia, endocarditis, dermatologic, urinary tract infection, various gastrointestinal infections.
II. Differential diagnosis ¹ , ² , ⁷ – ⁹ :
1. Intra-articular injury.
2. Osteomyelitis.
3. Inflammatory arthroplasty (rheumatoid arthritis, gout and pseudogout, reactive arthritis, systemic lupus erythematosus, Lyme arthritis, psoriatic arthritis).
4. Sickle cell disease.
5. Transient synovitis of the hip (pediatric).
6. Pigmented villonodular synovitis.
7. Hemarthrosis.
8. Neuropathic arthropathy.
9. Osteoarthritis.
10. Osteonecrosis of the femoral head.
11. Pediatric hip disorders (slipped capital femoral epiphysis, Legg–Calvé–Perthes, hip dysplasia, etc.).
12. Soft-tissue infection—septic bursa, psoas abscess, or cellulitis.
III. Pathophysiology ² , ⁹ :
1. Joint inoculation occurs in one of three ways:
  1. Bacteremia (e.g., pneumonia).
  2. Direct inoculation (e.g., trauma).
  3. Contiguous spread (e.g., nearby osteomyelitis—common with intra-articular metaphysis of the hip).
2. Seeding pathway:
  1. Bacteria enters through the highly permeable and vascular synovial membrane, depositing on the membrane:
    1. High vascularity and permeability allow for production of synovial fluid, exchange of nutrients, and waste removal.
  2. Lack of robust immunologic barriers and absence of a limiting membrane allows bacteria to seed the synovial fluid and precipitously proliferate in the nutrient-filled environment.
3. Bacterial proliferation results in release of destructive toxins and enzymes:
  1. Alpha, β, delta toxins in the Staphylococcus species break down cell membranes and proteins.
  2. Adhesins allow for bacterial adhesion, facilitating stability and growth.
  3. Cartilage degradation can occur within 8 hours and gross destruction is typically apparent within 1 week following an untreated infection.
4. Bacterial cell wall and intracellular proteins initiate the inflammatory cascade:
  1. B-cells, T-cells, and macrophages release inflammatory cytokines:
    1. B-cell: interleukin-1 (IL-1) and IL-10.
    2. T-cell: IL-4 and IL-10.
    3. Macrophage: IL-1, IL-10, and tumor necrosis factor-α (TNF-α).
5. Inflammatory response from host further contributes to cartilaginous breakdown via matrix metalloproteinases:
  1. Bacterial presence alters normal synovial fluid production and filtration:
    1. Gradual increase of toxic enzymes and inflammatory concentrations.
    2. Abnormal filtration results in increased intra-articular pressure, which further contributes to joint destruction and increases the risk of femoral head osteonecrosis.
6. Histological findings from acute to chronic inflammation show an increase from neutrophils to mononuclear leukocytes and lymphocytes:
  1. Lymphocytes are predominate cells by 3 weeks.
7. Blood supply:
  1. Robust pediatric blood supply of the hip renders infants and children more susceptible to hematogenous seeding:
    1. Medial femoral circumflex artery:
      - i. Dominant blood supply to the femoral head after 4 years of age.
    2. Lateral femoral circumflex artery:
      - i. Smaller contribution to femoral head as the child ages.
    3. Artery of the ligamentum teres:
      - i. Begins to regress at 4 years of age.
    4. Metaphyseal vessels:
      - i. Abundant supply to metaphysis.
IV. Microbiology ² , ⁹ , ¹⁰ :
1. Common organisms ⁹ , ¹¹ :
  1. Staphylococcus aureus (40–75%; Fig. 26.1 ):
    1. Most common pathogen, except for:
      - i. Young, healthy, sexually active adults (Neisseria gonorrhoeae—75%).
      - ii. Haemophilus influenza in unvaccinated infants and toddlers.
    2. Methicillin-sensitive S. aureus (MSSA).
      - i. Beta-lactamase confers penicillin resistance; however, it remains susceptible to methicillin.
      - ii. Antibiotic: methicillin (or similar penicillin derivative).
    3. Methicillin-resistant S. aureus (MRSA):
      - i. Bacteria carrying the mecA gene produce penicillin-binding protein 2A, which results in poor bacterial binding to penicillin. These bacteria are resistant to penicillin and methicillin (MRSA).
      - ii. Commonly hospital or health care acquired, although becoming more common in the public domain:
        
        Obtained from hospitals, surgery, catheters, advanced-care facilities.
        
        More commonly multiple drug-resistant forms.
      - iii. Community acquired; becoming a more common source:
        
        Typically less virulent with less drug resistance.
        
        At risk: intravenous (IV) drug users, athletes, military.
      - iv. Antibiotics: vancomycin, daptomycin, or linezolid.
        
        Fig. 26.1 Staphylococcus aureus.
  2. Other staphylococcal species:
    1. Uncommon in the setting of primary infection.
  3. Streptococcus species (20%):
    1. Group A most common form isolated.
    2. Group B: often found susceptible populations: infants, diabetics, and elderly.
  4. Gram negative (<5% of cases):
    1. Escherichia coli, Salmonella, Pseudomonas, Klebsiella, and Enterobacter species.
    2. IV drug users, neonates, and elderly are at highest risk.
  5. N. gonorrhoeae (10%; Fig. 26.2 ):
    1. Most common source in young, healthy, sexually active adults (75%):
      - i. Incidence of 3 to 5% of all patients infected with N. gonorrhoeae.
    2. Polyarticular and migratory with associated rash.
    3. Diagnosis typically made by polymerase chain reaction (PCR), as joint cultures are often negative:
      - i. Cultures from urethra or pharynx may be positive.
    4. Less morbid and destructive than most other pathogens.
    5. Responds quickly and well to antibiotics, and formal incision and drainage is often unnecessary.
  6. Special cases:
    1. Salmonella—more common with sickle cell disease.
    2. Bartonella henselae—common in HIV patients.
    3. Pseudomonas aeruginosa—often found in IV drug users.
    4. Pasteurella multocida—typically associated with a dog or cat bite.
    5. Eikenella corrodens—seen after a human bite injury.
2. Fungal:
  1. Unlike bacteria, fungal infections undergo granulomatous reactions, resulting in thickened synovium, effusions, and fibrin “rice bodies.”
    
    Fig. 26.2 Neisseria gonorrhoeae.
  2. Cartilage progressively destroyed via infiltration of granulation tissue.
  3. Risk factors: Found with substance abusers, immunocompromised, organ transplant patients, those on broad-spectrum antibiotics, and presence of an indwelling catheter (ref—Bariteau, JAAOS 2014).
V. Clinical presentation ² , ⁹ , ¹² :
1. Acute onset of pain, swelling, stiffness, and inability or unwillingness to bear weight through the affected extremity.
2. Pain is typically located in the groin:
  1. Be aware of referred pain to thigh and knee, especially in the pediatric population.
  2. Often will not allow the hip to be taken through any range of motion.
3. Fever, chills, malaise, erythema are variable in presence and severity.
4. Concurrent infection or sepsis.
5. Kocher’s criteria for pediatrics:
  1. White blood cell (WBC) greater than 12,000 cells/µL.
  2. Inability to bear weight in the affected extremity.
  3. Fever greater than 38.5°C (101.3°F).
  4. Erythrocyte sedimentation rate (ESR) greater than 40 mm/h.
  5. Sensitivity as high as 99.6% when all four criteria are met.
VI. Examination ² , ⁹ , ¹² :
1. Unable to bear weight or severe antalgic gait.
2. Hip held in flexion, abduction, external rotation: affords greatest capsular volume.
3. Significant pain with short arcs of motion.
4. Systemic physical examination for primary infectious source.
VII. Diagnosis ² , ⁶ , ⁷ , ⁹ , ¹⁰ , ¹² – ¹⁴ :
1. Combination of clinical history, examination, and diagnostic studies:
  1. Important criteria include fever → elevated inflammatory markers → refusal to walk/bear weight.
2. Serum laboratory:
  1. Serum WBC greater than 12,000/L.
  2. ESR greater than 30 mm/h.
  3. C-reactive protein (CRP) greater than 10.5 mg/L is predictive of infection.
3. Synovial fluid aspiration:
  1. Gold standard.
  2. Cell count and differential:
    1. WBC greater than 50,000 cells/µL:
      - i. High sensitivity, low specificity.
      - ii. Leukocyte counts greater than 28,000/µL or less in immunocompromised.
    2. Margaretten et al ⁹ report counts of less than 25,000/mm ³ , more than 25,000/mm ³ , more than 50 000/mm ³ , and more than 100 000/mm ³ gave a septic arthritis likelihood ratio of 0.32, 2.9, 7.7, and 28.0, respectively.
    3. Polymorphonuclear (PMN) neutrophils greater than 90% indicates infection (historically >75% considered positive).
    4. Glucose and protein have low sensitivity and specificity.
  3. Gram stain:
    1. Not a recommended tool for guidance of treatment due to variable sensitivity and specificity.
    2. Nonpyogenic arthritis often presents with false negatives.
  4. Synovial culture:
    1. Can be negative in up to 75% of cases.
    2. Obtained prior to administration of IV antibiotics.
    3. Blood cultures obtained in the cases of systemic sepsis.
  5. Crystal analysis:
    1. Presence of crystals does not necessarily rule out infection.
    2. Urate crystals are negatively birefringent and highly suggestive of gout.
    3. Calcium pyrophosphate dehydrate crystals are positively birefringent and are highly suggestive of pseudogout.
    4. Presence of crystals in the setting of concomitant septic arthritis is 1.5% of cases.
4. Aspiration technique:
  1. Sterile prep.
  2. Fluoroscopic guidance ( Fig. 26.3 ).
  3. An 18-gauge needle or larger, preferably 6 inches in length.
  4. Approaches: anterior, anterolateral, and lateral.
  5. Air arthrogram upon entering joint capsule.
    
    Fig. 26.3 Hip aspiration.
VIII. Imaging ² , ⁷ , ⁹ , ¹² :
1. Limited role in diagnosis.
2. Plain radiographs:
  1. Anteroposterior of the hip and pelvis.
  2. Lateral hip.
  3. May be used to monitor the response to treatment:
    1. Joint destruction or degeneration, osteomyelitis, bone loss, etc.
3. Ultrasound:
  1. Can determine location and extent of effusion.
  2. Echo-free effusion has low false-positive rate.
  3. Can also assist in aspiration.
4. Advanced imaging:
  1. Computed tomography (CT):
    1. Detects soft-tissue swelling, joint effusion, and abscess formation.
    2. Often utilized to guide joint aspiration in small or difficult-to-access areas.
    3. More readily obtained and less costly than MRI.
  2. Magnetic resonance imaging (MRI):
    1. Superior soft-tissue detail compared with CT and bone scans.
    2. Useful in differentiating between osteomyelitis, soft-tissue abscesses, and joint effusion.
    3. Costly and difficult to obtain in a timely fashion.
  3. Radionucleotide bone scan:
    1. Detect localized areas of inflammation.
    2. Areas with increased technetium-99m uptake are correlated with increased osteoblasts activity and vascularity:
      - i. Poor sensitivity and specificity when used alone.
    3. Gallium citrate indium-111 chloride are taken up rapidly of inflammation:
      - i. Overall poor sensitivity for septic arthritis when used alone (60%) with high incidence of false positives.
    4. Rarely indicated in the setting of acute septic arthritis.
  4. All advanced imaging modalities have the potential to delay appropriate treatment and are best reserved for instances of diagnostic uncertainty.
IX. Treatment ² , ⁸ , ¹⁰ , ¹⁵ – ¹⁸ :
1. Emergent condition that is indicated for prompt fluid evacuation, irrigation and debridement, and empiric antibiotic therapy.
2. Hip arthroscopy:
  1. Native hip arthroscopy with irrigation and debridement has been shown to be as effective as open arthrotomy.
  2. Less morbid procedure with more rapid discharge and return to function.
3. Open arthrotomy with irrigation and debridement:
  1. Current gold standard.
  2. Approach based upon surgeon preference and planned future interventions:
    1. Anterior-based approaches (direct anterior, Smith-Petersen, or anterolateral, Watson-Jones) allow easy access to the hip joint while better preserving the blood supply to the femoral head.
  3. Increased risk of instability regardless of approach utilized.
4. Resection arthroplasty:
  1. Necessary in the cases where the femoral head is extensively involved.
  2. May be definitive in the elderly, nonambulatory, and severely immunocompromised patients.
  3. Antibiotic spacer placement used when considering future arthroplasty:
    1. May also be used as definitive treatment in select individuals.
5. Two-stage arthroplasty:
  1. Conversion from resection arthroplasty with or without insertion of an antibiotic spacer.
  2. Second stage once:
    1. Laboratory results have normalized.
    2. Patient is offantibiotics for several weeks without reoccurrence.
    3. Repeat aspiration is negative for infection.
  3. Increased reinfection rate (7–14%) compared healthy patients without prior infection (<1%), but overall excellent outcomes.
6. Antibiotics:
  1. Empiric antibiotics begin immediately following aspiration and culture and are based on the clinical condition and/or the local antibiogram:
    1. Choice of coverage dictated by final culture.
    2. Broad spectrum with MRSA coverage preferable.
  2. Consultation with infectious disease for final recommendations.
  3. Length of treatment typically ranges from 4 to 6 weeks.
X. Outcomes ² , ¹⁵ , ¹⁶ , ¹⁹ :
1. Time to diagnosis remains most crucial element of treatment, as an exponential rise in joint pressure and destruction continues until treatment.
2. Delay or missed diagnosis carries serious consequences, both locally and systemically.
3. Recent literature has shown majority of patients (>95%) go on to have excellent functional outcomes when treated early with either open or arthroscopy techniques.
4. Negative consequences include:
  1. Joint contractures.
  2. Growth abnormalities—pediatrics.
  3. Osteonecrosis.
  4. Gait abnormalities.
  5. Postseptic arthritis degenerative joint disease.