20-39: Acute Pyogenic Osteomyelitis

Osteomyelitis is a serious infection that is often difficult to diagnose and treat. Infection of bone occurs as a consequence of (1) hematogenous dissemination of bacteria, (2) invasion from a contiguous focus of infection, and (3) skin breakdown in the setting of vascular insufficiency.

A. Symptoms and Signs

1. Hematogenous osteomyelitis

Osteomyelitis resulting from bacteremia is a disease associated with sickle cell disease, injection drug users, diabetes mellitus, or older adults. Patients with this form of osteomyelitis often present with sudden onset of high fever, chills, and pain and tenderness of the involved bone. The site of osteomyelitis and the causative organism depend on the host. Among patients with hemoglobinopathies such as sickle cell anemia, osteomyelitis is caused most often by salmonellae; S aureus is the second most common cause. Osteomyelitis in injection drug users develops most commonly in the spine. Although in this setting S aureus is most common, gram-negative infections, especially P aeruginosa and Serratia species, are also frequent pathogens. Rapid progression to epidural abscess causing fever, pain, and sensory and motor loss is not uncommon. In older patients with hematogenous osteomyelitis, the most common sites are the thoracic and lumbar vertebral bodies. Risk factors for these patients include diabetes, intravenous catheters, and indwelling urinary catheters. These patients often have more subtle presentations, with low-grade fever and gradually increasing bone pain.

2. Osteomyelitis from a contiguous focus of infection

Prosthetic joint replacement, pressure injury (formerly called pressure ulcer), neurosurgery, and trauma most frequently cause soft tissue infections that can spread to bone. S aureus and Staphylococcus epidermidis are the most common organisms. Polymicrobial infections, rare in hematogenously spread osteomyelitis, are more common in osteomyelitis due to contiguous spread. Localized signs of inflammation are usually evident, but high fever and other signs of toxicity are usually absent. Septic arthritis and cellulitis can also spread to contiguous bone.

3. Osteomyelitis associated with vascular insufficiency

Patients with diabetes mellitus and vascular insufficiency are susceptible to developing a very challenging form of osteomyelitis. The foot and ankle are the most commonly affected sites. Infection originates from an ulcer or other break in the skin that is usually still present when the patient presents but may appear disarmingly unimpressive. Bone pain is often absent or muted by the associated neuropathy. Fever is also commonly absent. Two of the best bedside clues that the patient has osteomyelitis are the ability to easily advance a sterile probe through a skin ulcer to bone and an ulcer area larger than 2 cm².

B. Imaging and Laboratory Findings

The ESR and serum CRP are almost always elevated and can be useful parameters to follow during the course of therapy.

The plain film is the most readily available imaging procedure to establish the diagnosis of osteomyelitis, but it can be falsely negative initially. Early radiographic findings may include soft tissue swelling, loss of tissue planes, and periarticular demineralization of bone (eFigure 20–29). About 2 weeks after onset of symptoms, erosion of bone and alteration of cancellous bone appear, followed by periostitis.

MRI, CT, and nuclear medicine bone scanning are more sensitive than conventional radiography. MRI is the most sensitive and is particularly helpful in demonstrating the extent of soft tissue involvement. Radionuclide bone scanning is most valuable when osteomyelitis is suspected but no site is obvious. Nuclear medicine studies may also detect multifocal sites of infection. Ultrasound is useful in diagnosing the presence of effusions within joints and extra-articular soft tissue fluid collections but not in detecting bone infections.

Identifying the offending organism is a crucial step in selection of antibiotic therapy. Bone biopsy for culture is required except in those with hematogenous osteomyelitis, who have positive blood cultures. Cultures from overlying ulcers, wounds, or fistulas are unreliable.

Acute hematogenous osteomyelitis should be distinguished from suppurative arthritis, rheumatic fever, and cellulitis. More subacute forms must be differentiated from tuberculosis or mycotic infections of bone and Ewing sarcoma or, in the case of vertebral osteomyelitis, from metastatic cancer. When osteomyelitis involves the vertebrae, it commonly traverses the disk—a finding not observed in cancer. Charcot arthropathy of the foot or ankle can mimic osteomyelitis, particularly in patients with diabetes but does not cause an elevated ESR or serum CRP.

Inadequate treatment of bone infections results in chronicity of infection, and this possibility is increased by delaying diagnosis and treatment. Extension to adjacent bone or joints may complicate acute osteomyelitis. Recurrence of bone infections often results in anemia of chronic disease, a markedly elevated ESR, weight loss, weakness and, rarely, amyloidosis or nephrotic syndrome. Pseudoepitheliomatous hyperplasia, squamous cell carcinoma, or fibrosarcoma may occasionally arise in persistently infected tissues.

Most patients require both debridement of necrotic bone and prolonged administration of antibiotics. Patients with vertebral body osteomyelitis and epidural abscess may require urgent neurosurgical decompression. Depending on the site and extent of debridement, surgical procedures to stabilize, fill in, cover, or revascularize may be needed. Oral therapy with quinolones (eg, ciprofloxacin, 750 mg twice daily) for 6–8 weeks has been shown to be as effective as standard parenteral antibiotic therapy for chronic osteomyelitis with susceptible organisms. When treating osteomyelitis caused by S aureus, quinolones are usually combined with rifampin, 300 mg orally twice daily.

If sterility of the lesion is achieved within 2–4 days, a good result can be expected in most cases if there is no compromise of the patient’s immune system. However, progression of the disease to a chronic form may occur. It is especially common in the lower extremities and in patients in whom circulation is impaired (eg, diabetics).