Last Updated on October 29, 2023
Pyogenic vertebral osteomyelitis is a type of spinal infection which may result from direct trauma, the spread of infection from adjacent structures or hematogenous spread from the distant focus of infection. It can have devastating complications if untreated which could be a pathological fracture, epidural infection, and compression of the neural structures.
Vertebral osteomyelitis is considered uncommon, there is a suggested increase in spinal infections because of increased use of vascular devices, other instrumentation and increasing rates of IV drug abuse.
Pathophysiology of Vertebral Osteomyelitis
The spine is column formed by stacking of vertebrae, intervertebral discs and associated joints stabilized by muscles, tendons, and ligaments. Cord and roots are contained in the vertebral column and it serves to protect them.
The spine starts below the skull and forms articulations with the skull for neck motion. It ends at the coccyx, a point palpable below the beginning of gluteal cleft posteriorly.
It has the following regions –
- Cervical spine – First seven vertebrae in the spinal column (C1-7)
- Thoracic – Next 12 vertebrae (T1-12) and is stabilized by the attached rib cage and intercostal musculature.
- Lumbar spine – Next five vertebrae (L1-5), located between the relatively immobile segments of the thoracic and sacral segments.
95% of pyogenic spinal infections involve the vertebral body, and only 5% involve the posterior elements of the spine. The difference of involvement is due to blood supply which is more in vertebral bodies.
A distant focus of infection provides an infective nidus from which bacteria spread by the bloodstream to the spinal column. The skin and the genitourinary tract are sites. Septic arthritis, sinusitis, subacute bacterial endocarditis, and respiratory, oral, or gastrointestinal infection could be other sources of infective agents.
[Approximately 30-70% of patients with vertebral osteomyelitis have no obvious prior infection.]
Circulating bacteriae may enter the vertebra or a disc space via small metaphyseal arteries arising from larger primary periosteal arteries that, or venous system.
Bone infarct may result from blockage of metaphyseal arteries by septic thrombi. The sequestrum facilitates colonization.
The disc is avascular and is secondarily invaded by bacteria from the endplate region after the metaphyseal bone is infected.
Retrograde seeding of venous blood via the Batson plexus can also cause the infection. During periods of increased intra-abdominal pressure, venous blood is shunted toward the vertebral venous plexus.
Spread of contiguous infection into the vertebrae and disc from a retropharyngeal abscess or a retroperitoneal abscess may cause resulting in osteomyelitis and discitis.
Pyogenic infection can affect any vertebra but most vertebral body infections occur in the lumbar spine because of the blood flow to this region of the spine. Tuberculosis has a predilection for the thoracic spine, and IV drug abusers are more likely to contract an infection of the cervical spine.
The combination of mechanical compression of the spinal cord by pus or granulation tissue can result in ischemia with spinal cord infarction, which accounts for the rapid neurologic progression.
Patients with a spinal epidural abscess may progress to complete paralysis within minutes to hours, even while receiving optimal antibiotic therapy.
Pathological fractures can occur due to the softening of the bone, and present with acute spinal cord compression.
Risk Factors for Vertebral Osteomyelitis
Risk factors for developing osteomyelitis include conditions that compromise the immune system, such as the following:
- Advanced age
- Intravenous (IV) drug use
- Diabetes mellitus
- Organ transplantation
- Malnutrition
- Congenital immunodepression
- Long-term systemic administration of steroids
- Cancer
- Surgical site infection
The common microorganisms that cause vertebral osteomyelitis are
- Staphylococci
- Enterococcus species
- Enterococcus species
- Pseudomonas aeruginosa
- Enterobacteriaceae
- Beta-hemolytic streptococci
- Propionibacterium acnes
- Tuberculosis
- Fungus
- Yeast
- Parasitic organisms
Clinical Presentation
Adult patients usually present with insidious onset back pain. There is often a history of back pain several weeks or months of gradually progressing neck or back pain that increases with movement.
The pain gradually increases in intensity and eventually becomes severe and unrelieved by medication and rest.
Neural signs are often not present until late.
The children present with more acute symptoms and discitis. [More about that here]
In most of the patients, there is only mild tenderness over the spinous process of the involved vertebra, and minimal spasm may be present.
The range of motion may be decreased. Fever is not present in 50% of the patients.
In advanced disease, bony collapse, the spread of the infection underneath the posterior longitudinal ligament, or frank epidural abscess may cause compression of the spinal cord or nerve roots.
Radicular signs followed by neural deficit suggests epidural abscess. [Spinal epidural abscess occurs in 5-18% of cases]
It may be noted that cervical vertebral osteomyelitis is associated with paralysis more commonly than either thoracic or lumbar infection.
A detailed motor and sensory examination should be performed
Sensorimotor examination suggests the level of the affliction of the spinal cord. [Neural deficits occur in about 15%]
Secondary sepsis may occur in uncontrolled infections.
Lab Studies
- Elevated ESR and CRP
- A minimal increase of leucocytes [Unlike other infections]
- Blood cultures for establishing the diagnosis
- Aspiration biopsy for cytology, culture, and sensitivity
- CT guided
- Positive only 60-70% of the time.
- Trocar Biopsy/open biopsy when does not yield material
Imaging Studies
X-rays
- Normal in the first 2-4 weeks
- Reduced disc space
- Destruction of the endplates around the disc
- Rarefaction, loss of bony trabeculation close to the cartilaginous plate, and an irregular narrowing of the vertebral disk space
- Vertebral body collapse
- Evidence of rapid bone regeneration
- Bone spurs
- Dense new bone
- Paravertebral soft-tissue shadow
CT
- Depicts osteomyelitis earlier
- Hypodensity at the site of infected discs
- Lytic fragmentation of the involved bone,
- Gas within an involved vertebra
- Decreased density of adjacent vertebrae
- Epidural and paraspinal extension of infection
MRI
- Destructive and expansile lesions involving two adjacent vertebrae and the in-between disc
- Low-density changes in bone and disc on T1- weighted images
- High-density changes are seen in these structures on T2-weighted images,
- Gadolinium enhancement shows the involved structures.
- Soft tissue infections are visualized better
- Paravertebral infection
- Collections under the posterior longitudinal ligament
- Epidural abscesses
Radionuclide scanning
Radionuclide scan findings become positive long before plain film changes are evident.
Treatment of Vertebral Osteomyelitis
Most patients with pyogenic vertebral osteomyelitis respond to medical management. Surgery is indicated where medical treatment is not successful.
Medical Treatment
The treatment of vertebral osteomyelitis must be individualized according to the patient’s condition. Underlying infections (eg, retropharyngeal, pelvic, decubital) require simultaneous treatment.
Initially, broad-spectrum antibiotics are given covering both gram-positive and gram-negative organisms, aerobes and anaerobes, including methicillin-resistant S aureus.
As S aureus is the most common agent, it should be covered by most of the antibiotics. Specific antibiotics can be instituted when culture and sensitivity reports are available.
With lack of response to antibiotics and negative cultures, less common organisms should be considered.
Antibiotics are given for 6-8 weeks.
Choice of antibiotics as per agent is given in the table below, as per IDSA guidelines
Microorganism |
First Choice |
Alternatives |
| Staphylococci, oxacillin susceptible |
|
|
| Staphylococci, oxacillin resistant | Vancomycin |
|
| Enterococcus species, penicillin susceptible |
|
|
| Enterococcus species, penicillin resistant | Vancomycin |
|
| Pseudomonas aeruginosa |
|
|
| Enterobacteriaceae |
|
Ciprofloxacin |
| ?-hemolytic streptococci |
|
Vancomycin |
| Propionibacterium acnes |
|
|
| Salmonella species | Ciprofloxacin | Ceftriaxone |
ESR and CRP are markers of the disease. Antibiotics can be withdrawn when the patient is without fever and pain, ESR has fallen to at least two-thirds of the pretherapy level, and there are not as neurologic deficits.
A persistent high ESR demands additional antibiotics. Repeat biopsy can be taken from the infected vertebra to see if organisms not susceptible to the chosen antibiotics.
Bracing is recommended for 6-12 weeks. It provides rest to spine, restrict motion and allows fusion of the vertebrae. A rigid brace is preferred.
A residual kyphosis after healing, if severe, may require corrective surgery later.
Surgical Treatment
Indications for surgery include the following:
- Significant bony involvement requiring debridement and stabilization
- Neural deficits
- Significant kyphosis
- Compression due to abscess/collapse
- Infection in the epidural space
- Infection not responding to antibiotics
Goals of surgery are the preservation of neural function and achievement of stable bony fusion without deformity.
The anterior disease is best addressed by an anterior or anterolateral surgical decompression and debridement. Debridement and drainage should be followed by extensive irrigation with antibiotic solution. In most cases, the closure can be done primarily, with a surgical drain left in place.
Patients with extensive vertebral destruction usually require instrumentation and fusion.
Postoperatively orthosis for a variable period is given. The antibiotics are adjusted according to the culture results.
The patient should be watched for decubitus ulcers, lung problems, and deep vein thrombosis.
Once the correct treatment is implemented, patients require neurologic monitoring to exclude progressive neurologic deterioration.
