Surgical Management of Diskospondylitis

Diskospondylitis is an infectious inflammatory disease affecting the intervertebral disc, vertebral endplates, and adjacent vertebral bodies. It is characterized by bacterial or fungal infection that typically begins in the vertebral endplate, spreads to the intervertebral disc, and may extend into the epidural space, causing spinal cord compression, nerve root compression, and vertebral instability. Surgical management is indicated for cases that fail medical therapy, have progressive neurological deficits, exhibit severe spinal pain unresponsive to analgesics, or present with vertebral instability, pathological fracture, or epidural abscess formation. The surgical goals are decompression of neural structures, debridement of infected tissue, stabilization of the affected vertebral segment, and collection of samples for microbiological and histopathological diagnosis. Surgical approaches vary by spinal location: ventral slot for cervical lesions, hemilaminectomy or dorsal laminectomy for thoracolumbar lesions, and dorsal laminectomy for lumbosacral lesions. Stabilization techniques include vertebral body plating, pins and polymethylmethacrylate (PMMA), and external skeletal fixation. Perioperative management includes broad-spectrum antimicrobial therapy, pain management, and strict activity restriction.

The most common causative agents are bacterial, with Staphylococcus pseudintermedius, Staphylococcus aureus, Streptococcus spp., Escherichia coli, and Brucella canis being frequently isolated. Fungal etiologies include Aspergillus spp., Paecilomyces spp., and Coccidioides immitis. Infection typically spreads hematogenously from a primary source such as the urinary tract, skin, oral cavity, or endocarditis. Direct inoculation can occur via penetrating wounds, spinal surgery, or migrating foreign bodies. Iatrogenic causes include prior spinal surgery or epidural injection. The infection initially localizes in the highly vascular vertebral endplate, then extends into the avascular intervertebral disc, leading to discitis and osteomyelitis. The thoracolumbar and lumbosacral regions are most commonly affected due to increased mechanical stress and blood flow. In some cases, diskospondylitis may be associated with immunocompromise, such as in dogs receiving chronic corticosteroid therapy or with concurrent endocrine disorders.

Diskospondylitis is most commonly diagnosed in dogs, with a reported prevalence of 0.2% to 2.8% in referral populations. Large-breed dogs, particularly German Shepherd Dogs, Labrador Retrievers, Rottweilers, and Doberman Pinschers, are overrepresented. There is no clear sex predilection, though some studies suggest a slight male predominance. The condition typically affects middle-aged to older dogs, with a mean age of 5 to 7 years. Cats are less commonly affected, but when present, they often have concurrent infections such as feline leukemia virus or feline immunodeficiency virus. Working and sporting dogs may be at increased risk due to higher exposure to trauma and environmental pathogens. The lumbosacral region is the most common site, followed by the thoracolumbar junction and cervical spine. Breed-specific anatomical factors, such as vertebral conformation and spinal mobility, may contribute to susceptibility.

The pathophysiology of diskospondylitis begins with hematogenous seeding of bacteria or fungi into the vertebral endplate, which has a rich blood supply. The microorganisms adhere to the bone and initiate an inflammatory response, leading to osteomyelitis. The infection then spreads through the subchondral bone into the intervertebral disc, which is avascular and lacks intrinsic immune defenses, allowing rapid bacterial proliferation. The disc becomes necrotic and may collapse, leading to loss of intervertebral disc height. The inflammatory process extends to the adjacent vertebral bodies, causing osteolysis, sclerosis, and new bone formation. As the infection progresses, it can extend dorsally into the vertebral canal, resulting in epidural abscess formation, spinal cord compression, and nerve root entrapment. Vertebral instability and pathological fractures can occur due to severe osteolysis. Chronic infection may lead to vertebral fusion and spinal deformity. The release of inflammatory mediators, such as cytokines and prostaglandins, contributes to pain and systemic signs. In fungal infections, granulomatous inflammation and fibrosis are more prominent, and the disease may progress more slowly.

Intrinsic predisposing factors include immunocompromise due to concurrent diseases (e.g., diabetes mellitus, hyperadrenocorticism, chronic renal failure), advanced age, and genetic susceptibility in certain breeds. Extrinsic factors include urinary tract infections, skin infections, dental disease, endocarditis, and any condition causing transient bacteremia. Prior spinal surgery or epidural injections can introduce pathogens directly. Trauma to the spine may create a nidus for infection. Poor nutritional status and poor husbandry can increase susceptibility. In working dogs, repetitive high-impact activity may cause microtrauma to the endplates, predisposing to bacterial seeding. The use of immunosuppressive drugs, such as corticosteroids, is a significant risk factor. Additionally, environmental exposure to fungal organisms, particularly in endemic areas, increases the risk of fungal diskospondylitis.

Clinical signs of diskospondylitis vary depending on the location and severity of the infection. The most common presenting sign is spinal pain, which may be severe and localized to the affected region. Dogs may exhibit reluctance to move, stiffness, kyphosis, and muscle spasms. Neurological deficits occur in approximately 30% to 50% of cases and can range from mild proprioceptive ataxia to paraplegia. Cervical lesions may cause neck pain, reluctance to lower the head, and tetraparesis. Thoracolumbar lesions often present with pelvic limb weakness and ataxia. Lumbosacral diskospondylitis can cause lumbar pain, pelvic limb lameness, and cauda equina syndrome, characterized by urinary and fecal incontinence, tail weakness, and perineal hypalgesia. Systemic signs such as fever, lethargy, and anorexia are present in about 30% of cases. In chronic cases, muscle atrophy and weight loss may be observed. Neurological examination may reveal spinal hyperesthesia, proprioceptive deficits, and reduced spinal reflexes. In severe cases, pathological fracture or epidural abscess can cause acute, non-ambulatory paraparesis or paraplegia.

Differential diagnoses for diskospondylitis include intervertebral disc disease (IVDD), vertebral neoplasia (e.g., osteosarcoma, multiple myeloma), spinal fracture or luxation, spinal epidural empyema, meningitis, and steroid-responsive meningitis-arteritis. IVDD typically presents with acute onset of pain and neurological deficits, but lacks systemic signs and radiographic changes of endplate lysis. Vertebral neoplasia may cause similar pain and neurological deficits, but imaging shows lytic or blastic lesions without disc space collapse, and biopsy is needed for definitive diagnosis. Spinal fractures or luxations are usually associated with trauma and show distinct radiographic abnormalities. Epidural empyema can mimic diskospondylitis but is often associated with a primary infection elsewhere and may require MRI for differentiation. Meningitis presents with fever, neck pain, and leukocytosis, but imaging does not show vertebral changes. Steroid-responsive meningitis-arteritis is an immune-mediated condition that responds to corticosteroids, whereas diskospondylitis requires antimicrobial therapy. Other differentials include discospondylitis due to fungal infection, which may have a slower progression and different imaging characteristics.

The diagnostic algorithm for diskospondylitis begins with a thorough history and physical examination, including a complete neurological assessment. If spinal pain or neurological deficits are present, survey radiographs of the spine are obtained. Radiographic findings suggestive of diskospondylitis include narrowing of the intervertebral disc space, irregularity and lysis of the vertebral endplates, and sclerosis of adjacent vertebral bodies. However, radiographs may be normal in early cases. If radiographs are inconclusive or if neurological deficits are progressive, advanced imaging with computed tomography (CT) or magnetic resonance imaging (MRI) is recommended. CT provides excellent bone detail and can detect early endplate changes, while MRI is superior for evaluating soft tissue involvement, including epidural abscesses and spinal cord compression. In cases where a specific organism is suspected, blood cultures and urine cultures should be obtained. If surgical intervention is planned, intraoperative samples of the affected disc and bone should be collected for aerobic and anaerobic bacterial culture, fungal culture, and histopathology. Serology for Brucella canis should be performed in endemic areas or in breeding dogs. The diagnostic algorithm should also include a complete blood count, serum biochemistry profile, and urinalysis to identify underlying systemic infections.

Laboratory findings in diskospondylitis are often non-specific. A complete blood count may reveal leukocytosis with a left shift, but this is not always present. Serum biochemistry may show mild hyperglobulinemia and hypoalbuminemia due to chronic inflammation. Urinalysis may reveal evidence of urinary tract infection, which is a common primary source. Blood cultures are positive in approximately 30% to 50% of cases, and urine cultures may be positive in up to 50% of cases. Inflammatory biomarkers such as C-reactive protein (CRP) and serum amyloid A (SAA) may be elevated. Synovial fluid analysis is not typically performed unless there is concurrent joint involvement. Coagulation panel (PT/aPTT) is recommended if surgery is planned, especially if there is concern for sepsis. In cases of suspected fungal infection, serology for Aspergillus or Coccidioides may be helpful. Histopathology of surgical biopsy samples is essential for definitive diagnosis and to differentiate from neoplasia.

Radiography: Survey radiographs of the spine are the initial imaging modality. Findings include narrowing of the intervertebral disc space, irregularity and lysis of the vertebral endplates, and sclerosis of the adjacent vertebral bodies. In chronic cases, there may be new bone formation and vertebral fusion. However, radiographs may be normal in early disease, and changes may take 2 to 4 weeks to become apparent. Stress radiographs may be used to assess vertebral instability, but are rarely necessary. CT: Computed tomography provides detailed bone evaluation and can detect early endplate erosion, osteolysis, and sclerosis. It is also useful for surgical planning, as it allows assessment of vertebral body dimensions and implant placement. 3D reconstructions can help visualize the extent of the lesion. MRI: Magnetic resonance imaging is the most sensitive modality for evaluating soft tissue involvement. It can detect bone marrow edema, disc degeneration, epidural abscess formation, and spinal cord compression. MRI is particularly useful in cases with neurological deficits. Ultrasonography: Not typically used for spinal imaging, but may be used to evaluate the urinary tract for infection. Arthroscopy: Not applicable. Angiography/Fluoroscopy: May be used intraoperatively to guide needle placement for biopsy or to assess vascular anatomy.

Cytology: Fine-needle aspiration of the affected disc or vertebral body may be performed under fluoroscopic or CT guidance. Cytological examination may reveal inflammatory cells, including neutrophils and macrophages, and may identify bacterial or fungal organisms. However, the yield is low, and negative results do not rule out infection. Histopathology: Surgical biopsy of the affected disc and vertebral endplate is the gold standard for diagnosis. Histopathological findings include osteomyelitis with necrosis, infiltration of neutrophils and macrophages, and fibrosis. In bacterial infections, Gram-positive or Gram-negative organisms may be identified with special stains. In fungal infections, fungal hyphae or spores may be seen with PAS or GMS stains. Histopathology also helps rule out neoplasia. Surgical margins should be evaluated to ensure complete debridement.

Medical management is the first-line treatment for diskospondylitis and consists of antimicrobial therapy and pain management. However, surgical management is indicated in cases that fail to respond to medical therapy after 2 to 4 weeks, have progressive neurological deficits, exhibit severe spinal pain, or have vertebral instability, pathological fracture, or epidural abscess. Surgical techniques vary by location. For cervical lesions, a ventral slot approach is used to access the affected disc and vertebral bodies. The infected tissue is debrided, and samples are collected for culture and histopathology. Stabilization is achieved using a ventral vertebral body plate or pins and PMMA. For thoracolumbar lesions, a hemilaminectomy or dorsal laminectomy is performed to decompress the spinal cord and allow debridement of the infected disc. Stabilization may be achieved with vertebral body plating, pins and PMMA, or external skeletal fixation. For lumbosacral lesions, a dorsal laminectomy is performed to decompress the cauda equina and debride the infected disc. Stabilization may be achieved with pins and PMMA or transilial bolts. Postoperative management includes continued antimicrobial therapy based on culture and sensitivity results, typically for 6 to 12 weeks. Pain management includes opioids, NSAIDs, and muscle relaxants. Strict activity restriction is essential for 6 to 8 weeks to allow bone healing. Physical rehabilitation may be initiated after the initial healing period.

The prognosis for diskospondylitis is generally good with appropriate medical or surgical management. Medical management alone is successful in approximately 70% to 80% of cases. Surgical management is successful in about 80% to 90% of cases, with resolution of pain and neurological deficits. However, the prognosis is guarded in cases with severe neurological deficits, pathological fractures, or fungal infections. Negative prognostic indicators include chronicity, severe spinal cord compression, and involvement of multiple sites. Recurrence rates are low but can occur if antimicrobial therapy is discontinued prematurely. Complications include implant failure, infection, and neurological deterioration. Overall, the long-term prognosis is favorable for most dogs, with many returning to normal function.

Postoperative follow-up is crucial for monitoring recovery and detecting complications. Sutures are typically removed 10 to 14 days after surgery. Serial radiographs are recommended at 4, 8, and 12 weeks postoperatively to assess bone healing and implant stability. Radiographic changes may lag behind clinical improvement, so clinical assessment is also important. Restricted activity is recommended for 6 to 8 weeks, with gradual return to normal activity over the following 4 to 6 weeks. Physical rehabilitation, including passive range of motion exercises and controlled leash walks, may be initiated after the initial healing period. Antimicrobial therapy should be continued for at least 6 to 12 weeks, and repeat blood and urine cultures may be performed to ensure resolution of infection. Long-term monitoring for recurrence of clinical signs is recommended, with repeat imaging if necessary.

Pearls: 1. Always obtain multiple tissue samples for culture (aerobic, anaerobic, fungal) and histopathology during surgery. 2. Use a surgical approach that provides adequate exposure for both decompression and stabilization. 3. Consider using autogenous cancellous bone graft to promote fusion after debridement. 4. In cervical lesions, the ventral slot approach provides excellent exposure, but care must be taken to avoid the vertebral arteries and spinal cord. 5. For lumbosacral lesions, a dorsal laminectomy allows decompression of the cauda equina and access to the disc space. Pitfalls: 1. Failure to identify and treat the primary source of infection can lead to recurrence. 2. Inadequate debridement of infected bone and disc can result in persistent infection. 3. Overlooking vertebral instability can lead to implant failure and neurological deterioration. 4. Using implants in an infected field increases the risk of implant-associated infection; therefore, strict aseptic technique and appropriate antimicrobial therapy are essential. 5. Postoperative activity restriction is critical to allow bone healing; premature activity can cause implant failure.

Perioperative antimicrobial therapy: Cefazolin (22 mg/kg IV) administered 30 minutes before incision and repeated every 90 minutes during surgery. Postoperative antimicrobial therapy should be based on culture and sensitivity results. If no culture is available, a broad-spectrum antimicrobial such as amoxicillin-clavulanate (13.75 mg/kg PO q8h) or enrofloxacin (10 mg/kg PO q24h) combined with metronidazole (15 mg/kg PO q12h) may be used. Antimicrobial therapy should be continued for 6 to 12 weeks. Pain management: Preoperative opioids such as methadone (0.2-0.5 mg/kg IV) or hydromorphone (0.05-0.1 mg/kg IV) are administered. Postoperative analgesia may include fentanyl CRI (2-5 mcg/kg/h IV) for 24 hours, followed by oral tramadol (2-5 mg/kg PO q8h) or gabapentin (10 mg/kg PO q8h). NSAIDs such as carprofen (2.2 mg/kg PO q12h) or meloxicam (0.1 mg/kg PO q24h) may be used if there are no contraindications. Muscle relaxants such as methocarbamol (15-20 mg/kg PO q8h) may be used to reduce muscle spasms. Chondroprotectants such as polysulfated glycosaminoglycan (4.4 mg/kg IM q7d) may be considered, but their efficacy is not well established. In cases of fungal infection, antifungal therapy with fluconazole (5-10 mg/kg PO q12h) or itraconazole (5 mg/kg PO q12h) should be initiated.

Several studies have evaluated the outcomes of surgical management of diskospondylitis. A retrospective study by Betbeze et al. (2006) reported successful outcomes in 85% of dogs undergoing surgical debridement and stabilization. Another study by Auger et al. (2016) found that dogs with diskospondylitis treated with surgery had a shorter time to resolution of pain compared to medical management alone. A consensus statement from the ACVS recommends surgical intervention for cases with progressive neurological deficits, severe pain, or vertebral instability. A study by Ruoff et al. (2017) reported that the use of autogenous cancellous bone graft improved fusion rates. The use of advanced imaging, particularly MRI, has been shown to improve diagnostic accuracy and surgical planning. Overall, the evidence supports surgical management as a viable option for cases that fail medical therapy, with good to excellent outcomes in most cases.