Diskitis is an inflammation of the vertebral disk space often related to infection. Infection of the disk space must be considered with vertebral osteomyelitis; these conditions are almost always present together, and they share much of the same pathophysiology, symptoms, and treatment.
Although diskitis and associated vertebral osteomyelitis are uncommon conditions, they are often the causes of debilitating neurologic injury. Unfortunately, morbidity can be exacerbated by a delay in diagnosis and treatment of this condition. The lumbar region is most commonly affected, followed by the cervical spine and, lastly, the thoracic spine.[1, 2, 3, 4, 5]
An infection does not ordinarily originate in the vertebra or disk space; rather, it typically spreads there from other sites via the bloodstream. Spinal arteries form two lateral anastomotic chains and one median anastomotic chain along the posterior surface of the vertebral bodies. The spinal arteries are the origins of the periosteal arteries, which in turn give rise to metaphyseal arteries.
In children, anastomoses between metaphyseal arteries are made by the intermetaphyseal arteries; however, in adults, the intermetaphyseal arteries degenerate, causing direct diffusion from the adjacent endplate to be the only source of nutrients for the disk. Septic emboli travelling through this arterial system enter the metaphyseal arteries, which have become end arteries in the adult, causing a large area of infarction. Infarction of the vertebral endplates is followed by localized infection that subsequently spreads through the vertebral body and into the poorly vascularized disk space. Infection can then spread to the epidural space or paraspinal soft tissues.
The other anastomotic vascular system of the spine is the venous system. The venous system of the spine, like the arterial system, forms an anastomotic plexus (Batson plexus) in the epidural space. This plexus drains each segmental level and is continuous with the pelvic veins. Retrograde flow through this plexus during periods of high intra-abdominal pressure has been postulated to allow the spread of infection from the pelvic organs.
Support for this hypothesis comes from the observation that pelvic disease is one of the most common primary sites of infection in patients with diskitis. Other authors take issue with this hypothesis, citing animal studies that show retrograde flow through the epidural venous plexus only at extremely high intra-abdominal pressures that are not physiologic.
Diskitis is thought to spread to the involved intervertebral disk via hematogenous spread of a systemic infection (eg, urinary tract infection [UTI]). Many sites of origin have been implicated, but UTI, pneumonia, and soft-tissue infection seem to be the most common. Direct trauma has not been conclusively shown to be related to diskitis. Intravenous (IV) drug use with contaminated syringes offers direct access to the bloodstream for a variety of organisms. Often, no other site of infection is discovered.
Staphylococcus aureus is the organism most commonly found; however, Escherichia coli and Proteus species are more common in patients with UTIs. Pseudomonas aeruginosa and Klebsiella species are other gram-negative organisms observed in IV drug abusers, although they are not seen as commonly as S aureus. Not surprisingly, medical conditions that predispose patients to infections elsewhere in the body are associated with diskitis. Diabetes, AIDS, steroid use, cancer, and chronic renal insufficiency are common comorbidities.[1]
Although rare, infection of the disk space can also occur following surgical intervention at the site. The infection rate after anterior cervical diskectomy has been quoted at 0.5% of cases; the infection rate for lumbar diskectomy is half that. In such cases, infection is transmitted through direct inoculation of the operative site. As in spontaneous diskitis, the most common organism is S aureus, but Staphylococcus epidermidis and Streptococcus species also should be considered.
Childhood diskitis has not been consistently associated with an initial causative infection elsewhere in the body. S aureus is the most common organism found.
In the United States, the incidence of diskitis ranges from 1 in 100,000 population to 1 in 250,000 population. In other developed nations, the incidence of diskitis is similar; however, in less developed nations, infectious diskitis is much more common. In some areas of Africa, it has been reported that 11% of all patients seen for back pain were diagnosed with diskitis.
A bimodal distribution of ages occurs with diskitis. Childhood diskitis affects patients with a mean age of 7 years. The incidence of diskitis then decreases until middle age, when a second peak in incidence is observed at approximately 50 years of age. Some authors argue that childhood diskitis is a separate disease entity and should be considered independently.
The predominance of diskitis in males is more pronounced in adults, with male-to-female ratios ranging from 2:1 to as high as 5:1. Childhood diskitis has a slight male prevalence, with a male-to-female ratio of 1.4:1.
Most patients are cured by a treatment protocol of antibiotics, either alone or in combination with surgery. Only 15% of patients experience permanent neurologic deficits. Recrudescence of infection occurs in 2-8% of patients.
Mortality associated with diskitis occurs from the spread of infection, either through the nervous system or through other organs. Mortality has been reported to be 2-12%.
Karadimas et al retrospectively analyzed the outcomes of a large series of patients treated for spondylodiskitis. Patients were divided into three groups: 70 who received nonoperative treatment (group A), 56 who underwent posterior decompression alone (group B), and 37 who underwent decompression and stabilization (group C).[6] At 12-month follow-up, treatment had failed in eight of the group A patients. Reoperation was necessary in 24 of the group B patients and in six of the group C patients. None of the group A patients had neurologic symptoms; 11 of the group B patients had neurologic deficits, five of whom benefited from surgery; and 11 of the group C patients had altered neurologic deficits.
The significance of antibiotic regimen compliance is the single most important factor in patient education. Incomplete treatment can lead to resistance with devastating results.
The importance of orthotic brace compliance must also be stressed.
Educate patients on early neurologic signs, and instruct patients to return for medical attention on detection of the slightest deficit.
Unfortunately, adult diskitis has a slow, insidious onset, which can cause diagnosis to be delayed for months. Neck or back pain with localized tenderness is the initial presenting complaint. Movement exacerbates these symptoms, which are not alleviated with conservative treatment (eg, analgesics or bed rest).
In patients who are chronically ill, a high incidence of epidural extension of the infection exists, causing lower-extremity weakness or plegia. Fever, chills, weight loss, and symptoms of systemic disease may be present, but they are not common.
In postoperative patients, symptoms usually begin days to weeks after surgery. Symptoms are similar to those experienced by patients with spontaneous diskitis, consisting of pain without neurologic abnormality. Limited movement and localized tenderness also occur; however, superficial signs of infection are rare (only 10% of cases). Diagnosis is rarely delayed in postoperative patients, which is the main reason that neurologic deficit is uncommon in these cases.
The disease has a more acute course in children. A sudden onset of back pain, refusal to walk, and irritability are the most common symptoms. Fever is often present, accompanied by local tenderness and limited back motion.
Localized tenderness over the involved area with concomitant paraspinal muscle spasm is the most common physical sign. If the cervical or lumbar segments are involved, restricted mobility secondary to pain occurs. Reported rates of neurologic deficit (eg, radiculopathy, myelopathy) vary widely, ranging from 2% to 70%. Cervical disease is associated with a much higher rate of neurologic deficit.
Elevations in the erythrocyte sedimentation rate (ESR) and the C-reactive protein (CRP) level are the most consistent laboratory abnormalities seen in cases of diskitis. The mean ESR for patients with diskitis is 85-95 mm/hr. The utility of the ESR can be extended by performing serial measurements during treatment. A 50% decline in the ESR can usually be expected with successful treatment, and the ESR often continues to decline after treatment. Frequently, the ESR may not return to normal levels despite adequate therapy.
Leukocytosis is often present in systemic disease but is frequently absent in diskitis cases. Diskitis is generally accompanied by a normal peripheral white blood cell (WBC) count if the primary site of infection has been treated.
Procalcitonin (PCT) has been evaluated as a diagnostic tool and monitoring parameter for spondylodiskitis and for discrimination between bacterial infection and aseptic inflammation of the spine, but a study by Maus et al did not find it to be useful for these purposes.[7] A study by Jeong et al found serum PCT to be less sensitive than serum CRP in patients with spinal infection.[8]
Blood cultures must be obtained on a frequent basis for any patient suspected of harboring an infected disk. Appropriate therapy may be instituted for positive blood cultures without the need for invasive tests. Unfortunately, blood cultures are positive in only one third to one half of diskitis cases.
Sputum and urine cultures are necessary to locate any other sources of infection, including respiratory and genitourinary sites.
Although radiographic films of the spine can be very useful in diagnosing diskitis, abnormalities are visible only after several weeks following the onset of disease. The most common early finding on plain films is disk-space narrowing, followed by irregularities and erosion of the adjacent endplates and calcification of the anulus around the affected disk. As osteomyelitis progresses, bone density decreases, with loss of the normal trabeculation of the vertebra. If bone destruction continues, subluxation (with possible instability of the spine) becomes evident.
Magnetic resonance imaging
The most sensitive and specific test for diskitis is magnetic resonance imaging (MRI). T1-weighted images (see the image below) show narrowing of the disk space and low signals consistent with edema in the marrow of adjacent vertebral bodies. T2-weighted images show increased signals in both the disk space and the surrounding vertebral bodies.
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Sagittal T1-weighted MRI of the lumbar spine in a 74-year-old man, revealing diskitis of the L4-L5 disk space. Note extensive destruction of the endpl....
MRI is very useful in helping distinguish between infectious diskitis, neoplasia, and tuberculosis. Diffusion-weighted imaging is useful in distinguishing between degenerative and infectious endplate abnormalities. Compared with positron emission tomography (PET), diffusion-weighted MRI costs less, has faster imaging times, and lacks ionizing radiation.[9]
Disk-space involvement directs attention toward infection; it only is involved late in tuberculosis and very rarely in neoplasia.
With the use of intravenous (IV) contrast (see the image below), MRI, like computed tomography (CT), can detect paraspinal disease (eg, paraspinal phlegmon or epidural abscess). A large amount of paraspinal soft-tissue swelling and a psoas abscess are often associated with spinal tuberculosis.
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Contrast-enhanced sagittal T1-weighted MRI image in a 55-year-old woman shows thoracic diskitis with an associated epidural abscess and spinal cord co....
Computed tomography
CT has the ability to detect diskitis earlier than plain radiography does. Findings include hypodensity of the intervertebral disk and destruction of the adjacent endplate and bone (see the image below), with edematous surrounding tissues.
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Axial CT scan in a patient with diskitis demonstrates extensive destruction of the vertebral endplate. Note the preservation of the posterior elements....
Certain bacterial organisms can also produce gas in the site that is easily detected on CT scans. However, this is not pathognomonic, because as it can be present in degenerative spine disease.
The advantage of CT over radiography is that it can also detect associated paraspinal disease, especially when combined with IV contrast or myelography. CT can serve as a supplement to MRI, in that it is better able to distinguish between bone and soft tissue than MRI. CT can help monitor successful treatment, which is accompanied by increased bone density and sclerosis.
Nuclear medicine
Gallium-67 and technetium-99m have been utilized in the detection of diskitis with similar results. Radionuclide scanning has demonstrated a high degree of sensitivity shortly after the onset of symptoms. Diffuse initial uptake is followed by more focal uptake on delayed scans. Technetium-99m has been recommended more often because of its lower cost and smaller radiation dose.
Because of the availability and sensitivity of other tests, radionuclide scans may be most useful in the workup of patients with fever of unknown origin.
Indium-111 WBC scintigraphy has been shown to have a low sensitivity for diskitis and is not the test of choice.
Bone scans are not specific for infection over inflammation; therefore, they are ineffective in postoperative patients.
Needle or trocar placement into the infected area is a minimally invasive test used to obtain histologic confirmation of the disease and tissue samples for culture. The yield and safety of the procedure are maximized by employing CT for guidance (see the image below). As in blood cultures, positive tissue cultures occur in only half of biopsies, especially if antibiotic therapy has already been initiated. In such cases, needle biopsy can be repeated, or the patient can be referred for open surgical biopsy.
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Trajectory of a needle in a biopsy of the infected disk space guided by CT scan. Care is taken to avoid the thecal sac and nerve roots.
Surgical biopsy
Open biopsy is the most invasive test. In some studies, it has been found to have the highest yield in terms of positive cultures and diagnosis confirmation.[10] Whereas some surgeons prefer to combine open biopsy with surgical debridement, no difference has been found between antibiotics and debridement when compared with antibiotics alone in cases of early diskitis.
The histologic findings of diskitis are similar to those of any bacterial pyogenic infection. Local destruction of the disk and endplates occurs with infiltration of neutrophils in the early stages. Later, a lymphocytic infiltrate predominates.
Antibiotic treatment must be tailored to the isolated organism and any other sites of infection. Broad-spectrum antibiotics must be used if no organism is isolated; however, this is very rare, and other disease processes (eg, spinal tuberculosis) must be considered in the face of persistently negative cultures.
Parenteral antibiotics are a requirement, even for outpatients. They are usually administered for 6-8 weeks. Before parenteral therapy is discontinued, the erythrocyte sedimentation rate (ESR) should have dropped by one half to one third, the patient should have no pain on ambulation, and there should be no neurologic deficits (see Complications and Long-Term Monitoring).[1, 3]
The use of oral antibiotics after intravenous (IV) treatment has not been shown to be of added benefit.
Any laboratory or clinical sign of persistent infection should prompt another biopsy and continued antibiotic therapy.
Immobilization
Immobilization is necessary, especially in the initial stages of the disease. The goal of immobilization is to provide the opportunity for the affected vertebrae to fuse in an anatomically aligned position.
Two weeks of bed rest should be followed by external immobilization with a brace when the patient gets out of bed. Any pain on ambulation is an indication for continued bed rest. Generally, bracing is used for 3-6 months following initiation of treatment; however, even with the use of appropriate antibiotics and bracing, collapse of the vertebral segments and kyphos formation may occur.
Pain control
Pain medications can be a useful adjunct to antibiotic therapy, in that they allow increased mobilization.[2]
Indications for surgery beyond open biopsy include the following:
Neurologic deficit
Spinal deformity
Disease progression
Noncompliance
Antibiotic toxicity
The goal of surgery are as follows:
To remove diseased tissue
To decompress neural structures
To ensure spinal stability
Although in most cases the vertebrae fuse spontaneously after diskitis and osteomyelitis, operative fusion can be a useful adjunct by allowing earlier mobilization of the patient. Despite early concerns, use of a fusion plug and metallic instrumentation in an infected field has not been shown to impede successful treatment.
Neurologic deficits develop in 13-40% of patients, especially those with diabetes or other systemic illnesses. Transfer to an institution with neurosurgical or orthopedic spinal care is warranted for any patient demonstrating neurologic decline for decompression and possible stabilization.
Long-term antibiotic therapy may lead to ototoxicity or renal toxicity.
No particular diet has been shown to have a clinical benefit in patients with diskitis.
Many authors believe that 2 weeks of bed rest with initial treatment helps prevent the development of a kyphotic deformity. Use of an orthotic brace to help stabilize the spine while spontaneous fusion takes place is recommended for 3-6 months. Ambulation is recommended only if the patient has neither pain nor radiographic signs of instability.
No specific deterrence is available for diskitis except treatment of the underlying disease (eg, diabetes, sepsis).
Sharma et al reported on the severe complication of diskitis following diskography.[11] They found that the available clinical evidence did not conclusively demonstrate that IV or intradiskal antibiotics during diskography decreased the rate of diskitis in comparison with sterile technique alone. Animal model research supports prophylactic antibiotic use when used before iatrogenic inoculation of intervertebral disks. Both single- and double-needle techniques when used with stylettes are superior to nonstyletted techniques, according to the authors.
Once the correct treatment is implemented, monitor patients to rule out progressive neurologic deficit.
A falling ESR is consistent with successful treatment. Although ESR values should fall by at least one third to one half, rarely do they return to preinfection levels. Reduction of C-reactive protein (CRP) levels has been shown to be more sensitive than ESR in some studies.
Serial radiographic examination is a necessity to detect bony collapse or deformity. Successful treatment is accompanied by appropriate changes, including sclerosis of the endplates, on plain radiography and computed tomography (CT). Nevertheless, radiographic findings are significantly slower than clinical response and cannot be used to assess eradication of infection.
Parenteral narrow-spectrum antibiotics should be prescribed according to the organism isolated. If cultures are consistently negative, administer broad-spectrum antibiotics for several weeks.
Clinical Context:
Potent antibiotic that is directed against gram-positive organisms and is active against Enterococcus species. Useful in the treatment of septicemia and skin structure infections. Indicated for patients who cannot receive or have failed to respond to penicillins or cephalosporins or who have infections with resistant staphylococci. For abdominal penetrating injuries, it is combined with an agent active against enteric flora and/or anaerobes.
To avoid toxicity, the current recommendation is to assay vancomycin trough levels after the third dose is drawn and a half an hour prior to the next dose. Use CrCl to adjust the dosage in patients diagnosed with renal impairment.
Used in conjunction with gentamicin for prophylaxis in patients who are allergic to penicillin and are undergoing gastrointestinal or genitourinary procedures.
Clinical Context:
Initial therapy for suspected penicillin-G–resistant streptococcal or staphylococcal infections. Use parenteral therapy initially for severe infections. Change to oral therapy as condition warrants.
Due to thrombophlebitis, particularly in the elderly, administer parenterally only for short term (1-2 d); change to oral route as clinically indicated.
Clinical Context:
Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin-binding proteins.
What is diskitis?What is the pathophysiology of diskitis?What causes diskitis?What is the prevalence of diskitis?What is the prognosis of diskitis?What should be included in patient education about diskitis?Which clinical history findings are characteristic of diskitis?Which physical findings are characteristic of diskitis?What conditions should be considered in the differential diagnoses of diskitis?What are the differential diagnoses for Diskitis?What is the role of lab testing in the diagnosis of diskitis?What is the role of plain radiography in the diagnosis of diskitis?What is the role of MRI in the diagnosis of diskitis?What is the role of CT scanning in the diagnosis of diskitis?What is the role of radionuclide scanning in the diagnosis of diskitis?What is the role of echocardiography in the diagnosis of diskitis?What is the role of needle biopsy in the diagnosis of diskitis?What is the role of surgical biopsy in the diagnosis of diskitis?Which histologic findings suggest diskitis?What is the role of antibiotics in the treatment of diskitis?What is the role of immobilization in the treatment of diskitis?What is the role of pain medications in the treatment of diskitis?What are indications for the surgical treatment of diskitis?What is the goal of surgery for diskitis?What is the efficacy of surgery for diskitis?What are the possible complications of diskitis?Which dietary modifications are used in the treatment of diskitis?Which activity modifications are used in the treatment of diskitis?How is diskitis prevented?Which specialist consultations are beneficial to patients with diskitis?What is included in the long-term monitoring of patients with diskitis?Which medications are used in the treatment of diskitis?Which medications in the drug class Antibiotics are used in the treatment of Diskitis?
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
William O Shaffer, MD, Orthopedic Spine Surgeon, Northwest Iowa Bone, Joint, and Sports Surgeons
Disclosure: Received royalty from DePuySpine 1997-2007 (not presently) for consulting; Received grant/research funds from DePuySpine 2002-2007 (closed) for sacropelvic instrumentation biomechanical study; Received grant/research funds from DePuyBiologics 2005-2008 (closed) for healos study just closed; Received consulting fee from DePuySpine 2009 for design of offset modification of expedium.
Chief Editor
Jeffrey A Goldstein, MD, Clinical Professor of Orthopedic Surgery, New York University School of Medicine; Director of Spine Service, Director of Spine Fellowship, Department of Orthopedic Surgery, NYU Hospital for Joint Diseases, NYU Langone Medical Center
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Medtronic, Nuvasive, NLT Spine, RTI, Magellan Health<br/>Received consulting fee from Medtronic for consulting; Received consulting fee from NuVasive for consulting; Received royalty from Nuvasive for consulting; Received consulting fee from K2M for consulting; Received ownership interest from NuVasive for none.
Additional Contributors
George I Jallo, MD, Professor of Neurosurgery, Pediatrics, and Oncology, Director, Clinical Pediatric Neurosurgery, Department of Neurosurgery, Johns Hopkins University School of Medicine
Sagittal T1-weighted MRI of the lumbar spine in a 74-year-old man, revealing diskitis of the L4-L5 disk space. Note extensive destruction of the endplates of the adjacent vertebral bodies. No compression of the thecal sac is present, which is an important consideration when contemplating surgical intervention.
Contrast-enhanced sagittal T1-weighted MRI image in a 55-year-old woman shows thoracic diskitis with an associated epidural abscess and spinal cord compression. Because of the significant cord compression, this patient underwent surgical decompression.
Axial CT scan in a patient with diskitis demonstrates extensive destruction of the vertebral endplate. Note the preservation of the posterior elements, including facet joints, lamina, and spinous process. This is characteristic for pyogenic diskitis and less common in tuberculosis (Pott disease).
Trajectory of a needle in a biopsy of the infected disk space guided by CT scan. Care is taken to avoid the thecal sac and nerve roots.
Axial CT scan in a patient with diskitis demonstrates extensive destruction of the vertebral endplate. Note the preservation of the posterior elements, including facet joints, lamina, and spinous process. This is characteristic for pyogenic diskitis and less common in tuberculosis (Pott disease).
Sagittal T1-weighted MRI of the lumbar spine in a 74-year-old man, revealing diskitis of the L4-L5 disk space. Note extensive destruction of the endplates of the adjacent vertebral bodies. No compression of the thecal sac is present, which is an important consideration when contemplating surgical intervention.
Contrast-enhanced sagittal T1-weighted MRI image in a 55-year-old woman shows thoracic diskitis with an associated epidural abscess and spinal cord compression. Because of the significant cord compression, this patient underwent surgical decompression.
Trajectory of a needle in a biopsy of the infected disk space guided by CT scan. Care is taken to avoid the thecal sac and nerve roots.
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