3.18 The infected spine

It is known that spinal infections have afflicted humans since early times. Osteomyelitic changes affecting the spine have been demonstrated in skeletons from 4000 bc found in the Nile Valley and in Egyptian mummies.

Classification is normally by the causative organism. Infective organisms may be pyogenic, granulomatous, or parasitic. Infection is usually either by direct implantation or secondary to a septic focus elsewhere in the body with spread into the vertebrae through Batson’s plexus of veins or the segmental arteries. Infection may affect the vertebral body, the intervertebral disc, the epidural space, and the posterior elements, but most commonly involves the anterior and middle columns.

Pyogenic infections may present acutely or chronically. The presentation depends on the age of the patient, the immune response, and the infecting organism. Almost any infective organism can cause vertebral infection under suitable conditions. The most common by far is Staphylococcus aureus, but in a significant minority of cases there is Escherichia coli, Proteus, and streptococcal involvement. The mode of spread is usually from other septic foci via the vascular system. The most common site is in the lumbar spine and multiple vertebral involvement is usual. Infection may track along tissue planes, and without early control will cause secondary abscess formation and pointing at distant sites. The vertebral canal may be invaded by pus and granulation tissue either directly from the disc space or through the exit foramenae causing meningitis or transverse myelitis. If this occurs, recovery is uncommon. Retropulsion of bone or disc causes neural compromise, and destruction of vertebral body and discs causes local instability and deformity. However, with effective control, healing occurs with fusion of adjacent vertebrae.

The incidence of pyogenic spinal infection is almost certainly increasing because of increased awareness, diagnostic improvements, and enlargement of the ‘at-risk’ group (HIV/AIDS, poor nutrition, the elderly, diabetes, and other comorbidity) Spinal infection represents 3–4% of all osteomyelitis, but the figure has been quoted as high as 16%. The population incidence is about 1 in 250 000. Spinal infection is involved in 10–11 per 10 000 hospital admissions for back pain. Epidural abscess is thankfully rare and represents about 1.2 per 10 000 hospital admissions.

The presence of associated ‘conditions’ tends to delay diagnosis and there is a higher risk of neurological compromise. Direct spread of infection also occurs with stab wounds, gunshot wounds, and surgical trauma to the spine.

Localized constant pain, often at an unusual site and exacerbated by movement and percussion, is the most common feature, and there is associated muscle spasm. Most patients do not present with acute pyogenic signs. Fever is present in only about a third of cases.

Neurological deficits may be present and careful evaluation is vital, especially where there is pre-existing pathology. Neurological signs, which will depend upon the nature and site of the spinal infection, will be present in 15% of patients. Quadriplegia is a presenting feature in cervical spine involvement, and paraplegia in the thoracic spine. Lumbosacral involvement is more likely to produce single or multiple root deficits.

Primary extradural abscesses have a predilection for the thoracic spine. The usual presentation is a history of severe local unremitting pain with single root symptoms. There is a tendency for the epidural abscess to spread throughout the epidural space causing rapid onset of neurological deterioration and paraplegia.

The erythrocyte sedimentation ratio (ESR) is usually above 50mm/h, and C-reactive protein (CRP) and alkaline phosphatase may be raised. These tests are non-specific and may be difficult to evaluate, particularly in children and patients with rheumatoid arthritis. CRP is best for postoperative infection. The white cell count is raised in less than half of cases. Blood cultures when the patient is febrile are more reliable. Urine culture may be valuable if urethral manipulation is considered to be causative.

Although plain radiography is imperative, it is of little value in early cases. Disc-space narrowing and occasionally paraspinal widening occurs after 2–3 weeks, and secondary bone changes may take up to 3 months to occur. The earliest changes are of loss of delineation of subchondral bone. Radiographic changes are progressive with time but may remain limited to the disc complex (Figure 3.18.1). Plain radiographs are not very useful in assessing response to treatment.

Technetium-99m bone scans can be positive as early as 2 days from the onset of symptoms; they have a high sensitivity (95%) but a lower specificity (75%). Positron emission tomography (PET) scanning is helpful but not widely available. Indium and gallium scans have proved less useful.

Computed tomography (CT) scanning (Figure 3.18.2) is useful for assessing the degree of bone destruction and examining the surrounding soft tissues.

Magnetic resonance imaging (MRI) scanning has become the most important investigation. It has a sensitivity of 96%, about the same as radionuclear scanning, but has a higher specificity (up to 95%)(Figure 3.18.3).

The diagnostic ‘yield’ from needle biopsy is disappointingly low. A histological diagnosis is almost invariably positive, but less than 50% produce a positive culture, particularly when antibiotics have been used. Pus from needle biopsy of the primary focus or from more distant abscess cavities gives 80–90% successful culture.

Needle biopsy can provide confirmatory material especially when culture is negative.

The most common differential is between infection and tumour. Haematomas may mimic epidural infection. Diagnosis of pyogenic infection within either the disc or the bony canal can be difficult after recent spinal surgery.

The principles of non-operative treatment are rest and appropriate antibiotics. When the diagnosis is certain, the organism is known, and there are no progressive neurological features, non-operative treatment is indicated. Bed rest and intravenous antibiotics may be required initially with the acute presentation, and this should be continued until pain reduces and a response can be confirmed. The patient may then be mobilized in a brace and continue on oral antibiotics.

The length of time required on antibiotics is arbitrary and depends on the organism, its sensitivity, and the patient’s clinical response. As a guide, intravenous antibiotics should be used for a period of 6–8 weeks followed by a similar period of treatment with oral antibiotics. Some recommend indefinite antibiotics to suppress infection. Serial ESR/CRP examination is usually of value and antibiotics should continue for a month after both symptoms and ESR have returned to normal. Radiographic and MRI evaluation is useful, but there is a distinct lag-time before healing can be confirmed.

Surgical management is indicated if there is a failure of conservative treatment, or the diagnosis and organism cannot be confirmed, or there is a significant neurological deficit, particularly when there is epidural spread. Mechanical instability may also be an indication for surgical management. The aims of surgery are to drain the abscess, make a definitive diagnosis, and decompress the neural tissue, either root or cord. Following this, it is necessary to achieve stability and rapid healing of the lesion by bone grafting and internal fixation. Surgery should always be directed to the area of pathology. Usually this involves an anterior approach to the spine. There is no place for decompressive laminectomy alone, which almost invariably produces instability, except in the rare cases of epidural abscess or where there is primary posterior involvement.

In the debilitated patient it is possible to drain an abscess by the posterolateral approach. It is difficult to achieve spinal stability by this approach, particularly if there has been significant vertebral destruction.

There is a significant mortality following surgery in the high-risk groups, where diagnosis has been delayed and destruction of soft tissue is extensive. Neurological recovery occurs in more than 80% of cases, particularly where there is neurological sparing preoperatively. Recovery may be delayed for many weeks, particularly in elderly patients.

Late deformity following pyogenic infection can present a formidable challenge. The neurological deficit which often accompanies severe deformity adds to the difficulty. Scarring in the neural canal and almost certainly long-standing vascular inadequacy makes correction and stabilization a high-risk procedure.

Although the term discitis was originally used solely for infection in children it has now come to describe any primary disc-space infection. There are two types of discitis, one occurring in children and the other occurring following endplate closure. In adults, haematogenous spread probably cannot occur through the intact endplate. Either an intradiscal procedure has been undertaken or there is a defect in the endplate.

Discitis in children is characterized by severe localized back pain and spasm, loss of disc-space height, and a raised ESR. In the pre-antibiotic era this condition was known as benign osteomyelitis, because discitis is usually self-limiting and heals without antibiotics to a bony ankylosis.

Children present with only mild toxaemia but with a constant well-localized back pain, muscle spasm, and stiffness. The child will often not weight-bear. Pain may be referred to the hips and upper thigh, particularly when the infection is in a lumbar disc. Delay in diagnosis is not uncommon. The white cell count is usually normal, but with a raised ESR or CRP. Blood cultures are usually negative. Initially there are no radiographic changes. After 2 weeks there is a progressive disc-space narrowing, and at about 2–3 months some endplate irregularity is apparent. Quite marked central erosions into the endplate may be produced.

MRI is usually diagnostic. Disc biopsy for culture and histology is usually unnecessary.

The mainstay of treatment is rest, initially strict bed rest, followed by mobilization in a well-fitting cast or brace as soon as the pain reduces, often after 2 or 3 days. Broad-spectrum intravenous antibiotics are usually given initially before progressing to oral treatment. This is despite the fact that it has been shown that this condition is usually self-limiting, even without antibiotics.

Surgery has a place only when pain persists, and in these cases there is often marked endplate destruction and sclerosis. Following curettage and grafting, healing is often rapid.

It is notable that late kyphosis rarely occurs in childhood discitis. However, in babies who develop vertebral infection in the first few months of life, vertebral destruction is rapid and is followed by the development of kyphosis (Figure 3.18.4).

Disc-space infection can occur following any invasive procedure on the disc. The avascular disc is prone to low-grade infection with only a small innoculum but can almost certainly be minimized by prophylactic antibiotics.

Postdiscectomy discitis is characterized by the onset of severe back pain a few days after an invasive procedure. The pain is continuous and may be referred to the hips. Tenderness is well localized and there is considerable spasm of the back muscles. The white cell count is often normal but the ESR and CRP is raised. MRI is usually positive. Rest and broad-spectrum antibiotics may be required even if the condition cannot be confirmed with certainty. Late erosive changes in the endplate are seen on both MRI scans and radiography.

The natural history is of resolution over a period of weeks and occasionally months. About 50% fuse spontaneously within 2 years.

Spinal surgery involving implants carries an infection risk of 3–4%. We found 95% involved either Propionibacteria or Staphylococcus aureus. The remainder involve Gram negative organisms. Prophylactic antibiotics should always be used when implanting metal. Effective treatment implies early diagnosis and drainage. As with implants elsewhere, the wound is opened thoroughly, debrided, and thoroughly irrigated, and the metal is left in place until fusion has occurred. Intravenous antibiotics may be required for 6–12 weeks followed by oral therapy. Cure can only be obtained with removal of the implants.

Granulomatous lesions are caused by organisms typified by the formation of a granuloma. The most common of these are tuberculosis and brucellosis, but fungi can also be a cause.

More than 30 million patients suffer from overt tuberculosis in the world today, of whom 2–3% have involvement of the skeletal system. Spinal tuberculosis accounts for roughly 50% of all cases. There are an estimated two million patients with active spinal tuberculosis in the world, and the numbers are likely to increase due to the poor economy and living standards of the developing nations, the increasing incidence of HIV-infected patients, and emergence of multidrug-resistant strains.

The organism usually responsible for spinal tuberculosis is Mycobacterium tuberculosis. Pulmonary tuberculosis is found in less than 10% of patients (Figure 3.18.5A). The spread of infection is mainly via the arterial vascular channels and Batson’s perivertebral venous plexus. More than 50% of lesions occur in the dorsolumbar region. Children show a higher incidence of cervical involvement than adults. About 5% of patients have skip lesions, which are separated by two or three normal vertebrae (Figure 3.18.5B).

The vertebral bodies are affected in the majority of the patients, but the appendices (pedicle, laminas, transverse process, or spinous process) are involved in less than 10%. Many types of body involvement are observed (Figure 3.18.6). Paradiscal infection is the most common type, especially in adolescents and young adults. The infection spreads through the epiphyseal arteries and there is narrowing of the disc space with involvement of the adjacent bodies. Disc-space narrowing is observed 2–3 months before any osseous changes are seen (Figure 3.18.6A).

Complete destruction of one or two vertebrae is more common in children below the age of 10 years. The anterior column deficit is enormous, and these children are specifically prone to severe deformity and late-onset paraplegia (Figure 3.18.6B). Posterior or the appendicial lesions may affect the pedicle, transverse process, laminas, or spinous process (Figures 3.18.7 and 3.18.8).

The natural history of untreated spinal tuberculosis is one of continued destruction of the vertebral bodies and progressive deformity with potential for neurological deficit due to compression of the neural structures by caseous and infective granulation tissue. Specific antituberculous chemotherapy can arrest the progress of the disease at any stage and hasten the healing and consolidation of the focus.

The disc is destroyed early in the course of the disease. The rate of bony fusion in spinal tuberculosis is high. In patients with severe disease, many vertebral bodies are destroyed and there is usually a severe collapse before contact of healthy bone can take place (Figure 3.18.9B). Deformity may progress to more than 60 degrees in about 5% of the patients, and there may be some neurological symptoms or signs in about 15–20%. Children who have a severe collapse of more then 90 degrees in the dorsal and the dorsolumbar vertebra are also prone to late-onset paraplegia in their second or third decade.

There is usually insidious, but sometimes acute onset of weight loss, loss of appetite, malaise, and evening rise of temperature, pain, and restriction of movement localized to the site of the lesion but soon becomes referred and aggravated with spinal movements. Tenderness to pressure over the involved vertebra is always present, and tapping on the spinous process causes referred pain. Deformity occurs as the involved vertebrae are softened. A retropharyngeal abscess causes difficulty in deglutition and phonation (Figure 3.18.10A). A cold abscess is present in more than half of patients (Figures 3.18.11 and 3.18.12).

Thoracic paravertebral abscesses may spread into the extrapleural space or may rupture into the pleura, resulting in empyema or track backwards along the intercostal vessels and nerves onto the chest wall. In lumbar lesions, the majority of cold abscesses enter the psoas sheath and form a psoas mass in the groin, the pelvis, the gluteal region, or the posterior aspect of the thigh or the popliteal region.

MRI is very useful for delineating the soft tissue masses in both the sagittal and coronal planes and for indicating the extent of the disease and the spread of the tuberculous debris (Figure 3.18.13). A relative lymphocytosis, an elevated ESR, and a positive tuberculin skin test are not infallible; skin test and ESR may be normal in more than 10% of patients. ESR may provide a rough guide for assessing response to therapy. Enzyme-linked immunoabsorbent assay (ELISA) for antibody to mycobacterial antigen-6 is also used in diagnosis and in differential diagnosis from other diseases such as brucellosis, typhoid, and syphylitic infections. CT is better for assessing bony destruction (Figure 3.18.14).

Chemotherapy using antituberculous drugs is the mainstay of treatment. Chemotherapy has also made surgery more successful by drastically improving wound healing and reducing secondary wound infections. Surgery is helpful in managing deformity, neurological involvement, and non-response to chemotherapy (Figure 3.18.15). Unless there is an emergency, it is safer to perform a definite surgical procedure after chemotherapy for 3–4 weeks and adequate improvement of the nutritional status of the patient. Treatment is summarized in Table 3.18.1.

The current recommended daily dosage for the treatment of adults, with or without HIV infection, is 300mg isoniazid, 600mg rifampin (rifampicin), and 20–30mg/kg pyrazinamide. In this intensive phase, which lasts for 2 months, ethambutol (or streptomycin for children who are too young to be monitored for visual acuity) should be included when the severity of the lesion is extensive and there are complicating factors like neurological involvement, in patients from a population where there is a high primary resistance to isoniazid, and if there is a suspicion of drug resistance. After the intensive phase of 2 months, with either the triple-drug or the four-drug regimen, a continuation phase using isoniazid and rifampin can be continued for a period of 9–12 months.

Late deformity can occur in two distinct phases: the active phase, which includes the changes in the first 18 months when the disease is still active, and the healed phase, which includes all changes in deformity after cure has been achieved. The extent of the collapse and its progress during a long-term follow-up has been found to depend on the age of the individual, the level of the lesion, and the presence of spinal instability. Paraplegia due to tuberculosis has traditionally been divided into two groups: early-onset paraplegia, which occurs within the first 2 years of the onset of the disease, and late-onset paraplegia, which usually occurs after many years.

Brucella is endemic in agricultural areas of the world, particularly where goats are common. Brucella melitensis is found in goat’s milk, although other milk- producing animals can act as a reservoir. Brucella abortus and B. suis are present in about 30% of the cattle in the United Kingdom but rarely cause disease. Brucellar infections present in a similar way to tuberculosis. Spinal Brucella is mainly found in the lumbar region and multiple sites are common. Presentation may be relatively acute, particularly if Brucella causes a meningitis. Brucella can also cause a local sacral ileitis. Diagnosis depends on considering the possibility of brucellosis and on bacterial culture and serology. The usual treatment is chemotherapy with a range of antibiotics (tetracycline, streptomycin, and rifampin (rifampicin)). Chemotherapy should be maintained for at least 3 months and possibly longer, and even then the recurrence rate is high. Surgical management is limited to patients who fail to resolve, particularly if there is neurological compromise.

Fungi may cause granulomatous lesions in the spine. Fungal infections include coccidioidomycosis blastomycosis, histoplasmosis, cryptococcosis, and aspergillosis. They all occur in endemic regions and are rarely seen in the United Kingdom except in cases of immunodeficiency. They are all difficult to identify and to treat.

Echinococcus is a very rare cause of spinal infection which presents with large expansile lytic lesions (hydatid cysts). Diagnosis is made by a positive complement fixation test as well as the typical radiological changes. Treatment is by radical surgery combined with mebendazole. Results are very poor with a high rate of recurrence and also a high rate of paraplegia.

Salmonella typhimurium can cause spinal infection in endemic areas and typically in patients with concomitant sickle cell disease. Other Salmonella species can cause spinal infection in the immunosuppressed. Commensals such as Serratia marcescens and Nocardia have been reported as causing spinal infection. These organisms have little relevance except in the immunocompromised.