Spondylogenic Back Pain: Osseous and Intervertebral Lesions
“The spine is a series of bones running down your back. You sit on one end of it and your head sits on the other.”
–Anonymous
Patients with severe pathologic processes involving the vertebrae (and the intervertebral joints), such as infections, neoplasms, and metabolic disorders, frequently present with pain in the back. Although there may be minor aggravation by activity, the significant distinguishing feature of these conditions is the fact that the pain is not relieved by rest. Major trauma resulting in fracture and fracture dislocations is not the thrust of this book. Low impact fractures are covered briefly as they can be a diagnostic dilemma with entities such as tumor and/or resulting in back pain as a tiresome sequel. The diagnosis of all of these conditions is largely dependent on radiographic findings, and treatment is along well-established lines. New computed tomography (CT) scanning and magnetic resonance imaging (MRI) techniques are giving us a better understanding of these various conditions and allowing, in some cases, for a more aggressive surgical treatment option.
Although these lesions constitute a relatively small percentage of the backaches seen in clinical practice, some aspects of each group are discussed very briefly.
Low Impact Traumatic Events Affecting the Lumbar Spine
The Osteoporotic Compression Fracture
The most common spine fracture you will see in the emergency department is the compression fracture in osteoporotic bone. Your patient will usually (but not always) be a woman and will describe the sudden onset of midback pain brought on by a simple maneuver such as a cough or lifting of a bag of groceries. In approximately 20% of the patients, the compression fracture will be asymptomatic and unrecognized until a radiograph is done for some other purpose.
Most patients will experience the sudden onset of pain so severe they will appear in the emergency department. Even though the fracture may be affecting a single vertebral level, the pain will be described as a diffuse discomfort; for example, a fracture of T9 will radiate widely, even to the lower lumbar region.
Careful palpation or percussion of the spinous processes will usually reveal the level of fracture. Rarely will there be evidence of radicular or cord involvement in simple compression fractures.
Plain radiographs will reveal one of three fracture patterns (Fig. 3-1). The anterior wedge is the fracture pattern most commonly seen in the thoracic vertebrae, with the biconcave endplate fracture being more common in the lumbar region. If there is any question that the middle column of the vertebrae is involved, a CT scan should be obtained to rule out a more serious, potentially unstable burst fracture. Measure the distance between the pedicles and the height of the posterior
vertebral body on the plain x-rays. If the interpedicular distance is wider than the average of the levels above or below, or the posterior body height is less than the average of the adjacent levels, then the middle column of the vertebral segment may have been fractured and compressed. A thin cut CT scan through the area will answer this question.
vertebral body on the plain x-rays. If the interpedicular distance is wider than the average of the levels above or below, or the posterior body height is less than the average of the adjacent levels, then the middle column of the vertebral segment may have been fractured and compressed. A thin cut CT scan through the area will answer this question.
FIGURE 3-1 The three varieties of compression fracture: left—wedge; middle—“codfish”; right—uniform compression, anterior and posterior. |
Most patients with benign compression fractures can be treated outside of the hospital. Occasionally the pain is so severe that admission becomes a necessity. The rare complications of ileus, urinary retention, and neurologic complications will require hospital admission. In this older population, excessive narcotic use (e.g., oxycodone and hydrocodone) will cause more problems than solutions. Often strong analgesia is needed in the first couple of days, but this should be quickly reduced as the patient is ambulated in corset support (Fig. 3-2). Bracing is especially important in ambulating these patients, but the design has to be simple to accommodate frailty and the often accompanying arthritic hands. Obviously, severe osteoporosis or osteoporosis in the younger patient
(younger than 65 years) requires redress. The 2004 U.S. Surgeon General’s Report on Osteoporosis (4) suggests that a patient sustaining a fragility fracture (such as a vertebral compression fracture) should have a bone densitometry performed and appropriate treatment instituted if necessary.
(younger than 65 years) requires redress. The 2004 U.S. Surgeon General’s Report on Osteoporosis (4) suggests that a patient sustaining a fragility fracture (such as a vertebral compression fracture) should have a bone densitometry performed and appropriate treatment instituted if necessary.
FIGURE 3-2 Brace support: Three points of support—one posterior below fracture, one on sternum, and one on the symphysis pubis. |
Healing is best followed by the patient’s symptoms, although serial radiographs will show any progressive collapse. It will take 6 to 12 weeks before patients are comfortable enough to shed their brace and increase their activities. Once a comfort level is achieved, the institution of an extension exercise program and low impact aerobics is important.
In patients who continue to have significant pain beyond a few weeks, stabilization by injection of bone cement into the vertebral body may be an option (Fig. 3-3) (6,7,11,14). There have been reports of reduction of the fracture and improvement in alignment with these injections (11,14).
FIGURE 3-3 Cement injection into a thoracic vertebral body for osteoporotic compression fracture. Ideal cement pattern with spread throughout the body and no leakage. |
Repeated compression fractures will lead to an increasing kyphotic deformity of the chest, with the ribs eventually settling on the pelvis. This causes discomfort and is associated with poor posture, a protuberant abdomen, respiratory compromise, and a very unhappy patient. There is little the physician can offer in this situation; thus, prevention is an important goal.
Osteoporotic Compression Fracture Versus Tumor
A constant dilemma in the emergency room is to decide whether the thoracic fracture you are looking at is occurring in osteoporotic bone or bone weakened by a tumor.
The following points suggest that you are dealing with a secondary malignant lesion (or primary hematopoietic neoplasm such as multiple myeloma):
The patient presents with severe pain, and any attempt to roll or sit up becomes a moment of agony.
Radicular pain and/or cord symptoms and signs are present.
Plain radiographs reveal:
Destruction of cortex.
Loss of pedicle (Fig. 3-4).
A compression fracture above T7 or below L2.
The patient has a history of a past malignancy.
An MRI (Fig. 3-4) reveals:
The marrow cavity is completely obliterated, with no fatty marrow left.
The cortical margins are gray and mottled, rather than black and distinct.
There is a soft tissue mass outside of the vertebral body such as cord effacement (Fig. 3-5).
There are skip lesions (Fig. 3-6).
Gadolinium injection on MRI is not a reliable way to sort out malignancy from benignity.
A bone scan is often helpful in distinguishing malignant from benign lesions (Fig. 3-7).
FIGURE 3-5 The soft tissue mass of tumor on MRI (sagittal T1) is pressing on the cauda equina (arrow). |
FIGURE 3-7 Bone scans in a fracture (A) and tumor (B). There is no difference in the intensity of the hot spot, but there are multiple “hot spots” in (B) indicative of metastatic tumor. |
If, after all of the considerations just mentioned, you have still not pinned down the diagnosis, a CT-guided biopsy will be required.
Infection
Spinal infections, despite their relative rarity, must be remembered as a potential source of back pain. For convenience of discussion, infections involving the vertebral column may be considered under the following clinicopathologic syndromes:
Vertebral osteomyelitis
Pyogenic
Granulomatous (tubercle bacillus)
Miscellaneous
Epidural abscess
Intervertebral disc “infection”
Pyogenic vertebral osteomyelitis and epidural abscess will be discussed together as they are often closely associated in clinical practice.
Pyogenic Vertebral Osteomyelitis
Although pyogenic spinal lesions may result from discography, discectomy, and open wounds, most vertebral osteomyelitis results from hematogenous spread through an arterial or venous route. Probably the most common source of infection is from a pelvic inflammatory lesion (e.g., bladder infection), with spread occurring through Batson’s (1) plexus (Fig. 3-8) sometimes after a surgical procedure such as cystoscopy.
The clinical features of vertebral osteomyelitis have altered from the preantibiotic era. Vertebral osteomyelitis used to be a disease of adolescence and was very acute in onset. The source of the infection was rarely known. Staphylococcus was by far the most common organism involved, and the disease had a dreadful mortality of approximately 60%.
Vertebral osteomyelitis is presently a disease of adults. The onset may still be acute, but more often than not the onset is insidious, and the course is chronic. This leads to more misdiagnoses than you can imagine; in fact, the first time you meet a patient with vertebral osteomyelitis, you will likely miss the diagnosis!
The source of infection can be localized in approximately 50% of patients and usually can be linked to infection or instrumentation of the genitourinary system. It is interesting to note that a significant portion of these patients are elderly, debilitated, or diabetic. Although Staphylococcus is still the most common infecting organism, Escherichia coli and other gram-negative organisms are increasing in frequency. Streptococcus can be seen in diabetics. The drug subculture has added a new dimension, with its own group of gram-negative organisms (Pseudomonas).
The lumbar spine is more commonly affected than the thoracic or cervical spine. Because the vertebral body has a richer vascular network than the posterior elements, the majority of infections involve the body. Commonly, two adjacent vertebrae and the intervening disc space are involved (Fig. 3-9). Varying degrees of vertebral body destruction and collapse occur. With the spread of the infection, an abscess may develop and extend either anteriorly or posteriorly.
Neurologic damage may result from the development of an angulatory kyphosis, an epidural abscess, or a sequestrated disc or bone fragments. Occasionally, the spinal cord may be destroyed by obliteration of its vascular supply.
Clinical Presentation
Backache is the most common presenting symptom: indeed, early in its course, the disease may be indistinguishable symptomatically from a mechanical backache. The insidious onset and the lack of radiographic changes account for the usual delay of often weeks in diagnosis. With progression of the disease, the back pain increases in intensity, becoming constant, and is particularly noticeable in bed at night. More often than not, the back pain has reached severe proportions before the diagnosis is made. On occasion, pain will be referred to the abdomen, leading to a search for intra-abdominal disease.
The patient may appear sick and will have a variable temperature elevation. The findings at examination vary with the stage and severity of the disease. All spinal movements and especially weight-bearing (sitting, standing, jarring) intensify the pain. Paravertebral muscle and hamstring spasms are sometimes severe. The patient may stand with a marked list of the spine to one side. Gross spinal rigidity is a characteristic feature. The spinous processes are usually tender on pressure. The back pain is intensified by percussion of the involved area. Straight leg raising (SLR) is restricted because of hamstring spasm. If the infection has spread to involve the meninges, SLR may be markedly reduced from the meningismus. On the rare occasion, neurologic findings of root compression will be detected, but every so often a delay in diagnosis will be followed by epidural
abscess formation, and either direct compression or a vascular lesion will damage the lower cord or cauda equina. If paralysis is the outcome, there is little chance for recovery from this tragic sequence of events.
abscess formation, and either direct compression or a vascular lesion will damage the lower cord or cauda equina. If paralysis is the outcome, there is little chance for recovery from this tragic sequence of events.
Laboratory
In half of the patients, the white blood count (WBC) will be within normal limits, and even when elevated, the WBC rarely rises above 15,000/mm<+>3. The erythrocyte sedimentation rate (ESR) and particularly the C-reactive protein (CRP), however, will be consistently elevated and are the most useful tests for monitoring disease activity and the efficacy of treatment. On occasion, a very debilitated patient will show no signs of fever, no elevated WBC, or no increased ESR. The CRP is the most sensitive test and usually is elevated. Blood cultures may be positive in up to 50% of patients, particularly in those who present with a markedly febrile clinical course.
Radiology
Radiologic evidence of the spinal disease lags 4 weeks or more behind the clinical manifestations. The earliest changes are localized rarefaction of the vertebral endplates (Fig. 3-10), followed rapidly by involvement of the adjacent vertebrae and narrowing of the disc spaces. With the increasing recognition of disc degeneration as a source of spondylogenic pain, there is an inherent danger of misinterpretation of the radiologic changes. The early specific radiologic features that distinguish the disc narrowing that is the result of infection from the disc narrowing that is associated with degenerative changes are very subtle and include fuzziness of the cortical endplate and a “divot” out of the anterior-superior or anterior-inferior portion of the vertebral body (Fig. 3-10).
This raises another distinguishing feature of infection versus tumor: early radiologic changes reflective of infection affect the endplate region and are anterior, whereas tumors affect the medullary/marrow space and tend to be posterior in the vertebral body.
The radiologist frequently is not provided with enough clinical information, and there is no reason why the minimal radiologic changes should make him or her suspicious of an infective lesion. So the diagnosis is suggested by the clinical findings: a sick patient with severe pain, a rigid back, fever, and an elevated WBC and ESR. Early plain radiologic changes are minimal but may give an indication of the site of the lesion. At this stage, the diagnosis is best made by an MRI (Fig. 3-9) (13). But even with these sophisticated tests, the diagnosis can be missed because of nonspecific changes.
Later in the course of infective disease, the plain radiographs reveal destructive erosion of the contiguous vertebral bodies, starting first and usually most extensive anteriorly (Fig. 3-11). Subsequently, there is sclerosis and the development of reactive bone. Evidence of soft tissue reaction is revealed on radiograph by distortion of the psoas shadow or by a localized paravertebral mass.
There may be some difficulty in distinguishing the radiologic changes of an infective lesion from those produced by a neoplasm, but as a general rule it may be said that with infection the disc space is the first structure to be destroyed, whereas with secondary metastatic tumor deposits in the vertebral body the disc space is spared (Fig. 3-12).
Diagnosis
It is essential to search for the causative organism. The triad of cultures blood, infection site, and potential source are to be completed before institution of antimicrobial therapy. The blood culture and source culture (e.g., urine or sputum) are readily obtained. A culture of the infection site often requires a percutaneous biopsy (Fig. 3-13) Securing tissue for culture is preferred because of the occasional case of blood cultures revealing organisms different from the actual organism cultured from the infected site.
Antibiotic treatment is absolutely dependent on the isolation of the organism and on the stage of the disease. No longer is it safe to presume that the infection is staphylococcal. Because of the increasing incidence of gram-negative infections and infections by more than one organism, the offending organism must be identified by blood culture and/or a vertebral biopsy and culture, in order that its sensitivity may be determined. If needle biopsy fails to obtain enough material to permit isolation of the organism, then an open biopsy is necessary.
Treatment
Intravenous antibiotics and bed rest to start are followed by bracing, oral antibiotics, and activity limitation. Treatment should be continued until the ESR has returned to normal. The brace should be worn for an arbitrary period of 3 months, and antibiotic coverage should be continued at least 6 weeks during this period of time, providing the clinical course allows. Serial ESRs and CRPs that return toward normal should be included in this regimen. Routine radiologic assessment should be carried out at 4- to 6-week intervals for at least 3 months. Fusion occurs in 50% of pyogenic disc space infections in approximately 1 year, and the majority of the remainder show bony obliteration of the disc space in 2 years. Routine radiologic reassessment is of importance to evaluate effectiveness of antibiotic treatment as measured by no ongoing bone destruction.
The endpoint in medical treatment has been reached when the patient’s pain and fever have resolved, there is radiographic evidence of fusion, and the ESR and CRP are back to normal for that patient. Remember, in a lot of elderly debilitated patients there is no such occurrence as “normal” ESR. When you have met these four criteria, administration of antibiotics can be stopped, the brace can be shed, and rehabilitation for lost function can start.
Surgery
The indications for surgical intervention are as follows:
Failure of medical management: Despite rest and massive intravenous antibiotics, the patient’s fever and pain persist.
A large abscess forms. Small abscesses, providing they are not in the epidural space, may be successfully treated with medical management. In general, never let the sun set on a large paraspinal or any size epidural abscess.
Progressive neurologic deficit. If the patient arrives on your service paraplegic, you must intervene on an emergency basis, but there is little likelihood of salvage. If on your watch (a neurologic examination every 2–4 hours), you detect an increasing deficit despite medical treatment, take the patient to the operating room without delay.
Biomechanical instability is a likely outcome (e.g., anticipated or actual kyphosis of >15 degrees).
Failure to obtain an adequate biopsy specimen sufficient to make a definitive diagnosis.
Type of surgery. The basic rule in spine infection (and almost any other spinal problem) is to go directly to the problem. Because these infections are in the vertebral body and disc space, the surgical approach is anteriorly. The only exception to this rule is an epidural abscess, which should be approached posteriorly (laminectomy).
The surgical goals anteriorly are adequate debridement, decompression of any material in the spinal canal, and stabilization of the interspace with rib strut grafts or tricortical iliac crest grafts. A satisfactory fusion rate with this approach, along with antibiotics and rest, is a very high likelihood.
Tuberculous Vertebral Osteomyelitis
Tuberculous infections of the lumbar spine usually have a clinical course that distinguishes them from pyogenic infections (Table 3-2). Skeletal tuberculosis is almost always secondary to a focus elsewhere, particularly the pulmonary and urinary tracts. The most frequent site of vertebral involvement is the lower thoracic and upper lumbar region. The vertebral body, as in pyogenic osteomyelitis, is the site of localization. The intervertebral disc is relatively resistant to tuberculous destruction and the infection simply migrates under the anterior longitudinal ligament to the adjacent vertebral body.
The disease is very insidious, and the time that elapses from the onset of symptoms to hospital admission is often well more than 6 months. This is further complicated by the fact that, in North America, tuberculosis is now a much rarer condition and is frequently overlooked in differential diagnosis. However, over the past decade, there has been an increase in the incidence of pulmonary tuberculosis, and it is reasonable to assume there will be a subsequent increase in tuberculous osteomyelitis.
In the younger child, irritability and refusal to sit or walk are presenting features. Older children and adults present with simple backache. The symptoms do not have the dramatic disability characteristic of the later stages of a pyogenic vertebral osteomyelitis.
A careful history will reveal the association of constitutional symptoms of intermittent fever, sweats, anorexia, weight loss, and easy fatigability. At examination, marked splinting of the spine can usually be demonstrated. Although the gross tenderness associated with pyogenic osteomyelitis is rarely apparent, localized bony deformity associated with vertebral collapse, presenting as gibbus, is common.
Because of the insidious nature of the disease and the consequent delay in seeking advice, the patient may present with evidence of neurologic impairment even when seen for the first time.
Laboratory and Radiograph
As in pyogenic lesions, the CRP and ESR are elevated. The WBC is variable, however, and may even be depressed. The plain radiographic features that distinguish the lesion from pyogenic osteomyelitis are as follows: (a) there may
be multiple vertebral bodies affected and (b) there may be scalloping of the anterior surface of the vertebral bodies by the tuberculous abscess (Fig. 3-15) (3). The disc space is usually spared until late in the disease, when it may rupture into the tuberculous cavities within the vertebral bodies or paraspinal abscesses. In fact, the vertebral body destruction in tuberculosis is not unlike that caused by neoplasm, except that tuberculous lesions tend to be anterior in the vertebral body, and neoplasms, especially secondaries, are more posterior in the vertebral body and invade the posterior elements.
be multiple vertebral bodies affected and (b) there may be scalloping of the anterior surface of the vertebral bodies by the tuberculous abscess (Fig. 3-15) (3). The disc space is usually spared until late in the disease, when it may rupture into the tuberculous cavities within the vertebral bodies or paraspinal abscesses. In fact, the vertebral body destruction in tuberculosis is not unlike that caused by neoplasm, except that tuberculous lesions tend to be anterior in the vertebral body, and neoplasms, especially secondaries, are more posterior in the vertebral body and invade the posterior elements.
As noted earlier, tuberculous infections of the lumbar spine are rarely primary. They are commonly secondary to foci either in the lungs or the genitourinary tract. Radiographs of the chest and bacteriologic examination of the urine must always be carried out in routine clinical assessment. The Mantoux test, when positive, can be regarded as suggestive but never diagnostic. As with pyogenic vertebral osteomyelitis, vertebral biopsy is essential for diagnosis.