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Diagnosis and Management of Pyogenic Vertebral Osteomyelitis in Adults Richard K. Osenbach, M.D., Patrick W. Hitchon, M.D., and Arnold H. Menezes, M.D. Department of Surgery, Division of Neurosurgery, University of lowa Hospitals and Clinics, Iowa City, Iowa
Osenbach RK, Hitchon PW, Menezes AH. Diagnosis and management of pyogenic vertebral ostcomyelitis in adults. Surg Neurol 1990;3'~:266-75.
Management of vertebral osteomyelitis remains controversial regarding optimum duration of antibiotic therapy and the role of surgery. Forty adults with vertebral nsteomyelitis were reviewed. Staphylococcus aureus was t h e most common pathogen isolated. Disk space narrowing with end-plate erosion was the earliest finding, followed by progressive vertebral body destruction. Magnetic resonance imaging proved extremely valuable in detecting spinal cord compression in patients with neuroiogic deficit. T r e a t m e n t should include at least 8 weeks of intravenous antibiotics combined with immobilization for pain reduction. Surgical intervention is indicated for all patients with neurologic deficit. Serial erythrocyte sedimentation r a t e s a r e valuable for following response to therapy. The value of magnetic resonance imaging in diagnosis is emphasized. KEY WORDS: Antibiotics; Epidural abscess; Magnetic resonance imaging; Neurologic deficit; Vertebral osteomyclitis
stability [ 1, I 1]. Therefore, early diagnosis is critical in obviating complications. Furthermore, treatment of vertebral osteomyelitis is not uniform and is controversial regarding the role of surgery and duration of antibiotic therapy. In an attempt to clarify some of these issues, we reviewed our experience with adult pyogenic spinal osteomyelitis.
Clinical Materials and Methods Between 1980 and 1987, 40 adults with pyogenic vertebral osteomyelitis were treated at University of Iowa Hospitals and Clinics and Iowa City Veterans Hospital. Data were collected by review of hospital and outpatient records along with review of radiographic studies. T h e r e were 32 men and 8 w o m e n from 25 to 85 years of age, with the mean ages of men and w o m e n being 60.6 and 59.4 years, respectively. Thirty patients (75C4) were over 50 years of age.
Clinical Presentation
Introduction Pyogenic infection of the vertebral column has traditionally been of little concern to neurosurgeons due to its relatively infrequent occurrence. However, neurologic complications are not u n c o m m o n and often warrant emergent surgical intervention. Unlike the pediatric population, in which the disorder is frequently acute in onset and associated with systemic illness, the adult variety more commonly presents insidiously and pursues an indolent clinical course, making early diagnosis difficult [2,7,16,24]. Consequently, affected individuals may present with neurologic findings related to paravcrtebral/epidural abscesses or spinal in-
Address reprint requests to." Richard K. Osenbach, M.D., Division of Neurosurgery, C42 General Hospital, University of Iowa Hospitals, Iowa City, Iowa 52242. Received October 20, 1989; accepted December 19, 1989. ¢~ 1990 by Elsc'vlcr Sci¢-nte Publishing Co., Inc.
The lumbar spine was most frequently involved (17), followed by the cervical (12) and thoracic (11) regions in descending order. Local spinal pain was present in 39 of 40 patients (98%), with 12 (30c'/c) also having a prominent radicular component. The single patient without pain had been rendered paraplegic in an unrelated accident several years earlier. Twenty patients (50%) were febrile at the time of diagnosis. The duration of symptoms ranged from 1 to 28 weeks, with a mean of 6 weeks. The average duration of symptoms was greater in patients who were neurologically intact (7.6 weeks) compared with patients with neurologic findings (4.2 weeks). Fourteen patients (35%) experienced symptoms for 6 weeks or longer. Physical examination uniformly revealed localized spinal tenderness, muscle spasm, and limited range of motion. Neurologic findings were present in 19 patients (48O;). Myelopathy occurred in 12 (635;), which included six patients with quadriparesis and six with paraparesis; five patients had a cauda equina syndrome; and 0090-~019.'90.'$3.~0
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F i g u r e 1. T i m e course of er,thro()te sedimentatton rate ~ESR, in patient~ u'ttb t ertebra/ osteom)dttt~. Thrre tJ a gradual decline tn the ESR u'itb treatt~tent.
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two patients had a radiculopathy. Neurologic deficit occurred in 8 of 12 (67¢;) patients with cervical disease, 6 of 11 (55C4) with thoracic inw>lvement, and 5 of 17 (29Ulvement. Risk factors or associated illnesses were present in 18 patients ( 4 5 ~ ) , including diabetes (8), chronic ethanol abuse (7), intravenous drug use (2/, and rheumatoid arthritis ( l }. Vertebral infection was believed to be secondary to hematogenous seeding in ~3 (83C/) cases, with a definite source of infection identified in 2 v patients (82C~). Soft tissue and urinary tract infections accounted for I0 and 6 cases, respectively; pulmonary infection ~3), subacute bacterial endocarditis (3), septic arthritis (2), purulent sinusitis ( 1 ), suppurative pharyngitis ( 1 ), and dental abscess (I) accounted for the remaining metastatic cases. Six metastatic cases could not be linked to a definite source. Seven cases (17%~) were considered to be the result of direct contamination from previous spinal surgery.
Laboratory Int'estigation The most c o m m o n laboratory abnormality and the most useful test was the erythrocyte sedimentation rate (ESR), which was uniformly elevated, ranging from 40 to 145 m m / h at diagnosis, with a mean value o f 8 5 m m / h (normal 0 - 2 0 mm/h). The ESR gradually declined during therapy to a mean of 25 m m / h by the termination ()f antibiotic therapy and to 12 m m / h by 16 weeks (Figure I ). While the ESR often failed to return to normal even in successfully treated patients, a declining trend was noted. By the end of antibiotic therapy, the ESR fell to at least 5()~ of original values in 9 4 ~ of patients, although
only 22% had normal values. By the end of 16 weeks, the ESR was normal in almost half the patients. In contrast to the ESR, peripheral leukocyte counts were normal or only slightly elevated. The white blood cell count showed no significant trend during therapy and in general was not helpful. Blood cultures were positive in 12 patients {.~0~) at the time of diagnosis.
Radiographic El,aluation Plain radiographs of the spine demonstrated a characteristic sequence of changes (Figure 2). Disk space narrowing with end-plate erosion was the earliest finding, followed by progressive vertebral body destruction and paravertebral inflammatory reaction. Sclerosis, new bone formation, and fusion occurred late as healing progressed. Plain films were normal in three patients, all with symptoms for less than 3 weeks. T w e n t y - o n e patients underwent computed t o m o g r a p h y (CT) scans, which revealed destructive changes of the vertebral body and delineated the inflammatory soft tissue reaction in all cases. C o m p u t e d tomography accurately identified six patients with psoas abscesses, which required drainage [ 15,19]. Percutaneous CT-guided aspiration/biopsy was peril>treed in 15 patients. Technetium bone imaging was performed in eight patients, which revealed increased uptake at the diseased level in all cases. Nine patients underwent myelography, which was normal in five and revealed extradural defects in four patients. The latter group included two patients with epidural abscess and two with postsurgical changes. Magnetic resonance imaging (MRI) in 14 patients revealed characteristic signal changes (Figure 3) and accurately identified six cervical epidural abscesses (Figure 4}.
2(~8
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()sc.nbach ct al
Figure 2. (A) l_atera/ lumbar .*ptn~ radiograph of a ~5-1car-o/d man 6 u t~ek, after the on,et ( , / h a ~ pazn. There L, .,ubt/e err,don of the .~upertor r~.rtehra/ end-p/at,. ,J L2 but l* oth,.rwt.~e unremarkah/e (13) l.atera/ /umbar ,pine lilm ~.*amepalsent, 6 month, Jollowzng tBe on,~.t e~lJ)mptnm* Hi.* ESR z~a, 65 mm/h. Bo~t~ d¢.itru~tto*t o~ the LI and 1.2 t'erlel)ra/ hod1¢..~ i~ now ,'z id*nt, f$a~leria/ ,u/tur~., o/ thi, /e,iopt o/J/,Jlpl~d /JV (. T-'4uz,/cd n~ed/; biop.,l ~qe/d,.d .Staph~./o~o, cu, aur, n*. (C) Lateral llvmhar *ptne/~/m l.*ame pattenl) o/2tatned .? month, after ~hal .,ho~ n in B. The palieplt ha.* h~.en immobilized in a thora~ o/umbar ortho.*l* and ha., recelt ed 6 week., o/)ntrare.nous antibzof it.*. The.re ha.* been ~e.,satlon of o.*teoclaJtic aclirily and znitiatton of./u~ion helu een t/oe inro/zt.d tertebra/ hodte*. The patient t~a.* asymptc, matic and h~* FSR u'a¢ .? ~ ram.;/;.
Vertebral ()stcomyclitis
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Figure 3. (A) Mid-sagttta/"['l-u'etRhtedMRl oj a .il-year-o]d man u'ho pre.~.nted u ith neck path aml radi~ulom3 elopath.; ,\'ot~ the decrea.~ed ~igna/ tntenjtty that ~o*l/tuent/r intolt'eJ the C4 and (55 t e~Yehral bodie., a n d intert'e*~tnx d i ~ . Ptvt'ertebral .,o]? tissue .~u'elling ~a*z he .*ee*l extending/rom (]2 to (.v t7"R l vO0. 7"E 120. J (B) ,~lid-.~agitta/T2u ei.~hted M R I t3ame patientJ ret'ea]., imreawd siR~lal inten.~it1 o] the i n t o h , d tertebral bodie~ and it~tert ertebra/ di~k. A]~o *tote the ventral ~pina/ cord conlpro ~io*l.
A
Microbiology and Isolation of Organism A causative organism was isolated in 36 (90C/c) patients (Table 1). Staphylococcu., aureus was the most c o m m o n organism, accounting for 67(7c of all cases and 86(?/c of all gram-positive isolates. Gram-negative infections occurred in 1 7 ~ of patients. T h e r e were four patients (10%) in which the causative organism could not be cultured. Only cultures obtained from the vertebral body, paravertebral tissues, or blood were considered
2(~9
signiticant. Diagnostic cultures were obtained from the vertebral body or contiguous tissues in 32 of 36 cases (89('~ 1:23 by an open procedure and 9 by CT-directed percutaneous biopsy. In four patients, organisms were identified only by blood cultures. Treatment
and Outcome
T r e a t m e n t consisted of spinal immobilization, antibiotics, and surgery. Bedrest was employed in 16 patients,
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ranging from 2 to 12 weeks, and was individualized fi)r each patient based on reduction in spinal pain. External immobilization was utilized in 30 patients, including all patients with cervical anti thoracic inw)lvement anti 13 of 17 with lumbar disease. In uncomplicated cases, bracing was continued for 2 - 3 months or until pain had resolved or significantly subsided. In case of frank spinal instability, immobilization was continued until there was radiographic confirmation of fusion anti stability. Thirty-six patients with nontuberculous infections received antibiotics (intravenous only or intravenous plus oral) for an average of 10.8 +- 5.3 weeks; two patients received antituberculous therapy for I year and two patients received no antibiotics. The route of administration and duration of therapy are summarized in Table 2. Surgery was p e r f o r m e d on 2 ~ patients (68C~). All patients (19/27) with neurologic deficit underwent surgery: 10 because of spinal deformity/instability and 9 because of epidural/paravertebral suppuration. An autologous bone fusion was simultaneously incorporated in 15 patients. T h e indications for surgery in the eight patients without neurologic deficit included diagnosis (5), drainage o f paravertebral abscess (2), and debridement of the diseased vertebral body ( 1 ). T h e operative
()scnbach ct al
Figure 4. ,Xlkl-,agittal T2-u ei×hhd ,~IRI o]a 6~-.;,ar-r,M man with a 2-w~t.k hi,tor~ o/ nrck paid and /et er u'hrJ prt,rnt~d quadrtpareti~ with a C4 .,en,or~ lete/. An epidural ab*c~.,, ~arrowj i., compre,~ing the .,pina/ cord zentra/]~ at C ~-C4. Tki., patient maJe a /)¢ll neure,/ogzc rec0ce*3]ol/ou tng l entral decompres,ion and/nterbod~//~.,i~,n.
approach was determined by the location of compression, degree of bony destruction, and potential for spinal instability. Eleven of 12 patients with cervical involvemerit underwent surgery. Ten had a traditional anterior approach while one patient had a laminectomy. Eight patients each with thoracic and lumbar disease underwent surgery. A posterolateral approach was used in four thoracic and six lumbar cases, respectively, while laminectomy was performed in four patients with thoracic disease and two with lumbar involvement. Patients treated with laminectomy were kept at bedrest until their spinal pain resolved. Thereafter, a suitable orthosis for the neck or thoracolumbar spine was prescribed where instability was suspected. The mean follow-up period was 1 year, with outcome based on the degree of neurologic and/or symptomatic improvement. There" were two deaths related to sepsis secondary to the primary illness. Twenty-seven of the
Vertebral Osteomyclitis
Surg Neurol 1990;55:266-75
Table l. Causatire Organism Cultured from 36 Patients Organism Grarn- positive Staphylococcus aureus
No. of patients
Percent of total
28
77.7 66.6 5.6 2.8
24
Streptococcus sp
Anaerobe B rucella
Gram-negative Mixed Single ~ Tuberculosis
2 i 1
2.8
6 a, 5 2
16. ~ 8.5 8.3 5.6
• Eschertcbta colt. 1: Pseudomonas. 1, Proteus sp, I
remaining 38 patients (71 c,'Jc) eventually were asymptomatic. T h e r e was no difference in symptomatic or neurologic outcome between the group treated with intravenous antibiotics only as compared with the group that received intravenous as well as oral antibiotics. No patient who was initially intact deteriorated during therapy. Eight of 19 patients with neurologic deficit regained normal function while nine improved, one was unchanged, and one died. The level of involvement had no bearing on the incidence of recovery. One patient with paraparesis secondary to a T6 lesion deteriorated neurologically following laminectomy but subsequently showed progressive improvement following posterior stabilization. T h e r e was a single recurrent infection after discontinuation of antibiotics. This individual had undergone drainage of a psoas abscess followed by 8 weeks of intravenous plus 8 weeks of oral antibiotics. His pain and neurologic deficit improved and his ESR fell from 140 to 45 mm/h. H e subsequently experienced recurrent progressive pain, and reevaluation revealed his ESR to be > I 0 0 mm/h. Radiographic evaluation revealed a recurrent psoas abscess. Following repeat drainage, he again received 8 weeks of intravenous followed by 8 weeks of oral antibiotics, which resulted in resolution of his pain and fusion. Thirty-two patients ( 8 0 ~ ) ultimately achieved radiographic evidence of bony fusion, 17 spontaneously and 15 surgically.
Discussion Vertebral osteomyelitis was previously believed to be uncommon and even today occurs infrequently in otherwise healthy adults [38]. In contrast to acute spontaneous disk space infection more common in children, pyogenie vertebral osteomyelitis primarily affects adults [38,44,45]. The two conditions have a slightly different pathogenesis due to differences in the vascular supply of the disk and vertebral bodies between children and adults [38,45,46]. Prior to age 20, vascular channels
271
perforate the vertebral end-plates providing bloodborne bacteria access to the intervertebral disk. Therefore, in children the disk is initially affected with secondary involvement of adjacent vertebral bodies [46]. Adults have no direct vascular communication between the vertebral body and disk. Consequently, hematogeneously disseminated bacteria lodge in avascular areas adjacent to the subchondral bone. The vertebral endplates are then eroded and the disk secondarily involved [38,45]. Hematogenous seeding of the vertebral body may occur in two ways. Direct arterial seeding occurs by nutrient arteries derived from the posterior spinal, intercostal, and lumbar arteries [45]. Alternatively, transient bacteremia from urinary sepsis or instrumentation may result in retrograde venous seeding through Batson's plexus, which shares numerous connections with the pelvic veins [6,14]. Certain conditions appear to predispose one to vertebral osteomyelitis. Most notable is diabetes, which has been noted in 19(¥ of patients with vertebral osteomyelitis [9,13,38,42,44]. Diabetics have a diminished host immune response, making them more prone to infection, particularly with staphylococci [4,34]. Intravenous drug users have increased vulnerability to infection, and this practice has become increasingly associated with pyogenic vertebral infection [18,31,38]. Chronic ethanol abuse has been implicated as a risk factor for vertebral osteomyelitis. However, the incidence of ethanol abuse in patients with vertebral osteomyelitis is only 2.3C4 [38], compared with 4~; in the general population [39]. Therefore, the role of alcohol may be affected by the patient population under consideration. Contrary to earlier belief[24], nonpenetrating trauma has no bearing on the subsequent development of vertebral infection [ 13,35,38]. Finally, the belief that steroids or other im-
Table 2. Route and Duration of Antibiotic Therapy
All p a t i e n t s i N = 4 0 ) IV only IV plus oral TB None N o deficit ( N = 2 l ) IV o n l y IV plus oral None W i t h deficit I N - 19) IV o n l y IV plus oral TB
No. of patients
Duration"
24 t60.05:; ) 12 150.0c'; ) 2 !5.0'7,'.; I 2 f 5.0~?~ )
8.2 +- 5.3 w e e k s 16.1 +- ,t.8 w e e k s 1 year --
13 ( 6 1 . 9 ( ; ; ) 6 ~28.6ff;: )
~.0 ~.: 2.5 w e e k s 14.(I _+ 4.(1 w e e k s
2 19.5ff; )
--
11157.9(:,; ) 6{51.6q4) 2 i 10.0(:,; 1
9 . 6 m 3.3 w e e k s 18.2 * 4 . 8 w e e k s 1 year
Abbreviations IV, intravenous; "I'B, antituberculosis therapy. • Average duration of therapy was 10.8 -+ 5. a, weeks excluding'l'B patients
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Surg Ncurol 1990;3 "E266- v 5
munosuppressive drugs increase the risk of vertebral osteomyelitis has not been substantiated [38]. Most cases of vertebral osteomyelitis result from a metastatic source of infection, most commonly the urinary tract [ 14,38]. Up to 60c?~ of metastatic infections related to urosepsis affect the skeleton, with 839~: of these involving the spine" [41]. Soft tissue infections often distant from the site of vertebral infection are a second important source of seeding [38]. Although three of our cases were related to subacute bacterial endocarditis (SBE), this association has been rare in the literature. This may reflect prompt diagnosis and treatment of SBE with simultaneous eradication of a subclinical osteomyelitis [8,26,37]. Less c o m m o n sources of metastatic infection include dental infections/proce'dures, thrombophlebitis, and respiratory infections. Infection related to previous spinal surgery results from direct contamination rather than hematogenous seeding. Nine of our cases were related to previous surgery. These cases did not represent uncomplicated discitis but had the entire picture of osteomyelitis. Elevation in the ESR, although nonspecific, is the most frequent laboratory abnormality, with mean values at diagnosis ranging from 40 to 87 m m / h [2,10,16,38]. An elevated ESR is not diagnostic of infection but is helpful in making or excluding the diagnosis in the appropriate clinical setting. The ESR is most valuable in monitoring therapy by observing the typical downward trend that occurs with successful treatment. However, absolute values of the ESR must be interpreted with caution because, despite successful therapy, the ESR may remain elevated to some degree for as long as 6 months in up to 7 5 ~ of patients [38]. In a large series of patients who underwent successful treatment, the ESR fell to two thirds of pretreatment values in all patients and to less than 5 0 ~ of pretreatment values in most patients by the completion of antibiotic therapy. Therefore, persistent elevation of the ESR does not necessarily indicate treatment failure and by itself should not dictate the need for further antibiotic therapy. In contrast, peripheral leukocyte counts are usually normal or only slightly elevated and show no significant trends with therapy [ 11,38,42]. Successful treatment depends on identifying the causative organism such that specific antibiotic therapy can be employed. Bacteriologic isolates should be considered diagnostic only if cultured from the affected vertebral body and contiguous paravertebral tissues or blood [38]. Cultures from the affected vertebra can be obtained by closed percutaneous aspiration/biopsy or open surgical biopsy. In a subgroup of patients with vertebral osteomyelitis, 70#~ of closed biopsies yielded positive cultures [36]. It is unclear what influence previous antibiotic therapy, inaccurate needle placement, or inadequate speci-
Osenbach et al
mens had on the 30c/c negative results. If an initial closed biopsy is negative, a repeat attempt is justified to ensure accurate needle localization and adequate specimens. Nine of 15 of our patients had diagnostic cultures obtained by closed biopsy. O f the six negative results, two patients had a diagnostic open biopsy, two received antibiotics based on positive blood cultures, and two were given empiric antibiotic therapy. If two attempts at closed biopsy fail to produce a positive culture, a decision must be made to proceed with empiric antibiotic therapy or to perform open biopsy. Blood cultures, which are positive in 14c),:-50()r/ of patients, especially during febrile periods, should be obtained routinely since" this may occasionally be the only source from which the pathogen can be isolated [38]. Staphylococcus aureus is the most c o m m o n pathogen causing vertebral osteomyelitis, accounting for 5BY of all cases and over 8()(X of all gram-positive isolates [2,13,38,42]. E~cherichia ,'oli is the most c o m m o n gramnegative organism, although Enterobacter. Proteus, and Pseudomonas are not uncommonly found, with Pseudomohas particularly frequent in intravenous drug users [18,27,38,40]. Anaerobic infection is relatively rare in vertebral osteomyelitis [38]. The incidence of tuberculous infection of the spine has sharply declined in this country, although in some parts of the world it remains the most c o m m o n pathogen [22,23]. Finally, a n u m b e r of rarer pathogens, such as syphilis, may cause vertebral osteomyelitis [20]. Classically, disk space narrowing is the earliest radiographic finding [2,10,24]. This may occur as early as 2 weeks following the onset of symptoms, but more frequently appears 6 - 8 weeks into the illness. During the early stages, tomograms may be helpful in visualizing changes not apparent on plain films [7]. Progressive vertebral body destruction follows, accompanied by paravertebral inflammatory reaction [13]. Sclerosis, new bone formation, and fusion occur late as healing occurs, although fusion may not be evident fi)r up to 1 year and in some cases may require 5 years [2]. In patients who fail to achieve bony fusion, a fibrous union usually functions equally effectively [43]. Although the sequence of plain film changes are characteristic of vertebral osteomyelitis, they often lag behind the clinical picture and are frequently not helpful in establishing an early diagnosis. Recently, MR1 has assumed an important role in the evaluation of spinal infection [3,32,33]. Magnetic resonance imaging has been shown to have a sensitivity, specificity, and diagnostic accuracy equivalent to combined technetium-gallium imaging in the diagnosis of vertebral osteomyelitis [33]. Furthermore, MRI is noninvasive and provides accurate information regarding the vertebral body, intervertebral disk, paravertebral tissues, and the spinal cord. Typically, T l-weighted images
Vertebral Osteomyelitis
reveal confluent decrease in signal in the affected vertebral body while T2 sequences reveal increased signal intensity. Disk involvement is invariably demonstrated, which helps to distinguish osteomyelitis from neoplasm [33]. Magnetic resonance imaging has been shown to delineate epidural abscesses with accuracy equivalent to myelography [3] and may eventually supplant the need for myelography. This accuracy is supported by our experience with MRI, which demonstrated all cervical epidural abscesses. The dosage, route, and duration of antibiotic therapy advocated by various investigators have been extremely variable [2,10,13,16,21,38]. Some authors have advocated 6-8 weeks of parenteral therapy only, while others have proposed 4-8 weeks of parenteral therapy followed by 2 months of oral therapy [ 16,29,31]. In Sapico and Montgomerie's [38] review of 162 patients with vertebral osteomyelitis, 33ff: of patients who received no antibiotics either died or suffered prolonged morbidity related to their disease. Furthermore, patients who received less than 4 weeks of parenteral therapy either failed treatment outright or relapsed significantly more often than those who received more than 4 weeks of parenteral antibiotics (P < 0.05 by X 2 analysis). We believe that 6-8 weeks of parenteral therapy is probably adequate in uncomplicated cases. We noted no difference in symptomatic and neurologic outcomes or recurrent infection between patients treated for 8 weeks compared with those treated longer than 8 weeks. Based on our own observations as well as those of others, the efficacy of complementary oral therapy at best remains unclear and is probably not indicated in most cases [35,38]. Spinal immobilization has traditionally played an integral role in the treatment of vertebral osteomyelitis. It is clearly indicated in cases of definite spinal instability. However, in the absence of overt spinal instability, the absolute need for and duration of immobilization is unclear [21,35]. The main goal of bracing in uncomplicated cases is to reduce pain and prevent postinfectious spinal deformity. Involvement of two adjacent vertebral bodies or more than a 50% reduction in height of a single body increases the risk of deformity [12]. We recommend that all patients have external bracing until pain is gone or minimal. The role of surgery, particularly in uncomplicated cases, remains controversial. Many authors believe that uncomplicated cases are effectively managed with antibiotics and immobilization with good results and minimum morbidity [ 10,13,16,35,45 ]. Others believe that surgery should play a primary role in treatment, citing a lower incidence of postinfectious spinal deformity, a reduction in recurrent infection, avoidance of neurologic deficit,
Surg Neurol 1990~33:266-75
273
and an earlier return to a functional capacity in support of their position [12,17,47]. On the other hand, it is generally agreed that surgery is mandatory in treating neurologic complications that occur in 3 f f - 4 0 % of patients with vertebral osteomyelitis [5,10,12,16,24,38]. The two primary causes of neurologic deficit are epidural abscess and spinal deformity/ instability. Epidural abscess complicates 5 % - 1 8 % of cases of vertebral osteomyelitis [ 1,24,38]. The 15% incidence of epidural abscess in our series is comparable. Any patient with vertebral osteomyelitis and neurologic deficit without significant spinal deformity should be suspected of harboring an epidural abscess. Epidural abscess causes spinal dysfunction by two mechanisms [ 1]. First, the localized accumulation of pus may cause mechanical spinal cord compression. Second, the epidural suppuration may lead to inflammatory thrombosis of the spinal vasculature that can eventually result in spinal cord infarction [30]. Evacuation of the abscess within 24-36 hours will often lead to complete neurologic recovery; however, once paralysis has occurred, spinal cord damage is likely irreversible. Although most spontaneous epidural abscesses are located dorsally, those associated with osteomyelitis are more often anterior to the dura mater. Inflammation begins beneath the posterior longitudinal ligament, progresses to subligamentous suppuration, and ultimately ruptures into the epidural space. The abscess may consist of either acute pus or dense granulation tissue in more chronic cases. Spinal deformity and instability affect 2 % - 2 8 % of patients with vertebral osteomyelitis and is the second major cause of neurologic deficit, although not all kyphotic deformities result in neurologic compromise [ 1]. Some degree of stability is usually maintained by intact posterior elements that are infrequently affected, thus preventing significant subluxation. Therefore, decompressive laminectomy is generally contraindicated as this may further destabilize the spine and result in increased neurologic deficit [ 1,11]. The goal of surgery is to relieve spinal cord compression, which is often ventral; therefore, the operative approach must provide adequate anterior exposure. The traditional anterior cervical approach is ideal for cervical lesions and readily allows simultaneous incorporation of a bony fusion [25,48]. Thoracic and lumbar lesions may be approached equally effectively by either an anterolateral [23,24,28] or posterolateral approach [ 1,11,25,30]. With either approach, the requirement for fusion depends on the extent of anterior bony destruction. If anterior bony destruction is minimal, decompression alone may be sufficient. However, extensive vertebral body destruction usually requires fusion either simultaneously or at a later time. The experience of a number
274
Surg N c u r o l 1990:3 ~:26()--5
of surgeons as well as our own has shown that bone fusion tan be performed safely and successfully in the presence of infection, provided the majority of purulent material is removed [1,I 1,22]. Fifteen of our patients underwent autologous bone fusion without complication. Others prefer to defer fusion until the infection has been eradicated [125]. Regardless of the approach, if spinal cord compression can be promptly relieved, the majority of patients fair quite well in terms of neurologic recovery.
Conclusion Prompt and accurate diagnosis of vertebral osteomyelitis remains a challenge that depends upon a thorough knowledge of the disease along with a high index of suspicion. Delay in diagnosis can result in neurologic complications related to spinal instability and/or suppuration. Definitive diagnosis relies upon positive identification of the causative organism in the appropriate clinical, laboratory, and radiographic setting. Magnetic resonance imaging provides an accurate method of detecting early disease and may become the procedure of choice for identifying epidural abscess. Optimal therapy should include 8 weeks of parenteral antibiotics supplemented by spinal immobilization for reduction of pain and assistance in bony healing. Surgical intervention is mandatory in patients with neurologic deficit and/or paravertebral suppuration. Despite the lengthy morbidicy often associated with this disease, timely diagnosis and appropriate management result in successful outcomes in the majority of patients. This study was supported m part by a Merit Review Grant lrom the Veterans Administration.
References I. Abramovitz I N , Batson RA, Yabhm JS. Vertebral osteom.velitis. The surgical management of neurologic complications. Spree 1986:11:4 lg-2(). 2. Ambrose GB, Alpcrt bt, Neer CS. Vertebral osteomyelitis. A diagnostic problem. J A M A 1966:19-: 101 -.i. ~. Antguaco EJC, McConnel JR, Chadduck WM, Flanigan S. MR imaging of spinal epidural sepsis. Am J Neuroradiol 198~:8:8~9-8.1. 4. BagdadeJD. Infection in diabetics: pre-disposing factors. Postgrad Med 19 .'6:59:160-,1. 5. Baker AS, Ojemann RG, Schwartz MN, Richardson I!P. Spinal epidural abscess. N EnglJ Med 19~5;29~:46';-8. 6. Batson OV. The function of the vertebral veins and their role in the spread of metastases. Ann Sure, 19,10:112:1 ~8-49. 7. Bonfiglio M, l.ange TA, Kim YM. Pyogenic vertebral osteomyelitis. Disc space infections. Clin Orthop 19~;96:2a,,i-.i ~.
O s c n b a c h ct al
8. Churchill MA, GeraciJt-, Hunder GG. Muscuh)skeletal manifestations of bacterial endocarditis. Ann Intern Med 1977;8~:-54-9. 9. Cooppan R, Schoenbaum S, Younger M, Friedberg S, D'Elia J. Vertebral osteomyelitis in insulin-dependent diabetics. S Afr Med J 19 "6;50:199~-6. 10 Digby JM. KersleyJB. Pyogenic non-tuberculous spinal infect/on. An analysis of thirty cases. J Hone Joint Surg 19"9;61B:,i7-55. 11. I'ismemt l~l. Bohhnan HB, Prasanna SL. Goldberg VM, Freehafer AA. Pyogenic and fungal vertebral osteomyelitis with paralysis..J Bone Joint Surg 198~:05A:19-29 12. Frederickson B, Yuan H, ()lans R. Management and outcome of pyogenic vertebral ostcomyelitis. (21m ()rthop 19=8:1 ~1:16()-7 15. Garcia A, Grantham SA. Hematogenous pyogenic vertebral osreomyelitis. J Bone Joint Surg 196():42A:,i29-30. Ii. Gcnster [-tG, Anderson MJ. Spinal osteomyclitis complicating urinary tract infecti(m. J Urol 19-2:10-:109-1 I. 15. Golimbu (., Firo()znia H, Rafii M. CT of osteomyelms of the spine. Am J Neuroradiol 198a,;.i:120--1 I. 16. Griffiths HED, .h)ncs DM. Pyogenic lnt)ction ()t" the spree. A review of twenty-eight cases. J Bone Joint Surg 19-1 ;5 a~g: '~8'~-91. 1 " Hodgson AR, Stock FE. Anterior spinal fusion for the treatment of tuberculosis of the spine: operative tindings and results of treatment in the first one hundred cases. J Bone Joint Surg 1960;i2A:295-~10. 18. t|olzman RS. gishko F. ()steomyelitis in heroin addicts. Ann Intern Med 19- I:-5:69~-6. 19. Jeffrey RIB, Cullcn PW, Fcderle alP. Computed tomography of psoas abscess. J Comput Assist Tomogr 1980:4:659-41. 20. Johns D. Syphilitic disorders of the spine. Report of two cases. J Bone Joint Surg 19-(1:52f3:'24- 51. 21. Jordan (2 Kirby WM. Pyogenic vertebral osteomyelitis treated with antimicroi~ial agents and bedrest. Arch Intern Med 19~ 1;128:.i05-10. 22. Kemp HBS, Jackson JW, Cook J, Cook J. Anterior fusion ot the spmc for infk'ctive lesions m adults. J Bone Joint Surg 19-3;55P,: "15-~4. 2/;. Kirkaldy-Willis WH, Thomas T G Anterior approaches in the diagnosis and treatment of infections of the vertebral bodies. J Bone Joint Surg 1965;,1~A:8 =-110. 24. KulowskiJ. Pyogenic osteomyclitis of the spine. J Bone Joint Surg 19 ~6:18: ';-i ';-64. 25. Larson SJ. Infi.'ction of the spine. In: Long D, ed. Current therapy m neurological surgery-2. Toronto: B.C. Decker, 1989:21)1)-1. 2(~. l.erner PI, Wemstein L Infk'ctive endocarditis in the antibiotic era. N I!nglJ Med 1966;2",1: 199-206,259-66, 32 a,-3 l, 3 8 8 - 9 k 2:. Lewis R, C,orbach S. Altner P. Spinal pseudomonas chondroosteomyelitis in heroin users. N Engl J Med 19 :2;286:1"~()'~-6. 28. l.oboskyJM, lqitchon PW. McDonnell DE. Transthoracic anterolateral dec
Surg N c u r o l 1990;-) a,:266-75
Diagnosis and Management of Pyogenic Vertebral Osteomyelitis in Adults Richard K. Osenbach, M.D., Patrick W. Hitchon, M.D., and Arnold H. Menezes, M.D. Department of Surgery, Division of Neurosurgery, University of lowa Hospitals and Clinics, Iowa City, Iowa
Osenbach RK, Hitchon PW, Menezes AH. Diagnosis and management of pyogenic vertebral ostcomyelitis in adults. Surg Neurol 1990;3'~:266-75.
Management of vertebral osteomyelitis remains controversial regarding optimum duration of antibiotic therapy and the role of surgery. Forty adults with vertebral nsteomyelitis were reviewed. Staphylococcus aureus was t h e most common pathogen isolated. Disk space narrowing with end-plate erosion was the earliest finding, followed by progressive vertebral body destruction. Magnetic resonance imaging proved extremely valuable in detecting spinal cord compression in patients with neuroiogic deficit. T r e a t m e n t should include at least 8 weeks of intravenous antibiotics combined with immobilization for pain reduction. Surgical intervention is indicated for all patients with neurologic deficit. Serial erythrocyte sedimentation r a t e s a r e valuable for following response to therapy. The value of magnetic resonance imaging in diagnosis is emphasized. KEY WORDS: Antibiotics; Epidural abscess; Magnetic resonance imaging; Neurologic deficit; Vertebral osteomyclitis
stability [ 1, I 1]. Therefore, early diagnosis is critical in obviating complications. Furthermore, treatment of vertebral osteomyelitis is not uniform and is controversial regarding the role of surgery and duration of antibiotic therapy. In an attempt to clarify some of these issues, we reviewed our experience with adult pyogenic spinal osteomyelitis.
Clinical Materials and Methods Between 1980 and 1987, 40 adults with pyogenic vertebral osteomyelitis were treated at University of Iowa Hospitals and Clinics and Iowa City Veterans Hospital. Data were collected by review of hospital and outpatient records along with review of radiographic studies. T h e r e were 32 men and 8 w o m e n from 25 to 85 years of age, with the mean ages of men and w o m e n being 60.6 and 59.4 years, respectively. Thirty patients (75C4) were over 50 years of age.
Clinical Presentation
Introduction Pyogenic infection of the vertebral column has traditionally been of little concern to neurosurgeons due to its relatively infrequent occurrence. However, neurologic complications are not u n c o m m o n and often warrant emergent surgical intervention. Unlike the pediatric population, in which the disorder is frequently acute in onset and associated with systemic illness, the adult variety more commonly presents insidiously and pursues an indolent clinical course, making early diagnosis difficult [2,7,16,24]. Consequently, affected individuals may present with neurologic findings related to paravcrtebral/epidural abscesses or spinal in-
Address reprint requests to." Richard K. Osenbach, M.D., Division of Neurosurgery, C42 General Hospital, University of Iowa Hospitals, Iowa City, Iowa 52242. Received October 20, 1989; accepted December 19, 1989. ¢~ 1990 by Elsc'vlcr Sci¢-nte Publishing Co., Inc.
The lumbar spine was most frequently involved (17), followed by the cervical (12) and thoracic (11) regions in descending order. Local spinal pain was present in 39 of 40 patients (98%), with 12 (30c'/c) also having a prominent radicular component. The single patient without pain had been rendered paraplegic in an unrelated accident several years earlier. Twenty patients (50%) were febrile at the time of diagnosis. The duration of symptoms ranged from 1 to 28 weeks, with a mean of 6 weeks. The average duration of symptoms was greater in patients who were neurologically intact (7.6 weeks) compared with patients with neurologic findings (4.2 weeks). Fourteen patients (35%) experienced symptoms for 6 weeks or longer. Physical examination uniformly revealed localized spinal tenderness, muscle spasm, and limited range of motion. Neurologic findings were present in 19 patients (48O;). Myelopathy occurred in 12 (635;), which included six patients with quadriparesis and six with paraparesis; five patients had a cauda equina syndrome; and 0090-~019.'90.'$3.~0
Vertebral Ostcomyclitis
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267
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F i g u r e 1. T i m e course of er,thro()te sedimentatton rate ~ESR, in patient~ u'ttb t ertebra/ osteom)dttt~. Thrre tJ a gradual decline tn the ESR u'itb treatt~tent.
i
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two patients had a radiculopathy. Neurologic deficit occurred in 8 of 12 (67¢;) patients with cervical disease, 6 of 11 (55C4) with thoracic inw>lvement, and 5 of 17 (29Ulvement. Risk factors or associated illnesses were present in 18 patients ( 4 5 ~ ) , including diabetes (8), chronic ethanol abuse (7), intravenous drug use (2/, and rheumatoid arthritis ( l }. Vertebral infection was believed to be secondary to hematogenous seeding in ~3 (83C/) cases, with a definite source of infection identified in 2 v patients (82C~). Soft tissue and urinary tract infections accounted for I0 and 6 cases, respectively; pulmonary infection ~3), subacute bacterial endocarditis (3), septic arthritis (2), purulent sinusitis ( 1 ), suppurative pharyngitis ( 1 ), and dental abscess (I) accounted for the remaining metastatic cases. Six metastatic cases could not be linked to a definite source. Seven cases (17%~) were considered to be the result of direct contamination from previous spinal surgery.
Laboratory Int'estigation The most c o m m o n laboratory abnormality and the most useful test was the erythrocyte sedimentation rate (ESR), which was uniformly elevated, ranging from 40 to 145 m m / h at diagnosis, with a mean value o f 8 5 m m / h (normal 0 - 2 0 mm/h). The ESR gradually declined during therapy to a mean of 25 m m / h by the termination ()f antibiotic therapy and to 12 m m / h by 16 weeks (Figure I ). While the ESR often failed to return to normal even in successfully treated patients, a declining trend was noted. By the end of antibiotic therapy, the ESR fell to at least 5()~ of original values in 9 4 ~ of patients, although
only 22% had normal values. By the end of 16 weeks, the ESR was normal in almost half the patients. In contrast to the ESR, peripheral leukocyte counts were normal or only slightly elevated. The white blood cell count showed no significant trend during therapy and in general was not helpful. Blood cultures were positive in 12 patients {.~0~) at the time of diagnosis.
Radiographic El,aluation Plain radiographs of the spine demonstrated a characteristic sequence of changes (Figure 2). Disk space narrowing with end-plate erosion was the earliest finding, followed by progressive vertebral body destruction and paravertebral inflammatory reaction. Sclerosis, new bone formation, and fusion occurred late as healing progressed. Plain films were normal in three patients, all with symptoms for less than 3 weeks. T w e n t y - o n e patients underwent computed t o m o g r a p h y (CT) scans, which revealed destructive changes of the vertebral body and delineated the inflammatory soft tissue reaction in all cases. C o m p u t e d tomography accurately identified six patients with psoas abscesses, which required drainage [ 15,19]. Percutaneous CT-guided aspiration/biopsy was peril>treed in 15 patients. Technetium bone imaging was performed in eight patients, which revealed increased uptake at the diseased level in all cases. Nine patients underwent myelography, which was normal in five and revealed extradural defects in four patients. The latter group included two patients with epidural abscess and two with postsurgical changes. Magnetic resonance imaging (MRI) in 14 patients revealed characteristic signal changes (Figure 3) and accurately identified six cervical epidural abscesses (Figure 4}.
2(~8
Surg Ncurol
()sc.nbach ct al
Figure 2. (A) l_atera/ lumbar .*ptn~ radiograph of a ~5-1car-o/d man 6 u t~ek, after the on,et ( , / h a ~ pazn. There L, .,ubt/e err,don of the .~upertor r~.rtehra/ end-p/at,. ,J L2 but l* oth,.rwt.~e unremarkah/e (13) l.atera/ /umbar ,pine lilm ~.*amepalsent, 6 month, Jollowzng tBe on,~.t e~lJ)mptnm* Hi.* ESR z~a, 65 mm/h. Bo~t~ d¢.itru~tto*t o~ the LI and 1.2 t'erlel)ra/ hod1¢..~ i~ now ,'z id*nt, f$a~leria/ ,u/tur~., o/ thi, /e,iopt o/J/,Jlpl~d /JV (. T-'4uz,/cd n~ed/; biop.,l ~qe/d,.d .Staph~./o~o, cu, aur, n*. (C) Lateral llvmhar *ptne/~/m l.*ame pattenl) o/2tatned .? month, after ~hal .,ho~ n in B. The palieplt ha.* h~.en immobilized in a thora~ o/umbar ortho.*l* and ha., recelt ed 6 week., o/)ntrare.nous antibzof it.*. The.re ha.* been ~e.,satlon of o.*teoclaJtic aclirily and znitiatton of./u~ion helu een t/oe inro/zt.d tertebra/ hodte*. The patient t~a.* asymptc, matic and h~* FSR u'a¢ .? ~ ram.;/;.
Vertebral ()stcomyclitis
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Figure 3. (A) Mid-sagttta/"['l-u'etRhtedMRl oj a .il-year-o]d man u'ho pre.~.nted u ith neck path aml radi~ulom3 elopath.; ,\'ot~ the decrea.~ed ~igna/ tntenjtty that ~o*l/tuent/r intolt'eJ the C4 and (55 t e~Yehral bodie., a n d intert'e*~tnx d i ~ . Ptvt'ertebral .,o]? tissue .~u'elling ~a*z he .*ee*l extending/rom (]2 to (.v t7"R l vO0. 7"E 120. J (B) ,~lid-.~agitta/T2u ei.~hted M R I t3ame patientJ ret'ea]., imreawd siR~lal inten.~it1 o] the i n t o h , d tertebral bodie~ and it~tert ertebra/ di~k. A]~o *tote the ventral ~pina/ cord conlpro ~io*l.
A
Microbiology and Isolation of Organism A causative organism was isolated in 36 (90C/c) patients (Table 1). Staphylococcu., aureus was the most c o m m o n organism, accounting for 67(7c of all cases and 86(?/c of all gram-positive isolates. Gram-negative infections occurred in 1 7 ~ of patients. T h e r e were four patients (10%) in which the causative organism could not be cultured. Only cultures obtained from the vertebral body, paravertebral tissues, or blood were considered
2(~9
signiticant. Diagnostic cultures were obtained from the vertebral body or contiguous tissues in 32 of 36 cases (89('~ 1:23 by an open procedure and 9 by CT-directed percutaneous biopsy. In four patients, organisms were identified only by blood cultures. Treatment
and Outcome
T r e a t m e n t consisted of spinal immobilization, antibiotics, and surgery. Bedrest was employed in 16 patients,
270
Surg Ncuro[ 1990;$ ";:266- '5
ranging from 2 to 12 weeks, and was individualized fi)r each patient based on reduction in spinal pain. External immobilization was utilized in 30 patients, including all patients with cervical anti thoracic inw)lvement anti 13 of 17 with lumbar disease. In uncomplicated cases, bracing was continued for 2 - 3 months or until pain had resolved or significantly subsided. In case of frank spinal instability, immobilization was continued until there was radiographic confirmation of fusion anti stability. Thirty-six patients with nontuberculous infections received antibiotics (intravenous only or intravenous plus oral) for an average of 10.8 +- 5.3 weeks; two patients received antituberculous therapy for I year and two patients received no antibiotics. The route of administration and duration of therapy are summarized in Table 2. Surgery was p e r f o r m e d on 2 ~ patients (68C~). All patients (19/27) with neurologic deficit underwent surgery: 10 because of spinal deformity/instability and 9 because of epidural/paravertebral suppuration. An autologous bone fusion was simultaneously incorporated in 15 patients. T h e indications for surgery in the eight patients without neurologic deficit included diagnosis (5), drainage o f paravertebral abscess (2), and debridement of the diseased vertebral body ( 1 ). T h e operative
()scnbach ct al
Figure 4. ,Xlkl-,agittal T2-u ei×hhd ,~IRI o]a 6~-.;,ar-r,M man with a 2-w~t.k hi,tor~ o/ nrck paid and /et er u'hrJ prt,rnt~d quadrtpareti~ with a C4 .,en,or~ lete/. An epidural ab*c~.,, ~arrowj i., compre,~ing the .,pina/ cord zentra/]~ at C ~-C4. Tki., patient maJe a /)¢ll neure,/ogzc rec0ce*3]ol/ou tng l entral decompres,ion and/nterbod~//~.,i~,n.
approach was determined by the location of compression, degree of bony destruction, and potential for spinal instability. Eleven of 12 patients with cervical involvemerit underwent surgery. Ten had a traditional anterior approach while one patient had a laminectomy. Eight patients each with thoracic and lumbar disease underwent surgery. A posterolateral approach was used in four thoracic and six lumbar cases, respectively, while laminectomy was performed in four patients with thoracic disease and two with lumbar involvement. Patients treated with laminectomy were kept at bedrest until their spinal pain resolved. Thereafter, a suitable orthosis for the neck or thoracolumbar spine was prescribed where instability was suspected. The mean follow-up period was 1 year, with outcome based on the degree of neurologic and/or symptomatic improvement. There" were two deaths related to sepsis secondary to the primary illness. Twenty-seven of the
Vertebral Osteomyclitis
Surg Neurol 1990;55:266-75
Table l. Causatire Organism Cultured from 36 Patients Organism Grarn- positive Staphylococcus aureus
No. of patients
Percent of total
28
77.7 66.6 5.6 2.8
24
Streptococcus sp
Anaerobe B rucella
Gram-negative Mixed Single ~ Tuberculosis
2 i 1
2.8
6 a, 5 2
16. ~ 8.5 8.3 5.6
• Eschertcbta colt. 1: Pseudomonas. 1, Proteus sp, I
remaining 38 patients (71 c,'Jc) eventually were asymptomatic. T h e r e was no difference in symptomatic or neurologic outcome between the group treated with intravenous antibiotics only as compared with the group that received intravenous as well as oral antibiotics. No patient who was initially intact deteriorated during therapy. Eight of 19 patients with neurologic deficit regained normal function while nine improved, one was unchanged, and one died. The level of involvement had no bearing on the incidence of recovery. One patient with paraparesis secondary to a T6 lesion deteriorated neurologically following laminectomy but subsequently showed progressive improvement following posterior stabilization. T h e r e was a single recurrent infection after discontinuation of antibiotics. This individual had undergone drainage of a psoas abscess followed by 8 weeks of intravenous plus 8 weeks of oral antibiotics. His pain and neurologic deficit improved and his ESR fell from 140 to 45 mm/h. H e subsequently experienced recurrent progressive pain, and reevaluation revealed his ESR to be > I 0 0 mm/h. Radiographic evaluation revealed a recurrent psoas abscess. Following repeat drainage, he again received 8 weeks of intravenous followed by 8 weeks of oral antibiotics, which resulted in resolution of his pain and fusion. Thirty-two patients ( 8 0 ~ ) ultimately achieved radiographic evidence of bony fusion, 17 spontaneously and 15 surgically.
Discussion Vertebral osteomyelitis was previously believed to be uncommon and even today occurs infrequently in otherwise healthy adults [38]. In contrast to acute spontaneous disk space infection more common in children, pyogenie vertebral osteomyelitis primarily affects adults [38,44,45]. The two conditions have a slightly different pathogenesis due to differences in the vascular supply of the disk and vertebral bodies between children and adults [38,45,46]. Prior to age 20, vascular channels
271
perforate the vertebral end-plates providing bloodborne bacteria access to the intervertebral disk. Therefore, in children the disk is initially affected with secondary involvement of adjacent vertebral bodies [46]. Adults have no direct vascular communication between the vertebral body and disk. Consequently, hematogeneously disseminated bacteria lodge in avascular areas adjacent to the subchondral bone. The vertebral endplates are then eroded and the disk secondarily involved [38,45]. Hematogenous seeding of the vertebral body may occur in two ways. Direct arterial seeding occurs by nutrient arteries derived from the posterior spinal, intercostal, and lumbar arteries [45]. Alternatively, transient bacteremia from urinary sepsis or instrumentation may result in retrograde venous seeding through Batson's plexus, which shares numerous connections with the pelvic veins [6,14]. Certain conditions appear to predispose one to vertebral osteomyelitis. Most notable is diabetes, which has been noted in 19(¥ of patients with vertebral osteomyelitis [9,13,38,42,44]. Diabetics have a diminished host immune response, making them more prone to infection, particularly with staphylococci [4,34]. Intravenous drug users have increased vulnerability to infection, and this practice has become increasingly associated with pyogenic vertebral infection [18,31,38]. Chronic ethanol abuse has been implicated as a risk factor for vertebral osteomyelitis. However, the incidence of ethanol abuse in patients with vertebral osteomyelitis is only 2.3C4 [38], compared with 4~; in the general population [39]. Therefore, the role of alcohol may be affected by the patient population under consideration. Contrary to earlier belief[24], nonpenetrating trauma has no bearing on the subsequent development of vertebral infection [ 13,35,38]. Finally, the belief that steroids or other im-
Table 2. Route and Duration of Antibiotic Therapy
All p a t i e n t s i N = 4 0 ) IV only IV plus oral TB None N o deficit ( N = 2 l ) IV o n l y IV plus oral None W i t h deficit I N - 19) IV o n l y IV plus oral TB
No. of patients
Duration"
24 t60.05:; ) 12 150.0c'; ) 2 !5.0'7,'.; I 2 f 5.0~?~ )
8.2 +- 5.3 w e e k s 16.1 +- ,t.8 w e e k s 1 year --
13 ( 6 1 . 9 ( ; ; ) 6 ~28.6ff;: )
~.0 ~.: 2.5 w e e k s 14.(I _+ 4.(1 w e e k s
2 19.5ff; )
--
11157.9(:,; ) 6{51.6q4) 2 i 10.0(:,; 1
9 . 6 m 3.3 w e e k s 18.2 * 4 . 8 w e e k s 1 year
Abbreviations IV, intravenous; "I'B, antituberculosis therapy. • Average duration of therapy was 10.8 -+ 5. a, weeks excluding'l'B patients
272
Surg Ncurol 1990;3 "E266- v 5
munosuppressive drugs increase the risk of vertebral osteomyelitis has not been substantiated [38]. Most cases of vertebral osteomyelitis result from a metastatic source of infection, most commonly the urinary tract [ 14,38]. Up to 60c?~ of metastatic infections related to urosepsis affect the skeleton, with 839~: of these involving the spine" [41]. Soft tissue infections often distant from the site of vertebral infection are a second important source of seeding [38]. Although three of our cases were related to subacute bacterial endocarditis (SBE), this association has been rare in the literature. This may reflect prompt diagnosis and treatment of SBE with simultaneous eradication of a subclinical osteomyelitis [8,26,37]. Less c o m m o n sources of metastatic infection include dental infections/proce'dures, thrombophlebitis, and respiratory infections. Infection related to previous spinal surgery results from direct contamination rather than hematogenous seeding. Nine of our cases were related to previous surgery. These cases did not represent uncomplicated discitis but had the entire picture of osteomyelitis. Elevation in the ESR, although nonspecific, is the most frequent laboratory abnormality, with mean values at diagnosis ranging from 40 to 87 m m / h [2,10,16,38]. An elevated ESR is not diagnostic of infection but is helpful in making or excluding the diagnosis in the appropriate clinical setting. The ESR is most valuable in monitoring therapy by observing the typical downward trend that occurs with successful treatment. However, absolute values of the ESR must be interpreted with caution because, despite successful therapy, the ESR may remain elevated to some degree for as long as 6 months in up to 7 5 ~ of patients [38]. In a large series of patients who underwent successful treatment, the ESR fell to two thirds of pretreatment values in all patients and to less than 5 0 ~ of pretreatment values in most patients by the completion of antibiotic therapy. Therefore, persistent elevation of the ESR does not necessarily indicate treatment failure and by itself should not dictate the need for further antibiotic therapy. In contrast, peripheral leukocyte counts are usually normal or only slightly elevated and show no significant trends with therapy [ 11,38,42]. Successful treatment depends on identifying the causative organism such that specific antibiotic therapy can be employed. Bacteriologic isolates should be considered diagnostic only if cultured from the affected vertebral body and contiguous paravertebral tissues or blood [38]. Cultures from the affected vertebra can be obtained by closed percutaneous aspiration/biopsy or open surgical biopsy. In a subgroup of patients with vertebral osteomyelitis, 70#~ of closed biopsies yielded positive cultures [36]. It is unclear what influence previous antibiotic therapy, inaccurate needle placement, or inadequate speci-
Osenbach et al
mens had on the 30c/c negative results. If an initial closed biopsy is negative, a repeat attempt is justified to ensure accurate needle localization and adequate specimens. Nine of 15 of our patients had diagnostic cultures obtained by closed biopsy. O f the six negative results, two patients had a diagnostic open biopsy, two received antibiotics based on positive blood cultures, and two were given empiric antibiotic therapy. If two attempts at closed biopsy fail to produce a positive culture, a decision must be made to proceed with empiric antibiotic therapy or to perform open biopsy. Blood cultures, which are positive in 14c),:-50()r/ of patients, especially during febrile periods, should be obtained routinely since" this may occasionally be the only source from which the pathogen can be isolated [38]. Staphylococcus aureus is the most c o m m o n pathogen causing vertebral osteomyelitis, accounting for 5BY of all cases and over 8()(X of all gram-positive isolates [2,13,38,42]. E~cherichia ,'oli is the most c o m m o n gramnegative organism, although Enterobacter. Proteus, and Pseudomonas are not uncommonly found, with Pseudomohas particularly frequent in intravenous drug users [18,27,38,40]. Anaerobic infection is relatively rare in vertebral osteomyelitis [38]. The incidence of tuberculous infection of the spine has sharply declined in this country, although in some parts of the world it remains the most c o m m o n pathogen [22,23]. Finally, a n u m b e r of rarer pathogens, such as syphilis, may cause vertebral osteomyelitis [20]. Classically, disk space narrowing is the earliest radiographic finding [2,10,24]. This may occur as early as 2 weeks following the onset of symptoms, but more frequently appears 6 - 8 weeks into the illness. During the early stages, tomograms may be helpful in visualizing changes not apparent on plain films [7]. Progressive vertebral body destruction follows, accompanied by paravertebral inflammatory reaction [13]. Sclerosis, new bone formation, and fusion occur late as healing occurs, although fusion may not be evident fi)r up to 1 year and in some cases may require 5 years [2]. In patients who fail to achieve bony fusion, a fibrous union usually functions equally effectively [43]. Although the sequence of plain film changes are characteristic of vertebral osteomyelitis, they often lag behind the clinical picture and are frequently not helpful in establishing an early diagnosis. Recently, MR1 has assumed an important role in the evaluation of spinal infection [3,32,33]. Magnetic resonance imaging has been shown to have a sensitivity, specificity, and diagnostic accuracy equivalent to combined technetium-gallium imaging in the diagnosis of vertebral osteomyelitis [33]. Furthermore, MRI is noninvasive and provides accurate information regarding the vertebral body, intervertebral disk, paravertebral tissues, and the spinal cord. Typically, T l-weighted images
Vertebral Osteomyelitis
reveal confluent decrease in signal in the affected vertebral body while T2 sequences reveal increased signal intensity. Disk involvement is invariably demonstrated, which helps to distinguish osteomyelitis from neoplasm [33]. Magnetic resonance imaging has been shown to delineate epidural abscesses with accuracy equivalent to myelography [3] and may eventually supplant the need for myelography. This accuracy is supported by our experience with MRI, which demonstrated all cervical epidural abscesses. The dosage, route, and duration of antibiotic therapy advocated by various investigators have been extremely variable [2,10,13,16,21,38]. Some authors have advocated 6-8 weeks of parenteral therapy only, while others have proposed 4-8 weeks of parenteral therapy followed by 2 months of oral therapy [ 16,29,31]. In Sapico and Montgomerie's [38] review of 162 patients with vertebral osteomyelitis, 33ff: of patients who received no antibiotics either died or suffered prolonged morbidity related to their disease. Furthermore, patients who received less than 4 weeks of parenteral therapy either failed treatment outright or relapsed significantly more often than those who received more than 4 weeks of parenteral antibiotics (P < 0.05 by X 2 analysis). We believe that 6-8 weeks of parenteral therapy is probably adequate in uncomplicated cases. We noted no difference in symptomatic and neurologic outcomes or recurrent infection between patients treated for 8 weeks compared with those treated longer than 8 weeks. Based on our own observations as well as those of others, the efficacy of complementary oral therapy at best remains unclear and is probably not indicated in most cases [35,38]. Spinal immobilization has traditionally played an integral role in the treatment of vertebral osteomyelitis. It is clearly indicated in cases of definite spinal instability. However, in the absence of overt spinal instability, the absolute need for and duration of immobilization is unclear [21,35]. The main goal of bracing in uncomplicated cases is to reduce pain and prevent postinfectious spinal deformity. Involvement of two adjacent vertebral bodies or more than a 50% reduction in height of a single body increases the risk of deformity [12]. We recommend that all patients have external bracing until pain is gone or minimal. The role of surgery, particularly in uncomplicated cases, remains controversial. Many authors believe that uncomplicated cases are effectively managed with antibiotics and immobilization with good results and minimum morbidity [ 10,13,16,35,45 ]. Others believe that surgery should play a primary role in treatment, citing a lower incidence of postinfectious spinal deformity, a reduction in recurrent infection, avoidance of neurologic deficit,
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and an earlier return to a functional capacity in support of their position [12,17,47]. On the other hand, it is generally agreed that surgery is mandatory in treating neurologic complications that occur in 3 f f - 4 0 % of patients with vertebral osteomyelitis [5,10,12,16,24,38]. The two primary causes of neurologic deficit are epidural abscess and spinal deformity/ instability. Epidural abscess complicates 5 % - 1 8 % of cases of vertebral osteomyelitis [ 1,24,38]. The 15% incidence of epidural abscess in our series is comparable. Any patient with vertebral osteomyelitis and neurologic deficit without significant spinal deformity should be suspected of harboring an epidural abscess. Epidural abscess causes spinal dysfunction by two mechanisms [ 1]. First, the localized accumulation of pus may cause mechanical spinal cord compression. Second, the epidural suppuration may lead to inflammatory thrombosis of the spinal vasculature that can eventually result in spinal cord infarction [30]. Evacuation of the abscess within 24-36 hours will often lead to complete neurologic recovery; however, once paralysis has occurred, spinal cord damage is likely irreversible. Although most spontaneous epidural abscesses are located dorsally, those associated with osteomyelitis are more often anterior to the dura mater. Inflammation begins beneath the posterior longitudinal ligament, progresses to subligamentous suppuration, and ultimately ruptures into the epidural space. The abscess may consist of either acute pus or dense granulation tissue in more chronic cases. Spinal deformity and instability affect 2 % - 2 8 % of patients with vertebral osteomyelitis and is the second major cause of neurologic deficit, although not all kyphotic deformities result in neurologic compromise [ 1]. Some degree of stability is usually maintained by intact posterior elements that are infrequently affected, thus preventing significant subluxation. Therefore, decompressive laminectomy is generally contraindicated as this may further destabilize the spine and result in increased neurologic deficit [ 1,11]. The goal of surgery is to relieve spinal cord compression, which is often ventral; therefore, the operative approach must provide adequate anterior exposure. The traditional anterior cervical approach is ideal for cervical lesions and readily allows simultaneous incorporation of a bony fusion [25,48]. Thoracic and lumbar lesions may be approached equally effectively by either an anterolateral [23,24,28] or posterolateral approach [ 1,11,25,30]. With either approach, the requirement for fusion depends on the extent of anterior bony destruction. If anterior bony destruction is minimal, decompression alone may be sufficient. However, extensive vertebral body destruction usually requires fusion either simultaneously or at a later time. The experience of a number
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of surgeons as well as our own has shown that bone fusion tan be performed safely and successfully in the presence of infection, provided the majority of purulent material is removed [1,I 1,22]. Fifteen of our patients underwent autologous bone fusion without complication. Others prefer to defer fusion until the infection has been eradicated [125]. Regardless of the approach, if spinal cord compression can be promptly relieved, the majority of patients fair quite well in terms of neurologic recovery.
Conclusion Prompt and accurate diagnosis of vertebral osteomyelitis remains a challenge that depends upon a thorough knowledge of the disease along with a high index of suspicion. Delay in diagnosis can result in neurologic complications related to spinal instability and/or suppuration. Definitive diagnosis relies upon positive identification of the causative organism in the appropriate clinical, laboratory, and radiographic setting. Magnetic resonance imaging provides an accurate method of detecting early disease and may become the procedure of choice for identifying epidural abscess. Optimal therapy should include 8 weeks of parenteral antibiotics supplemented by spinal immobilization for reduction of pain and assistance in bony healing. Surgical intervention is mandatory in patients with neurologic deficit and/or paravertebral suppuration. Despite the lengthy morbidicy often associated with this disease, timely diagnosis and appropriate management result in successful outcomes in the majority of patients. This study was supported m part by a Merit Review Grant lrom the Veterans Administration.
References I. Abramovitz I N , Batson RA, Yabhm JS. Vertebral osteom.velitis. The surgical management of neurologic complications. Spree 1986:11:4 lg-2(). 2. Ambrose GB, Alpcrt bt, Neer CS. Vertebral osteomyelitis. A diagnostic problem. J A M A 1966:19-: 101 -.i. ~. Antguaco EJC, McConnel JR, Chadduck WM, Flanigan S. MR imaging of spinal epidural sepsis. Am J Neuroradiol 198~:8:8~9-8.1. 4. BagdadeJD. Infection in diabetics: pre-disposing factors. Postgrad Med 19 .'6:59:160-,1. 5. Baker AS, Ojemann RG, Schwartz MN, Richardson I!P. Spinal epidural abscess. N EnglJ Med 19~5;29~:46';-8. 6. Batson OV. The function of the vertebral veins and their role in the spread of metastases. Ann Sure, 19,10:112:1 ~8-49. 7. Bonfiglio M, l.ange TA, Kim YM. Pyogenic vertebral osteomyelitis. Disc space infections. Clin Orthop 19~;96:2a,,i-.i ~.
O s c n b a c h ct al
8. Churchill MA, GeraciJt-, Hunder GG. Muscuh)skeletal manifestations of bacterial endocarditis. Ann Intern Med 1977;8~:-54-9. 9. Cooppan R, Schoenbaum S, Younger M, Friedberg S, D'Elia J. Vertebral osteomyelitis in insulin-dependent diabetics. S Afr Med J 19 "6;50:199~-6. 10 Digby JM. KersleyJB. Pyogenic non-tuberculous spinal infect/on. An analysis of thirty cases. J Hone Joint Surg 19"9;61B:,i7-55. 11. I'ismemt l~l. Bohhnan HB, Prasanna SL. Goldberg VM, Freehafer AA. Pyogenic and fungal vertebral osteomyelitis with paralysis..J Bone Joint Surg 198~:05A:19-29 12. Frederickson B, Yuan H, ()lans R. Management and outcome of pyogenic vertebral ostcomyelitis. (21m ()rthop 19=8:1 ~1:16()-7 15. Garcia A, Grantham SA. Hematogenous pyogenic vertebral osreomyelitis. J Bone Joint Surg 196():42A:,i29-30. Ii. Gcnster [-tG, Anderson MJ. Spinal osteomyclitis complicating urinary tract infecti(m. J Urol 19-2:10-:109-1 I. 15. Golimbu (., Firo()znia H, Rafii M. CT of osteomyelms of the spine. Am J Neuroradiol 198a,;.i:120--1 I. 16. Griffiths HED, .h)ncs DM. Pyogenic lnt)ction ()t" the spree. A review of twenty-eight cases. J Bone Joint Surg 19-1 ;5 a~g: '~8'~-91. 1 " Hodgson AR, Stock FE. Anterior spinal fusion for the treatment of tuberculosis of the spine: operative tindings and results of treatment in the first one hundred cases. J Bone Joint Surg 1960;i2A:295-~10. 18. t|olzman RS. gishko F. ()steomyelitis in heroin addicts. Ann Intern Med 19- I:-5:69~-6. 19. Jeffrey RIB, Cullcn PW, Fcderle alP. Computed tomography of psoas abscess. J Comput Assist Tomogr 1980:4:659-41. 20. Johns D. Syphilitic disorders of the spine. Report of two cases. J Bone Joint Surg 19-(1:52f3:'24- 51. 21. Jordan (2 Kirby WM. Pyogenic vertebral osteomyelitis treated with antimicroi~ial agents and bedrest. Arch Intern Med 19~ 1;128:.i05-10. 22. Kemp HBS, Jackson JW, Cook J, Cook J. Anterior fusion ot the spmc for infk'ctive lesions m adults. J Bone Joint Surg 19-3;55P,: "15-~4. 2/;. Kirkaldy-Willis WH, Thomas T G Anterior approaches in the diagnosis and treatment of infections of the vertebral bodies. J Bone Joint Surg 1965;,1~A:8 =-110. 24. KulowskiJ. Pyogenic osteomyclitis of the spine. J Bone Joint Surg 19 ~6:18: ';-i ';-64. 25. Larson SJ. Infi.'ction of the spine. In: Long D, ed. Current therapy m neurological surgery-2. Toronto: B.C. Decker, 1989:21)1)-1. 2(~. l.erner PI, Wemstein L Infk'ctive endocarditis in the antibiotic era. N I!nglJ Med 1966;2",1: 199-206,259-66, 32 a,-3 l, 3 8 8 - 9 k 2:. Lewis R, C,orbach S. Altner P. Spinal pseudomonas chondroosteomyelitis in heroin users. N Engl J Med 19 :2;286:1"~()'~-6. 28. l.oboskyJM, lqitchon PW. McDonnell DE. Transthoracic anterolateral dec
