SPINAL INFECTIONS. Anatomical Classification. Pathophysiology. Spine Infections. Microbiology. Sharad Rajpal, MD

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1 Anatomical Classification SPINAL INFECTIONS Sharad Rajpal, MD Vertebral column Intervertebral disc space Pyogenic vertebral osteomyelitis Spontaneous adult discitis Non pyogenic vertebral osteomyelitis Childhood discitis Postoperative adult discitis Spinal canal Epidural abscess Subdural Intramedullary abscess Adjacent soft tissues Cervical paraspinal lesions Thoracic paraspinal lesions Lumbar psoas muscle abscesses Pathophysiology Hematogenous spread (e.g. remote infections from indwelling catheters, urinary tract infections, IV drug use) Spread to adjacent structure Invasive procedure or instrumentation Source is not identified Predisposing factors IV drug abuse Diabetes mellitus Spinal trauma Alcoholism Chronic immunosuppression Renal insufficiency Spine Infections Sources of Low Back Pain (Jarvik and Deyo, Ann Intern Med 2002) Mechanical low back and leg pain 97% Neoplasms 0.7% Inflammatory arthritis 0.3% Infections 0.01% Other 2% Microbiology S. aureus is most common cause of osteomyelitis S. epidermidis common source of vertebral infections Gram negative organisms (E. coli, Proteus mirabilis, Enterococcus) more common in postoperative and immunocompromised patients Pseudomonas aeruginosa common among drug abusers Low virulent skin flora (Propionibacterium acnes, diphtheroids) source of delayed spinal infections Brucellosis individuals involved in animal husbandry and farming Fungal infections Coccidioidomycosis: endemic to the southwestern US, central valley of California, Central and South America; multiple lytic lesions and disc sparing Blastomycosis: endemic to mid and southwestern US; disc destruction Granulomatous infections: Mycobacterium tuberculosis Accuracy of Imaging Techniques for Spine Infections* Technique Plain MRI SPECT Radiography Sensitivity 82% 96% 90% Specificity 57% 92% 78% Positive Likelihood Ratio Negative Likelihood Ratio *Jarvik and Deyo, Ann Intern Med 2002

2 Spine Infection Multidisciplinary Management Project (SIMP) Imaging Diagnostic gold standard: MRI w/gadolinium PET/CT can help to differentiate between high stage degenerative inflammation and infection, if MRI doesn t help in diagnosis Evaluation of treatment efficacy: PET/CT at time 0 and after 2 4 wks. medical therapy or after 6 12 wks from surgery CT guided biopsy before the beginning of AB therapy in the stable patient for histologic and microbiologic diagnosis AB therapy Surgical treatment Wide abscess Progressive neurological signs Instability deformity Need for diagnosis Conservative treatment failure Pyogenic Vertebral Osteomyelitis Epidemiology Incidence 1/100,000 to 1/250, % of all cases of osteomyelitis A smaller peak at younger age than 20 and a larger peak between Vertebral bodies are involved more commonly than the posterior elements Lumbar region 13 83% Thoracic region 13 50% Cervical region 0 30% 9/24/2012 Change name of presentation in View > Header Footer 9 Pathophysiology and Etiology Vast majority are due to hematogenous spread secondary to bacteremia Starts in a highly vascular region, can spread to disc and adjacent body Untreated progress to abscess w/spread to paravertebral structures and into spinal canal Sources Genitourinary tract Soft tissues Respiratory tract Previous surgical intervention Open spinal trauma Almost always caused by Staphylococcus aureus Diagnosis Slow progression Gradual onset of symptoms for 2 to 3 months (range, 2 wks 2 yrs) Symptoms Local pain and tenderness Weight loss Fever Malaise Neurological symptoms are unusual initially Neurological signs can be observed in less than half patients (radicular, myelopathic) Spinal epidural abscess up to 20% of cases

3 Diagnostic Studies Laboratory tests ESR: mm/hr (range, ) Bacteriological tests Blood cultures should be obtained from all patients Radiology Plain radiography: not reliable CT: hypodensity of the involved disc, lytic fragmentation; demonstrate paraspinal and epidural involvement CT guided biopsy: bacteriological identification MRI: demonstrate early changes, diminished T1 and increased T2 signal; epidural and paraspinal involvement Treatment Conservative treatment is recommended Blood cultures or biopsy under x ray guidance IV AB therapy 6 8 wks Orthoses Medications for pain control Selective surgical treatment Draining of large paraspinal abscesses Kyphotic deformities may cause SC compression Neurologic deficit w/o x ray evidence of spinal deformity epidural space involvement may require urgent intervention Prognosis Spontaneous fusion is seen in about 50% after 1 year Less than 15% incidence of permanent deficits Tuberculous Vertebral Osteomyelitis (s. Pott Disease) 9/24/2012 Change name of presentation in View > Header Footer 16 Pott s Disease Has been documented in ancient mummies from Egypt and Peru 1779 classic description by Percivall Pott Rare in industrialized countries 2% of tuberculosis cases in developing countries Pathophysiology and Symptoms Route of infection Hematogenous Direct extension from lungs Paraspinal lymph nodes Symptoms Pain Fever and weight loss Two or 3 vertebral levels are usually involved Progressive bone destruction vertebral collapse and kyphosis Paraparesis in less than ¼of all patients due to abscesses, granulation tissue or direct dural invasion

4 Diagnosis Labs Skin tuberculin test PPD Elevated ESR (mean 44mm/hr) Microbiologic studies (bone tissue or abscess samples) CT guided biopsy Imaging Radionuclide scanning: non specific X ray changes present relatively late CT: diffuse anterior vertebral body destruction Sclerosis Large paraspinal mass w/thick nodular rim Extension along the spinal ligaments Calcification is common MRI Contrast enhanced MRIs are useful to differentiate tuberculous from pyogenic spondylitis

5 Treatment AB therapy Duration: 6 9 months (9 12 months if neurological or multiple vertebral involvement) 4 drug regimen: Isoniazid and Rifampin + first line drugs: pyrazinamide, ethambutol, streptomycin Second line drugs for resistant strains Combination chemotherapy and surgery Neurologic deficit Spinal deformity w/instability No response to medical therapy Large paraspinal abscess Spinal Canal Epidural Abscess (SEA) Spinal Epidural Abscess (SEA) First described by Morgagni in 1761 Walter Dandy (1926) Reported mortality rates of 83% Only 4 out of 25 patients were treated surgically Diagnosis was made at autopsy in the majority cases Incidence cases/10,000 hospital admissions (Reihsaus et al, Neurosurg Rev 2000) Mortality rates from 5 to 32% (Soehle and Wallenfang; Neurosurgery 2002) Outcomes remain poor approx. 45% achieve full recovery (Bostrom et al, Min Invasive Neurosurg 2008) 29

6 Clinical Presentation Localization Posterior hematogenous spread of remote infections Anterior spread of adjacent infection from discitis or osteomyelitis Symptoms Back pain Motor deficit Fever Elevated WBC, CRP, ESR Sepsis Meningeal involvement Bowel and bladder dysfunction Cord compression if not promptly treated Clinical Presentation Progression stages (Darouiche, N Engl J Med 2006) Stage 1: back pain localized to the affected vertebral level Stage 2: Radicular pain from the corresponding level Stage 3: Motor weakness, somatosensory deficit and sphincter dysfunction Stage 4: Paralysis The correct diagnosis was missed initially in 30 to 60% of cases (Darrouiche et al, Medicine 1992; Nussbaum et al, Surg Neurol 1992) Diagnosis MRI w/gadolinium is the test of choice Hypo (T1) or hyperintense (T2) mass w/diffuse homogeneous or slightly heterogeneous enhancement Peripherally enhanced fluid collection as the phlegmonous mass necroses CT myelography if MRI contraindicated Lumbar puncture is a relative contraindication Blood cultures are 60% positive Treatment Strategy Emergent surgical decompression IV AB therapy sometimes combined w/ct guided needle aspiration High risk of surgery patients Presumably irreversible paralysis that lasts > hrs AB therapy should cover gram positive cocci (staph, MRSA) and gram negative bacilli Symptoms-Guided Treatment Strategies* *Karikari et al, Neurosurgery 2009 Prognosis Clinical presentation Back pain/radiculopathy vs. paresis/plegia Duration of clinical signs and symptoms Surgery (if indicated) within hours is advised Surgical vs. medical treatment Location, extent and degree of the SC compression Lower limb motor deficits in general and complete paralysis in particular prognostic of poor outcome Complete paralysis outcomes are poor even if surgery is performed within 24 hours (Soehle et al, Neurosurgery 2002) Clinical outcomes Good clinical outcome 60 70% Severe disabilities 5 20%

7 Subdural Abscess (SSA) or Empyema Spinal Subdural Abscess (SSA) SSA is a rare condition Incidence is unknown First described by Sitting in 1927 Pathophysiology Hematogenous spread from distant infections (e.g. furuncles, otitis, pelvis infections, systemic sepsis) Direct extension of adjacent discitis or osteomyelitis is less frequent Complication of congenital dermal sinus Iatrogenic Pathogens Staphylococcus aureus is most common 37 Clinical Presentation Fever Spinal or radicular pain Neurologic deficit depending on location Motor deficit Sensory loss Sphincter disturbances Progression stages are similar to SEA The duration of symptoms prior to diagnosis (Bartels et al, J Neurosurg 1992) Acute: < 1 week Subacute: 2 to 8 wks Chronic: > 8 wks Diagnosis and Treatment Strategies Diagnosis MRI Myelogram or CT Immediate surgical decompression and drainage 32/39 (82.1%) patients survived* AB therapy 1/5 (20%) patients survived* *(Bartels et al, J Neurosurg 1992)

8 Iatrogenic Infections Invasive diagnostic procedures Lumbar discography: 0.6% infectious discitis (Gepstein & Eismont, in Garfin (ed): Complications of Spine Surgery, 1989) Surgical Lumbar discectomy: 1% infection rate PLIF 3 13% The greatest risk of infections in patients More than one operation during the same admission The presence of open drain postoperatively Internal fixation of a fracture Spinal fusion, if surgery lasted more than 5 hours Inadequate soft tissue coverage of the device Skin and muscle devascularization Comorbidities e.g. systemic diseases, severe malnutrition, immune compromise Diagnostic challenges in postoperative patients May not present with classic signs of infection Postoperative fever Patients with S. epidermidis or diphtheroids infections have delayed presentation RhBMP induced inflammatory response ESR, CRP may be elevated, but is non specific Tests MRI Deep wound aspiration Positive bacteriological cultures Pathological changes in tissue surrounding the instrumentation