24 Spondyloarthropathies

Amir Ahmadian and Fernando L. Vale

I. Key Points

– Spondyloarthropathies are subdivided into seronegative and seropositive arthropathies (positive vs. negative antinuclear antibody [ANA] or rheumatoid factor [RF]).

– A family of described disorders/syndromes with overlapping symptomology with varying human leukocyte antigen (HLA) associations, including ankylosing spondylitis (AS), psoriatic arthritis, enteropathic arthritis, Reiter syndrome, ossification of the posterior longitudinal ligament (OPLL), and rheumatoid arthritis (RA)

– RA with high incidence of C-spine involvement (>85%)¹

– In RA, atlantoaxial subluxation (AAS) classified by anterior atlantodental interval (ADI) ≤3 mm (stable) and posterior atlantodental interval (PADI) ≤14 mm (increased risk of injury)

– OPLL: Asians, mostly asymptomatic, surgical approach controversial. Computed tomography (CT) for evaluation of posterior longitudinal ligament (PLL) calcification/ossification.

– Diffuse idiopathic skeletal hyperostosis (DISH): sacroiliac sparing, osteophytic change, associated with globus and dysphagia

II. Ankylosing Spondylitis Seronegative Arthropathy

– Background

• Also called Marie-Strümpell disease.¹ Affects 0.1 to 0.2% of the population, with a male : female ratio of 3 : 1. Peak age of onset: teens to fourth decade of life.²

• A chronic systemic inflammatory disease (strongest correlation with HLA-B27). CD4, CD8, and cytokine (tumor necrosis factor [TNF]-α and -β) mediated.^3–5

• AS specifically involves the sacroiliac joints and progresses to involve the entire spine. It may also variably involve peripheral joints, eyes, skin, and the cardiac and intestinal systems.

• Increased risk (up to 20%) if there is a first-degree relative with HLA-B27 and AS⁶

• Enthesitis: chronic inflammation at the insertion point of tendons that leads to ossification⁵

• Enthesopathy leads to osteoporosis of vertebral bodies and disc with sparing of nucleus pulposus (bridging osteophytes), producing the so-called bamboo spine.1

– Signs, symptoms, and physical exam^1,5

• Initial nonradiating back pain and morning stiffness (>45 minutes) that improves with exercise/activity

• Stiffness of the gluteal and lumbosacral junction (sacroiliitis)

• Progression of symptoms to entire spinal axis

• Eventual decrease in range of motion (autofusion)

• Tendon/ligament involvement (plantar fasciitis/Achilles tendonitis)

• Differential diagnosis: rheumatoid arthritis (RF+), DISH (also called Forestier disease) (spares facet and sacroiliac [SI] joint, later age of onset than AS), psoriatic arthritis/Reiter syndrome (milder with asymmetric sacroiliitis)

• The Patrick or FABERE (flexion, abduction, external rotation, extension) test: flex hip, flex knee, and place the lateral malleolus on contralateral knee; then press the ipsilateral knee downward (by stressing the hip joint); will cause pain in bursitis, sacroiliitis, and other hip joint pathology

• Cauda equina syndrome: usually no obvious etiology or compression

• Unstable rotatory subluxation (occipitoatlantal or atlantoaxial joint)

• Myelopathy: due to bow stringing of cord

• Significant fractures with minimal trauma

– Workup

• Modified New York criteria (radiographic sacroiliitis and back pain >3 months, limited spine motion in sagittal/frontal planes, or limited chest expansion)

– Neuroimaging

• Plain x-rays (crucial for diagnosis): obtain x-rays of entire spine (bamboo spine) and pelvis (SI joint) (Fig. 24.1)

• Magnetic resonance imaging (MRI): for further evaluation of disc spaces and ligamentous changes

• Bone scan: increased uptake at SI joint

– Treatment

• Medical management with nonsteroidal antiinflammatory drugs (NSAIDs), sulfasalazine, TNF-α antagonists, and corticosteroids

• Stable fracture: treatment with rigid brace

• Surgical decompression for inpatients with unstable fractures and/or progressive neurologic deficit

– Surgical pearls1,5

• Special care needed with routine neck immobilization after trauma intraoperatively in patients with AS. These patients tend to have the neck fixed in flexed position. Forced inline fixation may be deleterious, so fix neck in natural position.

• If patient is placed in traction, special attention to degree of kyphosis is necessary. Traction must be in line with patient’s natural kyphosis and not directly horizontal.

• No consensus on treatment for cord injury in AS patients (halo vs internal fixation) without obvious compression

• Root/cord compression: laminectomy and fusion recommended

• Posterior approach should be strongly considered secondary to anterior bridging osteophytes and concerns with fixation of anterior plate for osteoporotic vertebral body.

• Consider posterior osteotomy and fusion for correction of severe kyphotic deformity

Fig. 24.1 “Bamboo spine” in ankylosing spondylitis.

III. Rheumatoid Arthritis

– Background

• Very high incidence of C-spine involvement (atlantoaxial subluxation [anterior > posterior], basilar impression, pannus granulation of odontoid)^5,7

• ADI: ≤3 mm for evaluation of integrity of the transverse ligament; does not correlate with risk of injury8

• PADI: essentially the amount of space for the cord at C1-C2; does correlate with risk of injury if ≤14 mm^5,8

• Look for basilar impression and cervicomedullary junction compression

– Neuroimaging

• Lateral C-spine x-ray: ADI (anterior aspect of odontoid to arch of C1) / PADI (posterior aspect of vertebral body to spinolaminar line)

• MRI for evaluation of degree of stenosis (pannus)

– Treatment

• Surgical treatment of asymptomatic AAS can be considered when ADI >6 to 10 mm.⁹

• AAS in RA will progress with time; therefore, treatment is recommended, especially if myelopathy exists.

• Rigid collar does not support C1-C2 and is therefore a poor option.

• Immobilization of the C1-C2 joint via halo or posterior fusion alone may reduce the size of pannus over time.

• May use halo traction to align the odontoid and return it to its neutral position (start with 5 lb).

– Surgical pearls⁵

• Anterior, posterior, or vertical subluxation: most cases will require 360 degrees of fusion.

• Rotational or lateral subluxation: posterior-only approach is adequate.

• Anterior approach: odontoidectomy. For transoral approach the patient’s mouth must be able to open at least 25 mm.1 Patient is to remain in halo traction until fusion.

• RA with concomicant basilar impression should first be reduced and then fused.

• Transoral approach is associated with higher morbidity and usually reserved as a second option to posterior fusion.

IV. Diffuse Idiopathic Skeletal Hyperostosis

– Background

• Significant osteophyte formation in absence of significant degeneration. Distinct from degenerative disease, OPLL, and AS (Fig. 24.2).¹⁰

• Males in seventh decade of life

• SI joint spared¹¹

• Osteophytes do not stabilize, and unfused they are unstable. Minor trauma can lead to significant injury.

– Signs, symptoms, and physical exam

• Morning stiffness (milder than with AS)

• Globus: sensation of lump in the throat, secondary to large anterior vertebral body osteophyte adjacent to esophagus

• Dysphagia with or without weight loss¹

– Neuroimaging/workup/treatment

• Dysphagia: speech therapy consult to rule out primary esophageal pathology, diet modification, barium swallow (to localize obstruction). Progressive dysphagia with weight loss may benefit from surgical debulking.⁵

• CT scan superior to x-ray for evaluation of osteophytic structures

• Conservative treatment unless mass effect on esophagus or surrounding structures causes significant health risk (i.e., weight loss from dysphagia, pneumonia, and respiratory difficulty)

• Initially a change in diet to soft mechanical may be beneficial.

– Surgical pearls

• Anterior approach, drill down osteophyte. Special attention needed for protection of surrounding structures.

• No instrumentation needed. Debulking only. Do not violate disc space.⁷

• Initially, postop patients may have increased dysphagia. Risk of gastrostomy tube requirement.¹

Fig. 24.2 Diffuse idiopathic skeletal hyperostosis in the cervical spine. Note the continuous osteophyte formation along the anterior border of the cervical spine.

• Increased incidence in Asian (Japanese) population (prevalence around 2%).5,12 Prevalence increases with age (average age at time of diagnosis is mid-50s).

– Signs, symptoms, and physical exam

• Most are asymptomatic but can progress to myelopathy over time.¹³

• Symptoms can range from subjective neck pain to severe myelopathy.

– Neuroimaging/workup

• Plain x-rays will miss the ossification. Therefore, CT is suggested when OPLL is suspected.

• MRI or CT with intrathecal contrast for evaluation of degree of stenosis

• MRI: ossified PLL is dark on T1 and T2.

• Surgeon’s prerogative as to whether or not to leave a thin rim of ossified PLL attached to the dura during decompression. Note that the ossification usually extends into the dura and is inseparable.1

• Anterior approach (corpectomy) as opposed to posterior (laminectomy/laminotomy) decompression is controversial because of the significant risk associated with resecting all of the OPLL.¹⁴ Leaving a thin layer of bone that is adherent to the dura is recommended. Nerve root decompression is required.⁷

• Somatosensory evoked potential (SSEP) monitoring highly recommended.

Related posts:

Tumors of the Spine Thoracic Pedicle Technique Posterior and Transforaminal Lumbar Interbody Fusion (PLIF/TLIF) (Open) Surgical Resection of Spinal Vascular Lesions Physical Examination Retroperitoneal Approaches to the Thoracolumbar Spine

Stay updated, free articles. Join our Telegram channel

Join