SPINE infective/inflammatory Flashcards
risk factors?
Entity. Def. Clinical presentation
Osteomyelitis, Discitis.
Def: infection of the bone involving the medullary cavity and the adjacent intervertebral disc.
Mainly due to pyogenic infection. Others: fungal, syphilis, tb.
Presentation:
Bimodal: paediatric patients and old adults.
Risk factors: IV drug user, HIV, Chronic disease (DM, chronic renal dysfunction, cirrhosis, IBD, cancer)
Which microorganism? rout of infection?
Pyogenic osteomyelitis/discitis:
Path, complications
Microorganism:
-Usually bacterial supurative:** S Aureus **most common.
-Ecoli if gram negative. Salmonella in sickle cell disase.
-Bacteriemia from extraspinal primary source (GU, GI, pulmonary, cardiac, mucocutaneous disease)
Rout:
-Hematogenous from extraspinal primary source (GU, GI, pulmonary, cardiac, mucocutaneous disease)
Targeted site: Vascularized subchondral bone adjacent to endplate seeded primarily
Secondary infection of intervertebral disc, adjacent vertebra
-Direct inoculation (trauma, surgery, procedures)
-Local extension (bowel infection, pyelonephritis, in DM patients)
Complications: spinal meningitis. Vascular compromise of cord and myelitis.
Prognosis/Treatment: medical and surgical.
Children: Intervertebral disc 1st site of infection due to presence of vascularity (isolated discitis. . Typically child with respiratory symptoms who suddenly presents with lumbar pain)
Complications: spinal meningitis. Vascular compromise of cord and myelitis.
Pyogenic osteomyelitis/discitis:
Morphology, Dx.
Morphology:
-Ill-defined T1 vertebral marrow
-loss of 2 adjacent endplate definition on both sides of disc (destruction of end plate cortex)
-Loss of disc height and **abnormal disc signal
-Vertebral collapse.**
-75% Paraspinal ± epidural infiltrative soft tissue ± loculated fluid collection = mass effect on thecal sac.
-Possible all spinal segments: L 48% > T 35% > cervical 6%
-Children: have direct supply to disc= can get isolated discitis, usually L. (scenario: kid 5yo w/upper respiratory infection now lumbar pain)
Dx:
**Best tool: MR T1 , T1 +C , T2/STIR . **
Avid enhancement of disc space and adjacent vertebral bodies (paraspinal and epidural involvement in 75%. DD with degenerative)
Xray: can be negative <2weeks. Irregular osteolysis followed by sclerotic endplates (not lytic). Loss of fat planes.
CT: Endplate osteolytic/sclerotic changes. Enhancing disc, marrow and paravertebral soft tissue.
Bone scan: 3-phase Tc-99m diphosphonate scan shows ↑ activity in all phases
SPECT Gallium scan: ↑ uptake of gallium citrate (Ga-67) (good alternative after MR)
WBC scan: often negative in patients with chronic osteomyelitis.
How often is this associated with other organ affection?
Etiology. Definition. Clinical presentation
Potts disease ( TB osteomyelitis)
Def: Caseating granulomatous infection of spine and adjacent soft tissue secondary to tuberculosis.
Concomitant with pulmonary disease 5-10%
Spine is most common MSK TB.
Presentation: pain, tenderness, fever, kyphosis, neurologic deficit.
Mid age adult 50yo.
More aggressive in children and more common intervertebral involvement due to rich vascularity.
Pott’s disease:
Path and complications
Path:
haematogenous or lymphatic spread.
Initial inoculum in anterior vertebral body.
Spread to noncontiguous vertebral bodies beneath anterior longitudinal ligamentsParaspinal, subarachnoid dissemination of disease
**Sparing of intervertebral disc **secondary to lack of proteolytic enzymes
Granulomatous destruction of spinal column with adjacent soft tissue infection = Gibbus deformity
Children: more common intervertebral involvement due to rich vascularity.
Complications:
Phlegmon (Diffusely enhancing soft tissue)
Abscess (Peripherally enhancing soft tissue). Epidural abscess./ Late stage can be “cold abscess”
Cord displacement/compression
Arachnoiditis
Intramedullary epidural abscess
Pott’s disease:
Morphology, Dx.
Morphology: Findings after weeks of infection onset.
Vertebral body involvement with sparing of disc space (spares due to absence of proteolytic enzimes)
Anterior vertebral body> Laminae > pedicles > spinous process > transverse process
Multilevel skip/non-contiguous lesions
Large paraspinal abscess (more than bony involvement) (posterior arch involvement is possible)
Gibbus deformity (late): focal short segment vertebral destruction resulting in kyphosis, spinal abscesses. Disc intact in early stage.
Mid-Thoracic and thoracolumbar most common > L or C.
Calcification in chronic paravertebral abscesses.
Atypical: posterior element and sacral involvement.
Dx:
-MR best: T1WI, T2WI, and T1 C+ with fat sat, most sensitive for bone marrow edema, epidural involvement
T1 , T2 , Post con enhancement.
DWI: Acute / chronic
-Bone scan: increased uptake, sensible but not specific. Gallium highly sensible and specific.
Predisposition factors?
Entity. Definition. clinical presentation
Epidural abscess/phlegmon
Def: Extradural spinal infection with abscess formation
Epidemio:
S. Aureus most common ~70%. TB 25%. Fungal less common case. 1/3 doest not have etiology.
Predisposing factors: IV drug users, immunocompromised, DM, chronic renal faillure, alcoholism.
Clinical: Old adults 60-70yo. Fever, pain, tenderness. Radiculopathy. Cord compression syndrome.
Epidural abscess,
Path, complications, associations
Path: Granulation tissue.
Local **direct inoculation **from penetrating trauma/surgery
Local spread: If anterior: arrises from adjacent discitis and vertebral osteomyelitis.
Haematogenous: posterior: GU or GI tract, lungs, cardiac, and mucous/
Cord ischemia from compromised epidural venous plexus.
Associations: infection in other location.
Prognosis/Treatment: irreversible neurologic deficit or death if untreated.
Epidural abscess,
Morphology, Dx
Morphology: Obscured posterior fat plane. Smooth borders from dura.
Spondilodyscitis with adjacent enhancing epidural phlegmen/abscess.
Location:
**Posterior 80%: **from GU, GI, lung cardiac
Anterior 20%: from adjacent discitis, osteomyelitis.
Circumferential
Lower thoracic and lumbar > upper thoracic and cervical
Signal alteration in spinal cord due to compression.
Dx: Best MR + C and fat sat.
T1 , T2 . DWI/ADC restriction.
Post con enhancement.
Phlegmon (Diffusely enhancing soft tissue, more solid)
Abscess (Peripherally enhancing soft tissue)
Subdural abscess,
Definition, predisposition, clinical profile
Def: presence of abscess located in the potential space between the dura and arachnoid mater. Intraspinal, extramedullary enhancing fluid collection.
Epidemio:
Predisposing factors: Intravenous drug abuse, immunocompromised state, diabetes, cirrhosis, renal failure, OH.
Clinical: old adults. F > M.
Fever, pain, tenderness, cord compression syndrome.
Subdural abscess,
Morphology , dx
Morphology:
Presence of clear epidural fat posteriorly.
The inner confines of a subdural haematoma are often concave and irregular, as opposed to the usual smooth contour of an epidural haematoma.
Thoracolumbar region most common
Dx:
Ring-enhancing intradural extramedullary collection outlined by epidural fat and CSF on axial imaging
Best: MRI.
T1 , T2 . Heterogeneous diffuse enhancement.
DD
S-inal cord abscess
-Cavernous malformation
-Hypervascular cord neoplasm (ependymoma, hemangioblastoma, astrocytoma, vascular emts rcc)
-MS
-Acute transverse/viral myelitis
Etiology. Definition. Clinical presentation.
Acute pyogenic meningitis
Def: Infection of spinal cord leptomeninges and subarachnoid space
Clinical: Newborn / Infant 3-8 months / Adults
Acute onset of fever, headache, and altered level of consciousness. Convulsion, neck stiffness, gait abnorm, urinary bladder dysfunction, paraparesia, paresthesia.
Acute spinal pyogenic meningitis,
Etiology and clinical presentation
-Acute meningitis: onset of symptoms < 24hs. Almost always bacterial.
-Newborn: Group B Streptococcus, gram-negative bacilli E Coli, Listeria monocytogenes
-2 months to 12 years: Haemophilus influenzae, Streptococcus pneumoniae, and Neisseria meningitides
-Adults: Above + streptococci + staphylococci, listeria
-Subacute: symptms develove 1-7 days.
Mostly viral (e.g., HIV-related CMV radiculomyelitis, enterovirus, influenza), some bacterial (e.g., Lyme disease)
-Chronic meningitis: fluctuating symptoms for > 7 days.
**TB, syphilis, fungal **(Coccidioidomycosis, cryptococcosis, and aspergillosis)
Path: Infection of **CSF and meningeal **coverings surrounding spinal cord. Initial acute inflammatory exudate in subarachnoid space.
Acute spinal pyogenic meningitis,
Mechanism of infection
Hematogenous dissemination from extraspinal focus of infection
Contiguous spread from adjacent spondylodiscitis, spinal epidural abscess
Direct inoculation through trauma or interventional procedures
Unexplained source of infection: Probably bacteria (meningococci) colonized in nasopharynx
Acute spinal pyogenic meningitis,
Associations?
-Spondylodiscitis
-Spinal epidural abscess, Subdural empiema, cord abscess
-Myelitis
-Syringomyelia (Blocked CSF flow results in increased pressure within cord and subsequent central canal expansion)
Acute spinal pyogenic meningitis,
Morphology, Dx
Morphology:
Diffuse/focal, extensive **subarachnoid enhancement. **
Smooth or irregular meningeal enhancement.
All spinal segments involved.
Diffuse CSF enhancement.
Dx:
Often negative in early spinal meningitis (positive if granulomatous or bacterial)
**Best: MR T1 C+ (Contrast mandatory for meningeal disease)
Best clue: Increased CSF SI on T1WI with diffuse postgadolinium enhancement **
-MR: T1: CSF intensity. Indistinct CSF/cord interface. Irregular cord outline. Clumped nerve roots.
-T2: Obliterated subarachnoid space. Nodular or band-like filling defects in subarachnoid space
Cord involvement: intensity
-T1 C+: Smooth or nodular leptomeningeal enhancement / root enhancement.
-CT: density of CSF. / CECT: Enhancing CSF + meninges.
Entity. Definition. Clinica
Facet Septic Arthritis.
Def: Suppurative bacterial infection of facet joint, adjacent soft tissue
Epidemio: old adults.
Clinical: **Acute or chronic **back pain. Tenderness, fever, spinal cord compression syndrome or radiculopathy.
Facet septic arthritis,
Path, assoc, complications
Path: Necrotic bone, suppurative and granulation soft tissue
Pathogen: S. Aureus 80%. Strep. 10%.
Most common route: Hematogenous. Also direct inoculation or local extension (from abdominal retroperitoneal inflammation)
Source: GU/GI, lungs, cutaneous.
Predisposition: IV drug, immunosuppressed, chronic disease (DB, cirrhosis, renal failure, OH, cancer, other)
Associations:
GI/GU primary source.
Epidural paravertebral abscess 25%, paraspinal abscess, spondylodiscitis, spinal meningitis.
Facet septic arthritis,
Morphology, dx.
Morphology:
Abnormal **enhancement within facet **joint with associated facet marrow, adjacent soft tissue edema
Typically single level, unilateral involvement
Facet joint widening
Ill-defined facet marrow signal alteration
Eroded facet cortex
80-90% Lumbar spine most common
Dx: Enhancing facet joint with juxtaarticular, paraspinal, or epidural phlegmon or abscess characteristic of septic facet joint arthritis
Best tool: MR
-Sagittal STIR or FSE T2 with fat saturation most sensitive for bone marrow edema and epidural involvement
-Post gadolinium T1WI with fat saturation better delineates extent of facet, epidural, and paraspinal involvement
T1hypo within facet. T2/STIR hyper. Post con enhancement.
-Xray: *may be negative 2-8 weeks *after onset infection. Instability in flexion/extension.
Osteolytic/sclerotic facets, periarticular soft tissue density.
-CT: rim enhancement within facet.
-NM: bone scan Tcc-9m. Gallium-67.
Recomm:
-Image-guided facet joint aspiration if blood culture negative
-Consider **scintigraphy **with marked leukocytes as posttreatment control (assess remote active septic foci, medical response)
Entity. Definition. Clinica.
Type 1 Arachnoiditis.
Def: Postinflammatory changes involving the meninges and subarachnoid space and nerve roots.
Clinica: simulates spinal stenosis and polyneruopathy. back pain or leg pain. Bladder bowel dysfunction, gait disorder, paraparesis, hyopestesia.
Arachnoiditis,
Types
Type 1: Thickening and clumping of nerve roots centrally in cauda equine = enlarged cords
Type 2: Adhesion of nerve roots to peripheral dura (empty sac sign)
Type 3: Soft tissue mass (pseudo mass) filling thecal sac
Arachnoiditis,
physiopath, etiology, associations.
Etiology:
Secondary to surgery
Infectious: meningitis (TB, syphilis, fungal, parasitic)
Inflammatory: intrathecal haemorrhage (thoracic)
Iatrogenic (contrast, medication), surgery
Other: trauma
Pathophysiology: Infection, perineural and leptomeningeal fibrosis, collagen deposition by fibroblasts, nerve roots adhere (to each other or thecal sac), CSF loculation.
Associations: Syringomyelia
Arachnoiditis
Morph, dx.
Morphology:
Abnormality extends > 2 vertebrae segments.
Type 1: Thickening and clumping of nerve roots centrally in cauda equine = enlarged cords
Type 2: Adhesion of nerve roots to peripheral dura (empty sac sign)
Type 3: Soft tissue mass (pseudo mass) filling thecal sac
Minimal to mild pial, dural enhancement: nodular, smooth, mass like.
/ intradural cysts (loculated CSF)
Nerve root calcification (rare) or calcific mass (arachnoiditis ossificans)
Lumbar sipne – cauda equine
Dx: Absent discrete nerve roots in thecal sac with clumping or empty sac sign highly suggestive of lumbar arachnoiditis
MR best tool. Contrast is mandatory.
Myelography.
Spinal MS,
Morph, Dx
Def: Primary acquired autoimmune demyelinating disease of CNS characterized by episodes of neurologic deficits separated in time, attributable to patchy white matter lesions that are separated in space (different regions)
Most common demyelinating disorder.
Epidemio: Young adults 20-40. F > M. Western European. Living away from equator.
Clinical: vision loss, motor or sensory abnormality, gait and balance abn.
Episodes of disease activity, separated in time, resulting from WM lesions separated in space.
Forms:
Relapsing remitting (RR) most common 70%. Symptoms, complete recovery.
Secondary progressive (SP) aprox 85% of RR enters this phase. (probable secondary to axon loss)
Primary progressive (PP) uncommon 10%. progressive accumulation of disability for >12 months
Progressive relapsing (PR) 15-50%. functionally active for over 15 years (retrospective dx)
Path: Gen + environmental
-Autoimmune, cell-mediated inflammatory disease targeting CNS myelin (WM) with loss of oligodendrocytes w/ relative preservation of axons (axonal degeneration is more typical of later stages).
-Genetic: Association with HLA-DR class II.
-Acquired trigger: infectious agent (e.g. EBV).
-Environmental: higher number of cases away from equator (lower vit D)
Associations:
-90% Concomitant intracranial lesions in periventricular, subcallosal, brainstem, or cerebellar white matter.
-NF 1
Complications:
Prognosis/Treatment:
Morphology: Isolated spinal cord in only 10-20%.
Isolated spinal cord disease (10-20%)
Cervical segment is most commonly affected
Dorsolateral aspect of cord
Short segment: < 2 vertebral segments in length
< 1/2 of cross-sectional area of spinal cord
Lesions typically oval, peripheral, & asymmetric
Does not respect GM/WM boundary
Wedge shaped on axial (apex directed centrally)
Cord: mild focal expansion + edema in active stage
Atrophy in late stage
Dx Dissemination in space and time (review McDonald Criteria 2017)
Space: 2 lesions w/ clinical evidence or
1 T2 (>3mm in long axis), characteristic, in 2 or more locations (periventricular, cortical or juxtacortical, infratentorial, spinal cord)
In time: clinical attacks or 1 with CSF specific oligoclonal bands, or
-a new T2 or G+ compared to previous baseline MR.
-simultaneous presence of G+ lesions and a non-enhancing T2 on any other MR.
Dx: Dx must be image + lab + clinical
Best clue: Concomitant T2 lesions in ≥ 2 of 4 areas of CNS: Periventricular, cortical or juxtacortical, infratentorial, & spinal cord
T1 iso hypo /T2-Flair-PD: hyperintense lesions + hyperintensity due to edema.
DWI restriction if active.
C+: variable: homogenous in acute and sub-acute. No enhancement in chronic.
Enhancement lasts 1-2 months but does not reflect disease progression
MRS: N-acetylaspartate (reduced within plaques, most common and remarkable), choline in acute.
MS,
Definition, Clinica,.
Def: Primary acquired autoimmune demyelinating disease of CNS characterized by episodes of neurologic deficits separated in time, attributable to patchy white matter lesions that are separated in space (different regions)
Most common demyelinating disorder.
Epidemio: Young adults 20-40. F > M. Western European. Living away from equator.
Clinical: vision loss, motor or sensory abnormality, gait and balance abn.
Episodes of disease activity, separated in time, resulting from WM lesions separated in space.
Forms:
Relapsing remitting (RR) most common 70%. Symptoms, complete recovery.
Secondary progressive (SP) aprox 85% of RR enters this phase. (probable secondary to axon loss)
Primary progressive (PP) uncommon 10%. progressive accumulation of disability for >12 months
Progressive relapsing (PR) 15-50%. functionally active for over 15 years (retrospective dx)
MS,
Path, assoc, complicatoins
Path: Gen + environmental
-Autoimmune, **cell-mediated **inflammatory disease targeting CNS myelin (WM) with loss of oligodendrocytes w/ relative preservation of axons (axonal degeneration is more typical of later stages).
-Genetic: Association with HLA-DR class II.
-Acquired trigger: infectious agent (e.g. EBV).
-Environmental: higher number of cases away from equator (lower vit D
Associations:
-90% Concomitant intracranial lesions in periventricular, subcallosal, brainstem, or cerebellar white matter.
-**NF 1 **
Complications: progressive multifocal leukoencephalopathy (PML)
