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11th Cycle Module 1. Spine Infections

Disclosure

• I do not have anything to disclose

Spine infections
Angel Sánchez-Montañez, MD
Pediatric Neuroradiology
Universitary Hospital Vall d’Hebron – Barcelona, Spain
angel.sanchez.idi@gencat.cat

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11th Cycle Module 1. Spine Infections 11th Cycle Module 1. Spine Infections
Index Objectives
• Objectives • Pathogens • To review the different spinal infections in pediatric population

• Introduction • Classification
• Embriology · Extradural • To discuss the different possible pathways and pathogens
• Anatomy · Intradural
• Variants · Intramedullary
• To focus on their neuroimaging findings and differential diagnosis
• Techniques • Differential diagnosis
• Pathways • Conclusions

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11th Cycle Module 1. Spine Infections 11th Cycle Module 1. Spine Infections
Introduction Embriology
• Spinal infectious disorders, although uncommon in children, can have devastating effects when not
recognized promptly, especially in immunocompromised, chronic illnesses…
• Gastrulation (2nd/3rd GW)
• Staphylococcus aureus is the most common pathogen. Others: Kingella kingae (6m-4y), virus, TB, … – Formation of the 3 embrionary layers  Neural Plate
Cultures of blood and biopsy specimens are frequently negative
• They may present back pain, irritability, weakness, areflexia or hyperreflexia, scoliosis, incontinence, • 1st Neurulation (3rd/4th GW):
sensory dysfunction, neuropathies, limp or refusal to walk/sit & paralysis – Neural Plate  Neural Canal  Neural Tube
• Neurological exam is usually absent or masked by prior administration of antibiotics +/- Gower sign

• Peripheral leukocytosis with a left-shift, and elevated ESR or C-reactive protein. Fever is inconsistent

• Difficult to differentiate from noninfective inflammatory diseases, degenerative & neoplasms

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Embriology Anatomy
• 2nd Neurulation (5th/6th GW) SC SP Subarachnoid space
Subarachnoid space Spinous process
– Caudal Cell Mass Condensation
Spinal Cord Meninges Conus medullaris
– Vacuolization Dentate
Ligaments
– Canalization & fusion
– Retrograde Differentiation (cellular apoptosis), forms:
• conus medullaris, ventriculus terminalis & filum
terminal Echogenic central complex
L1-L2
Intumescentia lumbalis Vertebral bodies Cauda equina nerve roots

Cauda Terminal
equina Filum
nerve (<2mm)
roots

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Variants Variants

Filar cyst: Incidental & common well-defined fusiform cystic image in the filum Transient central canal dilatation: firsts weeks of life (<5mm)

Pseudomass: grouped roots Dysmorphic angled coccix

Ventriculus terminalis (5V): Incidental & common ependymal-lined fusiform Others: synchondroses, posterior arches clefts, vertebral wedging, spina bifida occulta, vascular grooves, ring apophyses, pediculate
dilatation of the terminal central canal of the spinal cord within the CM thinning, spina bifida occulta, ossiculum terminale, bifid odontoid, ponticulus posticus, pseudosubluxation, “bone-within-bone”

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Techniques Sagittal T2WI-FS/ STIR + T1WIFS GD+ (S & S > 92%)
Techniques Sagittal T2WI-FS/ STIR + T1WIFS GD+ (S & S > 92%)
• MRI: Modality of choice. Sensitive and specific, especially for soft tissue and spinal cord • MRI: Modality of choice. Sensitive and specific, especially for soft tissue and spinal cord
> lesion conspicuity by suppressing epidural fat & vertebral marrow SI > lesion conspicuity by suppressing epidural fat & vertebral marrow SI
• CT: best shows the destruction of the bone in early stages  osteosclerotic changes Stage I (< 1 mo) Stage II (1–6 months)
Ossified vertebral body is oval Size and SI of ossified vertebral body increases
• US: the spinal cord is well seen in the first few months of life Large cartilaginous endplates T1WI SI of cartilaginous structures decreases
HyperSI T1WI endplates Decrease of SI gradually in vertebral body by 2 years
• X-Ray: low sensitivity. Negative <8w. Late phase: endplates sclerosis + disc narrowing
Hypointense T1WI BM & NP Vertebral bodies have a horizontal band with high SI
• NM: low sensitivity and specificity. May show abnormalities early (1 w after onset) Stage III (6 months–5 years)
– Bone scan 3-phase Tc-99m diphosphonate scan shows increased activity in all phases Vertebral bodies become rectangular
At 5 years the SI of vertebral bodies > discs on T1WI
– Gallium scan increased uptake of Ga67 citrate. > S&S with SPECT- Ga67 (alternative to MRI) (90%) Vertebral body BM have low SI, basivertebral plexus has high SI on T2WI
– WBC scan: Often false-negative in patients with chronic vertebral osteomyelitis Narrower intervertebral discs compared to adults
Posterior elements are cartilaginous initially with hyperSI T2WI compared to muscle
Ossification begins by 1st year and become relatively hypointense on T2WI

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Pathogens Pathways
· Bacterial: Staphylococci (aureus), Kingella, Streptococci, Brucella, N. meningitidis, Salmonella, Nocardia · Hematogenous spread: the most important. Arterial > Venous (Batson plexus)

· Myobacterial: Tubercullosis …
· Direct extension: specially when congenital dysraphism or dermal sinus tract, spinal catheters or prior
· Viral: Enterovirus, VZV, HSV, CMV, EBV, PV, WNV … COVID-19 … spinal surgery. Is the major mechanism for abscesses (paraspinal/epidural/subdural/medullary)

· Fungal: Candida, Aspergillosis, Coccidiosis, Cryptococcus …

· Cerebrospinal fluid: contiguity between intradural cranial vault and the thecal sac  direct communication
· Parasital: Cysticercosis, Schistosoma …

· Lymphatic spread: rare; may be seen in cases of mediastinal or retroperitoneal node enlargement
The course depends on the virulence of the
organism, the number of inoculating organisms,
and the immunologic status of the patient

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Classification Classification
Location Location
· Extradural infections · Extradural infections
Disc, vertebra, epidural space, facet joint Disc, vertebra, epidural space, facet joint

· Intradural extramedullary infections · Intradural extramedullary infections

Leptomeninges, subdural & subarachnoid spaces Leptomeninges, subdural & subarachnoid spaces

· Intramedullary infections · Intramedullary infections

Spinal cord Spinal cord

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Disc-Vertebra Discitis-osteomyelitis / spondylitis / spondylodiscitis Disc-Vertebra Discitis-osteomyelitis / spondylitis / spondylodiscitis
• Suppurative infection of vertebrae and intervertebral disc. Most common lumbar > thoracic > cervical • Endplates irregularity with narrowed disc space and often is of low intensity on T1 and T2WI. If the disc or the adjacent
• Pathophysiology is often not known, but hematogenous arterial spread through capillary tufts in the cartilaginous vertebral body is hyperintense on T2WI in a nonanatomic pattern, consider disc space abscess with adjacent OM
vertebral endplates and in the vascular channels of the immature intervertebral disc. Young children are more • Diffuse and irregular Gd enhancement of the adjacent vertebral body is strong evidence of vertebral osteomyelitis
susceptible because vessels are found in the disc annulus up to age 20 years and in the cartilaginous endplate up to 7y • Associated phlegmon may be identified extending into the epidural space, paravertebral regions and psoas muscles
• S. aureus is the most common organism. Salmonella is the classic in sickle cell disease. None is identified in up to 70%
MRI Disc Vertebra Phlegmon / Abscess
• If not detected early in the course of the disease, vertebral OM may result in vertebral collapse and spinal deformity

• Spondylitis may extend to and cause retropharyngeal abscess, mediastinitis, empyema, pericarditis, peritonitis… T1WI Hypointense Hypointense Isointense
S. aureus
T2WI-FS / STIR Hypo/hyperintense Hyperintense Hyperintense
T1WI-FS Gd+ +/- +++ ++ (diffuse / rim)
Proteolytic Enzymes
A>P (Hyaluronidase) DWI + + +++ (abscess)
Other Loss of height Irregularities, deformity Mass effect / Extension
Disc +/- Vertebral Lysis
Not in adults, the intervertebral disc is avascular (except if 2ary vascularization due to degenerative)

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Disc-Vertebra Discitis-osteomyelitis / spondylitis / spondylodiscitis Negative Disc-Vertebra Discitis-osteomyelitis / spondylitis / spondylodiscitis Negative
F 19m. Abdominal pain 1 month. Walk alteration & lumbar hyperlordosis. ESR: 102 mm/h - CRP: 0.1 mg/dL blood culture M 3yo. Sitting and walking rejection 72h , complaining and fever 12h. ESR 50mm/h - CRP 0’73 mg/dL blood culture

Segmental arteries supply 2 adjacent vertebral bodies and the intervening disc: typical SOM MRI pattern

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Disc-Vertebra Discitis-osteomyelitis / spondylitis / spondylodiscitis Disc-Vertebra Discitis-osteomyelitis / spondylitis / spondylodiscitis Candida
M 15yo. T-Acute Lymphoblastic Leukemia treated with chemotherapy 1,5 months ago. Lumbar pain & fever

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Disc-Vertebra Discitis-osteomyelitis / spondylitis / spondylodiscitis Candida Disc-Vertebra Discitis-osteomyelitis / spondylitis / spondylodiscitis Nocardia
M 16yo. Buttock pain (posterior hip pain) and walk intolerance

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Disc-Vertebra Discitis-osteomyelitis / spondylitis / spondylodiscitis Kingella Disc-Vertebra Discitis-osteomyelitis / spondylitis / spondylodiscitis
M 5yo. Lumbar pain and rejection of the march kingae

1 month follow up MR 9 months follow up MR

• Early empiric antibiotics, broad spectrum coverage until causative pathogen isolated 8w. Abscess may need surgery

• After treatment, changes in the vertebral body last for up to 24 months, and persists for up to 34 months in the disc

• The best predictor of favorable treatment response is the disappearance of associated phlegmon

• Improvement in imaging findings may lag behind clinical one: increasing T2 hyperSI may be seen within the adjacent
vertebral bodies in the face of improving symptoms and laboratory tests, so is not a reliable sign of treatment response

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Disc-Vertebra Nonpyogenic spondylitis – TB Spinal Osteomyelitis Disc-Vertebra Nonpyogenic spondylitis – TB Spinal Osteomyelitis
• TB SOM (Mycobact. tuberculosis) is common in children. Hematogenous spread from chest and/or GU tract infection M 14yo. Lumbar pain and fever. Arrived from Mali few weeks ago

• Most common onset (Pott’s disease): midthoracic / thoracolumbar junction infection in child 2-5yo with chronic pain
+/- neurological deficits (50%). Extensive anterior vertebral body’s osteolysis (Ddx Fungal: Coccidioides…) +/- collapse,
gibbus, relatively intact discs and large paravertebral abscesses (>60%). Possible isolated posterior elements affection

• Lumbosacral +/- calcified PV abscess (Ddx Brucellosis) and craniocervical (big abscesses and nodal disease) TB are rare

• Pediatric TB is more extensive/aggressive than in adults, w large abscess; however children seldom develop paraplegia

• Diagnosis is difficult confirmed only by histology and/or culture. Often is based on clinical, imaging and response to ABs
MRI Disc Vertebra Marrow Abscess
Posterior T1WI Isointense Hypointense Isointense
C T2WI-FS/STIR Isointense Hyperintense Hyperintense
T1WI-FS Gd+ +/- +++ +++
DWI +/- ++ +++
Paradiscal Other Usually spared Posterior elements Cord displacement

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Disc-Vertebra Pyogenic Osteomyelitis – TB Spinal Osteomyelitis Disc-Vertebra Differential Diagnosis
M 5yo. Lumbar pain 1 month disturbing night sleep
DDX Pyogenic SOM Tuberculous SOM
Pathogen S. aureus Mycobacterium tuberculosis
Laboratory Highly elevated Low / Moderate
Location Lumbar Midthorax / Thoracolumbar junction
Segments Monosegmental Polysegmental (non)contiguous
Vertebra Body (ventral part) Body or isolated posterior elements
Osteolysis + +++
Disc Narrowed (proteolytic enzymes) Relative Spared (>70%) – Late phase
Abscess +/- Large and extensive (calcified)
Course Acute Insidious / Chronic
Treatment Antibiotics 8w +/- surgery Antituberculostatics 1y +/- surgery
Langerhans Cell Histiocytosis

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Disc-Vertebra Differential Diagnosis Disc-Vertebra Differential Diagnosis

Bone infarction Fracture Oropharyngeal carcinoma Scheuermann’s disease

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Epidural Space Epidural Abscess/ Empyema Epidural Space Epidural Abscess/ Empyema
• Lower thoracic & lumbar. Hematogenous spread & SOM. S. aureus (>50%), M. tuberculosis (25%), Streptococ., Brucella • MRI 95% sensitive for diagnosis, rapid & accurate localization/extension, helping in planning & monitoring treatment

• Very rare in childhood (girls > boys), but is important to recognize because may lead to permanent neurologic injury • Iso-hypoSI T1WI, hyperSI T2WI/STIR + homo-heterogeneous enhancing phlegmon / rim Gd enhancing necrotic abscess

• Predisposing conditions in children: sepsis, indwelling vascular catheters and spinal instrumentation (fetal, scoliosis…) • Better prognosis in children than adults & lower levels / poorer when ≥50% canal stenosis or craniocaudal length >3cm

• Location: posterior aspect of the canal (80%) in blood-borne empyemas / anterior canal (20%, usually bellow L1) when
DDX Epidural Phlegmon Epidural Abscess
infection extends from the vertebral body (SOM). Focal / diffuse extending over many segments with skip lesions
Pathogen S. aureus, M. tuberculosis S. aureus, M. tuberculosis
• Epidural space anatomy (> in dorsal lumbosacral) limits empyema to vertical spread  extradural/paraspinal extension
Location Posterior Lumbar Posterior Lumbar
• Encroaching/compression on the thecal sac, spinal cord, spinal nerve roots  cord edema / ischemia / infection
Aspect Homogeneous Heterogeneous +/- gas
Loculated No Yes
Gd+ Uniform enhancement Rim enhancement
DWI +/- +++
Treatment Conservative Surgery (decompression)

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Epidural Space Differential Diagnosis Facet Joint Septic Facet Joint Arthritis
• Suppurative bacterial infection of facet joint. Typically lumbar spine (>90%), single level, unilateral involvement

• Very rare in children. Most common cause: hematogenous contamination. S. aureus (86%)

• Facet joint widening w abnormal enhancement, facet marrow SI alteration, eroded facet cortex and soft tissue edema

• Facet joint & facet marrow HypoSI T1WI and HyperSI T2WI/STIR + periarticular soft tissue edema +/- OM +/- abscess

• T1WI Gd+: enhancement within joint, facet marrow and soft tissue +/- fluid collection (contiguous/epidural/paraspinal)

• Favorable outcome: ABs +/- percutaneous drainage +/- surgery. Delay in follow-up MR findings with respect to clinical

Bleeding Neuroblastoma Courtesy of Alvaro Pontoni, MD, Chile

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Facet Joint Septic C1-C2 Sinovytis / Arthritis Classification
• 16 m old boy with cervical stiffness. High ESR. Normal pharynx. Blood cultures negative. AB treatment. Good evolution Location
· Extradural infections
Disc, vertebra, epidural space, facet joint

· Intradural extramedullary infections

Leptomeninges, subdural & subarachnoid spaces

· Intramedullary infections
Spinal cord

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Subdural Space Subdural Abscess/ Empyema Meninges Leptomeningitis / Subarachnoid space infection
• Extremely rare in children, indistinguisible from epidural abscess • The most common infectious spinal disorder in children. Hematogenous spread, direct (trauma), local extension (SOM)

• The underlying subarachnoid space is narrowed or obliterated

Classification Spinal meningitis occurs less frequently than intracranial meningitis

· Acute meningitis: Onset of symptoms < 24 hr. Almost always bacterial

– Newborn: Group B Streptococcus (50%), gram-negative bacilli (E. coli), Listeria monocytogenes
– 2 m - 12 yo: Haemophilus influenzae (40-60%), Neisseria meningitides, and Strept. pneumoniae
– >12 yo: Pneumococcus, Neisseria meningitides, plus other streptococci and staphylococci
· Subacute meningitis: symptoms develop in 1-7 days. Mostly viral, some bacterial (e.g., Lyme disease)
· Chronic meningitis: Fluctuating symptoms for > 7 days. Tuberculosis, Fungal (e.g., Aspergillosis)

• Diagnosed and treated on a clinical and physical examination basis. Imaging usually not required (exc.: complications)

• CSF lactate level → dis nguish bacterial infec on where lactate is ↑ from nonbacterial (viral) meningi s

• Tx & Px depend on severity, age, comorbidities. Bacterial mortality (20-90%) / Viral less severe full recovery within 2 w

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Meninges Leptomeningitis / Subarachnoid space infection Meninges Differential diagnosis
• T1WI: Increased CSF intensity, Indistinct cord-CSF interface, Irregular cord outline, Clumped nerve roots

• T2WI: Obliterated & loculated subarachnoid space with nodular or band-like filling defects  syringomyelia

• T1WI Gd+ (without FS): smooth or irregular leptomeningeal / nerve roots / subarachnoid CSF enhancement

• Spinal cord swelling and edema likely due to ischemia from vasculitis, venous congestion, &/or direct infection
M 7yo. Tick bite. Target erythematous macular lesion. Asthenia, anorexy, drowsiness and fever Borrelia burgdorferi
DLGNT

Carcinomatous Lepto. Guillain-Barré Syndrome Intracranial Hypotension Infl. Arachnoiditis

Primary CNS neoplasm Inflam. autoimmune Prior spinal procedure / trauma Idiophatic / prior
Metastatic (rare) demyelination or spontaneous surgery, trauma…
Thickened, blurred Following recent viral Increased dural venous Thickened nerve
nerve roots illness or vaccination engorgement roots  “mass”
Obliterated CSF Ascending palsy. Areflexia Cerebellar descent + effacement "Empty sac" sign
Focal or diffuse Diffuse conus and cauda Difuse smooth meningeal Nerve roots Gd
nodular Gd uptake equina uptake (ventral) thickening & uptake uptake & clumpling

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Classification Spinal Cord Medullary Abscess / Granuloma
Location • Spinal cord abscesses are extremely rare (begin as an untreated myelitis). Children account for up 20%–50% of cases
· Extradural infections • Pathogens: Staphylococci, Streptococci, Listeria, Mycobact. (TB), Schistosoma, Fungal (Candida, Aspergillus)
Disc, vertebra, epidural space, facet joint • Risk factors: spinal dysraphism (40%), dermal sinuses, congenital heart disease, immunocompr., intravascular access

· Intradural extramedullary infections • Cord infection  edema, perivascular inflammation & vascular compromise  thrombosis, ischemia & infarction

Leptomeninges, subdural & subarachnoid spaces • T2WI: initial mild edema  cord swelling +/- Gd uptake  edema & abscess + diffuse, patchy, or ring uptake & DWI+

• Infected syrinx may simulate an intramedullary abscess, particularly in children with congenital spinal malformations
· Intramedullary infections
• Fungal disease tends to produce multiple lesions that may be small, solid, or enhance in a ring-like pattern
Spinal cord
• Treatment: early surgical drainage and aggressive intravenous antibiotic therapy

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Spinal Cord Medullary Abscess / Granuloma Spinal Cord Medullary Abscess / Granuloma
M 14 m. Unknown fever origin and irritability. Sacral dimple.

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Spinal Cord Medullary Abscess / Granuloma Actinomyces Spinal Cord Medullary Abscess / Granuloma Actinomyces

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Spinal Cord Myelitis Spinal Cord Myelitis EV D68
• Acute infection/inflammatory insult of spinal cord due to direct viral infection or postviral immunologic attack F 20 m. Obnubilation, fever, ataxia, no response to orders and flaccid paralysis after upper respiratory tract’s infection

• Since near complete Polio eradication, other EV (EV71 & D68) most common etiology / Herpes virus / West Nile …

• Location: cervical > thoracic segments > isolated conus involvement

• Clinical: flaccid paralysis (poliomyelitis) or neurologic dysfunction due to WM afection (motor & sensory symptoms)

• MRI: nonspecific w considerable overlap. HyperSI T2WI swollen edematous spinal (particularly cervical & thoracic) cord
with segmental contiguous involvement, fusiform expansion & variable, patchy enhancement of involved cord segment

• The degree of enhancement and DWI + correlate with the clinical status. Most cases leave lasting residual effects

• Treatment: intravenous immunoglobulin in children with acute flaccid myelitis. Antiviral drugs. Corticosteroid therapy

DWI + (EVD68): sequelae and even death

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Spinal Cord Myelitis VZV Spinal Cord Myelitis Viral Specific diagnosis through viral titers or PCR on CSF
M 7yo. Leukemia. Corticotherapy. OTI + spontaneous mechanical ventilation. Areflexic flaccid tetraplegia. Muscular atrophy EV71 & D68 PV VZV HSV-2 CMV WNV
Brain stem (P) Poliomyelitis Viral latent Rapidly progressive Necrotizing Polyradiculomyelitis
cervical cord Flaccid asymmetric reactivation neurologic dysfunc. polyradiculomyelitis Poliomyelitis-like sd
Epidemic muscle weakness Vesicular rash (lower thoracic cord) Febrile illness - deficits
Poliomyelitis- Fecal-oral spread Affects dorsal Extensive spinal Radicular pain Multiple segments
like sd. Acute Infants. Poor hygiene root first and cord enlargement, Urinary retention Cord uptake
flaccid paralysis Uncommon today posterior horns necrosis & blood uncommon
Uni or bilateral HyperSI T2WI Unilateral Ascending / Rapidly progressive Unilateral or bilateral
hyperSI T2WI anterior horns along ipsilat. enlarged relapsing paraparesis in the HyperSI T2WI
anterior horns whole cord hemicord & Gd+ transverse myelitis lower extremities Cervical anterior horns

Occasional Anterior roots of Long segment Lumbosacral Cauda equina, conus Cauda equina Gd+ and
ventral nerve the cauda equina HyperSI T2WI radiculitis surface & meninges parenchymal spinal
root and horn may also enhance Dermatomal Long segment Gd+ thickened and Gd+ cord hyperSI T2WI
Gd+ uptake distribution
September 2020
HyperSI T1/T2WI

EV71 and D68, WNV  clinical poliomyelitis and exhibit tropism for the anterior gray matter columns

HIV  vacuolar myelopathy. MRI: N or dorsolateral high T2 signal over multiple segments with multifocal enhancement

Other: bacterial (Borrelia burgdorferi, Mycoplasma pneumoniae…), parasites (Schistosomiasis, Cysticercosis…), Echinococco

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Spinal Cord Myelitis COVID-19 Spinal Cord Differential diagnosis
·The first case of SARS-CoV-2 causing myelitis was published on March,
May 2021 2020, from Wuhan, China. Firsts report in pediatrics scenario
Result of direct viral infection or autoimmune phenomenon?
·Virus impacts vascular cells or disseminates into CNS via olfactory bulb
·Advanced stages: hypoxia, respiratory and metabolic acidosis sequels

Myelitis - NMO Myelitis - MS

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Spinal Cord Differential diagnosis Spinal Cord Differential diagnosis

Low Grade Astrocytoma SCIWORA Systemic Lupus Erythematosus Medullary Ischemia

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Differential Dx Conclusions
• Despite spinal infections remain uncommon in pediatric clinical practice, and in most cases, the diseases are mild /
Extradural Intradural Intramedullary resolve spontaneously, there is need to maintain awareness due to their potentially fatal evolution

LCH, Cordoma, Osteosarcoma, Leptomeningeal Astrocytoma, Ependymoma, • Non-specific clinical presentations may lead to missed or delayed diagnoses. Spinal dysraphisms should be considered
Lymphoma, Leukemia carcinomatosis Cavernous malformation
• It is crucial to identify the source of the infection, and to establish a microbiological diagnosis  PCR
AIJ Guillain-Barré Syndrome ADEM, MS, NMO, SLE
• Imaging approach in spinal infections: early MRI (T2WIFS/STIR & GD+) +/- CT-guided needle cultures and histology
Bone marrow changes Bleeding, Hemorrhage Ischemia, Trauma (SCIWORA)
Degenerative disease, Cobalamin / Cooper deficiency • Most patients diagnosed in early stages, have better outcomes, can be successfully managed conservatively with ABs
Scheuermann disease, Inflammatory arachnoiditis, Sjögren’s, Behçet’s disease,
Mucopolysaccharidosis Intracranial Hypotension Sarcoidosis, RT myelopathy • If instability, progressive neurological deficits, conservative treatment’s failure, spinal abscess, sepsis  surgery

Fractures, Krabbe’s disease, Mixed connective tissue disease,

Bone infarction Metabolic and Rheumatoid arthritis, Ankylosing
Degenerative CNS disorders spondylitis

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11th Cycle Module 1. Spine Infections

Thank you for

your attention!
Spine infections
Angel Sanchez-Montañez, MD Angel Sanchez-Montañez, MD
Pediatric Neuroradiology Pediatric Neuroradiology
Universitary Hospital Vall d’Hebron – Barcelona, Spain Universitary Hospital Vall d’Hebron – Barcelona, Spain
angel.sanchez.idi@gencat.cat angel.sanchez.idi@gencat.cat

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