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Morning Report Nolan Sandygren, PGY-2
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Case
10-month-old girl presenting with lower extremity weakness after a fall
yesterday
Fell from bed to carpeted floor, approximately 3 ft
Mother was present in room, but facing the other way
No LOC, immediately started crying after the fall
Initially appeared to be fine, but later became fussy, wanted to held
Gradually seemed to get weaker in LEs over next few hours
Became unable to support weight with legs
Previously able to stand with support and walk with assistance
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HPI
Otherwise behaving normally
Reportedly weaker cry than usual
No difficulty breathing or eating
One episode of emesis following evening feeding
No fever, cough, congestion, or diarrhea
Reported GI illness 5 weeks prior
Received influenza vaccine 4 weeks ago
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Outside Hospital
Taken to OSH ED
Plain films of T-spine, L-spine, pelvis, and bilaterallower extremities normal
Discharged home, advised to watch carefully
Parents concerned that not moving her legs at all
Brought to PCMC ED later that night
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History
PMHx:
Born full term, no complications
Reflux Development: Normal
PSHx: None
Meds: None
Allergies: NKDA
Immunizations:
Up to date, with flu vaccine 4 weeks ago
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History
Family Hx:
Mother with developmental delay, functions at 6 y.o. level
7 y.o. half brother with ADHD
Social Hx:
Lives with foster parents and their 2 y.o. child for past 6 months
Possible domestic violence in the home that she came from, butfoster parents dont think that she was directly physically abused
ROS otherwise negative
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Physical Exam
Vitals:
Weight 7.4 kg, Temp 36.8, HR 120, Resp 38, BP 97/54, SaO2 95% on RA
Exam:
General: awake, alert, interactive, no acute distress
HEENT: Atraum, normoceph, EOMI, PERRL, no conjunct, Nl TMs, nares clear, MMM, no oral lesions
Neck: supple without LAD, no tenderness or meningismus
CV: RRR, nl S1,S2, no MGR, cap refill < 2s
Lungs: CTAB, no WRR, nl WOB
Skin: No petechiae, purpura, jaundice, or cyanosis
Abdomen: S/ND/NTTP, nl BS, no HSM
Back: No bruising, tenderness, deformity, or bony step-off Extremities: No bruising, edema, or deformities of upper or lower extremities, normal ROM passively
Neuro: Makes eye contact and tracks, CN 2-12 grossly in tact. Moves both arms equally, reaches for objects, normal tone.Doesnt spontaneously move either leg at all, but withdraws both lower extremities to nailbed pressure. Decreased sensation in
LEs. No tone against gravity, doesnt support weight when held in standing position. 1+ patellar reflexes, 2+ achilles, biceps, and
triceps reflexes. Decreased rectal tone.
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10 m.o. girl presenting with lower extremity weakness x
1 day after a fall.
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Differential Diagnosis
Neuro:
Guillain-Barr syndrome (acute inflammatory demyelinating
polyradiculoneuropathy)
Acute disseminated encephalomyelitis (ADEM)
Multiple Sclerosis
Transverse myelitis Epilepsy
Migraine
Musculoskeletal:
Spinal cord injury or compression
Trauma
Malignancy:
Lymphoma
High grade glioma
Metabolic:
Vitamin deficiency (B12, folate)
Infectious:
Acute bacterial/viral encephalitis or meningitis
Viral myelitis
Lyme disease
West Nile virus
Syphilis
HIV
Inflammatory/Vasculitis:
Systemic lupus erythematosus
Antiphospholipid antibody syndrome
Behcet disease
Vascular:
Spinal cord infarction
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ED Course
C-spine XR, with overread of outside films -> no fx
Planned to admit to trauma, with MRI of T-spine and L-
spine pending
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MRI T and L spine wo
contrast
MRI initially read as normal, with no evidence of
traumatic injury
Pt transferred to pediatric service with neuro consult.
GBS was working diagnosis given MRI findings, and
time course and distribution of symptoms
MRI read changed later that evening
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MRI T and L spine wo
contrast MRI Thoracic Spine wo Contrast:
Long segment T2 hyperintensity and mild cord enlargement in
midthoracic spinal cord extending approximately 6 vertebrallevels, T4-10. No additional findings are noted to indicate a
traumatic thoracic spine injury.
MRI Lumbar Spine wo Contrast:
Normal imaging appearance of conus. No traumatic vertebral orposterior element fractures noted. No intervertebral disc herniation
Marked urinary bladder distention.
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Transverse Myelitis
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Acute Transverse Myelitis
Neuro-inflammatory spinal cord disorder
Presentation:
Rapid onset of signs and symptoms
Motor, sensory, and/or autonomic dysfunction
Annual incidence: one to eight new cases per million
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Classification
Acute partial TM
mild or asymmetric, extends 1-2 vertebral seg Acute complete TM
near complete symmetric, extends 1-2 vert seg
Longitudinally extensive transverse myelitis (LETM)
complete or incomplete, extending 3+ vert seg
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Etiology
Idiopathic TM
Typically occurs as post infectious complication, likely
autoimmune process
Secondary (disease-associated) TM
Systemic inflammatory autoimmune condition
MS, neuromyelitis optica, and acute disseminated
encephalomyelitis (ADEM)
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Diagnostic criteria
Sensory, motor, or autonomic dysfunction attributable to
spinal cord
Bilateral signs and/or symptoms
Clearly defined sensory level
No evidence of compressive cord lesion
Inflammation defined by CSF pleocytosis orelevated IgGindex orgadolinium enhancement
Progression to nadir between 4 hours and 21 days
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Symptoms
Motor
Rapidly progressing paraparesis that can involve UEs
Initial flaccidity followed by spasticity
Sensory
Pain
Dysesthesia (burning, wetness, itching, electric shock)
Paresthesia (pins and needles)
Autonomic
Increased urinary urgency
Bowel and bladder incontinence
Urinary retention, constipation
Sexual dysfunction
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Treatment
High-dose IV glucocorticoid treatment x 3-5 days
Methylprednisolone 15 mg/kg/day IV div q6h x 3days
Prednisolone 7.5 mg PO QD x 5 days, followed by
taper
Consider plasma exchange for patients with acute TM
complicated by motor impairment (5x QOD)
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Recovery
Most have at least a partial recovery within 1-3 months
Persistent symptoms in 40%
Rapid onset is associated with poorer outcomes
Recurrence
25-33% of pts with idiopathic TM
up to 70% of pts with disease associated
Pts with acute complete TM have 5-10% risk of MS
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Labs & Micro
CSF:
Protein: 12
Glucose: 55
Cell count: WBC
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Case development
Symptoms evolved during hospitalization and she
became hyporeflexic with decreasing sensation, then
more spastic.
Significant bladder distention requiring intermittent
catheterization q4-6h during hospital stay.
Started to regain strength after initiation of steroids, with
continued improvement in weight bearing as outpatient.
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References
Beh SC, Greenberg BM, Frohman T, Frohman EM. Transverse
myelitis. Neurol Clin 2013; 31:79.
Krishnan C, Kaplin AI, Pardo CA, et al. Demyelinating disorders:update on transverse myelitis. Curr Neurol Neurosci Rep 2006;
6:236.
Pidcock FS, Krishnan C, Crawford TO, et al. Acute transverse
myelitis in childhood: center-based analysis of 47 cases. Neurology
2007; 68:1474.
Wolf VL, Lupo PJ, Lotze TE. Pediatric acute transverse myelitis
overview and differential diagnosis. J Child Neurol 2012; 27:1426.