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Medical Student Morning Report Presentation

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... next morning, pt had 2nd seizure lasting ~10min with a 6 min post-ictal period. ... to the tissues and develop into cysticerci over a 3 wk 2 mo period. ... – PowerPoint PPT presentation

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Title: Medical Student Morning Report Presentation


1
Medical Student Morning Report Presentation
  • Jamison Strahan, Omar Hernandez, Toby Natividad,
    Tawana Smith, Justin McInnis

2
HPI
  • 17 y/o LAM with new onset seizure. Sz, observed
    by brother, lasted 12 min with post-ictal period
    of 6 min. Patient was evaluated at Clear Lake
    Medical, no laboratory or radiologic tests were
    performed, no meds prescribed, patient was D/C
    home.
  • At 6 am next morning, pt had 2nd seizure lasting
    10min with a 6 min post-ictal period. Following
    both seizures, patient was not aware of the
    incident, no encopresis, incontinence or biting
    of his tongue. No associated fevers, N/V,
    abdominal pain, diarrhea, no aura or HA prior to
    seizure.

3
History
  • PMH
  • HA approximately every 10 days since childhood,
    resolved with Advil/Tylenol, never formally
    evaluated.
  • Gastritis x 3 yrs.
  • Asthma at 10 yrs old-resolved.
  • Several episodes of inability to move his
    extremities when awakening from sleep
    (hypnopompic paralysis) during childhood.
  • FHx
  • Non-contributory, parents live in Guatemala.
  • Two brothers, five sisters, all healthy.
  • PSHx None
  • Developmental Hx Completed 6th grade.
  • Immunizations Unsure, last vaccination at age
    13 yrs.

4
History, Contd
  • Hospitalizations Fx left clavicle 6 yo, Fx right
    ankle 8 yo, no complications.
  • Social Hx Moved from Guatemala 2 yrs ago.
    Lives with brother (19), and two friends in an
    apt. No tobacco, alcohol, drug use. Denies any
    sexual activity ever. No sick contacts. No
    travel outside of country since moving here. No
    food from outside of country. Works as a bus boy
    at a Mexican restaurant.
  • Meds None. Takes herbal supplement Sukkol
    (Glutamic acid, Lecithin) qod x 1 month for
    memory and energy and Chamomile tea for
    gastritis.
  • Allergies NKA

5
OSH Labs
80N 14.8L 3.8M 0.8E
  • LFTs
  • SDS Digoxin 0.1, Acetaminophen lt 10,
    Salicylate lt 2.8, ETOH 0.003
  • UDS Neg
  • UA SG 1.020, Blood 1, pH 5, 0 LE, 0 Nit, WBC
    3-4, RBC 3-5, Bacteria 3
  • CT 7 cm low density intra-axial lesion in
    posterior right temporal lobe. 4 cm low
    density extra-axial lesion in left mid-cranial
    fossa.
  • EEG pending

6
Physical Exam
  • Ht 58 in (50th for 11.5 y/o) Wt 104 lbs (50th
    for 13.5 y/o)
  • T 37.6 po BP 104/59 P 86 R 24
  • Gen A O x 3, NAD, cooperative
  • HEENT PERRL, EOMI, MMM
  • Neck Supple, Brudzinski-Neg, no nuchal
    rigidity no LAD
  • CV RRR, Normal S1/S2, No M/R/G
  • Lung CTA bilaterally
  • Abd BS, NTND, soft, No HSM
  • GU Normal testicular exam (Tanner IV), Tanner IV
    ax hair
  • Skin No rashes, petechiae or lesions
  • Ext No C/C/E, LBP muscular origin
  • Neuro CN II-XII grossly intact. LE DTRs 2.
    Normal heel-shin test. Mild past pointing and
    decreased concentration with finger to nose test
    both UEs. No dysdiadochokinesia. Negative
    Rhomberg. Gait slight decrease in balance
    (secondary to Phos phenytoin infusion from OSH
    per subjective report).

7
Problem List?
Differential Diagnosis?
8
DDX for Pediatric Brain Mass
  • Neoplasm
  • Primary
  • Pilocytic Astrocytoma (24)
  • Medulloblastoma (16)
  • Ependymoma (10)
  • Hemangioblastoma
  • Craniopharyngioma
  • Glioblastoma multiforme
  • Tuberous Sclerosis
  • Pinealoma
  • Benign cyst
  • Choroid Plexus Papilloma
  • Secondary
  • Lymphoma (also 1)
  • Germ cell (testicular)
  • Blood/Vascular
  • Hemorrhage
  • AVM
  • Aneurysm
  • Pus
  • Infectious
  • Abscess
  • Toxoplasmosis
  • Neurocysticercosis
  • Tuberculosis
  • CMV
  • Amebic Meningoencephalitis
  • Lyme Disease
  • Toxocariasis
  • Trichinosis
  • Fungal Infx (Histoplasma/Blastomyces)
  • Inflammatory
  • Sarcoidosis
  • Other Granulomatous Dz
  • Vasculitis
  • Water (hydrocephalus)
  • Obstructive
  • Communicating

9
UTMB Labs
  • UA WNL
  • Urine Cx Negative.
  • EEG Very abnormal, 2 independent foci of
    underlying dysfunction (R frontal and R posterior
    regions) with potential epileptogenicity
  • Stool OP Endolimax nana, Entamoeba hartmanni,
    Dientamoeba fragilis, few Blastocystis homonis.

10
Image MRI
T1 Weighted Image
T2 Weighted Image
  • 1.1 cm rim enhancing cystic lesion in right
    temporal lobe with suspected scolex and
    surrounding edema highly suspicious for
    neurocysticercosis.

11
Image CT
Calcification?
  • Hypodense region - 1 cm in diameter in R
    temporal/parietal region which may have a tiny
    punctate calcification inferiorly, leading
    differential possibility is neurocysticercosis.

12
DiagnosisNeurocysticercosis
13
Diagnostic Criteria
  • Minor
  • Compatible lesion on image
  • Clinical manifestations
  • Positive CSF ELISA Ab/Ag
  • Other organ involvement demonstrated
  • Epidemiologic
  • Household contact
  • Immigrant from endemic area
  • Frequent travel to endemic area
  • Absolute
  • Confirmatory biopsy
  • Image of cyst w/ scolex
  • Funduscopic exam
  • Major
  • Highly suggestive lesion on image
  • Positive serum Ab
  • Cyst resolution after anti-parasitic med
  • Spontaneous resolution single cyst

14
Diagnostic Criteria
  • Definitive
  • 1 absolute OR
  • 1 major 2 minor 1 epidemiologic
  • Probable
  • 1 major 2 minor
  • 1 major 1 minor 1 epidemiologic
  • 3 minor 1 epidemiologic

Del Brutto, OH et al. Proposed diagnostic
criteria for neurocysticercosis. 2001 Neurology
57(2)177-183.
15
Neurocysticercosis Background
16
Epidemiology
  • Most common parasitic infection of the central
    nervous system
  • Affects 50 million people worldwide
  • Endemic to Mexico, Central and South America,
    sub-Saharan Africa and Asia
  • gt 1,000 cases per year in the United States,
    particularly in the Southwestern region where
    immigration is prevalent

17
Transmission
  • Humans develop NCC through ingestion of T. solium
    ova
  • Contaminated food (i.e. fruits and vegetables
    irrigated with water containing human feces)
  • T. solium carrier contaminating foods directly
    (carriers often contain eggs under fingernails)

18
Pathophysiology
  • Ingested ova develop into embryos in the small
    intestine and invade the bowel wall
  • The embryos then disseminate hematogenously to
    the tissues and develop into cysticerci over a 3
    wk 2 mo period.
  • The cysticerci that enter the central nervous
    system do not cause inflammation in surrounding
    tissues initially (asymptomatic) and can be
    parenchymal and extraparenchymal
  • The asymptomatic phase lasts an average of 3-5
    years but can last as long as gt 30yrs.
  • Neurologic symptoms occur when cysticeri
    die/degenerate and the human host mounts an
    associated inflammatory response

19
Pathogenesis
20
Morbidity and Mortality
  • NCC typically is benign most lesions resolve
    spontaneously within 2-3 months
  • Mortality depends on whether NCC is simple or
    complicated
  • Simple NCC occurs in children with only a single
    exposure to cysts most commonly seen in the U.S.
    and other non-endemic countries (few
    complications)
  • Complicated NCC occurs in children in endemic
    areas who are constantly re-exposed to ova (less
    favorable prognosis)

21
Clinical Manifestation
  • Seizures (particularly focal) (87)
  • Headache (32)
  • Nausea/Vomiting (32)
  • Altered Mental Status (13)
  • Cranial Nerve palsies, gait abnormalities,
    papilledema, decreased visual acuity (lt10)
  • Fever is uncommon
  • Physical exam is commonly normal

22
Labs
  • Enzyme-linked immuno-transfer blot assay (EITB)
  • Specificity is 100 and sensitivity 90 for
    children with gt2 lesions
  • Sensitivity only 50-70 in children with just 1
    lesion
  • Lumbar Puncture (contraindicated with increased
    ICP)
  • Reveals pleocytosis (often lymphocytic, but
    occasionally eosinophilic) in 50 of cases
  • Glucose- decreased
  • Protein- increased
  • Stool sample
  • 3 consecutive daily stool specimens
  • Presence of ova may be sole diagnostic
    confirmation
  • Stool test for T. Solium is rarely positive
  • Enzyme-linked immunosorbent assay (ELISA)
  • Serum or CSF sample
  • Can aid in diagnosis in cases with few lesions
    and mild disease
  • Sensitivity 75-80

23
Radiographic Correlation
24
Parasite Stages
  • Vesicular
  • No cellular response, prominent scolex
  • Colloidal
  • Cyst degenerating, mild inflammation
  • Nodular
  • Prominent inflammation, surrounding edema
  • Calcified
  • Resolving cellular response, calcified remnant

25
Vesicular Phase
  • MRI shows cysts having CSF-like density WITHOUT
    surrounding high-intensity signal
  • CT shows round hypodensities WITHOUT enhancement

Scolex
MRI with contrast
26
Colloidal Phase
  • Contrast-CT or MRI shows slight pericystic
    contrast uptake due to thickened capsule
  • Symptoms (Sz) may begin in this stage

MRI with contrast
27
Nodular Phase
  • Intense inflammation and surrounding edema cause
    typical ring-enhancement with contrast
  • Symptoms most prominent at this stage

MRI with contrast
28
Calcified Phase
  • Only calcified remnants
  • CT without contrast shows high intensity signal

CT w/o contrast
29
Treatment
30
Neurocysticercosis is not a single disease for
which one therapy can be recommended -Current
Consensus Guidelines for Treatment of
Neurocysticercosis. Clin Micro

Reviews. Oct 2002 pg 747-756
  • Factors Influencing Treatment
  • Number of parasites
  • single lesion
  • few lesions (lt5 cysts)
  • massive infection (gt100 cysts)
  • Location of Lesion (intra-parenchymal vs
    extra-parenchymal)
  • Parasite Viability
  • Growing, living, degenerating, calcified
  • Current Treatments Antihelminthics,
    Anticonvulsants, Anti-inflammatory and Surgery

31
Antihelminthic Therapy
  • Albendazole
  • - Inhibits microtubule synthesis in nematodes
  • - standard dosing is 15mg/kg/day given for 15
    days (several studies have shown similar
    efficacy for 3d and 8d courses)
  • Why?
  • - Standard course kills 75-90 of cysts
  • - More rapid cyst clearance from brain
  • Why not?
  • - Most Pt with NCC become symptomatic only when
    cyst begin to degenerate. This is secondary
    to development of edema and inflammation
    around dying cyst.
  • - Anti-helminthic drugs can worsen neurological
    problems due to rapid increase in number of
    degenerating cysts (risk of pericystic
    vasculitis/stroke).
  • Praziquantel
  • - Interacts with both steroids and
    anticonvulsants (P450)
  • - Poor CNS penetration
  • - New studies show 75-100mg/kg given in 3
    divided doses 2hrs apart have similar efficacy
    as standard Albendazole therapy

32
Anti-Inflammatory Therapy (Steroids)
  • Should be given concomitantly with Albendazole
  • Dexamethasone 12-16 mg/day or Prednisolone 30-40
    mg/day (up to 1 mg/kg/day) x 5 days then a 2 week
    taper.
  • Primary management for chronic cysticercosis and
    cysticercosis encephalitis

33
Anticonvulsant Therapy
  • Carbamazepine and Phenytoin 1st line.
  • Risk of seizure greatest during degenerative
    phase
  • Calcified cysts can serve as epileptic focus
    after active infection cleared.
  • Current practice Anticonvulsant therapy for 1yr.
    Medication can be stopped if Pt has been seizure
    free.

34
Guidelines for Intra-parenchymal Cysts
  • Growing cysts Always treat with antihelminthics
    (AH) and steroids especially when there is risk
    of ventricular involvement
  • Live cysts
  • Few - AH /- steroids or Neuroimaging f/u only
  • Moderate(gt5) - AH steroids
  • Heavy(gt100) - AH high dose steroids or chronic
    steroid management with neuroimaging follow-up
  • Degenerating Cysts
  • Few to Moderate - Neuroimaging f/u
  • Heavy (cysticercosis encephalitis) - high dose
    steroids and osmotic diuretics to decrease ICP.
  • Calcified Cysts No treatment regardless of
    number

35
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