Transcript KCMC Case Presentation: A 20 year

KCMC Case Presentation:
A 20 year-old male with
Altered Mental Status
Jesse Waggoner
Resident, Internal Medicine
International Health Elective
History of Present Illness
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20 y/o male with no known past medical
history
Brought to ED by family for 1 month of
malaise and worsening headache
Recently, pt had become lethargic and slow
to respond to questions at home
Over the 3 days prior to admission, patient
had been vomiting and became
unresponsive
No previous history of such episodes
Further History
ROS: per family members report, no
fevers, chills or night sweats; no
diarrhea; no weight loss
 Social History: unknown sexual
history, no known EtOH abuse or
IVDU, worked as a farmer near Moshi
 Family History: no significant family
medical history known
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Physical Exam
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Vitals: 36.8 115/75 82 15 on 2L NC
Gen: pt lying in bed, responds to pain, GCS 8 (eyes
open, withdraws to pain)
Neuro:
 CN: pupils 5mm, sluggish, corneal reflexes and gag
in-tact
 Motor: bulk nml, tone decreased
 Reflexes: 2+ DTRs, toes downgoing
HEENT: Fundi show papilledema, op clear
Lungs: CTAB, no w/r/r, limited by pt cooperation
CV: RRR, nl s1 and s2, no m/r/g
Abd: soft, NTND, +bs, no HSM
Ext: no c/c/e, 2+ peripheral pulses
Skin: no rashes or lesions
Laboratory Data
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Chemistry:
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Cr 78 (0.9)
Full Blood Picture:
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Hgb 4, WBC 0.6, Plts 25
Rapid HIV: negative x 2
 Blood culture: no growth
 LP not obtained given results of
funduscopic exam
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Imaging
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CT brain (on admission):
3 cm ring enhancing lesion in the R
parietal and occipital lobes with
surrounding edema and mass effect
 No evidence of sinusitis or site for
direct extension of infection
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Chest X-ray:
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No infiltrate, nml cardiac silhouette, no
bony lesions
Differential Diagnosis
Brain Abscess: no site for direct
spread
 Tuberculoma
 Toxoplasmosis
 Primary CNS lymphoma
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Clinical Course
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Pt initially treated with chloramphenicol and
ampicillin without clinical deterioration
Following results of CT, antibiotic coverage
changed to ceftriaxone and metronidazole
Pt continued to worsen clinically and 4 drug
TB therapy (INH, RIF, PZA, EMB) was
added along with prednisolone 60 mg/day
Over the following week, pt became more
alert per family members’ report
Neurosurgery consulted and felt patient was
a poor candidate for surgery
Diagnosis
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Final diagnosis remains unclear – pt did
appear to respond to therapy for TB, though
this included high dose steroids
Etiology of pancytopenia is also unknown
and leukopenia would have predisposed
him to opportunistic pathogens not covered
in the treatment regimen
His clinical stability and advanced stage at
presentation combined with available
diagnostic tests limited our ability to make a
definitive diagnosis
Discussion
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Brain abscess
Microbiology
 Diagnosis
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CNS Tuberculosis
Meningitis and Tuberculomas
 Treatment
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Brain Abscess
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Can result from direct spread (sinusitis,
otitis, neurosurgical procedure) or from
hematogenous spread (more often multiple
abscesses)
Most common location for hematogenous
spread: frontal or temporal lobes, frontalparietal, or parietal
Typically results from a bacterial infection,
though in immunocompromised hosts,
causes include fungi and other opportunistic
pathogens
Microbiology of Brain Abscesses
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Anaerobes
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Anaerbic streptococci
Bacteroides fragilis
Prevotella
melaninogenica
Propionibacterium
Fusobacterium
Eubacterium
Veillonella
Actinomycetes
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Aerobes
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Viridans Strep
Strep milleri
Pneumococcus (rare)
Staph aureus
Klebsiella pneumoniae
Psudomonas
Eschericia coli
Proteus
Microbiology of Brain Abscesses
in Specific Hosts
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Immunocompromised
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Toxoplasma
Rhodococcus equi
Listeria
Nocardia
Mycobacteria
Aspergillus
Cryptococcus
Coccidioides
Candida
Zygomycosis
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Travelers/Immigrants
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Cysticercosis
Entamoeba
Schistosoma japonicum
Paragonimus
Brain Abscess (continued)
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Pts often present with worsening unilateral
headache
Changes in mental status develops with
worsening cerebral edema and portends a poor
prognosis
Exam: fever only present in 50% of cases; focal
neurological deficits develop after the headache
Imaging: MRI more sensitive than CT and can
differentiate abscess from neoplastic lesions
Diagnosis often comes after guided aspiration
or surgery
CNS Tuberculosis
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Three clinical manifestations:
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Meningitis
Tuberculoma
Spinal arachnoiditis
Small tubercules (Rich foci) form during
bacteremia following primary or reactivation
disease
These can form in the brain or meninges
Development of meningitis or tuberculoma
results from progression and possible
rupture of these lesions
Epidemiology of CNS Tb
Around 1% of Tb cases will develop
CNS Tb (6.3% of extrapulm cases)
 Signs of Tb outside the CNS are only
present in ~50% of cases
 In adults, risk factors for developing
CNS Tb include: alcoholism,
malignancy, immunosuppressive
agents, & HIV
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Tuberculoma
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Can present as single or multiple ringenhancing lesions
Usually present as a mass lesion but can
occur in the setting of Tb meningitis (after
one ruptures into the subarachnoid space)
More common in developing countries than
in the United States
Tb brain abscess is a rare complication – do
not see classic granulomas on pathology
Diagnosis
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CSF classically shows lymphocytic pleocytosis, elevated
protein, & hypoglycorrachia in Tb meningitis
Micro:
 CSF AFB smears: sensitivity 20-35% for one sample, up
to 85% with consecutive samples
 Culture: sensitivity 71%
No nucleic acid amplification tests currently approved in
US for detection of Tb in CSF
ADA in the CSF cannot reliably distinguish Tb meningitis
from bacterial meningitis; also no standard cutoffs
Contrasted MRI more sensitive for findings of CNS Tb
than CT
 Basal meningeal enhancement
 Hydrocephalus
 Supratentorial infarctions
Treatment
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No RCTs have been performed to show the optimal
drug regimen, dosage and duration of therapy
Current guidelines recommend initial 4 drug therapy
for 2 months followed by 7-10 months of continued 2
drug therapy
 INH: good CNS penetration
 RIF: penetrates inflamed meninges
 PZA: good CNS penetration
 EBM: lower CSF concentrations
Glucocorticoids: shown to benefit adults in one RCT,
particularly those with less severe disease (study used
dexamethasone)
References
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Kent SJ et al. Tuberculous meningitis: a 30-year review. Clin Infect Dis, 1993; 17: 987-994.
Kumar R et al. Tuberculous brain abscess: clinical presentation, pathophysiology, and
treatment (in children). Child’s Nerv Syst, 2002; 18:118-123.
Leonard, J. Central nervous system tuberculosis. UpToDate, acessed 5/20/2009.
Pai et al. Diagnostic accuracy of nucleic acid amplification tests for tuberculous
meningitis: a systematic review and meta-analysis. Lancet Infect Dis, 2003; 3: 633643.
Rock RB et al. Central nervous system tuberculosis: pathogenesis and clinical
aspects. Clin Micro Rev, 2008; 21: 243-261.
Seydoux C et al. Bacterial brain abscesses: factors influencing mortality and
sequelae. Clin Infect Dis, 1992; 15: 394-401.
Southwick FS. Pathogenesis, clinical manifestations, and diagnosis of brain abscess.
UpToDate, accessed 5/20/2009.
Tattevin P et al. Bacterial brain abscesses: a retrospective study of 94 patients
admitted to an intensive care unit (1980 to 1999). Am J Med, 2003; 115: 143-146.
Thwaites GE et al. Dexamethasone for the treatment of tuberculous meningitis in
adolescents and adults. NEJM, 2004; 351: 1741-1751.
Thwaites GE et al. Improving the bacteriological diagnosis of tuberculous meningitis.
J Clin Micro, 2004; 42: 378-9.
Thwaites GE et al. Effect of antituberculosis drug resistance on response to
treatment and outcome in adults with tuberculous meningitis. J Infect Dis, 2005; 192:
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