KCMC Case Presentation: A 20 Year-Old Male With Altered Mental Status

KCMC Case Presentation:
A 20 year-old male with

Altered Mental Status
Jesse Waggoner
Resident, Internal Medicine
International Health Elective
History of Present Illness
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
Physical Exam
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 intact
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
Chemistry:
Cr
78 (0.9)
Full Blood Picture:

Hgb
4, WBC 0.6, Plts 25
Rapid HIV: negative x 2

Blood culture: no growth
LP not obtained given results of
funduscopic exam
Imaging
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
Chest X-ray:
No
infiltrate, nml cardiac silhouette, no

bony lesions
Differential Diagnosis
Brain Abscess: no site for direct
spread
Tuberculoma
Toxoplasmosis
Primary CNS lymphoma
Clinical Course
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
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
Brain abscess
Microbiology
Diagnosis
CNS Tuberculosis
Meningitis
Treatment
and Tuberculomas
Brain Abscess
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
Anaerobes
Anaerbic streptococci
Bacteroides fragilis
Prevotella
melaninogenica
Propionibacterium
Fusobacterium
Eubacterium
Veillonella
Actinomycetes
Aerobes
Viridans Strep
Strep milleri
Pneumococcus (rare)
Staph aureus
Klebsiella pneumoniae
Psudomonas
Eschericia coli
Proteus
Microbiology of Brain Abscesses

in Specific Hosts
Immunocompromised
Toxoplasma
Rhodococcus equi
Listeria
Nocardia
Mycobacteria
Aspergillus
Cryptococcus
Coccidioides
Candida
Zygomycosis
Travelers/Immigrants
Cysticercosis
Entamoeba
Schistosoma japonicum
Paragonimus
Brain Abscess (continued)
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
Three clinical manifestations:

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
Tuberculoma
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
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
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
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
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). Childs 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: 79-88

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KCMC Case Presentation:

A 20 year-old male with

History of Present Illness

20 y/o male with no known past medical

Vitals: 36.8 115/75 82 15 on 2L NC

Full Blood Picture:

4, WBC 0.6, Plts 25

Rapid HIV: negative x 2

CT brain (on admission):

cm ring enhancing lesion in the R

infiltrate, nml cardiac silhouette, no

Pt initially treated with chloramphenicol and

Final diagnosis remains unclear pt did

Can result from direct spread (sinusitis,

Microbiology of Brain Abscesses

Microbiology of Brain Abscesses

Brain Abscess (continued)

Pts often present with worsening unilateral

Three clinical manifestations:

Small tubercules (Rich foci) form during

Can present as single or multiple ringenhancing lesions

CSF classically shows lymphocytic pleocytosis, elevated

No RCTs have been performed to show the optimal

Leonard, J. Central nervous system tuberculosis. UpToDate, acessed 5/20/2009.

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