Transcript Rheumatology Conference - MEDICINE DEPARTMENT of MMC

MEDICAL GRANDROUNDS
Kathryn Hazel C. Trinidad M.D.
First Year Medical Resident
OBJECTIVES



To be able to present a known case of SLE who
developed seizure during the course of illness
To be able to know the diagnosis, treatment, and
prognosis of NPSLE
To be able to know the latest updates with regards
to NPSLE
THE CASE
H.M
 35 year old G3P2 (1112) female
 right-handed
 known case of SLE maintained on Prednisone
20mg 2x/day
 known case of APAS, maintained on ASA 80mg OD
 housewife

Seizure
CHIEF COMPLAINT
INTERVAL HISTORY

May 2002  experienced on-off fever
(Tmax 40C), malar rash, joint pains,
vomiting, photosensitivity, and oral
ulcers. diagnosed with SLE; started on
Prednisone 5mg OD; regular OPD
follow-up

Nov 2007  (+) miscarriage;
OPD follow-up for clearance prior
to dilatation and curettage
INTERVAL HISTORY
• Feb 2008  diagnosed with APAS based
on history and lab results:
Test
Results
N.V.
Kaolin Clotting Time
79 sec
50 – 90 sec
APTT
32 sec
25 – 40 sec
DRVVT
37 sec
31 – 44 sec
ACA IgG
18.8 GPL units/mL
up to 15.0 GPL
units/mL
ACA IgM
11.72 MPL units/mL
up to 12.5MPL
units/mL
She was started on ASA 80mg OD
INTERVAL HISTORY
9 months PTA(July 2008)  1st prenatal checkup at 7wks AOG. No rashes, joint pains, and
oral ulcers; Started on Heparin 5,000 IU SQ
OD Prednisone 5mg OD and ASA 80mg OD
continued.
Monthly prenatal check-up with both
Rheumatology and OB-GYN services
INTERVAL HISTORY

2 months PTA(March 2009)  gave birth to
a live preterm male via LTCS; Discharged
with ASA 80mg OD and Heparin 5,000
IU/mL; Prednisone was not resumed
HISTORY OF PRESENT ILLNESS


11days PTA, OPD ff up
with
(+)occasional upper
back pain, grade I
bipedal edema, raised
macules on both face
and upper extremities.

Prednisone 5mg OD
was resumed. CBC,
urinalysis and ESR
were requested.
HISTORY OF PRESENT ILLNESS

4 days PTA  (+) diffuse headache & joint
pains; (+) fever; inc. rashes in face &
extremities; consult done  Prednisone inc.
to 20mg BID; Advised ff up of lab requests

3 days PTA  pancytopenia: (Hgb-9.5 hct30.1 wbc-2,640 plt-120,000) and
proteinuria(+4) hematuria(1171/hpf),
pyuria(335/hpf) bacteriuria(404); ESR was
elevated at 111. Ciprofloxacin 500mg BID
HISTORY OF PRESENT ILLNESS

7 hrs PTA  severe headache
(10/10)slightly relieved by Paracetamol. (-)
vomiting nor blurring of vision

30 mins PTA tonic-clonic seizure ~ 30
minutes
MMC ER  Admission
PAST MEDICAL HISTORY





Non-hypertensive
Non-diabetic
s/p CS (2001)
s/p dilation and curettage November 2007
No history of travel outside of Metro Manila.
Family History:
 No hypertension
 No diabetes
 No connective tissue disease.
Personal and Social History:
 Non-smoker
 Non-alcoholic beverage drinker
 Worked as a bank teller prior to being
diagnosed with SLE
 Currently stays at home and takes care of
her children; can do light household
chores
PHYSICAL EXAM



Gen. Survey: Drowsy, not in cardio-respiratory
distress
Vital signs: BP = 200/100  170/100
HR 81
RR 20
Temp 36.7C
Skin: raised macules on the face and both upper
extremities
• HEENT: Anicteric sclerae, pink palpebral
conjunctivae, (+) subconjunctival
effusion, no tonsillopharyngeal discharge,
no cervical lymphadenopathy
• Chest: Symmetrical chest expansion, no
retractions, clear breath sounds
PHYSICAL EXAMINATION



Heart: Adynamic precordium, distinct S1 and S2,
normal rate and rhythm, no murmurs
Abdomen: Flabby abdomen, soft, non-tender,
normoactive bowel sounds
Extremities: Full and equal pulses, no cyanosis and no
edema
NEUROLOGICAL EXAM


MSE: Drowsy, opens eyes to verbal
stimulation but non-sustained, does not
follow commands
Cranial Nerves: Pupils 3mm EBRTL; Full
EOMS; (+) visual threat on all planes; (-) facial
asymmetry; (+) gag





Sensory: Withdraws to pain in all extremities
MMT: Moves all extremities non-purposely
Reflexes: +2 in all reflexes
Pathologic Reflexes: No Babinski
Meninges: Supple neck
SALIENT FEATURES






35 year old G3P2 (1112) female
known case of SLE on Oral steroids
Steroids on hold for 1 month; resumed
~ 1 week prior to onset of symptoms
known case of APAS, maintained on
ASA 80mg OD
Came in for tonic-clonic seizure
History of fever, headache, rashes,
and joint pains few days prior to
seizure
SALIENT FEATURES


Proteinuria, pyuria on urinalysis
sample done few days PTA
On PE:







Drowsy, does not follow commands,
opens eyes to verbal stimulation (GCS ~ 9
– 10)
Elevated BP upon admission
Raised macules on the face and both upper
extremities
Withdraws to pain on stimulation
Moves extremities non-purposely
Intact reflexes
Supple neck
ADMITTING IMPRESSION






Neuropsychiatric SLE
R/O CNS infection
Lupus nephritis
Hypertension, secondary
UTI
APAS
COURSE IN THE WARD
UPON ADMISSION
CBC, Urinalysis, C3, 24hour urine, ESR,
antiSmith, antidsDNA
 Complete Blood Count revealed improvement in
pancytopenia
 Hydrocortisone 100mg IV q8
 Referral to neurology service
 NGT feeding started

UPON ADMISSION….
3 episodes of
seizures at ER
– Midazolam
5mg IV
 Loading dose
Phenytoin
300mg IV x 2
doses 1 hour
apart

Phenytoin
100mg IV q8
Citicholine 1g IV
q12
Mannitol 20%
75ml IV q6
UPON ADMISSION
Urinalysis

Co- amoxiclav 1.2 g IV every
8 hours
UPON ADMISSION
Lumbar tap
done
 CT Scan
revealed
normal
 EEG

Methylprednisolone 1
g IV in D5W 500mL x
4hours for 3 days
UPON ADMISSION…

BP 180-200/100



Cardiology referral
Nicardipine drip started
ECG, CXR, 2Decho were
normal
2ND HOSPITAL DAY




(-)seizures
(-)headache
still drowsy but
opens eyes to
verbal stimuli,
moves all
extremities
spontaneously
BP was 140150/100mmHg

Phenytoin was shifted to
Leviteracetam(Keppra)
500mg ½ tablet BID

Nicardipine overlapped
w/ Amlodipine 5mg OD
3RD HOSPITAL DAY


(-) seizures/headache
Awake, conversant



Mannitol was tapered
down to 50mL Q8 then
later D/C
Last dose
Methylprednisolone
pulse therapy
Hydrocortisone 100mg
IV q8
3RD HOSPITAL DAY



24 hr urine collection
proteinuria with a
creatinine clearance of
83.5mL/min.
Serum complement C3,
anti-SM and anti-dsDNA
were requested which
showed low C3 levels
and positive anti-SM
and anti-dsDNA
Urine culture – no
growth



Nephrology referral
Imidapril 5mg OD
UTZ guided kidney
biopsy contemplated
4TH HOSPITAL DAY



(-) seizures/headache
Awake, conscious,
coherent
Tolerated soft diet, NGT
removed


Placed on full diet
Hydrocortisone shifted
to Prednisone 25mg BID
5TH HOSPITAL DAY

No recurrence of
seizures, headache, no
fever

Co- Amoxiclav IV was
shifted to oral CoAmoxiclav 625mg BID

ASA discontinued
anticipating kidney
biopsy
Leviteracetam continued

6TH HOSPITAL DAY



No recurrence of
seizures, headache,
no fever
Decrease in raised
macules on face
and UE
CBC showed
decrease in platelet
to 80,000


Prednisone increased
to 30mg BID
Kidney biopsy to be
done as outpatient
7TH HOSPITAL DAY

No recurrence of
seizures, headache, no
fever, significant
decrease in malar rash
and macules on upper
extremities

Patient cleared
for discharge from
all services
8TH HOSPITAL DAY

Patient discharged improved and stable
FINAL DIAGNOSIS





NPSLE
Lupus Nephritis
Hypertension, secondary
Urinary Tract Infection, resolved
APAS
DISCUSSION
BACKGROUND

Systemic lupus erythematosus (SLE)





multisystem autoimmune connective tissue
disorder with various clinical presentations
Affects many organ systems, including the
central and peripheral nervous systems and
muscles.
90% of patients are women of childbearing age
Incidence is 12-39 cases per 100,000 people
With full access to medical care, overall survival
for SLE is 85% at 5 years and 63% at 15 years
Harrison’s Principles of Internal Medicine 17th Ed.
PATHOPHYSIOLOGY

SLE is caused by interactions between
susceptible genes and environmental factor
resulting in abnormal immune response
1. Hyper-reactivity and hypersensitivity of T
and B lymphocytes
2. Ineffective regulation of antigen availability
and ongoing antibody response
Harrison’s Principles of Internal Medicine 17th Ed.
PATHOPHYSIOLOGY

End result: sustained production of pathogenic autoantibodies and formation of immune complexes that
bind target tissues, resulting in:
1. Sequestration and destruction of Ig-coated
circulating cells
2. Fixation and cleaving of complement proteins
3. Release of chemotaxins, vasoactive peptides, and
destructive enzymes into tissues
ARA CRITERIA FOR DIAGNOSIS:
Malar rash
Discoid rash
Photosensitivity
Oral ulcers
Fixed erythema, flat or raised, over malar eminence
Erythematous circular raised patches with adherent
keratotic scaling and follicular plugging; atropic scarring
may occur
Exposure to UV light causes rashes
Oral or nasopharyngeal
Arthritis
Nonerosive, involving 2 or more joints
Serositis
Pleuritis: + pleuritic pain or rub, OR pleural effusion, OR
pericardial effusion
Renal disorder
Neurologic disorder
Persistent proteinuria OR cellular casts
Seizures or psychosis
Hematologic disorder
Hemolytic anemia with reticulocytosis OR Leukopenia <
4000 OR lymphopenia < 1,500 OR thrombocytopenia <
100,000
ANA
Positive; if negative, check for anti-SSA (Ro) antibodies
Anti-dsDNA or antismith antibody
Positive; highly specific for SLE
Harrison’s Principles of Internal Medicine 17th Ed.
NEUROPSYCHIATRIC SLE
HISTORICAL BACKGROUND

Hebra and Kaposi (1875)  Noted first
neurologic involvement in SLE
Over the last 3 decades, appreciation of
• Baum
(1904)
 Related
active delirium,
Clinical
significance
of antineuronal,
aphasia
and hemiparesis
to probable
antiribosomal
P, and antiphospholipid
disseminated
LE
antibodies as well as advances in brain
• Dalyhave
(1945)
 altered
conducted
1st modern
Imaging
again
our concept
of
study of NP-SLE
NP-SLE
• Lewis (1954)  1st to focus on
importance of EEG findings and
psychometric testing in patients with
NP-SLE
Joseph FG, Lammie AG, Scolding NG. CNS lupus: A study of 41 patients. Neurology. 2007
CLASSIFICATION AND CLINICAL
PRESENTATION

Incidence of neuropsychiatric manifestations in
SLE ranges from 14 – 75%
• Patients with NP-SLE can present with a
myriad of diffuse and/or focal symptoms and
signs involving the brain, spinal cord, or
peripheral nervous system
PATHOLOGIC CLASSIFICATION OF
CNS CHANGES OBSERVED IN SLE

Vasculopathy





Hyalinization
Peripheral

inflammation w/o
infection
 Microinfarcts

Endothelial
proliferation w/o
 Large infarcts 
infection
Thrombosis

Vasculitis
Infarction
Hemorrhage
 Infection
Subarachnoid
 Meningitis
Microhemorrhages
 Subdural  Perivascular
 Intracerebral inflammation with
infection
 Septic
hemorrhages
 Focal cerebritis
 Vasculitis with
infection
Joseph FG, Lammie AG, Scolding NG. CNS lupus: A study of 41 patients. Neurology. 2007
PATHOPHYSIOLOGY OF NERVOUS SYSTEM
INVOLVEMENT
1.
2.
3.
Vasculopathy
Auto-antibodies
Others
Schur PH, Khoshbin S. Neurologic manifestations of systemic lupus erythematosus. www.Uptodate.com
1. VASCULOPATHY





characterized by small to
moderate perivascular
accumulation of mononuclear
cells, without destruction of the
blood vessel.
May have small infarcts
Pathogenesis not known
Antiphospholipid antibodies may
play a role
Accelerated atherosclerosis may
contribute to the risk of stroke in
patients with SLE
Schur PH, Khoshbin S. Neurologic manifestations of systemic lupus erythematosus. www.Uptodate.com
Joseph FG, Lammie AG, Scolding NG. CNS lupus: A study of 41 patients. Neurology. 2007
2. AUTO-ANTIBODIES



(+) Antineuronal antibodies found in one report in 45
percent of patients with CNS lupus
Cognitive dysfunction associated with lymphocytotoxic
antibodies
Antiphospholipid antibodies  increase the risk of
stroke syndromes, recurrent seizures and abnormal
findings on MRI
Schur PH, Khoshbin S. Neurologic manifestations of systemic lupus erythematosus. www.Uptodate.com

Antiribosomal P protein antibodies  associated with
lupus psychosis and depression but not with cognitive
dysfunction or psychologic distress

High levels of autoantibodies to a 50 kDa antigen
located in the plasma membrane of brain synaptic
terminals in 19 of 20 patients with SLE who had CNS
involvement
•Antiribosomal-P autoantibodies from psychiatric lupus target a novel neuronal surface protein causing calcium influx and apoptosis
Soledad Matus,1,2,4 Patricia V. Burgos,1,2,4 Marcela Bravo-Zehnder,1,2,4 Regine Kraft,6 Omar H. Porras,5
3. OTHERS
Cytokines
 Neuropeptides
 Oxidative stress
 Nitric oxide
 Interference with neurotransmission
 Genetic heterogeneity

Schur PH, Khoshbin S. Neurologic manifestations of systemic lupus erythematosus. www.Uptodate.com
PATHOGENIC MECHANISMS CAUSING
NEUROPSYCHIATRIC SYMPTOMS IN SLE

Primary
•
•
•
•
•
Vascular
occlusion/hemorrhage
Auto-antibodymediated
Choroid Plexus
dysfunction
Cytokine effects
Other mechanisms
• Secondary
•
•
•
•
•
•
•
•
•
•
•
•
Infection
Medications
TTP
Hypertension
Uremia
Electrolyte imbalances
Fever
Thyroid disease
Atherosclerotic strokes
Subdural hematoma
Cerebral lymphoma
Reactive depression
Schur PH, Khoshbin S. Neurologic manifestations of systemic lupus erythematosus. www.Uptodate.com
DIAGNOSTIC APPROACH TO MANIFESTATIONS OF NEUROPSYCHIATRIC LUPUS
Confirm diagnosis of lupus according to ARA criteria
Careful history and PE
Diagnostics
• Monitoring:
•If patient improves: monitor history and PE
•If patient gets worse: PET scan/MRI, LP
Schur PH, Khoshbin S. Diagnostic approach to the neuropsychiatric manifestations of systemic lupus erythematosus . www.Uptodate.com
DIAGNOSTICS:
1.
Blood tests:
a.
Complete blood cell count including
platelet count and smear

b.
c.
d.
e.
f.
g.
h.
i.
j.
may demonstrate a hemolytic anemia with reticulocytosis or
reductions of neutrophils, lymphocytes, or platelets
Creatinine or creatinine clearance
Urinalysis
Liver function tests
Electrolytes
C3, C4, or CH50
Anti-dsDNA antibodies
Erythrocyte sedimentation rate or Creactive protein
Antiphospholipid antibodies
Lipid profile, glucose
Ramachandran T, Grisola JS. Systemic Lupus Erythematosus. www.e-medicine.com
DIAGNOSTICS:
2.
CSF Studies:
a.
b.
c.
d.
e.
f.
g.
h.
Cell count
Protein
Glucose
Cultures
Gram stain and other special stains
VDRL
IgG index
Oligoclonal bands
Ramachandran T, Grisola JS. Systemic Lupus Erythematosus. www.e-medicine.com
DIAGNOSTICS:
3.
Imaging:
a.
b.
CT Scan
indicated for suspected acute hemorrhage and in
patients with contraindications to MRI
(intracranial metal, pacemakers, etc.)
MRI
 more sensitive and used to define site and
extent of lesions.
 A negative MRI result does not rule out CNS
lupus, and MRI abnormalities may not be
diagnostic of NPSLE.
 Follow-up MRIs may be indicated to document
progression, improvement, or significance of
lesions
Ramachandran T, Grisola JS. Systemic Lupus Erythematosus. www.e-medicine.com
DIAGNOSTICS
Positron emission tomography (PET) and single
photon emission computed tomography (SPECT)
have also been explored as functional imaging tools
in lupus and both appear to be more sensitive in
detecting subtle brain changes in NPSLE
DIAGNOSTICS:
4.
EEG


Standard EEG indicated in seizures and
encephalopathies.
Evoked potentials are performed for suspected
demyelinating disease.
5.
Psychologic Testing
6.
Others: 2D echo
Ramachandran T, Grisola JS. Systemic Lupus Erythematosus. www.e-medicine.com
DIAGNOSTIC APPROACH FOR SPECIFIC SIGNS AND SYMPTOMS




Stroke - CT scan, blood tests for coagulopathy
(including lupus anticoagulant), MRI,
echocardiogram, carotids ultrasonography
Seizures – EEG
Neuropathy – EMG
Psychosis - MRI, EEG, lumbar puncture
• Cognitive abnormalities - Psychometric
testing, MRI, EEG, blood tests for
coagulopathy, antibrain antibody
• Anxiety or depression - Psychometric testing
Meningitis/fever - lumbar puncture
Schur PH, Khoshbin S. Diagnostic approach to the neuropsychiatric manifestations of systemic lupus erythematosus . www.Uptodate.com
TREATMENT:


High-dose IV corticosteroid regimens
consist of methylprednisolone 1-2 g
daily for 3-6 doses, followed by oral
prednisone 60 mg daily, then
tapering according to clinical recovery
Various steroid-sparing strategies
have evolved for long-term use,
including cyclophosphamide 0.5-2
mg/kg/d, azathioprine 1-2 mg/kg/d,,
permitting gradual reduction or
elimination of chronic steroid therapy.
Ramachandran T, Grisola JS. Systemic Lupus Erythematosus. www.e-medicine.com
TREATMENT:

Intravenous cyclophosphamide (at an
initial dose of 500 mg per square meter
of body surface area) is given in the ff:
1.
2.
3.
Acute or recent onset of neurologic
symptoms such as seizures or organic brain
syndromes in the absence of another
cause.
Evidence of active inflammation in the brain
such as increased cells and protein in the
cerebrospinal fluid, brain swelling on MRI or
CT scan.
Failure to respond to a one to two week
course of high dose oral corticosteroids (eg,
prednisone in a dose of 1 to 2 mg/kg per
day) or to pulse methylprednisolone (1000
mg/day for three days).
Ramachandran T, Grisola JS. Systemic Lupus Erythematosus. www.e-medicine.com
CLINICAL UPDATES
IV CYCLOPHOSPHAMIDE VS
METHYLPREDNISOLONE

Patients and methods:



RCT at two tertiary care centres of patients with
SLE with severe NP manifestations such as
seizures, optic neuritis, peripheral or cranial
neuropathy, coma, brainstem disease, or
transverse myelitis.
Induction treatment with 3 g of IV
methylprednisolone (MP) followed by either IV
monthly cyclophosphamide (Cy) versus IV MP
bimonthly every 4 months for 1 year and then IV
Cy or IV MP every 3 months for another year.
The primary end point was response to
treatment: at least 20% improvement from basal
conditions on clinical, laboratory, or specific
neurological testing variables.
RESULTS
 Of the 32 patients studied, 18/19 receiving
Cy and 7/13 receiving MP responded to
treatment (p,0.03)
CONCLUSIONS
 Cy was significantly more effective than
MP.
 Cy was clearly better in patients with
seizures, peripheral neuropathy, optic
neuritis, and brainstem disease, while
differences were not clear in coma and
transverse myelitis
CLINICAL UPDATES
EFFICACY OF RITUXIMAB (ANTI-CD20) FOR
REFRACTORY SLE INVOLVING CNS


Study describes the results of treatment of patients
with NPSLE who had previously failed to respond to
various immunosuppressants.
Rituximab  anti-CD20 antibody
 a chimeric antibody that directly targets B cells
 a biological preparation that eliminates B cells
through a variety of mechanisms such as
antibody-dependent cellular cytotoxicity,
complement-dependent cytotoxicity and apoptosis.
 has recently been used for the treatment of a
variety of SLE disease conditions and good
therapeutic response has been reported
EFFICACY OF RITUXIMAB (ANTI-CD20) FOR
REFRACTORY SLE INVOLVING CNS

Inclusion Criteria:
1.
2.

Presence of a highly active disease
CNS lesions resistant to conventional
treatment. such as intravenous
cyclophosphamide pulse treatment (IV-CY),
cyclosporine A (CsA), PE and
immunoadsorption therapy
Treatment Protocol:
•
•
•
•
Patients 1–5 and 10  treated with 375
mg/m2 rituximab once a week for 2 weeks
Patient 9  treated with single dose of 375
mg/m2 rituximab
Patients 6 and 7  treated with 500 mg
rituximab once a week for 4 weeks
Patient 8  treated with 1000 mg once
biweekly for 4 weeks.
RESULTS




Treatment with rituximab resulted in rapid
improvement of central nervous system-related
manifestations, particularly acute confusional
state.
Rituximab also improved cognitive dysfunction,
psychosis and seizure, and reduced the SLE
Disease Activity Index Score at day 28 in all 10
patients.
These effects lasted for >1 year in five patients.
Flow cytometric analysis showed that rituximab
down regulated CD40 and CD80 on B cells and
CD40L, CD69 and inducible costimulator on
CD4+ T cells.
CONCLUSION
Rituximab rapidly improved refractory
NPSLE, as evident by resolution of
various clinical signs and symptoms
and improvement of radiographic
findings.
 The down regulation of functional
molecules on B and T cells suggests
that rituximab modulates the
interaction of activated B and T cells
through costimulatory molecules.
 These results warrant further analysis
of rituximab as treatment for NPSLE

THANK YOU
COMPLETE BLOOD COUNT
4/24/09
4/28/09
5/4/09
Hgb
9.5
11.2
10.1
Hct
30.1
35.9
31.7
WBC
2,640
5,160
7,730
Seg
72
65
75
Lym
19
24
13
Mono
9
11
8
Platelet
Count
120,000
140,000
80,000
COMPLETE BLOOD COUNT
4/24/09
4/28/09
5/4/09
Hgb
9.5
11.2
10.1
Hct
30.1
35.9
31.7
WBC
2,640
5,160
7,730
Seg
72
65
75
Lym
19
24
13
Mono
9
11
8
Platelet
Count
120,000
140,000
80,000
BLOOD CHEMISTRIES
ESR
4/24/09
4/28/09
111
77
4/29/09
4/30/09
5/4/09
Na
143
140
K
3.4
4.2
BUN
Crea
0.9
RBS
120
CRP
Neg
19.99
25.01
1.2
0.9
C3
30.3
Anti-SM
+
dsDNA
+
Albumin
2.3
URINALYSIS
4/24/09
4/28/09
Color
Yellow
Yellow
Transparency
Hazy
Hazy
pH
6.0
6.5
Spec. Grav
1.02
1.02
Sugar
Negative
Negative
CHON
+4
+3
Ketones
Negative
Negative
Nitrites
Negative
Negative
Leucocyte
Esterase
Negative
Negative
RBC
1,171.50/uL
2,123.00/uL
WBC
335.50/uL
236.50/uL
Epithelial Cells
16.50/uL
11.0/uL
Bacteria
404.06/uL
245.16/uL
CSF Analysis
CSF GS/CS
AFB
No microorganism seen; Pus
cells 0 – 1/OIF
No acid fast bacilli seen
VDRL
Non-reactive
CALAS
Negative for Streptococcus
Group
B,
Streptococcus
pneumoniae,
Haemophilus
influenzae type B, Neisseria
meningitides ABCY W135 and
E. coli K1 antigens
Negative
India Ink
Negative
KOH
No fungal elements seen
Color
Non-xanthochromic
Transparency
Clear
RBC
13/uL
WBC
Lymphocytes
Protein
1/uL
1%
Total CHON: 88.8 mg% (NV
15 – 45)
Glucose 59 mg% (NV 40 – 75)
Phadebact
Sugar
Urine CS
No growth in 48 hours
Urine chemistry
Urine Protein
Urine Creatinine
Total Volume
535.2 mg% = 8563.2 /24 hours (Ref
Value: 0 – 149.1mg/24hrs)
90.2 mg% = 1443.2mg /24 hours (Ref
Value: 600 – 2500 mgs/24hrs)
1600mL / 24hrs
IMAGING STUDIES
CXR
Cranial CT Scan
normal
Normal non-contrast CT
2D Echo
Normal LV dimension with normal wall
thickness, motion and contractility.
Color flow and Doppler study showed
trace MR and PR with mild TR. There
was also a note of decreased
relaxation based on prolonged IVRT.
EEG
Abnormal EEG due to epileptiform
discharges
on
the
right
frontocentrotemporal region suggestive
of a tenderncy towards localization
related seizure, on top of mild diffuse
slowing of background activity at 7 – 8
Hz