A Case of CVA with Polyserositis

AN INTERESTING CASE OF CVA DR.AMUDHAN M3 UNIT

A 35Y/FEMALE WAS BROUGHT TO THE HOSPITAL WITH H/O DIMINISHED CONSCIOUSNESS- 1 DAY LOSS OF SPEECH

MORNING SHE WAS NOTICED TO HAVE DIMINISHED CONSIOUSNESS & LOSS OF SPEECH. NOT ASSOC.WITH LOC,HEADACHE OR VOMITING NOT ASSOC WITH BLURRING OF VISION NOT ASSOC.WITH CHEST PAIN ASSOC.WITH SPEECH DIFFICULTY

H/O PRESENT ILLNESS H/O WEAKNESS IN USING RT UL AND LL H/O DEV.OF ANGLE OF MOUTH TO LEFT SIDE NO H/O BLURRING OF VISION NO H/O VERTIGO/TINNITUS NO H/O LOSS OF SENSATION OVER THE FACE NO H/O NASAL REGURGITATION NO H/O DEV OF TONGUE NO H/O BLADDER AND BOWEL INCONTINENCE

PAST HIST K/C/O RHD/MS/POST CMC STATUS/AF/PHT 2 ½ YRS ON TREATMENT K/C/O CONSTRICTIVE PERICARDITIS PERICARDECTOMY DONE 3 YEARS BACK. DETAILS NOT AVAILABLE. ADMITED 2 MONTHS AGO WITH FEATURES OF FAILURE AND MASSIVE PLEURAL EFFUSION AND INVESTIGATED AND STARTED ON EMPIRICAL ATT. NO H/O T2DM/SHT/IHD NO H/O SIMILAR ILLNESS IN FAMILY

PERSONAL H/O MIXED DIET NO ANTI SOCIAL HABITS BOWEL & BLADDER HABITS NORMAL

General Examination O/E PT. DROWSY, DISORIENTED AFEBRILE ANEMIC, BPPE + NO CL/ CY/J NO NEUROCUTANEOUS MARKER NO PERIPHERAL NERVE THICKENING ORAL ULCERS PRESENT

VITAL SIGNS PULSE 78/MIN,IRREGULAR,NO VESSEL WALL THICKENING,NO RADIOFEMORAL DELAY RR-18/MIN BP-140/90mm Hg TEMP-NORMAL PUPIL-3MM ERRLA

CNS EXAMINATION Pt DROWSY APHASIC HMF- COULD NOT BE ASSESED CRANIAL NERVES RIGHT UMN VII N PALSY. OTHER CN-NORMAL

MOTOR FUNCTIONS RT LT BULK UL N N LL N N TONE UL EXT. HYPERTONIA N LL FLEX. HYPERTONIA N POWER UL 3 5 LL 4- 5 DTR BICEPS J 3+ 3+ TRICEPS J 3+ 3+ SUP. J 3+ 3+ KNEE 3+ 3+ ANKLE + + PLANTAR B/L EXTENSOR

SENSORY SYSTEM-COULD NOT BE TESTED CEREBELLUM-COULDN’T BE TESTED GAIT-HEMIPARETIC GAIT CVS - S1S2 +,S1 VARIABLE,MDM + APEX WITHOUT PRESYSTOLIC ACCENTUATION RS - NVBS+ BS DIMINISH IN LEFT INFRA AXILLARY & INFRASCAPULAR P/A DISTENDED. FF+ NO ORGANOMEGALY

PROVISIONAL DIAGNOSIS RHD/ MS/ POST CMC/ AF/ CVA / RIGHT HEMIPARESIS/LEFT PLEURAL EFFUSION /ASCITES FOR EVALUATION ? EMBOLIC STROKE R/O CTD

INVESTIGATIONS CBC – HB 8 SR. ELECTROLYTES TC 6700 Na-124 DC N48L50E2 K-3.7 ESR 6/15 CL-98 PCV 25 HCO3-23 MCV 98 URINE MCH 28 ALB-++ MCHC 30 SUG-NIL RBC 3LAC DEP-1-3PUS CELS PLATLETS 1.5 24 hrs urine protein-608 mg/day RFT- SUGAR 96 URINE PCR-1.8 UREA 26 P. SMEAR- normocytic , normochromic CREATININE 0.7

CT BRAIN HYPODENSE LESION IN B/L PARIETAL LEFT TEMPORAL LEFT CAUDATE LEFT CORONA RADIATA RIGHT OCCIPITAL FEATURES SUGGESTIVE OF ‘’ MULTI INFARCT STATE’’

CT CHEST LEFT PLEURAL EFFUSION WITH MULTIPLE LOCULATION WITH UNDRELYING LUNG COLLAPSE.

LFT TOTAL BILIRUBIN-1mg/dl IDB-0.6 DB-0.4 SERUM ALBUMIN-3.6mg/dl SERUM ALP-WNL SERUM ALT.AST-WNL

ECHOCARDIOGRAM RHD (Post CMC) MVA 1.7Cm 2 MS- Mod. MR- Mild TR- Mild PHT-Mild AR – Trivial No LA Clot Normal LV SYS. Function NO PERIC.EFFUSION

Ascitic fluid Analysis C/S-No Growth GM Stain-No Org. TC- 100 Cells/m3 Lymp.-40%N-30% Reactive mesothel.-30% Sugar-76 Protein-3 AFB-Negative

Pleural Fluid Analysis TC-30 CELL LYMP.-90% REACTIVE MESOTHEL.-10% CYTOLOGY SHEETS OF LYMPHOCYTES & REACTIVE MESOTHEL.CELLS IN PROTEINACEOUS BACKGROUND S/O REACTIVE EFFUSION.

OTHER INVESTIGATIONS RA - NEGATIVE CRP -12U VDRL -NEGATIVE ANA - POSITIVE 1 : 100+VE RIM PATTERN ANTI DS DNA - POSITIVE .

ORAL ULCER POLY SEROSITIS PROTEINURIA in a women of child bearing age with STROKE IMMUNOLOGICAL EVIDENCE

FINAL DIAGNOSIS RHD/ MS/ POST CMC STATUS/ AF/ CVD / RIGHT HEMIPARESIS/ SYSTEMIC LUPUS ERYTHREMATOSUS

DEFINITION SLE is an autoimmune disease in which organs and cells undergo damage mediated by tissue binding autoantibodies and immune complexes. 99% are women of child bearing years.

EPIDEMIOLOGY Prevalence influenced by age, gender, race, and genetics Prevalence: 1:2000 Peak incidence 14-45 years Black > White (1:250 vs. 1:1000) Female predominance 10:1 HLA DR3 association, Family History Severity is equal in male and female

Etiology Genetic (HLA DR3 association) Abnormal immune response Environmental UV Viruses Hormones (Estrogen)

PATHOGENESIS Gene-environment interaction Abnormal immune response Induces pathogenic autoantibodies and immune complexes. Activates complement causing inflammation Irreversible organ damage.

GENE ENVIRONMENT INTERACTION GENES … C1q,c2,c4 HLA-D2,3,8 MBL FcR 2A,3A,2B MCP-1 . ENVIRONMENT FACTORS UV LIGHT,gender ?infection ?EBV

ABNORMAL IMMUNE RESPONSE 1) Activation of innate immunity by DNA/RNA 2)Lowered threshold of adaptive immunity cells. 3) ineffective regulatory and inhibitory CD4+ and CD8+TCELLS. 4)reduced clearence of apoptotic cells.

INFLAMMATION Immune activation of cells Increased proinflammatory factors like TNFalpha,IFN,IL10 Sustained production of pathogenic autoantibodies and immune complexes. Activation of compliment and phagocytic cells leading to irreversible tissue damage.

Overactive B-cells Estrogen is a stimulator of B-cell activity Lupus is much more prevalent in females of ages 15-45 Height of Estrogen production IL-10, also a B-cell stimulator is in high concentration in lupus patient serum. High concentration linked to cell damage caused by inflammation

AUTOANTIBODIES IN SLE ANTIBODY CLINICAL IMPORTANCE 1)ANTINUCLEAR(ANA) 2)ANTI-DsDNA 3)ANTI_SM BEST SCREENING TEST(98%PREVALENCE) SLE SPECIFIC, CORRELATES WITH DISEASE ACTIVITY, NEPHRITIS,VASCULITIS SPECIFIC FOR SLE

ANTIBODIES CLINICAL IMPORTANCE 4)ANTI-RNP 5)ANTI-RO(SS-A) NOT SPECIFIC ASSOC.WITH SICCA SYNDR,SUBACUTE CUTANEOUS LUPUS,NEONATAL LUPUS WITH CONG.HEART BLOCK,DECREASED RISK OF NEPHRITIS

ANTIBODIES CLINICAL IMPORTANCE 6)ANTI-La(SS-B) 7)ANTI HISTONE 8)ANTIPHOSPHOLIPID ASSOC.WITH ANTI-RO,DECREASED RISK OF NEPHRITIS IN DRUG INDUCED LUPUS PREDISPOSE TO THROMBOCYTOPENIA, FETAL LOSS

ANTIBODIES CLINICAL IMPORTANCE 9)ANTI ERYTHROCYTE 10)ANTIPLATELET 11)ANTI NEURONAL 12)ANTIRIBOSOMAL P MEASURED AS DIRECT COOMBS TEST ASSOC.WITH THROMBOCYTOPENIA ACTIVE CNS LUPUS DEPRESSION OR PSYCHOSIS

DIAGNOSTIC CRITERIA MALAR RASH-ERYTHEMA OVER MALAR EMINENCE DISCOID RASH-ERYTHEMATOUS RAISED PATCH WITH FOLLICULAR PLUGGING PHOTOSENSITIVITY ORAL ULCERS ARTHRITIS-NONEROSIVE ARTHRITIS SEROSITIS-PLEURITIS , PERICARDITIS RENAL DISORDER-PROTEINURIA>0.5G/DAY OR CAST HEMATOLOGICAL DISORDER-HEMOLYTIC ANEMIA OR LEUCOPENIA OR THROMBOCYTOPENIA IMMUNOLOGICAL DISORDER-ANTIBODIES ANA NEUROLOGICAL- PSYCOSIS, SEIZURES

CLASSIFICATION CRITERIA Must have 4 of 11 for Classification Sensitivity 75% Specificity 95% Like RA, diagnosis is ultimately clinical Not all “Lupus” is SLE Discoid Lupus Overlap syndrome Drug induced lupus Subacute Cutaneous Lupus

CLINICAL FEATURES: Neurologic Behavior/Personality changes, depression Cognitive dysfunction Psychosis Seizures Stroke Chorea Pseudotumor cerebri Transverse myelitis Peripheral neuropathy Total of 19 manifestations described May be difficult to distinguish from steroid psychosis or primary psychiatric disease

CLINICAL FEATURES: Gastrointestinal & Hepatic Uncommon SLE manifestations mesenteric vasculitis, resembling medium vessel vasculitis (PAN) Diverticulitis may be masked by steroids Hepatic abnormalities more often IATROGENIC than to SLE itself

T reatment. Mild cases : NSAID, local treatment, hydroxy-chloroquin Cases of intermediate severity : corticosteroid (12-64 mg methylprednisolon), azathioprin, methotrexat

SLE – treatment Severe, life-threatening organ involvements : High dose IV corticosteroid + iv.cyclophosphamide .P lasmapheresis or iv. Immunoglobulin . Some cases of nephritis (especially membranous), myositis, thrombocytopenia: cyclosporine

WOMEN OF CHILDBEARING AGE MULTISYSTEM INVOLVEMENT NO RELATED CAUSE EVEN WITH SUBTLE MANIFESTATION EVALUATE C T D RULE OUT S L E

A Case of CVA with Polyserositis

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