Your SlideShare is downloading. ×
0
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

A Case of CVA with Polyserositis

1,148

Published on

Published in: Health & Medicine, Technology
0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total Views
1,148
On Slideshare
0
From Embeds
0
Number of Embeds
3
Actions
Shares
0
Downloads
11
Comments
0
Likes
0
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide
  • fhh
  • Transcript

    • 1. <ul><li>AN INTERESTING CASE OF CVA </li></ul><ul><li>DR.AMUDHAN </li></ul><ul><li>M3 UNIT </li></ul>
    • 2. <ul><li>A 35Y/FEMALE WAS BROUGHT TO THE HOSPITAL WITH </li></ul><ul><li>H/O DIMINISHED CONSCIOUSNESS- </li></ul><ul><li>1 DAY </li></ul><ul><li>LOSS OF SPEECH </li></ul>
    • 3.  
    • 4. <ul><li>MORNING SHE WAS NOTICED TO HAVE DIMINISHED CONSIOUSNESS & LOSS OF SPEECH. </li></ul><ul><li>NOT ASSOC.WITH LOC,HEADACHE OR VOMITING </li></ul><ul><li>NOT ASSOC WITH BLURRING OF VISION </li></ul><ul><li>NOT ASSOC.WITH CHEST PAIN </li></ul><ul><li>ASSOC.WITH SPEECH DIFFICULTY </li></ul>
    • 5. H/O PRESENT ILLNESS <ul><li>H/O WEAKNESS IN USING RT UL AND LL </li></ul><ul><li>H/O DEV.OF ANGLE OF MOUTH TO LEFT SIDE </li></ul><ul><li>NO H/O BLURRING OF VISION </li></ul><ul><li>NO H/O VERTIGO/TINNITUS </li></ul><ul><li>NO H/O LOSS OF SENSATION OVER THE FACE </li></ul><ul><li>NO H/O NASAL REGURGITATION </li></ul><ul><li>NO H/O DEV OF TONGUE </li></ul><ul><li>NO H/O BLADDER AND BOWEL INCONTINENCE </li></ul>
    • 6. PAST HIST <ul><li>K/C/O RHD/MS/POST CMC STATUS/AF/PHT 2 ½ YRS ON TREATMENT </li></ul><ul><li>K/C/O CONSTRICTIVE PERICARDITIS PERICARDECTOMY DONE 3 YEARS BACK. DETAILS NOT AVAILABLE. </li></ul><ul><li>ADMITED 2 MONTHS AGO WITH FEATURES OF FAILURE AND MASSIVE PLEURAL EFFUSION AND INVESTIGATED AND STARTED ON EMPIRICAL ATT. </li></ul><ul><li>NO H/O T2DM/SHT/IHD </li></ul><ul><li>NO H/O SIMILAR ILLNESS IN FAMILY </li></ul>
    • 7. PERSONAL H/O <ul><li>MIXED DIET </li></ul><ul><li>NO ANTI SOCIAL HABITS </li></ul><ul><li>BOWEL & BLADDER HABITS NORMAL </li></ul>
    • 8. General Examination <ul><li>O/E </li></ul><ul><li>PT. DROWSY, DISORIENTED </li></ul><ul><li>AFEBRILE </li></ul><ul><li>ANEMIC, BPPE + </li></ul><ul><li>NO CL/ CY/J </li></ul><ul><li>NO NEUROCUTANEOUS MARKER </li></ul><ul><li>NO PERIPHERAL NERVE THICKENING </li></ul><ul><li>ORAL ULCERS PRESENT </li></ul>
    • 9. VITAL SIGNS <ul><li>PULSE 78/MIN,IRREGULAR,NO VESSEL WALL THICKENING,NO RADIOFEMORAL DELAY </li></ul><ul><li>RR-18/MIN </li></ul><ul><li>BP-140/90mm Hg </li></ul><ul><li>TEMP-NORMAL </li></ul><ul><li>PUPIL-3MM ERRLA </li></ul>
    • 10.  
    • 11. CNS EXAMINATION Pt DROWSY APHASIC HMF- COULD NOT BE ASSESED CRANIAL NERVES RIGHT UMN VII N PALSY. OTHER CN-NORMAL
    • 12. <ul><li>MOTOR FUNCTIONS </li></ul><ul><li> RT LT </li></ul><ul><li>BULK UL N N </li></ul><ul><li> LL N N </li></ul><ul><li>TONE UL EXT. </li></ul><ul><li>HYPERTONIA N </li></ul><ul><li> LL FLEX. </li></ul><ul><li>HYPERTONIA N </li></ul><ul><li>POWER UL 3 5 </li></ul><ul><li>LL 4- 5 </li></ul><ul><li>DTR BICEPS J 3+ 3+ </li></ul><ul><li>TRICEPS J 3+ 3+ </li></ul><ul><li>SUP. J 3+ 3+ </li></ul><ul><li>KNEE 3+ 3+ </li></ul><ul><li>ANKLE + + </li></ul><ul><li>PLANTAR B/L EXTENSOR </li></ul>
    • 13. <ul><li>SENSORY SYSTEM-COULD NOT BE TESTED </li></ul><ul><li>CEREBELLUM-COULDN’T BE TESTED </li></ul><ul><li>GAIT-HEMIPARETIC GAIT </li></ul><ul><li>CVS - S1S2 +,S1 VARIABLE,MDM + APEX </li></ul><ul><li>WITHOUT PRESYSTOLIC ACCENTUATION </li></ul><ul><li>RS - NVBS+ BS DIMINISH IN LEFT INFRA </li></ul><ul><li>AXILLARY & INFRASCAPULAR </li></ul><ul><li>P/A DISTENDED. FF+ </li></ul><ul><li>NO ORGANOMEGALY </li></ul>
    • 14. PROVISIONAL DIAGNOSIS <ul><li>RHD/ MS/ POST CMC/ AF/ CVA / RIGHT HEMIPARESIS/LEFT PLEURAL EFFUSION /ASCITES FOR EVALUATION </li></ul><ul><li>? EMBOLIC STROKE </li></ul><ul><li>R/O CTD </li></ul>
    • 15. INVESTIGATIONS <ul><li>CBC – HB 8 SR. ELECTROLYTES </li></ul><ul><li>TC 6700 Na-124 </li></ul><ul><li>DC N48L50E2 K-3.7 </li></ul><ul><li>ESR 6/15 CL-98 </li></ul><ul><li>PCV 25 HCO3-23 </li></ul><ul><li>MCV 98 URINE </li></ul><ul><li>MCH 28 ALB-++ </li></ul><ul><li>MCHC 30 SUG-NIL </li></ul><ul><li>RBC 3LAC DEP-1-3PUS CELS </li></ul><ul><li>PLATLETS 1.5 24 hrs urine protein-608 mg/day </li></ul><ul><li>RFT- SUGAR 96 URINE PCR-1.8 </li></ul><ul><li>UREA 26 P. SMEAR- normocytic , normochromic </li></ul><ul><li>CREATININE 0.7 </li></ul>
    • 16.  
    • 17.  
    • 18. CT BRAIN <ul><li>HYPODENSE LESION IN B/L PARIETAL </li></ul><ul><li> LEFT TEMPORAL </li></ul><ul><li> LEFT CAUDATE </li></ul><ul><li> LEFT CORONA RADIATA </li></ul><ul><li> RIGHT OCCIPITAL </li></ul><ul><li>FEATURES SUGGESTIVE OF </li></ul><ul><li>‘’ MULTI INFARCT STATE’’ </li></ul>
    • 19.  
    • 20.  
    • 21. CT CHEST <ul><li>LEFT PLEURAL EFFUSION WITH MULTIPLE LOCULATION WITH UNDRELYING LUNG COLLAPSE. </li></ul>
    • 22. <ul><li>LFT </li></ul><ul><li>TOTAL BILIRUBIN-1mg/dl </li></ul><ul><li>IDB-0.6 </li></ul><ul><li>DB-0.4 </li></ul><ul><li>SERUM ALBUMIN-3.6mg/dl </li></ul><ul><li>SERUM ALP-WNL </li></ul><ul><li>SERUM ALT.AST-WNL </li></ul>
    • 23. ECHOCARDIOGRAM <ul><li>RHD (Post CMC) </li></ul><ul><li>MVA 1.7Cm 2 </li></ul><ul><li>MS- Mod. </li></ul><ul><li>MR- Mild </li></ul><ul><li>TR- Mild </li></ul><ul><li>PHT-Mild </li></ul><ul><li>AR – Trivial </li></ul><ul><li>No LA Clot </li></ul><ul><li>Normal LV SYS. Function </li></ul><ul><li>NO PERIC.EFFUSION </li></ul>
    • 24. Ascitic fluid Analysis <ul><li>C/S-No Growth </li></ul><ul><li>GM Stain-No Org. </li></ul><ul><li>TC- 100 Cells/m3 </li></ul><ul><li>Lymp.-40%N-30% </li></ul><ul><li>Reactive mesothel.-30% </li></ul><ul><li>Sugar-76 </li></ul><ul><li>Protein-3 </li></ul><ul><li>AFB-Negative </li></ul>
    • 25. Pleural Fluid Analysis <ul><li>TC-30 CELL </li></ul><ul><li>LYMP.-90% </li></ul><ul><li>REACTIVE MESOTHEL.-10% </li></ul><ul><li>CYTOLOGY </li></ul><ul><ul><li>SHEETS OF LYMPHOCYTES & REACTIVE MESOTHEL.CELLS IN PROTEINACEOUS BACKGROUND </li></ul></ul><ul><ul><li> S/O REACTIVE EFFUSION. </li></ul></ul>
    • 26. OTHER INVESTIGATIONS <ul><li>RA - NEGATIVE </li></ul><ul><li>CRP -12U </li></ul><ul><li>VDRL -NEGATIVE </li></ul><ul><li>ANA - POSITIVE 1 : 100+VE </li></ul><ul><li>RIM PATTERN </li></ul><ul><li>ANTI DS DNA - POSITIVE . </li></ul>
    • 27. <ul><li>ORAL ULCER </li></ul><ul><li>POLY SEROSITIS </li></ul><ul><li>PROTEINURIA </li></ul><ul><li>in a women of child bearing age </li></ul><ul><li>with </li></ul><ul><li>STROKE </li></ul><ul><li>IMMUNOLOGICAL EVIDENCE </li></ul>
    • 28. FINAL DIAGNOSIS <ul><li>RHD/ MS/ POST CMC STATUS/ AF/ CVD / RIGHT HEMIPARESIS/ SYSTEMIC LUPUS ERYTHREMATOSUS </li></ul>
    • 29. DEFINITION <ul><li>SLE is an autoimmune disease in which organs and cells undergo damage mediated by tissue binding autoantibodies and immune complexes. </li></ul><ul><li>99% are women of child bearing years. </li></ul>
    • 30. EPIDEMIOLOGY <ul><li>Prevalence influenced by age, gender, race, and genetics </li></ul><ul><ul><li>Prevalence: 1:2000 </li></ul></ul><ul><ul><li>Peak incidence 14-45 years </li></ul></ul><ul><ul><li>Black > White (1:250 vs. 1:1000) </li></ul></ul><ul><ul><li>Female predominance 10:1 </li></ul></ul><ul><ul><li>HLA DR3 association, Family History </li></ul></ul><ul><li>Severity is equal in male and female </li></ul>
    • 31. Etiology <ul><li>Genetic (HLA DR3 association) </li></ul><ul><ul><li>Abnormal immune response </li></ul></ul><ul><li>Environmental </li></ul><ul><ul><li>UV </li></ul></ul><ul><ul><li>Viruses </li></ul></ul><ul><ul><li>Hormones (Estrogen) </li></ul></ul>
    • 32. PATHOGENESIS <ul><li>Gene-environment interaction </li></ul><ul><li>Abnormal immune response </li></ul><ul><li>Induces pathogenic autoantibodies and immune complexes. </li></ul><ul><li>Activates complement causing inflammation </li></ul><ul><li>Irreversible organ damage. </li></ul>
    • 33. GENE ENVIRONMENT INTERACTION <ul><li>GENES … C1q,c2,c4 </li></ul><ul><li>HLA-D2,3,8 </li></ul><ul><li>MBL </li></ul><ul><li>FcR 2A,3A,2B </li></ul><ul><li>MCP-1 </li></ul><ul><li>. ENVIRONMENT FACTORS </li></ul><ul><li>UV LIGHT,gender </li></ul><ul><li>?infection </li></ul><ul><li>?EBV </li></ul>
    • 34. ABNORMAL IMMUNE RESPONSE <ul><li>1) Activation of innate immunity by DNA/RNA </li></ul><ul><li>2)Lowered threshold of adaptive immunity cells. </li></ul><ul><li>3) ineffective regulatory and inhibitory CD4+ and CD8+TCELLS. </li></ul><ul><li>4)reduced clearence of apoptotic cells. </li></ul>
    • 35. INFLAMMATION <ul><li>Immune activation of cells </li></ul><ul><li>Increased proinflammatory factors like TNFalpha,IFN,IL10 </li></ul><ul><li>Sustained production of pathogenic autoantibodies and immune complexes. </li></ul><ul><li>Activation of compliment and phagocytic cells leading to irreversible tissue damage. </li></ul>
    • 36. Overactive B-cells <ul><li>Estrogen is a stimulator of B-cell activity </li></ul><ul><ul><li>Lupus is much more prevalent in females of ages 15-45 </li></ul></ul><ul><ul><ul><li>Height of Estrogen production </li></ul></ul></ul><ul><li>IL-10, also a B-cell stimulator is in high concentration in lupus patient serum. </li></ul><ul><ul><li>High concentration linked to cell damage caused by inflammation </li></ul></ul>
    • 37. AUTOANTIBODIES IN SLE <ul><li>ANTIBODY </li></ul><ul><li>CLINICAL IMPORTANCE </li></ul><ul><li>1)ANTINUCLEAR(ANA) </li></ul><ul><li>2)ANTI-DsDNA </li></ul><ul><li>3)ANTI_SM </li></ul><ul><li>BEST SCREENING TEST(98%PREVALENCE) </li></ul><ul><li>SLE SPECIFIC, CORRELATES WITH DISEASE ACTIVITY, NEPHRITIS,VASCULITIS </li></ul><ul><li>SPECIFIC FOR SLE </li></ul>
    • 38. <ul><li>ANTIBODIES </li></ul><ul><li>CLINICAL IMPORTANCE </li></ul><ul><li>4)ANTI-RNP </li></ul><ul><li>5)ANTI-RO(SS-A) </li></ul><ul><li>NOT SPECIFIC </li></ul><ul><li>ASSOC.WITH SICCA SYNDR,SUBACUTE CUTANEOUS LUPUS,NEONATAL LUPUS WITH CONG.HEART BLOCK,DECREASED RISK OF NEPHRITIS </li></ul>
    • 39. <ul><li>ANTIBODIES </li></ul><ul><li>CLINICAL IMPORTANCE </li></ul><ul><li>6)ANTI-La(SS-B) </li></ul><ul><li>7)ANTI HISTONE </li></ul><ul><li>8)ANTIPHOSPHOLIPID </li></ul><ul><li>ASSOC.WITH ANTI-RO,DECREASED RISK OF NEPHRITIS </li></ul><ul><li>IN DRUG INDUCED LUPUS </li></ul><ul><li>PREDISPOSE TO THROMBOCYTOPENIA, FETAL LOSS </li></ul>
    • 40. <ul><li>ANTIBODIES </li></ul><ul><li>CLINICAL IMPORTANCE </li></ul><ul><li>9)ANTI ERYTHROCYTE </li></ul><ul><li>10)ANTIPLATELET </li></ul><ul><li>11)ANTI NEURONAL </li></ul><ul><li>12)ANTIRIBOSOMAL P </li></ul><ul><li>MEASURED AS DIRECT COOMBS TEST </li></ul><ul><li>ASSOC.WITH THROMBOCYTOPENIA </li></ul><ul><li>ACTIVE CNS LUPUS </li></ul><ul><li>DEPRESSION OR PSYCHOSIS </li></ul>
    • 41. DIAGNOSTIC CRITERIA <ul><li>MALAR RASH-ERYTHEMA OVER MALAR EMINENCE </li></ul><ul><li>DISCOID RASH-ERYTHEMATOUS RAISED PATCH WITH FOLLICULAR PLUGGING </li></ul><ul><li>PHOTOSENSITIVITY </li></ul><ul><li>ORAL ULCERS </li></ul><ul><li>ARTHRITIS-NONEROSIVE ARTHRITIS </li></ul><ul><li>SEROSITIS-PLEURITIS , PERICARDITIS </li></ul><ul><li>RENAL DISORDER-PROTEINURIA>0.5G/DAY OR CAST </li></ul><ul><li>HEMATOLOGICAL DISORDER-HEMOLYTIC ANEMIA OR LEUCOPENIA OR THROMBOCYTOPENIA </li></ul><ul><li>IMMUNOLOGICAL DISORDER-ANTIBODIES </li></ul><ul><li>ANA </li></ul><ul><li>NEUROLOGICAL- PSYCOSIS, SEIZURES </li></ul>
    • 42. CLASSIFICATION CRITERIA <ul><li>Must have 4 of 11 for Classification </li></ul><ul><ul><li>Sensitivity 75% </li></ul></ul><ul><ul><li>Specificity 95% </li></ul></ul><ul><li>Like RA, diagnosis is ultimately clinical </li></ul><ul><li>Not all “Lupus” is SLE </li></ul><ul><ul><li>Discoid Lupus </li></ul></ul><ul><ul><li>Overlap syndrome </li></ul></ul><ul><ul><li>Drug induced lupus </li></ul></ul><ul><ul><li>Subacute Cutaneous Lupus </li></ul></ul>
    • 43. CLINICAL FEATURES: Neurologic <ul><li>Behavior/Personality changes, depression </li></ul><ul><li>Cognitive dysfunction </li></ul><ul><li>Psychosis </li></ul><ul><li>Seizures </li></ul><ul><li>Stroke </li></ul><ul><li>Chorea </li></ul><ul><li>Pseudotumor cerebri </li></ul><ul><li>Transverse myelitis </li></ul><ul><li>Peripheral neuropathy </li></ul><ul><li>Total of 19 manifestations described </li></ul><ul><ul><li>May be difficult to distinguish from steroid psychosis or primary psychiatric disease </li></ul></ul>
    • 44. CLINICAL FEATURES: Gastrointestinal & Hepatic <ul><ul><li>Uncommon SLE manifestations </li></ul></ul><ul><ul><li>mesenteric vasculitis, resembling medium vessel vasculitis (PAN) </li></ul></ul><ul><ul><li>Diverticulitis may be masked by steroids </li></ul></ul><ul><ul><li>Hepatic abnormalities more often IATROGENIC than to SLE itself </li></ul></ul>
    • 45.  
    • 46. T reatment. <ul><li>Mild cases : NSAID, local treatment, hydroxy-chloroquin </li></ul><ul><li>Cases of intermediate severity : corticosteroid (12-64 mg methylprednisolon), azathioprin, methotrexat </li></ul>
    • 47. SLE – treatment <ul><li>Severe, life-threatening organ involvements : </li></ul><ul><li>High dose IV corticosteroid + iv.cyclophosphamide .P lasmapheresis or iv. Immunoglobulin . </li></ul><ul><li>Some cases of nephritis (especially membranous), myositis, thrombocytopenia: cyclosporine </li></ul>
    • 48. <ul><li>WOMEN OF CHILDBEARING AGE </li></ul><ul><li>MULTISYSTEM INVOLVEMENT </li></ul><ul><li>NO RELATED CAUSE </li></ul><ul><li>EVEN WITH SUBTLE MANIFESTATION </li></ul><ul><li>EVALUATE C T D </li></ul><ul><li>RULE OUT S L E </li></ul>
    • 49. <ul><li>THANK U </li></ul>

    ×