A Case of Infective Endocarditis

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A Case of Infective Endocarditis

  1. 1. A case of infective endocarditis By Dr P. Arul M4, Prof P. Vijayaraghavan’s unit
  2. 2.  46 year old male presented with c/o ◦ Fever 3 weeks duration ◦ Slurring of speech 1 day ◦ Weakness of left upper and lower limbs 1 day  History of present illness: ◦ Fever  3 weeks duration  Intermittent  High grade  Not associated with chills, rigors.
  3. 3. ◦ Patient suddenly developed an episode of sudden loss of consciousness which lasted for 2 minutes and recovered spontaneously, following which he noticed difficulty in standing and walking due to weakness of his left lower limb. His family members also noticed that his speech was slurred. ◦ No h/o seizure ◦ No h/o bladder, bowel disturbance ◦ No h/o regurgitation of feeds
  4. 4. ◦ No h/o burning micturition, increased frequency. ◦ No h/o abdominal pain, vomiting, diarrhea. ◦ No h/o cough with expectoration, breathlessness ◦ No h/o skin ulcers, rash, jaundice
  5. 5.  Past history: ◦ Was diagnosed to have cardiac valvular lesion (?RHD) 1 yr back and on drugs since then. ◦ Not a known diabetic, hypertensive, epileptic, COPD, PT, IHD. ◦ No previous similar episodes.  Personal history: ◦ Not a smoker, drinks alcohol occasionally
  6. 6.  Family history: ◦ No family h/o cardiac ailment  Treatment history: ◦ Patient consulted a private practitioner 1 yr back for reduced exercise tolerance and was evaluated for cardiac causes. Echo picked up mitral regurgitation and patient was put on penicillin prophylaxis along with T. lasix.
  7. 7. General Examination  Conscious  Oriented  Afebrile  No cyanosis  No clubbing  No pallor  Not icteric  No pedal edema  No petichiae  No Splinter hemorrhages  No Oslers node  No Janway lesion  Retinal hemorrhage+ -Roth’s spot
  8. 8.  CVS: ◦ S1, S2 heard, ◦ A pan systolic murmur with a musical quality heard in the mitral area, ◦ P2 loud.  RS: ◦ Normal vesicular breath sounds heard  P/A ◦ Soft, no organomegaly
  9. 9.  CNS ◦ HMF  Conscious  Orientation  Time +  Place +  Dysarthria with Anomic Aphasia(difficulty in naming persons and objects)  Memory intact
  10. 10. ◦ Cranial nerves  I-VI – normal  VII – UMN type facial palsy on left side  VIII-XII – normal ◦ Motor system  Grade 4/5 power in both left lower and upper limb  Deep tendon reflex brisk in the left side  Tone – mild increase in the left side  Babinski positive on the left side
  11. 11. ◦ Sensory system:  Normal ◦ Cerebellar functions:  Normal ◦ Spine and cranium:  Normal ◦ No meningeal signs  Imp:- RHD – mitral regurgitation/ infective endocarditis/ embolic CVA – left hemiparesis
  12. 12. Investigations  ECG – NSR, WNL  CXR - NAD  CBC ◦ Hb 11.2g/dl ◦ PCV 31 ◦ TC 8600 ◦ DC P74 L24 E2 ◦ ESR 4/12 ◦ Platelets 1.8 lakhs  Blood sugar 108  Blood urea 24  Sr. creatinine 0.9
  13. 13.  Lipid profile: ◦ TC ◦ TGL ◦ LDL ◦ HDL  CT Brain: ◦ Normal  MRI: ◦ Multiple small infarcts in the frontal lobe, parietal lobe and basal ganglia
  14. 14.  Blood culture ◦ Sample A no growth ◦ Sample B no growth ◦ Sample C coagulase negative Staphylococci  Repeat blood culture (5th day): ◦ coagulase negative Staphylococci  Echo: ◦ Mitral regurgitation – moderate ◦ Rupture of chordae tendinae ◦ Valvular vegitations+
  15. 15. Treatment  Inj Vancomycin 1g IV BD x 4weeks  Inj Gentamycin 80mg BD x 5days
  16. 16.  Cardiologist opinion: ◦ Continue antibiotics repeat echo weekly for assessing reduction in size of vegetations.
  17. 17. Follow up  Repeat blood culture (3rd week) ◦ No growth  ECHO ◦ Mitral regurgitation (moderate) ◦ Rupture of chordae tendinae
  18. 18. Discussion  Infective endocarditis is microbial infection of cardiac valves.  The features of infective endocarditis have changed dramatically during the past three decades.  Patients with classic manifestations such as fever, splenomegaly, changing murmurs, signs of peripheral embolization and multiple positive blood cultures have become distinctly unusual.  Originally endocarditis was classified as acute or sub-acute depending on the duration of the disease.
  19. 19.  Patients dying within 8 weeks were said to have acute form while those surviving more than 8 weeks were said to have sub-acute form.  Patients with endocarditis due to staphylococcus aureus, Neisseria meningitidis, Hemphilus influenzae or Streptococcus pyogenes were considered to have the acute form.  Streptococcus viridans or staphylococcus epidermidis were associated with the sub acute form.
  20. 20. Incidence  0.16 to 5.4 per 1000 hospital admissions.  Mean age is between 55 and 57 years.  Uncommon in the first decade.  When it occurs in infants it is of the acute variety involving normal cardiac valves.  Men predominate with a ratio of 2:1 to as high as 9:1 in older age group.
  21. 21. Predisposing conditions  72% of patients have a preexisting structural cardiac abnormality.  Isolated valvular aortic stenosis was the congenital defect most often associated with IE followed by VSD, TOF, idiopathic subaortic stenosis and ASD (uncommon).  In patients with valvular lesion mitral valve is involved most often followed by aortic valve, tricuspid valve involvement is uncommon (1%).  Cardiac prosthetic valves and parentral narcotic drug constitutes a major risk for IE.
  22. 22. Relative risk of various predisposing conditions High risk Intermediate risk Low/negligible risk Prosthetic valves Mitral valve prolapse Degenerative heart disease Aortic valve disease Mitral stenosis ASD Mitral regurgitation Tircuspid valve disease Luetic Aoritis (syphiis) PDA HOCM CABG AV fistula Calcific aortic stenosis Surgically corrected congenital lesions VSD TOF Pacemakers Coarctation of Aorta Non valvular intra- cardiac prosthesis Previous IE Marfan’s syndrome
  23. 23. Etiology Native valves Narcotic addicts Prosthetic valves Streptococcus viridans 30-40 Saphylococcus aureus 50-60 Saphylococcus Epidermidis 20-30 Saphylococcus aureus 10-30 Streptococci 8-15 Saphylococcus aureus 15-20 Saphylococcus Epidermidis 1-3 Saphylococcus Epidermidis 2-5 Streptococcus Viridans 5-20 Enterococci 5-15 Enterococci 8-10 Enterococci 5-10 Other streptococci 15-20 Other streptococci 10-15 Other streptococci 1-5 Gram -ve bacilli 2-10 Gram -ve bacilli 4-8 Gram -ve bacilli 10-20 Fungi 2-4 Fungi 4-5 Fungi 5-15 Culture negative 5-10 Culture negative 5-8 Culture negative <5
  24. 24. Pathogenesis  Source of infection ◦ The bacteremia or fungemia that initiates the infection is transient and arises form the oropharynx, genitourinary or gastrointestinal mucosa ◦ Bacteremia following dental procedures occurs in 60% patients, 85% following suction abortion, 30% following tonsillectomy , 16% following nasotracheal intubation, 15% following bronchoscopy and10% after UGI scopy. ◦ Staphylococcus aureus endocarditis are more likely to have a demonstrable source of infection.
  25. 25. Invasive predisposing factors to bacterial endocarditis Dental procedures Oral and upper respiratory tract surgery Certain gastrointestinal procedures Genitourinary surgery Cardiac surgery Certain trauma Alimentation catheters in the right heart Intravenous drug use
  26. 26. Cardiac pathology  Endocarditis develops following implantation of a microorganism on a preexisting sterile thrombotic vegetation present at a point of structural endocardial abnormality.  It has been shown experimentally that bacteria are often deposited in areas of high blood flow velocity. Consequently vegetations develop more frequently in a regurgitant valve.
  27. 27. Valve affected Site of vegetation/complication Mitral valve Along chordae tendinae toward papillary muscle causing their rupture Aortic valve Develop ring abscess VSD Right ventricular wall, the site of jet impact Regurgitant mitral lesion Wall of left atrium in the area termed MacCallum’s patch Regurgitant Aortic lesion Chordae tendinae of anterior mitral leaflet
  28. 28. Extracardiac pathology  Systemic embolism is reported to occur in over 50% cases in autopsy studies.  Most common sites are kidneys, skin, spleen, eye and CNS.  There is increasing evidence to show that embolic phenomena actually represent “immune complex” deposition in small systemic arteries.
  29. 29. Clinical manifestations Symptoms % Fever 84 Chills 41 Weakness 38 Dyspnoea 36 Sweats 24 Anorexia 24 Malaise 24 Cough 24 Skin lesion 21 Stroke 18 Nausea, vomiting 17 Chest pain 16
  30. 30. Physical findings % Heart murmurs 89 Fever 77 Embolic events 50 Skin manifestations 50 Splenomegaly 28 Septic complications 19 Mycotic aneurisms 18 Glomerulonephritis 15 Digital clubbing 12 Retinal lesions 9
  31. 31.  Heart murmurs ◦ Was the sine qua non for the diagnosis ◦ It has been found that 15% don’t have murmurs at initial diagnosis, however most develop a murmur during the course of the disease ◦ Changing murmurs – factors other than valvular integrity like change in cardiac output, temperature, hematocrit may play a role. However new onset regurgitant murmur in a setting of acute sepsis is virtually diagnostic.
  32. 32.  Cutaneous manifestations ◦ Petichiae (20-40%) ◦ Subcunjunctival and subungual splinter hemorrhages due to lipid microembolism. ◦ Osler nodes  Tender, purplish erythematous papules in pulp of distal fingers  Due to hypersensitive angitis – cultures are negative ◦ Janeway lesions  Erythematous, non-tender nodules on palms or soles. ◦ Clubbing found only in 10-20%.  Ocular manifestations ◦ Roth spot- flame shaped hemorrhage occasionally takes the form of cotton wool spot.
  33. 33. Complications  Congestive heart failure  Extravalvular cardiac manifestations  Systemic and pulmonary embolism  Mycotic aneurism  Neurologic – stroke, neuropsychiatric syndromes  Renal – glomerulonephritis, renal infarcts  Hematological – anemia, TTP
  34. 34. Diagnosis – duke’s criteria  Major Criteria  1. Positive blood culture  Typical microorganism for infective endocarditis from two separate blood cultures or  Persistently positive blood culture, defined as recovery of a microorganism consistent with infective endocarditis from blood cultures drawn >12 h apart or  Single positive blood culture for Coxiella burnetii or phase I IgG antibody titer of >1:800  2. Evidence of endocardial involvement ◦ Positive echocardiogram  Oscillating intracardiac mass on valve, or  Abscess, or  New partial dehiscence of prosthetic valve, or ◦ New valvular regurgitation
  35. 35.  Minor Criteria  1. Predisposition: ◦ Predisposing heart condition or ◦ Injection drug use  2. Fever ≥38.0°C (≥100.4°F)  3. Vascular phenomena: ◦ Major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions  4. Immunologic phenomena: ◦ Glomerulonephritis, Osler’s nodes, Roth’s spots, Rheumatoid factor  5. Microbiologic evidence: ◦ Positive blood culture but not meeting major criterion as noted previously or ◦ Serologic evidence of active infection with organism consistent with infective endocarditis  Documentation of two major criteria, of one major and three minor criteria, or of five minor criteria allows a clinical diagnosis of definite endocarditis
  36. 36. Treatment -medical
  37. 37. Surgical treatment
  38. 38. THANK YOU

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