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Case presentation Dr. Kailash Raj
Case History 35 yr old female KHAIRUNNISA was admitted thru ER on 19oct 2010 with; 	Fever	  		6 months 	Generalized weakness According to patient; she was in her usual state of health 6 months back that she started having low grade, on and off  fever; associated with generalized weakness that patient’s routine activities were disturbed. For that she visited many general practitioners but got no ultimate relief. Besides that, from last 1 week she started having high grade fever that was associated with rigors, chills, headache and nausea.  There is no h/o of joint pain, sore throat, palpitation, sweating, shortness of breath, skin rash, dysuria, hematuria, diarrhea and vomiting.
Case History PM Hx:	Not significant PS Hx:	Not significant Personal Hx: 		Appetite---Good 		Bowel Habits---Regular 		Micturition ---- Normal 		Thirst---- Normal 		Weight loss--- No Family Hx: No history of T.B, D.M, HTN, Asthma 	Parents: Healthy 	Siblings: Healthy 	4 Children: Healthy  Socio-economic Hx: 	Fair
Physical examination 35 year old female of average height& built, lying comfortably on bed; oriented to time place and person Pulse: 98/min	B.P: 130/80	Resp: 16/min 	Temp:103F Gen:  Anxious and worried, Anemia+ve, Jaundice –ve, Dehydration –ve, Cyanosis –ve, Clubbing –ve, osler nodes -ve, splintterhemmorhage-ve, janeway lesion -ve  .    Neck: No JVD or hepatojugular reflux & no lymph nodes palpable Cardiovascular: S1 and S2 audible, murmurs audible Pulmonary: B/L NVB, No wheeze, crepts Abd: Soft, non tender, hepato-spleenomegaly
Physical examination CNS: GCS 15/15 and neck stiffness-ve, other signs of meningeal irritation -ve At time of presentation CNS was fully intact; unfortunately on 3rd day of admission here in hospital she developed left sided weakness with dysarthria Bulk --- B/L Normal Power ---1/5 Lt side & 5/5 Rt side Tone ---Dec Lt side Reflexs--- Diminished Lt side Plantars--- Rt ↓ ----- Lt- ↑
Laboratory Findings
Laboratory Findings
Differentials
Treatment Being Given Inj. Benzyl penicillin Ҳ 3mega units Ҳ TID Inj. Genticin 120mg Ҳ OD Inj. Arbinin 500 md Ҳ TID Inj. Risek 40mg Ҳ OD Inj. Lasix 20mg × BD Tb. Panadol × PRN Tb. Folic acid 5mg ×OD Tb. Lowplat 75mg × OD Tb. Ascard 75mg × OD Tb. Lexotanil 1.5mg × HS
Infective Endocarditis
Definition Infective Endocarditis (IE): A bacterial or fungal infection of the valvular or endocardial surface of heart Microbial infection of the endothelial lining of the heart
Classification Classified into four groups:  Native Valve IE Prosthetic Valve IE Intravenous drug abuse (IVDA) IE Nosocomial IE
Further Classification Acute Affects normal heart valves Rapidly destructive Metastatic foci Commonly Staph. If not treated, usually fatal within 6 weeks Subacute Often affects damaged heart valves Indolent nature If not treated, usually fatal by one year
Pathophysiology Turbulent blood flow disrupts the endocardium making it “sticky” Bacteremia delivers the organisms to the endocardial surface  Adherence of the organisms to the endocardial surface Eventual invasion of the valvular leaflets
Epidemiology Incidence difficult to ascertain and varies according to location, Estimated incidence: 1.6 to 6.0 / 100,000 person-per year. Much more common in males than in females, Male:female ratio is 1.7:1. May occur in persons of any age and increasingly common in elderly; 50% of cases are over 60yrs of age. Mortality ranges from 20-30%
Risk Factors Intravenous drug abuse Artificial heart valves and pacemakers  Acquired heart defects Calcific aortic stenosis Mitral valve prolapse with regurgitation Congenital heart defects Intravascular catheters
Infecting Organisms Common bacteria S. aureus Streptococci  Enterococci Not so common Fungi Pseudomonas HACEK
Symptoms Acute High grade fever and chills SOB Arthralgias/ myalgias Abdominal pain Pleuritic chest pain Back pain Subacute Low grade fever Anorexia Weight loss Fatigue Arthralgias/ myalgias Abdominal pain
Signs Fever  Heart murmur Nonspecific signs – petechiae, subungal or “splinter” hemorrhages, clubbing, splenomegaly, neurologic changes More specific signs - Osler’s Nodes, Janeway lesions, and Roth Spots
Petechiae Nonspecific Often located on extremities  	or mucous membranes
Splinter Hemorrhages Nonspecific Nonblanching Linear reddish-brown lesions found under the nail bed Usually do NOT extend the entire length of the nail
Osler’s Nodes ,[object Object]
4 P’s:
Pink
Painful
Pea-sized
Pulp of the fingers/toes.
Immunologic originMore specific Painful and erythematous nodules Located on pulp of fingers and toes More common in subacute IE
Janeway Lesions More specific Erythematous, blanching macules  Nonpainful Located on palms and soles Septic emboli
Lab findings Hematology ,[object Object],Thrombocytopenia (5-15%) Leukocytosis (20-30%) Histiocytes (>25%) Elevated ESR, with mean value of 57mm/hr (90-100%) Hypergammaglobulinemia (20-30%) Urinalysis Proteinuria (50-65%) Microscopic hematuria (30-60%) Red cell casts (12%)
Lab findings Serology Rheumatoid factor (40-50%) Circulating immune complexes Antinuclear antibodies Complement Blood culture Most important lab test Positive cultures in 97% of cases
Imaging Chest x-ray  Look for multiple focal infiltrates and calcification of heart valves EKG Rarely diagnostic Look for evidence of ischemia, conduction delay, and arrhythmias Echocardiography
Indications for Echocardiography Transthoracic echocardiography (TTE) First line if suspected IE Native valves is rapid, noninvasive specificity: 98% sensitivity: <60% Transesophageal echocardiography (TEE) Prosthetic valves Intracardiac complications higher ultrasonic frequencies, improve spatial resolution specificity: 94% (prosthetic valve: 88-100%) sensitivity: 76-100% (prosthetic valve: 86-94%)
Making the Diagnosis Pelletier and Petersdorf criteria (1977) Classification scheme of definite, probable, and possible IE Reasonably specific but lacked sensitivity Von Reyn criteria (1981) Added “rejected” as a category Added more clinical criteria Improved specificity and clinical utility Duke criteria (1994) Included the role of echocardiography in diagnosis Added IVDA as a “predisposing heart condition”
Duke Criteria for IE diagnosis
Duke Criteria for IE diagnosis
Modified Duke Criteria Definite IE Microorganism (via culture or histology) in a valvular vegetation, embolized vegetation, or intracardiac abscess Histologic evidence of vegetation or intracardiac abscess Possible IE 2 major 1 major and 3 minor 5 minor Rejected IE Resolution of illness with four days or less of antibiotics
Therapy ,[object Object],1. The infection exists in an area of impaired host defense and is tightly encased in a fibrin meshwork 2. The bacteria reach very high population densities, such that the organism may exist in a state of reduced metabolic activity and cell division ,[object Object],[object Object]
Parenteral antibiotics are recommended over oral drugs
Bacteriostatic antibiotics are generally ineffective
Antibiotic combinations should produce a rapid effect
Selection of antibiotics should be based on susceptibility tests, and treatment should be monitored clinically and with antimicrobial blood levels
Blood cultures should be obtained during the early phase of therapy to ensure eradication
Use of anticoagulants during therapy for native valve IE is not recommended.  With mechanical valves, anticoagulation should be maintained (if indicated) within therapeutic range,[object Object]
>2 serious systemic embolic episode

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infective endocarditis krm

  • 1. Case presentation Dr. Kailash Raj
  • 2. Case History 35 yr old female KHAIRUNNISA was admitted thru ER on 19oct 2010 with; Fever 6 months Generalized weakness According to patient; she was in her usual state of health 6 months back that she started having low grade, on and off fever; associated with generalized weakness that patient’s routine activities were disturbed. For that she visited many general practitioners but got no ultimate relief. Besides that, from last 1 week she started having high grade fever that was associated with rigors, chills, headache and nausea. There is no h/o of joint pain, sore throat, palpitation, sweating, shortness of breath, skin rash, dysuria, hematuria, diarrhea and vomiting.
  • 3. Case History PM Hx: Not significant PS Hx: Not significant Personal Hx: Appetite---Good Bowel Habits---Regular Micturition ---- Normal Thirst---- Normal Weight loss--- No Family Hx: No history of T.B, D.M, HTN, Asthma Parents: Healthy Siblings: Healthy 4 Children: Healthy Socio-economic Hx: Fair
  • 4. Physical examination 35 year old female of average height& built, lying comfortably on bed; oriented to time place and person Pulse: 98/min B.P: 130/80 Resp: 16/min Temp:103F Gen: Anxious and worried, Anemia+ve, Jaundice –ve, Dehydration –ve, Cyanosis –ve, Clubbing –ve, osler nodes -ve, splintterhemmorhage-ve, janeway lesion -ve . Neck: No JVD or hepatojugular reflux & no lymph nodes palpable Cardiovascular: S1 and S2 audible, murmurs audible Pulmonary: B/L NVB, No wheeze, crepts Abd: Soft, non tender, hepato-spleenomegaly
  • 5. Physical examination CNS: GCS 15/15 and neck stiffness-ve, other signs of meningeal irritation -ve At time of presentation CNS was fully intact; unfortunately on 3rd day of admission here in hospital she developed left sided weakness with dysarthria Bulk --- B/L Normal Power ---1/5 Lt side & 5/5 Rt side Tone ---Dec Lt side Reflexs--- Diminished Lt side Plantars--- Rt ↓ ----- Lt- ↑
  • 9. Treatment Being Given Inj. Benzyl penicillin Ҳ 3mega units Ҳ TID Inj. Genticin 120mg Ҳ OD Inj. Arbinin 500 md Ҳ TID Inj. Risek 40mg Ҳ OD Inj. Lasix 20mg × BD Tb. Panadol × PRN Tb. Folic acid 5mg ×OD Tb. Lowplat 75mg × OD Tb. Ascard 75mg × OD Tb. Lexotanil 1.5mg × HS
  • 11. Definition Infective Endocarditis (IE): A bacterial or fungal infection of the valvular or endocardial surface of heart Microbial infection of the endothelial lining of the heart
  • 12. Classification Classified into four groups: Native Valve IE Prosthetic Valve IE Intravenous drug abuse (IVDA) IE Nosocomial IE
  • 13. Further Classification Acute Affects normal heart valves Rapidly destructive Metastatic foci Commonly Staph. If not treated, usually fatal within 6 weeks Subacute Often affects damaged heart valves Indolent nature If not treated, usually fatal by one year
  • 14. Pathophysiology Turbulent blood flow disrupts the endocardium making it “sticky” Bacteremia delivers the organisms to the endocardial surface Adherence of the organisms to the endocardial surface Eventual invasion of the valvular leaflets
  • 15. Epidemiology Incidence difficult to ascertain and varies according to location, Estimated incidence: 1.6 to 6.0 / 100,000 person-per year. Much more common in males than in females, Male:female ratio is 1.7:1. May occur in persons of any age and increasingly common in elderly; 50% of cases are over 60yrs of age. Mortality ranges from 20-30%
  • 16. Risk Factors Intravenous drug abuse Artificial heart valves and pacemakers Acquired heart defects Calcific aortic stenosis Mitral valve prolapse with regurgitation Congenital heart defects Intravascular catheters
  • 17. Infecting Organisms Common bacteria S. aureus Streptococci Enterococci Not so common Fungi Pseudomonas HACEK
  • 18. Symptoms Acute High grade fever and chills SOB Arthralgias/ myalgias Abdominal pain Pleuritic chest pain Back pain Subacute Low grade fever Anorexia Weight loss Fatigue Arthralgias/ myalgias Abdominal pain
  • 19. Signs Fever Heart murmur Nonspecific signs – petechiae, subungal or “splinter” hemorrhages, clubbing, splenomegaly, neurologic changes More specific signs - Osler’s Nodes, Janeway lesions, and Roth Spots
  • 20. Petechiae Nonspecific Often located on extremities or mucous membranes
  • 21. Splinter Hemorrhages Nonspecific Nonblanching Linear reddish-brown lesions found under the nail bed Usually do NOT extend the entire length of the nail
  • 22.
  • 24. Pink
  • 27. Pulp of the fingers/toes.
  • 28. Immunologic originMore specific Painful and erythematous nodules Located on pulp of fingers and toes More common in subacute IE
  • 29. Janeway Lesions More specific Erythematous, blanching macules Nonpainful Located on palms and soles Septic emboli
  • 30.
  • 31. Lab findings Serology Rheumatoid factor (40-50%) Circulating immune complexes Antinuclear antibodies Complement Blood culture Most important lab test Positive cultures in 97% of cases
  • 32. Imaging Chest x-ray Look for multiple focal infiltrates and calcification of heart valves EKG Rarely diagnostic Look for evidence of ischemia, conduction delay, and arrhythmias Echocardiography
  • 33. Indications for Echocardiography Transthoracic echocardiography (TTE) First line if suspected IE Native valves is rapid, noninvasive specificity: 98% sensitivity: <60% Transesophageal echocardiography (TEE) Prosthetic valves Intracardiac complications higher ultrasonic frequencies, improve spatial resolution specificity: 94% (prosthetic valve: 88-100%) sensitivity: 76-100% (prosthetic valve: 86-94%)
  • 34. Making the Diagnosis Pelletier and Petersdorf criteria (1977) Classification scheme of definite, probable, and possible IE Reasonably specific but lacked sensitivity Von Reyn criteria (1981) Added “rejected” as a category Added more clinical criteria Improved specificity and clinical utility Duke criteria (1994) Included the role of echocardiography in diagnosis Added IVDA as a “predisposing heart condition”
  • 35. Duke Criteria for IE diagnosis
  • 36. Duke Criteria for IE diagnosis
  • 37. Modified Duke Criteria Definite IE Microorganism (via culture or histology) in a valvular vegetation, embolized vegetation, or intracardiac abscess Histologic evidence of vegetation or intracardiac abscess Possible IE 2 major 1 major and 3 minor 5 minor Rejected IE Resolution of illness with four days or less of antibiotics
  • 38.
  • 39. Parenteral antibiotics are recommended over oral drugs
  • 40. Bacteriostatic antibiotics are generally ineffective
  • 41. Antibiotic combinations should produce a rapid effect
  • 42. Selection of antibiotics should be based on susceptibility tests, and treatment should be monitored clinically and with antimicrobial blood levels
  • 43. Blood cultures should be obtained during the early phase of therapy to ensure eradication
  • 44.
  • 45. >2 serious systemic embolic episode
  • 47. physiologically significant valve dysfunction as demonstrated by echo
  • 50. most cases of prosthetic valve IE (caused by more antibiotic-resistant pathogens)
  • 51.
  • 54. CHF
  • 56. Rupture of a mycotic aneurysm
  • 57. Lack of response to antimicrobial therapy
  • 59.
  • 60. Embolic Complications Occur in up to 40% of patients with IE Predictors of embolization Size of vegetation Left-sided vegetations Fungal pathogens, S. aureus, and Strep. Bovis Incidence decreases significantly after initiation of effective antibiotics
  • 61. Embolic Complications Stroke Myocardial Infarction Fragments of valvular vegetation or vegetation-induced stenosis of coronary ostia Ischemic limbs Hypoxia from pulmonary emboli Abdominal pain (splenic or renal infarction)
  • 64. Local Spread of Infection Heart failure Extensive valvular damage Paravalvular abscess (30-40%) Most common in aortic valve, IVDA, and S. aureus May extend into adjacent conduction tissue causing arrythmias Higher rates of embolization and mortality Pericarditis Fistulous intracardiac connections
  • 65. Local Spread of Infection Acute S. aureus IE with perforation of the aortic valve and aortic valve vegetations. Acute S. aureus IE with mitral valve ring abscess extending into myocardium.
  • 66. Metastatic Spread of Infection Metastatic abscess Kidneys, spleen, brain, soft tissues Meningitis and/or encephalitis Vertebral osteomyelitis Septic arthritis
  • 67. Summary IVDA and the elderly are at greatest risk of developing IE. The signs and symptoms of IE are nonspecific and varied. A thorough but timely evaluation (including serial blood cultures, adjunct labs, and an echo) is crucial to accurately diagnose and treat IE. Beware of life-threatening complications.