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A case of infective
endocarditis
By Dr P. Arul
M4, Prof P. Vijayaraghavan’s unit
 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.
◦ 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
◦ 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
 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
 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.
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
 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
 CNS
◦ HMF
 Conscious
 Orientation
 Time +
 Place +
 Dysarthria with Anomic Aphasia(difficulty in
naming persons and objects)
 Memory intact
◦ 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
◦ Sensory system:
 Normal
◦ Cerebellar functions:
 Normal
◦ Spine and cranium:
 Normal
◦ No meningeal signs
 Imp:- RHD – mitral regurgitation/
infective endocarditis/ embolic CVA –
left hemiparesis
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
 Lipid profile:
◦ TC
◦ TGL
◦ LDL
◦ HDL
 CT Brain:
◦ Normal
 MRI:
◦ Multiple small infarcts in the frontal lobe,
parietal lobe and basal ganglia
 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+
Treatment
 Inj Vancomycin 1g IV BD x 4weeks
 Inj Gentamycin 80mg BD x 5days
 Cardiologist opinion:
◦ Continue antibiotics repeat echo weekly
for assessing reduction in size of
vegetations.
Follow up
 Repeat blood culture (3rd week)
◦ No growth
 ECHO
◦ Mitral regurgitation (moderate)
◦ Rupture of chordae tendinae
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.
 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.
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.
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.
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
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
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.
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
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.
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
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.
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
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
 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.
 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.
Complications
 Congestive heart failure
 Extravalvular cardiac manifestations
 Systemic and pulmonary embolism
 Mycotic aneurism
 Neurologic – stroke, neuropsychiatric
syndromes
 Renal – glomerulonephritis, renal
infarcts
 Hematological – anemia, TTP
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
 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
Treatment -medical
Surgical treatment
THANK YOU

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A Case of Infective Endocarditis

  • 1. A case of infective endocarditis By Dr P. Arul M4, Prof P. Vijayaraghavan’s unit
  • 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. ◦ 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. ◦ 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.  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.  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. 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.  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.  CNS ◦ HMF  Conscious  Orientation  Time +  Place +  Dysarthria with Anomic Aphasia(difficulty in naming persons and objects)  Memory intact
  • 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. ◦ Sensory system:  Normal ◦ Cerebellar functions:  Normal ◦ Spine and cranium:  Normal ◦ No meningeal signs  Imp:- RHD – mitral regurgitation/ infective endocarditis/ embolic CVA – left hemiparesis
  • 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.  Lipid profile: ◦ TC ◦ TGL ◦ LDL ◦ HDL  CT Brain: ◦ Normal  MRI: ◦ Multiple small infarcts in the frontal lobe, parietal lobe and basal ganglia
  • 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. Treatment  Inj Vancomycin 1g IV BD x 4weeks  Inj Gentamycin 80mg BD x 5days
  • 16.  Cardiologist opinion: ◦ Continue antibiotics repeat echo weekly for assessing reduction in size of vegetations.
  • 17. Follow up  Repeat blood culture (3rd week) ◦ No growth  ECHO ◦ Mitral regurgitation (moderate) ◦ Rupture of chordae tendinae
  • 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.  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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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.  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.  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. 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. 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.  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
  • 37.
  • 38.