• Congestive heart failure
• Embolic events – Coronary, Cerebral, renal, visceral, pulmonary
• Periannular extension of abscess
• Arrythmia development – New onset heart block
• Prosthetic valve dysfunction
• Metastatic infection
• Persistent bacteremia or Fungemia
• Mycotic aneurysms
• Renal failure
Congestive Heart Failure
In native-valve IE, acute CHF occurs more frequently in aortic-valve infections (29 per cent) than with mitral (20 per cent) or tricuspid disease (8 per cent). CHF may develop acutely from:
• Perforation of a native-or bioprosthetic-valve leaflet,
• Rupture of infected mitral chordae,
• Valve obstruction from bulky vegetations,
• Sudden intracardiac shunts from fistulous tracts or prosthetic dehiscence. CHF may also develop more insidiously, despite appropriate antibiotics, as a result of a progressive worsening of valvular insufficiency and ventricular dysfunction.
• CHF in IE, irrespective of the course or mechanism, signifies a grave prognosis with medical therapy alone and is also the most powerful predictor of poor outcome with surgical therapy.
• The decision to operate on the patient with IE is driven primarily by the severity of CHF.Medical and surgical management decisions can be guided by echocardiographic detection of abscesses, fistulae, prosthetic dehiscence, obstructive vegetations, or flail leaflets, none of which will resolve with medical therapy alone. Delaying surgery to the point of frank ventricular decompensation dramatically increases operative mortality, from 6 per cent to 11 per cent for patients without CHF and 17 per cent to 33 per cent for patients with CHF.
Poor surgical outcome is predicted by preoperative New York Heart Association class III or IV CHF, renal insufficiency, and advanced age. In any patient, a decision to delay surgery to extend pre-operative antibiotic treatment carries with it the risk of permanent ventricular dysfunction.The incidence of reinfection of newly implanted valves in patients with active IE has been estimated to be 2 per cent to 3 per cent, far less than the mortality rate for uncontrolled CHF.
Risk of Embolization
Systemic embolization occurs in 22 per cent to 50 per cent of cases of IE. Emboli often involve major arterial beds, including lungs, coronary arteries, spleen, bowel, and extremities. Up to 65 per cent of embolic events involve the central nervous system, and 90 per cent of central nervous system emboli lodge in the distribution of the middle cerebral artery. The highest incidence of embolic complications is seen with aortic- and mitral-valve infections and in IE due to S aureus and Candida species and HACEK and Abiotrophia organisms. Emboli can occur before diagnosis, during therapy, or after therapy is completed, although most emboli occur within the first 2 to 4 weeks of antimicrobial therapy. The rate of embolic events drops dramatically during the first 2 weeks of successful antibiotic therapy, from 13 to .2 embolic events per 1000 patient-23days. In general, mitral vegetations, regardless of size, are associated with higher rates of embolization (25 per cent) than aortic vegetations (10 per cent). The highest embolic rate (37 percent) has been seen in the subset of patients with mitral vegetations attached to the anterior rather than the posterior mitral leaflet and with vegetation size > 1 cm in diameter. Staphylococcal or fungal IE appears to carry a high risk of embolization, i.e., independent of vegetation size. Large vegetations independently predict embolic events only in the setting of streptococcal IE. The embolic event rate among patients with IE and increasing vegetation size was twice that of patients with static or decreasing vegetation size over 4 to 8 weeks of therapy.
The indications for surgery for persistent vegetation after systemic embolization are:
1) Anterior mitral leaflet vegetation, particularly with size > 10 mm
2) One or more embolic events during first 2 weeks of antimicrobial therapy
3) Two or more embolic events during or after antimicrobial therapy
4) Increase in vegetation size after 4 weeks of antimicrobial therapy
Periannular Extension of Infection
Occur in 10 per cent to 40 per cent of all native-valve IE, and complicates aortic IE more commonly than mitral or tricuspid IE. Periannular infection is of even greater concern with prosthetic-valve IE, occurring in 56 per cent to 100 per cent of patients. Perivalvular abscesses are particularly common with prosthetic valves because the annulus, rather than the leaflet, is the usual primary site of infection. In native aortic-valve IE, this generally occurs through the weakest portion of the annulus, which is near the membranous septum and atrioventricular node.
Clinical parameters for the diagnosis of perivalvular extension in a patient with IE who is taking adequate antibiotics are:
• Persistent bacteremia or fever
• Recurrent emboli
• Heart block
• CHF
• New pathological murmur
Only aortic-valve involvement and recent IVDA have been prospectively identified as independent risk factors for perivalvular abscess. On ECG, new atrioventricular block has an 88 per cent positive predictive value for abscess formation but has a low sensitivity (45 per cent).The sensitivity of TTE to detect perivalvular abscess is low (18 per cent to 63 per cent in prospective and retrospective studies, respectively). TEE improves the sensitivity for defining periannular extension of IE (76 per cent to 100 per cent) while retaining excellent specificity (95 per cent) and positive and negative predictive values (87 per cent and 89 per cent, respectively).
When it is combined with spectral and color Doppler techniques, TEE can demonstrate the distinctive flow patterns of fistulae and pseudoaneurysms and can rule out communications from unruptured abscess cavities. Surgery for patients with perivalvular extension of IE directed toward eradication of the infection as well correction of hemodynamic abnormalities. Drainage of abscess cavities, excision of necrotic tissue, and closure of fistulous tracts often accompanies valve-replacement surgery. Human aortic homografts, when available, can be used to replace the damaged aortic valve as well as to reconstruct the damaged aorta. Those pts who do not have heart block, echocardiographic evidence of progression of abscess during therapy, valvular dehiscence, or insufficiency can be managed with out surgical intervention. Such patients should be monitored closely with serial TEE, and TEE should be repeated intervals of 2, 4, and 8 weeks after completion of antimicrobial therapy.
Splenic Abscess
Splenic infarction is a common complication of left-sided IE (40 per cent of cases). Only 5 per cent of patients with splenic infarction will develop splenic abscess. This infection develops via 1 of 2 mechanisms Bacteremic seeding of a bland infarction, created via splenic artery occlusion by embolized vegetations, or direct seeding of the spleen by an infected embolus also originating from an infected valvular vegetation. Viridans streptococci and S aureus each account for 40 per cent of cases in which splenic abscess cultures are positive, whereas the enterococci account for 15 per cent of cases. Aerobic Gram-negative bacilli and fungi are isolated in, 5 per cent of cases. Clinical splenomegaly, present in up to 30 per cent of cases of IE, is not a reliable sign of
splenic infarction or abscess. Splenic infarction delineated by imaging techniques is often asymptomatic Back, left-flank, or left-upper-quadrant pain or abdominal tenderness, when present, may be associated with either splenic infarction or abscess. Splenic rupture with hemorrhage is a rare complication of infarction. Persistent or recurrent bacteremia, persistent fever, or other signs of sepsis are suggestive of splenic abscess, Abdominal CT or MRI appear to be the best tests for diagnosis of splenic abscess, with sensitivities and specificities of 90 per cent to 95 per cent. On ultrasonography, a sonolucent lesion suggests abscess. Infarcts are generally associated with clinical and radiographic improvement during appropriate antibiotic therapy.
Ongoing sepsis, recurrent positive blood cultures, and persistence or enlargement of splenic defects CT or MRI suggest splenic abscess, which responds poorly to antibiotic therapy alone.Definitive treatment is splenectomy with appropriate antibiotics. Percutaneous drainage or aspiration of splenic abscess is an alternative to splenectomy for the patient who is a poor surgical candidate. Splenectomy should be performed before valve-replacement surgery because of the risk of infection of the valve prosthesis as a result of the bacteremia from abscess.
Mycotic Aneurysms
They result from septic embolization of vegetations to the arterial vasa vasorum or the intraluminal space, with subsequent spread of infection through the intima and outward through the vessel wall. Arterial branching points favour the impaction of emboli and are the most common sites of MA development. MAs due to IE occur most frequently in the intracranial arteries, followed by visceral arteries and arteries of the lower and upper extremities.
Intra Cranial Mycotic Aneurysms
The reported occurrence of ICMAs is 1.2 per cent to 5 per cent of cases. Streptococci and S.aureus account for 50 per cent and 10 per cent of cases, respectively, and are seen with increased frequency among IVDA patients with IE. The distal middle cerebral artery branches are most often involved, especially the bifurcations. ICMAs are multiple in 20 per cent of cases.Mortality rates are similar for multiple or single distal ICMAs. The overall mortality rate among IE patients with ICMAs is 60 per cent. Among those without rupture, the mortality rate is 30 per cent; this approaches 80 per cent if rupture occurs. Clinical presentation is variable Headache,altered sensorium, FND, SAH or IVH. CSF is sterile and contains erythrocytes, leucocytes and elevated protein. Imaging procedures to detect ICMAs are indicated in IE patients with localized or severe headaches, “sterile” meningitis, or focal neurological signs. Contrast-enhanced CT may provide useful initial information. This technique has a 90 per cent to 95 per cent sensitivity for intracerebral bleed and may thus indirectly identify the location of the MA. Magnetic resonance angiography is a promising new technique for the detection of ICMAs, although its sensitivity for aneurysms smaller than 5 mm is inferior to conventional 4-vessel cerebral angiography.
Conventional angiography remains the diagnostic imaging of choice. ICMAs may heal with medical therapy: ICMAs resolved between an initial and follow-up angiogram in 52 per cent of patients treated with effective antibiotic therapy. A decrease in ICMA size was seen in an additional 29 per cent. In 19 per cent of patients, however, the ICMA increased in size by the time of the second angiogram, and a new ICMA was discovered in 10 per cent. Currently, there are no data that precisely identify at risk for imminent rupture, and decisions concerning medical versus surgical therapy must be individualized. It is generally felt that a Single ICMA distal to the first bifurcation of a major artery (e.g., middle cerebral artery) and Multiple ICMAs should be monitored with frequent serial angiograms and excised promptly if the aneurysm enlarges or bleeds.
Extra Cranial MAs
Intrathoracic or intra-abdominal MAs are often asymptomatic until leakage or rupture occurs.Most extracranial MAs (ECMAs) will rupture if not excised. The appearance of a tender, pulsatile mass in a patient with IE should suggest an ECMA. Hematemesis, hematobilia, and jaundice suggest rupture of a hepatic artery MA; Arterial hypertension and hematuria suggest rupture of a renal MA; Massive bloody diarrhea suggests the rupture of an ECMA into the small or large bowel. Proximal and distal ligation with excision of all infected material and revascularisation with interposed vascular grafts or autologous venous grafts is ideal.Mortality among patients with IE and ECMA is high, which is attributable to suture line infection with vessel or graft rupture.
Anticoagulation Issues
Anticoagulation is contraindicated in native-valve endocarditis because of the risk of intracerebral hemorrhage. Patients with prosthetic valve endocarditis who normally take maintenance anticoagulation, however, are usually maintained on anticoagulant therapy during treatment of IE, provided there is no evidence of cerebral events.
Surgical Treatment of Infective Endocarditis
Cardiac surgical intervention has an increasingly important role in the treatment of intracardiac complications of endocarditis. Retrospective data suggest that mortality is unacceptably high when these complications are treated with antibiotics alone, whereas mortality is reduced when treatment combines antibiotics and surgical intervention.It encompasses both radical valve replacement and more conservative vegetectomy and valve repairs. Surgery is necessary in 25–30 per cent of cases during acute infection, and in 20–40 per cent in later phases. The final outcome has little relation to the duration of previous antibiotic therapy. Results of studies on surgery for active infective endocarditis indicate mortality rates of 8–16 per cent, with actuarial survival at 5 years of 75–76 per cent and at 10 years of 61 per cent.
Cardiac Surgery in Patients with Infective Endocarditis Absolute Indications
1) Moderate to severe congesive heart failure due to valve dysfunction.
2) Unstable prosthesis.
3) Unconrolled infection despite optimal antimicrobial therapy.
4) Unavailable effective antimicrobial therapy; endocarditis due to fungi, Brucellae,pseudomonas aeruginosa (aortic or mitral valves).
5) Staphylococcus aureus PVE with an intracardiac complication.
6) Relapse of PVE after optimal therapy.
Relative Indications (Surgery commonly required for optimal outcome)
• Perivalvular extension of infection, intracardiac fistula
• Poorly responsive S. aureus NVE (aortic or mitral valves)
• Relapse of NVE after optimal antimicrobial therapy
• Culture-negative NVE or PVE with persistent fever (> 10 d)
• Large (> 10 mm diameter) hypermobile vegetation (with or without prior arterial embolus)
• Endocarditis due to highly antibiotic resistant enterococci.
Mortality Rates
• NVE – 16 –27 per cent
• PVE - Early - 50-60 per cent
Late - 33 – 45 per cent
• Treated NVE – survival is 88 per cent at 5 years and 81 per cent at 10 yrs
• Treated PVE – 50 –80 per cent at 4 – 6 years.
Mortality rates associated with various organisms are:
• Viridans streptococci – 4-16 per cent
• Enterococci - 15-25 per cent
• S.aureus – 25-47 per cent
• C.burnetti- 5-37 per cent
• P.aeruginosa and Fungi - > 50 per cent
Death due to IE has been a/w:
• Old age > 65 yrs
• CHF
• Aortic valve infection
• Renal failure
• Neurological complications
Relapse and Recurrence
Relapse of infective endocarditis usually occurs within two months of the discontinuation of antimicrobial therapy. The relapse rate for patients with native-valve endocarditis caused by penicillin-susceptible viridans streptococcus who have been treated with one of the recommended courses of therapy is generally less than 2 per cent.The relapse rate for patients with enterococcal native-valve endocarditis after standard therapy is 8 to 20 per cent. Among patients with infective endocarditis caused by Staph.aureus,
Enterobacteriaceae, or fungi, treatment failure often occurs during the primary course of therapy.Positive culture at the time of valve-replacement surgery, particularly in patients with staphylococcal endocarditis, is a risk factor for subsequent relapse. The relapse rate in prosthetic-valve endocarditis is approximately 10 to 15 per cent, and relapse of infection may be an indication for combined medical and surgical therapy. Recurrence rate of NVE and PVE is around 4.5 – 7 per cent. In IVDA recurrent IE is around 43 per cent.
• Embolic events – Coronary, Cerebral, renal, visceral, pulmonary
• Periannular extension of abscess
• Arrythmia development – New onset heart block
• Prosthetic valve dysfunction
• Metastatic infection
• Persistent bacteremia or Fungemia
• Mycotic aneurysms
• Renal failure
Congestive Heart Failure
In native-valve IE, acute CHF occurs more frequently in aortic-valve infections (29 per cent) than with mitral (20 per cent) or tricuspid disease (8 per cent). CHF may develop acutely from:
• Perforation of a native-or bioprosthetic-valve leaflet,
• Rupture of infected mitral chordae,
• Valve obstruction from bulky vegetations,
• Sudden intracardiac shunts from fistulous tracts or prosthetic dehiscence. CHF may also develop more insidiously, despite appropriate antibiotics, as a result of a progressive worsening of valvular insufficiency and ventricular dysfunction.
• CHF in IE, irrespective of the course or mechanism, signifies a grave prognosis with medical therapy alone and is also the most powerful predictor of poor outcome with surgical therapy.
• The decision to operate on the patient with IE is driven primarily by the severity of CHF.Medical and surgical management decisions can be guided by echocardiographic detection of abscesses, fistulae, prosthetic dehiscence, obstructive vegetations, or flail leaflets, none of which will resolve with medical therapy alone. Delaying surgery to the point of frank ventricular decompensation dramatically increases operative mortality, from 6 per cent to 11 per cent for patients without CHF and 17 per cent to 33 per cent for patients with CHF.
Poor surgical outcome is predicted by preoperative New York Heart Association class III or IV CHF, renal insufficiency, and advanced age. In any patient, a decision to delay surgery to extend pre-operative antibiotic treatment carries with it the risk of permanent ventricular dysfunction.The incidence of reinfection of newly implanted valves in patients with active IE has been estimated to be 2 per cent to 3 per cent, far less than the mortality rate for uncontrolled CHF.
Risk of Embolization
Systemic embolization occurs in 22 per cent to 50 per cent of cases of IE. Emboli often involve major arterial beds, including lungs, coronary arteries, spleen, bowel, and extremities. Up to 65 per cent of embolic events involve the central nervous system, and 90 per cent of central nervous system emboli lodge in the distribution of the middle cerebral artery. The highest incidence of embolic complications is seen with aortic- and mitral-valve infections and in IE due to S aureus and Candida species and HACEK and Abiotrophia organisms. Emboli can occur before diagnosis, during therapy, or after therapy is completed, although most emboli occur within the first 2 to 4 weeks of antimicrobial therapy. The rate of embolic events drops dramatically during the first 2 weeks of successful antibiotic therapy, from 13 to .2 embolic events per 1000 patient-23days. In general, mitral vegetations, regardless of size, are associated with higher rates of embolization (25 per cent) than aortic vegetations (10 per cent). The highest embolic rate (37 percent) has been seen in the subset of patients with mitral vegetations attached to the anterior rather than the posterior mitral leaflet and with vegetation size > 1 cm in diameter. Staphylococcal or fungal IE appears to carry a high risk of embolization, i.e., independent of vegetation size. Large vegetations independently predict embolic events only in the setting of streptococcal IE. The embolic event rate among patients with IE and increasing vegetation size was twice that of patients with static or decreasing vegetation size over 4 to 8 weeks of therapy.
The indications for surgery for persistent vegetation after systemic embolization are:
1) Anterior mitral leaflet vegetation, particularly with size > 10 mm
2) One or more embolic events during first 2 weeks of antimicrobial therapy
3) Two or more embolic events during or after antimicrobial therapy
4) Increase in vegetation size after 4 weeks of antimicrobial therapy
Periannular Extension of Infection
Occur in 10 per cent to 40 per cent of all native-valve IE, and complicates aortic IE more commonly than mitral or tricuspid IE. Periannular infection is of even greater concern with prosthetic-valve IE, occurring in 56 per cent to 100 per cent of patients. Perivalvular abscesses are particularly common with prosthetic valves because the annulus, rather than the leaflet, is the usual primary site of infection. In native aortic-valve IE, this generally occurs through the weakest portion of the annulus, which is near the membranous septum and atrioventricular node.
Clinical parameters for the diagnosis of perivalvular extension in a patient with IE who is taking adequate antibiotics are:
• Persistent bacteremia or fever
• Recurrent emboli
• Heart block
• CHF
• New pathological murmur
Only aortic-valve involvement and recent IVDA have been prospectively identified as independent risk factors for perivalvular abscess. On ECG, new atrioventricular block has an 88 per cent positive predictive value for abscess formation but has a low sensitivity (45 per cent).The sensitivity of TTE to detect perivalvular abscess is low (18 per cent to 63 per cent in prospective and retrospective studies, respectively). TEE improves the sensitivity for defining periannular extension of IE (76 per cent to 100 per cent) while retaining excellent specificity (95 per cent) and positive and negative predictive values (87 per cent and 89 per cent, respectively).
When it is combined with spectral and color Doppler techniques, TEE can demonstrate the distinctive flow patterns of fistulae and pseudoaneurysms and can rule out communications from unruptured abscess cavities. Surgery for patients with perivalvular extension of IE directed toward eradication of the infection as well correction of hemodynamic abnormalities. Drainage of abscess cavities, excision of necrotic tissue, and closure of fistulous tracts often accompanies valve-replacement surgery. Human aortic homografts, when available, can be used to replace the damaged aortic valve as well as to reconstruct the damaged aorta. Those pts who do not have heart block, echocardiographic evidence of progression of abscess during therapy, valvular dehiscence, or insufficiency can be managed with out surgical intervention. Such patients should be monitored closely with serial TEE, and TEE should be repeated intervals of 2, 4, and 8 weeks after completion of antimicrobial therapy.
Splenic Abscess
Splenic infarction is a common complication of left-sided IE (40 per cent of cases). Only 5 per cent of patients with splenic infarction will develop splenic abscess. This infection develops via 1 of 2 mechanisms Bacteremic seeding of a bland infarction, created via splenic artery occlusion by embolized vegetations, or direct seeding of the spleen by an infected embolus also originating from an infected valvular vegetation. Viridans streptococci and S aureus each account for 40 per cent of cases in which splenic abscess cultures are positive, whereas the enterococci account for 15 per cent of cases. Aerobic Gram-negative bacilli and fungi are isolated in, 5 per cent of cases. Clinical splenomegaly, present in up to 30 per cent of cases of IE, is not a reliable sign of
splenic infarction or abscess. Splenic infarction delineated by imaging techniques is often asymptomatic Back, left-flank, or left-upper-quadrant pain or abdominal tenderness, when present, may be associated with either splenic infarction or abscess. Splenic rupture with hemorrhage is a rare complication of infarction. Persistent or recurrent bacteremia, persistent fever, or other signs of sepsis are suggestive of splenic abscess, Abdominal CT or MRI appear to be the best tests for diagnosis of splenic abscess, with sensitivities and specificities of 90 per cent to 95 per cent. On ultrasonography, a sonolucent lesion suggests abscess. Infarcts are generally associated with clinical and radiographic improvement during appropriate antibiotic therapy.
Ongoing sepsis, recurrent positive blood cultures, and persistence or enlargement of splenic defects CT or MRI suggest splenic abscess, which responds poorly to antibiotic therapy alone.Definitive treatment is splenectomy with appropriate antibiotics. Percutaneous drainage or aspiration of splenic abscess is an alternative to splenectomy for the patient who is a poor surgical candidate. Splenectomy should be performed before valve-replacement surgery because of the risk of infection of the valve prosthesis as a result of the bacteremia from abscess.
Mycotic Aneurysms
They result from septic embolization of vegetations to the arterial vasa vasorum or the intraluminal space, with subsequent spread of infection through the intima and outward through the vessel wall. Arterial branching points favour the impaction of emboli and are the most common sites of MA development. MAs due to IE occur most frequently in the intracranial arteries, followed by visceral arteries and arteries of the lower and upper extremities.
Intra Cranial Mycotic Aneurysms
The reported occurrence of ICMAs is 1.2 per cent to 5 per cent of cases. Streptococci and S.aureus account for 50 per cent and 10 per cent of cases, respectively, and are seen with increased frequency among IVDA patients with IE. The distal middle cerebral artery branches are most often involved, especially the bifurcations. ICMAs are multiple in 20 per cent of cases.Mortality rates are similar for multiple or single distal ICMAs. The overall mortality rate among IE patients with ICMAs is 60 per cent. Among those without rupture, the mortality rate is 30 per cent; this approaches 80 per cent if rupture occurs. Clinical presentation is variable Headache,altered sensorium, FND, SAH or IVH. CSF is sterile and contains erythrocytes, leucocytes and elevated protein. Imaging procedures to detect ICMAs are indicated in IE patients with localized or severe headaches, “sterile” meningitis, or focal neurological signs. Contrast-enhanced CT may provide useful initial information. This technique has a 90 per cent to 95 per cent sensitivity for intracerebral bleed and may thus indirectly identify the location of the MA. Magnetic resonance angiography is a promising new technique for the detection of ICMAs, although its sensitivity for aneurysms smaller than 5 mm is inferior to conventional 4-vessel cerebral angiography.
Conventional angiography remains the diagnostic imaging of choice. ICMAs may heal with medical therapy: ICMAs resolved between an initial and follow-up angiogram in 52 per cent of patients treated with effective antibiotic therapy. A decrease in ICMA size was seen in an additional 29 per cent. In 19 per cent of patients, however, the ICMA increased in size by the time of the second angiogram, and a new ICMA was discovered in 10 per cent. Currently, there are no data that precisely identify at risk for imminent rupture, and decisions concerning medical versus surgical therapy must be individualized. It is generally felt that a Single ICMA distal to the first bifurcation of a major artery (e.g., middle cerebral artery) and Multiple ICMAs should be monitored with frequent serial angiograms and excised promptly if the aneurysm enlarges or bleeds.
Extra Cranial MAs
Intrathoracic or intra-abdominal MAs are often asymptomatic until leakage or rupture occurs.Most extracranial MAs (ECMAs) will rupture if not excised. The appearance of a tender, pulsatile mass in a patient with IE should suggest an ECMA. Hematemesis, hematobilia, and jaundice suggest rupture of a hepatic artery MA; Arterial hypertension and hematuria suggest rupture of a renal MA; Massive bloody diarrhea suggests the rupture of an ECMA into the small or large bowel. Proximal and distal ligation with excision of all infected material and revascularisation with interposed vascular grafts or autologous venous grafts is ideal.Mortality among patients with IE and ECMA is high, which is attributable to suture line infection with vessel or graft rupture.
Anticoagulation Issues
Anticoagulation is contraindicated in native-valve endocarditis because of the risk of intracerebral hemorrhage. Patients with prosthetic valve endocarditis who normally take maintenance anticoagulation, however, are usually maintained on anticoagulant therapy during treatment of IE, provided there is no evidence of cerebral events.
Surgical Treatment of Infective Endocarditis
Cardiac surgical intervention has an increasingly important role in the treatment of intracardiac complications of endocarditis. Retrospective data suggest that mortality is unacceptably high when these complications are treated with antibiotics alone, whereas mortality is reduced when treatment combines antibiotics and surgical intervention.It encompasses both radical valve replacement and more conservative vegetectomy and valve repairs. Surgery is necessary in 25–30 per cent of cases during acute infection, and in 20–40 per cent in later phases. The final outcome has little relation to the duration of previous antibiotic therapy. Results of studies on surgery for active infective endocarditis indicate mortality rates of 8–16 per cent, with actuarial survival at 5 years of 75–76 per cent and at 10 years of 61 per cent.
Cardiac Surgery in Patients with Infective Endocarditis Absolute Indications
1) Moderate to severe congesive heart failure due to valve dysfunction.
2) Unstable prosthesis.
3) Unconrolled infection despite optimal antimicrobial therapy.
4) Unavailable effective antimicrobial therapy; endocarditis due to fungi, Brucellae,pseudomonas aeruginosa (aortic or mitral valves).
5) Staphylococcus aureus PVE with an intracardiac complication.
6) Relapse of PVE after optimal therapy.
Relative Indications (Surgery commonly required for optimal outcome)
• Perivalvular extension of infection, intracardiac fistula
• Poorly responsive S. aureus NVE (aortic or mitral valves)
• Relapse of NVE after optimal antimicrobial therapy
• Culture-negative NVE or PVE with persistent fever (> 10 d)
• Large (> 10 mm diameter) hypermobile vegetation (with or without prior arterial embolus)
• Endocarditis due to highly antibiotic resistant enterococci.
Mortality Rates
• NVE – 16 –27 per cent
• PVE - Early - 50-60 per cent
Late - 33 – 45 per cent
• Treated NVE – survival is 88 per cent at 5 years and 81 per cent at 10 yrs
• Treated PVE – 50 –80 per cent at 4 – 6 years.
Mortality rates associated with various organisms are:
• Viridans streptococci – 4-16 per cent
• Enterococci - 15-25 per cent
• S.aureus – 25-47 per cent
• C.burnetti- 5-37 per cent
• P.aeruginosa and Fungi - > 50 per cent
Death due to IE has been a/w:
• Old age > 65 yrs
• CHF
• Aortic valve infection
• Renal failure
• Neurological complications
Relapse and Recurrence
Relapse of infective endocarditis usually occurs within two months of the discontinuation of antimicrobial therapy. The relapse rate for patients with native-valve endocarditis caused by penicillin-susceptible viridans streptococcus who have been treated with one of the recommended courses of therapy is generally less than 2 per cent.The relapse rate for patients with enterococcal native-valve endocarditis after standard therapy is 8 to 20 per cent. Among patients with infective endocarditis caused by Staph.aureus,
Enterobacteriaceae, or fungi, treatment failure often occurs during the primary course of therapy.Positive culture at the time of valve-replacement surgery, particularly in patients with staphylococcal endocarditis, is a risk factor for subsequent relapse. The relapse rate in prosthetic-valve endocarditis is approximately 10 to 15 per cent, and relapse of infection may be an indication for combined medical and surgical therapy. Recurrence rate of NVE and PVE is around 4.5 – 7 per cent. In IVDA recurrent IE is around 43 per cent.
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