Valvulopathies and infective endocarditis (IE)
Anatomical reminder:
Heart valves are elastic, non-contractile structures that prevent the backflow of blood from one heart chamber to another. There are four of them:
- the aortic valve, located between the left ventricle and the ascending aorta ;
- the mitral valve , between the left atrium and ventricle, composed of a small valve and a large valve. The latter are connected by cords (elastic fibers) to the heart muscle via the pillars;
- the tricuspid valve between the right atrium and the right ventricle;
- and the pulmonary valve between the right ventricle and the pulmonary artery.
Normally, the heart’s valves help control the flow of blood through the heart’s chambers.
Epidemiology :
An American study shows that nearly 2% of the adult population has valvulopathy, the most common being mitral insufficiency.
This prevalence increases with age with a prevalence of between 10 and 15% in patients over 75 years of age 1 , and is expected to continue to increase with the aging of the population.
Valvulopathy occurs when one or more heart valves do not work properly.
Cause :
In Western countries, the frequency of rheumatic valvulopathies is decreasing in favor of an increase in degenerative valvulopathies.
While in developing countries, rheumatic disease predominates.
Various valvular disorders;
In case of valvulopathy, it may happen that a valve does not close correctly (or is incompetent) and this is called insufficiency or leakage or does not open completely and this is called stenosis.
Sometimes the valve balloons back into the previous heart chamber (a phenomenon called valve prolapse).
Any heart valve can become stenotic or insufficient (or incompetent) and cause hemodynamic changes long before symptoms. These failures affect blood flow and can force the heart to work harder with each beat.
Most often , valvular stenosis or insufficiency affects one valve in isolation , but polyvalvular disorders can coexist and a valve can be both stenosing and insufficient and we speak of disease (mitral, aortic, tricuspid, etc.).
Heart valve disorders include
- Aortic insufficiency : Insufficiency is due to the valves not sealing properly, causing blood to flow back from the aorta into the left ventricle during diastole.
- Aortic stenosis: Aortic stenosis is the reduction in the surface area of the aortic valve creating an obstacle to the ejection of blood from the left ventricle into the aorta during systole.
- Mitral regurgitation : Insufficiency of the mitral valve causing blood flow from the left ventricle to the left atrium during ventricular systole.
- Mitral stenosis : is a narrowing of the mitral orifice that blocks blood flow from the left atrium to the left ventricle.
- Valve prolapse : mitral: ballooning of the mitral valves into the left atrium during systole
- Pulmonary valve insufficiency or reflux : failure of the valve to seal, causing blood to flow back from the pulmonary artery into the right ventricle during diastole
- Pulmonary stenosis (lung narrowing) : narrowing of the pulmonary outflow tract resulting in obstruction of blood flow from the right ventricle to the pulmonary artery during systole
- Tricuspid regurgitation : loss of sealing of the tricuspid valve resulting in blood flowing back from the right ventricle to the right atrium during systole
- Tricuspid stenosis : A narrowing of the tricuspid orifice that obstructs flow from the right atrium to the right ventricle
Infectious endocarditis (IE):
Definition :
It is a septicemia caused by bacteria or yeast grafting onto the endocardium of a healthy or pathological heart.
Interest of the question:
Etiopathogenic:
It includes 04 elements:
Underlying heart disease except for acute AEs.
The front door.
The land of occurrence.
Infectious agent.
Anapathomogic:
1Endocardial lesions:
They are mainly represented by vegetations and ulcerations.
2Arterial lesions: we have bacterial embolisms (of the cerebral vessels, limbs, spleen) and so-called mycotic aneurysms.
Severity:
Indeed, the severity of IE persists despite advances in medical and surgical treatment. It is fatal in 6% to 25% of subacute IEs and 30% to 50% of acute IEs.
Efforts should focus on early diagnosis and treatment of the disease.
Prevention:
It remains the best weapon to prevent the occurrence of IE. It is well codified according to the level of risk.
Clinical manifestations (subacute Osler EI):
This is the most common and represents 70% of IEs.
Circumstances of discovery:
Fever is a major sign, it is constant.
Headaches, arthromyalgia.
Hemiplegia or transient deficit accident.
Cerebral or limb arterial embolism, cerebromeningeal hemorrhage, intracerebral hematoma.
Pain in the left hypochondrium.
Clinical examination:
Infectious syndrome:
Fever is the major symptom and is almost always present.
Splenomegaly is present in 20% to 40% of cases and can be painful.
Any fever in a subject with a heart murmur should raise the diagnosis of IE and blood cultures should be performed.
Cardiac signs:
The appearance or modification of a heart murmur is the second sign of IE, especially suggestive when it is a regurgitation murmur.
The association of fever with heart murmur has great diagnostic value.
Other cardiac manifestations are rarely inaugural but can occur during the course.
Heart failure in all its forms should raise the diagnosis when it is associated with fever.
More rarely, coronary or pericardial involvement.
Extracardiac manifestations:
Skin signs:
Osler’s false whitlow: very specific, these are reddish nodules on the pulp.
Janeway erythema: early painless palmoplantar.
Frequent and late digital clubbing should suggest the diagnosis of IE when associated with fever.
Vascular purpura.
Neurological manifestations:
Cerebral infarctions – cerebral hemorrhages. They have a poor prognostic value.
Paraclinical examinations:
1) orientation examinations:
They are nonspecific and may be absent.
FNS: -normochromic normocytic anemia.
-inconstant hyperleukocytosis.
Increased ESR and CRP.
A polyclonal hypergamma.
The presence of rheumatoid factors FR, immune complexes CI, cryoglobulinemia.
Hematuria-proteinuria.
2) The 02 decisive exams:
Blood cultures:
This is the first reference examination in EI. 03 – 04 blood cultures performed at 01 hour intervals, before any antibiotic therapy, at fever peaks or chills.
In case of antibiotic treatment, a therapeutic window must be carried out before blood cultures.
Culture is carried out in aerobic and anaerobic environments.
It takes 01 to sometimes more than 03 weeks to isolate bacteria that are difficult to grow, germs of the HACEK group, deficient streptococci and yeasts.
Cardiac ultrasound:
It has a triple interest:
Diagnosis: combined with blood cultures allows the diagnosis to be confirmed with a sensitivity of 90%. The main sign of endocarditis is vegetation.
Prognosis:
By assessing the severity of vascular damage and the hemodynamic impact, the mobility of the vegetations.
Therapeutic:
Element of therapeutic decision and to specify the time and type of surgery.
The positive diagnosis:
It is based on the durack criteria:
The EI is certain in the presence of 02 major criteria or 1 major criterion and 03 minor criteria.
The main criteria:
*Positive blood cultures:
02 blood cultures positive for non-groupable streptococcus, streptococcus bovis, HACEK group bacteria or in the absence of an identified focus, staphylococcus or enterococcus.
Persistently positive blood cultures for the same organism.
*Endocardial involvement:
By the presence of clinical and ultrasound signs.
Clinical:
New-onset valvular leak murmur.
Vegetation.
Abscess.
New periprosthetic leak.
Minor criteria:
Predisposing heart disease or drug addiction.
Fever above 38ºc.
Vascular phenomena (arterial embolism, mycotic aneurysm, pulmonary infarction, conjunctival hemorrhage, cerebral).
Immunological phenomena: glomerulonephritis, Osler’s nodule, Roth’s spot).
Minor microbiological criteria: positive blood cultures without entering into the definition of the major criterion positive serology for an organism responsible for endocarditis.
Minor ultrasound criteria: ultrasound compatible without entering into the definition of the major criterion.
Once the diagnosis of IE is made, the search for and treatment of the entry point is systematic.
The front door (PE):
It is only formally identified in 50% of cases.
The oral-dental entry point is by far the most frequent; the germ in question is streptococcus, transmitted most often during dental care accompanied by bleeding.
PE ENT (otitis – sinusitis).
Genitourinary (surgery): enterococcus or BGN.
Digestive common in the elderly: streptococcus bovis or enterococcus.
Cutaneous: rarer staphylococcus aureus or epidermidis.
Iatrogenic PE: increasingly frequent catheter pacemakers cardiac surgery.
Complications of EI:
1heart complications:
Heart failure – coronary embolisms – cardiac conduction disorders – supraventricular and ventricular arrhythmias – septic pericarditis.
Extracardiac complications:
Neurological stroke (CVA).
Renal: renal failure; renal infarction.
Splenic: infarction, abscess.
Peripheral mycotic arterial embolisms and aneurysms.
Osteoarticular: osteoarthritis.
Special forms:
EI of the elderly subject:
It is clearly increasing due to the increase in life expectancy. It occurs on degenerative valvulopathy or on intracardiac material.
The hospital mortality rate is higher compared to young adults.
EI on valve prosthesis:
It represents more than 20% of AEs. We contrast early AEs, appearing 02 months after the intervention which are very serious (virulence of the germ, heart already operated), with late AEs of the order of 0.5% patient/year.
They are serious due to embolic complications and surgical difficulties.
EI of drug addicts:
It is increasing. They are observed in young subjects. The tricuspid localization is usual, the left valves are as affected as the tricuspids.
Staphylococcus is responsible for 65% of these AEs. The prognosis for tricuspid involvement alone is good.
Evolution and prognosis:
It is variable, it depends on the type of germ, the precocity of the diagnosis, the existence of heart failure and the terrain.
Differential diagnosis:
Collagenosis such as systemic lupus.
In case of pre-existing heart disease:
Positive blood cultures: eliminating contamination.
Negative blood cultures: rule out cardiac rheumatism; thromboembolic disease, pulmonary superinfection.
Following heart surgery, eliminate a parietal infection.
Valvulopathies and infective endocarditis (IE)
Treatment:
Aim:
Its aim is to eradicate the infection and prevent cardiac and extracardiac complications.
Management of extensive and destructive cardiac lesions and extracardiac focal complications.
Means:
Hospitalization.
Medical treatment:
It is based on the combination of bactericidal antibiotics which must be administered early, most often by prolonged intravenous route at a high dose.
Treatment must be adapted and prolonged.
Surgical treatment: this is valve replacement.
Directions:
| STREPTOCOCCUS VIRIDANS OR BOVIS | PENNI G OF CHOICE + AMINOSIDE GENTAMYCIN 20 M- 30 M/D 3MG/KG/D PD 4WEEK PD 02WEEK IF ALLERGY TO PENNICILLIN: CEPHALOSPORIN, VANCOMYCIN 30MG/KG/D WITHOUT EXCEEDING 2GR/D IF EI ON PROSTHESIS: DURATION OF TRT 6TH IF STREPTOCOCCUS NOT GROUPABLE: SAME AS ENTEROCOCCUS TRT |
| STREPTOCOCCUS PYOGENIS PNEUMONIA GROUP ABG | SURGERY IS FREQUENTLY REQUIRED GROUP A STREPTO: PENNI G PD 4 WEEKS PENNI-RESISTANT PNEUMO: CEFTRIAXONE + VANCOMYCIN BCG GROUP STREPTO: PENNI GA HIGH DOSE PD 4 WEEKS + GENTAMYCIN 05 DAYS |
| ENTEROCOCCUS | PENNI GA HIGH DOSE OR AMPICILLIN 12 G/D PD 6 WEEKS GENTAMYCIN PD 02 WEEKS OTHERWISE VANCOMYCIN + AMINOSIDES |
| STAPHYLOCOCCUS | ON NATIVE VALVES: NON-METHICILLIN-RESISTANT: OXACILLIN 2G/4H OR CEFAZOLINE 2G/8H PD 4-6WK METHICILLIN-RESISTANT STAPH: VANCOMYCIN 30 MG/KG/DAY ON PROSTHESIS: TRT OF AT LEAST 6WK RIFAMPICIN -VANCOMYCIN METHYL SENSITIVE STAPH: OXACILLIN -RIFAMPICIN – AMINOSIDE |
Systematic treatment of PE:
Indication for surgical treatment:
Heart failure resistant to medical treatment.
EI is emboligenic.
When the infection resists antibiotic treatment.
Treatment monitoring:
Disappearance of fever and inflammatory syndrome are necessary but not sufficient elements to confirm recovery.
Blood cultures should become negative promptly after treatment initiation and remain negative at the end of treatment.
Preventive treatment:
Its importance stems from all the elements previously mentioned. It consists on the one hand of the eradication of all the foci likely to be at the origin of an IE and on the other hand of the judicious prescription of an antibiotic which will prevent possible bacteremia during medical-surgical procedures.
Identification of patients at risk is necessary.
Heart diseases associated with a risk of IE:
1 IE prophylaxis is recommended :
High risk:
Valve prosthesis
History of EI
Cyanotic congenital heart disease
Surgical shunts
Medium risk:
Other congenital heart diseases
Acquired valvulopathies
Hypertrophic cardiomyopathy
Mitral valve prolapse with leak and/or valve thickening
2 IE prophylaxis not recommended
Low risk:
Atrial communication
Left right shunt operated
Coronary artery bypass grafting
Mitral valve prolapse without leakage with thin valves
Paces makers
Actions justifying prophylaxis:
Esophageal dilatations, sclerosis of esophageal varices
Colonoscopy with biopsies
Intratracheal intubation
Urinary tract surgery
Intervention on infected skin tissue.
Some IEs are the consequence of a periodontal infection responsible for spontaneous bacteremia.
Their prophylaxis consists of rigorous oral hygiene.
Recommendations for at-risk individuals are as follows:
Root treatment: it is done under three conditions.
In one session.
Performed under sterile operating field.
Entire endodontium easily accessible.
-scaling is possible; however, implants and periodontal surgery are not recommended.
-in patients at high risk of IE:
Pulp diseases, periodontal diseases and trauma require extraction.
Prostheses on teeth to be pulped, implants and periodontal surgery are strongly discouraged.
-when preparing for valve replacement surgery, patients fall into the high-risk category for IE. Only teeth with pulp or perfect periodontal treatment without Desmontal enlargement dating back more than one year and with intact periodontium would be retained.
In all other situations, extraction will be performed at least 15 days before surgery.
-With the exception of superficial caries and bloodless supragingival prosthetic preparations on pulped teeth which do not require any special precautions, all authorized procedures must be performed under antibiotic prophylaxis and immediate preoperative local asepsis.
Valvulopathies and infective endocarditis (IE)
Antibiotic prophylaxis of IE during dental care and upper respiratory tract procedures – outpatient care.
| PRODUCT | DOSAGE – ROUTE OF ADMINISTRATION SINGLE TAKEN WITHIN 1 HOUR PRECEDING THE PROCEDURE | |
| NO ALLERGY TO B LACTAMS | AMOXICILLIN | 3 GR PER OS |
| ALLERGY TO B LACTAMS | CLINDAMYCIN OR PRISTINAMYCIN | 600 MG PERS OR 1 GR PEROS |
Antibiotic prophylaxis of IE during dental care and procedures involving the upper respiratory tract – general anesthesia
| PRODUCT | DOSAGE AND ROUTE OF ADMINISTRATION | |
| AMOXICILLIN | BEFORE THE HOUR PRECEDING THE GESTURE | AFTER (6 HOURS LATER) |
| 02 GR IV PERFUSION in 30 MIN in the hour preceding the procedure | 1 GR PER OS | |
| VANCOMYCIN OR TERICOPLAMIN | 1 GR HOURLY INFUSION 400 MG DIRECT IV within the hour preceding the procedure | NO 2ND DOSE |
If the treatment requires several sessions, they should be spaced out if possible by at least ten days if the practitioner uses antibiotic prophylaxis .
Valvulopathies and infective endocarditis (IE)
Conclusions:
IE is a serious disease, early diagnosis and treatment are necessary to reduce morbidity and mortality.
The real treatment is prophylactic treatment in at-risk populations.
Reference :
– Pr François Delahaye, Dr André Mercusot, Dr Marie Célard et al. Infectious endocarditis. Practitioner’s review 2005:55 I-7-Q80.
-Jp. Delahaye, R Loire, F Delahaye, F Vandenesch, B Hoen. Infectious endocarditis. EMC 11-013-B-10.
-Prevention of Bacterial Endocarditis-Tables, scientific statement.
-Gilbert Habib, Gérald ROUL. Infectious endocarditis. July 2001.
Dental alvulsions and prevention of infective endocarditis: current recommendations Internal Medicine Department, Beaujon Hospital, 100, boulevard du Général-Leclerc, 92110 Clichy, France Received March 13, 2007; accepted August 3, 2007
Valvulopathies and infective endocarditis (IE)
Wisdom teeth can be painful if they are misplaced.
Composite fillings are aesthetic and durable.
Bleeding gums can be a sign of gingivitis.
Orthodontic treatments correct misaligned teeth.
Dental implants provide a permanent solution for missing teeth.
Scaling removes tartar and prevents gum disease.
Good dental hygiene starts with brushing twice a day.