INFECTIOUS ENDOCARDITIS
- DEFINITION
It is an infection of one or more heart valves of bacterial origin. The germs most often involved are Streptococcus; Staphylococcus; Gram-negative bacilli and Pneumococcus.
- EPIDEMIOLOGY
Endocarditis is currently affecting increasingly older people. After the disappearance of acute articular rheumatism and rheumatic valvulopathies, other predisposing factors have appeared:
- Drug addiction IV
- Valve prosthesis
- Degenerative valvular sclerosis
- Invasive gestures
- Intracardiac devices
III-PHYSIOPATHOLOGY
1. LESIONS: progressive lesions of increasing severity are described.
- Proliferative lesions by sterile fibrino-platelet deposits
- If bacteremia with adhesion and multiplication of germs
- Development of infected vegetation
- Valvular destruction lesions and ulcerations
2-CONSEQUENCES:
Depending on the stage of the disease, we can have:
- Appearance or worsening of valvulopathy
- Appearance or increase of a murmur
- Heart failure
- Appearance of vegetation causing secondary septic outbreaks
3-HIGH-RISK HEART DISEASES:
Certain heart diseases present a risk of endocarditis such as:
- Mitral insufficiency and stenosis
- Mitral valve prolapse
- Congenital heart disease
- Valve prostheses
4- RISKY ACTIONS:
Invasive procedures are a gateway for germs leading to endocarditis; it is found in half of the cases. These are mainly surgical procedures such as extracorporeal circulation, placement of intravenous catheters, pacemakers, implantable chambers, hemodialysis and dental care.
IV-CLINIC
- Fever :
Its degree and type are variable. It perhaps more readily takes on an undulating aspect that a careful interview should seek to highlight, especially since between the febrile periods there may be phases of almost total apyrexia. This probably explains why the diagnosis of this condition has sometimes been made after a surprisingly long delay. But the fever is sometimes reduced to a simple low fever; it may even only be objectified by taking the temperature every three hours. In fact, very often, it is the prolongation, the tenacity of this fever that worries the patient and leads him to consult.
- The other general signs are clearly in the background:
– a suggestive sign: pallor whose degree classically exceeds that of anemia.
– misleading signs: myalgia and arthralgia which have, in certain cases, led to talk of true “rheumatic forms” of Osler’s disease.
– finally, forms with significant weight loss have been reported which, especially in elderly subjects, can wrongly lead to a diagnosis of latent cancer.
- Heart signs
These are most often murmurs whose organicity will need to be checked in these febrile and anemic subjects. They frequently reflect aortic or mitral valvulopathy, but endocarditis can be grafted onto other heart diseases.
On the electrocardiogram, look for atrioventricular conduction disorders which, if attributable to endocarditis, suggest a septal abscess.
Echocardiography and Doppler can highlight vegetations on the valves but also allow a precise assessment of valvulopathy and even a study of ventricular function.
- Extracardiac signs
Three orders of signs must be sought because their presence has considerable diagnostic value:
– Splenomegaly: its often moderate nature should prompt a long search for it by making the patient breathe well; painful, it could indicate a splenic infarction.
– Skin signs:
Bluish or pinkish nodules, always painful, located on the pulp of the fingers or toes, must be examined systematically. In fact, their fleeting nature makes them above all a sign of interrogation.
Petechial purpura, which develops in bursts, is most often located on the conjunctiva, particularly the lower eyelid, on the oral mucosa (palatine vault), on the skin of the clavicular region, and sometimes on the lower limbs. It is necessary to compare this, at the funduscopy, with the possible existence of shuttle-shaped petechiae alongside whitish Roth spots.
The false whitlow
– Respiratory signs: cough, dyspnea
– Ophthalmic signs: conjunctival purpura
-Neurological signs: cerebral or cerebromeningeal hemorrhages, cerebral abscess
-Rheumatologic signs: arthralgia of the limbs, myalgia
-Renal damage: renal failure due to glomerular damage
V-DIAGNOSTIC
1. Blood cultures
This is the key examination, they are carried out about ten times in three days, preferably at the time of a fever or shivering attack, on aerobic and anaerobic media, on penicillinase if necessary; the blood cultures will be kept in the incubator for at least a month with periodic subcultures because it may be a slowly growing germ.
Identification of the germ: The most frequently encountered are streptococci:
Streptococcus viridans (notably S. sanguis and S. mitis) mainly, but also streptococcus D (S. bovis and enterococcus).
Other germs: meningococcus, pneumococcus, salmonella, brucella, and even yeasts (candida endocarditis).
The seriousness of staphylococcal endocarditis must be emphasized given the frequent resistance of this germ to antibiotics.
2.Biology
Blood count: It reveals moderate hyposideraemic anemia of the inflammatory type, a slight hyperleukocytosis with polynucleosis; a certain degree of monocytosis has sometimes been observed. The platelet count is usually normal.
The sedimentation rate is constantly increased but must be interpreted taking into account the anemia. The protein profile generally shows hypoalbuminemia with hyperalpha2globulinemia.
Immune assessment: This includes the possible presence in the serum of rheumatoid factor (positivity of latex and Waaler-Rose reactions) in about half of the patients seen after an evolutionary period of at least 6 weeks. It would disappear in the majority of cases, in parallel with healing by antibiotic treatment. The presence of circulating immune complexes, cryoglobulins has also been reported.
Other biological signs: renal damage, proteinuria, but especially microscopic hematuria (Addis count) knowing that it is inconstant, late, intermittent (repeat the tests).
3. Finding the front door:
As with any septicemia, it should be the subject of a methodical investigation, especially stomatological (clinical and radiological examination with panoramic incidence supplemented by retrodental incidences), urological (prostate by digital rectal examination, cytobacteriological examination of urine and, at the slightest doubt, ultrasound and/or intravenous urography), gynecological, ENT, cutaneous.
In the case of streptococcus D endocarditis, renal ultrasound and/or intravenous urography should be systematic, as well as endoscopic examination of the digestive tract (especially colonoscopy if Streptococcus bovis) without forgetting ultrasound of the biliary tract.
In some contexts, the entry point is obvious: traumatic maneuvers, prolonged venous catheterization; in the latter case, the catheter must be sent to the bacteriology laboratory to “inoculate” it.
VI-EVOLUTION AND COMPLICATIONS
The evolution is often favorable when the diagnosis is early, allowing early antibiotic therapy on a sensitive germ. The improvement is evident as evidenced by the defervescence and transformation of the general condition, the progressive disappearance of clinical signs, the normalization of the biological syndrome, the negativity of control blood cultures.
Complications: Their risk is present at all times and in all cases.
- Heart failure in subacute bacterial endocarditis is directly related to mutilating lesions: valvular perforations, especially aortic and mitral, ruptures of mitral chordae, and more rarely, perforation of the interventricular septum or the sinus of Valsalva. The evolution of this heart failure can be galloping despite medical treatment.
- Renal complications: (glomerulonephritis, embolisms) the sudden onset of low back pain and macroscopic hematuria immediately suggests the diagnosis of renal infarction, but since antibiotic therapy, this manifestation has become much rarer than subacute segmental and focal or diffuse glomerulopathy that electron microscopy and immunofluorescence studies have shown to be linked to deposits, along the basement membrane, and following a granular type distribution, of immunoglobulins and complement. This glomerulopathy may have a clinical translation or be totally latent. Interstitial nephropathy is also possible. However, it should be emphasized that the evolution of renal manifestations during subacute bacterial endocarditis treated early is very rarely unfavorable.
- Other complications: Cerebral, renal, splenic, pulmonary septic embolisms; neurological complications such as cerebral embolisms or meningitis, and cardiac complications: arrhythmias and conduction disorders
VII- TREATMENT
- Curative medical treatment
The choice, dose, type of combination of antibiotics, duration of treatment will be determined based on the identification of the germ, the antibiogram, and the study of the bactericidal power (MIC) of the antibiotics alone and in combination.
When it comes to viridans streptococcus (mitis, sanguis, and other “non-groupable” streptococci) Penicillin G, 20 million units per day for 4 weeks combined for the first 15 days with an aminoglycoside. Penicillin G can be replaced by amoxicillin, 200 mg/kg/day which has the advantage of being able to be administered orally. In case of allergy to beta-lactams: Vancomycin, 10 mg/kg every 8 hours
Enterococcus: Penicillin G, 30 million combined with gentamicin, for 45 days.
Staphylococcus: Staphylococcus sensitive to methicillin: Oxacillin, 150 mg/kg for 45 days combined with an aminoside for 15 days.
Methicillin-resistant staphylococcus: Vancomycin, 10 mg/kg every 8 hours, for 45 days.
Treatment of the entry point It is essential in all cases, accompanied by antibiotics.
- Surgical treatment
Emergency surgery may be indicated in cases of acute pulmonary edema due to rupture of the mitral chordae or destruction of the aortic sigmoids, for example. This may sometimes be due to a syndrome of valvular obstruction due to a large vegetation.
- Preventive treatment
1) Dental care, ENT procedures (outpatient)
– AMOXICILLIN 3g orally 1 hour before.
–IF ALLERGY TO BETA-LACTAMS: PRISTINAMYCIN 1g per os
2) Dental care, ENT procedures (under AG)
– AMOXICILLIN 2g IV (perf. 30min) 1 H BEFORE 1g orally 6 H after.
– IF ALLERGY TO BETA-LACTAMS: VANCOMYCIN 1g IV (perf. > 60min.) 1 hour before
3) UROGENITAL AND DIGESTIVE INTERVENTIONS
– AMOXICILLIN 2g IV (perf. 30min.) 1 HOUR BEFORE. Then GENTAMICIN 1.5mg/kg IV (perf. 30min.), AMOXICILLIN 1g per os 6 HOURS AFTER
– IF ALLERGY TO BETA-LACTAMS: VANCOMYCIN 1g IV (perf. > 60min.) 1 hour before. Then GENTAMICIN 1.5mg/kg IV (perf. 30min.) or IM