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91 2019/11/19

Medically compromised patient

Infective Endocarditis
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 Infective endocarditis (IE):
• is defined as a microbial infection of the endothelial surface of the heart or
heart valves that most often occurs in proximity to congenital or acquired
cardiac defects. Its intra-cardiac effects include severe valvular insufficiency,
which may lead to intractable congestive heart failure and myocardial
abscesses, therefore, emphasis has long been directed toward its prevention.

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• Although bacteria most often cause these diseases, fungi
and other microorganisms may also cause infection; thus,
the term infective endocarditis (IE) is used to reflect this
multi-microbial origin.  

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 Classification
• IE classification based on:
1. The causative microorganism (e.g, streptococcal
endocarditis, staphylococcal endocarditis; candidal
endocarditis)
2. The type of valve that is infected (e g., native valve
endocarditis [NVE], prosthetic valve endocarditis [PVE)
3. The source of infection; Whether community acquired
or hospital acquired, or Whether the patient is an
intravenous (IV) drug user or not.

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 Etiology
1. Streptococci are the most common cause of IE 30%-65%, of Which
streptococci viridians (alpha-hemolytic streptococci), which are
normal constituents of the oral flora and gastrointestinal tract,
remain the most common cause of community acquired NVE.

2. Staphylococci are the cause of at least 3000-4000 of cases of IE;

mostly coagulase-positive Staphylococcus aureus which is the
most common pathogen in IE associated With IV drug abuse, it is
also the most common pathogen in non-valvular cardiovascular
device infections.

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3. Other microbial agents that less commonly cause IE
such as the HACEK group (Haemophilus, Actinobacillus,
Cardiobaeterium, Eikenella, Kingella}, Pseudomonas
aeruginosa, Corynebacterium, Bacteroides fragilis, and
fungi.

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 Predisposing conditions attributed to IE include:
1.  Mitral valve prolapses 25%- 30%.
2. Aortic valve disease 12%- 30%.
3. Congenital heart disease 10%-20%
4. Prosthetic valve 10%- 30%
5. Intravenous drug abuse 5-%20%
6. No identifiable condition 25% -47%

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 Pathophysiology
• IE is thought to be the result of a series of complex
interactions of several factors involving endothelium,
bacteria, and the host immune response. The sequences
of events include:
1. Injury or damage to an endothelial surface, most often of
a cardiac valve leaflet.
2. Fibrin and platelets then adhere to the roughened
endothelial surface and form small clusters or masses
called nonbacterial thrombotic endocarditis (NBTE), these
masses are sterile and do not contain microorganisms.

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3. With the occurrence of a transient bacteremia, bacteria
can be seeded into and adhere to the mass.
4. Additional platelets and fibrin are then deposited onto the
surface of the mass, which serves to protect the bacteria
that undergo rapid multiplication within the protection of
the vegetative mass. .

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5. The clinical outcome results from:
A. Local destructive effects of intra-cardiac (valvular) lesions.
B. Embolization of vegetative fragments to distant sites, resulting in
infarction or infection.
C. Hematogenous seeding of remote sites during continuous
bacteremia
D. Antibody response to the infecting organism with subsequent
tissue injury caused by deposition of preformed immune
complexes or antibody complement interaction with antigens /
deposited in tissues.
 

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 Signs and symptoms
• The clinical presentation may be varied, the interval
between the presumed initiating bacteremia and the
onset of symptoms, of IE is estimated to be less than 2
weeks in more than 80% of patients.
1.  Fever (most common).
2. Heart murmur.
3. Petechiae of the palpebral conjunctiva, the buccal and
palatal mucosa, and extremities.
4. Osler's nodes (small, tender, subcutaneous nodules that
develop in the pulp of the digits). They are caused by
immune-complex deposition.
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5. Janeway lesions (small, erythematous or hemorrhagic, macular
nontender lesions on the palms and soles). They are caused by
septic emboli which deposit bacteria, forming micro-abscesses of
the dermis with marked necrosis and inflammatory infiltrate not
involving the epidermis.
6. Splinter hemorrhages in the nail beds
7. Roth spots (oval retinal hemorrhages with pale centers) Caused by
immune complex mediated vasculitis.

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8.  Splenomegaly
9. Clubbing of the digits.
10. Positive blood cultures in most cases. Although up to
30% of cases of IE are initially found to be “culture
negative,” especially in patients who have taken
antibiotics prior to the diagnosis of IE.

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 Diagnosis :
• Duke criteria were developed to facilitate diagnosis of IE.
These criteria are categorized as major and minor.
Major criteria:
1. Positive blood cultures
2. Evidence of endocardial involvement (e.g., positive
echocardiography, presence of new valvular
regurgitation.

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 Minor criteria:
1. Predisposing heart condition or IV drug use.
2. Fever.
3. Vascular phenomena.
4. Immunologic phenomena.
5. Microbiologic evidence other than positive blood
culture.
 Definitive diagnosis of IE requires the presence of two
major criteria+ one minor or one major and three minor
criteria, or five minor criteria.
•  
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 Complications
1. Heart failure as a result of severe valvular dysfunction.
2. Embolization of vegetation fragments leads to stroke,
Ml, pulmonary embolism. Emboli also may involve
other systemic organs, including the liver, spleen,
kidney, and abdominal mesenteric vessels.
3. Renal dysfunction is also common and may be due to
immune complex glomerulonephritis or infarction.

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 Medical Management :
• Generally it consists of antibiotics and surgery. The most
widely used antibiotics include penicillin, ceftriaxone,
gentamicin and vancomycin while most staphylococcus
aureus organisms that produce betalactamase respond
to nafcillin and oxacillin and for strains resistant to
oxacillin, vancomycin is combined with rifampin and
gentamicin.
• Surgical intervention may be necessary to facilitate a cure
for IE or to repair damage caused by the infection.
•  

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 Dental management
- The dentist should identify from history taking those
patients with cardiac conditions that increase risk for IE
and should remain alert and refer the patient With signs
or symptoms of IE to physician. This would apply
whether or not the patient has received prophylactic
antibiotics for dental procedures.
 

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- The basic assumption is that IE is most often due to a
bacteremia that results from an invasive dental
procedure, and that through the administration of
antibiotics prior to those procedures, IE could be
prevented. But studies have shown that bacteremia can
also result from many normal daily activities such as
tooth brushing, flossing, using toothpicks, using oral
water irrigation devices, and chewing .

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 Cardiac Conditions Associated With the Highest Risk of Adverse
Outcome From Endocarditis for Which Prophylaxis With Dental
Procedures Is Recommended:
1. Prosthetic cardiac valve
2. Previous infective endocarditis
3. Congenital heart disease (CHD)
4. Unrepaired cyanotic CHD, including those With palliative shunts
and conduits
5. Completely repaired CHD With prosthetic material or device by
surgery or catheter intervention during the first 6 months after
the procedure. Prophylaxis is reasonable because
endothelialization of prosthetic material occurs Within 6 months
after the procedure.

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6. Repaired CHD with residual defects at the site or
adjacent to the site of a prosthetic patch or prosthetic
device, which inhibits endothelialization
7. Cardiac transplantation recipients who develop cardiac
valvulopathy.

- (IE antibiotic prophylaxis is recommended only for

patients listed above who undergo any dental procedure
that involves the manipulation of gingival tissues or the
periapical region of a tooth and for those procedures
that perforate the oral mucosa. )

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 The following procedures and events do not need prophylaxis:
1. Routine anesthetic injections through non-infected tissue.
2. Restorative dentistry.
3. Taking dental radiographs.
4. Placement of removable prosthodontic or orthodontic
appliances.
5. Adjustment of orthodontic appliances.
6. Placement of orthodontic brackets.
7. Shedding of deciduous teeth.
8. Suture removal.
9. Fluoride treatment .
10. Bleeding from trauma to the lips or oral mucosa.
 
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 Antibiotic prophylaxis regimens
Situation Agent Regimen: Single dose
30-60 ‘ Minutes before Procedure
Adult Child
Oral Amoxicillin 2g 50 mg /kg
Unable to take oral Ampicillin 2g IM or IV 50 mg / kg
medication Cefazolin or 1 g IM or IV or 50 mg/ kg m IM
Ceftriaxone or IV
Allergic to Penicillin Cephalexin 2g 50 mg/ kg
or Ampicillin (Oral) Clindamycin 600 mg 20 mg/kg
Azithromycin or 500 mg 15 mg/kg
Clarithromycin
Allergic to Penicillin Cefazolin or 1 g IM or IV 50 mg/ kg IM or IV
or Ampicillin but he Ceftriaxone
cant take oral  

Or Clarithromycin 600 mg IM or IV 20 mg/ kg IM or IV

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• Cephalosporins should not be used in an individual with a history
of anaphylaxis, angioedema, or urticaria with penicillin's or
ampicillin.
• Preoperative use of 0.02 Chlorhexidine mouth washes is
advisable.
- In patients who are already taking penicillin or amoxicillin for
eradication of an infection or for long-term secondary prevention
of rheumatic fever are likely to have streptococcus viridians that
are relatively resistant to penicillin or amoxicillin. Therefore:
Clindamycin, azithromycin, or clarithromycin should be selected
for prophylaxis if treatment is immediately necessary.
Cephalosporin's should be avoided because of cross resistance.

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• An alternative approach is to wait for at least 10 days
after completion of antibiotic therapy before
administering prophylactic antibiotics. In this case, the
usual regimen can be used
• in case of prolonged dental procedures (longer than 6
hours) it is advisable to administer an additional
prophylactic dose.
• Prior to cardiac valve surgery or replacement or repair
of congenital heart disease, it is recommended that
preoperative dental evaluation be performed and
necessary dental treatment provided whenever possible
in: an effort to decrease the incidence of late PVE
caused by viridians group .Streptococci.
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 Rheumatic fever and rheumatic heart
disease
• Rheumatic fever is an autoimmune inflammatory process
that develops after pharyngeal infection with group A
beta-hemolytic streptococci (streptococcus pyogenes). It
predominantly affects children between 5-15 years.
Rheumatic fever may occasionally be followed by chronic
rheumatic cardiatis with permanent cardiac valvular
damage that appears to be immunologically mediated
tissue damage, which may lead to fibrosis and distortion
of the cardiac valves (chronic rheumatic heart disease).

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 Clinical manifestations
•  The clinical manifestations of acute rheumatic fever are so variable that the
diagnosis is made only if at least two of the major criteria are fulfilled

Diagnostic Criteria
Major Minor
Carditis pyrexia
Polyarthritis Arthralgia
Chorea Previous rheumatic
fever
Erythema Raised ESR and C-
marginatum reactive protein
Subcutaneous Characteristic ECG
nodules changes

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- A sore throat may be followed after about 3 weeks by an
acute febrile illness with multiple Joints pain (migratory
arthralgia) which heals Without permanent damage in
about 3 weeks.
- Cerebral involvement causing spasmodic involuntary
movements (Sydenham Chorea, St. Vitus dance)
- A characteristic rash (erythema marginatum).
- Lung involvement
- Subcutaneous nodules (usually around the-elbows).

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 Medical management
1. Prompt antimicrobial treatment of streptococcal sore
throat (Within 24 hours of onset) prevents the
development of rheumatic fever in most cases.
2. After an attack of rheumatic carditis, there is a risk of
recurrence and continuous antibiotic prophylaxis
becomes necessary to lessen the risk Of permanent
cardiac damage. The drug of choice is usually oral
phenoxymethyl penicillin until the age of 20 years . For
those allergic to penicillin, sulfadimidine should be
given.

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 Dental management
- Acute rheumatic fever patients are exceedingly unlikely
to be seen during an attack but emergency dental
treatment may be necessary.
- Patients with history of rheumatic fever but without
cardiac involvement are treated as a normal person.
•  

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3. Most patients with chronic rheumatic heart diseases
are anticoagulated and they should be managed after
determining their prothrombin time and INR and the
treatment can be done under local anesthesia with
vasoconstrictor in consultation With the physician.
Conscious sedation with nitrous oxide may be given if
cardiac function is good and with the approval of the
physician.
4. Indications for prophylactic antibiotics are only for the
high risk patients mentioned in the dental management
‘of IE.

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 Congenital heart diseases
• Congenital heart diseases (CHD) are the most common
type of cardiac diseases present in children. They can
broadly be classified as Cyanotic  and A cyanotic
(noncyanotic).

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 Cyanotic CHDs
• The cyanosis results from shunting of deoxygenated blood
from the right ventricle into the left side of the heart and
the systemic circulation (right to left shunt) leading to
chronic hypoxemia, they include:
1. Eisenmenger syndrome
2. Fallot's tetralogy
3. Pulmonary atresia.
4. Pulmonary valve stenosis.
5. Total anomalous venous drainage.
6. Transposition of great vessels.
7. Tricuspid
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atrasia.
• Patients may crouch to improve venous return, but
eventually polycythemia With hemorrhagic and
thrombotic tendencies develop, finger and toe clubbing
develops but after 3 months of age. If untreated, 4000 of
patients with cyanotic CHD die within 5 years.

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 A cyanotic CHDs
• They are further divided into those with no shunt like;
Aortic stenosis, bicuspid aortic valve, coarctation of the
aorta, dextrocardia and mitral valve prolapse. The other
division of the A cyanotic CHD is those diseases with left
to right shunt and these include; Atrial septal defects
(ASD), Ventricular septal defects (VSD) and patent ductus
arteriosus (PDA). Some CHD start as Acyanotic diseases
and become cyanotic with time. Most of these cardiac
defects are well tolerated in utero, and it is only after
birth that their anatomic and hemodynamic
abnormalities‘ become evident.
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• CHD is most commonly diagnosed through
echocardiography, and confirmed by cardiac magnetic
resonance imaging (MRI).

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 Dental management
- The most important aspect for dentists to consider is
how well the patient’s heart condition is compensated.
Consultation with the physician is recommended.
- Patients with heart disease should take their medications
as usual on the day of the dental procedure, and should
bring all their medications to the dental office for review
at the time of the first appointment.
- Patients with stable heart disease receiving atraumatic
treatment under local anesthesia can receive treatment.

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- Late morning or early afternoon appointments are advisable.
- Stress-reduction and good analgesia should be provided.
- Limited use of vasoconstrictor with aspirating syringes.
- Retraction cords containing adrenalin should be avoided.
- Conscious sedation preferably with nitrous oxide can be given with
the approval of the physician. General anesthesia should only be
provided by expert anesthetists in hospital.
- Bleeding tendencies due to platelet dysfunction or coagulation
defects should be evaluated and. managed accordingly.
• There may be susceptibility to infective endocarditis, so
prophylactic antibiotics should be used in the following cases:

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•  Unrepaired cyanotic CHD, including those With
palliative shunts and conduits ‘
• Completely repaired CHD with prosthetic material or
device by surgery or catheter intervention during the
first 6 months after the procedure. Prophylaxis is
reasonable because endothelialization of prosthetic
material Occurs within 6 months after the procedure.
•  Repaired CHD with residual defects at the site or
adjacent to the site of a prosthetic patch or prosthetic
device, which inhibits endothelialization.

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 Prior to cardiac valve surgery or replacement or repair of
congenital heart disease it is reCommended that
preoperative dental evaluation be performed and
necessary dental treatment provided whenever possible in
an effort to decrease the incidence of late PVE caused by
viridans group streptococci.

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