IM Lec 4 by Hanan Musle7

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IM Lec 4 by Hanan Musle7

Post by Sura on 25/10/2011, 11:39 pm

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Sura

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Re: IM Lec 4 by Hanan Musle7

Post by Shadi Jarrar on 4/11/2011, 7:43 pm

Internal Medicine
Infective Endocarditis
Lecture #5
Dr. Hanna
Oct. 18, 2011
Infective Endocarditic is extremely important and relevant in the field of dentistry. We need to understand all the basics related to this topic.
What is infective endocarditic??
It is an infection of the heart's endocardial surface.

**The layers of the heart: the outermost layer is the pericardium, beneath it is the epicardium; which contains the coronary vessels, then beneath it is the myocardium; which is the muscle, and finally the inner part of the heart is the endocardium; which includes the inner part of the chambers plus the valves.

The most recent classification concerning Infective Endocarditis:
Ò native valve endocarditis: the word native denotes that this is the valve that we're born with, not a prosthetic valve.
Ò prosthetic valve endocarditis
Ò intra venous drug abusers endocarditis (IVDA)
Ò Nosocomial endocarditis: with the increase in the number of procedures being done; procedures such as pacemakers, intracardiac defibrillators…. accompanying this is an increase in the number of infections occurring; so nosocomial infective endocarditis is becoming a significant group.
When the patient has a native valve (which is one of the most common groups), this can be classified into acute and subacute.
{The acute type of IE in the native valve patient:
It is usually caused by Staph.aureus. In this case, the heart valve is normal, the person goes to the dentist and then one week later they're suddenly in heart failure or they're very sick all of a sudden…
It usually affects normal heart valves, it's rapidly destructive, can lead to metastatic fossi, the common organism is Staph. Aureus, if not treated it's usually fatal within 6 weeks.
{The subacute type of IE in the native valve patient:
The patient usually has rheumatic heart disease, mitral regurgitation …..so it often affects damaged heart valves. It has an indolent nature, this means that it needs time to develop, weeks/months. If not treated it's usually fatal by one year.
The incidence of infective endocarditis is difficult to ascertain and varies with location, more common in males than in females, may occur in any age mostly the elderly. More than 50% of patients are older than 50 years old.
Male:female ratio ranges from about 2:1 and 9:1,so 1.7:1 is the smallest ratio.
Aortic and mitral valves are the most commonly affected valves and this is age dependent, mitral valve usually more so in young females, while the aortic valve is usually a senile format and is usually affected in elderly patients.
The tricuspid valve is the most common valve involved in the drug abusers, it’s a right-sided heart valve; and that’s what usually gets affected in the IVDA. Why? Because the venous system drains into the right atrium and goes to the right ventricle , so in a recurrent IVDA, the infection most commonly goes to the right side of the heart. Pulmonary exceedingly rare. But since we don’t see many IVDA in Jordan, the involvement of the tricuspid valve isn’t that significant. But out of 100 IVDA's the tricuspid valve would be highly affected.
{Risk factors for infective endocarditis:
Ó IVDA
Ó Pacemakers
Ó Artificial heart valves
Ó Acquired heart defects: calcific aortic stenosis, mitral valve prolapse with regurgitation (Mitral valve prolapse (MVP) is a valvular heart disease characterized by the displacement of an abnormally thickened mitral valve leaflet into the left atrium during systole…._Wikipedia)
Ó Congenital heart defects
Ó Intravascular catheters
The most common organisms that affect the heart are Staph.Aureus, Streptococci, and enterococci. There are other organisms which aren't as common as the previous ones and they are; fungi, pseudomonas, HACEK organisms (Haemophilus, actinobacillus, Cardiobacterium, Eikenella, Kingella) they are slow growers, their growth in cultures takes about 4 weeks. They grow on chocolate agar 5% CO2.

In a series that contains 2800 patients , there are 2 groups; the native valve endocarditis and the nosocomial endocarditis; which includes the prosthetic valve and other devices.






{How does Infective Endocarditis happen??

A turbulence in the blood flow develops, from for example VSD (A ventricular septal defect (VSD) is a defect in the ventricular septum, the wall dividing the left and right ventricles of the heart….._Wikipedia) or mitral regurgitation or aortic regurgitation, so there's a turbulence in the flow, consequently there's a murmur, when the blood passes through an orifice that’s not functionally normal, there will be turbulence and this turbulence affects the endocardium , this disrupts the endocardium making it sticky and this results in a good location for platelets and fibrin to adhere and form a mesh. If there is bacteremia that developed from whatever cause; tooth brushing/ flossing/ dental work/other unrelated procedures….this bacteremia will result in the bacteria residing in the mesh and then it'll spread, because the bacteria itself will add more platelets to the vegetation, so the vegetation is made up of platelets, fibrin and bacteria, and it creates a shell around itself and it propagates until there's a large amount of bacteria and then the damage to the valves begins. After the bacteria is in the system, adherence of the organisms to the endocardium occurs, and invasion of the valvular leaflets.

A common term in the early stage of infective endocarditis is NBTE (non-bacterial thrombotic endocarditis); which is the deposition of small sterile vegetations on valve leaflets, this happens in the early stage of infective endocarditis resulting from the Venturi effect (The Venturi effect is the reduction in fluid pressure that results when a fluid flows through a constricted section of pipe….._Wikipedia)
NBTE causes damage to the endocardium which results in the deposition of platelets and fibrin.

"Non-bacterial Thrombotic

Endocarditis

Sterile vegetations are found on the heart valves in rheumatic

carditis and rarely in systemic lupus erythematosus. They

consist of platelets and fibrin and are deposited on the

surface of an acutely inflamed valve. But sterile vegetations

are sometimes also found on valves that are not grossly

diseased. This condition is called non-bacterial thrombotic

endocarditis, and it affects the mitral and aortic valves predominantly.

At the most the changes are confined to a slight
degeneration of the collagen framework of the valve.'…_ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1800100/pdf/brmedj02655-0015a.pdf)
˜™Causes of endocardial damage include:
Valvular heart disease or mitral valve prolapsed…..something that caused turbulence in the flow.
A pressure gradient is required in producing a high velocity jet, the high flow results in Venturi effect which is a low pressure area adjacent to the area of high flow, which allows the bacteria to settle in that area (the area of low pressure).
The area preceding the stenosis is under high pressure (when you apply pressure on a hose, the pressure increases proximally, and distally its low) the infection, mesh, and bacterial vegetation is subsequent to that stenotic area; which is the low pressure Venturi effect.
{The prevalence of transient bacteremia that results from the following procedures:
Ò Dental procedures (extractions): about 85%
Ò Chewing gum: 26%
Ò Tooth brushing: up to 50%
Ò Upper airway procedures:15%
Ò GI procedures much lower
Ò Urological procedures: 10-30%
The platelet-fibrin complex provides a protective environment (it resembles a shell), so phagocytes are incapable of entering the area where the bacteria resides, due to the platelet fibrin shield surrounding the mesh. This means our own immunological system can't get rid of the bacteria in this case.
The presence of the bacteria induces platelet aggregation and the colony count reaches up to billions 10^9-10^11 bacteria/gram of tissue.
{Antibiotic Prophylaxis:
The guidelines for prophylaxis changed in 2009/2010, they have shifted dramatically. The authorities in the US and other western countries decided that antibiotic prophylaxis will only be given to certain groups from now on, and for everyone else they canceled the prophylaxis (for example all patients with mitral regurgitation, according to these new guidelines aren't given antibiotic prophylaxis anymore). Then the results will be observed to determine whether or not prophylaxis contributed in the prevention of infective endocarditis for those groups.
The efficacy of prophylaxis has never been proven, no study has been conducted. We can't do a placebo (a placebo is a sham or simulated medical intervention……_Wikipedia), because you can't go to people and tell them we want to have a trial done on you, where we don’t give you antibiotics so we can tell if antibiotics have a positive effect in preventing the occurrence of infective endocarditis, since you have mitral regurgitation (or any other risk factor of infective endocarditis). There is no way you can do a trial on a group of patients who are at risk. So universally, this antibiotic prophylaxis is given regardless (even though there is no definite answer as to whether or not it helps in the prevention of this disease) since no trial has ever been conducted.
The risk of one dental procedure causing infective endocarditis is about 1:400, so the benefit of prophylaxis is minimal, to prove efficacy we need a huge study to be conducted (which we already said can't be done ).

˜™ There's an emphasis in the AHA guidelines that came out in 2007: "an under emphasis on maintenance of good oral hygiene and access to routine dental care which are likely more important in reducing the lifetime risk of infective endocarditis than the administration of prophylactic antibiotics."

Oral hygiene is so important , certain diet, fluoride…
There is no relationship between bleeding during dental procedures and the occurrence of bacteremia.
There is no need for IV antibiotics, 1 gram of amoxicillin given 1 hour before the procedure is enough, only for certain high risk groups; patients with prosthetic valves, prior endocarditis, or congenital heart disease, there is another rare group which is the transplanted heart that has valvulopathy, but this is rare. Whereas patients that suffer from mitral regurgitation, aortic regurgitation, VSD (left to right shunt), hypertrophic cardiomyopathy all these diseases that were included in the guidelines before 2009 are no longer part of the risk groups that should be given antibiotic prophylaxis.
{Again we as dentists, according to the guidelines that came out after 2009, only give antibiotic prophylaxis to the following risk groups:
Ò prosthetic heart valve patients
Ò patients with prior endocarditis
Ò patients with congenital heart disease (and not all cases of congenital heart disease are included, only certain specific ones that we'll mention later on in this lecture)
We use bacteriocidal drugs (bacteriostatic are of no effect), generally the incubation period is less than 2 weeks, time of onset of symptoms until treatment is about 4 weeks. History of fever is the most common, it happens in 80% and fatigue is common
{The most common presenting symptoms in infective endocarditis:
Ò fever
Ò chills
Ò weakness
Ò sweating
Ò anorexia, weight loss
Ò malaise
Ò cough
Ò arthralgia
Ò back pain

{What ABOUT THE SIGNS??
Fever, heart murmur, embolic phenomena, skin manifestations, splenomegaly, clubbing, retinal lesions
What are the skin manifestations?
Osler nodes, splinter hemorrhage, petechia, and Janeway lesions

{Skin manifestations:



Petechia on mucosa



Petechia on skin




Splinter Hemorrhage, which is a nonspecific, non-blanching, linear, reddish brown lesion found under the nail bed. It usually does not extend the entire length of the nail, just at the tip.




Osler nodes, which are painful and erythematous nodules on the pulps of the fingers. They're more common in subacute infective endocarditis.

Osler Ouch…..Osler is painful







Janeway lesions: erythematous, blanching macuoles, that are nonpainful, located on the palms and soles.

Janeway is not painful.







The lab tests needed to confirm infective endocarditis are: CBC, ESR, CRP, complement level is low, rheumatoid factor, urine analysis, base-like chemistry (which I assume is the blood chemistry test…), coagulation cascade.

Imaging: chest x-ray, ECG, echocardiography,
{Echocardiography, there are 2 types: transthoracic echo (TTE) and transesophageal echo (TEE) .

˜ Transthoracic: it's done externally, we place the probe on the chest.

™ Transesophegeal echo: just like endoscopy, on the tip of the probe there's a camera that gives us a closer look to the heart valves.



The TTE is the first choice if we suspect infective endocarditis, especially in native valve endocarditis, with prosthetic valve endocarditis we go right away to TEE , if we suspect intracardiac complications we use TEE, if the TTE is inadequate: for example in an obese person, or a smoker, where it's difficult to see the heart we use TEE, if you suspect fungal or staph.aureus bacteremia then you go for TEE.

There are lots of criteria in diagnosing infective endocarditis, the most recent is the modified DUKE (duke is an institution in the USA).

{The modified duke for the diagnosis of infective endocarditis:
Definite and Possible

ÓDefinite:

2 major

1 major and 3 minor

5 minor

ÓPossible:

1 major and 1 minor

3 minor

{Major:

1) positive blood cultures with typical organisms; staph.aureus, strep.viridans

Positive Q fever serology or single positive blood culture for COXIELLA BURNETII, this is an atypical organism



2) echo(TEE/TTE): if the echo shows a mobile mass on the valve

{Minor:

If the patient has any predisposing conditions, such as IVDA, fever >38 degrees, vascular phenomena; like Janeway lesions , Osler nodes, petechia, rough spots in the retina, immunological phenomena, single positive blood culture with typical organism

So 1 positive blood culture is considered a minor, whereas 2 separate positive blood cultures are needed to be considered a major.

The TTE has a sensitivity of about 60-65%, whereas TEE is about 90-100% sensitive and can detect vegetations less than 10 mm and is helpful in assessing the need for surgery , it detects perivalvular extension , we use it in the initial evaluation for suspected infective endocarditis.

Treatment is either via parenteral IV antibiotics or surgery , surgery is usually done if there is no response to the medication, or if there is a complication from the infective endocarditis

{Complications that could happen:

Ó Embolic infection (the vegetation itself embolizes and causes problems such as MI, stroke , mesenteric ischemia, peripheral occlusion which causes acute leg ischemia

Ó Local spread of the infection which causes localized damage to the heart, such as mitral regurgitation or heart failure

Ó Metastatic spread of the infection, the infected source spreads and results in osteomyelitis, renal infection, immune complex glomerular nephritis , and arthritis as a result of the presence of auto-antibodies that cause GN and arthritis



™ Embolic complications; one of the major complications that occur in infective endocarditis , occurs in up to 40%. The predictors of embolization: if the size of the vegetation is more than 1 cm, then there's a higher chance for it to embolize, if it’s a left-sided vegetation, if there's a fungal pathogen strep.bovis. Its incidence decreases significantly after initiation of effective antibiotics

™ Embolic complications: stroke, MI, ischemic limbs, hypoxia from PE(pulmonary embolism), Abdominal pain resulting from mesenteric infarction.



Septic pulmonary emboli






The local spread of the infection can cause extensive valvular damage, which could lead to parvalvular abscesswhich is most commonly seen in the aortic valve and in intravenous drug abusers and the organism is staph.aureus, may extend into adjacent conduction tissue causing arrhythmia, higher rate of embolization, and mortality. Also pericarditis may result from the local spread and fistulous intracardiac connections.





Staph.aureus infection with perforation of the aortic valve.


Acute staph.aureus infection with aortic valve ring, it's an absess extending into the myocardium.










The metastatic spread can cause infections in the kidney, spleen, the soft tissue of the brain causing meningitis and encephalitis, vertebral osteomyelitis, and septic arthritis.

{The following are poor prognostic factors in infective endocarditis:

Ó Being a female, although we already said that the incidence is lower for females.

Ó Staph.aureus

Ó Vegetation size

Ó Aortic valve, this usually has a worse prognosis.

Ó Prosthetic valve

Ó Older age

Ó Diabetics

Ó Low serum albumin

Ó APACHE II Smug"Acute Physiology and Chronic Health Evaluation II") is a severity-of-disease classification system, one of several ICU scoring systems. It is applied within 24 hours of admission of a patient to an intensive care unit…._Wikipedia)

Ó Heart failure

Ó Paravalvular abscess

Ó Embolic events



™ IVDA's and the elderly are at the greatest risk of developing infective endocarditis.

The signs and symptoms of infective endocarditis are non specific and varied, a thorough but timely evolution including blood cultures and echo is crucial and beware of life threatening complications.



˜™What matters to us as dentists; is when should we give a patient antibiotic prophylaxis??

{We give prophylaxis to patients with:

Ó Prosthetic valve.

Ó History of infective endocarditis

Ó Certain congenital heart diseases:

1.) unrepaired cyanotic heart diseases; for example someone who has PDA (Patent Ductus Arteriosus) with left to right shunt

2.) or non- cyanotic within the first 6 months preceding the repair; whereas after the repair by 6 months or more there is no need to give prophylaxis,

3.) or he had his heart condition repaired, but it wasn't completely repaired (repaired congenital heart with residual defect

Ó Transplanted heart (there is no transplant program anymore in Jordan)

{In what dental procedures do we give prophylaxis??

Ó Extraction

Ó Periodontal probing

Ó Scaling

Ó Root planning and surgery

Ó Biopsy

Ó Suture removal

Ó Subgingival restorations

Ó Orthodontic band placement
All these previous procedures need prophylaxis.

{When don’t we give prophylaxis?

Ó Taking an x-ray

Ó Removable appliances

Ó Orthodontic Brackets

Ó Shedding of primary teeth

Ó Trauma to the lips or oral mucosa
Best of luck
Done by:Hanan Musleh
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Shadi Jarrar
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عدد المساهمات : 997
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تاريخ التسجيل : 2009-08-28
العمر : 26
الموقع : Amman-Jordan

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