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Posts Tagged ‘infective endocarditis’

When do you call a infected heart as healed ?

Should the vegetation disappear to call it a cure ?

Vegetation’s rarely disappear following treatment . Very small vegetation may dissolve – 20% . Many times it regress in size .

Often  our aim should be  restricted  to sterilise the vegetation. This invariably happens in most of the patients who receive complete course of antibiotic. But healing and sterilizing is not enough in many vulnerable patients.If the vegetation is large the embolic risk is still there even with a healed vegetation.

So if there is a relatively large  (>1.5cm) vegetation it is always better to remove by surgery.

Interventional  techniques may   soon  allow  capturing these vegetation by basket catheters .When technology is there to retrieve small bits of a thrombus inside a coronary artery it should be possible to remove a large vegetation with temporary aortic filters in place.

Also read

https://drsvenkatesan.wordpress.com/2011/01/12/what-is-the-natural-history-of-infective-endocarditis-vegetation/

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Modern  day cardiology can do wonders. It can revive a sinking  patient in cardiogenic shock with IABP , LV  assist ,   multivessel angioplasty and bring back  life . On  the other  hand  , a young man with an infected mitral valve who is put on  intensive  antibiotic  regimen   , progressively deteriorates  throws an emboli into brain ,  raise his urea  creatinine  , cardiac   failure worsens and finally succumbs .

This is a clear case of failure  of medical therapy in infective endocarditis .  It is almost certain  surgery would have saved him .

Why  the delay ?

So the question that is been debated for so long is   “When to intervene with surgery in IE”  ?

While we show extreme  urgency for ACS , the same is not shown  with IE.This is going to change in the future .Thanks to the  EASE trial (Early surgery  in  endocarditis )  This land mark study from Korea  is likely to revolutionise  the way we will look into the  problem  of infective endocarditis. It was presented in the just concluded AHA annual scientific sessions  in Orlando

This was  our  observation  too . The issue was discussed in  the year 2008 .It reminds me ,  every  learned  thought or opinion is in fact a paper  but unfortunately modern science does not accept a  fact without evidence of a  study . Until then  it remains  as a crap !

I am glad  to note   genuine concepts will some day  get ratified . Kudos to the Korean team.It is a great study to do with  many ethical issues.

Click below to read the related article

Link to EASE Trial  http://www.theheart.org/article/1313215.do

Next question  on the cards

Should there be  a time window above which medical therapy should be   deemed (Doomed !) to have  failed  , so that the patient becomes a default candidate for surgery.

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What happens to vegetation following  successful therapy ?

  1. It regresses almost completely  and become sterile
  2. It regresses about 50 % volume   but continue to harbor  live  viable bacteria
  3. Gets sterile   but  does not regress ,
  4. Vegetation vanishes completely .Gets dissolved circulation as micro particles.
  5. Appears slightly bulky.

Answer.

Each of the above statement can be true in different patients  at  / different times.  However No  1, is generally the dominant theme.

  • Most of the small vegetations disappear fully.
  • Large vegetations (>2 cm) almost never disappear fully .
  • Fungal vegetation is notoriously known  for a long haul battle
  • Systemic embolism is an important mode of  vegetation clearance from heart.
  • Size of vegetation is an independent indication for surgery .
  • Combination of vegetation with super added layer of  thrombus is common.The thrombus lyses in due course , mimicking thrombus regression.
  • Paradoxically healed vegetations may appear dense in  2 D echocadiography ,which may be wrongly interpreted as a growing vegetation.
  • The risk of recurrent vegetation formation remains till the raw area is completely endothelised.Hence antibiotics are given up to 4-6 weeks.

Persistent  culture negativity may be a  good index  for  successful management . But a negative blood culture  does not in any – way imply  absence of vegetation.

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Retrieve&list_uids=7985602&dopt=abstractplus

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Mitral regurgitation jets can take many shapes

  • Symmetrical
  • Central
  • Eccentric

The direction of the jet depends upon

  • The angle of co-optation
  • The  plane of  orientation of regurgitant  orifice . It  can be entirely off track with  physiological  mitral orifice .
  • Degree of prolapse or shortening /subvalvular  fusion.
  • Flail valve tips can guide the jet selectively into anterior/superior  or posterior aspect of LV

Rheumatic mitral valve showing poor leaflet co-optation.Patient is having significant tachycardia

 

Perpendicular 90 degree MR jets

 

In rheumatic heart disease  eccentric jets are more common. In dilated cardiomyopathy MR jets are often symmetrical and central as the pathology is annular dilatation.

What are  the significance of eccentric MR jets ?

  • Anterior jets clinically mimic aortic stenosis as the murmur is  often well conducted to neck
  • Murmurs of  posterior jets well conduct to axilla .
  • Eccentric jets are often acute and compromise hemodynamics
  • Suspect early infective endocarditis.Carefully look for vegetation.
  • Eccentric jets make it difficult /risky  for PTMC (Note : In Mitral stenosis  +  grade 1  MR   with central jets  one can safely do PTMC)
  • Severe eccentric jets can flood one of the pulmonary veins and result in unilateral or regional pulmonary hypertension or even lobar /segmental pulmonary edema

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Infective endocarditis continues to be a challenge for the cardiac physicians.

While we have innovated too much( More than what is required !)  in the interventional arena little is progressed in the last few decades on  this vital  area  of  “Infections of heart”.

Globally , deaths continue to occur in prime ages due to rampant infections of the heart valves.

Prevention of IE was recently deglamorised by diluting the criteria for prophylaxis by ACC/AHA (Cost issues ,  overwhelming science ? )

So, what is left in the war against IE ?

Early diagnosis and recognition

How to diagnose it early ?

Suspicion is the key  . . .

When to suspect ?

Suspect in all with fever and h/o heart disease . So far  no case of afebrile IE reported !

Get rid of the common myths

  • You don’t require vegetations to diagnose IE
  • Blood culture need not be positive
  • Fever can be low grade
  • Rarely severe fatigue is the only sign

This effectively means , one can diagnose IE without a major criteria of Dukes.

One can diagnose IE with 5 minor criterias

If you wait for a major criteria to develop to start treatment , it could be a  costly miss .

So have a open mind, suspect IE, treat early.

Do not unduly worry about , overuse of antibiotics in case of  false diagnose of IE.This  attempt is worth in weight  of gold !


Million ton of antibitics are used indiscrininately in this world by all walks of physcinas for simple cold and surgeions  non existing peripopertaive infections .

While , the global medical community has  accepted this concept with total submission (Intentional harm condoned !) , it is funny to ask for 100% appropriateness in the therapy for a  deadly infection of heart.

It is absolute necessity  to  inject an  anticipatory antibiotic in all cases of suspected IE with high risk valve lesions. (Of course ,  it need to be a reasonably appropriate antibiotic with microbiologists consultation to avoid interference in the subsequent culture evaluation !)

Minor only infective endocarditis.

Please note IE can be diagnosed with the following 5 minor criteria

  1. Predisposing lesion
  2. Fever >38c
  3. Immunological / Vascular lesion
  4. Culture eqivocal
  5. No clear cut vegetation , but high suggestion of vegetaion, New valve regurgitation

A related article in this blog

Vegetation negative infective endocarditis .

Final message

Never hesitate to start empirical antibiotic therapy in suspected high risk IE

Let us err . . . for the patient’s sake  !

Fever + New murmur*= IE until proven otherwise (Oxford handbook of  clinical medicine  P 136 7th Edition )

*It can be read as , presumably new murmur to increase the sensitivity.

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Infective endocarditis (IE) continues to be a dreaded  medical problem. The clinical outcome has not improved much , in spite of  availability of powerful antibiotics. Early surgery in eligible patients  could provide the best possible results.

One of the major determinants of morbidity and mortality  in IE  is the renal involvement.

Kidney gets affected in almost all the patients  with IE.  As IE is a  a systemic illness and  immunological activation is  the  norm ,  some degree of renal involvement is universal. Microscopic hematuria confirms this. This is due to clogging and  globulin mediated  damage to glomerular membranes. There is a linear co relation between  the size of the vegetation and degree of renal involvement.

The following  mechanisms are attributed   for  rapid deterioration of renal function in patients with IE .

  1. Renal arterial emboli-occlusion-renal infarct
  2. Immune complex mediated  focal nephritis .
  3. Diffuse ,  rapidly progressive glomerulonephritis
  4. Drug induced renal dysfunction, especially with  aminoglycosides, vancomycin etc
  5. Finally &  most importantly , the underlying cardiac condition, which result in refractory cardiac failure  may either be primarily responsible for the renal compromise or aggravate the situation.
  6. Combination of each of the above can occur

How to manage renal failure and IE ?

This forms a deadly combination.  Aggressive  planning  & implementation  is  required. Cardiologists, cardiothoracic surgeons, nephrologists  should  discuss the strategies  together.  A microbiologist  is also welcome !

  • If it is purely a pre -renal failure due to CHF, there is no major worry.The  patient should  do well with cardiac failure management.
  • The role of CT surgeon is always vital, since 75% of times , IE patients require  valve replacement or vegetation/abscess  removal  in  an  emergency or semi emergency basis.
  • Pre operative and peri-operative dialysis will  improve the results.
  • Renal replacement therapy , combined with valve  replacement may be the ultimate therapy .It  could be the most heroic way to save a patient but carries near death mortality.

If ,  there is strong  evidence  to suggest  immune activation ,there could be a role for steroid administration. Literature  does not address this issue . Long term follow up of renal function is required in these patients .

Final message

Renal failure in IE is common and the underlying mechanisms are often complex.Early intervention is the key as there is  almost  “no  option” for   conservative management in this situation.

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Yes , we can .         Abstract : Link to Indian heart journal

b1

Vegetation Negative Infective-Endocarditis

S Venkatesan, G Gnanavelu, G Karthikeyan, V Jaganathan,  R Alagesan,
M Annamalai, S Shanmugasundaram, S Geetha, A Balaguru, G Anuradha

Madras Medical College, Chennai


The definitive diagnosis of infective endocartitis (IE) remains a contentious clinical issue. Many diagnostic criteria have been advanced. However, none has withstood the test of time. Currently Duke’s criteria is considered as de facto standard. Documentation of vegetation within the cardiac chambers and positivity of blood culture is the sine qua non of IE and evidently they constitute the major criteria. Ironically, according to Duke’s criteria, IE could still be diagnosed in the absence of vegetation, provided it fulfils other major criteria of culture positivity. In this context, we report our analysis of patients with IE without vegetation. Out of 24 patients admitted between 2004-2005 in our hospital with the diagnosis of IE, 4 patients failed to show vegetations. All had rheumatic heart disease (RHD) and presented with prolonged fever. All had severe eccentric mitral regurigitation (MR). One had severe aortic regurgitation (AR) also. One had flail posterior mitral leaflet (PML). All had blood culture positive – 3 for staphylococcus auerus 1 for pseudomonas. None had vegetations on the first echocardiographic examination. Transesophageal echcardiography (TEE) also failed to detect a vegetation or abscess. The diagnosis of IE was made on the basis of Duke’s criteria (1 major and 3 minor features). Treatment was started based on culture positivity and sensitivity. All patients underwent serial echocardiography every week for 6 weeks. New mobile vegetation was detected in 1 patient in anterior mitral leaflet (AML) measuring 12 mm after 2 weeks. Three patients never showed any evidence of vegetation. One patient developed cerebral vasculitis and another renal insufficiency during the course of treatment. Two patients stabilized with medical management. One expired and other had refractory cardiac failure and was referred for emergency surgery. The mechanism of absence of vegetation in IE could be varied. Simple temporal dissociation between appearance of vegetation and the clinical syndrome should be the first possibility. Further, vigorous antimicrobial treatment might have prevented the formation of vegetation. But, as we have seen in few patients, it never appeared. This was possibly due to layered vegetation like that of a thrombus on the surface of the valve or adjacent myocardium. The process of vegetation formation need not be endoluminal, it can burrough into the tissue plane intramurally without projecting into the cavity. Spontaneous rupture of chordae secondary to inflammation without any vegetation is another possibility.

We conclude , even though vegetations are considered sine quo non of IE in many clinical situations, IE occurs without vegetation. The mechanisms could be varied.

Download full  PPT presentation

infective-endocarditis-csi-2005

infective-endocarditis-csi-2005

infective-endocarditis-vegetation-csi-2005

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