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Posts Tagged ‘infective endocarditis’

Pericardial effusion is often detected in patients with Infective endocarditis. Incidence can be as high as 25% . Most often it is mild, can be moderate in few.

Mechanism

  1. Sympathetic effusion in response to endocardial infection. It’s never more than minimal. (Evidence ? it’s only an assumption)
  2. IE related cardiac failure (Raised systemic venous pressure to which pericardial veins drain)
  3. Local sepsis, Abcess formation tracks to pericardial space through transmural lymphatics
  4. Fungal , granulomatous , Tuberculous IE (Rare) Here IE and PE  share the same pathology
  5. Part of systemic sepsis activated Immune mechanism (Polyseroists)
  6. Renal Involvement of IE-Renal failure
  7. Postoperative pericardial effusion in Prosthetic valve IE (Common, often loculated)

Clinical Implication

  • If the pericardial effusion is more than mild, it often denotes worse outcome. This implies more extensive infection or a marker of extracardiac causes of effusion like renal dysfunction.
  • Effusion may predispose to local dissemination of infection and ends up as peri-annular abscess is whether it is a cause or effect of effusion remains to be understood.It is often exudate as one would expect, but transudative  effusions also occur and would indicate more benign course.
  • The sterility of pericardial fluid has not been proven. Culture studies are rarely done from effusions associated with IE.
  • Pericardial effusions appear more often seen in IE of right heart valves. They turn out to be  IV drug abusers.
  • Contained rupture of an abscess needs to be differentiated from effusion

Can we give steroids for PE associated with IE?

Steroids can rapidly plug the inflammatory pores in the from the pericardial surface.It may also prevent future constriction. Currently, routine steroid therapy is not advised in infective pathology . If the infection is confirmed and is being taken care of by antimicrobial therapy there could be a role for steroids with user discretion.

Final message

During the echocardiographic evaluation of IE, the presence of pericardial effusion should be specifically looked for. These patients should be flagged and will require monitoring as the prognosis of PE complicating IE is a concern unless proved benign.

Reference

Two studies one from Spain and other from Egypt looked into this issue specifically.

 

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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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                                                   Infective endocarditis is a serious clinical cardiac problem. The disease has evolved over many decades and now we are witnessing the  most virulent forms of the disease . Infection of heart , can occur in a native healthy valve, native diseased valve, or a prosthetic valve. Further, IE can occur either as  an acute (usually non diseased valve) , or sub acute form (usually in diseased valve).The changing microbial pattern has made this entity very complex. The vigorous   treatment protocols are available for IE. Still  the  prognosis and outcome with medical management is  dismal even in best centers.So the role of surgery in IE has increased over the years.We propose here,  a radically different approach to the problem.

 Traditionally there is a set of criteria for surgery in IE  :  These include

  •  Abscess formation
  •  Worsening valve lesion
  •  Refractory cardiac failure
  •  Persistent fever even after  2 weeks of  appropriate and adequate anti microbial therapy .
  •  Vegetation of more than 10mm size.
  •  Failed medical treatment

(The list is not exclusive)

In any large tertiary  hospital  series, if you  apply the above rule  more than 50 % of all patients with IE will be the candidates for  immediate surgery.

In the remaining 50% the mortality in medical management is very high. The reason being,  the  medical treatment is often prolonged over weeks. Many  of the complications occur  during the course of medical treatment.The common ones are abscess formation, embolic episodes, renal failure etc.Once a complication set in we call it as failed medical treatment and ask our surgical colleagues  to operate.By this time patient’s  general condition  deteriorates and either the surgeon refuses to take  up the case or  patient dies on the table.

So the key point  is , failure of medical treatment  is so common , it is simply not acceptable  to delay  the surgery in these patients as  majority of  them are  doomed to  fail  the trial of medical therapy.

What is the incidence of failed medical management, how to recognise it ? what is the impact of recognising it late ?

  • Failed medical therapy is around 60-70%  even in best centers.
  • Failed medical patients  constitute the greatest  surgical risk .
  • So it is proposed all IE patients should be triaged  early and the  dominant theme should be surgery (Commonly valve replacement, or valve repair)   .
  • If there is large vegetation surgery may be done for the sole purpose of physical removal of the vegetation*.

Final message

In Infective endocarditis experience has taught us, surgery  should be the default management protocol and medical therapy should be offered  to selected few who don’t require surgery.This is especially true in preexisting  rheumatic valve disease.

*The fundamental principle of management of infectious diseases, state that when there is a  resistant focus of infection .Always  remove the focus whenever possible.

 

 

 

 

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Infective endocarditis  remains a  major cardiac emergency.

Medical management has an initial role and  the many will require some form of surgery

( Mainly valve  replacement). But the surgeons request a realtively stable patients to operate upon as

surgical mortality is high in patients with uncontrolled infection and destabilsed CHF.

Even though there are battery of antibiotics, and volumes of texts written on the medical management

of infective endocarditis the medical therapy fails in bulk of the patients.

We have observed  emprical (Scientific guess work ) therapy has helped many patients .

While rifampicin according to scientific worls it’s useful only in prosthetic valve endocardtis

we have found it quiet useful in all resistant IE patients.

IE being a chronic inflammatory state rifampicin might work 

also as an anti inflammatory or immune   modulator.

This paper was presented in Cardiological society of India , Annual scientific sessions at  Mumbai 2005 . Download PPT

 

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