Stevens diagnosis is confirmed as Streptococcus Infective Endocarditis.
What is endocarditis?
What causes endocarditis?
What are the symptoms of endocarditis?
- fever,
- fatigue,
- chills,
- weakness
- aching joints and muscles,
- night sweats,
- edema (fluid collection) in the leg(s), foot (feet), and abdomen,
- malaise,
- shortness of breath, and
- occasionally, scattered small skin lesions.
Who is at risk for endocarditis?
How is endocarditis diagnosed?
How is endocarditis treated?
http://www.medicinenet.com/endocarditis/article.htm
Infective Endocarditis (IE)
IE produces both intracardiac effects, eg valvular insufficiency and a wide variety of systemic effects, both from emboli (sterile and infected) and a variety of immunological mechanisms.
It is a disease that is easily overlooked or misdiagnosed and clinicians should be vigilant and well versed in the manifestations of IE to avoid missing the diagnosis.
Epidemiology
The incidence of infective endocarditis is approximately 1.7-6.2 cases per 100,000 patient years, although rates are higher in at-risk cohorts such as intravenous drug users.[1] Incidence has remained constant for 50 years despite changes in the factors affecting incidence.[2]Figures for incidence are similar between countries. It is 3 times more common in men and increasing in elderly patients (25-50% of cases occur in the over 60s) often associated with other disease, eg diabetes, cancer, alcoholism.
Risk factors
- Previous IE with valvular damage
- Invasive vascular procedures
- Recreational drug abuse
- Rheumatic heart disease (fewer than 20% of cases of IE)
- Elderly patients with calcific aortic stenosis
- Congenital heart disease accounts for 15% of cases (bicuspid aortic valve being the most common)
- Prosthetic valve implants
Pathogenesis
All cases have a nonbacterial thrombotic endocarditis (a sterile fibrin-platelet vegetation) as the prerequisite for adhesion and invasion. The site of this thrombus is influenced by the Venturi effect, with deposition of thrombus on the low pressure side.There are differences in the different clinical situations:
- Acute IE:
The thrombus may be produced either by the invading organism or by valvular trauma (pacing wires, catheters, etc.). - Subacute IE:
Sufficient inoculum of bacteria required to allow invasion of the thrombus, bacteria clumping with production of agglutinating antibodies. - Nonbacterial thrombotic endocarditis:
This can result from, for example, renal failure, neoplasia, systemic lupus erythematosus (SLE) or malnutrition.
- Mitral valve
- Aortic valve
- Combined mitral and aortic valve
- Tricuspid valve
- Pulmonary valve - rare
The organisms responsible for infective endocarditis
- Staphylococcus aureus:
The most common cause of IE overall (acute and subacute); most common with prosthetic valves, acute IE, and IE related to intravenous drug abuse. High mortality rate.
Coagulase negative S. aureus: causes subacute disease similar to Streptococcus viridans. Accounts for 30% of IE associated with prosthetic valves. - Streptococci:
- S. viridans:
50-60% of subacute IE cases. - Group D streptococci:
Usually subacute and the third most common cause of IE. - Streptococcus intermedius:
Acute and subacute infection. Causes 15% of all cases of IE. - Group A, C and G streptococci:
Acute IE is similar to that with S. aureus. High mortality (up to 70%). - Group B streptococci:
Acute disease, high mortality often requiring valve replacement. Occurs in pregnancy and the elderly particularly.
- S. viridans:
- Pseudomonas aeruginosa:
Usually acute IE and requires surgery for cure. - HACEK organisms (Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae):
Usually subacute disease and about 5% of all IE. - Fungi:
Cause subacute disease. - Enterococci.
Presentation
- Early disease subtle and nonspecific
- Indolent process which may include:
- Fatigue
- Low-grade fever
- Flu-like illness
- Polymyalgia-like symptoms
- Loss of appetite
- Back pain
- Pleuritic pain
- Abdominal symptoms (may be pain, vomiting and appendicitis-like symptoms)
- Symptoms akin to rheumatic fever
- Weight loss
- Cerebrovascular accident - less common
- Congestive cardiac failure - less common
- May be history of:
- Invasive procedures (see above)
- Recreational drug use
- Dental disease
- Gingivitis - most cases caused by transient bacteraemia from this
- Symptoms usually arise 2 weeks after invasive procedures but diagnosed after 6 weeks
- Fewer than half of patients have previously-diagnosed valvular disease
- Developing disease produces a myriad of further clinical features of
embolic or immunological origin when treatment/diagnosis delayed for
weeks/months:
- Acute meningitis - signs and symptoms but with sterile CSF
- Hemiplegia from emboli in the middle cerebral artery (50% of patients may be first manifestation; has high mortality)
- Renal infarcts causing painless haematuria
- Splenic infarction causing pain
- Blindness from retinal artery occlusion
- Myocardial infarction from emboli in the coronary artery
- Pulmonary emboli
- Interstitial nephritis or proliferative glomerulonephritis from deposition of circulating immune complexes
- Renal failure may result
- Musculoskeletal symptoms (nearly half of patients) often from immunologically mediated synovitis
- Immune-mediated vasculitis (causing Osler's nodes and Roth's spots)
- Palpitations from immune-mediated myocarditis
- Back pain (15% of patients) may have origin in immune complex deposition in disc spaces
Examination
- Fever: elderly, chronically ill patients with subacute IE may not have fever, but the majority do
- Heart murmurs:
- Most patients have a murmur
- Exception is right-sided IE where one third have murmurs
- Only 15% have the classic 'changing murmur'
- Most common murmur is aortic regurgitation
- Petechiae:
- Conjunctivae
- Hands and feet (dorsum)
- Chest and abdominal wall
- Oral mucosae and soft palate
- Splinter or subungual haemorrhages: Linear and red
- Osler's nodes: small tender red-to-purple nodules pulp of terminal phalanges fingers and toes
- Clubbing: only 10% of cases and usually in longstanding subacute IE
- Roth's spots: retinal haemorrhages with pale centres
- Janeway's lesions: irregular painless erythematous macules on the thenar and hypothenar eminence (usually with acute IE and S. aureus)
- Arthritis:
- With subacute IE usually asymmetric and up to 3 joints affected (fluid sterile)
- Acute IE can give acute septic monoarticular arthritis
- Splenomegaly: most often observed in longstanding subacute disease and often persists after treatment
- Meningism/meningitis: purulent disease occurs in acute IE and aseptic variety in subacute IE
Differential diagnosis
The differential diagnosis could include all those conditions which occur as a complication or with progression of the disease.Some of the more unusual diseases which may also have similar complex and varied manifestations are:
- SLE
- Atrial myxoma and other cardiac neoplasms
- Lyme disease
- Antiphospholipid syndrome
- Polymyalgia rheumatica
- Reactive arthritis
Investigations
Blood cultures
- Blood cultures are used to demonstrate bacteraemia of 30 minutes or more duration
- Draw 3 to 5 sets of blood cultures over 24 hours
- In acute IE, 3 sets drawn from different venepuncture sites over 30 minutes demonstrates continuous bacteraemia
- If cultures are negative 24 hours after stopping antibiotics, repeat after 7 days and, if still negative, reconsider IE diagnosis
- Blood should not be drawn from IV lines (unless diagnosing line infection when simultaneous line and peripheral vein sampling may be used)
- Prior use of antibiotics commonly gives false negative results
- Probably 50% of culture results are estimated to be falsely positive
- Fastidious organisms may require special culture media or prolonged incubation
- HACEK organisms may require 3 weeks of culture and brucella organisms up to 6 weeks
Serological tests
These may be necessary to detect some organisms, eg legionella, chlamydia, brucella and coxiella species.Imaging studies
Echocardiography is the indirect investigative method of choice. Note in general terms that:- Echocardiography is particularly useful in the elderly
- Echocardiography is especially of use when clinical picture of IE but negative cultures
- Echocardiography is useful to predict complications such as embolisation:
- Larger vegetations (>10 mm diameter)
- Multiple vegetations
- Pedunculated vegetations
- Prolapsing vegetations
- Diagnosis of IE can never be excluded with negative echocardiogram (of whatever type)
- Echocardiography should not be used to screen for IE because of high (15% plus) false positive rate (caused by thickened valves, etc.)
- TTE is the initial technique of choice for investigating infective endocarditis.[1]
- Can detect vegetations in 60% of native valve endocarditis but much less often in prosthetic valves
- TTE is good enough for most cases of IE
- In high risk groups, TEE, with its higher sensitivity and specificity, may be needed if the TTE is normal and suspicion of infective endocarditis remains high[1]
- Was developed to visualise prosthetic valves and right-sided pathology
- It detects over 90% of all vegetations
- TEE is better at detecting myocardial abscesses and vegetations on pacemaker leads
- This may help in diagnosis but also in predicting risk of embolisation
- Useful for visualising jet lesions and cusp perforation
Electrocardiogram is useful to detect the 10% of patients who will develop conduction defects.
Diagnostic criteria
The Duke criteria - for definitive clinical
diagnosis requires either 2 major or 1 major and 3 minor or 5 minor
criteria from the list below:[3]
- Major blood culture criteria:
- 2 positive blood cultures for typical IE organisms
- Persistently positive cultures for such organisms drawn >12 hours apart
- 3 or more positive cultures drawn at least 1 hour apart
- Major echocardiographic criteria:
- Positive result and no alternative explanation
- Myocardial abscess
- Partial dehiscence of prosthetic valve
- New valvular regurgitation
- Positive molecular assays for specific gene targets
- Positive serology for Coxiella burnetii, Bartonella spp., or Chlamydophila psittaci
- Minor criteria:
- Predisposing cardiac condition
- Intravenous drug use
- Fever (38°C or over)
- Elevated C-reactive protein or erythrocyte sedimentation rate
- Vascular lesions
- Immunological phenomenon
- Positive cultures less than 'major'
- Positive echocardiographic results but insufficient for major criteria
- Definitive pathological diagnosis from tissue
Management
Have a high index of suspicion:- Admit the patient to hospital for full investigation:
- Blood cultures
- Temperature records
- Basic haematology and biochemistry investigations
- ECG and CXR
- Comprehensive TTE
- Blood cultures:
- With a sick patient (acute IE) take 3 sets of cultures at >1 hour intervals.
- Less obvious IE (sub-acute presentation) requires 6 sets of cultures over 24-48 hours.
- Cultures negative for the commoner organisms should be checked for unusual slow-growing organisms and fungi.
- Referral:
- When blood cultures are positive to a cardiologist.
- At the outset to a microbiologist.
- TTE or TEE:
- If TTE difficult or suboptimal.
- In order further to assess vegetations, abscesses or valvular perforations.
- In all patients with prosthetic valve endocarditis (PVE).
- Serological testing:
- If the diagnosis is still suspected but cultures negative after 7 days.
- Tests for Coxiella burnetii, Bartonella spp. and chlamydial organisms are available and should be performed.
- Testing of biopsied tissue with special techniques to identify bacteria and fungi are being developed.
Antimicrobial therapy
Stevens antibiotic treatment is Vancomycin, Gentamicin, Rifampicin, lasting for 6 weeks, in hospital via drip.
Guidelines have been produced for treating IE.[Treatment of infective endocarditis: guidelines from the RCP. | |||
|---|---|---|---|
| Type or variety of IE/ organism | Antibiotic | Dose/route | Duration of treatment |
| IE due to penicillin-sensitive viridans streptococci and S. bovis (MIC*<0.1 mg/l) in adults |
Benzylpenicillin and gentamicin (b) | Benylpenicillin: 7.2-12 g iv/24 hours in 4-6 divided doses Gentamicin: 3-5 mg/kg iv daily in 2-3 divided doses (max 240 mg/day) |
4-6 weeks (a) 2 weeks |
| As above but allergic to penicillin | Vancomycin and gentamicin (b) | Vancomycin: 30 mg/kg iv in 24 hours infused in 2 divided doses over 2 hours Gentamicin: as above |
4 weeks 2 weeks |
| IE due to penicillin-relative resistant viridans streptococci and S. bovis (MIC*>0.1 mg/l) in adults |
Benzylpenicillin and gentamicin (b) | Benzylpenicillin: 12-14 g iv/24 hours in 4-6 divided doses Gentamicin as above |
4-6 weeks (a) 2 weeks(a) |
| As above but allergic to penicillin | Vancomycin and gentamicin (b) | Vancomycin and gentamicin as above | Vancomycin and gentamicin as above |
| IE due to staphylococci on native valve: penicillin-sensitive (non-beta-lactamase producers) |
Benzylpenicillin and gentamicin (b) | Benzylpenicillin: 12-14 g regime as above. Gentamicin as above |
6 weeks benzylpenicillin 3-5 days of gentamicin only |
| IE due to staphylococci on native valve: methicillin-sensitive staphylococci (beta-lactamase producer) |
Flucloxacillin and gentamicin (b) | Flucloxacillin: 8-12 g iv/24 hours in 4 divided doses Gentamicin as above |
6 weeks flucloxacillin 3-5 days of gentamicin only |
| IE due to staphylococci on native valve: methicillin-resistant staphylococci (c) |
Vancomycin (d) and gentamicin (b) | Vancomycin: 30 mg/kg iv in 24 hours in 2 divided doses (infused over 2 hours) Gentamicin as above |
6 weeks vancomycin 3-5 days of gentamicin only |
| As above but allergic to penicillin | Vancomycin (d) and gentamicin (b) | As above for V and G | As above for V and G |
| IE due to enterococci in adults: gentamicin-sensitive or low level resistant organism (MIC*<500 mg/l) |
Benzylpenicillin or ampicillin or amoxicillin and gentamicin (f), (b) | Benzylpenicillin: 10-12 g iv/24 hours in 4-6 divided doses Amp/amox: 12 g iv/24 hours in 4-6 divided doses Gentamicin as above |
All 4-6 weeks with 6 weeks if symptoms for more than 3 months of amox and amp (e) |
| As above but allergic to penicillin | Vancomycin (d) and gentamicin (b) | As above for V and G | As above for V and G |
| (a) Adjust duration according to response and microbiologist advice. (b) Check gentamicin levels regularly. (c) Linezolid or Synercid® may be used with MRSA. (d) Monitor peak and trough levels with advice. (e) 6 weeks for symptoms over 3 months. (f) Strains highly resistant to gentamicin seek microbiology advice. *MIC = minimum inhibitory concentration. |
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Surgical care
Surgery is needed in approximately 50% of patients who develop infective endocarditis and careful timing is essential to ensure a good outcome:[1]- In most stable patients surgery is best delayed until antibiotics are completed to reduce the risk of perioperative complications and early prosthetic valve endocarditis.
- Unstable patients with haemodynamic or perivalvular complications have a poor prognosis and are best transferred to a specialist centre at the earliest opportunity.
Complications
These are an inherent part of the progression of the disease. Patients should be monitored for:- Valve dysfunction
- Myocardial abscesses
- Embolic phenomena
- Heart failure
- Metastatic infection
- Immunological disease and organ dysfunction
- Complications even after bacteriological cure
- Conduction defects (patients with IE should have daily ECGs)
Prognosis
This varies markedly according to a variety of factors. The following outlines the range of prognosis when managed appropriately:- Native valve endocarditis:
- S. viridans 98% cure rate
- S. aureus 60-90% cure rate with worse results in occurring in those NOT abusing intravenous drugs
- Fungal infections - cure rate less than 50%
- PVE:
- Cure rates at least 10% lower than above for each variety
- Surgery needed more often
Streptococci are the commonest causes of bacterial endocarditis. However, Streptococcus mutans, a member of this group associated with dental caries which might be expected to be commonly associated with endocarditis, has only rarely been reported. This is possibly because of difficulties in isolation and identification. Differing blood culture media may affect the chances of isolation of these organisms, and, though brain-heart infusion, thiol, tryptic soy, and glucose-brain infusion broths have all proved satisfactory, subcultures may require increased CO2 concentrations for growth. Plemorphism in the resultant colonies and in the individual organisms may give rise to a hazardous misinterpretation of this appearance as contamination. Strep. mutans and the similarly penicillin sensitive Strep. bovis may be differentiated from the penicillin resistant enterococci by their lincomycin sensitivity and intolerance of 6-3 per cent sodium chloride. Precise differentiation of streptococci in bacterial endocarditis is of value both epidemiologically and in the management of the disease.
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