![\"Splinter](\"https:\/\/i0.wp.com\/drcrunch.co.uk\/blog\/wp-content\/uploads\/2013\/10\/photo.jpg\")
<\/a>On palpation there was splenomegaly.<\/p>\n
On auscultation there was a loud pansystolic murmur radiating to the axilla.<\/p>\n
Bloods confirmed a normocytic anaemia with a WCC of 10.1 and a CRP of 53. His U&Es, LFTs and Coagulation were all normal.<\/p>\n
A urine dipstick showed haematuria (+++).<\/p>\n
A transthoracic echo showed a mitral valve oscillating vegetation, with severe mitral regurgitation and normal LVEF.<\/p>\n
Three sets of blood cultures returned two days later which all grew strep viridans sensitive to benzylpenicillin.<\/p>\n
What is actually going on in IE?<\/b><\/p>\n
As the under review HPA guidelines on blood cultures states: Why did this man get IE?<\/b><\/p>\n Intact valvular endothelium is normally quite resistant to colonisation. The rheumatic fever caused some degree of valve damage, which makes it easier for any bacteria that happens to be in the blood to make a camp there.<\/p>\n What bugs are most likely in this case?<\/b><\/p>\n According to the UK guidelines (2012), the most common causes of NVE in non-intravenous drug users are currently S. aureus (28%), coagulase-negative staphylococci (CoNS; 9%), streptococci (35%) and enterococci (11%); 9% are culture-negative.<\/p>\n The main times staph aureus dominates over streptococci is healthcare associated IE, IVDU associated IE and in the first year following a prosthetic valve placement. Staph aureus is the second most common cause of IE in prosthetic valves in the first year after coagulase negative staphylococci. In fact, the closer it is now to the time of the prosthetic valve placement, the more likely that any IE the patient is currently having on that valve is caused by coagulase negative staphloccoci.<\/p>\n How should cultures be taken?<\/b><\/p>\n According to the UK guidelines<\/a>:<\/p>\n \u201cIn patients with a chronic or subacute<\/b> presentation, three sets of optimally filled blood cultures should be taken from peripheral sites with \u22656 h between them prior to commencing antimicrobial therapy.\u201d<\/p>\n It adds:<\/p>\n \u201cThere is no evidence to support the commonly perpetuated view that blood cultures should be taken from different sites. All skin surfaces are colonized by bacteria and adequate skin disinfection is key to reducing contamination. Taking blood cultures at different times is critical to identifying a constant bacteraemia, a hallmark of endocarditis.\u201d<\/p>\n In practice, this means it would be 12 hours from your first suspicion of IE to giving your first set of IV antibiotics in a patient with a chronic or subacute<\/b> presentation.<\/p>\n But the sepsis six! Each hour\u2019s delay results in a 7.8% increase in mortality<\/a>! What should I do if the patient is septic with IE?<\/b><\/p>\n According to the same guidelines:<\/p>\n \u201cIn patients with suspected IE and severe sepsis or septic shock at the time of presentation, two sets of optimally filled blood cultures should be taken at different times within 1 h prior to commencement of empirical therapy, to avoid undue delay in commencing empirical antimicrobial therapy.\u201d<\/p>\n If you spoke to a sepsis champion, they would feel very uncomfortable about knowingly delaying giving antibiotics in any patient with severe sepsis or septic shock. In fact, the guidance from the sepsis world is to give fluids, oxygen and antibiotics ASAP and only take cultures before giving antibiotics if this would not delay giving antibiotics.<\/p>\n I\u2019ll have to cross check what to do in this situation with a sepsis don.<\/p>\n <\/b>What is the most common extracardiac manifestation of IE?<\/b>\u00a0<\/b><\/p>\n Though this man had a splinter haemorrhage, this could be related to his occupation as a builder. The patient was unsure if this line in his nail was new or old. Splinter haemorrhages are a pretty rare feature of IE in the developed world, where the presentation is usually fairly early. Janeway lesions, Osler nodes and clubbing are all subacute signs, and are also quite rare in the developed world.<\/p>\n Cerebral complications are the most severe extracardiac complications of infective endocarditis, as well as the most frequent (occurring in 15 to 20% of patients<\/a>). A haemorrhagic or ischaemic stroke may result. In other words, if a patient has an unexplained stroke, we may question whether or not there is underlying IE (after dealing with the stroke).<\/p>\n To TOE or not to TOE?<\/b><\/p>\n Same guidelines:<\/p>\n What should the first line antibiotics be whilst awaiting culture results in this case?<\/b><\/p>\n
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\n\u201cIE is infection of the heart valves and\/or other areas of the endocardium. It usually occurs at the site of a predisposing cardiac lesion or congenital defect where there is turbulent blood flow, encouraging endocardial damage and adhesion of platelets. A fibrin clot is deposited on the damaged endocardial surface and becomes colonised with organisms which have entered the bloodstream, so forming infected vegetation. Viable bacteria may be present deep within the vegetation as well as on the surface making antimicrobial treatment difficult.\u201d<\/p>\n<\/a>