Infective Endocarditis

Infective endocarditis (IE) is relatively rare in the UK. However, delays in diagnosis and treatment can lead to serious complications, and be fatal. Thus, it is important to be aware of the condition and its management. This article is a practical guide aiming to help you manage IE patients on ward cover and on their first presentation in A&E.

Disease process

The clinical picture is easier to remember if you bear in mind what happens in IE. Bacteria settle on a heart valve (more to less common: mitral -> aortic -> tricuspid), creating a vegetation. Pre-existing valve disease is a major risk factor, but virulent organisms (e.g. Staph Aureus) can sometimes affect previously healthy valves. Pathogens gradually damage the valve, interfering with its function, and small pieces of it (septic emboli) are thrown into circulation. Although we will concentrate on infective causes, less commonly ‘non-bacterial thrombotic endocarditis’ may occur secondary to CKD, malignancy, rheumatological conditions and malnutrition.

Signs & Symptoms

The above process may result in the following symptoms:

  • Feeling fatigued, generally unwell, getting ‘chills’
  • Shortness of breath and cough
  • Palpitations
  • Night sweats

…and produce the following signs:

  • Fever: body’s response to the present infection (occurs in 90%)
  • New heart murmur: mitral/tricuspid/aortic regurgitation
  • Signs of heart failure: due to damaged valve
  • Splinter haemorrhages, Janeway lesions (painless) and splenomegaly: septic emboli
  • Osler’s nodes (painful), hematuria and Roth’s spots on the retina: Ag & Ab complex deposits (due to body’s immune reaction to the infection)

As you can see, symptoms are very unspecific, and similar to the whole array of other conditions, so thorough examination and focused investigations are crucial.

Remember to check for IE risk factors – this will help you to build the case for or against IE:

  • History of heart surgery – especially valve replacement
  • Past medical history – especially cardiac, including congenital conditions, and IBD
  • Recent surgeries/procedures and any indwelling lines
  • Immunosuppressive drugs, or diagnosed immune deficiency
  • Recent hospital admissions – especially to ITU
  • Illicit substance use history – especially IV
  • Dental hygiene and recent dental procedures

A full systematic enquiry is equally important for other potential sources of infection. Ask about chest, urine, abdominal and skin infection symptoms.

Depending on the pathogen, endocarditis is sub-divided into acute and sub-acute:

BacteriaVirulent (e.g. Staph)Non-virulent (e.g. Strep Viridans)
Major risk factorIVDUPre-existing heart disease
Pre-morbid heartHeart might be normalValvular disease likely
Risk of septic emboliHighLow
TreatmentValve replacement often neededAntibiotics may be enough

Immediate investigations

Most important is to take cultures prior to starting any antibiotics – gold standard is 3 sets of cultures from 3 different sites a couple of hours apart (remember – meticulous aseptic technique is essential!). In patients with septic shock where antibiotics cannot be delayed take two sets of cultures from different sites within 1 hour of starting antibiotics.

In addition:

  • Standard bloods and a VBG
  • Chest X-ray – check for pulmonary oedema or pneumonia (another cause of fever and SOB)
  • ECG – for new blocks or arrhythmias (a prolonged PR interval in aortic valve endocarditis may indicate an aortic root abscess)
  • Consider urine dip, especially if a patient reports haematuria – to check for blood and protein (septic emboli or immune complex deposits may lead to kidney damage)
  • Book an urgent echocardiogram – if possible, trans-oesophageal
  • Call a cardiologist and microbiologist who will advise further. They will likely use the ‘Modified Duke criteria’ to establish the diagnosis

On call scenarios

IE patients are usually managed with long term antibiotics by cardiologists and microbiologists working together. You will not ever be expected to start or alter that management yourself. However, you might be expected to manage IE’s acute complications. The most common are stroke, ACS, pulmonary oedema and AKI.

a) Bleep! Patient with known IE suddenly developed arm/leg/face weakness

Ask the nurse to:

  • Put the patient NBM until you assess them
  • Hold anticoagulation or antiplatelets if they are due
  • Do a full set of observations and an ECG


  • Stroke secondary to septic embolus is most likely
  • …could be caused by something else, e.g. carotid plaques, but it won’t alter management
  • Could potentially be hypoactive delirium – sometimes hard to tell the difference!

Assess the patient:

  • ABCDE approach – address issues as you go (see ABCDE article)
    • Make sure to ask for BM, especially if the patient is drowsy
  • Take a focused history
    • When symptoms started, and whether resolved
    • Any chest pain/palpitations/SOB
    • Any speech, vision or balance (e.g. vertigo) problems
  • Full neuro examination (sorry!)
    • Check for any suggestion of unsafe swallow
    • Record GCS and whether they are orientated to person, place and time
  • Go through the notes to establish the patient’s history and background, including their escalations plan and presence of DNAR form.


  • Assess the ECG for signs of new arrhythmia or ischaemic changes
  • Book urgent CT head – remember to hold anticoagulation until then!
  • +/- ABG or VBG if the patient is unwell, desaturating due to drowsiness or is tachypnoeic

Treatment and escalation:

  • Escalate NOW to your registrar
  • Then dial acute stroke team – they will advise on further management
b) Patient with suspected/known IE desaturates and becomes tachypnoeic

Ask the nurse to:

  • Do a full set of obs and an ECG
  • Ask to start them on oxygen; aim sats > 94% unless known CO2 retainer (not just COPD!); aim 94% and above if unsure, but assess this once you are there


  • Pulmonary oedema – most likely, in the context of a compromised valve
  • ACS with secondary heart failure – also high on the list
  • Pulmonary embolus – somewhat less likely as the majority of patients receive thromboprophylaxis, but still possible. Doses might be missed, the patient might be thrombophilic, etc. Those with tricuspid or pulmonary valve IE are at highest risk.
  • HAP – less likely as IE antibiotics should be covering for this, but also possible

Assess the patient:

  • ABCDE manner – address issues as you go
    • Make sure to examine legs for signs of DVT
  • Focused history
    • Questions should aim to distinguish between differentials above
    • Timeline of symptoms
    • Assess for chest pain, its character, radiation etc.
    • Presence of cough, sweatiness, pain elsewhere
  • Go through the notes and drug chart to understand the patient’s background


  • Examine the ECG for signs of new ischaemia or arrhythmia
  • New or increased O2 demand, unless minimal & the patient feels well, calls for an ABG:
    • Check they do not retain CO2 and adjust O2 accordingly
    • Check if they are acidotic and whether lactate is high
  • Do a full set of bloods including inflammatory markers +/- troponin if you suspect ACS
  • Order a chest X-ray asap

Treatment and escalation:

  • If the patient is unstable, requires a high amount of oxygen or ABG is very abnormal, call your senior whatever you think the cause is – severe cases might require ITU admission, but this would be the registrar’s call in most trusts
  • If the patient is stable, requires low flow oxygen and X-ray suggests pulmonary oedema, IV diuretics (e.g. Furosemide) might be sufficient
  • If you suspect PE or ACS, discuss the patient with your senior and follow the local protocols for their respective management
  • If the patient is septic, and/or CXR shows consolidation, try to get in touch with a microbiologist. The patient is likely to be on antibiotics already, so you would most likely need advice to decide if you need to add anything. If they are unavailable out of hours – call your senior.
c) …same patient (what a night!) is now having new haematuria

Ask the nurse to:

  • Do a full set of obs
  • Hold anticoagulation till review


  • In the context of IE, this could be glomerulonephritis caused by immune complex deposits in glomeruli
  • …however, patients could have two independent things going on, especially if they are elderly – so consider your usual haematuria causes too

Assess the patient:

  •   Check the obs, and make sure their blood pressure and heart rate are stable
    • Assess in ABCDE if they are unwell
  • Take a focused history
    • Timing of the symptoms, and whether happened before
    • Check if they have any pain, which would point towards stones or infection
    • If recently catheterized, mild haematuria is common
  • Examine abdomen – in particular, for distended bladder and flank tenderness
  • If they are catheterised, look: is there pure blood, or blood-tinged urine (usually described as rosé)? If you can easily see through it, it is rosé; if not –blood.

Treatment and escalation:

  • Take bloods – U&Es, FBC (for Hb) and clotting.
  • Consider stopping anticoagulation – depending on the patient’s state and degree of blood loss
  • If there is a large Hb drop, do a group and save and call your senior – the patient might need a transfusion. IE glomerulonephritis should not cause profound bleeding. There is probably another reason, and the patient should be reviewed by a urologist.
  • Check renal function, and if AKI is present, follow your usual treatment protocol.
  • Consider discussing patient with the renal team in the day time.

Useful links and Further Reading

Written by Dr Varvara Bashkirova (FY1) & Dr Khudaim Mobeen (SHO)

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