Infective Endocarditis Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Thompson is a 66-year-old retired farmer who presents with a 10-day history of fever, night sweats, progressive exertional dyspnoea, and a transient episode of left arm weakness 3 days ago. [1]

His past history includes:

• Rheumatic mitral regurgitation requiring mechanical mitral valve replacement 6 years ago
• Atrial fibrillation
• He is on warfarin for his mechanical valve, INR target 2.5 to 3.5 [1]

On examination he is febrile at 38.6 degrees, tachycardic in atrial fibrillation at 96, hypoxic at 92% on room air. There is a loud prosthetic mitral click with a new pansystolic murmur at the apex radiating to the axilla. The JVP is elevated 4 cm with bibasal crackles. There is a painful tender nodule on the pad of his right index finger consistent with an Osler node, several painless erythematous macules on his right palm consistent with Janeway lesions, and splenomegaly 3 cm below the costal margin. [1]

Three sets of blood cultures grew Staphylococcus aureus. His INR is 2.8. Transthoracic echo shows a vegetation on the prosthetic mitral valve with new paravalvular regurgitation. Creatinine is 145. [1]

His main problems are:

1. Prosthetic valve infective endocarditis due to methicillin-sensitive Staphylococcus aureus — definite by Duke criteria
2. New paravalvular regurgitation with heart failure and pulmonary oedema — a surgical indication
3. Transient ischaemic attack — an embolic neurological complication
4. Acute kidney injury — multifactorial
5. Anticoagulation management of his mechanical valve during acute illness and surgery
6. Need to identify the portal of entry for his Staphylococcus aureus bacteraemia" [1]

Examiner probing questions and model answers

Q1: "Apply the Modified Duke criteria to this patient." [1]

"He meets definite IE. Two major criteria: first, typical organism — Staphylococcus aureus — in blood cultures from three separate sites, which is a major criterion regardless of whether a primary focus is identified. Second, echo evidence of endocardial involvement — a vegetation on his prosthetic mitral valve with new paravalvular regurgitation. He also has multiple minor criteria: predisposition (prosthetic valve), fever above 38 degrees, vascular phenomena (Janeway lesions), and immunological phenomena (Osler node). Two major criteria establish definite IE. The key modification in the 2000 Li criteria was elevating Staphylococcus aureus bacteraemia to a major criterion even when nosocomial, and adding Coxiella serology as a major criterion." [1]

Q2: "What is your immediate management priority?" [1]

"My first priority is to assess and treat his heart failure, because that is the strongest surgical indication and the leading cause of death in IE. He has pulmonary oedema with hypoxia — I would sit him upright, give high-flow oxygen, and start intravenous frusemide. I would confirm the severity of regurgitation with urgent transoesophageal echocardiography, which is mandatory in all prosthetic valve IE because TTE has low sensitivity. I would ensure he is on appropriate antibiotics — flucloxacillin 2 g IV 4-hourly for MSSA prosthetic valve IE, with rifampicin to be added once bacteraemia clears and gentamicin to be considered cautiously given his AKI. And I would refer immediately to the Endocarditis Team — cardiology, infectious diseases, and cardiac surgery." [1]

Q3: "Does he need surgery, and if so when?" [1]

"Yes. He has multiple surgical indications. Heart failure from a surgically correctable paravalvular lesion is the single strongest indication — stronger than organism, vegetation size, or embolic history. He also has prosthetic valve Staphylococcus aureus IE, which has high medical-therapy failure rates, and a new paravalvular regurgitation suggesting possible dehiscence. The timing is complicated by his neurological event. I would order an urgent CT head to determine whether his transient left arm weakness was a TIA or a completed infarct, and whether there is any haemorrhage. If it is a TIA with no infarct, surgery can proceed urgently. If there is an ischaemic infarct, I would ideally defer surgery 2 to 4 weeks to reduce the risk of haemorrhagic transformation under cardiopulmonary bypass. But if his heart failure is refractory and life-threatening, I would proceed with early surgery after neurosurgical consultation — the mortality of deferring surgery exceeds the neurological risk." [1]

Q4: "How will you manage his warfarin?" [1]

"He has a mechanical mitral valve requiring lifelong anticoagulation. In the setting of acute IE with a recent embolic event and planned cardiac surgery, I would stop his warfarin and convert to an unfractionated heparin infusion — it has a short half-life and is fully reversible, allowing rapid reversal before surgery and rapid re-establishment after. I would monitor his INR down to below 1.5 before surgery. A critical point: rifampicin, which he will need for prosthetic valve staphylococcal IE, is a potent hepatic enzyme inducer that markedly increases warfarin clearance. If warfarin is continued postoperatively, the dose will need to approximately double or triple. Using heparin during the rifampicin phase avoids this interaction. I would absolutely not switch him to a DOAC — mechanical valves require warfarin, and the RE-ALIGN trial showed harm with dabigatran in mechanical valves." [1]

Q5: "Why is Staphylococcus aureus more destructive than viridans streptococci in endocarditis?" [1]

"Staphylococcus aureus possesses multiple virulence factors that viridans streptococci lack. First, it expresses MSCRAMMs — microbial surface components recognising adhesive matrix molecules — including fibronectin-binding proteins A and B and clumping factors A and B, which mediate direct adherence to endothelial cells and to vegetations, even on a previously normal valve. Viridans streptococci require a pre-existing non-bacterial thrombotic vegetation to colonise; Staph aureus can colonise healthy endothelium. Second, Staph aureus produces enzymes — proteases, lipases, hyaluronidase — that destroy tissue, causing valve perforation, abscess, and paravalvular extension. Third, it can form biofilms on prosthetic material, making eradication with antibiotics alone difficult. Fourth, it causes metastatic infection — vertebral osteomyelitis, psoas abscess, epidural abscess. This explains why Staph aureus IE is more acute, more destructive, and carries higher mortality than viridans streptococcal IE." [1]

Q6: "What is the role of the Endocarditis Team?" [1]

"The Endocarditis Team is a multidisciplinary group — cardiology, infectious diseases, cardiac surgery, microbiology, imaging, anaesthetics, clinical pharmacy, and specialist nursing — that meets regularly to make collective decisions on every IE patient. The 2023 ESC guideline reinforced it as the standard of care. The evidence shows that patients managed within an Endocarditis Team structure have lower mortality, shorter hospital stays, and more appropriate use of surgery. The team makes the surgical timing decision together — weighing the cardiac, neurological, infectious, and anaesthetic factors — rather than each specialty acting independently. Complex IE — prosthetic valve, cardiac device, complicated course, pregnancy, IVDU — should be managed in or referred to a Heart Valve Centre with on-site cardiac surgery." [1]

Q7: "He develops acute severe headache and confusion on day 3. What do you do?" [1]

"I am concerned about an intracranial complication — either haemorrhagic transformation of his earlier embolic infarct, rupture of a mycotic aneurysm, or a new embolic stroke. I would order an urgent CT head and CT angiography of the cerebral vessels. Mycotic aneurysms in IE are typically distal middle cerebral artery aneurysms caused by septic embolisation to the vasa vasorum; they can rupture with catastrophic subarachnoid haemorrhage. If a mycotic aneurysm is found, I would involve neurosurgery and interventional neuroradiology — some are managed endovascularly, some surgically. His anticoagulation would need to be held immediately. This complication would further complicate his surgical timing — if he has an intracranial haemorrhage, valve surgery is deferred by approximately 4 weeks unless heart failure dictates otherwise." [1]

Q8: "What is his prognosis?" [1]

"Prosthetic valve infective endocarditis carries in-hospital mortality of 20 to 30%, and Staphylococcus aureus IE carries mortality of 20 to 25%. His adverse prognostic factors are prosthetic valve, Staphylococcus aureus, heart failure, embolic event, acute kidney injury, and age. With prompt surgery and appropriate antibiotics, his prospects are better, but he still faces significant mortality risk. I would discuss prognosis honestly with him and his family, emphasising the team approach, the planned surgery, and the prolonged antibiotic course. I would also initiate advance care planning discussions, appropriate given the gravity of his presentation." [1]

Short Case Discussion

Scenario: "Examine this patient's hands and then the cardiovascular system"

Candidate presentation (model): [1]

"On general inspection, the patient is comfortable at rest at 45 degrees. There is no cyanosis, pallor, or clubbing. [1]

Examining the hands, I note several splinter haemorrhages in the distal third of the nail beds of the index and middle fingers bilaterally. There are painful, pea-sized, tender nodules on the pads of the right index and middle fingers, consistent with Osler nodes. On the palms, there are several painless, erythematous macules consistent with Janeway lesions. There is no clubbing or peripheral stigmata of endocarditis-related chronicity at this stage. [1]

The pulse is regular at 88 beats per minute, normal volume and character. Blood pressure is 120/70. The hands are warm and well perfused. [1]

Examining the cardiovascular system, the JVP is not elevated. The apex beat is not displaced. On auscultation, there is a normal first heart sound and a soft second heart sound. There is an ejection systolic murmur at the aortic area radiating to the carotids, grade 3 out of 6, with an associated early diastolic murmur at the left sternal edge, consistent with aortic stenosis and regurgitation. [1]

In summary, these findings — splinter haemorrhages, Osler nodes, and Janeway lesions — are the peripheral stigmata of infective endocarditis, and the aortic valve murmur suggests the likely valve involved." [1]

Examiner: "Distinguish Osler nodes from Janeway lesions." [1]

"Osler nodes are painful, tender, pea-sized nodules found on the pads of the fingers or toes. They are immunological in origin — caused by immune complex deposition in the dermal vessels — and they are a Duke minor criterion for immunological phenomena. They are not septic emboli. Janeway lesions are painless, flat, erythematous macules found on the palms or soles. They are septic microemboli — caused by deposition of bacteria and microabscess formation in the dermis — and they are a Duke minor criterion for vascular phenomena. The single discriminating feature at the bedside is pain: Osler nodes are painful, Janeway lesions are painless." [1]

Examiner: "What are Roth spots?" [1]

"Roth spots are retinal haemorrhages with a pale or white centre, visible on fundoscopy. They were traditionally attributed to infective endocarditis, but they are also seen in leukaemia, anaemia, diabetes, hypertension, and connective tissue disease. In the context of IE, they are immunological — caused by immune complex-mediated capillary rupture in the retina, with the white centre representing fibrin or white cells. They are NOT septic emboli. They are classified as a Duke minor criterion for immunological phenomena, the same category as Osler nodes and glomerulonephritis." [1]

Examiner: "Why does this patient have splenomegaly?" [1]

"Splenomegaly in infective endocarditis is a sign of chronicity — it reflects prolonged immune activation and is seen in approximately 15 to 50% of subacute cases. It indicates that the infection has been present for weeks rather than days. Splenomegaly is not a Duke criterion, but it is a useful clinical marker of disease duration. In some cases, splenic infarction or splenic abscess may occur from septic embolisation to the spleen — this presents with left upper quadrant pain, referred to the left shoulder, and peritonism, and requires CT imaging and sometimes splenectomy." [1]

Examiner: "What is the significance of clubbing in this context?" [1]

"Clubbing in infective endocarditis is a late sign — it appears after 6 to 8 weeks of untreated disease. Like splenomegaly, it indicates chronicity. In the modern era of early diagnosis and treatment, clubbing is rarely seen, but its presence in an exam patient suggests that the IE has been subacute and indolent. It is caused by chronic cytokine-mediated effects on the nail bed, similar to clubbing in other chronic suppurative conditions like bronchiectasis and lung abscess." [1]