Complications
Patients who develop acute heart failure from valvular dysfunction require immediate evaluation by cardiovascular surgery. Several studies have demonstrated that heart failure is the single greatest impact on prognosis.[93] Despite a higher operative mortality rate, patients with heart failure who undergo operative intervention have a markedly reduced mortality compared with patients who have medical therapy alone.[92]
As populations age, IE is becoming more frequent in those aged over 70 years,[94] with trends towards worsening outcomes.[29] Mortality of older patients with IE is higher than that of younger patients: age, cerebral embolism, and prosthetic valve endocarditis have been shown to be risk factors for the increased mortality.[85]
Systemic embolisation occurs in 22% to 50% of patients with IE.[95] There is a significant increase in the risk of embolisation if the vegetation is >10 mm.[96] Other risk factors for embolisation include intravenous drug use, Staphylococcus aureus infection and mitral valve vegetation.[97] Emboli often involve the lungs, spleen, joints, brain, and coronary arteries. Up to 65% involve the central nervous system, the majority of which involve the middle cerebral artery distribution presenting as facial droop, unilateral hemiparesis, and aphasia or neglect, depending on dominance. The indication for valvular surgery for prevention of systemic emboli have traditionally been >2 prior major embolic events.[98] There has been much debate regarding whether patients with IE require anticoagulation. Given the underlying pathophysiology of endothelial damage, platelet aggregation, and superimposed thrombus, it seems intuitive that anticoagulation may prevent systemic emboli; however, several studies have not been able to demonstrate this benefit and, in fact, have found a trend toward increased bleeding in patients treated with aspirin.[99][100][101]
Acute kidney injury (AKI) occurs in up to 30% of patients with IE. In this context, AKI may be caused by:
Immune complex and vasculitic glomerulonephritis
Renal infarction, which is usually due to septic emboli and may occur at any time during the course of IE
Haemodynamic instability in a patient with heart failure or sepsis or after cardiac surgery
Antibiotic toxicity (acute interstitial nephritis), particularly if the patient is being treated with aminoglycosides, vancomycin (which has synergistic toxicity when given with aminoglycosides), or high-dose penicillin
Nephrotoxicity due to contrast agents used for imaging purposes.
Renal replacement therapy may be required if the patient has severe AKI.[102] Mild AKI is usually reversible.
To mitigate against the risk of AKI, adjust antibiotic doses according to creatinine clearance and monitor serum antibiotic levels carefully.[7] If the patient is haemodynamically unstable, or has previously had AKI, avoid imaging with nephrotoxic contrast agents if possible.
The role of surgical intervention to prevent systemic emboli is controversial and should be targeted to each individual patient. Surgical intervention yields the greatest benefit during the early phase of IE when embolic rates are highest.[103]
Valvular dehiscence or fistulisation occurs most commonly in patients with prosthetic valve involvement or in those with invasive Staphylococcus aureus infection. It is recommended that these patients have early surgical intervention to prevent onset of acute congestive heart failure.[36]
This is a rare complication of IE. It occurs via bacterial seeding of a bland splenic infarct or direct septic emboli to splenic arteries. Computed tomography and magnetic resonance imaging scans are the best diagnostic tools. Definitive therapy is splenectomy but percutaneous drainage can be performed in patients who are poor surgical candidates.
These are also rare complications of IE and result from septic embolisation to the arterial vasa vasorum with subsequent spread of the infection through the intima and outward through the vessel wall. They most commonly occur in the intracranial arteries.[104] Patients may present with non-specific findings or focal neurological deficits. Some aneurysms may rupture and produce intracerebral haemorrhage or meningeal irritation. Computed tomography or magnetic resonance imaging scans are 90% to 95% specific for detecting intracranial mycotic aneurysms, but the diagnostic standard remains cerebral angiography.[105]
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