Focal neurological deficit with tricuspid endocarditis and patent foramen ovale

Dear Editor, We describe the case of a 49-year-old woman admitted to the ICU for convulsive status epilepticus. Two weeks before, she had suffered chest pain, dyspnoea and arthralgia. Her medical history was uneventful. Infective endocarditis was suspected and transoesophageal echocardiography showed several mobile tricuspid vegetations (15 9 21 mm) (Fig. 1a) with tricuspid regurgitation (Fig. 1b) and a patent foramen ovale (Fig. 1c). A Staphylococcus aureus strain was isolated from blood cultures. On the 12th day, she suffered posterior headache, vomiting and bilateral amaurosis, and she experienced a generalized tonic–clonic seizure followed by coma (GCS 4) requiring endotracheal intubation. She was normotensive (114/74 mmHg). An emergency CT scan revealed bilateral occipital hypodense lesions compatible with embolic stroke (Fig. 1d). MRI showed bilateral subcortical hyperintense lesions on diffusionweighted images in the occipital and parietal lobes (Fig. 1e). Increased diffusion on ADC maps (Fig. 1f) was related to vasogenic oedema. These results were consistent with posterior reversible encephalopathy syndrome (PRES). Ischaemic stroke due to paradoxical embolism or cerebral bleeding was excluded and cerebral vasospasm was ruled out by a transcranial Doppler scan. Cardiac surgeons replaced the tricuspid valve (St Jude prosthetic valve) and fixed the patent foramen ovale. Two days later, clinical neurological examination was normal (except anterograde amnesia that eventually regressed). The patient was discharged home on the 21st day after surgery and the follow-up CT scan no longer showed occipital hypodense lesions (Fig. 2). We describe the unusual association between PRES and S. aureus sepsis in a patient whose clinical features converged to an ischaemic stroke as the culprit for neurological impairment. The clinical picture of PRES is characterized by a combination of acute encephalopathy with headache, seizures, focal neurological deficits and visual impairment [1, 2]. Predisposing factors are hypertension, immunosuppressive therapy and antineoplastic drugs. The clinical evolution, the MRI patterns and the CT follow-up were consistent with the diagnosis of PRES. The increased diffusion obtained on ADC mapping led us to identify the vasogenic oedema involving the subcortical white matter of the occipital poles and parietal lobes [1, 2]. The occurrence of PRES during sepsis has already been described, and gram-positive cocci were reported in the majority of patients (84 %) [3]. According to the ‘‘ENDOcardite en REAnimation’’ study, S. aureus infective endocarditis is independently associated with neurological complications (OR 1.45, 95 % CI 1.02–2.05) [4]. According to the classic hypertension and hyperperfusion theory, a hypertensive status promotes brain hyperperfusion and blood–brain barrier (BBB) disruption [3] in susceptible occipital vessels. In our normotensive patient, a massive inflammatory response could have impaired local vascular tone regulation and endothelium permeability, which are increased by major oxidative stress [5]. In conclusion, our case highlights the importance of MRI in deciding the best therapeutic approach. Indeed, if ischaemic stroke or a ruptured mycotic aneurysm were the cause of the neurological disorder, valve surgery should have been postponed: a ruptured BBB carries the risk of haemorrhagic transformation during cardiopulmonary bypass. On the contrary, PRES associated with infective endocarditis urged a surgical procedure to eradicate the septic loci and allow neurological recovery. Intensivists should be aware of this rare clinical manifestation of infective endocarditis and systematically request an MRI scan in patients with a focal neurological deficit.