Ischaemic Stroke Complicating Infective Endocarditis: Microbleeds Are the Diagnostic Clue ()
1. Introduction
Infective endocarditis (IE) is a bacterial attack on the endocardium, responsible for valvular lesions, most frequently the mitral valve (43.3%), followed by the aortic valve (26.3%) with a significant risk of heart failure and septic embolism.
Staphylococci are currently the most frequently isolated organisms in IE. The diagnosis is based on a combination of clinical, microbiological and echocardiographic evidence.
Janeway lesions are haemorrhagic, irregular and non-painful palmoplantar macules. They are seen with the acute form of bacterial endocarditis and are part of the modified DUKES minor criteria [1].
Ischaemic strokes are the most common neurological complications. They are most often manifested by a sudden focal neurological deficit (hemiparesis, hemianesthesia, hemianopsia, etc.), permanent or transient, and occurring in a febrile context. However, some of them may be completely asymptomatic and detected only on the occasion of a systematic imaging examination.
2. Case Presentation
A 32-year-old woman, a mother of 4 children and without any particular history, presented on 09 August 2021 with a fever of 40, headaches and vomiting, and the appearance of very painful skin lesions in the form of nodules located on the soles of the feet, some of which are purplish in color (Figure 1: photos taken by the husband), characteristic of Janeway nodules.
On 21 September 2021, the patient suddenly developed weakness of the right hemicbody with the suspension of speech, in the context of fever. The general examination results are fever 40, BP = 140/07, tachycardia 120, and polypnoea 30 cycles/min. The neurological examination found a conscious patient with total right hemiplegia 0/5, global aphasia, and an NHISS score of 14. The cardiovascular examination showed a heart murmur in all 4 foci. Finally, the dermatological examination noted scarring lesions with significant desquamation on the soles of the feet.
Brain MRI without and with gadolinium (21 September 2021) was in favor of ischemic stroke (Figure 2) associated with an occlusion of the intracranial left internal carotid artery (Figure 3) and multiple bi-hemispheric cortical and sub tentorial microbleeds (Figure 4). The echocardiography showed mobile elements in the aortic valve of 10 mm and 6 mm in favor of infective endocarditis on aortic valve disease. Blood culture returned positive with isolation of Staphylococcus aureus. The cerebrospinal fluid (CSF) analysis was in favour of bacterial meningitis with positive culture for Staphylococcus aureus (210 GB (40% PNN, 60% lymphocytes) and Proteinorachy at 0.33 g/l, glycorrhaphy at 0.67 g/l,). The patient was put on Ampicillin 12 g/day associated with gentamycin 160 mg/day for 6 weeks. The patient continued to improve neurologically with the beginning of recovery of the motor deficit, on the cardiological aspect a surgical intervention is planned.
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Figure 2. Axial DWI brain MRI: Hypersignal DWI in the fronto-parieto-insular regions corresponding to ischemic stroke of the superficial and deep MCA territory.
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Figure 3. T2 axial brain MRI: T2-Falair hypersignal of the left internal carotid artery in its intra petrous segment (red arrow), in favour of an occlusion of the left intracranial internal carotid artery.
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Figure 4. SWI axial brain MRI: Multiple microbleeds in the cortico-subcortical and subtentorial areas (cerebellum and brainstem).
3. Discussion
Neurological manifestations are the most frequent extracardiac complication in IE. They are most often of cerebrovascular origin, resulting from the migration of a fragment of vegetation (ischaemia) or the rupture of a weakened arterial wall (haemorrhage). They are asymptomatic in 30% to 50% of cases. Symptomatic stroke is the second most common cause of death from IE [2].
The incidence of embolic events in IE is estimated to be between 10% - 50% [3]. In addition, ischaemic stroke accounts for approximately 70% of cerebrovascular events in patients with bacterial endocarditis who have a stroke. Risk factors for cerebral embolisation include S. aureus endocarditis, large vegetation, increased mobility of vegetation, and mitral valve involvement [4]. Haemorrhagic strokes account for about 30% of cerebrovascular complications. They are due to haemorrhagic transformation of cerebral infarction, primary intracerebral haemorrhage, or ruptured cerebral mycotic aneurysm [5].
The frequency of microbleeds has been estimated at 57% in patients who had brain MRI within seven days of hospital admission for IE [6]. These microbleeds are preferentially cortical in distribution, but deep involvement is possible [7].
The pathophysiological process involved in the formation of these microhemorrhages is still to be clarified. The cortical location of microbleeds may reflect a preferential mode of entry of septic emboli across the blood-brain barrier at the cortico-pial junction. Microbleeds may also be due to a subacute process, either due to immunological vasculitis and/or an embolic process in the vasa vasorum [8].
The prognostic value of cerebral microbleeds has been assessed in several studies. All concluded that the presence and the number of CMBs, particularly two or more microbleeds, was an independent predictor of the development of intracerebral haemorrhage. Based on all these arguments, several authors propose to include microbleeds in the diagnostic criteria for infective endocarditis.
The performance of valve surgery in the acute phase of EI and the delay in the procedure pose a problem in the event of neurovascular complications. Indeed, there is a cerebral haemorrhagic risk directly related to the extracorporeal circulation, and to the curative anticoagulation necessary after the intervention. The inclusion of microbleeds may be useful to evaluate the risk of IE patients developing major postoperative cerebral bleeding [9].
4. Conclusion
Stroke is the most frequent extracardiac complication during IE. The presence of microbleeds is increasingly reported in studies and may contribute to early diagnosis, especially in asymptomatic forms, as does the clinical presence of nodular Janeway skin lesions. Brain MRI should be performed systematically in cases of bacterial IE, even in the absence of neurological signs, to detect asymptomatic lesions and guide the therapeutic strategy.
Acknowledgements
We thank our colleagues from the Neurology A and Neuropsychology department as well as the Neuroradiology team of the Hospital of Specialties, Ibn Sina University Hospital for their and expertise that greatly assisted our research.