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Brief Communications
B R I E F C O M M U N I C AT I O N S
Intravenous thrombolysis is unsafe in stroke due to infective endocarditis W. J. Brownlee,1 N. E. Anderson1 and P. A. Barber1,2 1
Department of Neurology, Auckland City Hospital and 2Centre for Brain Research, Faculty of Medical and Health Sciences, University of Auckland,
Auckland, New Zealand
Key words stroke, thrombolysis, infective endocarditis. Correspondence Wallace Brownlee, Department of Neurology, Auckland District Health Board, Park Road, Grafton, Auckland 1142, New Zealand. Email: [email protected]
Abstract Embolic stroke is the most common neurological complication of infective endocarditis and a major source of morbidity and mortality. Septic embolism is considered a contraindication to intravenous thrombolysis in patients with ischaemic stroke because of concerns over an increased risk of intracranial haemorrhage. We describe a patient with occult endocarditis who was treated with thrombolysis for acute stroke and review other cases reported in the literature.
Received 24 July 2013; accepted 28 October 2013. doi:10.1111/imj.12343
A 27-year-old woman presented following the sudden onset of dysphasia and right hemiparesis (National Institutes of Health Stroke Scale (NIHSS) score 15). She had been in good health with no relevant prior medical history until she collapsed at home. On admission, she was afebrile with no heart murmurs or peripheral embolic phenomena. Routine blood tests showed raised inflammatory markers with an erythrocyte sedimentation rate of 44 mm/h and C-reactive protein of 56 mg/L. A computed tomography (CT) brain scan showed loss of grey-white matter differentiation in the left insular cortex and hyperdensity in the M2/M3 branches of the left middle cerebral artery that were shown to be occluded on CT angiography. She was treated with intravenous tissue plasminogen activator (tPA) 0.9 mg/kg 2 h and 35 min after symptom onset. An hour later, she deteriorated with headache, drowsiness and worsening right-sided weakness (NIHSS score 20). Repeat CT brain scan showed no intracerebral haemorrhage (ICH). A magnetic resonance imaging brain scan 7 h and 35 min after symptom onset showed a 3-cm area of restricted diffusion in the left perisylvian/insular regions and additional areas of restricted diffusion in the right temporoparietal lobe, right superior parietal lobe and cerebellum (Fig. 1).
Funding: None. Conflict of interest: None. © 2014 The Authors Internal Medicine Journal © 2014 Royal Australasian College of Physicians
Review of the earlier CT brain scan and angiogram did not show involvement of these areas prior to treatment with tPA. Later the same day, she became febrile. An urgent echocardiogram showed vegetations on the anterior leaflet of the mitral valve with mild-to-moderate mitral regurgitation. Blood cultures grew Streptococcus sanguis. She was treated with a 4-week course of intravenous penicillin, initially with gentamicin. Extensive dental work was undertaken for poor dentition. She was transferred to a rehabilitation facility and improved. Six months later, she was neurologically normal apart from minor right hand clumsiness. Infective endocarditis (IE) remains an important clinical problem. There has been little change in the incidence of IE over the past 30 years with declining rates of rheumatic heart disease offset by increasing rates of IE among patients with prosthetic heart valves, intravenous drug use and elderly patients with degenerative valvular disease.1 Stroke due to cerebral embolism occurs in 10% of patients with IE and in half is the presenting problem.2 Risk factors for ischaemic stroke include Staphylococcus aureus infection, larger vegetation size and mitral valve position.2 Patients with IE are also at high risk of ICH because of septic and immune-complex-mediated arteritis, haemorrhagic transformation of infarcts, infiltration of meningeal vessels and rupture of mycotic aneurysms. Antiplatelet therapy is harmful in the primary prevention of embolic complications in patients with IE with an 195
Brief Communications
Figure 1 Magnetic resonance brain scan 4 h after completion plasminogen activator showing restricted diffusion in multiple territories.
excess of ICH,3 and thrombolysis for myocardial infarction, a much rarer embolic complication, has been associated with fatal ICH.4 Accordingly, patients with IE were excluded from registration trials of tPA for acute
imaging of tissue areas of vascular
ischaemic stroke, and IE is listed as a contraindication to thrombolysis in most guidelines. Seven patients with stroke due to IE treated with thrombolysis have now been reported (Table 1).5–8 The
Table 1 Patients treated with intravenous tPA for ischaemic stroke complicating infective endocarditis Patient
Age/sex
Presentation
Baseline NIHSS
Time to tPA
Time to IE diagnosis
IE risk factors
Complications
Follow-up NIHSS
15
56/M
15
2 h, 36 min
48 h
None
None reported
4
26 36
46/M 65/F
15 21
1 h, 50 min 2 h, 0 min
Brief Communications
B R I E F C O M M U N I C AT I O N S
Intravenous thrombolysis is unsafe in stroke due to infective endocarditis W. J. Brownlee,1 N. E. Anderson1 and P. A. Barber1,2 1
Department of Neurology, Auckland City Hospital and 2Centre for Brain Research, Faculty of Medical and Health Sciences, University of Auckland,
Auckland, New Zealand
Key words stroke, thrombolysis, infective endocarditis. Correspondence Wallace Brownlee, Department of Neurology, Auckland District Health Board, Park Road, Grafton, Auckland 1142, New Zealand. Email: [email protected]
Abstract Embolic stroke is the most common neurological complication of infective endocarditis and a major source of morbidity and mortality. Septic embolism is considered a contraindication to intravenous thrombolysis in patients with ischaemic stroke because of concerns over an increased risk of intracranial haemorrhage. We describe a patient with occult endocarditis who was treated with thrombolysis for acute stroke and review other cases reported in the literature.
Received 24 July 2013; accepted 28 October 2013. doi:10.1111/imj.12343
A 27-year-old woman presented following the sudden onset of dysphasia and right hemiparesis (National Institutes of Health Stroke Scale (NIHSS) score 15). She had been in good health with no relevant prior medical history until she collapsed at home. On admission, she was afebrile with no heart murmurs or peripheral embolic phenomena. Routine blood tests showed raised inflammatory markers with an erythrocyte sedimentation rate of 44 mm/h and C-reactive protein of 56 mg/L. A computed tomography (CT) brain scan showed loss of grey-white matter differentiation in the left insular cortex and hyperdensity in the M2/M3 branches of the left middle cerebral artery that were shown to be occluded on CT angiography. She was treated with intravenous tissue plasminogen activator (tPA) 0.9 mg/kg 2 h and 35 min after symptom onset. An hour later, she deteriorated with headache, drowsiness and worsening right-sided weakness (NIHSS score 20). Repeat CT brain scan showed no intracerebral haemorrhage (ICH). A magnetic resonance imaging brain scan 7 h and 35 min after symptom onset showed a 3-cm area of restricted diffusion in the left perisylvian/insular regions and additional areas of restricted diffusion in the right temporoparietal lobe, right superior parietal lobe and cerebellum (Fig. 1).
Funding: None. Conflict of interest: None. © 2014 The Authors Internal Medicine Journal © 2014 Royal Australasian College of Physicians
Review of the earlier CT brain scan and angiogram did not show involvement of these areas prior to treatment with tPA. Later the same day, she became febrile. An urgent echocardiogram showed vegetations on the anterior leaflet of the mitral valve with mild-to-moderate mitral regurgitation. Blood cultures grew Streptococcus sanguis. She was treated with a 4-week course of intravenous penicillin, initially with gentamicin. Extensive dental work was undertaken for poor dentition. She was transferred to a rehabilitation facility and improved. Six months later, she was neurologically normal apart from minor right hand clumsiness. Infective endocarditis (IE) remains an important clinical problem. There has been little change in the incidence of IE over the past 30 years with declining rates of rheumatic heart disease offset by increasing rates of IE among patients with prosthetic heart valves, intravenous drug use and elderly patients with degenerative valvular disease.1 Stroke due to cerebral embolism occurs in 10% of patients with IE and in half is the presenting problem.2 Risk factors for ischaemic stroke include Staphylococcus aureus infection, larger vegetation size and mitral valve position.2 Patients with IE are also at high risk of ICH because of septic and immune-complex-mediated arteritis, haemorrhagic transformation of infarcts, infiltration of meningeal vessels and rupture of mycotic aneurysms. Antiplatelet therapy is harmful in the primary prevention of embolic complications in patients with IE with an 195
Brief Communications
Figure 1 Magnetic resonance brain scan 4 h after completion plasminogen activator showing restricted diffusion in multiple territories.
excess of ICH,3 and thrombolysis for myocardial infarction, a much rarer embolic complication, has been associated with fatal ICH.4 Accordingly, patients with IE were excluded from registration trials of tPA for acute
imaging of tissue areas of vascular
ischaemic stroke, and IE is listed as a contraindication to thrombolysis in most guidelines. Seven patients with stroke due to IE treated with thrombolysis have now been reported (Table 1).5–8 The
Table 1 Patients treated with intravenous tPA for ischaemic stroke complicating infective endocarditis Patient
Age/sex
Presentation
Baseline NIHSS
Time to tPA
Time to IE diagnosis
IE risk factors
Complications
Follow-up NIHSS
15
56/M
15
2 h, 36 min
48 h
None
None reported
4
26 36
46/M 65/F
15 21
1 h, 50 min 2 h, 0 min
