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Neurological Sequelae of Infectious Endocarditis: Differential Diagnoses & Workup

Author: Aiesha Ahmed, MD, Fellow, Department of Neuromuscular Medicine, Pennsylvania State University, Milton S Hershey Medical Center
Coauthor(s): Kevin Hargrave, MD, Consulting Staff in Medicine/Neurology, Comprehensive Neurologics and Sleep; Justin R Fisher, MD, Fellow, Department of Neurophysiology, Penn State Milton S Hershey Medical Center; Milind J Kothari, DO, Professor and Vice-Chair, Department of Neurology, Pennsylvania State University College of Medicine; Consulting Staff, Department of Neurology, Hershey Medical Center
Contributor Information and Disclosures

Updated: Feb 17, 2009

Differential Diagnoses

Aphasia
Dissection Syndromes
Aseptic Meningitis
Herpes Simplex Encephalitis
Cardioembolic Stroke
Lacunar Syndromes
Cavernous Sinus Syndromes
Lumbar Puncture (CSF Examination)
Cerebellar Hemorrhage
Metastatic Disease to the Brain
Cerebral Aneurysms
Primary CNS Lymphoma
Cerebral Venous Thrombosis
Spinal Epidural Abscess
Complex Partial Seizures
Subarachnoid Hemorrhage

Other Problems to Be Considered

Computed tomography in neurovascular diseases
Depression
EEG in neurologic infections
Epidural abscess
Gastrointestinal discomfort
Heart failure
Orbital cellulitis
Psychosis
Weight loss
Carotid disease and stroke

Workup

Laboratory Studies

  • Blood cultures
    • Unless the patient is overtly toxic, the current recommendation is to obtain 3 blood cultures in the first 24 hours and prior to starting antibiotics.
    • In two thirds of patients, all culture samples are positive.
    • Approximately 5% are culture negative (50% of fungal BE is culture negative).
  • Cerebrospinal fluid examination: See Meningeal processes in the Pathophysiology section for an outline of CSF findings in infective endocarditis.
  • Complete blood cell count
    • Anemia is present in 70-90% of patients and is usually normochromic and normocytic.
    • The peripheral white blood cell count is elevated in a minority of patients with SBE.
    • Marked leukocytosis is not uncommon in acute infective endocarditis.
  • Erythrocyte sedimentation rate
    • The erythrocyte sedimentation rate (ESR) is elevated in 90% of patients with infective endocarditis, with a median ESR on admission of 65 mm/h.
    • The C-reactive protein is more helpful to assess therapeutic efficacy since it falls much sooner than the ESR, which can stay elevated for 3-6 months following successful therapy.
  • Rheumatoid factor: The rheumatoid factor is more commonly positive in SBE (approximately 50%) than in ABE.
  • Urinalysis
    • Urinalysis demonstrates either increased protein or red blood cells (RBCs) in 50% of patients.
    • Immunoglobulin complexes also can deposit in the kidney and cause nephropathy.

Imaging Studies

  • Echocardiography
    • Transthoracic echocardiography identifies 60-77% of valvular vegetations; transesophageal echocardiography identifies approximately 96% of vegetations.
  • Echocardiography may not be positive, since vegetations are often less than 2 mm in diameter.
  • In a series of 212 patients, 113 underwent transthoracic echo, and 53% had visualized vegetations.
  • At least one study suggests that vegetations confirmed by echocardiography do not correlate significantly with an increased risk of embolism. However, vegetation size greater than 10 mm does correspond with increased risk of embolism.
  • Angiography
    • For patients with infective endocarditis and focal neurologic deficits, the Cleveland Clinic has recommended 4-vessel angiography at a point between 2 days and 2 weeks from the onset of symptoms.
    • Others do not pursue routine angiography to search for occult aneurysms but reserve it for those with established subarachnoid hemorrhage or persistent headache after the infection is controlled.
  • Brain imaging
    • Computed tomography (CT) of the brain may be normal in infective endocarditis with CNS involvement, but magnetic resonance imaging (MRI) usually reveals multiple focal areas of ischemia even in the absence of clinical manifestations of a CNS disorder (in 33 out of 35 patients in one study).
    • In one neuroimaging report, 2 patients were presented who were transferred with mental status changes.7 Both had normal contrast-enhanced CT scans, but subsequent cranial MRI scans were abnormal. One patient was agitated and confused but had no neurologic focal or lateralized deficit. The echocardiogram was normal, but CSF subsequently was abnormal. The second patient was hemiparetic, but contrast and noncontrast CT scans were normal. The ESR was normal despite demonstrable mitral valve vegetations by echocardiogram. Thus, a normal ESR does not completely exclude infective endocarditis.
    • Regions are as follows:
      • A recent series showed that of 12 patients with endocarditis and neurologic dysfunction, 10 had multiple brain lesions. These most frequently were found in the distal MCA territory and at the gray-white junction.
      • Most were less than 1 cm2 in diameter and enhanced with contrast.
      • Orbital cellulitis was reported in 2 patients in this series.
    • Diffusion-weighted MRI imaging (DWI) is very sensitive in revealing evidence of ischemic cerebral lesions in patients with infective endocarditis. In one study, DWI images revealed ischemic lesions in 33 of 35 patients with infective endocarditis and neurologic symptoms.

Histologic Findings

Macroscopic brain abscesses are rare in patients with SBE (0.5%). Microscopic abscesses (also termed focal cerebritis) are more common (4%) and often are discovered at autopsy. For mass lesions (abscess and/or focal cerebritis), surgery is rarely necessary since these lesions usually improve and occasionally resolve after antibiotic therapy.

In one series, 9 abscesses were found, with staphylococci the predominant organisms (8 of 9 abscesses were <1 cm). Abscesses larger than 1 cm usually are not associated with endocarditis. Epidural abscesses can occur in patients with infective endocarditis. One such case in the Massachusetts General Hospital series was unsuspected and was discovered at lumbar puncture.2

More on Neurological Sequelae of Infectious Endocarditis

Overview: Neurological Sequelae of Infectious Endocarditis
Differential Diagnoses & Workup: Neurological Sequelae of Infectious Endocarditis
Treatment & Medication: Neurological Sequelae of Infectious Endocarditis
References
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Further Reading

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Keywords

infectious endocarditis, bacterial endocarditis, BE, acute bacterial endocarditis, ABE, subacute bacterial endocarditis, SBE, nonbacterial thrombotic endocarditis, NBTE, marantic endocarditis, IE

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Contributor Information and Disclosures

Author

Aiesha Ahmed, MD, Fellow, Department of Neuromuscular Medicine, Pennsylvania State University, Milton S Hershey Medical Center
Aiesha Ahmed, MD is a member of the following medical societies: American Academy of Neurology and American Association of Neuromuscular and Electrodiagnostic Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Kevin Hargrave, MD, Consulting Staff in Medicine/Neurology, Comprehensive Neurologics and Sleep
Kevin Hargrave, MD is a member of the following medical societies: American Academy of Neurology and American Medical Association
Disclosure: Nothing to disclose.

Justin R Fisher, MD, Fellow, Department of Neurophysiology, Penn State Milton S Hershey Medical Center
Justin R Fisher, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Neurology
Disclosure: Nothing to disclose.

Milind J Kothari, DO, Professor and Vice-Chair, Department of Neurology, Pennsylvania State University College of Medicine; Consulting Staff, Department of Neurology, Hershey Medical Center
Milind J Kothari, DO is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, and American Neurological Association
Disclosure: Nothing to disclose.

Medical Editor

Edward L Hogan, MD, Professor, Department of Neurology, Medical College of Georgia; Emeritus Professor and Chair, Department of Neurology, Medical University of South Carolina
Edward L Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Neurological Association, American Society for Biochemistry and Molecular Biology, Phi Beta Kappa, Sigma Xi, Society for Neuroscience, and Southern Clinical Neurological Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Florian P Thomas, MD, MA, PhD, Drmed, Director, Spinal Cord Injury Unit, St Louis Veterans Affairs Medical Center; Director, National MS Society Multiple Sclerosis Center; Professor, Department of Neurology and Psychiatry, Associate Professor, Institute for Molecular Virology, and Department of Molecular Microbiology and Immunology, St Louis University
Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology, American Paraplegia Society, and National Multiple Sclerosis Society
Disclosure: Nothing to disclose.

CME Editor

Matthew J Baker, MD, Consulting Staff, Collier Neurologic Specialists, Naples Community Hospital
Matthew J Baker, MD is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.

Chief Editor

Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Nicholas Y Lorenzo, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Neurology
Disclosure: Nothing to disclose.

 
 
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