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ArtikelDelayed cerebral thrombosis after initial good recovery from pneumococcal meningitis  
Oleh: Schut, E. S. ; Brouwer, M. C. ; Gans, J. de
Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Neurology (Official Journal of The American Academy of Neurology) vol. 73 no. 23 (Dec. 2009), page 1988-1995.
Topik: Glasgow Coma Scale; transforming growth factor beta receptor II
Ketersediaan
  • Perpustakaan FK
    • Nomor Panggil: N11.K.2009.08
    • Non-tandon: 1 (dapat dipinjam: 0)
    • Tandon: tidak ada
    Lihat Detail Induk
Isi artikelObjective: To report an unusual clinical course in 6 patients with community-acquired acute bacterial meningitis and to compare clinical features with cases reported in the literature. Methods: Case series from Dutch hospitals from 2003 to 2008. Results: Five out of six patients were male, age ranged from 30 to 73 years (mean age, 47 years). All patients had pneumococcal meningitis, received adjunctive dexamethasone treatment on admission, and made a good or excellent initial recovery. After 7 to 19 days, patients suddenly deteriorated, developing headache, fever, a decreased level of consciousness, brainstem signs, or hemiparesis. Imaging studies showed infarctions involving the thalamus or brainstem in all patients. Repeated lumbar puncture showed a pleocytosis, but CSF cultures were sterile. Five patients were treated with high-dose steroids on deterioration. Outcome was poor: 4 patients died and 2 remained disabled. Autopsies, performed in 2 patients, showed infarctions predominantly involving the posterior circulation territory, thrombosis in penetrating arteries, but no evidence of vasculitis. We identified 5 meningitis cases with delayed vasculopathy in the literature, but these patients did not exactly resemble the clinical course of our patients. Conclusions: Delayed cerebral thrombosis may occur in patients with excellent recovery from pneumococcal meningitis. All patients were treated initially with adjunctive dexamethasone therapy, suggesting a dexamethasone-associated effect. Pathology suggests an immunologic reaction targeting cerebral blood vessels.
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