Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085437 (bacterial meningitis)
4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We presented atypical manifestations in tuberculous meningitis (TbM) and herpes simplex encephalitis (HSE), lymphocytic dominant cerebrospinal fluid pleocytosis in bacterial meningitis, and a hitherto easily overlooked critical illness polyneuropathy (CIP) associated with sepsis. 1) We presented 2 TbM patients with atypical manifestations. One patient was a 25-year-old man who exhibited polymorphonuclear (PMN) dominant pleocytosis in CSF throughout his clinical course. He died the next day after a CSF culture yielded the growth of tuberculous bacilli, before receiving appropriate anti-TBM therapy. This was a rare TbM example of persistent PMN dominant CSF pleocytosis. The other patient was a 39-year-old woman whose CSF pleocytosis changed from lymphocytic dominant to PMN dominant about 1 month after the initiation of antituberculous chemotherapy. This CSF change was followed by multiple cerebral infarcts due to vauculitis caused by TbM. Administration of prednisolone caused marked improvement of the patient's symptomatology. Tuberculomas appeared transiently during anti-TbM therapy, consistent with paradoxical progression of tuberculoma. 2) A few patients with HSE may show atypical CSF findings such as PMN dominant pleocytosis, absence of pleocytosis, and low sugar value. Our national survey of HSE patients showed following percentages of these atypical findings: PMN dominant pleocytosis observed in 10% of the patients in the early stage and at the time of exacerbation, no pleocytosis in 0.9% (1 patient), and low sugar value in 4%. 3) Bacterial meningitis typically causes PMN dominant CSF pleocytosis. However, Listeria meningitis (LM) may cause lymphocytic dominant pleocytosis in 30% of the patients, particularly in elderly ones. We showed one such 69-year-old patient with persistent lymphocytic dominant CSF pleocytosis throughout the clinical course. 4) CIP, septic encephalopathy and critical illness myopathy are 3 major complications associated with sepsis. CIP is a frequent cause of neuromuscular weakness due to axonal dysfunction, which occurs to critically ill patients with sepsis, particularly when multiple organ dysfunctions are present. We showed our CIP patient associated with acute bacterial endocarditis and multiple organ failure. We should bear in mind these atypical manifestations, and frequent and important complications associated with sepsis such as CIP, to provide appropriate management to patients with neuro-infection and sepsis.
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PMID:[Neuro-infections to be borne in mind]. 1223 30

In 2010 Critical Care published a large number of articles on critical care aspects of neurologic and neurosurgical conditions. These aspects included investigation of diagnostic criteria for bacterial meningitis, critical illness myopathy and their relationship to systemic inflammation. A number of studies investigated the biology of sepsis-related delirium, its biomarkers, its relationship to inflammation and its impact on outcome. Other teams reported on the use of magnetic resonance imaging, biomarkers and electroencephalogram to predict outcome in patients who were comatose following cardiac arrest. Our understanding of the pathophysiology as well as management of subarachnoid hemorrhage was addressed in several papers. Topics included the effect of hemodynamic treatment of delayed cerebral ischemia, pulmonary edema and the impact of subarachnoid hemorrhage on endocrine function. Finally, outcome from neurocritical care and patients' retrospective willingness to consent to the treatment they received were reported.
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PMID:Year in review 2010: Critical Care--Neurocritical care. 2214 75