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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The metabolic basis of the encephalopathy associated with acute bacterial meningitis is unknown. The presence of cerebrospinal fluid lactic acidosis and hypoglycorrhachia suggests that intracellular acidosis or cellular energy depletion may play a role. Phosphorus magnetic resonance spectroscopy allows for the noninvasive determination of intracellular pH and relative amounts of phosphate-containing metabolites in humans. In seven normal volunteers, the intracellular pH of a mixed volume of gray and white matter was 7.00 +/- 0.04 (mean +/- SD). The apparent relative intensities of resonances from adenosine triphosphate, phosphocreatine, phosphodiesters and phosphomonoesters, and inorganic phosphate were measured. An encephalopathic patient with pneumococcal meningitis who had severe cerebrospinal fluid lactic acidosis was studied. Brain intracellular pH and relative phosphate metabolite concentrations were normal. Intracellular acidosis and bioenergetic compromise are therefore not causes of encephalopathy in this disease. This also demonstrates that the human brain can maintain tight control of intracellular pH even in the presence of marked extracellular metabolic acidosis.
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PMID:Brain phosphorus magnetic resonance spectroscopy in acute bacterial meningitis. 277 14

The stress response in humans commonly includes elevations in plasma concentrations of glucocorticoids, catecholamines, glucagon, growth hormone, aldosterone, and renin, resulting in alterations in the metabolism of glucose and other energy substrates, and in increased sodium and water retention. In severe illness, triiodothyronine and sometimes thyroxine are decreased without evidence of clinical hypothyroidism. Antidiuretic hormone may be elevated in bacterial meningitis and other central nervous system disorders, as well as in acute asthma, chronic ventilator therapy, pneumothorax, atelectasis, and postoperatively. Increased ADH concentration can lead to significant hypoosmolality and hyponatremia with adverse effects on the patient. In the setting of severe intracerebral insults, ADH may be inappropriately low, resulting in diabetes insipidus. Insulin concentrations may be inappropriately low for serum glucose concentration, or insulin may have diminished receptor responsiveness in seriously stressed patients. Either situation leads to hyperglycemia. Disturbances in calcium, phosphorus, and magnesium homeostasis may occur relatively frequently in the critically ill patient in response to therapeutic interventions, or illness-induced altered metabolism. It is not always clear when an altered metabolic or hormonal state is an appropriate response to a stress, or represents decompensation of the body's mechanisms for coping with that stress. It is important, however to recognize the common responses of the organism to severe illness, and to monitor for treatable abnormalities which occur.
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PMID:Endocrine manifestations of critical illness in the child. 354 20