{'fraction_non_alphanumeric': 0.020308692120227456, 'fraction_numerical': 0.008123476848090982, 'mean_word_length': 5.695652173913044, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Neuron-specific enolase as a marker of fatal outcome in patients with severe sepsis or septic shock.

To the Editor:—The mortality rate of septic patients increases progressively with increasing severity of encephalopathy caused by sepsis. Several mechanisms have been suggested as the cause of septic encephalopathy, including direct central nervous system infection, endotoxin and cytokine effects on the brain, inadequate cerebral perfusion, metabolic derangements, or complications of medical therapy. Neuropathologic examinations of 12 septic patients who died during protracted, severe septic encephalopathy showed microabscesses in eight cases and vascular lesions in approximately half. We assessed the ability of the neuron-specific enolase (NSE), the neuronal isomer of the glycolytic enzyme 2-phospho-D-glycerate hydrolase, and the central nervous system–specific isoforms of S100 to predict mortality in patients with severe sepsis or septic shock. Both NSE and S100 have been shown to be specific parameters for the assessment of Table 2. Comparison of Tidal Volume and Peak Inspiratory Pressure When Sealing between Laryngeal Mask Airway and Endotracheal Tube and/or Laryngeal Mask Airway Cuff Inflation was Performed