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Study Objectives: Investigators have been using severity-of-illness indexes such as APACHE II (acute physiology and chronic health evaluation score II) to describe patients with prolonged critical illness. However, little is known about the utility of these indexes for this patient population. We evaluated the ability of four severity-of-illness indexes to predict mortality rates in 182 patients with prolonged critical illness.Design: Retrospective inception cohort study.Setting: A single, urban, long-term, acute-care hospital in Chicago.Patients: One hundred eighty-two patients transferred from 37 acute-care hospital ICUs.Measurements and Results: We assessed four indexes: the acute physiology and chronic health evaluation II, the simplified acute physiology score II, the mortality prediction model II, and the logistic organ dysfunction system using variables measured on admission to the long-term acute-care hospital ICU. We found that none of these indexes distinguished well between the patients who lived and the patients who died (area under ROC [receiver operating characteristics] curve < 0.70 for all), nor did they assign correct probabilities of death to individual patients (Hosmer-Lemeshow goodness-of-fit statistics, p < 0.01 for all).Conclusions: Investigators and clinicians should use caution in using severity-of-illness measures developed for acutely ill patients to describe critically ill patients admitted to long-term care units. As clinical practice and research focus more on these latter patients, development of adequately performing severity-of-illness measures appropriate to this patient population will be needed. [ABSTRACT FROM AUTHOR]

BACKGROUND: There are conflicting data on the effects of antipsychotic medications on delirium in patients in the intensive care unit (ICU). METHODS: In a randomized, double-blind, placebo-controlled trial, we assigned patients with acute respiratory failure or shock and hypoactive or hyperactive delirium to receive intravenous boluses of haloperidol (maximum dose, 20 mg daily), ziprasidone (maximum dose, 40 mg daily), or placebo. The volume and dose of a trial drug or placebo was halved or doubled at 12-hour intervals on the basis of the presence or absence of delirium, as detected with the use of the Confusion Assessment Method for the ICU, and of side effects of the intervention. The primary end point was the number of days alive without delirium or coma during the 14-day intervention period. Secondary end points included 30-day and 90-day survival, time to freedom from mechanical ventilation, and time to ICU and hospital discharge. Safety end points included extrapyramidal symptoms and excessive sedation. RESULTS: Written informed consent was obtained from 1183 patients or their authorized representatives. Delirium developed in 566 patients (48%), of whom 89% had hypoactive delirium and 11% had hyperactive delirium. Of the 566 patients, 184 were randomly assigned to receive placebo, 192 to receive haloperidol, and 190 to receive ziprasidone. The median duration of exposure to a trial drug or placebo was 4 days (interquartile range, 3 to 7). The median number of days alive without delirium or coma was 8.5 (95% confidence interval [CI], 5.6 to 9.9) in the placebo group, 7.9 (95% CI, 4.4 to 9.6) in the haloperidol group, and 8.7 (95% CI, 5.9 to 10.0) in the ziprasidone group (P = 0.26 for overall effect across trial groups). The use of haloperidol or ziprasidone, as compared with placebo, had no significant effect on the primary end point (odds ratios, 0.88 [95% CI, 0.64 to 1.21] and 1.04 [95% CI, 0.73 to 1.48], respectively). There were no significant between-group differences with respect to the secondary end points or the frequency of extrapyramidal symptoms. CONCLUSIONS: The use of haloperidol or ziprasidone, as compared with placebo, in patients with acute respiratory failure or shock and hypoactive or hyperactive delirium in the ICU did not significantly alter the duration of delirium. (Funded by the National Institutes of Health and the VA Geriatric Research Education and Clinical Center; MIND-USA ClinicalTrials.gov number, NCT01211522.). [ABSTRACT FROM AUTHOR]

Purpose: The Health Care Financing Administration's guidelines for billing and documentation by attending physicians have increased the amount of time that attending physicians spend documenting the services that they provide for patients. This study assessed the impact of these guidelines on attending physicians' teaching of housestaff on inpatient medical wards., Method: A survey of 92 housestaff from the department of medicine at one teaching hospital was conducted in 1998 to determine how attending physicians' billing and documentation requirements, clinic responsibilities, teaching styles, and inpatient census affected the quantity and quality of their teaching. The questionnaire included a rank-order analysis of factors affecting quantity and quality of attending physicians' teaching, as well as a five-point Likert scale assessing the quality of attending physicians' teaching., Results: All housestaff responded. A total of 39% of housestaff perceived billing and documentation requirements to be the major detriment to quantity of teaching by attending physicians, and 30% perceived these requirements to be the major detriment to quality of teaching by attending physicians. Housestaff perceived more teaching and higher-quality teaching on services where attending physicians did not perform billing and documentation during teaching rounds., Conclusion: Billing and documentation requirements are a major detriment to the quantity of teaching on inpatient services, especially when faculty attempt to meet these requirements during teaching rounds.

Long-term acute-care (LTAC) hospitals are facilities exempt from the Medicare prospective payment system and which provide care to patients suffering from prolonged critical illness. From August 1, 1995 to July 31, 1996, we studied the outcomes of 133 mechanically ventilated patients who were consecutively admitted to a large urban LTAC hospital from intensive care units (ICUs) of acute-care hospitals. Survival and functional status within 1 yr after the index admission were measured, and specific patient variables were used to develop a predictive model for survival at 1 yr. Of the 133 patients studied, 66 (50%) died prior to discharge. Of discharged patients, 70% had been successfully liberated from mechanical ventilation. One year after LTAC hospital admission, 103 (77%) of the patients had expired, typically after spending the majority of their days in acute care or long-term care facilities. Eleven 1-yr survivors (8%) were fully functional, whereas the remainder had significantly reduced functional status. Patients older than 74 yr, and patients older than 64 yr and not functionally independent before admission, had a 95% (confidence interval [CI]: 84% to 99%) 1-yr mortality; patients without these characteristics had a 56% (CI: 41% to 71%) 1-yr mortality (p < 0.001). We demonstrate characteristics predicting the poorest prognoses for patients requiring prolonged mechanical ventilation. These characteristics may be identifiable before transfer to an LTAC hospital.

We studied 118 patients with prolonged critical illness to determine if there would be a difference in outcome between patients managed by university-based (UB) or community-based (CB) intensivists. Patients consecutively admitted to a long-term acute care hospital were assigned in an arbitrary manner to the UB service or CB service. Patient survival, length of stay, and success and length of time required for liberation from mechanical ventilation (MV) were compared using survival analysis, logistic regression, and analysis of variance techniques. Patients on the UB service were liberated from MV in 32% fewer days (39 versus 57 d, p = 0.02) and were marginally more likely to be liberated from MV (46% versus 30%, p = 0.14). UB physicians were more likely to write do not resuscitate orders (59% versus 33%, p < 0.01) and to withdraw life-sustaining therapy (12% versus 2%, p = 0.09). There were no detectable differences in survival between the two groups. Estimated reimbursement for CB physicians ($6,797/patient) was 46% greater than for UB physicians ($4,651/patient) for discharged patients (p = 0.03). We conclude that patients experiencing prolonged critical illness may experience different outcomes based on their physician provider. In our study, patients were liberated more quickly from MV, were withdrawn from life support more readily, and were managed at lower cost by UB intensivists than by CB intensivists.

This study was performed to test the hypothesis that activated eosinophils or their secretory products can directly stimulate sensory neurons to release their neuropeptides. Neurons derived from neonatal rat dorsal root ganglia (DRG), which synthesize and store sensory neuropeptides, were placed in primary cell culture and were exposed to eosinophils or their bioactive mediators. The resultant release of substance P (SP) was measured by enzyme-linked immunosorbent assay and was expressed as a percent (mean +/- SE) of total neuronal SP content. Eosinophils were isolated from human volunteers with a history of allergic rhinitis and/or mild asthma and were activated by incubation with cytochalasin B (5 micrograms/ml) and N-formyl-methionyl-leucyl-phenylalanine (FMLP, 1 microM). Activated eosinophils [6 x 10(6)/ml, suspended in Hanks' buffered salt solution (HBSS)] applied to cultured DRG neurons for 30 min increased basal SP release 2.4-fold compared with HBSS-exposed neurons (activated eosinophils 11.10 +/- 2.48% vs. HBSS 4.59 +/- 0.99%; P = 0.002), whereas neither nonactivated eosinophils nor cytochalasin B and FMLP in HBSS influenced SP release. Additional cultured DRG neurons were exposed to soluble products made by eosinophils. Compared with SP release under control conditions (2.37 +/- 0.34%), major basic protein (MBP) increased release in a concentration-related fashion (e.g., 3 microM MBP: 6.23 +/- 0.67%, P = 0.006 vs. control), whereas neither eosinophil cationic protein (3 microM), eosinophil-derived neurotoxin (3 microM), leukotriene D4 (500 nM), platelet-activating factor (100 nM), nor H2O2 (100 microM) affected SP release. These studies demonstrate that activated eosinophils can stimulate cultured DRG neurons directly and suggest that MBP may be the responsible mediator.

Several authors have investigated the interaction of noise and aspirin in hearing loss, with conflicting results. We studied the combined effects of noise and high doses of aspirin on hearing in rats. Thirty-eight Sprague-Dawley rats were divided into the following five groups: (1) controls; (2) aspirin only; (3) noise only; (4) 8-day per 200 mg of aspirin per noise; and (5) 12-day per 200 mg of aspirin per noise. Auditory brain-stem-evoked responses were measured in each animal prior to, 24 hours after, and 3 weeks after aspirin and noise exposure. The animals were killed and hair cells were counted in 200-micron segments and expressed graphically. Results showed significant differences in permanent threshold shift and hair cell loss between all noise-exposed animals and non-noise-exposed animals. There was also a significantly greater amount of hair cell loss in group 5 when compared with groups 3 or 4. The 12-day per 200 mg of aspirin per noise regimen (group 5) also proved to be fatal for 6 of 15 of these animals, and caused significant weight loss in the survivors. No weight loss or deaths were noted in any other group.