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Biomedical subjects

M A Moskowitz

Publications and source records attributed to M A Moskowitz.

At least 127 records · Page 7Linked to original sources
PubMed1997

The impact of alcohol-related diagnoses on pneumonia outcomes.

BACKGROUND: There is controversy regarding the role of alcoholism as a prognostic factor in hospitalized patients with pneumonia. OBJECTIVE: To assess the impact of alcohol abuse on hospitalization charges, length of hospital stay, intensive care unit use, and in-hospital mortality. METHODS: We studied a cohort of all adults hospitalized in 1992 in Massachusetts with a principal diagnosis of pneumonia, and all Massachusetts residents hospitalized for pneumonia in 6 bordering states. RESULTS: For the 23,198 pneumonia cases the mean total hospitalization charges were $9925, mean length of hospital stay was 9.6 days, 12% of the cases had intensive care unit stays, and 10% of the cases died during the hospitalization. In bivariate analyses, pneumonia cases with alcohol-related diagnoses had higher charges (mean, $11,232 vs $9877, P = .07), had shorter length of hospital stay (9.2 vs 9.6 days, P = .02), were more likely to experience an intensive care unit stay (19% vs 12%, P < .001), and had lower in-hospital mortality (6.0% vs 10.2%, P < .001). Multivariable analyses adjusting for comorbidity, pneumonia etiology, and demographics revealed that for pneumonia cases with alcohol-related diagnoses, risk-adjusted hospital charges were $1293 higher (adjusted mean, $11,179 vs $9888, P < .001), length of hospital stay was 0.6 days longer (10.1 vs 9.5 days, P = .001), intensive care unit use was higher (18% vs 12%; adjusted odds ratio, 1.63; 95% confidence interval, 1.33-1.98), and mortality was no different (10% with or without an alcohol-related diagnosis). CONCLUSIONS: Having an alcohol-related diagnosis is associated with more use of intensive care, longer inpatient stays, and higher hospital charges. To understand resource utilization in cases of pneumonia, alcohol abuse is a comorbid factor that must be considered.

Aged↗
PubMed1997

Hospital cost of complications associated with coronary artery bypass graft surgery.

We identified 6,791 coronary artery bypass grafting (CABG) cases using the Massachusetts hospital discharge data to quantify the contribution of complications to the cost of a hospitalization for CABG. After adjusting for in-hospital mortality and baseline clinical severity as other contributors to cost, the additional costs associated with complications were substantial.

Aged↗
PubMed1997

Inhibition of interleukin 1beta converting enzyme family proteases reduces ischemic and excitotoxic neuronal damage.

The interleukin 1beta converting enzyme (ICE) family plays a pivotal role in programmed cell death and has been implicated in stroke and neurodegenerative diseases. During reperfusion after filamentous middle cerebral artery occlusion, ICE-like cleavage products and tissue immunoreactive interleukin 1beta (IL-1beta) levels increased in ischemic mouse brain. Ischemic injury decreased after intracerebroventricular injections of ICE-like protease inhibitors, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD.FMK), acetyl-Tyr-Val-Ala-Asp-chloromethylketone, or a relatively selective inhibitor of CPP32-like caspases, N-benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone, but not a cathepsin B inhibitor, N-benzyloxycarbonyl-Phe-Ala-fluoromethylketone. z-VAD.FMK decreased ICE-like cleavage products and tissue immunoreactive IL-1beta levels in ischemic mouse brain and reduced tissue damage when administered to rats as well. Only z-VAD.FMK and acetyl-Tyr-Val-Ala-Asp-chloromethylketone reduced brain swelling, and N-benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone did not attenuate the ischemia-induced increase in tissue IL-1beta levels. The three cysteine protease inhibitors significantly improved behavioral deficits, thereby showing that functional recovery of ischemic neuronal tissue can follow blockade of enzymes associated with apoptotic cell death. Finally, we examined the effect of z-VAD.FMK on excitotoxicity and found that it protected against alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate-induced or to a lesser extent N-methyl-D-aspartate-induced excitotoxic brain damage. Thus, ICE-like and CPP32-like caspases contribute to mechanisms of cell death in ischemic and excitotoxic brain injury and provide therapeutic targets for stroke and neurodegenerative brain damage.

Animals↗
PubMed1997

Expression of a dominant negative mutant of interleukin-1 beta converting enzyme in transgenic mice prevents neuronal cell death induced by trophic factor withdrawal and ischemic brain injury.

To explore the role of the interleukin (IL)-1 beta converting enzyme (ICE) in neuronal apoptosis, we designed a mutant ICE gene (C285G) that acts as a dominant negative ICE inhibitor. Microinjection of the mutant ICE gene into embryonal chicken dorsal root ganglial neurons inhibits trophic factor withdrawal-induced apoptosis. Transgenic mice expressing the fused mutant ICE-lacZ gene under the control of the neuron specific enolase promoter appeared neurologically normal. These mice are deficient in processing pro-IL-1 beta, indicating that mutant ICEC285G blocks ICE function. Dorsal root ganglial neurons isolated from transgenic mice were resistant to trophic factor withdrawal-induced apoptosis. In addition, the neurons isolated from newborn ICE knockout mice are similarly resistant to trophic factor withdrawal-induced apoptosis. After permanent focal ischemia by middle cerebral artery occlusion, the mutant ICEC285G transgenic mice show significantly reduced brain injury as well as less behavioral deficits when compared to the wild-type controls. Since ICE is the only enzyme with IL-1 beta convertase activity in mice, our data indicates that the mutant ICEC285G inhibits ICE, and hence mature IL-1 beta production, and through this mechanism, at least in part, inhibits apoptosis. Our data suggest that genetic manipulation using ICE family dominant negative inhibitors can ameliorate the extent of ischemia-induced brain injury and preserve neurological function.

Animals↗
PubMed1997

Statewide quality improvement initiatives and mortality after cardiac surgery.

BACKGROUND: Recent reports from New York and northern New England claim that statewide quality improvement initiatives and outcome reporting are leading to decreased mortality following coronary artery bypass graft (CABG) surgery. OBJECTIVE: To compare trends in mortality after CABG surgery in Massachusetts (a state that has not instituted statewide outcome reporting) with the decreases reported from New York and northern New England. DESIGN: Surgical cohorts from 1990, 1992, and 1994 were used to evaluate the risk-adjusted mortality trend for Massachusetts. We present this trend along with the published trends from New York and northern New England. For comparison, we also present unadjusted Medicare mortality trends from Massachusetts, New York, northern New England, and the entire United States. SETTING: All 12 Massachusetts hospitals performing cardiac surgery (excluding a Veterans Affairs hospital). PATIENTS AND DATA SETS: Massachusetts administrative data were used to identify all patients undergoing isolated CABG surgery in 1990, 1992, and 1994. MAIN OUTCOME MEASURES: Observed and risk-adjusted in-hospital mortality. RESULTS: Observed mortality rates in Massachusetts decreased from 4.7% in 1990 to 3.5% in 1992 and to 3.3% in 1994. The corresponding risk-adjusted mortality reductions for 1992 and 1994 (relative to 1990) were 35% and 42%, respectively. The mortality reduction seen in Massachusetts is comparable to the reductions seen in New York and northern New England over similar periods. Unadjusted Medicare mortality trends were generally similar in the states under study, and in the United States as a whole. CONCLUSIONS: In-hospital mortality after CABG surgery has decreased in Massachusetts despite the absence of statewide outcome reporting. Direct program evaluations are needed to better characterize the efficacy of the ongoing statewide outcome studies in New York and northern New England.

Aged↗
PubMed1997

Neuronal nitric oxide synthase mutant mice show smaller infarcts and attenuated apparent diffusion coefficient changes in the peri-infarct zone during focal cerebral ischemia.

Diffusion-weighted MRI at 2 T was used to monitor and assess tissue damage after permanent middle cerebral artery occlusion (MCAO) in wild-type (WT) and mice deficient in nitric oxide synthase gene expression (nNOS-). The ischemic lesion was evaluated 3 h after occlusion and subdivided into the lesion core and peri-infarct zone based on the magnitude of the apparent diffusion coefficient (ADC) change. Infarct volume, measured by using histochemical staining 24 h after MCA occlusion, correlated best with MRI infarct volume as assessed by an ADC threshold of 25% decrease from baseline at 3 h. For ADC thresholds of greater than 25% decrease, lesion size was not significantly different in nNOS- and WT mice. However, brain tissue showing ADC decreases of 10-25% was significantly smaller in the ipsilateral hemisphere of mutants (27 +/- 2% and 21 +/- 2% in WT and nNOS-, respectively; P < 0.05). These findings occurred independently of infarct volume and are consistent with a smaller peri-infarct zone in nNOS- mice. We postulate that the smaller peri-infarct zone is a reflection of less severe metabolic disturbance after ischemia in nNOS- mice, possibly related to diminished production of nitric oxide (NO) or a related product. We conclude that magnetic resonance techniques previously used to assess ischemic damage in larger animals can be extended to the mouse, raising the possibility that the molecular mechanisms leading to ischemic damage can be examined by using genetically engineered mice.

Animals↗
PubMed1997

Physician characteristics: do they influence the evaluation and treatment of breast cancer in older women?

BACKGROUND: To determine if physician specialty, length of time in practice, and fear of malpractice influence the diagnosis and management of breast cancer in older women. METHODS: We used a fractional factorial design that controlled for patient age (65 or 80 years), race, socioeconomic status, mobility, comorbidity, and assertive behavior through 2 videotaped scenarios (a potential breast cancer [no. 1] and a known stage IIA breast cancer [no. 2]). One hundred twenty-eight white male physicians equally divided by specialty (surgeon versus nonsurgeon) and time in practice (< or = 15 or >15 years) viewed the videotapes and made recommendations. RESULTS: The physician subjects saw 46 patients per week, 59% female, and 47% age > or = 65. Their concern over malpractice was 4.7 (on a 10-point Likert scale with a higher score indicating more concern) and did not differ by specialty or time in practice (P values > 0.7). After viewing scenario no. 1, surgeons were less likely than nonsurgeons to consider breast cancer as the principal diagnosis (odds ratio [OR] = 0.4, 95% confidence interval [CI] = 0.2 to 0.9) and to obtain a tissue diagnosis (OR = 0.3, 95% CI = 0.1 to 0.9). However, in scenario no. 2, surgeons were more likely to offer reconstruction (OR = 3.8, 95% CI = 1.4 to 10.4). Physicians in practice < or = 15 years were more likely than those in practice <15 years to obtain a tissue diagnosis in scenario no. 1 (OR = 6.1, 95% CI = 1.9 to 19.2) and to perform full primary therapy in scenario no. 2 (OR = 2.8, 95% CI = 1.2 to 6.9). Physicians who performed an extensive metastatic evaluation (bone or computer tomography [CT] scan) had greater concern over malpractice than those who did not, as did physicians who performed an axillary node dissection (OR = 2.1, 95% CI 1.3 to 3.4 and OR = 1.8, 95% CI = 1.1 to 3.0). CONCLUSIONS: With the uncertainty of how to diagnose and treat older women with breast cancer, physician specialty, length of time in practice, and concern over malpractice do influence clinical decisions.

Age Factors↗
PubMed1997

Menopausal hormone therapy: physician awareness of patient attitudes.

BACKGROUND: Physicians need to be aware of their patients' attitudes toward menopause when counseling women regarding hormone therapy, because menopausal attitudes may affect women's satisfaction with their decisions to use or not to use hormone therapy. Our objectives were to assess physician awareness of patient attitudes on issues surrounding the menopause and hormone therapy, and to determine the prevalence and correlates of hormone use. METHODS: This cross-sectional survey study was conducted in the primary care outpatient practices of an academic medical center. Surveys were simultaneously administered to female patients aged 50 to 70 years (n = 182) and their primary care physicians immediately after clinical encounters. The surveys contained questions from four established (five-point) attitudinal scales (autonomy, desire for information, philosophy of the menopause, barriers to use of hormone therapy), and questions addressing patients' degree of concern about developing various conditions. Physicians were asked to estimate their patients' attitudes. PATIENTS AND METHODS: Physicians were generally aware of patients' desire for autonomy (3.2 versus 3.2, P = 1.0), but tended to underestimate patients' desire for information (3.7 versus 4.5, P = 0.0001) and patients' perceptions of barriers to using hormone therapy (3.2 versus 3.4, P = 0.0001). They also underestimated the extent to which patients view menopause as a medical problem (3.0 versus 3.2, P = 0.0001). Physicians overestimated patients' general concern about heart disease (scale difference 0.40, P = 0.0001) and breast cancer (difference 0.23, P = 0.02). Physicians were less aware of their patients' attitudes when they were male (versus female), interns/residents (versus faculty/fellows), and less knowledgeable about menopausal hormone therapy (versus more knowledgeable). The significant predictors of hormone use on multivariate analysis were past hysterectomy, urinary incontinence, alcohol intake, and possession of knowledge regarding hormone therapy. CONCLUSIONS: Physicians incorrectly estimate some aspects of their patients' attitudes regarding menopause and hormone therapy, and certain physician characteristics may be associated with decreased awareness. To optimize hormone therapy counseling, physicians may need to increase their attention to patients' menopausal attitudes.

Adult↗
PubMed1997

The 5-HT1D receptor antagonist GR-127,935 prevents inhibitory effects of sumatriptan but not CP-122,288 and 5-CT on neurogenic plasma extravasation within guinea pig dura mater.

The aim of this study was to examine whether GR-127,935, a 5-HT1B/1D receptor antagonist, blocks the inhibitory effects of sumatriptan, CP-122,288 and 5-carboxamidotryptamine (5-CT) on plasma protein extravasation, within guinea pig and rat dura matter, following electric stimulation of the trigeminal ganglion. Binding studies first established that GR-127,935 shows a 500-fold selectivity for 5-HT1D binding sites (labeled by [3H]L-694,247) versus 5-HT1F binding sites (labeled by [3H]sumatriptan in the presence of 50 nM 5-carboxamidotryptamine) in guinea pig forebrain homogenates (pKD +/- SD = 7.0 +/- 0.2 at 5-HT1F sites and 9.7 +/- 0.1 at 5-HT1D sites). In guinea pigs, GR-127,935 showed partial agonist activity and inhibited dural plasma protein extravasation. Increasing doses of GR-127,935 reversed the effect of sumatriptan, but did not affect the action of 5-CT and CP-122,288 (at a dose as high as 2 mumol/kg). Sumatriptan, CP 122,288 and 5-CT dose-responsively inhibited plasma protein extravasation. At a dose of 2 mumol/kg (but not at 0.2 mumol/kg), GR-127,935 right-shifted the dose-response curve of sumatriptan. No significant rightward shift was observed in the dose-response of CP-122,288 and 5-CT. In rats, GR-127,935 did not show any significant partial agonist activity. A dose of 0.2 mumol/kg was sufficient to right-shift the dose-response curve of sumatriptan. These data suggest that sumatriptan inhibits neurogenic inflammation via 5-HT1D alpha receptors in guinea pigs and 5-HT1D beta (5-HT1B) receptors in rats. Additional receptor subtypes are likely to be involved in the inhibition of plasma extravasation by CP-122,288 and 5-CT. Pertussis toxin reduced the inhibitory effects of both sumatriptan and 5-CT, but not of muscimol, known to act at GABAA receptors. These results suggest that 5-CT, as well as sumatriptan, act at a receptor linked to an inhibitory G-protein.

Animals↗
PubMed1997

Possible mechanisms of valproate in migraine prophylaxis.

Valproate has been shown to be an effective prophylactic treatment in migraine. Investigation of the mechanism of its antimigraine action is difficult due to the broad range of its biochemical effects and the complex nature of migraine pathophysiology. Valproate increases brain GABA levels and, in doing so, may suppress migraine-related events in the cortex, perivascular parasympathetics or trigeminal nucleus caudalis. There is experimental evidence that it suppresses neurogenic inflammation and directly attenuates nociceptive neurotransmission. In addition, valproate reportedly alters levels of excitatory and inhibitory neurotransmitters and exerts direct effects on neuronal membranes in vitro. Valproate's observed effect may ultimately result from a combination of actions at different loci.

Animals↗
PubMed1997

Isoflurane-induced cerebral hyperemia in neuronal nitric oxide synthase gene deficient mice.

BACKGROUND: Nitric oxide (NO) has been reported to play an important role in isoflurane-induced cerebral hyperemia in vivo. In the brain, there are two constitutive isoforms of NO synthase (NOS), endothelial NOS (eNOS), and neuronal NOS (nNOS). Recently, the mutant mouse deficient in nNOS gene expression (nNOS knockout) has been developed. The present study was designed to examine the role of the two constitutive NOS isoforms in cerebral blood flow (CBF) response to isoflurane using this nNOS knockout mouse. METHODS: Regional CBF (rCBF) in the cerebral cortex was measured with laser-Doppler flowmetry in wild-type mice (129/SV or C57BL/6) and nNOS knockout mice during stepwise increases in the inspired concentration of isoflurane from 0.6 vol% to 1.2, 1.8, and 2.4 vol%. Subsequently, a NOS inhibitor, N omega-nitro-L-arginine (L-NNA), was administered intravenously (20 mg/kg), and 45 min later, the rCBF response to isoflurane was tested again. In separate groups of wild-type mice and the knockout mice, the inactive enantiomer, N omega-nitro-D-arginine (D-NNA) was administered intravenously in place of L-NNA. Brain NOS activity was measured with radio-labeled L-arginine to L-citrulline conversion after treatment with L-NNA and D-NNA. RESULTS: Isoflurane produced dose-dependent increases in rCBF by 25 +/- 3%, 74 +/- 10%, and 108 +/- 14% (SEM) in 129/SV mice and by 32 +/- 2%, 71 +/- 3%, and 96 +/- 7% in C57BL/6 mice at 1.2, 1.8, and 2.4 vol%, respectively. These increases were attenuated at every anesthetic concentration by L-NNA but not by D-NNA. Brain NOS activity was decreased by 92 +/- 2% with L-NNA compared with D-NNA. In nNOS knockout mice, isoflurane increased rCBF by 67 +/- 8%, 88 +/- 12%, and 112 +/- 18% at 1.2, 1.8, and 2.4 vol%, respectively. The increase in rCBF at 1.2 vol% was significantly greater in the nNOS knockout mice than that in the wild-type mice. Administration of L-NNA in the knockout mice attenuated the rCBF response to isoflurane at 1.2 and 1.8 vol% but had no effect on the response at 2.4 vol%. CONCLUSIONS: In nNOS knockout mice, the cerebral hyperemic response to isoflurane is preserved by compensatory mechanism(s) that is NO-independent at 2.4 vol%, although it may involve eNOS at 1.2 and 1.8 vol%. It is suggested that in wild-type mice, eNOS and nNOS contribute to isoflurane-induced increase in rCBF. At lower concentrations (1.2 and 1.8 vol%), eNOS may be involved, whereas at 2.4 vol%, nNOS may be involved.

Anesthetics, Inhalation↗
PubMed1997

Attenuation of transient focal cerebral ischemic injury in transgenic mice expressing a mutant ICE inhibitory protein.

We used transgenic mice expressing a dominant negative mutation of interleukin-1 beta converting enzyme (ICE) (C285G) in a model of transient focal ischemia in order to investigate the role of ICE in ischemic brain damage. Transgenic mutant ICE mice (n = 11) and wild-type littermates (n = 9) were subjected to 3 h of middle cerebral artery occlusion followed by 24 h of reperfusion. Cerebral infarcts and brain swelling were reduced by 44% and 46%, respectively. Neurological deficits were also significantly reduced. Regional CBF, blood pressure, core temperature, and heart rate did not differ between groups when measured for up to 1 h after reperfusion. Increases in immunoreactive IL-1 beta levels, observed in ischemic wild-type brain at 30 min after reperfusion, were 77% lower in the mutant strain, indicating that proIL-1 beta cleavage is inhibited in the mutants. DNA fragmentation was reduced in the mutants 6 and 24 h after reperfusion. Hence, endogenous expression of an ICE inhibitor confers resistance to cerebral ischemia and brain swelling. Our results indicate that downregulation of ICE expression might provide a useful therapeutic target in cerebral ischemia.

Animals↗
PubMed1997

[3H]L-NG-nitroarginine binding after transient focal ischemia and NMDA-induced excitotoxicity in type I and type III nitric oxide synthase null mice.

We investigated the density and distribution of nitric oxide synthase (NOS) binding by quantitative autoradiography using [3H]L-NG-nitroarginine ([3H]L-NNA) after transient focal ischemia or intrastriatal injection of N-methyl-D-aspartate (NMDA) in wild-type (SV-129 and C57black/6) and type I (neuronal) and type III (endothelial) NOS-deficient mice. The middle cerebral artery (MCA) was occluded by an intraluminal filament for 3 h followed by 10 min to 7 days of reperfusion. Specific [3H]L-NNA binding, observed in the wild-type and type III mutant mouse at baseline, increased by 50-250% in the MCA territory during ischemia and the first 3 h of reperfusion. The density of binding sites (Bmax), but not the dissociation constant (Kd), increased significantly during the ischemic period as did type I NOS mRNA as detected by quantitative reverse transcription polymerase chain reaction. [3H]L-NNA binding after intrastriatal NMDA injection also increased by 20-230%. In the type I NOS-deficient mouse, [3H]L-NNA binding was low and only a very small increase was observed after ischemia or excitotoxicity. Under conditions of this study, [3H]L-NNA did not bind to type II NOS as there was no difference in the distribution or density of [3H]L-NNA binding in the rat spleen obtained after lipopolysaccharide treatment despite induction of NOS type II catalytic activity. Our data suggest that an ischemic/excitotoxic insult up-regulates type I NOS gene expression and [3H]L-NNA binding and that this up-regulation may play a pivotal role in the pathogenesis of ischemic/excitotoxic diseases.

Animals↗
PubMed1997

Ischemic brain injury is mediated by the activation of poly(ADP-ribose)polymerase.

Poly(ADP-ribose)polymerase (PARP, EC 2.4.2.30), an abundant nuclear protein activated by DNA nicks, mediates cell death in vitro by nicotinamide adenine dinucleotide (NAD) depletion after exposure to nitric oxide. The authors examined whether genetic deletion of PARP (PARP null mice) or its pharmacologic inhibition by 3-aminobenzamide (3-AB) attenuates tissue injury after transient cerebral ischemia. Twenty-two hours after reperfusion following 2 hours of filamentous middle cerebral artery occlusion, ischemic injury was decreased in PARP-/- and PARP+/- mice compared with PARP+/+ litter mates, and also was attenuated in 129/SV wild-type mice after 3-AB treatment compared with controls. Infarct sparing was accompanied by functional recovery in PARP-/- and 3-AB-treated mice. Increased poly(ADP-ribose) immunostaining observed in ischemic cell nuclei 5 minutes after reperfusion was reduced by 3-AB treatment. Levels of NAD--the substrate of PARP--were reduced 2 hours after reperfusion and were 35% of contralateral levels at 24 hours. The decreases were attenuated in PARP-/- mice and in 3-AB-treated animals. Poly(ADP-ribose)polymerase cleavage by caspase-3 (CPP-32) has been proposed as an important step in apoptotic cell death. Markers of apoptosis, such as oligonucleosomal DNA damage, total DNA fragmentation, and the density of terminal deoxynucleotidyl transferase dUTP nick-end-labelled (TUNEL +) cells, however, did not differ in ischemic brain tissue of PARP-/- mice or in 3-AB-treated animals versus controls, although there were differences in the number of TUNEL-stained cells reflecting the decrease in infarct size. Thus, ischemic brain injury activates PARP and contributes to cell death most likely by NAD depletion and energy failure, although the authors have not excluded a role for PARP in apoptotic cell death at earlier or later stages in ischemic cell death. Inhibitors of PARP activation could provide a potential therapy in acute stroke.

Animals↗
PubMed1997

Variations in the performance of hip fracture procedures.

OBJECTIVES: Hip replacement is the preferred treatment for displaced femoral neck fractures, whereas other less expensive procedures are preferred for nondisplaced fractures. The authors determined whether there was geographic variation in the use of hip replacement to treat displaced and nondisplaced fractures. METHODS: The authors studied 332 patients, age 65 years or older, hospitalized with a femoral neck fracture in three cities. RESULTS: The population was 55% over age 80, 80% female, and lived in Houston (17%), Pittsburgh (29%), and Minneapolis (54%). Rates of hip replacement varied by city (Houston-84%, Pittsburgh-77%, Minneapolis-63%; P = 0.002), with great variability among patients with nondisplaced fractures (Houston-88%, Pittsburgh-77%, and Minneapolis-56%; P = 0.0001), and no variation among those with displaced fractures (P = 0.72). Other factors associated with hip replacement are history of hip fracture (P = 0.003) and cerebrovascular disease (P < or = 0.10), APACHE II-APS score (P = 0.09), and impacted fracture (P = 0.001). Sociodemographic and functional status (perceived health; activities of daily living and instrumental activities of daily living dependencies) were not associated with hip replacement (P > 0.10). In a logistic model controlling for prior history, APACHE II-APS, and fracture characteristics, city remained a significant predictor of hip replacement (P < 0.001). CONCLUSIONS: Despite an absence of evidence supporting its appropriateness and a much higher cost, hip replacement is used to treat nondisplaced fractures much more frequently in Houston and Pittsburgh than in Minneapolis.

APACHE↗