Referral selection bias in the Medicare hospital mortality prediction model: are centers of referral for Medicare beneficiaries necessarily centers of excellence?

OBJECTIVE: Although the Health Care Financing Administration (HCFA) uses Medicare hospital mortality data as a measure of hospital quality of care, concerns have been raised regarding the validity of this concept. A problem that has not been fully evaluated in these data is the potential confounding effect of illness severity factors associated with referral selection and hospital mortality on comparisons of risk-adjusted hospital mortality. We address this issue. DATA SOURCES AND STUDY SETTING: We analyzed the 1988 Medicare hospitalization data file (MEDPAR). We selected data on patients treated at the two Mayo Clinic-associated hospitals in Rochester, Minnesota, and a group of seven other hospitals that treat many patients from large geographic areas. These hospitals have had observed mortality rates substantially lower than those predicted by the HCFA model for the period 1987-1990. STUDY DESIGN: Using the multiple logistic regression model applied by HCFA to the 1988 data, we evaluated the relationship between distance from patient residence to the admitting hospital and risk-adjusted hospital mortality. PRINCIPAL FINDINGS: Among patients admitted to Mayo Rochester-affiliated hospitals, residence outside Olmsted County, Minnesota was independently associated with a 33 percent lower 30-day mortality rate (p < .001) than that associated with residence in Olmsted County. When patients at Mayo hospitals were stratified by residence (Olmsted County versus non-Olmsted County), the observed mortality was similar to that predicted for community patients (9.6 percent versus 10.2 percent, p = .26), whereas hospital mortality for referral patients was substantially lower than predicted (5.0 percent versus 7.5 percent, p = < .001). After incorporation of the HCFA risk adjustment methods, distance from patient residence to the hospitals was also independently associated with mortality among the Mayo Rochester-affiliated hospitals and seven other referral center hospitals. CONCLUSIONS: The HCFA Medicare hospital mortality model should be used with extreme caution to evaluate hospital quality of care for national referral centers because of residual confounding due to severity of illness factors associated with geographic referral that are inadequately captured in the extant prediction model.

State rate regulation and inpatient mortality rates.

Most research on hospital rate regulation has focused on costs, but concern about its consequences for quality of care, particularly mortality rates, has also been raised. In this study mortality rates and standardized mortality ratios (SMR) were computed to estimate any effect on quality, using data about Medicare beneficiaries hospitalized during 1986. Regulated states had lower SMRs for both patients and the general population than unregulated states and admitted significantly fewer patients. We found no basis for concluding that rate regulation is adversely related to patient mortality or population mortality, despite lower admission rates.

Potential effectiveness of quality assurance screening using large but imperfect databases.

To examine the effect of imprecise classification of patient risk (severity of illness) on an otherwise highly accurate quality assurance screening technique, data on clinical outcomes were generated for a simulated hospital system consisting of 108 facilities treating approximately 565,000 patients a year. In these simulations, marked differences in facility size, casemix distribution, and quality of care were combined with random variations in outcome. Pooled data for all 108 facilities were used to create algorithms that combined 468 discrete patient risk classifications into either ten or three groups with broad, overlapping ranges of patient-specific risks of unfavorable clinical results. When derived algorithms were applied to independently generated facility-specific data, the ability to identify hospital systems with and without quality of care problems was maintained with ten, but not with three, risk groups. However, even three moderately heterogeneous risk groups were sufficient to preserve a high degree of sensitivity and specificity in screening for potential quality of care problems within individual facilities. Thus, outcome-based quality assurance screening can be highly accurate in actual health care situations in which only imprecise estimations of patient-specific risk can be achieved.

Potential effectiveness of comparative casemix-corrected adverse outcome rates as quality monitors in a simulated hospital system.

To facilitate outcome-based medical quality assurance, a screening technique was developed which corrected facility-specific data for casemix using mean outcome rates from pooled data to establish norms for "uniform-risk groups" of patients. A stimulated health care system (108 facilities treating over 500,000 annually) was created to evaluate this technique's ability to distinguish between systems whose adverse outcomes were determined solely by casemix and random variations and those with true differences in quality of care. Specificity and sensitivity of quality of care decisions for individual facilities also were assessed. The screening technique achieved excellent differentiation between "homogeneous" systems and those with facility-specific variations in quality of care. No more than 3% of facilities without quality of care problems were ever inaccurately labeled, unless systematic or random errors in patient risk classification were introduced. Sensitivity in detecting substandard facilities was 35% when true deviation from standard was 2.5%, and rose to virtually 100% when deviation was 25% or greater. Thus, simulation can serve as an efficient method of testing the potential performance of casemix-corrected quality assurance screening under a wide variety of circumstances.

Cerebrospinal fluid ions in metabolic acidosis in dogs: effects of acetazolamide.

We hypothesized that, during isosmotic isonatremic HCl acidosis with maintained isocapnia in cisternal cerebrospinal fluid (CSF), acetazolamide, by inhibiting carbonic anhydrase (CA) in the central nervous system (CNS), should produce an isonatric hyperchloric metabolic acidosis in CSF. Blood and CSF ions and acid-base variables were measured in two groups of anesthetized and paralyzed dogs with bilateral ligation of renal pedicles during 5 h of HCl acidosis (plasma [HCO3-] = 11 meq/l). Mechanical ventilation was regulated such that arterial PCO2 dropped and CSF Pco2 remained relatively constant. In group I (control group, n = 6), CSF [Na+] remained unchanged, [HCO3-] and strong ions difference (SID) fell, respectively, 6.1 and 5 meq/l, and [Cl-] rose 3.5 meq/l after 5 h of acidosis. In acetazolamide-treated animals, (group II, n = 7), CSF [Na+] remained unchanged, [HCO3-], and SID fell 11 and 7.1 meq/l, respectively, and [Cl-] rose 7.1 meq/l. We conclude that during HCl acidosis inhibition of CNS CA by acetazolamide induces an isonatric hyperchloric metabolic acidosis in CSF, which is more severe than that observed in controls.

Excess mortality and morbidity associated with right bundle branch and left anterior fascicular block.

Excess mortality and morbidity associated with right bundle branch and left anterior fascicular block were evaluated in 108 patients with block (age 74 +/- 10 years, 69% male) and 108 age- and sex-matched control patients with normal conduction. Clinical characteristics were similar initially except for more congestive heart failure in patients with block. Life table analysis revealed a higher 12 year mortality with block, even after omitting patients with moderate or severe congestive heart failure (risk ratio 1.47, p less than 0.05). Compared with control subjects, the group of patients with block had more sudden death and deaths of unknown cause, but a similar number of noncardiac and diagnosed cardiac deaths. More patients with block developed new second and third degree atrioventricular block or new overt coronary artery disease, but this finding did not support prophylactic pacing in asymptomatic patients. The importance of internal controls in assessing the natural history of clinical and electrocardiographic abnormalities is emphasized.

Verapamil versus placebo in relieving stable angina pectoris.

Verapamil and placebo were compared in patients with stable, effort-induced angina. Single-blind dose titration (240, 360 and 480 mg/day) preceded a double-blind crossover. Among the 18 patients who completed graded exercise stress tests with reproducible pretreatment effort-limiting angina, exercise duration increased from 348 +/- 127 seconds (SD) before treatment to 494 +/- 182 seconds after verapamil (p less than 0.001), but did not change after placebo. Compared with placebo, verapamil reduced the weekly number of anginal episodes from 4.54 +/- 5.03 to 2.44 +/- 3.30 (p less than 0.05) and reduced nitroglycerin consumption from 3.46 +/- 5.30 to 1.55 +/- 2.89 tablets per week (p less than 0.05). Of 26 patients who completed the single-blind dose titration, 16 were improved (greater than 1 minute) at a dosage of 240 or 360 mg/day. No patient improved (greater than 1 minute) on 480 mg/day who had not already improved on a lower dose, but side effects requiring reduction in dosage occurred in seven patients receiving 480 mg of verapamil per day. Verapamil is an effective antianginal drug that appears most efficacious at a dose of 360 mg/day, but side effects are common at a dose of 480 mg/day.

Hydrostatic forces limit swelling of rat ventricular myocardium.

To study ventricular cellular volume regulation when cell membranes and ion pumps cannot prevent swelling, rat ventricular sections were incubated in modified Krebs-Henseleit solutions in which 1) potassium was substituted for sodium, ion for ion; or 2) sodium chloride was reduced to decrease osmolarity to 228, 171, or 114 mosM. Ventricular water, [3H]inulin and [3H]mannitol spaces, potassium, sodium, chloride, and protein contents, and resting transmembrane potentials were measured. Increases in ventricular cellular volume were less than 30% in potassium-substituted and extremely dilute media (114 mosM), in contrast to increases of over 100% in identically treated renal cortical slices. In potassium-substituted solution, the fluid gained by ventricular cells during incubation was hypertonic with respect to the bathing medium. In dilute solution (171 and 114 mosM), ventricular, cellular, and extracellular osmolarities equilibrated only after substantial losses of cellular ions had occurred. These findings support the existence of mechanical limitations to ventricular cellular swelling, which may be caused by a unique network of interstitial collagen present in ventricular myocardium.

Sodium permeability and myocardial resistance to cell swelling during metabolic blockade.

The role of cell membrane permeability to sodium in cell volume regulation during inhibition of the sodium-potassium exchange pump with ouabain and during total metabolic blockade was evaluated in sections of guinea pig renal cortex, ventricle, and atrium incubated in Krebs-Henseleit solution. In all tissues, 2 and 3 h of ouabain and metabolic blockade resulted in similar marked losses of potassium and parallel continuous reductions in resting membrane potentials. Only metabolic blockade of renal cortex increased cell water, chloride, and total monovalent cations (potassium plus sodium) significantly. Compared to ouabain, metabolic blockade markedly increased the rate of cellular washout of 24Na+ from renal cortex (t 1/2 reduced by 47%), which was significantly greater than reductions in t 1/2 from ventricle (16%) and atrium (15%). Thus, inhibition of sodium-potassium exchange pump activity was not sufficient to produce cell swelling unless associated with marked increases in cell membrane permeability to sodium, in which case sodium influx exceeded potassium loss and substantial increases in monovalent cations, chloride, and water occurred.

Anion exchange and volume regulation during metabolic blockade of renal cortical slices.

1. The development of swelling of rat and guinea-pig renal cortical slices was studied after metabolic blockade (hypoxia plus glycolytic blockade with iodo-acetic acid) and/or exposure to 'isotonic' high potassium, no sodium solution. 2. Swelling was greater after exposure to oxygenated high potassium solution than after metabolic blockade in physiologic Krebs-Henseleit solution. Swelling was reduced after metabolic blockade in high potassium solution compared to incubation in oxygenated high potassium solution. Increasing periods of transient metabolic blockade in Krebs-Henseleit solution progressively blunted swelling when slices were subsequently incubated in oxygenated high potassium solution. 3. Metabolic blockade in Krebs-Henseleit solution resulted in marked reductions in potassium and increases in sodium. Incubation in high potassium solution resulted in marked increases in potassium and similar low levels of sodium regardless of associated interventions. Metabolic blockade in both media resulted in significantly greater increases in renal cortical chloride than in monovalent cations (potassium plus sodium). Incubation in oxygenated high potassium solution was associated with similar increases in renal cortical chloride and total monovalent cations. 4. Renal cortical losses of solids and protein and increases in renal cortical inulin space were greater after metabolic blockade than after incubation under oxygenated conditions regardless of the incubation media. 5. These data support the conclusion that during metabolic blockade there is a significant replacement of larger intracellular anions by extracellular chloride. The loss of osmotically active intracellular anions limits the increase in renal cortical volume during metabolic inhibition and exposure to high potassium solution.

Resistance of contracting myocardium to swelling with hypoxia and glycolytic blockade.

The interrelationship of myocardial metabolism, performance and tissue hydration was examined in isolated contracting rat, guinea pig and dog myocardium. Myocardial metabolism was altered by blocking aerobic, and both aerobic and anaerobic metabolism. Myocardial water content and distribution were measured in rat myocardium using 3H-inulin and 51Cr-EDTA as extracellular markers. Myocardial hydration was also evaluated by light and electron microscopy. The relative susceptibility of non-contracting slices of rat and guinea pig myocardium and kidney to swelling secondary to these interventions was also explored. Hypoxia resulted in a partially reversible reduction in mechanical function; hypoxia plus glycolytic blockade led to irreversible severe contracture and total loss of tension development. Neither hypoxia nor hypoxia plus glycolytic blockade resulted in increased total tissue or extracellular water in previously contracting preparations or in non-contracting slices of myocardium. On the other hand, there were significant increases in cellular water in similarly treated kidney slices after each intervention. Thus, despite severe, irreversible derangements of mechanical function, myocardium did not swell under conditions which produced swelling in renal cortex.

Aortic valve replacement with the De Bakey valve.

De Bakey prostheses were inserted in 29 patients with aortic valve disease between October, 1970, and May, 1972. Ten patients have died, but all but one of the remaining 19 have beel followed for a minimum of 19 months. Evaluation of the results in these subjects indicates that the function of the De Bakey valve compares favorably with that of other aortic valve prostheses.