The death of managed care: a regulatory autopsy

On the heels of widespread patient protection legislation in the states, the managed care industry abandoned or greatly scaled back the core elements of gate-keeping, utilization management, and financial incentives, which are the very targets of this legislation. This article explores whether, and to what extent, the industry's abrupt change in course can be attributed to these laws. Based on extensive interviews with key informants in six representative states, the article concludes that these laws were not the primary driver of changes in managed care practices. However, patient protection laws interacted with other social and market forces, through complex forms of feedback and reinforcement, to bring about more thoroughgoing change than would have otherwise occurred.     

Reporting recidivism rates: The criterion and follow-up issues

Although the topic of recidivism invariably elicits much interest, there appears to be considerable conflict and uncertainty as to even crude estimates of the recidivism rate for persons released from prison. The purpose of this research was to examine the extent to which this apparent confusion may be explained by different methodological choices of criterion measure or length of follow-up. Through the cooperation of the Federal Bureau of Investigation, rap sheet follow-up information for a six-year period was obtained for a relatively large random sample of federal prisoners released in 1970. This data enabled calculation of recidivism rates using various criterion measures and follow-up periods applied to the same sample. The effect of varying these definitions on the recidivism rate obtained can then be directly observed.     

Error Reduction, Patient Safety and Institutional Ethics Committees

Institutional ethics committees remain largely absent from the literature on error reduction and patient safety. In this paper, the author endeavors to fill the gap. As noted in the Hastings Center's recent report, "Promoting Patient Safety," the occurrence of medical error involves complex web of multiple factors. Human misstep is certainly one such factor, but not the only one. This paper builds on the Hastings Center's report in arguing that institutional ethics committees ought to play an integral role in the transformation of a "culture of blame" to a "culture of safety" in healthcare delivery.     

A laboratory incubation method for determining the rate of microbiological degradation of skeletal muscle tissue in soil

A controlled laboratory experiment is described, in principle and practice, which can be used for the of determination the rate of tissue decomposition in soil. By way of example, an experiment was conducted to determine the effect of temperature (12 degrees, 22 degrees C) on the aerobic decomposition of skeletal muscle tissue (Organic Texel x Suffolk lamb (Ovis aries)) in a sandy loam soil. Measurements of decomposition processes included muscle tissue mass loss, microbial CO2 respiration, and muscle tissue carbon (C) and nitrogen (N). Muscle tissue mass loss at 22 degrees C always was greater than at 12 degrees C (p < 0.001). Microbial respiration was greater in samples incubated at 22 degrees C for the initial 21 days of burial (p < 0.01). All buried muscle tissue samples demonstrated changes in C and N content at the end of the experiment. A significant correlation (p < 0.001) was demonstrated between the loss of muscle tissue-derived C (Ct) and microbially-respired C (Cm) demonstrating CO2 respiration may be used to predict mass loss and hence biodegradation. In this experiment Q10 (12 degrees C-22 degrees C) = 2.0. This method is recommended as a useful tool in determing the effect of environmental variables on the rate of decomposition of various tissues and associated materials.     

Cerebrospinal fluid analysis in fatal thallium poisoning: evidence for delayed distribution into the central nervous system

The neurologic manifestations of thallium poisoning include a severely painful ascending peripheral neuropathy, autonomic dysfunction, cranial nerve abnormalities, and a toxic encephalopathy. Although thallium has a short half-life, these neurologic manifestations commonly progress, even as the blood concentration of thallium decreases. This suggests either that thallium persists in neuronal tissues or that it initiates an injury cascade that takes time to fully manifest. As the latter mechanism is consistent with many toxin exposures, the concept of a central nervous system reservoir for thallium is often discounted. A recent case provided a unique opportunity to evaluate this possibility. A 48-year-old man was acutely and chronically thallium poisoned by his common-law wife. During his initial exposures, only gastrointestinal symptoms manifested. Following an acute ingestion, hospitalization was required. Over 3 days, his symptoms rapidly progressed from a severely painful neuropathy to slurred speech, ptosis, confusion, coma, respiratory insufficiency, and death. Because of considerations of alternative diagnoses, 2 lumbar punctures were performed, one on admission and another on the day of his death. Serum thallium concentrations obtained from stored blood samples were paired with spinal fluid concentrations from the same days. On day 1, serum and spinal fluid concentrations were 8700 mu/L and 1200 mu/L, respectively. On day 3, although the serum concentration had fallen to 7200 mu/L, the spinal fluid concentration had increased to 2100 mu/L. This case provides evidence to support the hypothesis that thallium distributes into the central nervous system more slowly than the blood compartment, and this may in part account for the progression of neurologic findings in the setting of decreasing serum concentrations.