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Biomedical subjects

J Dempsey

Publications and source records attributed to J Dempsey.

At least 55 records · Page 3Linked to original sources
PubMed1991

How can hospital autopsy rates be increased?

Autopsy studies have provided the foundation of our knowledge of clinical medicine. Despite the acknowledged value of this postmortem procedure, hospital autopsy rates have fallen to only 10% of deaths. New diseases and therapeutic modalities are in danger of not being properly evaluated. A number of proposals have been made to increase autopsy rates. While many of these proposals are excellent, the key to increasing autopsy rates is direct reimbursement by third-party payers.

Attitude of Health Personnel↗
PubMed1990

Duplex Doppler examination of a perinephric abscess in a renal transplant.

Perinephric abscess has no characteristic ultrasonic appearance or location. Differentiation from urinoma, lymphocele, or hematoma depends on clinical and laboratory findings. Therapy consists of percutaneous catheter drainage, surgical drainage, and antibiotic therapy. Acute rejection is the most common cause of decreased diastolic flow during the immediate postoperative period. Acute tubular necrosis does not usually alter blood flow unless it is severe. Duplex doppler ultrasonic assessment of the renal transplant during the immediate postoperative period may provide a valuable baseline for comparison if complications develop. Baseline and follow-up ultrasonography to evaluate diastolic flow can help determine whether a posttransplant patient should receive emergency or conservative therapy for complications.

Abscess↗
PubMed1990

Hospital wars.

According to the author, marketing warfare precipitated by increased competition and recent public policy decisions is a distinct possibility in the health care environment. Since the military marketing metaphor has been useful in describing the current situation, Dr. Dempsey presents clear explanations of both attack and defense strategies with examples of organizations that have used them.

Economic Competition↗
PubMed1990

Health care costs: the other point of view.

Health care delivery in America is not efficient. Hospitals are not efficient and many are still wasteful. Some of the most blatant wastes in hospitals are staffing patterns that developed during the years of cost reports. Spending patterns become the norm, rather than excess, when they continue unabated for years. There are many reasons for cost increases in health care and specifically in hospitals. However, it is difficult to make these reasons add up to the total cost increase. No one has the answers; observation can only be made of what has been occurring and what continues to occur. Whatever the reason for the increase in health care costs, the consumer will bear the burden because of the circular flow of income and expenditures between the business sector and the household sector. Increased health care costs are passed on to the consumer in the form of increased expenditures for household goods and services or taxes. Ford Motor Company President Mr. Peterson says that $1,500 of every new automobile represents employee health care costs. The American consumer created the demand for health care services, and only the consumer can control the demand. One solution would be to let the consumer bear health care costs directly and remove the inefficiencies created by third party insurance carriers. This hypothesizes that the health care consumer is the most efficient shopper for health care services, and that third party insurance carriers are an important source of inefficiency in the health care delivery system. Many other solutions have been proposed by the government and by the insurance and health care industries, but most have only increased the cost of health care. Perhaps some day the health care industry will learn how to control the dynamics of this four-party purchasing decision. Until then, costs will continue to grow dramatically, and the executives of the industries who compete in the two-party purchasing system will wonder why the process is so complicated.

Costs and Cost Analysis↗
PubMed1986

Lymphadenopathy due to fatal histiocytic proliferative disorder containing Michaelis-Gutmann bodies.

A 59-year-old white man had generalized lymphadenopathy, fever, weight loss, and hypercalcemia. Histologic examination of seven lymph nodes from three different anatomic sites revealed a diffuse histiocytic infiltrate containing numerous typical Michaelis-Gutmann (MG) bodies. Histochemical and immunohistochemical results confirmed the histiocytic nature of the predominant cell within the infiltrate. Approximately equal numbers of residual normal B-cells, T-helper, and T-suppressor cells were present. Electron microscopy revealed extracellular and intracellular MG bodies, many of which were membrane-bound. Special stains, electron microscopy, and lymph node culture did not demonstrate microorganisms. The histologic features of the infiltrate were those of malacoplakia. However, the disease behaved like a lymphoma, with the occurrence of lymphadenopathy and a fatal outcome.

B-Lymphocytes↗
PubMed1986

First trimester chorionic villi sampling and direct chromosome preparations.

Chorionic villi sampling was performed on 52 patients prior to elective termination of their pregnancies. Villi were obtained in 42, and direct chromosome preparations were successful in 41 of them. The use of a mixture of 0.075 M potassium chloride and 1% sodium citrate in the ratio of 2:1 for hypotonic treatment and 40% acetic acid for cell dispersal yielded chromosomes with good morphology and G-bands.

Biopsy, Needle↗
PubMed1985

Small bowel capillary dilatation in portal hypertension.

A patient with small bowel capillary dilatation and cirrhosis is reported. This patient had persistent, unexplained gastrointestinal bleeding. Small bowel capillary dilatation appears to be unique to patients with portal hypertension. The possible role of small bowel capillary dilatation in causing gastrointestinal bleeding is discussed.

Adult↗
PubMed1983

Mechanisms of hypoxia-induced periodic breathing during sleep in humans.

Ventilation was studied during wakefulness and sleep in six healthy humans in normoxia (mean barometric pressure (PB) = 740 torr), and in hypobaric hypoxia (PB = 455 torr). Hypoxia caused hyperventilation and hypocapnic alkalosis (delta Pa,CO2 = -7 torr) during wakefulness and in all sleep states. Periodic breathing was the predominant pattern of breathing in all stages of non-rapid eye movement (non-r.e.m.) sleep in hypoxia, but was rarely observed during wakefulness or r.e.m. sleep. Periodic breathing was composed of repetitive oscillations of reproducible cycle length characterized by clusters of breaths with augmented inspiratory effort (VT/TI) and highly variable distribution of breath-to-breath minute ventilation (VE) and tidal volume (VT), which alternated regularly with prolongations of the expiratory pause of the last breath of each cluster (apnea duration = 5-18 sec). Hypoxia-induced periodic breathing was eliminated by: (a) acute restoration of normoxia coincident with a 3-6 torr increase in Pa,CO2; and (b) augmented FI,CO2 (at constant arterial oxygen saturation) which rapidly and reversibly eliminated apneas and stabilized breathing pattern with a less than 2 torr increase in Pa,CO2. If hypocapnia was prevented (by augmented FI,CO2) during acute induction of hypoxia in non-r.e.m. sleep, periodic breathing was also prevented. We propose that the genesis of hypoxia-induced periodic breathing requires the combination of hypoxia and hypocapnia. Periodicity results from oscillations in CO2 about a CO2-apnea threshold whose functional expression is critically linked to sleep state.

Adult↗
PubMed1982

Determinants and consequences of ventilatory responses to competitive endurance running.

Pulmonary ventilation and pattern, arterial blood gases, and [H+] were studied in 15 highly trained runners [maximum O2 consumption (VO2 max) 53--82 ml . kg-1 . min-1] during road racing (24 km, n = 5) and 60--70 min of treadmill running (70--75% VO2 max, n = 13). The predominant response throughout prolonged treadmill running and especially road running was a tachypneic, respiratory alkalosis (-5 to -12 Torr PaCO2) that was evident early in the exercise. Time-dependent increases in breathing frequency (10--40%, 6--60 min work), expired ventilation, and dead space ventilation were common in prolonged work; these were especially evident in two subjects even as VO2 fell during road racing under hot humid conditions. The tachypneic hyperventilation was 1) most often accompanied by alkaline [H+]a, 2) associated with time-dependent elevation in rectal temperature (1--1.5 degrees C) and circulating norepinephrine (5--20 x rest), 3) quickly alleviated via hyperoxia after 60--70 min of exercise, and 4) was shown to result from increased running velocity in separate experiments that compared walking vs. running at similar CO2 excretion and [HCO-3]a. In highly trained runners competing under favorable environmental conditions and optional pace selection, we view the net effects of the hyperventilatory response to be truly advantageous, whereby the benefits to pulmonary gas exchange and [H+] regulation outweigh the expense of some inefficiency in ventilatory work and pattern and a departure from steady-state homeostasis.

Adult↗
PubMed1982

Limitations to exercise capacity and endurance: pulmonary system.

The response of the pulmonary system to exercise is well-documented to be quite precise in its homeostatic regulation, highly efficient in terms of its physiologic cost, and operating well within its maximum reserves. Two exceptions to these generalizations are documented here in the highly-trained athlete: 1) the arterial hypoxemia observed in short-term work at a VO2 greater than 4-5 l . min-1, and 2) the tachypneic hyperventilation of long-term, heavy exercise in varying environmental conditions. The potential causes and consequences of these responses are discussed with reference to so-called exercise "limitations". The trained state as a cause of pulmonary limitations is emphasized.

Carbon Dioxide↗