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Biomedical subjects

M Keegan

Publications and source records attributed to M Keegan.

27 records · Page 2Linked to original sources
PubMed1989

The misconception of trauma reimbursement.

As health care costs increase, hospital reimbursement from trauma victims is decreasing. Thus, the number of institutions dedicated to trauma care continues to decrease in this country. Two hundred eight consecutive patients admitted to a level 1 trauma center were evaluated during a 10-month period. The total bill for 207 patients was $4,044,156, averaging $19,537 per patient. Total reimbursement 6 months after billing was $2,054,090, 51% of the total bill. Methods to improve reimbursement include increasing the ratio of blunt to penetrating trauma victims and by assembling a team knowledgeable in reimbursement options. However, because a major portion of trauma reimbursement comes under federal government regulation, topics such as diagnostic related groups and other classification criteria of critically injured patients need to be reevaluated, or underpayment for trauma patients will continue to be a national plague.

Adolescent↗
PubMed1987

Disposition of nalbuphine in patients undergoing general anaesthesia.

The pharmacokinetics of nalbuphine 20 mg i.v. were studied in 10 patients undergoing lower abdominal or body surface surgery. Blood sampling was carried out for 600 min after injection and drug concentrations were measured by HPLC using electrochemical detection. Disposition was best described as a triexponential function, with a mean elimination half-life of 135.5 min. Mean residence time, clearance, and volumes of distribution, Vss and V beta, were determined by a model independent method, and gave mean values of 149.7 min (MRT), 1095 ml min-1 (ClP), 159.9 litre (Vss) and 207.1 litre (V beta).

Adult↗
PubMed1986

Proactive and retroactive effects of repeated electroconvulsive shock on passive avoidance retention in rats.

In spite of technical modifications, the therapeutic administration of electroconvulsive shock (ECS) to humans is still associated with significant memory impairment. Studies aimed at elucidating the neurobiologic basis of this impairment and developing appropriate treatment approaches have been limited by the absence of an appropriate animal model. We report here that ECS administered daily for 1-7 days to male albino rats (ECS X 1-ECS X 7) cumulatively impaired retention of passive avoidance when animals were trained 24 hours after the last ECS and tested 24 hours after training. Retention was directly proportional to the interval between training and testing; animals trained 24 hours after ECS X 7 and tested 1 hour later showed no deficit while animals tested after 24 hours showed maximal impairment. Retention was significantly improved by 10 days following the last of ECS X 7 and intact by 21 days. These findings parallel the effects of ECS on memory function in humans. The retrograde effects of ECS also paralleled those demonstrated in humans; while retention of a passive avoidance task learned 24 hours before ECS X 7 was grossly impaired, retention was intact if learning took place 7 days before the ECS course. The application of these findings as an animal model of ECS-induced memory impairment in humans, is discussed.

Amnesia↗
PubMed1986

Pulmonary infections due to Legionella in immunocompromised patients.

At present, 11 different species of Legionella have been implicated in human disease. It has become apparent that disease caused by Legionella is acquired from a variety of environmental sources and that water is the factor that links many of them. Patients who are immunosuppressed, such as individuals receiving cancer chemotherapy or therapy designed to prevent organ rejection, are particularly susceptible to such environmental sources. It appears that intact cell-mediated immunity is more important in host defense than are adequate numbers of granulocytes or immunoglobulin concentrations. Diagnostic steps should be undertaken in all patients developing nosocomial pneumonia who present with a picture suspicious for this disorder. In the meantime, appropriate antimicrobial therapy with erythromycin and rifampin should be begun. If clusters of cases are detected in a hospital, immediate steps should be taken to attempt to isolate the organism from any aqueous environmental sources, and if found appropriate, steps taken. Awareness of the threat of legionnaires' disease must be maintained among clinicians and hospital epidemiologists because it is unlikely that the problem of nosocomial legionnaires' disease will disappear.

Anti-Bacterial Agents↗
PubMed1982

Mechanism of enhancement of blood group antibody reactions in low ionic strength.

When the ionic strength of blood samples is reduced, blood group antibodies bind to red blood cells that lack the corresponding antigen. Upon normalization of the ionic strength, the antibodies elute into the supernatant fluid. We compared, in semiquantitative terms, this nonspecific and reversible binding of various blood group antibodies. Studied with anti-CD antibodies showed that the nonspecific binding increased when the ion strength was progressively lowered. In 1/10 normal ionic strength, practically all of a high-titer anti-CD antibody bound to Rh(D)-negative RBC (phenotype ce). The majority of the other antibodies studied (anti-C, -c, -Fya, -Fyb, and -S) behaved similarly in 1/10 normal ionic strength, but the binding of some (anti-E, -s, and -Jka) was, at times, less complete. Most examples of anti-K antibodies, however, demonstrated very poor nonspecific binding to K-negative RBC in low ionic strength (LIS). The authors propose that the augmentation of specific blood group antibody reactions in LIS is the direct result of this nonspecific binding, and that the failure of these conditions to support the nonspecific binding of anti-K antibodies might explain the lack of augmentation (and, at times, even the impairment) of the reactions of anti-K with its antigen.

Antibody Specificity↗