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T A Raffin

Publications and source records attributed to T A Raffin.

At least 37 records · Page 2Linked to original sources
PubMed1998

Ethical decision-making in critical care in Hong Kong.

OBJECTIVES: Biomedical ethics has assumed an increasingly important role in medicine over the past 30 yrs, and its development has served the important goal of protecting patients' rights and interests. However, medical ethics has evolved within a Western tradition, and conflict often arises when trying to apply Western medical ethics to patients from other cultures. Using Hong Kong as an example, this article reviews the nature and sources of cross-cultural conflict in the intensive care unit setting that often arises between physicians trained in Western medicine and patients from a Chinese cultural background. DATA SOURCES: This article draws on the first author's experience as a critical care physician in Hong Kong, and on a review of the literature on cross-cultural interactions in medicine. STUDY SELECTION: Studies were selected that contrasted the approaches of different cultures to common ethical dilemmas in medicine. Review articles examining the relationship between culture and ethics were also selected. CONCLUSIONS: Hong Kong presents an interesting case study because of the coexistence of Western and Chinese medicine in a predominantly Chinese population that practices many Chinese cultural traditions. Whereas contemporary Western medical ethics focuses on individual rights, autonomy, and self-determination, traditional Chinese societies place greater emphasis on such community values as harmony, responsibility, and respect for parents and ancestors. Specific areas of cross-cultural conflict include: the role of the patient and family in medical decision-making; the disclosure of unfavorable medical information to critically ill patients; the discussion of advance directives or code status with patients; and the withholding or withdrawal of life support.

China↗
PubMed1998

Effects of the lazaroid, tirilazad mesylate, on sepsis-induced acute lung injury in minipigs.

OBJECTIVE: To assess the effects of the lazaroid, tirilazad mesylate, a potent lipid peroxidation inhibitor, in an animal model of Pseudomonas sepsis. DESIGN: Comparison of four experimental groups: a) saline control; b) Pseudomonas sepsis control; c) tirilazad mesylate control; and d) sepsis with tirilazad mesylate pre treatment. SETTING: University animal laboratory. SUBJECTS: Hanford minipigs (20 to 25 kg), anesthetized with pentobarbital and mechanically ventilated on an FIO2 of 0.4. INTERVENTIONS: Sepsis was induced by infusing Pseudomonas aeruginosa at 1 x 10(6) colony-forming units/kg/min over 120 mins. The tirilazad mesylate-treated group received a 5-mg/kg bolus 30 mins before, and a 3-mg/kg bolus 3 hrs after, the onset of sepsis. Hemodynamics, PaO2, and neutrophil counts were measured for 6 hrs. Thiobarbituric acid reactive material (TBARM) in tissue (lung, liver, and intestine), lung wet/dry weight ratio, lung myeloperoxidase activity, plasma tumor necrosis factor (TNF)-alpha concentrations, protein content, and percent neutrophils in bronchoalveolar lavage fluid were evaluated at the time the animals were killed (6 hrs). MEASUREMENTS AND MAIN RESULTS: Sepsis induced significant systemic hypotension, pulmonary hypertension, hypoxemia, and neutropenia. Sepsis also significantly increased TBARM content, lung wet/dry weight ratio, myeloperoxidase activity, plasma TNF-alpha concentrations, and bronchoalveolar lavage neutrophil percentage. Treatment with tirilazad mesylate significantly attenuated hypoxemia and decreased TBARM content, lung wet/dry weight ratio, myeloperoxidase activity, bronchoalveolar lavage protein, and bronchoalveolar lavage neutrophil percentage, but did not affect sepsis-induced hemodynamics, including systemic hypotension and pulmonary hypertension, plasma TNF-alpha concentrations, or neutropenia. CONCLUSIONS: Pretreatment with the tirilazad mesylate did not change P. aeruginosa sepsis-induced hemodynamic consequences. However, tirilazad mesylate attenuated sepsis-induced acute lung injury.

Animals↗
PubMed1998

The dying thoracic patient.

Health care providers should understand that the practice of good medicine includes not only diagnosing and curing diseases, but also effectively communicating with patients and families and helping terminally ill patients die a peaceful and dignified death. Patients in America come from varied backgrounds, and it is important for physicians to consider cultural and religious issues. Physicians should combine their clinical judgment with objective outcome data to provide optimal care for patients. Informed consent should be obtained from patients after offering a detailed plan of care that would include appropriate interventions and the consequences of no intervention. The physician should then assist the patient in making a decision that would provide the best possible future for that individual. The four fundamental principles of biomedical ethics, namely beneficence, nonmaleficence, autonomy, and justice, should be considered when analyzing an ethical problem. Voluntary active euthanasia, which means performing a deliberate act (e.g., administering a lethal injection) to end a patient's life, should not be performed by a physician. Withholding and withdrawing basic and advanced life support constitutes passive euthanasia. Good communication with patients early in the clinical course whenever possible results in an ethically correct decision. A nonconfrontational, sympathetic, and compassionate approach to family members and legal surrogates facing the immediate death of their loved ones leads to the best possible outcome. It is the duty of the physician to assure the patient and the family that he or she will not abandon the patient. Effective communication is the key to solving almost all ethical dilemmas when caring for the dying thoracic patient.

Death↗
PubMed1997

The effects of post-treatment with lisofylline, a phosphatidic acid generation inhibitor, on sepsis-induced acute lung injury in pigs.

The effects of lisofylline [(R)-1-(5-hydroxyhexyl)-3,7-dimethylxanthine] (LSF), an inhibitor of de novo phosphatidic acid (PA) generation, on sepsis-induced acute lung injury was studied using Hanford minipigs weighing 18 to 25 kg. Sepsis was induced by an intravenous infusion of Pseudomonas aeruginosa (1 x 10(6)/colony-forming units/kg/min over 2 h). Saline was used as the control vehicle. Six groups were studied: saline control group (SALINE: n = 5); sepsis control group (SEPSIS: n = 5); LSF control group (LSF: n = 5), which received a 25-mg/kgbolus of LSF 30 min before time zero followed by continuous infusion of 10 mg/kg/h throughout the study; LSF-treated septic groups, which were treated with LSF 30 min prior to sepsis (Pre: n = 5), 1 h postonset (Post-1 h: n = 8) or h postonset (Post-2 h: n = 8) of the bacterial infusion. Hemodynamics PaO2, neutrophil counts, and plasma porcine tumor necrosis factor-alpha concentrations were monitored for 6 h. After the minipigs were killed, lung tissue was sampled to measured wet-to-dry weight ratio (W/D), tissue albumin index (TAI), thiobarbituric acid-reactive material content (TBARM), and myeloperoxidase (MPO) activity. Compared with the SALINE group, the SEPSIS group showed significant systemic hypotension, pulmonary hypertension, arterial hypoxemia, neutropenia, and increase in TNF-alpha, MPO activity, W/D, TBARM, and TAI. LSF treatment attenuated sepsis-induced pulmonary hypertension, neutropenia, and hypoxemia, and increased MPO activity and lung injury measurements in the Pre and Post-1 h groups, but its efficacy was blunted in the Post-2 h group. Plasma TNF-alpha was decreased only in the Pre group. Thus, inhibition of intracellular PA generation through de novo pathways attenuates sepsis-induced acute lung injury.

Adjuvants, Immunologic↗
PubMed1997

Physician virtues and communicating with patients.

The growth of profit-driven medicine and managed care as well as the increasingly technologic focus of Western medicine have stimulated much reflection on the fundamental values of the medical profession and on the meaning of being a "good doctor." Many patients and many in the medical community have grown concerned about the fate of the doctor-patient relationship. In practicing medicine, physicians must be guided both by the basic principles of biomedical ethics and by Beauchamp's and Childress's four fundamental virtues: compassion, trustworthiness, discernment, and moral integrity. In addition, physicians must make the commitment to develop strong communication skills, for it is through communicating with patients that we forge a relationship with them and make them feel cared for. Good communication skills not only improve patient satisfaction and facilitate resolving the difficult ethical problems that arise in critical care but have also been shown to improve certain health outcomes. Unfortunately, studies have repeatedly shown physicians to have poor communication skills. In this article we identify key elements in preserving medicine's "covenant of trust" and in establishing good communication and rapport in critical care settings. We identify specific obstacles to good communication and propose strategies for overcoming them.

Clinical Competence↗
PubMed1997

Report of the Northern California Conference for Guidelines on Aid-in-Dying: definitions, differences, convergences, conclusions.

In September 1996, the Stanford University Center for Biomedical Ethics convened a conference entitled "Comprehensive Care of the Terminally Ill: The Northern California Consensus Development Conference for Guidelines on Aid-in-Dying." The regionally based, multidisciplinary conference gathered people from a variety of disciplines and diverse perspectives on physician aid-in-dying. This report documents important points of convergence, disagreement, and uncertainty that emerged from the conference and provides commentary on crucial issues: the definition of terminal illness, ensuring adequate palliative care, psychiatric challenges, coping with family pressures, the doctor-patient relationship, the managed care context, the role of ethics committees, and institutional challenges. Should physician aid-in-dying become a legal practice in California, the report will provide guidance to health care organizations, health professionals, and public policy officials engaged in local or state guideline or policy development.

California↗
PubMed1996

Whose death is it, anyway?

As medicine has increasingly gained the power to prolong life in the face of devastating illness, patients have increasingly become concerned about maintaining some control over how and when death arrives. Competent patients have the legal right to refuse treatment, but critically ill patients are frequently unable to participate in decision making. Advance directives were designed to help patients establish the level of care they would receive if they were to be rendered incompetent; yet, as the case discussed in this essay shows, even a valid advance directive does not guarantee that unwanted medical interventions will not be forced on us. The problem of physicians ignoring their patients' wishes goes beyond issues of communication and reflects an ongoing ambivalence about power and control in the physician-patient relationship. Unfortunately, many physicians find it easier to define success in terms of life and death than to try to determine what sort of existence is meaningful to an individual patient.

Attitude to Death↗
PubMed1996

The effects of recombinant human thrombomodulin on endotoxin-induced multiple-system organ failure in rats.

Activation of the coagulation system is postulated to play an important role in the pathogenesis of endotoxin-induced tissue injury. Thrombomodulin (TM) is an endothelial cell membrane glycoprotein receptor for thrombin. Once bound to TM, thrombin loses its procoagulant activity, which results in decreased clotting. In addition, the binding of thrombin to TM activates the endogenous anticoagulant pathway through protein C. We studied the effect of recombinant human TM (rh-TM) on endotoxin-induced multiple-system organ failure (MSOF) in Sprague-Dawley rats weighing 400 to 450 g: 2 mg/kg of rh-TM was injected (T1/2 = 4.5 h) 30 min prior to intravenous injection of 20 mg/kg of Escherichia coli endotoxin. The study presented here consisted of three separate experiments. Experiment 1: 24-h survival study. Experiment 2: multiple-system organ microthrombi study in which 125I-human fibrinogen was injected 30 min prior to an endotoxin or saline injection and tissue microthrombi formation was assessed by measuring the percentage of organ radioactivity (lung, heart, liver, and kidney) against total injected radioactivity (microthrombi index, MI) 2.25 h after an endotoxin or saline injection. Experiment 3: endotoxin-induced MSOF study in which 125I-rat albumin was injected 5 h after an endotoxin or saline injection, and endotoxin-induced organ injury was evaluated by measuring tissue wet-to-dry ratios (W/D) and tissue-to-plasma 125I-rat albumin concentration ratios (T/P) 8 h after the endotoxin or saline injection. Blood contamination in samples from Experiments 2 and 3 was corrected by using 131I-rat albumin measurements. Pretreatment with rh-TM improved the survival from 12 h through 23 h as compared with that of the endotoxin control group (p < 0.05). However, at 24 h, after essentially all injected rh-TM had been eliminated, there was no difference in survival. Significant reductions in MI, W/D, and T/P in the organs sampled were observed in the rh-TM pretreated groups (p < 0.05). In conclusion, rh-TM improved short-term but not overall survival and decreased MSOF in endotoxemic rats.

Albumins↗