The role of the therapist's critical parent

The need for nurse therapists to be aware of their own feelings, beliefs, and attitudes is all-important if treatment is to be effective. In this paper, the author uses the concept of the therapist's Critical Parent (from Berne's 1961 Transactional Analysis model) to explore countertransference reactions. Clinical examples from the author's professional experience are employed to demonstrate the interplay of ego states between therapist and client and how understanding of the effect of the therapist's Critical parent can enhance his or her ability to intervene effectively.     

Involvement of calcium and iron in Quin 2 toxicity to isolated hepatocytes

When treated with the cytosolic Ca++ indicator Quin 2-acetoxymethyl ester (Quin 2-AM), isolated hepatocytes exhibited signs of toxicity, such as extensive lipid peroxidation and vitamin E loss and release of lactate dehydrogenase. Lipid peroxidation induced by this agent was blocked completely by cotreatment of the cells with ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid, EDTA, ruthenium red, carbonyl cyanide m-chlorophenylhydrazone, desferal and trifluoperazine, and was partially inhibited by quinacrine and indomethacin. With the exception of carbonyl cyanide m-chlorophenylhydrazone and quinacrine, these agents also inhibited lactate dehydrogenase leakage. Although the results with ruthenium red suggested that Quin 2-AM may cause toxicity by altering handling of Ca++ by mitochondria, mitochondrial membrane potential was not altered in cells treated with Quin 2-AM until after toxicity occurred. Evidence of a direct, potentiative effect of Quin 2 on iron-induced lipid peroxidation was gained from experiments with liposomes. Treatment of cells with Quin 2-AM did not enhance nitro blue tetrazolium reduction, suggesting that Quin 2 did not stimulate O2- production by the cells. Direct chelation of Ca++ did not appear to be involved in the mechanism of Quin 2 toxicity, for an analog of Quin 2 that is virtually nonhydrolyzable, which greatly limits the binding of Ca++, also caused lipid peroxidation and cell death. These results suggest that Quin 2 causes toxicity by chelating iron or by activating some cellular process(es) that is dependent on the presence of iron or Ca++.     

The role of plasmapheresis in critical illness

In this article, the authors review the current recommendations from the American Society for Apheresis regarding the use of plasmapheresis in many of the diseases that intensivists commonly encounter in critically ill patients. Recent experience indicates that therapeutic plasma exchange may be useful in a wide spectrum of illnesses characterized by microvascular thrombosis, the presence of autoantibodies, immune activation with dysregulation of immune response, and some infections.     

Strategies to reduce late-stage drug attrition due to mitochondrial toxicity

Mitochondrial dysfunction is increasingly implicated in the etiology of drug-induced toxicities and negative side-effect profiles. Early identification of mitochondrial liabilities for new chemical entities is therefore crucial for avoiding late-stage attrition during drug development. Limitations of traditional methods for assessing mitochondrial dysfunction have discouraged routine evaluation of mitochondrial liabilities. To circumvent this bottleneck, a high-throughput screen has been developed that measures oxygen consumption; one of the most informative parameters for the assessment of mitochondrial status. This technique has revealed that some, but not all, members of many major drug classes have mitochondrial liabilities. This dichotomy encourages optimism that efficacy can be disassociated from mitochondrial toxicity, resulting in safer drugs in the future.     

The role of the clinical forensic nurse in critical care

Forensic nursing deals with the population of people whose lives have been affected by societal violence. The clinical forensic nurse (CFN) is seen as a means of coping with the resultant increased complexity of nursing practice, society, and the law. Critical care areas are clinical forensic domains where the CFN addresses the needs of living forensic patients through activities involving physical and non-physical evidence collection, crisis intervention, and documentation. Within a health care team, the CFN enhances patient care management, resulting in clinical service, legal order, and forensic protocol.     

The role of technology in critical care nursing

Title.  The role of technology in critical care nursing.
Aim.  This paper is a report of a study to identify the meaning for critical care nurses of technology related to weaning from mechanical ventilation and to explore how that technology was used in practice.
Background.  The literature concerned with the development of critical care (intensive care and high dependency units) focuses mainly on innovative medical technology. Although this use of technology in critical care is portrayed as new, it actually represents a transfer of technology from operating theatres.
Method.  An ethnographic study was conducted and data were collected on one critical care unit in a large teaching hospital over a 6-month period in 2004. The methods included participant observation, interviews and the collection of field notes.
Findings.  The overall theme 'The nursing–technology relation' was identified. This comprised three sub-themes: definition of technology, technology transferred and technology transformed. Novice nurses took a task-focussed approach to weaning, treating it as a 'medical' technology transferred to them from doctors. Expert nurses used technology differently and saw its potential to become a 'nursing technology'.
Conclusion.  Nurses need to examine how they can adapt and to 'reconfigure' technology so that it can be transformed into a nursing technology. Those technologies that do not fit with nursing may have no place there. Rather than simply extending and expanding their roles through technology transfer, nurses should transform those technologies that preserve the essence of nursing and can contribute to a positive outcome for patients.     

Mechanisms of acetaminophen-induced hepatotoxicity: role of oxidative stress and mitochondrial permeability transition in freshly isolated mouse hepatocytes

Freshly isolated mouse hepatocytes were used to determine the role of mitochondrial permeability transition (MPT) in acetaminophen (APAP) toxicity. Incubation of APAP (1 mM) with hepatocytes resulted in cell death as indicated by increased alanine aminotransferase in the media and propidium iodide fluorescence. To separate metabolic events from later events in toxicity, hepatocytes were preincubated with APAP for 2 h followed by centrifugation of the cells and resuspension of the pellet to remove the drug and reincubating the cells in media alone. At 2 h, toxicity was not significantly different between control and APAP-incubated cells; however, preincubation with APAP followed by reincubation with media alone resulted in a marked increase in toxicity at 3 to 5 h that was not different from incubation with APAP for the entire time. Inclusion of cyclosporine A, trifluoperazine, dithiothreitol (DTT), or N-acetylcysteine (NAC) in the reincubation phase prevented hepatocyte toxicity. Dichlorofluorescein fluorescence increased during the reincubation phase, indicating increased oxidative stress. Tetramethylrhodamine methyl ester perchlorate fluorescence decreased during the reincubation phase indicating a loss of mitochondrial membrane potential. Inclusion of cyclosporine A, DTT, or NAC decreased oxidative stress and loss of mitochondrial membrane potential. Confocal microscopy studies with the dye calcein acetoxymethyl ester indicated that MPT had also occurred. These data are consistent with a hypothesis where APAP-induced cell death occurs by two phases, a metabolic phase and an oxidative phase. The metabolic phase occurs with GSH depletion and APAP-protein binding. The oxidative phase occurs with increased oxidative stress, loss of mitochondrial membrane potential, MPT, and toxicity.     

The role of the senior health care worker in critical care

This article identifies that the introduction of the support worker role in the critical care team facilitates flexibility when organizing and managing patient care. Qualified nurses' time can be used more effectively, enhancing the quality of the patient care delivered. Aspects of the qualified nurses' workload in critical care can be shared and delegated successfully to unqualified staff. It is our view that staffing levels in critical care environments need to be reviewed with more flexible working practices to meet the current and future demands of critical care. There is a need for national consensus amongst qualified nurses to clarify and define the role of the support worker and develop a critical care competency framework to standardize training. To ensure proficiency, adequate training and appropriate accountability, support workers require regulation by a nationally recognized body.