Getting work done: a grounded theory study of resident physician value of nursing communication

ABSTRACT

Poor communication between nurses and physicians results in patient injury and increased healthcare costs. While multiple attempts have been made to improve communication between the two professions, evidence confirms little progress has been made. Previous research focused on standardizing communication processes and protocols between nurses and physicians rather than examining the relational component of these human interactions. The purpose of this study was to explore physician valuing of nursing communication in the context of patient care. Interviews were conducted with 15 internal medicine resident physicians. A constructivist grounded theory approach was used to develop the substantive theory of Getting Work Done. Getting Work Done incorporated three major categories: discerning the team, shifting communication, and accessing nurse knowledge and abilities. Hierarchical behaviors and language, and nurse collusion in both, characterized nurse-physician communication and situated the nurse outside the decision-making team. Complex work environments further devalued nurse-physician communication. Interprofessional education and practice must advance the unique and essential role of all health care professionals such that mutual valuing replaces hierarchical actions with collaborative systems for determining the most effective approaches to patient care.     

Delayed esophageal perforation after pneumatic dilatation for the treatment of achalasia

Two cases of delayed esophageal perforation following a pneumatic dilatation for the treatment of achalasia are presented. Esophagrams obtained immediately after pneumatic dilatation failed to reveal a perforation. Increasing symptoms prompted repeat contrast studies, at which time an esophageal perforation was demonstrated. The occurrence of delayed esophageal perforation after pneumatic instrumentation is emphasized. An ischemic etiology for this delayed perforation is postulated.     

Incidence of complications in intrahospital transport of critically ill patients – experience in an Austrian university hospital

BACKGROUND: During the past decade, considerable changes and advances have been made in intrahospital transport of critically ill patients. Despite the fact that intrahospital transport is nowadays regarded an extension of the intensive care continuum, it still poses a risk for the patient. MATERIALS AND METHODS: This prospective, observational study was designed to determine the occurrence rate of transport-related complications in the altered setting of intrahospital transports and to identify possible confounding sources of increased risk. In an eight-month period, adults and infants from anesthesiologic intensive care units were analyzed. RESULTS: A total of 226 patients underwent 452 intrahospital transports. The overall rate of critical incidents was low (4.2%) and no direct association between mortality and intrahospital transport was observed. In addition to the known risk factors of ventilatory support with positive end-expiratory pressure and requirement for catecholamine support, the necessity for intrahospital transport in the acute vs. elective situation was found to significantly increase the risk of complications. CONCLUSIONS: We conclude that advances in the management of intrahospital transport of critically ill patients have led to an overall decrease of complications. However, an undeniable risk remains, especially in relation to disease severity and the urgency of such transports.     

Diversification of ?T Cell Responses to Carboxy-terminal Determinants within the 65-kD Heat-shock Protein Is Involved in Regulation of Autoimmune Arthritis

The T cell response to the 65-kD mycobacterial heat-shock protein (Bhsp65) has been implicated in the pathogenesis of autoimmune arthritis. Adjuvant arthritis (AA) induced in the Lewis rat (RT-1^l) by injection of Mycobacterium tuberculosis serves as an experimental model for human rheumatoid arthritis (RA). However, the immunological basis of regulation of acute AA, or of susceptibility/resistance to AA is not known. We have defined the specificity of the proliferative T cell responses to Bhsp65 during the course of AA in the Lewis rat. During the early phase of the disease (6–9 d after onset of AA), Lewis rats raised T cell responses to many determinants within Bhsp65, spread throughout the molecule. Importantly, in the late phase of the disease (8–10 wk after onset of AA), there was evidence for diversification of the T cell responses toward Bhsp65 carboxy-terminal determinants (BCTD) (namely, 417–431, 441–455, 465–479, 513–527, and 521–535). Moreover, arthritic rats in the late phase of AA also raised vigorous T cell responses to those carboxy-terminal determinants within self(rat) hsp65 (Rhsp65) that correspond in position to the above BCTD. These results suggest that the observed diversification is possibly triggered in vivo by induction of self(Rhsp65)-reactive T cells. Interestingly, another strain of rat, the Wistar Kyoto (WKY/NHsd) rat (RT-1^l), with the same major histocompatibility complex class II molecules as the Lewis rat, was found to be resistant to AA. In WKY rats, vigorous responses to the BCTD, to which the Lewis rat responded only in the late phase of AA, were observed very early, 10 d after injection of M. tuberculosis. Strikingly, pretreatment with the peptides comprising the set of BCTD, but not its amino-terminal determinants, provided significant protection to naive Lewis rats from subsequent induction of AA. Thus, T cell responses to the BCTD are involved in regulating inflammatory arthritis in the Lewis rat and in conferring resistance to AA in the WKY rat. These results have important implications in understanding the pathogenesis of RA and in devising new immunotherapeutic strategies for this disease.Rheumatoid arthritis (RA)¹ is an autoimmune disease of unknown etiology (1, 2). In the past several years, considerable interest has been generated in the role of the 65-kD mycobacterial heat-shock protein (Bhsp65) in the pathogenesis of autoimmune arthritis both in experimental animals (3, 4) as well as in humans (5–7). In RA patients, an association between T cell responses to Bhsp65 and early stages of joint inflammation has been observed (8–10), suggesting that Bhsp65-reactive T cell responses are involved in the pathogenesis of this disease. Adjuvant arthritis (AA) can be induced in the inbred Lewis rat after immunization with Mycobacterium tuberculosis in oil (11–13). The disease can also be transferred to naive Lewis rats by T cell lines reactive to peptide 180–188 of Bhsp65 (3, 14). Although arthritic Lewis rats develop vigorous T cell responses to native Bhsp65 and to peptide 180–188 of Bhsp65, neither of these is arthritogenic when injected in protein or peptide form, respectively (15, 16). Interestingly, pretreatment with Bhsp65 can protect naive Lewis rats from development of arthritis upon subsequent immunization with M. tuberculosis (4, 17), suggesting that Bhsp65 contains protective as well as disease-inducing determinants. T cell lines specific for Bhsp65 have also been shown to protect against AA (14, 18). Similarly, Lewis rats afflicted with AA are resistant to reinduction of AA (13). Neither the mechanism of natural regulation of the acute inflammatory phase of AA nor the mechanism of protection from subsequent induction of AA is known. Likewise, the immunological basis of susceptibility or resistance to AA of different rat strains has not been revealed.In the present study, we have defined the changing pattern of specificity of the T cell responses of Lewis rats to determinants within Bhsp65 during the course of AA. Arthritic Lewis rats in the early and late phase of the disease revealed distinct patterns of T cell responses to Bhsp65. Importantly, with progression of the disease, there was evidence for diversification of the T cell responses toward Bhsp65 carboxy-terminal determinants (BCTD). (The phenomenon of spreading of the T cell responses to new determinants within an antigen, after priming with a single determinant of the same antigen, has been previously described as determinant spreading [19]. On the other hand, we have termed the induction of T cell responses to new determinants after priming with the whole, multideterminant antigen as diversification [20, 21]). Moreover, arthritic Lewis rats in the late phase of AA also raised significant responses to certain carboxy-terminal determinants within self(rat) hsp65 (Rhsp65). (Rat hsp60 [22] has been referred to as rat hsp65 in this study to emphasize its relationship with Bhsp65.) These self-determinants correspond in position precisely to that of the BCTD, suggesting that diversification of response to Bhsp65 observed in vitro, might be triggered in vivo by self-hsp65. In contrast with AA-susceptible Lewis rats, MHC class II–identical, Wistar Kyoto (WKY/NHsd = WKY) rats (23, 24) were found to be resistant to induction of AA after immunization with M. tuberculosis. In fact, M. tuberculosis-immunized WKY rats raised early and vigorous responses to the BCTD to which the Lewis rats only respond during the late phase of the disease. Pertinently, pretreatment of naive Lewis rats with peptides comprising the BCTD, but not its amino-terminal determinants (BNTD), induced significant protection from AA. These results suggest that T cell responses to the BCTD are involved in regulation of acute inflammatory arthritis. Our study suggests one of the immunological bases for natural regulation of acute AA, and of protection (resistance) from development of AA.     

Pharmacogenomics: a clinician's primer on emerging technologies for improved patient care

Pharmacogenomics is a term recently coined to embody the concept of individualized and rational drug selection based on the genotype of a particular patient. Customization of drug therapy offers the potential for optimal safety and efficacy in an individual patient. Such a process contrasts current prescribing practices, which use medications shown to be safe and effective in patient populations or based on anecdotal experiences. Within patient populations, medications vary in their efficacy among individual patients. More importantly, a medication that is safe and effective in one patient may be ineffective or even harmful in another. Underlying many of these phenotypic differences are genotypic variants (polymorphisms) of key enzymes and proteins that affect the safety and efficacy of a drug in an individual patient. An understanding of these polymorphisms has the potential to enhance patient care by allowing physicians to customize the selection of medication to meet individual patient needs. Pharmacogenomics may also lead to improved compliance and shorter time to optimal disease management, thereby reducing morbidity and mortality. Significant cost savings could result from reductions in polypharmacy as well as from fewer physician encounters and hospitalizations for exacerbations of underlying illness and because of adverse drug reactions.     

The influence of high versus normal impedance ventricular leads on pacemaker generator longevity

As pacemaker generator longevity is dependent on current consumption and resistance of the pacing lead, the use of a high impedance pacing lead theoretically results in an extension of battery longevity. Therefore, the effect of high versus standard impedance ventricular leads on generator longevity was studied. In 40 patients (21 women, age 73 +/- 13 years) with a standard dual chamber pacemaker indication, a bipolar standard impedance ventricular lead was implanted in 20 patients, the remaining patients received a bipolar high impedance lead in a randomized fashion. All patients received identical pacemaker generators and atrial leads. The estimated longevity of the generator was calculated automatically by a programmed pacemaker algorithm. After a mean follow-up of 39 +/- 4.8 months, no significant differences were observed with respect to mean pacing and sensing thresholds of the atrial and ventricular leads in both groups. However, the high impedance leads displayed a significantly higher impedance and a significantly lower current drain as compared to standard impedance leads (1,044 +/- 139 vs 585 +/- 90 Omega, and 2.2 +/- 0.4 vs 4.3 +/- 1.1 mA). The extrapolated generator longevity was significantly longer in the high impedance lead group, as compared to the standard impedance lead group (107.3 +/- 8.5 vs 97.6 +/- 9.0 months; P = 0.02). In conclusion, implantation of a high impedance lead for ventricular pacing results in a clinically relevant extension of generator longevity.