An exploration of nurse-physician perceptions of collaborative behaviour

Interprofessional collaboration is a key element in providing safe, holistic patient care in the acute care setting. Trended data at a community hospital indicated opportunities for improvement in collaboration on micro, meso, and macro levels. The aim of this survey study was to assess the current state of collaboration between frontline nurses and physicians at a non-academic acute care hospital. A convenience sample of participants was recruited with a final respondent sample of 355 nurses and 82 physicians. The results indicated that physicians generally perceived greater collaboration than nurses. Physician ratings did not vary by primary practice area, whereas nurse ratings varied by clinical practice area. Nurse ratings were the lowest in the operating room and the highest in the emergency department. Text-based responses to an open-ended question were analysed by role and coded by two independent research teams. Emergent themes emphasised the importance of rounding, roles, respect, and communication. Despite recognition of the need for improved collaboration and relational behaviours, strategies to improve collaborative practice must be fostered at the meso level by organisational leaders and customised to address micro-level values. At the study site, findings have been used to address and improve collaboration towards the goal of becoming a high reliability organisation.     

Comparison of M-mode and cross-sectional echocardiography in infective endocarditis.

Cross-sectional and M-mode echocardiograms were performed on 23 consecutive patients with infective endocarditis. Both M-mode and cross-sectional echocardiography identified vegetations in 18 patients, 10 of whom required valve replacement within 1 month of presentation. Cross-sectional echocardiography alone identified a vegetation in one patient with a prosthetic valve. Neither technique identified vegetations in five instances. The size and shape of a vegetation on cross-sectional echocardiography did not accurately predict the need for early valve replacement of the incidence of major peripheral emboli.     

Stress echocardiography with transesophageal atrial pacing: preliminary report of a new method for detection of ischemic wall motion abnormalities

We performed two-dimensional echocardiography in 19 patients with significant coronary artery disease and in six normal volunteers at rest and during transesophageal atrial pacing. Technically adequate resting echocardiograms were obtained in 18 of the 19 patients and in all six normal volunteers. In two subjects, atrial capture was not possible, and in one subject, discomfort from the pacing at the beginning of the study precluded its completion. In all subjects (n = 21) who completed the protocol satisfactory two-dimensional echocardiograms were obtained during pacing. Wall motion was normal at rest and during atrial pacing in five normal volunteers. New transient wall motion abnormalities developed in 13 of the 16 patients during pacing. Twelve of the 13 patients had significant coronary lesions in the coronary arteries supplying the abnormal wall segment. Only three of the patients developed significant ST segment depression during pacing. We conclude that stress echocardiography with transesophageal atrial pacing is safe and practical and can be used in patients who cannot perform dynamic exercise, this technique can detect ischemic segmental wall motion abnormalities corresponding to the distribution of coronary arterial obstruction, and the technique provides high-quality echocardiographic images during stress and thus may expand the usefulness of resting two-dimensional echocardiography in patients who have ischemic heart disease.     

Noncirrhotic portal hypertension associated with didanosine: a case report and literature review

Noncirrhotic portal hypertension (NCPH) has recently been reported as a liver complication in human immunodeficiency virus (HIV)-infected patients and has been found to be associated with exposure to didanosine. Here, we describe the case of an HIV-infected patient with portal hypertension who initially presented with massive ascites and portal vein thrombosis. The patient's HIV-1 infection was well-controlled with highly active antiretroviral therapy (lamivudine/didanosine plus nevirapine) for 3 years since its diagnosis in 2007. He had no history of alcoholism, drug abuse, or liver diseases. An extensive work-up for other possible causes of liver disease was performed, but the results were inconclusive. In addition to reporting this case, we have reviewed the literature on didanosine-related NCPH and analyzed the findings of 61 similar previously reported cases.     

Homozygosity for a HERG potassium channel mutation causes a severe form of long QT syndrome: identification of an apparent founder mutation in the Finns

OBJECTIVES

We studied the clinical characteristics and molecular background underlying a severe phenotype of long QT syndrome (LQTS).

BACKGROUND

Mutations of cardiac ion channel genes cause LQTS, manifesting as increased risk of ventricular tachycardia and sudden death.

METHODS

We studied two siblings showing prolonged QT intervals corrected for heart rate (QTc), their asymptomatic parents with only marginally prolonged QTc intervals and their family members. The potassium channel gene HERG was screened for mutations by deoxyribonucleic acid sequencing, and the electrophysiologic consequences of the mutation were studied in vitro using the whole-cell patch-clamp technique.

RESULTS

A novel missense mutation (L552S) in the HERG channel, present in the homozygous state in the affected siblings and in the heterozygous state in their parents, as well as in 38 additional subjects from six LQTS families, was identified. One of the homozygous siblings had 2:1 atrioventricular block immediately after birth, and died at the age of four years after experiencing unexplained hypoglycemia. The other sibling had an episode of torsade de pointes at the age of two years. The mean QTc interval differed significantly (p < 0.001) between heterozygous symptomatic mutation carriers (500 ± 59 ms), asymptomatic mutation carriers (452 ± 34 ms) and noncarriers (412 ± 23 ms). When expressed in vitro, the HERG-L552S formed functional channels with increased activation and deactivation rates.

CONCLUSIONS

Our data demonstrate that homozygosity for a HERG mutation can cause a severe cardiac repolarization disorder without other phenotypic abnormalities. Absence of functional HERG channels appears to be one cause for intrauterine and neonatal bradycardia and 2:1 atrioventricular block.     

Dexamethasone downregulated the expression of CSF 14-3-3β protein in mice with eosinophilic meningitis caused by Angiostrongylus cantonensis infection

Angiostrongylus cantonensis is the main causative agent of human eosinophilic meningitis in Southeast Asia and the Pacific Islands. A previous study demonstrated that the 14-3-3β protein is a neuropathological marker in monitoring neuronal damage in meningitis. Steroids are commonly used in patients with eosinophilic meningitis caused by A. cantonensis infection. However, the mechanism by which steroids act in eosinophilic meningitis is unknown. We hypothesized that the beneficial effect of steroids on eosinophilic meningitis is partially mediated by the down-regulation of 14-3-3β protein expression in the cerebrospinal fluid (CSF). In this animal study, we determined the dynamic changes of 14-3-3β protein in mice with eosinophilic meningitis. The 14-3-3β protein in serum and CSF was increased in week 2 and 3 after infections. Dexamethasone administration significantly decreased the amounts of CSF 14-3-3β protein. By developing an in-house ELISA to measure 14-3-3β protein, it was found that the amounts of 14-3-3β protein in the CSF and serum increased over a three-week period after infection. There was a remarkable reduction of 14-3-3β protein in the CSF after 2 weeks of dexamethasone treatment. In conclusion, the administration of corticosteroids in mice with eosinophilic meningitis decreased the expression of 14-3-3β protein in the CSF.