Search

Background: Interpersonal and communication skills are core competencies for nursing students. Empathetic, patient-centred communication improves patient outcomes and the care experience. Nursing trainees have reported a lack of preparation and confidence in communication and interpersonal skills with patients and members of the health care team. Acting-based hands-on training may provide a novel approach to develop communication in nursing students., Approach: The corresponding author worked as a professional actor before pursuing a medical career. He created an acting-based workshop, inspired by classic acting exercises taught in drama conservatories for decades, to develop core communication and interpersonal skills for health care professionals. The course creator and an instructor with no acting background each facilitated the workshops. The initiative was taught to over 200 preclinical baccalaureate freshmen and sophomore nursing students as part of their clinical skills courses at one institution., Evaluation: Participants were asked to rate their self-efficacy for skills developed in the workshop using a 5-point Likert scale. A 4 or 5 rating was considered agreement. Most participants agreed the workshop developed their skills of self-awareness, observation, teamwork, flexibility, nonverbal and verbal communication, trust, mindfulness, body language awareness, active listening, and sensitivity to emotions expressed by others., Implications: An acting-based teaching intervention is efficacious in instilling core communication and interpersonal skills to preclinical nursing students based on participants' self-efficacy ratings. This innovative way to teaching communication provides students with an experiential environment conducive to learning. Similar ratings between sessions suggest that health professions educators with no formal acting training can successfully teach this course., (© 2022 The Authors. The Clinical Teacher published by Association for the Study of Medical Education and John Wiley & Sons Ltd.)

Non-cardiac chest pain (NCCP) is a common presenting complaint which can be better managed. This requires the recognition of clinical sub-groups with investigation and treatment tailored accordingly. The aim of this paper is to encourage more accurate diagnoses and the better recognition of the source of chest pain. We discuss the appropriate investigations and management of each clinical sub-group.

A simple clinical approach to patients presenting with chest pain is outlined, which is easily taught and can be quickly applied. This approach was demonstrated in a large cohort of patients and this article discusses the characteristics of the various diagnostic sub-groups.

Pregnancy has not hitherto been known to influence the course of Churg-Strauss syndrome. We describe a case where relapse occurred in four successive pregnancies. The disease proved fatal in the last pregnancy when aggressive treatment failed to reverse fulminant cardiac disease.

The presentation of Churg-Strauss syndrome is most distinctive, permitting diagnosis on clinical grounds. It is a phasic disorder with allergic rhinitis and asthma initially, often followed by peripheral blood eosinophilia with eosinophilic tissue infiltrates. The vasculitic illness is the life-threatening phase, but it can be effectively suppressed by prompt treatment.

A 13 year old girl with catatonia resulting from cerebral lupus is described. She had concurrent minor epileptic status, but abolition of her seizure activity failed to influence her catatonic state. She recovered after treatment with corticosteroids and immunosuppressive agents. Cerebral lupus should be considered in the differential diagnosis in patients presenting with catatonia.

Although many similarities exist between the Churg-Strauss syndrome and the hypereosinophilic syndrome, these two disorders have hitherto been characterized by different types of cardiac disease. Two cases of the Churg-Strauss syndrome are described where the typical endomyocardial lesion of the hypereosinophilic syndrome dominated the clinical picture.

The in vitro heparin sensitivity of 18 nephrotic children was compared with that of 10 normal children and 13 children with other renal diseases. The influence of age on the heparin sensitivity of 52 normal subjects (aged 12 to 85 years) was also studied. The heparin sensitivity was calculated from the dose-response curve obtained when increasing amounts of heparin were added to plasma and the kaolin partial thromboplastin time (KPTT) was measured. There was a significantly-reduced heparin sensitivity in nephrotic children compared to the control children and a progressive decline in heparin sensitivity with age. In the nephrotic syndrome heparin-sensitivity correlated with albumin and triglyceride concentrations but not with antithrombin III, platelet factor 4, cholesterol, fibrinogen, heparin cofactor II or histidine-rich glycoprotein. Addition of exogenous albumin did not restore the heparin sensitivity of nephrotic plasma. Four patients with Type II hyperlipidemia had a normal sensitivity to heparin. The decreased sensitivity to heparin thus does not appear to be a consequence of the nephrotic state, and may be a reflection of an underlying disturbance of charged macromolecules in steroid-responsive nephrotic syndrome.

Cardiac tumours can mimic collagen vascular disease and they are often accompanied by profound systemic upset. Both benign and malignant tumours may present in this way. Three cases of cardiac tumour, two malignant and one benign, are reported with just such a presentation. A review of fifteen similar case reports showed that a spectrum of different collagen vascular diseases was diagnosed and treated before the true diagnosis emerged. In half of these cases the cardiac tumour was only diagnosed at necropsy. The diagnosis of collagen vascular disease should not be made in the absence of corroborative laboratory data. In cases of malignant cardiac tumour, and less commonly with atrial myxoma, M mode and cross sectional echocardiography may not exclude the diagnosis. There may be a good response to steroid treatment in cases of suspected but not confirmed collagen vascular disease in which the true diagnosis is cardiac tumour.

Fifty-two patients with systemic lupus erythematosus (SLE) were examined by fluorescein angiography, and retinopathy was detected in 15. Three patterns of retinopathy were discerned: 4 patients had disc vasculitis, 6 had multiple cotton-wool spots, and 5 had a normal fundal appearance but fluorescein leakage on angiography. One patient had arterial occlusive disease with retinal neovascularisation and another had extensive venous disease. With 3 exceptions retinopathy was found only in patients with active SLE. No association was discovered between retinopathy and cerebral disease; in particular, fluorescein angiography did no assist the diagnosis of mild cerebral lupus.

A 23 year old Englishman presented with keratoconjunctivitis sicca and was found to have systemic amyloidosis. Five members of his family in two generations also had non-neuropathic amyloid particularly affecting the kidneys. This conforms to the Ostertag type of hereditary amyloidosis. Amyloid deposits in the proband showed permanganate-sensitive Congophilia and positive immunofluorescence staining for P component, but were negative for amyloid A and prealbumin. These observations suggested that the fibril protein in this patient was immunochemically distinct from the amyloid fibrils characterized hitherto.

Two patients with lupus erythematosus and renal vein thrombosis are described. Both patients had the "lupus anti-coagulant" in their serum. It is postulated that in these patients the clotting tendency could be favoured by a cross reaction of the "lupus anti-coagulant" with phospholipids in the endothelial cell membrane, resulting in inhibition of prostacyclin release.

Serial blood samples were taken from eight patients with systemic lupus erythematosus and five normal controls before and after a standard meal containing 20 g of protein. The samples were assayed for circulating immune complexes by the fluid-phase C1q, monoclonal rheumatoid factor and conglutinin-binding assays. No significant differences were seen in the post- as compared to the pre-prandial levels of circulating immune complexes. In neither controls nor patients did circulating complexes appear for the first time within 90 min after starting the meal. We conclude that if systemic antigen--antibody reactions occur soon after a protein meal they are not detected by the polyethylene glycol-dependent tests in current use and do not appear to influence the immediate clearance of endogenous immune complexes.

Drawing on our experience of 16 cases and a review of the English literature, we propose that CSS is under-diagnosed because of exclusive emphasis upon pathologic recognition of the disorder. The classical histological picture comprises a necrotizing vasculitis, eosinophilic tissue infiltration and extravascular granulomas, but it is only found in a minority of cases, and is not pathognomonic of the condition (69, 108). On the other hand, the clinical pattern of the disorder is most distinctive, and CSS can be readily identified on clinical grounds. Typically, it begins with allergic rhinitis, which is often complicated by nasal polyposis and sinusitis. Asthma and peripheral blood eosinophilia are essential features, often accompanied by pulmonary infiltrates. The systemic vasculitis of CSS resembles that of PAN, but severe renal disease is uncommon (the typical renal lesion is a focal segmental glomerulonephritis), and cardiac involvement accounts for 50% of deaths. Diagnostic difficulties arise from the close relationship of CSS to other granulomatous, vasculitic and eosinophilic disorders. CSS is usefully regarded as a point of overlap between these three disease spectrums (Fig. 5). Individual components of each spectrum can occur in the course of CSS; hence cases may be reported as PAN developing as a complication of Löffler syndrome or eosinophilic gastroenteritis (37, 57, 66). The hypereosinophilia of CSS tends to be less severe and more steroid-responsive than in HES, and evidence of eosinophil degranulation was not found in the patients we studied. Complement abnormalities are not a prominent feature of the disorder, and circulating immune complexes were detected in only two cases; both contained IgM. This may be of pathogenetic significance as IgM deposition was a dominant feature in four of the five cases with positive renal immunofluorescence. IgE levels were elevated in all patients studied during the vasculitic phase, and skin-prick tests were positive in 8 of 10 patients tested. CSS responds well to treatment with steroids, although some patients benefit from the addition of immunosuppressive agents. The vasculitic illness is usually of limited duration, but relapses can occur, and should be detected and treated early. Major problems in the post-vasculitic phase stem from hypertension and persisting peripheral nerve damage. Allergic upper and lower respiratory tract disease is an important cause of morbidity in the pre- and post-vasculitic periods.

A young woman with recurrent deep venous thromboses and spontaneous abortions was studied. She suffered an ovarian infarction followed by aortic thrombosis and renal failure. Evidence for deficient prostacyclin production was found and she responded to treatment with a prostacyclin infusion. This syndrome is identical with that seen in women with the lupus anticoagulant, but the lupus anticoagulant was not detected and no other cause was identified.

A case is described where a symmetrical polyarthritis followed a febrile illness due to Chlamydia psittaci infection. The arthritis abated after treatment with tetracosactrin.

Two children of mothers with systemic lupus erythematosus had congenital heart block and subsequently developed connective tissue diseases. This association has only been described in 2 individuals previously.

Serum amyloid-A protein (SAA) is the putative precursor of amyloid-A (AA) protein which forms the fibrils in reactive systemic or secondary amyloidosis. By means of a novel immunoradiometric assay, the concentration of SAA was found to be greatly elevated in patients with rheumatoid arthritis and juvenile chronic arthritis and correlated with activity of their primary disease. However, in patients with systemic lupus erythematosus SAA levels were only modestly raised, even in those with severe active disease, unless significant intercurrent microbial infection was also present. In Crohn's disease SAA levels showed a pattern similar to that seen in rheumatoid arthritis, whereas in ulcerative colitis it resembled that of systemic lupus erythematosus. The level of SAA response in these different disorders corresponds with the incidence of reactive systemic amyloidosis in them. These observations support the view that major increases in SAA levels are a necessary condition for the deposition of this form of amyloid and suggest that prospective monitoring of the SAA concentration in predisposing diseases may help to identify those individuals who are most at risk for amyloidosis.