Is breathlessness what the professional says it is? Analysis of patient and professionals’ assessments from a German nationwide register

Purpose

Breathlessness is a common and distressing symptom in patients with advanced disease. Patients’ self-report is deemed to be the most valid method of symptom assessment. When patients are not capable of self-assessment, professionals’ assessment is often used as alternative but evidence on the validity is conflicting. The aim of this study was to compare self- and professionals’ assessment of breathlessness regarding presence and severity in patients with advanced disease.

Methods

Secondary analysis of a cross-sectional, multi-centre and nationwide register (HOspice and Palliative Care Evaluation (HOPE)). Documented inpatients from hospices and palliative care units from 2006 to 2008 who completed the self-assessed MInimal DOcumentation System (MIDOS) were included. Professionals’ assessment were based on the integrated symptom and problem checklist (symptom scores, 0–3). Cohen’s kappa (κ) was used to estimate the ‘level of agreement’ (LoA).

Results

Two thousand six hundred twenty-three patients (mean age, 66.9 (SD, 12.8); 54.4 % female; median Eastern Cooperative Oncology Group score, 3; 95.9 % with malignant disease) were analysed. Prevalence of breathlessness was 53.4 % (1,398 patients) by professionals’ and 53.1 % (1,410 patients) by self-assessment. Presence was correctly evaluated by professionals in 80.9 % of cases (sensitivity, 81.8 %; specificity, 79.8 %). Severity of breathlessness was correctly estimated in 65.7 % of cases. LoA was good (κ?=?0.62) for the evaluation of presence of breathlessness and moderate (κ?=?0.5) for the estimation of severity. The proportion of over- or underestimated scores was similar.

Conclusions

If patient’s self-rating, the gold standard of symptom assessment, is not possible, professionals’ assessment might be a valid alternative, at least for assessing the presence of breathlessness.     

Pyridostigmine-mediated growth hormone release: evidence for somatostatin involvement.

Pyridostigmine (PD), a cholinesterase inhibitor, has been shown to elicit GH release when given alone and to potentiate the GH response to GH-releasing hormone (GHRH) in man. Numerous experiments have indirectly indicated that somatostatin (SS) inhibition is its likely mechanism of action. This study sought to establish the ability of PD to induce GH release in the rat, determine the dose-response relationship, and test the hypothesis that SS inhibition is the method of action. Three experiments were performed to monitor the GH response to PD. I) Five groups of male rats were food deprived for 72 h. The groups were then treated iv with saline, SS antibody (SS-ab), and 10, 100, and 1000 micrograms/kg PD, respectively. Blood samples were drawn before and after treatment. II) Two groups of male rats were pretreated iv with GHRH antibody (GHRH-ab) and either SS-ab or normal sheep serum (NSS). Blood samples were drawn every 30 min for 8.5 h, during which time each animal was injected with PD (10 micrograms/kg) in the third hour and again in the sixth hour. III) Male rats received a PD injection (10 micrograms/kg, iv) during a spontaneous GH trough period and a second PD injection during a spontaneous GH peak period. Blood samples were drawn at regular intervals preceding and following treatments. In Exp I, PD induced a clear 4- to 5-fold increase in GH concentrations in food-deprived rats. The maximal GH responses occurred after the 10 and 100 micrograms/kg doses, although the pattern and duration were different with these two doses. In Exp II, PD induced an approximately 2-fold increase in GH values in animals pretreated with GHRH-ab and NSS, but failed to induce a change in GH in the animals treated with GHRH-ab and SS-ab. In Exp III, PD failed to induce any change in GH concentration when administered during spontaneous GH peaks or troughs. The first two experiments suggest that PD increases GH secretion in the rat via inhibition of SS. The failure of PD to alter GH during a spontaneous peak is consistent with the current hypothesis that the level of SS is low at this time. Its failure to alter GH during trough periods may be related to very high SS tone. In conclusion, our results support the hypothesis that PD acts via inhibition of SS secretion.     

Modulation of Allergic Airway Inflammation by the Oral Pathogen Porphyromonas gingivalis

Accumulating evidence suggests that bacteria associated with periodontal disease may exert systemic immunomodulatory effects. Although the improvement in oral hygiene practices in recent decades correlates with the increased incidence of asthma in developed nations, it is not known whether diseases of the respiratory system might be influenced by the presence of oral pathogens. The present study sought to determine whether subcutaneous infection with the anaerobic oral pathogen Porphyromonas gingivalis exerts a regulatory effect on allergic airway inflammation. BALB/c mice sensitized and subsequently challenged with ovalbumin exhibited airway hyperresponsiveness to methacholine aerosol and increased airway inflammatory cell influx and Th2 cytokine (interleukin-4 [IL-4], IL-5, and IL-13) content relative to those in nonallergic controls. Airway inflammatory cell and cytokine contents were significantly reduced by establishment of a subcutaneous infection with P. gingivalis prior to allergen sensitization, whereas serum levels of ovalbumin-specific IgE and airway responsiveness were not altered. Conversely, subcutaneous infection initiated after allergen sensitization did not alter inflammatory end points but did reduce airway responsiveness in spite of increased serum IgE levels. These data provide the first direct evidence of a regulatory effect of an oral pathogen on allergic airway inflammation and responsiveness. Furthermore, a temporal importance of the establishment of infection relative to allergen sensitization is demonstrated for allergic outcomes.A causative relationship between decreased microbial exposure and infection in recent decades and the concurrent increase in asthma prevalence in developed countries has been suggested and is thought to be attributable, at least in part, to a phenomenon known as the hygiene hypothesis (30). Originally put forth by Strachan (32), the hypothesis proposes that increased cleanliness of modern industrialized societies has resulted in decreased exposure to bacterial, viral, and other immunomodulatory organisms and their products, particularly in early life, and that this has in turn resulted in a loss of potentially protective effects of these exposures on the development of allergic diseases. Accumulating clinical and experimental evidence largely supports the hygiene hypothesis as it relates to asthma, although a consensus has not been reached. As reviewed recently (31), a variety of infections of a viral, bacterial, and parasitic nature influence the host immune response, such that regulation of the Th1-Th2 balance is modified to promote Th1 responses and impede Th2 responses, thereby reducing Th2-mediated allergic outcomes. However, this is likely a simplistic view of the effects of infections on immune system development and responses, and other factors, including host genetic makeup and timing of exposures to the infective agent relative to allergen exposure, undoubtedly contribute to the overall allergic phenotype.In addition to the influence of environmental exposure to microbes, the potential regulation of allergic diseases by the microflora of the host is receiving increased attention. Evidence suggests that the composition of the gastrointestinal microflora differs between individuals with and without allergy (reviewed in reference 25), and disruption of the normal gut microflora by antibiotic administration leads to allergic airway responses following allergen challenge in mice not previously sensitized to the allergen (24). Moreover, although similar benefits have not yet been demonstrated in humans, the oral administration of probiotic bacteria was recently shown to decrease allergic airway inflammation in mice (8, 9).As in the gut, the microenvironment of the oral cavity is complex and comprises hundreds of bacterial species. Porphyromonas gingivalis, a Gram-negative opportunistic periodontal pathogen, can initiate periodontal lesions in nonhuman primates when introduced into the periodontal microbiota (15) and is a major etiological agent in severe forms of periodontal disease such as chronic periodontitis (21). Interest in chronic oral infections and their potential role in adverse systemic health effects has been heightened by observations of positive associations between serum concentrations of antibodies to oral pathogens such as P. gingivalis and the incidence of cardiovascular diseases and renal dysfunction (3, 19, 28, 29). Recently, however, an inverse relationship between serum concentrations of antibodies to P. gingivalis and the prevalence of asthma, wheeze, and hay fever was observed in a representative sample of the population of the United States (2). Furthermore, a significant inverse association between periodontitis and the incidences of hay fever and allergy to house dust mites was reported for a northeast German population, with a borderline significant inverse association between periodontitis and asthma also observed (10). While limitations of these observational studies include potential recall bias pertaining to asthma symptoms and the inability to directly assess cause and effect, these findings nonetheless suggest a potential protective effect of infection with oral pathogens such as P. gingivalis on asthma pathogenesis.In order to examine the influence of oral pathogens on the development of allergic airway disease under controlled experimental conditions, the present study sought to determine whether infection with P. gingivalis modified allergic outcomes in a murine model of asthma. To accomplish this, a subcutaneous chamber model was employed wherein mice were subjected to a local infection with live P. gingivalis either before or after sensitization to allergen, and the effects of this infection on subsequent responses to allergen challenge were assessed. The results indicate that P. gingivalis infection exerts a modulatory effect on allergic airway responses and that this effect is dependent on the timing of infection relative to allergic sensitization.     

Non-cancer patients in specialized palliative care in Germany: what are the problems?

To determine the role of non-cancer palliative care in inpatient services in Germany, data from the Hospice and Palliative Care Evaluation (HOPE) were analysed. Since 1999, a three-month census has been conducted annually in German palliative care units. Pooled data from 2002-2005 were tested for differences between non-cancer patients (NCs) and cancer patients (Cs). A total of 4182 patients (NC: 3.5%; C: 96.5%) were documented; functional status (using Eastern Cooperative Oncology Group (ECOG) measures) in NCs was lower compared to Cs (p?=?0.009). NCs suffered more often from dyspnoea (40%; C: 29%; p?=?0.004), weakness (92,3%; C: 84,5%; p?=?0.011) and tiredness (75.4%; C: 66.7%; p?=?0.03) and less from nausea (17.1%; C: 28.9%; p?=?0.002), vomiting (8.2%; C: 19.4%; p?=?0.001) or loss of appetite (55.5%; C: 67.9%; p?=?0.002). There were no differences in pain and constipation. Other problems (nursing, psychological) were more frequent for NCs, in particular the need for support in the activities of daily life (90.3%; C: 72.8%; p?相似文献   

Discontinuation of mechanical ventilation in patients with amyotrophic lateral sclerosis

Mechanical ventilation, both invasive and non-invasive, may be an effective means of improving the quality of life and prolonging the survival of patients suffering from amyotrophic lateral sclerosis (ALS). However, the attitude towards this palliative measure varies greatly between different centres and countries. One of the arguments cited against this procedure is the fear that a patient might request the physician to discontinue life support. We believe that the question of withdrawal of mechanical ventilation can only be meaningfully addressed in the general context of palliative care. Here, we review possible modes of action in response to a patient’s request for life support withdrawal and their medical, legal and ethical implications. We propose that the following goals should be pursued: (1) prevention of unwanted ventilation by early, open discussion with patient and relatives, (2) delivery of optimal palliative care by the caring team, (3) recognition of the patient’s right to withdraw his/her consent to an invasive medical procedure. If these goals have been met, it may be medically, legally and ethically justified for the physician to take all necessary steps to ensure a peaceful death after discontinuation of life support. Received: 24 November 1997 Received in revised form: 3 April 1998 Accepted: 5 April 1998     

Palliative care in amyotrophic lateral sclerosis

The poor prognosis of amyotrophic lateral sclerosis (ALS) makes palliative care a challenge for the neurologist. Most disabilities associated with progressive disease can be ameliorated by symptomatic treatment. Prognosis and treatment options should be openly discussed with the patient and his/her relatives. Nutritional deficiency due to pronounced dysphagia can be efficiently relieved by a percutaneous enterogastrostomy. Respiratory insufficiency can be treated by non-invasive ventilation at home, provided the familial environment is supportive. Adequate assistance and palliative treatment in the terminal phase is of paramount importance.