Practice versus knowledge when it comes to pressure ulcer prevention

Purpose: This study was completed to determine the current knowledge and documentation patterns of nursing staff in the prevention of pressure ulcers and to identify the prevalence of pressure ulcers.Methods: This pre-post intervention study was carried out in three phases. In phase I, 67 nursing staff members completed a modified version of Bostrom's Patient Skin integrity Survey. A Braden Scale score, the presence of actual skin breakdown, and the presence of nursing documentation were collected for each patient (n = 43). Phase II consisted of a 20-minute educational session to all staff. In phase III, 51 nursing staff completed a second questionnaire similar to that completed in phase I. Patient data (n = 49) were again collected using the same procedure as phase I.Results: Twenty-seven staff members completed questionnaires in both phase I and phase III of the study. No statistically significant differences were found in the knowledge of the staff before or after the educational session. The number of patients with a documented plan of care showed a statistically significant difference from phase I to phase III. The number of patients with pressure ulcers or at risk for pressure ulcer development (determined by a Braden Scale score of 16 or less) did not differ statistically from phase I to phase III.Conclusion: Knowledge about pressure ulcers in this sample of staff nurses was for the most part current and consistent with the recommendations in the Agency for Health Care Policy and Research guideline. Documentation of pressure ulcer prevention and treatment improved after the educational session. Although a significant change was noted in documentation, it is unclear whether it reflected an actual change in practice.     

Massive intraoperative pulmonary embolism: it may not be as bad as it looks...

An elderly patient suffered a cardiac arrest while undergoing repair of a pathological femoral fracture. Intraoperative transoesophageal echocardiography demonstrated massive pulmonary embolism. Pulmonary embolectomy was considered inappropriate in view of her underlying terminal disease, so a decision was made to withdraw all further supportive measures. Despite this, the patient's haemodynamics improved spontaneously. The embolic material was presumed to be bone marrow fat. Fat may traverse the pulmonary circulation; hence the clinical consequences (and management implications) of massive intraoperative pulmonary embolism may vary, depending on the composition of the embolic material. As there are no reliable means of determining the composition of embolic material intraoperatively, the clinical suspicion of fat embolism poses a management dilemma. Should these cases be managed surgically or conservatively?     

Postburn impaired cell-mediated immunity may not be due to lazy lymphocytes but to overwork.

After major trauma, including burns, patients develop a multitude of immunologic alterations, including impaired cellular immunity (CMI). Because of conflicting reports on the relationship of in vitro lymphocyte activity to the clinical course of burn patients, we studied CMI in 29 patients with a mean burn size of 41% and a mean age of 32 years. The patients' cellular response to the mitogen phytohemagglutinin and the ability of the patients' serum to suppress a normal lymphocyte mitogenic response were measured. The endogenous level of lymphocyte activity spontaneous blastogenic transformation (SBT) was measured immediately after the cells were harvested from the blood. During the first 72 hours postburn, the ability of the patients' cells to respond to mitogens in vitro decreased, while the endogenous activity (SBT) increased. Subsequent changes in the SBT, but not the mitogen-stimulated response, predicted sepsis. Although the patients' serum was mildly suppressive, these changes were not of statistical or clinical significance. It is postulated that the in vivo and in vitro CMI defects are not primarily due to a defect in the ability of the cell to be activated, but instead are due to exhaustion, desensitization, or down-regulation of these in vivo-activated cells.