No abstract

The aim of this study was to determine the prevalence, severity, location, aetiology, treatment and healing of medical device-related pressure ulcers (PUs) in intensive care patients for up to 7 days. A prospective repeated measures study design was used. Patients in six intensive care units of two major medical centres, one each in Australia and the USA, were screened 1 day per month for 6 months. Those with device-related ulcers were followed daily for up to 7 days. The outcome measures were device-related ulcer prevalence, pain, infection, treatment and healing. Fifteen of 483 patients had device-related ulcers and 9 of 15 with 11 ulcers were followed beyond screening. Their mean age was 60·5 years, and most were men, overweight and at increased risk of PU. Endotracheal (ET) and nasogastric (NG) tubes were the cause of most device-related ulcers. Repositioning was the most frequent treatment. Four of 11 ulcers healed within the 7-day observation period. In conclusion, device-related ulcer prevalence was 3·1%, similar to that reported in the limited literature available, indicating an ongoing problem. Systematic assessment and repositioning of devices are the mainstays of care. We recommend continued prevalence determination and that nurses remain vigilant to prevent device-related ulcers, especially in patients with NG and ET tubes.

No abstract

To determine the diagnostic accuracy of state, minimally invasive clinical and physical signs (or sets of signs) to be used as screening tests for detecting impending or current water-loss dehydration, or both, in older people by systematically reviewing studies that have measured a reference standard and at least one index test in people aged 65 years and over. 1 Clinical and physical signs for identification of impending and current water-loss dehydration in older people (Protocol)

Critically ill patients often have distressful episodes of severe thirst, but the underlying complex biochemical, neurohormonal regulatory controls that regulate this primal sensation have rarely been addressed by clinicians. Subtle changes in plasma osmolality are the most potent stimulus for thirst. In response to increases in osmolality, osmoreceptors activate release of the neurohormone vasopressin (also known as antidiuretic hormone). The released vasopressin acts on the kidneys to conserve water to correct the hyperosmolar state. If this compensatory mechanism is unsuccessful, thirst arises to promote drinking. Thirst induced by marked volume loss, in contrast, is more closely related to the volemic and pressure changes regulated by the renin-angiotensin aldosterone system. Understanding the physiological mechanisms of thirst will help in understanding the pathophysiological consequences of underlying thirst-related disease and treatments in critically ill patients. Further clinical research is needed to elucidate the multiple inhibitory and excitatory neurohormonal stimuli that motivate patients’ intense desire for water.