Sleep in Critically ill

Sleep in critically ill

The sleep deprivation among patients hospitalized in ICU is extremely common, it creates(causes) a subjective discomfort and clinical consequences not yet fully clarified, there may be among them: increased delirium, immune dysfunction, delayed weaning from mechanical ventilation.
The reasons for the dysfunction of sleep during critical illness are certainly multifactorial: environmental causes (which accounted for approximately 20% of nocturnal awakenings) plus the clinical causes, including mechanical ventilation and usage of drugs that causes worsening of sleep’s quantity and quality (vasoactive amines, beta-blockers, corticosteroids, antibiotics, gastroprotective drugs, opioids, benzodiazepines, etc.). The severity of underlying disease at admission in ICU may lead to a profound alteration of the sleep / wakefulness.
The difficulties in getting enough a great sleep’s quantity is witnessed both by objective measures such as polysomnography, both by subjective measures such as questionnaires in which patients describe the stressors of their admission to ICU: the inability to satisfactorily sleep is shown always as a major factor(stresssor), often more important than thirst, or pain, or the presence of intubation tube.
Among the possible interventions that can be designed to improve the sleep of critically ill patients at first it must establish a good habits of "sleep hygiene"as discouraging daytime sleep, taking a day early physical therapy, avoidance of not necessaries medical procedures / nursing night time, decrease the volume of the bedside monitor’s alarms during the night, allowing patients - if possible - to see the light of the sun through the disposition of hospital beds, minimizing the sounds and turning on artificial lights during the night, providing eye masks or earplugs, if required.
About the pharmacological interventions often used to "induce sleep," must be specified that the appearance of a sleeping patient through the administration of propofol or benzodiazepines often does not correspond to a satisfactory refreshing sleep for the patient, as remains the activation of subcortical neural circuits, resulting in a drastic reduction in sleep’s slow wave and REM sleep, more restorative. Unlike sedative drugs, administration of exogenous melatonin could play a role more similar to(akin) physiological ipnoinduction ; preliminary monocentric studies have shown a possible usefulness of melatonin for increase sleep night time even for patients hospitalized in ICU.