June, 20th – 27th, 2016
June, 20th – 27th, 2016
June, 20th – 27th, 2016
Deep sedation is known to be associated with poor long-term outcomes in critically ill patients, including cognitive and psychological complications and increased mortality. Yet many patients still receive high levels of sedation, particularly during the early days of their intensive care unit (ICU) stay. The eCASH (early Comfort using Analgesia, minimal Sedatives and maximal Humane care) concept is a three-pronged approach to minimize sedation in ICU patients by ensuring adequate and timely analgesia is received; patient-centred care is encouraged, including communication aids, noise reduction to facilitate good sleep patterns, early mobilization, and family involvement; and, when needed, sedation is targeted to individual needs and regularly reassessed, with patients kept calm, comfortable and able to cooperate.
Key words: analgesia, communication, sleep, mobilization
Antioxidants are molecules that inhibit oxidation which under certain conditions leads to the production of free radicals, highly reactive species characterized by an unpaired electron which enter into further chain reactions that lead to cell damage. (1) In biological systems these include reactive oxygen species (ROS) which include the hydroxyl radical (OH.), hydrogen peroxide (H2O2) and the superoxide anion (O2.-) among others. The generation of such species may trigger a variety of pathological responses and any disequilibrium between production of ROS and the ability to attenuate the damage that such species may incur is referred to as oxidative stress. Oxidative stress may result in damage to any component of the cell and may result in DNA damage through base damage as well as strand breaks and also some ROS may act as cellular messengers causing disruption in cellular signaling. Cellular protection against oxidative stress may be through chelation of trace metals involved in free radical generation or through the actions of antioxidants. Antioxidants are broadly classified into two groups, depending on whether they are soluble in water (hydrophilic), such as vitamin C or fat soluble such as Vitamin E (lipophilic). Hydrophilic antioxidants are thought to predominantly react with oxidants in the cell cytosol and plasma whereas lipophilic antioxidants protect cell membranes from oxidation: a process termed lipid peroxidation. (2) The synergism between different antioxidant systems is complex. Indeed, both vitamin C and vitamin E were shown to have a direct interaction with vitamin C “repairing” the α-tocopherol radical with rates approaching diffusion limited outlining the reactivity of these species. (3)
One of the areas that has attracted considerable interest with regard to the role of oxidative stress is the host response to sepsis. (4) Sepsis remains a major cause of death worldwide affecting over 18 million people annually with a mortality rate approaching 80% in those individuals with multi-organ failure and in the US hospital costs total over $24 billion dollars. (5, 6) Therapy for severe sepsis is predominantly supportive with the relatively recent introduction of care bundles including antibiotic therapy being introduced. However, the precise pathogenesis of sepsis-induced organ failure remains elusive and although likely multifactorial in nature certainly microvascular dysfunction appears to be central to the process. (7) Microvascular dysfunction involves impairment of arteriolar reactivity, derangement of endothelial barrier integrity and microthombi induced plugging of the capillaries thus any therapy that addresses these issues may translate into improved outcomes.
Key words: sepsis, antioxidants, resuscitation
Mortality rates from critical illness are decreasing worldwide, but survivors suffer from significant functional disability as a result of muscle wasting. In the short-term the functional effects are seen in increased time of mechanical ventilation, and increased length of stay. Muscle wasting is the most common complication of critical illness, occurring in 25-50% of patients. In a longitudinal observational study, daily loss of muscle mass averaged 2-3% over the first 10 days. The scale of wasting was related to the severity of organ failure and of acute lung injury.
Changes in muscle mass are underpinned by alterations in muscle protein homeostasis. In stable isotope infusion experiments, muscle protein synthesis was reduced to levels of fasted controls despite the initiation of enteral feed. Protein synthetic levels recovered variably over the first week to levels comparable to fed controls. As a result, muscle protein breakdown was increased relative to muscle protein synthesis, leading to a net catabolic state.
There is a need for secondary prevention measures to be instituted in current practise. Increased nutritional delivery cannot be recommended at this stage during acute critical illness and early mobilisation has been demonstrated to increase functional status. This is best achieved through the ABCDEF bundle. This bundle constitutes a co-ordinated package of care with sedation control to facilitate spontaneous breathing and decreasing delirium. This facilitates early mobilisation, which is currently the only preventative measure with an evidence base to decrease skeletal muscle wasting associated functional disability.
Key words: muscle wasting, critical illness, muscle mass