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Intensive Care Unit-Acquired Weakness (ICU-AW)(ICU-AW)

Pressure Ulcer Risk Assessment

5.2 Intensive Care Unit-Acquired Weakness (ICU-AW)(ICU-AW)

In the past few years, critical illnesses in ICU (from myocardial infarction to surgical complications) required a mandatory com- plete immobility. ICU staff believed that bed rest could reduce the oxygen consumption, improve the tissue oxygenation, main- tain the correct alignment of spine and bones, and decrease to a minimum the effects of trauma. However, the adverse effects of prolonged immobility are now well known and concern all the body systems (Fig. 5.1). Early mobilization may help to reduce some of these adverse effects [6].

ICU-AW is defined as a “syndrome of generalized limb weakness that develops while the patient is critically ill and for which there is no alternative explanation other than the critical illness itself” [7]. The etiology of ICU-AW is multifactorial, with several studies establishing independent risk factors for its development [1].

The reported incidence of ICU-AW varies according to the different definitions given to this syndrome, the diagnostic

Physiological Harms of Prolonged Immobilization Burden of Severe Critical Illness

Cardiovascular Orthostatic intoleranceHypoxiaICUAWThrombolism Insulin resistance Pressure ulcers Increased atrial natriuretic peptide Aldosterone and plasma renin

Polynueropathy Polynueromyopathymyopathy muscle atrophy Bone densityJoint contractures

Atelectasis Pneumonia Mechanical ventilatory dependence

MIP and FVC

Stroke volume Cardiac output Muscle bulk, strengthPTSD Cognitive impairment Depression Anxiety Delirium

Fatigue Entrapment nueropathy Joint immobility Pain (eg, chest/feeding tube insertion site) Peak VO2

Microvascular dysfunction

Peripheral vascular resistance Physical DisabilityNon-Physical DisabilityOther QOL Issues

RespiratoryNeuromuscularOther Effects

ICU Admission Short-term Morbldity Increased ICU and hospital LOS Long-term Morblidity&

Caregiver burnout Financial strain Fig. 5.1Physiological sequelae of immobilization and the burden of severe critical illness. FVC, forced vital capacity; ICU-AW, ICU-acquired weakness; MIP, maximum inspiratory pressure; PTSD, post-traumatic stress disorder; VO2, oxygen consumption [7]

modalities used, and the specific population studied. A key issue in determining the incidence of ICU-AW is the struggle in ascertaining the development of neuromuscular weakness dur- ing the ICU stay, as opposed to weakness due to a preexisting condition (e.g., myasthenia gravis) and/or a specific etiology (e.g., new cerebrovascular accident). ICU-AW may be unrecog- nized in general critically ill populations, but it is prevalent in the chronic critically illnesses and in patients requiring pro- longed MV [8].

Among the risk factors for the development of the ICU-AW, there are the disease severity, the presence of systemic inflam- matory response syndrome (SIRS), and an organ failure associ- ated with neuromuscular disorders. Also, MV duration, ICU-LOS, blood biochemical alterations (such as hypo- and hyperglycemia), and the administration of total parenteral nutri- tion (TPN) increase the risk of ICU-AW development.

Furthermore, using of potentially myotoxic or neurotoxic medi- cations, such as corticosteroids and non-depolarizing neuromus- cular blocking agents, has been associated with neuromuscular abnormalities [1].

Mechanisms leading to the ICU-AW are complex and involve many physiopathological processes. On healthy sub- jects, for example, bed rest leads to a reduction in quadriceps force of around 1–1.5% a day [9], and this percentage increases significantly in sick or elderly subjects. In addition to the immo- bility, critical care patients often show signs of malnutrition during their ICU stay, because of malabsorption due to primary pathology, hypercatabolic and hypermetabolic stress, leading to protein loss [10]. Malnutrition is considered as a contributing factor to the occurrence of ICU-AW. Therefore, nutritive sup- port in ICU is essential to correct nutritional deficits.

Patients with ICU-AW have an increased duration of MV and LOS. After 7 days of MV, 25–33% of patients experience clini- cally evident neuromuscular weakness [1].

5.2.1 Prevention and Treatment of Immobility

There are few treatment options to prevent or treat the ICU-AW. A proper glycaemia control seems to be the only intervention related to the decrease in the onset of this syndrome [11]. Minimizing patient’s exposure to corticosteroids and/or neuromuscular block- ing agents may be prudent until future studies will clarify the role of these medications in the development of ICU-AW [12].

A potential therapeutic option to reduce ICU-AW is the avoidance of bed rest via early mobilization in the ICU setting.

Mobility is a basic nursing care, which is essential in maintain- ing patients’ safety and prevention of bed rest induced compli- cations. Mobility can improve gas exchanges, decrease incidence of ventilator-associated pneumonia and the occurrence of MV support, and decrease ICU and hospital LOS [12].

Physiotherapy carried out in ICU varies from hospital to hos- pital and among different typologies of ICUs. Furthermore, there is a wide range of interventions that can be carried out ranging from passive physiotherapy to kinetic therapy, or transferring the patient from bed to chair. In some case, patients are helped to brief walk within the ICU [8]. Usually more challenging physio- therapy (e.g., walking) is rarely performed in ICU because of the huge nurses’ workload and the reduced number of physiothera- pists dedicated to this activity [8].

Physiotherapy is also affected by the level of sedation: criti- cal care patients are often deeply sedated especially if mechani- cally ventilated. Deep sedation is related to the increasing number of MV days that prevents their participation to the activities [13]. Periodic interruptions of sedation and the imple- mentation of awakening tests can improve an early mobilization (see Chap. 17). Also, a multidisciplinary focus to perform an early mobilization program after the physiologic stabilization (Fig. 5.2) from cardiological, respiratory, and neurological impairments is desirable [14].

5.3 Skin and Pressure Ulcer Risk Assessment