Chapter 14: ICU-Acquired Weakness and Early Mobilization in the Intensive Care Unit

The decreasing mortality from critical illness over recent decades has led to an increasing number of intensive care unit (ICU) survivors.^1,2,3 As a result, there has been a shift in focus from short-term mortality to longer-term morbidities within the field of critical care. Neuromuscular complications, leading to ICU-acquired weakness (ICUAW) and impaired physical function, are common in survivors of critical illness, with a prevalence ranging from 9% to 87%.⁴ Furthermore, these complications are frequently severe and persistent, contributing to functional decline and significant decrements in health-related quality of life.^{5,6,7,8,9,10,11}

Reasons for muscle weakness following critical illness are multifactorial, including premorbid weakness associated with chronic diseases. Recently, there has been growing recognition that both critical illness and its associated treatments are toxic to muscles and nerves and contribute to the development of ICUAW.^1,2 Unfortunately, there are limited interventions to prevent or treat ICUAW. There is currently evidence from observational studies and small randomized controlled trials that establishes proof-of-principle that early mobilization (EM) may improve patient outcomes. This chapter will focus on the development, detection, and outcomes of ICUAW, with a particular emphasis on the role of EM in the critically ill. We will also discuss the barriers to EM in the ICU, the safety considerations for EM, strategies for measuring outcomes, and setting goals that include both the patient and their families.

Bed Rest, Immobilization, and Disuse Muscle Atrophy

Prolonged bed rest and immobilization is common in many ICU patients and may contribute to the development of ICUAW.³ A meta-analysis of 39 randomized trials examining the effects of bed rest on 15 different medical conditions and procedures demonstrated that bed rest was not beneficial, and may be associated with harm.⁴

Prolonged bed rest leads to decreased muscle protein synthesis, increased muscle catabolism, and decreased muscle mass, especially in the lower extremities.^5,6 In healthy volunteers, muscle atrophy can begin within hours of immobility,⁷ resulting in a 4% to 5% loss of muscle strength for each week of bed rest.⁸ Immobility results in the activation of specific biochemical pathways that lead to enhanced proteolysis and decreased protein synthesis, resulting in a net loss in muscle mass, cross-sectional muscle area, and contractile strength.^9,10,11,12 Moreover, there is a general shift from slow twitch (type I) to fast twitch (type II) muscle fibers, with reduced muscle endurance due to fewer fatigue-resistant (type I) fibers.^13,14,15 Consequently, disuse atrophy results in deleterious effects on muscle strength, with nearly 2% of quadriceps' strength lost for each day of bed rest in healthy individuals.^16,17 In a multisite study of patients with acute respiratory distress syndrome (ARDS), the duration of bed rest during critical illness was the only risk factor consistently associated with weakness throughout the entire follow-up, with each additional day of bed rest having up to an 11% relative decrease in muscle strength at 24-months post-ARDS.¹⁸ In addition, the interaction of bed rest and critical illness appears to result in more significant muscle loss than bed rest alone.^19,20,21 Furthermore, short-term immobility may impair microvascular function and induce insulin resistance, both of which may further potentiate injuries to muscle and nerves in the critically ill.²²

In addition to its direct effects on muscle, immobility can lead to a proinflammatory state via increased proinflammatory cytokines.^23,24 This cytokine shift may potentiate the systemic inflammatory milieu commonly observed during critical illness leading to further muscle damage and loss.²⁵ The proinflammatory state associated with bed rest also may cause increased production of reactive oxygen species (ROS), with a concomitant decrease in antioxidative defenses.^26,27 ROS play a role in oxidization of myofilaments, resulting in contractile dysfunction and atrophy.^28,29 This concomitant increase in ROS and imbalance in the cytokine profile can further disrupt the balance between muscle synthesis and proteolysis, with a net loss of muscle protein and subsequent muscle weakness.

Finally, bed rest may produce indirect consequences that lead to further intolerance of physical activity. Immobility may lead to increased postural hypotension and tachycardia due to alterations in baroreceptor function.^30,31 Furthermore, prolonged physical inactivity can result in generalized pain and changes in mood which may limit physical function.³² Even in healthy adults, the effects of prolonged immobilization and disuse atrophy alone are often persistent, and require extensive physical reconditioning to allow a return to their baseline level of functioning.^30,31

Critical Illness Polyneuropathy and Critical Illness Myopathy

Critical illness polyneuropathy (CIP) is a diffuse and symmetric sensorimotor axonal neuropathy that was first described in 1984.³³ Electrophysiologic changes, detected with nerve conduction studies (NCS) and electromyography (EMG), can occur within 24 hours after the onset of critical illness.³⁴ The development of primary axonal degeneration in CIP is likely multifactorial, but a number of mechanistic hypotheses have been posited.^35,36,37 Critical illness myopathy (CIM) represents metabolic, inflammatory, and bioenergetic derangements in muscle similar to those seen in CIP.³⁸ These changes result in early and rapid skeletal muscle wasting during the first week of critical illness.³⁹ Functional inactivation of the remaining muscle may occur due to membrane inexcitability from acquired ion-channel dysfunction.^40,41,42 CIP and CIM share many pathologic mechanisms, often coexist, and may represent a form of neuromuscular organ dysfunction from systemic critical illness.¹ As such, similar emphasis should be placed on prevention and recovery as would be for ICU patients that develop acute kidney injury or lung injury.⁴³

Although immobilization and the effects of critical illness traditionally have been considered to predominantly affect peripheral muscles groups, recent preclinical and clinical studies have suggested diaphragmatic involvement, including reduced muscle force and increased muscle atrophy.^44,45,46 A preliminary study in humans suggests that even short-term diaphragmatic inactivity and controlled mechanical ventilation (with effective functional denervation) can result in marked diaphragmatic atrophy.⁴⁷ A “two-hit” combination of immobilization and the early development of subclinical CIP/CIM may contribute to the rapid development of muscle atrophy.⁴⁸

Although many studies have investigated risk factors for ICUAW, most have been limited by small sample size, retrospective design, and single-center experiences.⁴⁹ Furthermore, lack of comparable patient populations and standard definitions for ICUAW makes comparisons across studies difficult.^43,49 Thus, although there are a number of commonly cited risk factors for ICUAW, many lack support from rigorous clinical investigations.⁴³

Hyperglycemia

A recent systematic review found that hyperglycemia is the most consistently identified risk factor for ICUAW.⁴⁹ Two large randomized controlled trials (RCTs) of intensive insulin therapy for tight glycemic control in the ICU,^50,51 and associated subanalyses,^37,52 demonstrated a substantial decrease in the incidence of ICUAW in patients randomized to intensive insulin therapy. However, the overall safety and efficacy of intensive insulin therapy and tight glycemic control in a heterogeneous population of critically ill patients remains controversial,^53,54,55 and clinicians should be cautious in using the results of these secondary analysis to support the use of tight glycemic control for the prevention of ICUAW.

Sepsis and Systemic Inflammation

Given the potential mechanistic relationship between systemic inflammation (ie, the systemic inflammatory response syndrome [SIRS]), with or without concomitant infection (ie, sepsis), and the development of ICUAW, several studies have examined this issue.^56,57,58 Two prospective studies reported a significant association of ICUAW with the presence of SIRS⁵⁷ and the duration of SIRS (odds ratio [OR] 1.05; 95% confidence interval [CI] 1.01-1.15 for each day in the first week).⁵⁶ However, another prospective study demonstrated no association between the presence of sepsis and ICUAW.⁵⁸

Corticosteroids and Neuromuscular Blocking Agents

There has been substantial controversy regarding the role of systemic corticosteroids in the development of ICUAW. A prospective study reported that exposure to corticosteroids was the single largest risk factor for the development of weakness (OR 14.9; 95% CI 3.2-69.8).⁵⁹ However, this study revealed no relationship between the dose or duration of corticosteroid therapy and the development of weakness. A number of other clinical studies, including a systematic review, have failed to demonstrate a consistent association between corticosteroids and ICUAW.^{18,37,49,56,57,58,60,61,62,63,64} Conversely, a recent study demonstrated decreased ICUAW in patients randomized to intensive insulin therapy who also received corticosteroids in the ICU (OR 0.91; 95% CI 0.86-0.97).⁵² The investigators suggested that the deleterious effects of corticosteroids on the neuromuscular system may be mediated through hyperglycemia, such that when blood glucose is strictly controlled, the anti-inflammatory effects of corticosteroids may be protective against ICUAW.

Despite early reports of persistent weakness following prolonged administration of neuromuscular blockade, 5 prospective trials,^{18,37,49,56,57} an RCT (which demonstrated at significant reduction in 28-day mortality)⁶⁵ and a systematic review⁶⁶ did not find a significant association between their use and the development of ICUAW. However, 2 other studies did find a significant association, possibly due to larger doses and longer duration of neuromuscular blockade use.^52,61 Thus, clinicians should consider the use of corticosteroids or neuromuscular blocking agents on a case-by-case basis, weighing the potential risks and benefits based on the individual patient characteristics.⁶⁷

ICUAW is often difficult to diagnose in critically ill patients during the acute phase of their illness due to the frequent use of deep sedation. As a result, ICUAW is usually recognized in 2 distinct contexts: (1) prolonged or failed weaning from mechanical ventilation, despite otherwise global improvement in other organ systems; or (2) profound bilateral weakness in an awake patient recovering from critical illness.⁶⁸ In either scenario, neuromuscular dysfunction is usually detected after the recovery of other organ systems as the patient wakes.

Typically, symmetric motor weakness is observed in all limbs, ranging from mild paresis to frank quadriplegia. In noncooperative patients, noxious stimuli may be applied to each extremity in order to grossly evaluate the strength of patient withdrawal. Since facial muscles are typically spared in patients with ICUAW, patients may have normal facial grimacing with application of noxious stimuli.

Physical Examination

The bedside physical examination of the neuromuscular system in a critically ill patient is often difficult due to deep sedation or delirium. The standard physical examination of individual muscle groups is typically done using the Medical Research Council (MRC) Manual Muscle Test scale,⁶⁹ which is dependent on patient effort and cooperation. This scale evaluates muscle strength with a score ranging from 0 (no muscle contraction) to 5 (normal strength). Physical examination of 3 muscle groups in each limb, yielding a composite MRC score, has demonstrated excellent inter-rater reliability within specific non-ICU patient populations,⁷⁰ with very good inter-rater reliability in ICU patients and survivors.⁷¹ Clinically detectable muscle weakness has been arbitrarily defined as a composite MRC score less than 80% of normal (eg, composite MRC score less than 48 out of a maximum score of 60 for 3 muscle groups in each limb).^59,70,72 Other methods of volitional muscle testing that could be employed in these patients include handheld or handgrip dynamometry.

Similar to the motor examination, a sensory examination is often limited by sedation, altered sensorium, as well as peripheral edema. Deep tendon reflexes may be diminished or absent, but normal reflexes do not rule out ICUAW. Hyperreflexia and/or associated spasticity should suggest an alternative diagnosis (eg, central nervous system etiology), and further investigations (eg, brain and spinal cord imaging) should be obtained.

Electrophysiology and Muscle Biopsy

Given the limitations of physical examination, there has been growing interest in the use of electrodiagnostic testing (ie, motor/sensory NCS and needle EMG) for the diagnosis of ICUAW. In patients with CIP, NCS often reveal a mixed sensorimotor axonopathy manifested by a reduced amplitude of the compound muscle action potential (CMAP) and sensory nerve action potential (SNAP) with relative preservation of the nerve conduction velocity.³⁶ The electrophysiologic changes seen in CIP can be detected as early as 24 to 48 hours following the onset of critical illness, and often precede clinical findings in these patients.^73,74,75 Despite their potential utility in sedated or comatose patients, there are still certain technical factors, including local edema and limb temperature, which can interfere with NCS.²

In patients with CIM, prolongation of CMAP duration on NCS can be seen and suggests the presence of a myopathic process (ie, not due to muscle denervation). On needle EMG, CIM will manifest as short-duration, low-amplitude motor unit action potentials (MUAP) with early recruitment of MUAPs on volitional contraction. Furthermore, abnormal spontaneous activity, including fibrillation potentials and positive sharp waves, may be present.⁷⁶ Therefore, diagnosis of CIM with EMG requires a cooperative patient that can perform voluntary contraction, and an experienced clinician to interpret the results.

Definitive diagnosis of an underlying myopathy requires histologic confirmation with a muscle biopsy. Histopathologic findings consistent with CIM include muscle fiber atrophy (with preferential loss of type II fibers), occasional fiber necrosis and regeneration, and selective loss of myosin filaments (pathognomonic for CIM).³⁸

Diagnostic Strategy

Despite its limitations, routine bedside physical examination should be the starting point for the identification of ICUAW. Given the relative cost, invasiveness, and need for specialist physicians and technicians, comprehensive electrophysiology studies and muscle biopsy should be reserved for weak patients with slower-than-expected improvement on serial clinical examination.⁶⁸

Weaning From Mechanical Ventilation

Prolonged or failed weaning from mechanical ventilation is a common manifestation of ICUAW in patients recovering from critical illness. Involvement of both chest wall muscles and the diaphragm in ICUAW likely contribute to the difficulty with weaning from mechanical ventilation. In a recent systematic review, 12 of 13 studies that evaluated ICUAW and the duration of mechanical ventilation revealed that ICUAW was associated with prolonged mechanical ventilation in patients with ICUAW.⁴⁹ In one study, the presence of ICUAW was the only significant predictor of failure to wean from mechanical ventilation (OR 15.4; 95% CI 4.6-52.3).⁷⁷

Patient Outcomes After ICU Discharge

A recent systematic review was inconclusive regarding differences in patient outcomes with CIP versus CIM.⁴⁹ Existing evidence is also inconclusive regarding whether ICUAW is associated with increased hospital mortality.^49,61,78 In survivors of critical illness, recovery from ICUAW is possible, with a majority (94%) of patients in one cohort demonstrating meaningful clinical recovery of muscle strength at 9 months.⁵⁹ However, in some patients, ICUAW may persist and result in severe and prolonged functional deficits,^18,79,80,81 with concomitant decrements in health-related quality of life.^18,82,83

There are currently few options for the prevention and/or treatment of ICUAW. During critical illness, exposure to hyperglycemia and certain medications (eg, corticosteroids and neuromuscular blocking agents) may be associated with the development of ICUAW. At present, the strongest evidence for the prevention of ICUAW is tight glycemic control with intensive insulin therapy, which may decrease neuromuscular abnormalities in critically ill patients who are mechanically ventilated for more than or equal to 7 days. However, the potential benefits of intensive insulin therapy should be carefully weighed against the possibility of serious hypoglycemia, as demonstrated in recent clinical trials.^55,84 Finally, despite a strong evidence base, maintenance of electrolyte homeostasis (eg, phosphate, magnesium) and adequate nutrition to ameliorate muscle catabolism may be reasonable clinical recommendations for minimizing ICUAW.⁸⁵

Beneficial Effects of Exercise in ICU

A potential therapeutic option to reduce ICUAW is avoidance of bed rest via EM in the ICU setting. EM in the ICU is a candidate intervention to improve muscle strength, physical function, and quality of survival.⁸⁶ EM is the intensification and acceleration of the usual physical therapy (PT) that is administered to critically ill patients, along with additional novel concepts that include the mobilization of patients requiring mechanical ventilation and the use of novel techniques such as cycle ergometry and electrical muscle stimulation.⁸⁶ EM is applied with the intention of maintaining or restoring musculoskeletal strength and function and thereby, potentially, improving functional, patient-centered outcomes.⁸⁷

Usual Physical Therapy in ICU

The management of critically ill patients appears to vary widely within countries and internationally.^88,89 This is partly due to cultural differences, funding differences (eg, staffing ratios of nurses to patient), and partly due to differences in medical management as a result of local practice. To date there is no published data comparing the practice of early mobilization in ICUs internationally. However, there are 2 multicenter point prevalence studies of EM in ICU that may be informative. The first studied all patients from 38 ICUs in Australia and New Zealand at a single time on a single day in 2009 and 2010.⁸⁸ Of the 514 patients included, 45% were mechanically ventilated. Overall, mobilization activities were classified into 5 categories that were not mutually exclusive: 140 patients (28%) completed an in-bed exercise regimen, 93 (19%) sat over the side of the bed, 182 (37%) sat out of bed, 124 (25%) stood and 89 (18%) walked. Adverse events occurred on 24 occasions (5%). Importantly, none of the mechanically ventilated patients sat out of bed or walked on the day of the study. The main barrier to mobilization was that the patient was unconscious (20%) or deeply sedated (17%).

A similar study was conducted in 116 German ICUs including 783 mechanically ventilated patients.⁸⁹ Overall, 185 patients (24%) were mobilized out of bed which was defined as sitting on the edge of the bed or a higher level of mobilization. Among patients with an endotracheal tube, tracheostomy, and noninvasive ventilation, 8%, 39%, and 53% were mobilized out of bed, respectively. This study identified cardiovascular instability (17%) and deep sedation (15%) as the main barrier to mobilization, however mobilization out of bed was not associated with a higher frequency of complications.

Safety

Clinical practice guidelines endorsed by the European Society of Intensive Care Medicine (ESICM) on the safety of EM have been published and serve as a guide to clinicians working in the ICU.⁹⁰ Active mobilization of a critically ill patient, particularly if they require mechanical ventilation, involves a complex assessment that has not been standardized and may differ between ICUs and individual patients. In part this may be due to the heterogeneity of critical illness, the changing stability of the patient and the cointerventions; however it is also affected by the individual response to EM.⁹¹

The decision to actively mobilize a patient, both in bed and out of bed, should be made by the multidisciplinary ICU team, preferably during the morning rounds. The decision should include the individual assessment of the patient's past medical history and exercise tolerance, respiratory and cardiovascular stability over the previous 24-hour period, management of lines and tubes, consideration of orthopedic and neurologic conditions, medications that may affect the patients' safety during mobilization, and the available staff and equipment to ensure patient safety. Occasionally medical staff outside the ICU may need to be consulted about the safety of mobilization, for example in a polytrauma patient with lower leg injuries, an orthopedic surgeon may need to be contacted regarding the lower limb weight-bearing status if it is not clearly documented in the patient history.

Ideally, each ICU would formulate a protocol to guide EM, where decisions are predetermined about the safety criteria acceptable within that ICU to commence mobilization and the safety criteria to cease if the patient deteriorates during mobilization.

Cardiovascular Reserve

Cardiovascular stability is determined by assessing the heart rate and rhythm, blood pressure, requirement and dose of vasoactive or antiarrhythmic drugs, and other major cardiac conditions or support (eg, intra-aortic balloon pump, extracorporeal membrane oxygenation [ECMO]).⁹⁰ The blood pressure and heart rate should be considered stable by the medical staff, with minimal variability (< 20%) over the preceding hours and stable requirements of vasoactive drugs. If there is any doubt about cardiovascular stability, the medical team should be consulted prior to mobilization.

Respiratory Reserve

Respiratory stability is determined by the respiratory rate and pattern, the fraction of inspired oxygen and the arterial oxygen concentration measured either with blood gases or a pulse oximeter and the ventilator settings if the patient is on mechanical ventilation, including the rate, pressure, volume, and requirement for positive end-expiratory pressure (PEEP). In general, the respiratory rate and oxygen requirements should not have increased in the preceding hours prior to mobilization and the patient should have a clear airway with minimal work of breathing.⁹⁰ The oxygen saturation should be greater than 90% and the fraction of inspired oxygen 0.6 with PEEP less than 15 cm H₂O. The respiratory rate should be less than 30 breaths/min.

Prior to each episode of mobilization, an appropriate ICU staff member should check the position of the artificial airway and ensure that the artificial airway is secure (ie, an orotracheal, nasotracheal, or tracheostomy tube). Additionally, if the plan is to move away from the bed, any supplementary gas supply required by the patient during mobilization should be available and there should be adequate reserve for the expected duration of the mobility session, and a little extra reserved for any unexpected additional requirements.

Neurologic Stability

Ideally, prior to mobilization, the patient is awake, calm, and able to follow instructions. This can be assessed with standardized tools, such as the Richmond Agitation and Sedation Scale (RASS), where a score of –1 to +1 is ideal. Delirium is common in the ICU and can also be assessed using the Confusion Assessment Method for the ICU (CAM-ICU). Other neurologic precautions for EM include active treatment for intracranial hypertension, craniectomy, open lumbar drains, spinal precautions, or the presence of an acute spinal injury.

Other Considerations

Medical Conditions—Patients should also be assessed with regards to oxygen carrying capacity (Hb > 7 g/dL and stable), white cell and platelet count, deep vein thrombosis or pulmonary embolus, body temperature, unstable fractures, skin grafting, and open surgical wounds. If there is any doubt about the safety of mobilization, the senior consultant or surgeon should be asked to make a final decision prior to commencing EM.

Staffing—There must be adequate trained staff and equipment to ensure safe mobilization of an ICU patient. In the case of a mechanically ventilated patient, one person should always be designated to ensure the security of the airway during mobilization. The patient should be assessed for strength prior to mobilizing out of bed, for example using the MRC manual muscle test, and if there is significant weakness the patient may not be strong enough to mobilize against gravity or they may require specific equipment designed to assist with EM. This may include a hoist, standing lifter or a walking frame designed to include a pole (to attach intravenous fluids), and a stand for the mechanical ventilator and oxygen tank (Figure 14–1).

Other Lines, Drains, and Attachments—Each ICU may differ in its policy regarding attachments that are safe for mobilization, or attachments that are contraindicated for mobilisation. Discussion about the safety of various patient lines and attachments must be considered on an individual basis. There is some evidence that femoral catheters, including femoral catheterization for hemofiltration, should not be a contraindication to EM in the ICU.⁹² Similarly, some extracorporeal devices are considered safe for EM with adequately trained staff conducting the activities.⁹³

In a recent systematic review of physiotherapy in intensive care, 17 observational studies of EM reported outcomes regarding feasibility, safety, and physiologic effects.⁹¹ Mobilization activities were reported as both safe and feasible, with the frequency of serious adverse events reported to be less than or equal to 1%. There were occasional short-term physiologic changes associated with EM that requires careful assessment throughout the mobilization activity.

Clinical Evidence—Early mobilization in ICU is an emerging new focus of intensive critical care research, representing a potentially lower-cost, high-impact intervention. However, there are few RCTs evaluating its efficacy.

Three RCTs^94,95,96 and a number of observational studies^{97,98,99,100,101,102} have provided data on the safety and preliminary efficacy of the concept of mobilizing patients dependent on ventilatory support. In the first observational study, the authors described 1449 activity events in 103 patients. Overall, 53% of these events included ambulating patients that were dependent on positive pressure ventilation via an endotracheal tube or tracheostomy; there was less than 1% adverse events related to EM. This treatment was resourced from within the existing ICU staff structure, including ICU nurses, technicians, physical therapists (PTs), and respiratory therapists. In a further study, the same authors describe a before-and-after cohort study in 104 patients with respiratory failure who were transferred from another ICU to their respiratory ICU. Transfer to the study respiratory ICU with a culture of EM increased the probability of ambulation (P < 0.0001) during ICU stay.

Schweikert and colleagues reported findings from a prospective, outcome assessor-blinded, randomized trial of early physical therapy (PT) and occupational therapy (OT) from two centers in the USA.⁹⁵ In this study, patients who were mechanically ventilated for less than 72 hours and expected to stay ventilated in the next 24 hours were randomized either to an EM protocol which progressed from passive range of motion (PROM), active range of motion (AROM), bed mobility, sitting balance, standing, standing transfers, and gait reeducation during sedation interruption, or a control group which underwent PT and OT as prescribed by standard care. This trial demonstrated safety and feasibility for EM, as well as improved functional outcomes with early intervention.

Sedation

The aim of sedation management in ICU is to keep patients awake and comfortable where appropriate¹⁰³ and to use sedation when medically indicated in the following manner:

1. Target therapy to a desired sedation score (eg, RASS)

2. Use analgesic therapy over sedative/hypnotic therapy

3. Limit excessive doses of sedative and analgesic medications

4. Reduce the incidence of medication-induced delirium

5. Promote daily sedation interruption to facilitate early mobilization

Analgesic and sedative infusions are routinely used in the ICU in patients requiring mechanical ventilation.¹⁰⁴ Although these infusions are often required for patient comfort, to facilitate procedures and for patient-ventilator synchrony, heavy sedation (RASS ≤ –3) is commonly used. There are some circumstances when heavy sedation is required (eg, to control raised intracranial pressure [ICP]). However, it is now understood that excessive sedation may result in delayed extubation and prolonged ICU length of stay, as well as a decrease in sleep quality, an increase in delirium, and even an increase in mortality.¹⁰⁴

Targeted sedation protocols involve the use of a validated sedation scale. Treating teams determine a required level of sedation and then titration algorithms are used to maintain the patient's level of sedation within the target range. Targeted sedation protocols have been shown to reduce time to arousal and decrease the duration of mechanical ventilation, as well as limiting exposure to benzodiazepines without an increase in self-extubation rates. A recent survey of Australian and New Zealand ICUs found that although 74% of ICUs used continuous infusions as the primary means of sedation and 70% used a sedation scale, only 48% of units had a written sedation policy.¹⁰⁴

Delirium

Assessment for delirium is recommended using either the CAM-ICU or the Intensive Care Delirium Screening Checklist (ICDSC). Delirium is known to be associated with the use of sedative medications and there is evidence that the use of a sedation protocol can decrease the number of days with delirium. The CAM-ICU tool should be used daily if the RASS score is greater than or equal to –2. A delirious patient may be unsafe when mobilized out of bed, and particular caution is required as their behavior may be unpredictable.

Pre-ICU Level of Function

It is important to set realistic goals for mobilization based on previous levels of physical function. Communication with the family and caregivers of the patient is essential to determine premorbid level of physical function, including whether the patient could transfer from bed to chair independently prior to the critical illness. For instance, it is essential to determine if the patient previously walked independently or with a gait aid, whether they could walk outside, on uneven surfaces, to the mailbox, around the shops, or further? Patients who were unable to walk independently or transfer independently prior to ICU admission will require increased supervision and increased staff numbers when attempting mobilization. This reduces the risk of injury to both patients and staff.

Mobility milestones are the most commonly reported outcome measure in ICU research projects of early mobilization.¹⁰⁵ Several studies have reported mobility milestones, such as sitting, standing, or walking, as an important indication of patient physical function in ICU.^97,99,101 They have not reported the level of assistance required to achieve the mobility milestone and they have not reported the same milestones. A recent systematic review described measures of physical function used in studies investigating EM in the ICU.¹⁰⁵ The ability to perform activities of mobility, or mobility milestones, was the most common end point reported in these studies. However, between these studies there was no consensus on the functional activities that should be included in measures of mobility in the ICU, or reports of the feasibility or inter-rater reliability of such measures.¹⁰⁵

ICU Mobility Scale

The IMS is an 11-point ICU mobility scale (Table 14–1).¹⁰⁶ The IMS was based on functional patient activities that can reasonably be achieved across the spectrum of recovery while in the ICU. Moreover the reliability assessment was conducted at 2 large ICUs with a varied clinical case mix, including surgical, medical, and trauma patients, and included nurses and junior and senior PTs. Despite the busy ICU environment, the IMS was administered with ease. The inter-rater agreement in the scale was excellent between PTs and good between nursing staff and PTs. This simple scale of mobility milestones will not replace other tests of physical function, but may assist as a daily record of mobility for both clinical and research purposes in order to allow greater standardization and comparability across time and between ICUs.

Other measures of mobilization have been developed for specific patient groups. For example, the Surgical Intensive Care Unit Optimal Mobility Score (SOMS) consists of a simple numeric scale that describes patients' mobilization capacity in a surgical ICU. A SOMS of 0 indicates that no mobilization should be considered. This score was assigned to patients who were either moribund or had an unstable head or spinal cord injury; those in whom any change in position led to profound respiratory or hemodynamic changes; and those with elevated ICPs (> 20 cm H₂O). A SOMS of 1 was used to describe patients receiving PROM exercises while in bed, and SOMS 2 was given to patients who were able to sit up in bed greater than 45° or in a chair. A SOMS 3 described patients who were able to stand with or without assistance, and a SOMS of 4 was assigned to patients able to ambulate. The SOMS demonstrated that in surgical critically ill patients presenting without preexisting impairment of functional mobility, it is a reliable and valid tool to predict mortality and ICU and hospital length of stay.¹⁰⁷

Protocols

Several types of protocols have been suggested to allow mobilization in the ICU to occur as early as possible.^99,107 All protocols include a stepwise prescription of mobilization activity based on the physical capacity of the patient (Figure 14–2). Protocols such as these have been safely and effectively introduced into clinical practice. Further to this, a protocol that considers both the cognitive and the physical capacity of the patient has been implemented in one center in the United States, and resulted in patients walking at least 3 days sooner, an adverse event occurrence of less than 1% and an increase in mobility of up to 2-fold.¹⁰⁸ In another US center, an increase in routine mobilization occurred.⁹⁵

Goal Setting

Setting goals for rehabilitation, particularly EM, is important to patients, family, and the staff in ICU. Functional rehabilitation can be progressed based on the clinical assessment discussed previously in this chapter and may be an important motivation for critically ill patients to recover. Family and friends often express delight at finding the patient out of bed, standing, or walking, even while attached to mechanical ventilation. Concerns about safety of early mobilization may arise from visitors to the ICU and it is important for clinicians prescribing and delivering exercise to explain the physiologic response expected in these circumstances and the safety precautions utilized by ICU staff.

Goals of EM should be clearly documented and progress reported. This is required both for hospital records and for patients and their families to celebrate progress. Diaries, journals, photographs, and documentation of progress made available to the patients and their families may be beneficial for physical and psychological recovery.^106,109,110

The S.T.A.N.D. Principle

• Safety and stability: Assess the respiratory, hemodynamic and neurologic stability, muscle strength, and cooperation of the patient. Most importantly, discuss this with the ICU team if any concerns are raised prior to mobilization.

• Teamwork: Early mobilization requires a team of people to work together with clear communication and an understanding of the safety requirements of the ICU. One person should be appointed as the leader of the team to direct the mobilization activity. The leader ensures that everyone in the team knows their role, including one person to be dedicated to protecting the airway.

• Airway management: Airway management is the main priority during mobilization. One person is dedicated to maintaining the airway. Emergency equipment and portable oxygen supplies are checked and should remain easily accessible at all times. The patient should be suctioned prior to mobilizing and suction equipment should be available during EM.

• Number of lines/tubes/attachments and equipment: Prepare the environment by double checking that all lines and tubes are secure, the area is clear of hazards, and the equipment required for mobilization is prepared.

• Determine an alternate plan: If the patient does not tolerate the mobilization activity, have an alternative plan for repositioning the patient into sitting or supine. Be prepared for bowel movements and ensure there is adequate staff around to assist if the patient becomes unstable.

ICU survivors recovering from a prolonged critical illness often have severe muscle weakness and functional impairment. Future studies are needed to further elucidate the various mechanisms that lead to ICUAW, and to find and develop therapeutic targets for this morbid ICU complication. Early mobilization is a promising intervention to prevent or attenuate ICUAW and requires a coordinated, interprofessional team approach to assess readiness to mobilize and to optimize the progression of patient activity. Observational studies and small randomized trials evaluating EM suggest safety and feasibility, but are mostly single center in design with limited external validity. These studies also suggest that EM has the potential to improve functional outcomes in these survivors, reduce readmissions, and reduce health care costs. Further research is warranted to define baseline standard practice, identify risk factors that predict patients at risk of weakness, and define an intervention and intervention dose for EM.

• ICUAW is common, occurs early in critical illness, and is associated with significant long-term morbidity, and potentially mortality.

• Despite its limitations, routine bedside physical examination should be the starting point for the identification of ICUAW. Given the relative cost, invasiveness, and need for specialist physicians and technicians, comprehensive electrophysiology studies and muscle biopsy should be reserved for weak patients with slower-than-expected improvement on serial clinical examination.

• Early mobilization is a promising intervention to prevent or attenuate ICUAW.

• Early mobilization requires a coordinated, interprofessional team approach to assess readiness to mobilize and to optimize the progression of patient activity.