Probably the most obvious and readily recognizable changes in patients immediately after discharge from the ICU are the physical impairments that are the result of the actual critical illness or the direct or indirect side-effects of interventions to treat the disease. An individual patient may lie at a particular point in the spectrum of physical disability according to the patient’s age, level of functioning prior to the onset of critical illness, and the burden of co-morbid conditions. At one end of this spectrum, clinicians encounter young, previously working and highly functional patients who develop a severe catastrophic illness. The middle range includes patients who are older and have a greater burden of comorbidities than the previous group. Finally, the opposite end of this spectrum includes those patients who have experienced chronic critical illness, or the very elderly, in whom ICU-level of care may not alter their ultimate outcome but may instead contribute to incremental disability and constitute part of a downward functional trajectory driven by progression of chronic illness.
It has been shown that in critical illness leading to respiratory failure, particularly in acute respiratory distress syndrome (ARDS), that lung function is decreased soon after recovery but improves to normal or near-normal over 6 months to 5 years. The diffusing capacity for carbon monoxide (DLCO) is the lung function parameter that seems to be mostly affected as DLCO values still remain mildly reduced or low-normal even after 5 years of follow-up.2 This persistent impairment in gas transfer is probably due to injury at the capillary level, which promotes thickening in alveolar capillary interfaces, pulmonary fibrosis, and pulmonary vascular remodeling.
Anatomical changes in the lung are also observed in follow-up imaging studies of ARDS survivors. Localized changes in the nondependent lung zones including reticular changes, ground-glass opacities and minor pulmonary fibrosis are seen on high-resolution computer tomography (CT) scans.3 The association between the severity of lung injury and length of mechanical ventilation may reflect ventilator-associated lung injury. However, the relationship between the development of lung fibrosis after ARDS and any possible risk factor is not straightforward. Some studies have found significant correlation between CT scan impairment and duration of mechanical ventilation, level of positive end-expiratory pressure (PEEP), and oxygen fraction. These data may only reflect greater severity of ARDS, which can be responsible per se for lung fibrosis.
It is interesting to note that the severity of the patient’s dyspnea after recovery from ARDS does not seem to correlate with actual lung dysfunction but may reflect extrapulmonary muscle weakness and sometimes psychological impairments.
Chronic Respiratory Failure
The onset of respiratory failure requiring prolonged mechanical ventilation is associated with increased morbidity, mortality, and health care costs. ICU admission for pneumonia, ARDS, neuromuscular disease, head trauma, or postoperative intracerebral hemorrhage is one of the strongest predictors of prolonged mechanical ventilation.4 ICU-acquired weakness (ICU-AW) has also been shown to be a predictor of failure to be liberated from the ventilator. The mechanism that is responsible for a majority of ventilator dependence can be explained by an increase in respiratory load coupled with decreased respiratory muscle performance. Chronic ventilator dependence may result in complications similar to those receiving short-term mechanical ventilation. These include infections, tracheal bleeding or malformations, renal failure, pneumothorax, volume overload, ileus, and seizures.
The overall mortality in patients with ventilator-dependent chronic respiratory failure is high and up to 52% at one year from the initial hospitalization.5 Chronic irreversible neurologic diseases and presence of skin breakdown has been associated with increased risk for mortality. These patients may be discharged to home, long-term acute care (LTAC) facilities, skilled nursing facilities or hospice care centers. The QOL tends to be low but may improve over the years. In particular, ARDS survivors who require prolonged mechanical ventilation have poorer QOL than other ARDS survivors.6 Health care resource utilization in these patients have been shown to be exceeding high and much of this is spent on ongoing and recurrent medical care.
Another important aspect of the physical impairment after recovery from critical illness is weakness. Potential contributors to weakness in survivors of critical illness are listed in Table 86–1. Risk factors for the development of weakness after critical illness are enumerated in Table 86–2. Several contrasting studies have shown variable association between the development of weakness and the severity of illness on ICU admission (eg, SAPS-2, APACHE II/III, SOFA). High blood glucose has been identified as a risk factor through an unknown mechanism while intensive insulin therapy has been shown to be a preventive factor against critical illness-associated weakness and to decrease the risk of critical illness polyneuropathy. The data on the association of corticosteroids with the development of weakness has been conflicting; however one study reported decreased neuromuscular dysfunction in patients on intensive insulin therapy while on corticosteroids, suggesting that when euglycemia is maintained, the anti-inflammatory effect of steroids may benefit the neuromuscular system.7 Low doses of neuromuscular blockers (eg, paralytics) do not seem to be associated with weakness but larger doses may be independently associated.
Table 86–1Contributors to weakness in survivors of critical illness. ||Download (.pdf) Table 86–1Contributors to weakness in survivors of critical illness.
|Chronic disease |
|Acute neurologic syndrome, eg, Guillian-Barre syndrome, myasthenia gravis |
|Persistent organ dysfunction, eg, heart failure, chronic respiratory failure, acute kidney injury |
|Neuro-muscular pathology, eg, CIP, CIM, ischemic or compression mononeuropathies |
|Muscle atrophy from prolonged immobility |
|Psychological disturbances |
Table 86–2Risk factors for weakness. ||Download (.pdf) Table 86–2Risk factors for weakness.
|Female sex |
|Advanced age |
|Severity of illness |
|Neuromuscular blockers |
Formerly described by different entities such as critical-illness polyneuropathy (CIP), critical-illness myopathy (CIM), and critical-illness neuromyopathy, ICU-AW is the prototypical functional impairment that has been the subject of intense research even prior to the recognition of the other domains of PICS. The incidence of ICU-AW varies from 30% to 90%. It may be missed during the acute phase of critical illness when the patient is sedated, restrained and unable to communicate. Difficulty liberating from mechanical ventilation may be the first indication of an impairment.
CIP is an axonal polyneuropathy that affects both sensory and motor nerves. The causes of axonal degeneration include the systemic inflammatory response syndrome (SIRS), ischemia to nerves from hypotension, microthrombosis, changes in microcirculation, endoneural edema, inflammation, mitochondrial dysfunction causing bioenergetic failure, neurotoxic meds, and metabolic abnormalities. Physical examination may reveal distal sensory deficits, distal weakness, and preserved deep-tendon reflexes (DTRs). Electromyography-Nerve Conduction Velocity (EMG-NCV) studies demonstrate decreased amplitudes of sensory and motor nerve action potentials with normal motor unit potentials and excitability. Pathologic evaluation reveals fiber loss and primary axonal degeneration of both motor and sensory nerve fibers, most severe distally.
CIM includes flaccid tetraparesis with depressed or absent DTRs but sensory function is not affected. The causes include increased muscle breakdown, decreased protein production and abnormal muscle repair, derangement of energy delivery, changes in the muscle membrane with primary inexcitability of muscle fibers, inflammation, steroids, and immobility. NCV studies reveal decreased amplitudes of compound muscle action potentials with preserved sensory nerve action potentials. Direct muscle stimulation demonstrates reduced or absent muscle excitability. Pathology most commonly reveals loss of thick filaments with atrophy of the type II fibers.
In terms of assessing weakness, the six-minute walk test (6MWT) is most widely used as it is an integrated outcome parameter that is dependent on the motor, pulmonary, and circulatory function. This test has proven to be a simple but useful test of global physical recovery in former ICU patients.