“It is in moments of illness that we are compelled to recognize that we live not alone but chained to a creature of a different kingdom, whole worlds apart, who has no knowledge of us and by whom it is impossible to make ourselves understood: our body.” —Marcel Proust
On completion of this chapter, the student/practitioner will be able to:
Define critical illness and its two subsets: critical illness polyneuropathy and critical illness myopathy.
Demonstrate an understanding of the relationship between critical illness and critical illness polyneuropathy and critical illness myopathy.
Apply knowledge of critical illness polyneuropathy and critical illness myopathy to the development of a valid rehabilitation assessment and goal-oriented intervention schema.
Critical illness polyneuropathy (CIP) and critical illness myopathy (CIM) are two major complications of critical illness. CIP and CIM affect many aspects of the therapeutic intervention spectra of critical illness. These include the progression and success of ventilator weaning; the initiation and progression of physical, emotional, and vocational rehabilitation; and the risk of idiopathic and iatrogenic complications of long-term bedrest. Etiological factors for CIP and CIM include sepsis, acute respiratory failure, systemic inflammatory response syndrome (SIRS), and multiple organ failure. This chapter focuses on the epidemiology, diagnostics, pathophysiology, risk factors, clinical consequences, and potential therapeutic interventions to reduce the incidence and severity of CIP and CIM. This chapter is written for the rehabilitative clinician but may also benefit residents, interns, primary care physicians, nurse practitioners, hospital-based nurses, and critical care physicians.
CIP and CIM were first described by Bolton et al. in 19841 and further elucidated by Bolton et al. in 1986.2 Five patients admitted to an acute care hospital in London, Ontario, Canada, with multiple primary diagnoses all complicated by multisystem organ failure and sepsis were described as having difficulties in weaning from the ventilator when the primary illness had subsided and development of flaccid and areflexic limbs. Early electroneurodiagnostic studies, especially the needle examination, provided definitive evidence of an acute, systemic motor neuropathy. Bolton et al.1 described the symptoms as “a primary axonal polyneuropathy with sparing of the central nervous system.” These investigators believed that nutritional issues may have provided the etiology of the motor loss because, as they noted, symptoms appeared to have improved with the addition of total parenteral nutrition. Williams et al.3 reported similar findings in children.
CIM and CIP have similar symptoms, signs are often difficult to differentiate, and they frequently co-occur. Combined electroneurophysiological testing and histological studies often show the overlap.4 From an interventional standpoint, these illnesses are often treated together—hence the often used diagnostic interpretation of CIM/CIP. Because the relationship of CIP and CIM is so intertwined in the literature dealing with etiology, pathogenesis, and ...