There is a myriad of causes that can lead to acute weakness in a patient in the intensive care unit (ICU). These include diseases affecting the central nervous system (CNS), the peripheral nervous system (PNS), the neuromuscular junction (NMJ), and the muscles (myopathic disorders). Other etiologic causes include the effects of drugs/medication and injuries. A patient may have acute onset weakness that necessitates admission to the ICU or develop weakness over the course of the critical illness. A thorough history and physical exam are critical in identifying the etiology of weakness, accompanied by relevant diagnostic studies such as computed tomography, lumbar puncture, electrophysiologic studies, and complete laboratory assessment. Physical exam should include evaluation for upper and lower motor neuron signs of impairment, which can be helpful in directing the clinician toward a CNS or PNS problem. An exhaustive review of causes for acute weakness is beyond the scope of this chapter, with selected conditions described subsequently.
Patients being treated in an ICU can present with an acute onset of weakness caused by an ischemic or hemorrhagic stroke. An acute focal change in neurologic status, such as facial droop, arm and/or leg weakness, and speech difficulties, ought to be recognized as a potential stroke. A noncontrast head CT should be performed as soon as possible to assess the situation (eg, ischemic stroke vs hemorrhage) and determine the need for additional imaging and specific interventions (eg, intravenous tPA, intra-arterial tPA, mechanical recanalization, and external ventricular drain).
Infections (including meningitis and meningoencephalitis) and abscesses of the CNS are other causes that could lead to acute weakness in patient who is in ICU. Although multiple clinical manifestations frequently accompany such an infection, including confusion, high fever, and/or seizure, weakness may be one of the presenting signs. For example, patients with herpes simplex virus encephalitis can present with focal neurologic deficits including hemiparesis, in addition to altered mental status. A small percentage of patients with West Nile virus develop rapidly progressive weakness, similar to poliomyelitis, in the context of destruction to the anterior horn cells of the spinal cord. Careful evaluation of the serum lab work, cerebrospinal fluid (CSF) studies, and brain imaging is required to reach a diagnosis. Treatment will be goal directed (eg, antibiotics, antiviral meds, surgical treatment for abscesses).
Symptoms of progressive tetraparesis along with dysarthria, dysphagia, weakness of respiratory muscles, and decreased level of consciousness, presenting in the setting of a recent rapid serum sodium correction, should prompt the clinician to think of osmotic demyelination syndrome (ODS). Symptoms typically present 2 to 6 days after an overly rapid correction of serum sodium. An overly rapid serum sodium correction is not likely to occur in patients experiencing severe hyponatremia for a few hours but demonstrates an increasingly higher incidence when it has been present for more than 2 to 3 days. Although the exact mechanism of ODS is unclear, the natural process by which the brain adapts to hyponatremia in the early stages to prevent cerebral edema makes the brain much more susceptible to a decrease in brain volume and demyelination in prolonged hyponatremia during an overly rapid serum sodium correction. Demyelination primarily occurs in the pons, but extrapontine demyelination could occur in locations such as the cerebellum, basal ganglia, corpus callosum, and internal capsule. MRI would confirm the diagnosis. Supportive therapy is the primary approach to treatment, with other interventions such as early relowering of sodium still being studied.