Measurement of maximal inspiratory force and expiratory vital capacity usually suffices for the bedside estimation of diaphragmatic strength and respiratory function. The trend of these measurements is a guide to the likelihood of respiratory failure. As had been observed in poliomyelitis, the strength of the neck muscles and trapezii, which share the same segmental innervation as the diaphragm, tends to parallel diaphragmatic power. A rough estimate of breathing capacity may be obtained by having the patient count quickly on one deep breath. The ability to reach 20 generally corresponds to a vital capacity of greater than 1.5 L. If a downward trend in these measurements is recognized and the vital capacity diminishes to below about 10 mL/kg, endotracheal intubation and mechanical ventilation are usually necessary (see further on). However, a fairly severe impairment of ventilation may occur before the first sign of dyspnea appears and before there is elevation of arterial carbon dioxide content. Incipient respiratory failure may be evident by tachypnea and a decrease in arterial oxygen tension (Po2 less than 85 mm Hg) reflecting pulmonary atelectasis. When respiratory failure arises gradually as the patient weakens over days, there is slight tachycardia, diaphoresis, restlessness, and tachypnea. Attempts to forestall intubation and positive-pressure ventilation by using negative-pressure cuirass-type devices have been unsatisfactory in our experience. Patients with oropharyngeal weakness require intubation even earlier so as to prevent aspiration, but full mechanical ventilation is not always necessary at the same time. Patients in these circumstances should obviously be admitted to an intensive care unit staffed by personnel skilled in maintaining ventilation and airway patency.
The other major aspects of the treatment in severely affected patients involve the management of autonomic instability and the prevention of the many general medical problems that attend any immobilizing critical illness. Hypotension from dysautonomia, which occurs in approximately 10 percent of paralyzed patients and a smaller proportion with lesser degrees of weakness, is treated by intravenous infusions of saline and by the use of vasopressor agents for brief periods. Extremes of hypertension are managed by short-acting and titratable antihypertensive medications, such as intravenous labetalol. The choice and dosing of an antihypertensive drug is important, as episodes of hypertension may be rapidly succeeded by precipitous declines in pressure. Severe autonomic problems are difficult to anticipate, but provocative maneuvers such as ocular pressure to elicit heart block are used in some units to identify patients at risk.
In patients who are bedbound, prevention of electrolyte imbalances, gastrointestinal hemorrhage, and particularly pulmonary embolism (by the use of subcutaneous heparin or pneumatic compression boots) requires careful attention. Adynamic ileus is a problem in some cases, manifest by abdominal pain coincident with nasogastric tube feeding and by bloating; it may lead to bowel perforation even if feeding is discontinued. As mentioned, a number of patients become hyponatremic, usually from SIADH but occasionally from a natriuresis, and the drop in sodium is exaggerated by positive-pressure mechanical ventilation. The distinction between the two conditions that cause hyponatremia determines the course of treatment: fluid restriction in the case of SIADH or salt replacement in the case of sodium loss. Many patients have bizarre waking dreams or hallucinations after weeks of immobilization (oneiric hallucinations). A dependable mode of communication should be established by the nursing staff, preferably before the patient is intubated. A Plexiglas or opaque board with letters and phrases is useful for this purpose.