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ДИАГНОСТИКА ПАРАЛИЧЕЙ ДИАФРАГМЫ
ДИАГНОСТИКА ПАРАЛИЧЕЙ ДИАФРАГМЫ
Resting arterial blood gas is usually normal in unilateral diaphragmatic paralysis. In bilateral diaphragmatic paralysis, the PO2 may be normal or may be decreased as a result of shunting of blood past atelectatic lung. Likewise, the PCO2 may be normal, decreased, or increased. Often, the atelectasis and hypoxemia that result from diaphragmatic paralysis lead to increased minute ventilation and a fall in PCO2. However, in some patients, diaphragmatic paralysis results in decreased tidal volumes, alveolar hypoventilation, and therefore increased PCO2. Hypercapnia usually occurs when overall respiratory muscle strength [maximal inspiratory pressure (MIP)] is <30% predicted and when vital capacity (VC) falls to <55% of predicted.22 Supine arterial blood gases are more sensitive for diaphragmatic paralysis. A fall in PCO2 by 5 to 25 mmg Hg and a rise in PCO2 by an average of 5 mm Hg can be expected when the patient lies supine.4 With significant diaphragmatic weakness, pulmonary function test findings are characterized by a restrictive pattern and decreased diffusing capacity of the lung for carbon monoxide (DLCO) but normal DLCO/alveolar volume (AV). In one study of patients with isolated diaphragm weakness, the average total lung capacity (TLC) was 67±11% predicted and D lco was 65±12% predicted with a normal or increased DLCO/AV.10 VC is often used as a predictor of hypercapnic respiratory failure due to neuromuscular disease, but it is an insensitive measure of lesser degrees of diaphragmatic weakness, in addition to being nonspecific. In unilateral diaphragmatic paralysis, VC in the upright position is usually around 75% of predicted and decreases by 15 to 25% with supine positioning. The effect of supine positioning on the VC is greater when the right hemidiaphragm is paralyzed, as a result of displacement of the liver into the chest.23,24 With bilateral diaphragmatic paralysis, VC can be reduced to <50% of predicted.9 However, seated VC is an insensitive measure of diaphragmatic weakness and doesn’t fall until weakness becomes significant. Upright VC only weakly correlates with measurements of diaphragmatic strength. This is because the shape of the pressure-volume curve flattens at both low and high volumes, so that moderate degrees of weakness only have a small effect on lung volumes.1 If there is significant weakness, a fall in lung volumes will be seen. With supine positioning, there is a further decrease in VC. The normal fall in VC with supine positioning is <20%; in patients with obstructive lung disease, it can be somewhat higher. A fall in VC >25% with normal lung function or >35% associated with obstructive lung disease should raise suspicion for diaphragmatic weakness. 25 In patients with bilateral diaphragmatic paralysis, the vital capacity may fall by up to 50% when they are supine.1,4 Unlike the upright VC, the supine fall in VC has been shown to correlate with direct measurements of diaphragmatic strength.1 In addition to VC, MIP is often used to assess patients for diaphragmatic weakness. In fact, the MIP has been shown to correlate with transdiaphragmatic pressure, the gold standard for the measurement of diaphragmatic weakness.1 However, this is highly nonspecific because it is an effort-dependent maneuver. Furthermore, the sensitivity of the MIP is limited by the fact that the compensatory actions of the accessory muscles can achieve a normal MIP. MIP reflects global inspiratory strength rather than isolated diaphragmatic function. Maximal expiratory force is usually normal in diaphragmatic paralysis, as expiration is achieved primarily by accessory muscles without contribution from the diaphragm. The 12-s maximum voluntary ventilation can also be low, and has been shown to correlate with transdiaphragmatic pressure.10 The chest radiograph classically reveals elevated hemidiaphragms or low lung volumes in diaphragmatic weakness, but these are neither sensitive nor specific. In bilateral diaphragmatic paralysis, the symmetric elevation of both hemidiaphragms, often with subsegmental atelectasis at the bases of the lungs, is easily interpreted as low lung volumes. Fluoroscopy is commonly used to assess for diaphragmatic weakness. Classically, paradoxical upward movement of diaphragm is seen during sniff inspiration. A threshold of 2 cm is often used because normal subjects may have paradoxical upward movement of the diaphragm during inspiration up to 2 cm. The sniff test is much more sensitive for the diagnosis of unilateral diaphragmatic paralysis, in which paradoxical elevation of the affected hemidiaphragm with inspiration is seen in >90% of patients.26 In bilateral diaphragm paralysis, the abdominal muscles can contract during expiration, pushing the diaphragm up. Then, during inspiration, the diaphragm can passively descend to a resting position, leading to a false-negative sniff test. In addition, when the accessory muscles achieve upward movement of the thoracic cage during inspiration, there can appear to be a relative downward displacement of the diaphragm.27 Finally, the test can give false-negative results if it is not performed in the supine position, which can be difficult for patients with true diaphragmatic paralysis. Historically, measurement of chest and abdominal dimensions were done during respiratory cycle to assess for paradoxical movement. This is known as the Konna and Mead model. The anterior-posterior (AP) diameter of the rib cage and the abdominal wall can be measured by placing magnetometers on the body surface. Magnetometer coils are attached at the level of the fifth intercostal space to measure the rib cage AP diameter. Another magnetometer is attached 2 cm above the umbilicus to measure the abdominal AP diameter. Expansion of the rib cage and abdominal wall can be measured during quiet tidal breathing or during inspirations to TLC, both in the upright and supine positions.1 A normal breathing pattern is characterized by an increase in the AP diameter of both the rib cage and abdomen during inspiration. In diaphragmatic weakness, the abdomen is pulled inward due to expansion of the thorax and passive upward displacement of the weak diaphragm.27 The gold standard for the diagnosis of diaphragamatic weakness is the maximal transdiaphragmatic pressure (Pdimax). While MIP assesses global inspiratory muscle activity, Pdimax specifically assesses the strength of the diaphragm. A nasogastric catheter is inserted with one balloon pressure sensor in the esophagus and one in the stomach. Esophageal pressure estimates pleural or intrathoracic pressure (Ppl), and gastric pressure represents intraabdominal pressure (Pab). Then, Pdi = Pab — Ppl. • At FRC, transdiaphragmatic pressure (Pdi) is zero. • With an intact diaphragm muscle, which descends during inspiration, Pab increases and Ppl decreases during inspiration. Therefore, Pdi is positive. A normal Pdi is >25 cm H2O. • In diaphragmatic paralysis, the negative intrathoracic pressure generated by the accessory muscles is transmitted across a flaccid diaphragm, because the thorax and abdomen effectively act as one compartment. In this case, Ppl = Pab, and Pdi is zero. • In diaphragm weakness, rather than complete paralysis, Pdi is reduced but greater than zero. • A decline in Pdimax over a short period of time (eg, hours) suggests diaphragmatic fatigue. Pdi can be measured during slow inspirations to TLC, maximal static inspiratory efforts, and a maximal sniff maneuver. Sniff Pdi produces the maximal and most reproducible values.1 Maximal and reproducible values of the Pdi measurement are achieved by the visual feedback technique, in which the subject watches Ppl and Pab fluctuate on a monitor. Transdiaphragmatic pressure can also be measured after electrical stimulation of the phrenic nerve in the neck, a measurement that is independent of effort.28 Pdi has been shown to correlate with the level of dyspnea, orthopnea, abdominal paradox, and fall in vital capacity with supine positioning. One study derived an equation to predict Pdi (in cm H2O) on the basis of noninvasive tests of diaphragmatic strength1: Pdi = 36.1 — [0.828(supine fall VC)] + [0.634(Pimax)] where Pimax is maximal static inspiratory mouth pressure (correlation, 0.80; p<0.0001). Pdi is reduced in some patients with unilateral diaphragmatic paralysis20,23 and should be highly sensitive for bilateral diaphragmatic paralysis. EMG can be used to conclusively diagnose complete diaphragmatic paralysis. An EMG can be done during tidal breathing, during maximal inspiratory maneuvers, and after phrenic nerve stimulation. The phrenic nerve is stimulated by percutaneous electrodes in the neck, where the nerve lies in a relatively superficial position just under the sternocleidomastoid. The muscle activity is then measured with surface electrodes placed over the lower rib cage, where the diaphragm contacts the inner ribs. A negative EMG signal confirms diaphragm paralysis. Esophageal electrodes may also be used to measure action potentials in the crural diaphragms without any effect of the intercostal and abdominal muscles. True diaphragmatic paralysis is diagnosed if phrenic nerve stimulation does not result in a diaphragmatic action potential. Of course, decreased action potential of the diaphragm after stimulation of the phrenic nerve is not specific for phrenic neuropathies: myopathies and disorders of the neuromuscular junction will give similar results. However, the EMG pattern and the nerve conduction time distinguish neuropathic from myopathic causes of diaphragmatic paralysis. Nerve conduction time -the time from the nerve stimulation to the EMG potential- can help with the diagnosis of phrenic neuropathies.29 If an action potential is present, Pdi can be measured after phrenic nerve stimulation to assess the mechanical response of the muscle to a successfully transmitted impulse.28–30 In disease processes with generalized weakness, the diagnosis may be made by EMG or muscle biopsy of muscles that are more easily accessible than the diaphragm. For example, diseases of the anterior horn cells, neuromuscular junction, and muscle itself affect strength outside of the diaphragm, and the diagnosis can be made by EMG or biopsy of more easily affected muscles. Also, blood tests such as thyroid-stimulating hormone, cortisol, electrolytes, creatine kinase, and rheumatologic serologies can be useful. Similar to plain film, the chest CT usually reveals small lung volumes and basilar atelectasis. Alternatively, myelography may be helpful in the diagnosis of spinal cord lesions. Additional testing that may be performed to workup the etiology of diaphragmatic paralysis includes cervical spine MRI. A sleep study is helpful to assess for worsening hypoxemia arising from atelectasis and hypoventilation in the supine position, as a positive study would alter treatment. |
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