PMC5457923_01
Chest computed tomography (CT) obtained during the patient's first admission to our hospital. CT showed no emphysematous changes or space-occupying lesions.
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To determine the cause of SIADH, additional brain MRI, abdominal CT and MRI, and chest CT (Fig. 1) were performed; however, they showed no significant findings.
The clinical course, laboratory data, and treatment of the present case. CO2: carbon dioxide, NPPV: non-invasive positive pressure ventilation
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The patient's clinical course during his second admission is shown in Fig. 2. After the initiation of NPPV, his hypercapnia improved, and he became alert (day 66) (Fig. 2). Subsequently, his serum sodium level was normalized and maintained within the normal range, even after NPPV, despite the state of inflammation associated with pneumonia, which was followed by tapering and the discontinuation of tolvaptan on day 74 (Fig. 2). After NPPV, the patient's serum ADH levels were maintained at a low level (<0.8 pg/mL), and his urinary sodium excretion decreased (Fig. 2).
Chest radiographs of the inspiratory and expiratory phases of breathing. Bilateral movement of the diaphragm was only observed between one intercostal margin.
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Chest radiographs during the inspiratory and expiratory phases showed bilateral movement of the diaphragm only between one intercostal margin (Fig. 3).
Progressive atrophy of the paraspinal and rotator cuff muscles.
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A whole-body CT revealed atrophy of the paraspinal muscles in addition to the atrophy of muscles that had been observed on physical examination on the second admission (Fig. 4). Based on these findings and the patient's progressive clinical course (Fig. 4), a diagnosis of ALS was established.