Sleep Apnea, Hypothyroidism and Pulmonary Edema
1990; Elsevier BV; Volume: 97; Issue: 3 Linguagem: Inglês
10.1378/chest.97.3.763b
ISSN1931-3543
AutoresAna M. López, José A. Lorente, Vicente Jerez, J.A. Julia,
Tópico(s)Chronic Obstructive Pulmonary Disease (COPD) Research
ResumoTo the Editor: We read with interest the article by Willms and Shure1Willms D Shure D Pulmonary edema due to upper airway obstruction in adults.Chest. 1988; 94: 1090-1092Abstract Full Text Full Text PDF PubMed Scopus (118) Google Scholar in which they review 25 cases of pulmonary edema associated with upper airway obstruction. Recently, we treated a 62-year-old patient with obstructive sleep apnea who developed pulmonary edema due to upper airway obstruction. We found signs of hypothyroidism and low thyroid hormones. The patient had a seven-year history of intermittent episodes of “noisy breathing” during sleep that were treated with bronchodilator therapy. The patient had an active life. The day of admission, the patient had one of these episodes which was more severe than usual. Brought to the hospital by his family, he was in obvious respiratory distress with minimal respiratory excursions. The patient was transferred to the ICU. The trachea was intubated and controlled mechanical ventilation initiated. Arterial blood gases (on a FIO2 of 1) were: PO2 197 mm Hg, PCO2 87, pH 6.96, HCO3 18.6 meq/L, HBco 1.2 percent, and HBO2 97 percent. Blood pressure was 90/60 mm Hg, pulse rate 100 bpm, temperature 37° C. A Swan Ganz catheter was inserted: pulmonary artery pressure was 14/6 mm Hg, pulmonary capillary pressure 5, central venous pressure 1. Therapy with cristalloids (2.5 L), methylprednisolone (40 mg), erythromicin (500 mg) and theophylline was administered. A chest x-ray film showed diffuse infiltrates (Fig 1). Echocardiogram was normal. Twelve hours later, arterial blood gases (on FIO2 of 0.4) were: PO2 124 mm Hg, PCO2 57, pH 7.35, HCO3 29.8 meq/L. On the second day the patient was extubated. Arterial blood gases (with 02.3 L per min by nasal prongs) were: PO2 88, PCO2 52, pH 7.37, HCO3, 30. Blood chemistry showed: Na 137 meq/L, K 3.8 meq/L, creatinine 1.2 g/dl, glucose 95 mg%, Hb 14.2 g/L, WBC 16,100, prothrombine time 100 percent. A chest x-ray film (Fig 2) was normal. A consultant in otolaryngology performed a laryngoscopy examination which disclosed hypertrophic chronic laryngitis. A fibrobronchoscopy was performed, which showed hypertrophic vocal cords. Spirometry showed an FEV1 of 1.32 (56 percent, predicted 2.42) and FVC of 1.85 (61 percent, predicted 3.03). A consultant in endocrinology found signs of hypothyroidism (dry skin, constipation) and thyroid hormone studies were performed: T4 was 7.5 μg/dl (normal 8 to 12), T3 0.56 ng/ml (normal 0.8 to 2 ng/ml), TSH 4.41 μU/Ml (normal less than 4). The patient was begun on therapy with thyroxine and bronchodilators; six months after discharge he is doing well.Figure 2View Large Image Figure ViewerDownload (PPT) Hypothyroidism is occasionally associated with sleep apnea,2Grusntein RR Sullivan CE Sleep apnea and hypothyroidism: mechanisms and management.Am J Med. 1988; 85: 775-779Abstract Full Text PDF Scopus (131) Google Scholar and mucoprotein deposition in the oropharynx is a proposed mechanism of obstructive apnea in these patients. Possibly, the mild hypothyroidism of our patient was playing a role in the development of upper airway obstruction and pulmonary edema.
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