J C Ayus1, A I Arieff. 1. Department of Medicine, Baylor College of Medicine, Houston, TX.
Abstract
OBJECTIVE: To determine the causes of hypoxia in patients with hyponatremic encephalopathy. DESIGN: Retrospective cohort study. SETTING: Consultation and referral service of two university medical centers and community hospitals. PATIENTS: Forty adults with postoperative hyponatremic encephalopathy and hypoxia of whom 30 had noncardiogenic pulmonary edema and 10 had hypercapnic respiratory failure. MAIN MEASUREMENTS: We evaluated the chest radiographs and measured plasma electrolytes, arterial blood gas values, pulmonary artery pressure, pulmonary capillary wedge pressure (PCWP), cardiac output, and net fluid retention. RESULTS: Forty patients with hyponatremic encephalopathy had hypoxia (arterial PO2 below 70 mm Hg), of whom 30 had pulmonary edema and 10 had hypercapnia (PCO2 above 50 mm Hg). Among the 30 patients with pulmonary edema, the serum sodium (+/- SD) was 114 +/- 7 mmol/L, arterial pH was 7.24 +/- 0.16, PCO2 was 45 +/- 15 mm Hg, and PO2 was 42 +/- 16 mm Hg. The cardiac index was 3.6 +/- 0.4 L/min/M2, pulmonary artery pressure was 26/16 mm Hg, and PCWP was 12 +/- 6 mm Hg. There was pulmonary edema, with normal heart size. The hypoxic patients who did not have pulmonary edema had significant hypercapnia (PCO2 = 91 +/- 29 mm Hg, p < 0.001). CONCLUSIONS: Patients with postoperative hyponatremic encephalopathy can develop hypoxia by at least two different mechanisms: noncardiogenic pulmonary edema or hypercapnic respiratory failure.
OBJECTIVE: To determine the causes of hypoxia in patients with hyponatremic encephalopathy. DESIGN: Retrospective cohort study. SETTING: Consultation and referral service of two university medical centers and community hospitals. PATIENTS: Forty adults with postoperative hyponatremic encephalopathy and hypoxia of whom 30 had noncardiogenic pulmonary edema and 10 had hypercapnic respiratory failure. MAIN MEASUREMENTS: We evaluated the chest radiographs and measured plasma electrolytes, arterial blood gas values, pulmonary artery pressure, pulmonary capillary wedge pressure (PCWP), cardiac output, and net fluid retention. RESULTS: Forty patients with hyponatremic encephalopathy had hypoxia (arterial PO2 below 70 mm Hg), of whom 30 had pulmonary edema and 10 had hypercapnia (PCO2 above 50 mm Hg). Among the 30 patients with pulmonary edema, the serum sodium (+/- SD) was 114 +/- 7 mmol/L, arterial pH was 7.24 +/- 0.16, PCO2 was 45 +/- 15 mm Hg, and PO2 was 42 +/- 16 mm Hg. The cardiac index was 3.6 +/- 0.4 L/min/M2, pulmonary artery pressure was 26/16 mm Hg, and PCWP was 12 +/- 6 mm Hg. There was pulmonary edema, with normal heart size. The hypoxicpatients who did not have pulmonary edema had significant hypercapnia (PCO2 = 91 +/- 29 mm Hg, p < 0.001). CONCLUSIONS:Patients with postoperative hyponatremic encephalopathy can develop hypoxia by at least two different mechanisms: noncardiogenic pulmonary edema or hypercapnic respiratory failure.