Pulmonary Complications of Hyponatremic Encephalopathy

Noncardiogenic Pulmonary Edema and Hypercapnic Respiratory Failure

¹ From the Department of Medicine, Baylor College of Medicine, Houston
² From the Department of Medicine, Geriatrics Section, Veterans Affairs Medical Center and University of California at San Francisco

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±29mm 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.

Key Words: cerebral edema • encephalopathy • hypercapnia • hyponatremia • hypoxia • pulmonary edema • respiratory failure

Submitted on March 14, 1994
Accepted on July 15, 2007

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