Case of Pulmonary edema secondary to severe hypalbuminemia in a young woman: a case report

Published On 2019-09-05 12:30 GMT   |   Update On 2019-09-05 12:30 GMT

Dr Daniel Tuchscherer at Department of Intensive Care, University Hospital Basel, Spitalstrasse 21, Basel, Switzerland and colleagues have reported a rare case of Pulmonary edema secondary to severe hypalbuminemia in a young woman.The case has appeared in the Journal of Medical Case Reports.


A 29-year-old Caucasian woman in respiratory distress was referred for initiation of parenteral nutrition because of chronic malabsorption and malnutrition. She had a history of bariatric gastric bypass surgery 10 years prior with multiple revisions over the following decade due to persisting steatorrhea. Her nutritional history revealed a voluntarily reduced protein intake of 25 g per day. She smoked one pack of cigarettes per day (13 pack-years). Alcohol and recreational drugs were negated. Family history was insignificant.


Her blood pressure (BP) was 132/58 mmHg, pulse rate was 120 beats per minute, respiratory rate 28 breaths per minute, and oxygen saturation 80% on room air. Auscultation revealed normal heart sounds and clear lungs. Lower extremity edema was noted and her right calf was tender on palpation. The rest of her clinical examination was unremarkable.


Routine laboratory analyses were normal except for hypalbuminemia (8 g/L, normal range 35–52 g/L), elevated B-natriuretic peptide (BNP; 844 ng/L, normal value < 177 ng/L), and C-reactive protein (CRP; 40 mg/L, normal value < 10 mg/L). Arterial blood gas analysis (BGA) confirmed hypoxemia: partial pressure of oxygen in arterial blood (PaO2) of 8 kPa. A computed tomography (CT) scan of her chest revealed bilateral central pulmonary embolism and ground glass opacities (Fig. 1a) [3]. Echocardiography showed dilatation of her right ventricle with normal right ventricular function, while her left ventricle showed systolic D-shaping with normal systolic function [4]. Systolic pulmonary artery pressure (PAP) was estimated at 54 mmHg. Transpulmonary thermodilution and pulse contour cardiac output (Pulsion Medical Systems©) displayed a normal cardiac index (4 L/minute per m2), a slightly increased extravascular lung water index (10 ml/kg, normal range 3–7 ml/kg), and a central venous pressure of 17 mmHg. Because of a worsening gas exchange over 3 days on non-invasive ventilation (NIV), a repeat CT scan was performed and profound ground-glass opacities (Fig. 1b) were noted. Bronchoalveolar lavage (BAL) remained sterile.


We diagnosed PE secondary to severe hypalbuminemia under excessive respiratory drive and treated her with thrombolysis, controlled mechanical ventilation, and albumin replacement.


In conjunction with severe hypalbuminemia, even the negative intrathoracic pressure swings of respiratory distress may cause pulmonary edema. Detrimental consequences of non-invasive ventilation due to uncontrolled tidal volume and pressure swings need to be considered when treating patients in hypoxemic respiratory failure with low serum albumin.


Fo further reference log on to :

https://jmedicalcasereports.biomedcentral.com/articles/10.1186/s13256-019-2169-6
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