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Cardiovascular Disease |

Acute Pulmonary Edema Due to Hyperbaric Oxygen Therapy

Manveen Dassan, MD; Vishesh Paul, MD; Sameer Chadha, MD; Nidhi Aggarwal, MD; Yizhak Kupfer, MD; Sidney Tessler, MD
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Maimonides Medical Center, Brooklyn, NY


Chest. 2014;145(3_MeetingAbstracts):74A. doi:10.1378/chest.1824043
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Abstract

SESSION TITLE: Cardiovascular Case Report Posters II

SESSION TYPE: Case Report Poster

PRESENTED ON: Sunday, March 23, 2014 at 01:15 PM - 02:15 PM

INTRODUCTION: Some important indications for use of hyperbaric oxygen therapy include treatment of diabetic ulcers, air embolism, carbon monoxide poisoning, and gas gangrene. It is usually well tolerated with very few side effects. We describe a case of acute pulmonary edema precipitated by hyperbaric oxygen treatment.

CASE PRESENTATION: An 80-year-old male with Ischemic Cardiomyopathy (ejection fraction- 25%), diabetes mellitus and peripheral vascular disease was admitted because of severe dyspnea. He was getting hyperbaric oxygen treatment for a non-healing ulcer on his foot. His vitals were stable and he was breathing comfortably before the start of therapy. Towards the end of treatment, he developed rapidly worsening dyspnea. EMS was called and he was brought to the hospital on 100% oxygen via non-rebreather mask. His vitals were: T: 98.8 F, HR: 110/min, RR: 30/min, BP: 138/74 mm Hg, SaO2: 92%. Examination was significant for diffuse inspiratory and expiratory crackles. Due to severe distress, he required intubation and mechanical ventilation. EKG didn’t show any ischemic changes. Cardiac biomarkers were negative, but his BNP was significantly elevated at 1568 pg/mL. There were pink frothy secretions in the endotracheal tube and chest X-ray showed severe pulmonary edema. Diagnosis of acute respiratory failure secondary to pulmonary edema was made, and he was admitted to the cardiac ICU. He received ventilator care and intravenous diuretics, and was successfully extubated 3 days later.

DISCUSSION: Hyperbaric oxygen (HBO) therapy has been shown to improve the rate of healing of diabetic foot ulcers. Suggested mechanisms include improved wound tissue hypoxia, enhanced perfusion, and down-regulation of inflammatory cytokines (1). Some side effects of HBO that are described include: otic barotrauma, visual changes and possible CNS oxygen toxicity. Very few cases of pulmonary edema due to HBO treatment have been described. Weaver et al described three cases in 2001- all of them had pre-existing cardiac disease, and two of them were diabetic (2). Yildiz et al demonstrated that HBO treatment led to increase of N-terminal pro-B-type natriuretic peptide (NT pro-BNP) levels in diabetics by mean of 100 pg/mL (3). Proposed mechanisms for this include: HBO induced hyperoxia leading to increased peripheral vasoconstriction and thus cardiac afterload, increased oxidative myocardial stress, decreased LV compliance by oxygen radical-mediated reduction in nitric oxide and increased pulmonary capillary permeability (2). Any of these can precipitate acute pulmonary edema in a patient with pre-existing heart disease. Treatment remains primarily supportive with diuretics, supplemental oxygen and occasionally ventilatory support.

CONCLUSIONS: Acute pulmonary edema is a rare but serious side effect of hyperbaric oxygen therapy in patients with pre-existing heart disease. Thus caution should be observed in treating patients with heart disease with hyperbaric oxygen therapy.

Reference #1: Cardiovascular and blood gas responses to hyperbaric oxygenation. Whalen RE et al. Am J Cardiol1965; 15,638-646

Reference #2: Pulmonary edema associated with hyperbaric oxygen therapy. Weaver LK et al. Chest 2001; 120(4): 1407-1409.

Reference #3: N-terminal pro-B-type natriuretic peptide levels increases after hyperbaric oxygen therapy in diabetic patients. Yildiz et al. Clinical & Investigative Medicine 31.5 (2008): E231-E235.

DISCLOSURE: The following authors have nothing to disclose: Manveen Dassan, Vishesh Paul, Sameer Chadha, Nidhi Aggarwal, Yizhak Kupfer, Sidney Tessler

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