Acute Exacerbation of Chronic Obstructive Pulmonary Disease Treated by Extracorporeal Carbon Dioxide Removal

Acute Exacerbation of Chronic Obstructive Pulmonary Disease Treated by Extracorporeal Carbon Dioxide Removal

Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is a critical condition that often necessitates mechanical ventilation support. However, mechanical ventilation, while life-saving, is associated with significant side effects, including barotrauma, ventilator-induced lung injury, and difficulties in weaning patients off the ventilator. These complications can lead to treatment failure and poor patient outcomes. In recent years, extracorporeal carbon dioxide removal (ECCO2R) has emerged as a promising alternative or adjunct to mechanical ventilation, particularly for patients who fail non-invasive positive-pressure ventilation (NPPV) or require assistance in weaning from invasive positive-pressure ventilation (IPPV). This technique involves diverting blood through an artificial membrane lung, where carbon dioxide is removed and oxygenation is achieved without the need for mechanical ventilation. While ECCO2R has been widely used in other countries, its application in China has not been officially reported until now. This article presents two cases of AECOPD patients successfully treated with ECCO2R, highlighting the technical details, clinical outcomes, and potential benefits of this innovative approach.

Case 1: A 69-Year-Old Male Patient

The first patient was a 69-year-old male with a 20-year history of chronic obstructive pulmonary disease (COPD). He was hospitalized in March 2017 due to severe respiratory distress. The patient had previously undergone two episodes of endotracheal intubation and invasive positive-pressure ventilation (IPPV). Upon admission, arterial blood gas analysis revealed severe hypercapnia and respiratory acidosis, with a pH of 7.25, arterial partial pressure of carbon dioxide (PaCO2) of 92 mmHg, arterial partial pressure of oxygen (PaO2) of 90 mmHg, bicarbonate (HCO3) level of 45.8 mmol/L, and base excess (BE) of 15.4 mmol/L. Despite eight days of non-invasive positive-pressure ventilation (NPPV), the patient’s condition did not improve, and he was subsequently intubated and placed on IPPV for four days. After extubation, his PaCO2 levels rose dramatically to 130 mmHg within 12 hours, necessitating re-intubation and IPPV.

Given the patient’s desire to avoid prolonged endotracheal intubation, ECCO2R was initiated to facilitate weaning from IPPV and support early rehabilitation. A 22F double-lumen venous catheter was inserted into the right internal jugular vein, with an insertion depth of 17 cm. The catheter was connected to an extracorporeal membrane oxygenation (ECMO) system (Maquet, Rotaflow, Germany). The pump blood flow was set between 1.0 to 1.5 L/min, and the gas flow was maintained at 4 L/min. Heparin was administered at a rate of 400–600 U/h for anticoagulation, with the activated partial prothrombin time maintained at 60 seconds and the activated clotting time at approximately 160 seconds.

Within one hour of ECCO2R initiation, the patient’s peripheral arterial PaCO2 decreased to 45.8 mmHg, and his pH normalized to 7.42. Concurrently, his ventilation parameters were reduced, with pressure support set at 10 cmH2O, fraction of inspired oxygen (FiO2) at 0.4, and positive end-expiratory pressure (PEEP) at 5 cmH2O. Sedation and analgesia were discontinued, and the endotracheal tube was removed the following day. NPPV was administered intermittently, and airway clearance techniques were used to assist with sputum drainage. The patient was also encouraged to begin assisted exercise. Over the course of treatment, the gas flow was gradually reduced from 4 L/min to 500 mL/min, and NPPV support was gradually restored to the patient’s usual levels (IPAP 18–20 cmH2O, EPAP 14 cmH2O, FiO2 0.4). ECCO2R was successfully discontinued after five weeks, with no significant complications observed during the treatment period.

Case 2: An 81-Year-Old Male Patient

The second patient was an 81-year-old male with a 20-year history of COPD, who had not received regular treatment. He was hospitalized in April 2017 after experiencing severe dyspnea, cough, and expectoration for 15 days. The patient also developed bilateral pneumothorax and extensive subcutaneous emphysema, which extended from the neck to the chest, abdomen, waist, and bilateral upper limbs. A thoracic drainage tube was placed in the right thoracic fourth intercostal space. Initial arterial blood gas analysis (FiO2 0.35) showed a pH of 7.43, PaCO2 of 46 mmHg, PaO2 of 73 mmHg, HCO3 level of 31.2 mmol/L, and BE of 5.6 mmol/L.

After admission, the patient’s condition worsened, with increased dyspnea and subcutaneous emphysema. Repeat arterial blood gas analysis (FiO2 0.5) revealed a pH of 7.26, PaCO2 of 66 mmHg, and PaO2 of 120 mmHg. ECCO2R was initiated using the same procedure and anticoagulation protocol as in the first case. NPPV was also administered (IPAP 6 cmH2O, EPAP 4 cmH2O, FiO2 0.4). However, due to weak cough and hypoxemia, the patient required endotracheal intubation and IPPV. The endogenous positive end-expiratory pressure (PEEPi) was measured at 19 cmH2O, indicating significant gas entrapment and increased intrathoracic pressure. IPPV parameters were set in assist/control mode, with a tidal volume of 170 mL, respiratory rate of 15 breaths/min, PEEP of 3 cmH2O, and FiO2 of 0.35.

Over the next four days, the patient’s subcutaneous emphysema improved, and the PEEPi decreased to 8 cmH2O. His pH remained stable between 7.43 and 7.51, and PaCO2 was maintained between 35 to 45 mmHg. After 11 days of effective treatment, the endotracheal tube was removed, and ECCO2R was successfully discontinued two days later. During the treatment, the patient experienced a slight increase in transaminase and bilirubin levels, as well as subcutaneous congestion at the puncture site.

Discussion

Traditional mechanical ventilation, while essential for managing AECOPD, is associated with numerous challenges, including NPPV treatment failure, barotrauma, and difficulties in weaning patients off the ventilator. ECCO2R offers a promising alternative by providing extracorporeal support for carbon dioxide removal and oxygenation, thereby reducing the need for mechanical ventilation and its associated complications. The two cases presented here demonstrate the potential benefits of ECCO2R in managing AECOPD patients who fail NPPV or require assistance in weaning from IPPV.

The first patient successfully weaned from IPPV with the assistance of ECCO2R, enabling early rehabilitation and avoiding prolonged intubation. The second patient experienced significant improvement in barotrauma and subcutaneous emphysema during ECCO2R treatment, ultimately allowing for successful extubation and discontinuation of ECCO2R. Both cases highlight the importance of carefully selecting patients for ECCO2R, particularly those who meet the criteria for NPPV failure or have failed multiple weaning attempts from IPPV.

However, ECCO2R is not without limitations. Tracheal intubation may still be necessary in cases of severe hypoxemia or difficulty in expectoration. Additionally, the risk of bleeding and the need for effective respiratory therapy must be carefully managed. Despite these challenges, ECCO2R represents a valuable tool in the management of AECOPD, offering a new respiratory support strategy that can improve patient outcomes and serve as a bridge to lung transplantation.

Conclusion

ECCO2R is a promising technique for managing AECOPD patients who fail NPPV or require assistance in weaning from IPPV. The two cases presented here demonstrate the potential benefits of ECCO2R in reducing the need for mechanical ventilation, improving barotrauma, and supporting early rehabilitation. While further research is needed to establish standardized protocols and optimize patient selection, ECCO2R offers a valuable alternative to traditional mechanical ventilation, with the potential to significantly improve outcomes for AECOPD patients.

doi.org/10.1097/CM9.0000000000000461

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