Transtracheal oxygen and positive airway pressure: A salvage technique in overlap syndrome
A 63-year-old white man with a history of hypercarbic-hypoxemic respiratory failure due to moderate COPD and with mild SAHS, presented with worsening fatigue, dyspnea, and development of peripheral edema. His initial polysomnography 10 years earlier revealed obstructive sleep apnea (OSA) with an AHI of 13.4/hour with oxygen desaturations to 62% on room air, entirely due to obstructive hypopneas. He was completely compliant with CPAP therapy at 11 cm of water pressure in addition to oxygen at 4 liters per minute (LPM), which had been demonstrated to adequately correct his sleep disordered breathing in the sleep laboratory. He was found to have emphysema with an forced expiratory volume in the first second (FEV1) of 67% of predicted. He quit smoking and was compliant with his bronchodilators and medical therapy for diastolic dysfunction.\nDespite medical compliance, 8 years later he complained of worsening fatigue. Daytime oxygen requirements while walking rose to 6 LPM and nocturnal oxygen saturations fell to 70% on 5 LPM of oxygen with CPAP. He had to stop working because it was impractical for him to have such high oxygen flows at work. Repeat polysomnography was performed for retitration of CPAP therapy. This demonstrated correction with CPAP at 15 cm of water pressure and 4 LPM of O2, yielding an AHI of 0 with saturations >90%.\nEchocardiography and cardiac catheterization showed diastolic dysfunction and no obstructive coronary artery disease or valvular disease. Diuretic therapy was intensified without improving oxygenation or symptoms. Computerized tomography of the chest with contrast showed baseline emphysema and no pulmonary emboli. Repeat pulmonary function was unchanged with FEV1 at 67% of predicted and stable lung volumes. Awake resting arterial blood gas on oxygen at 5 LPM was at baseline (pH: 7.45, PaCO2: 54 torr, PaO: 61 torr). A repeat nocturnal oximetry demonstrated desaturations to 75% on CPAP at 15 cm of water pressure with oxygen at 5 LPM. Interestingly, he never had erythrocytosis with a hemoglobin level of 13.6 g/dl.\nHe refused suggested tracheostomy in order to initiate nocturnal mechanical ventilation with a positive pressure ventilator, but agreed to have to TTOT in order to improve nocturnal oxygenation. A SCOOP® TTOT catheter was placed using a modified Seldinger technique. Subsequently, CPAP at 15 cm of water pressure was continued with TTOT at 4 LPM. Nocturnal oximetry on these settings showed no desaturations below 87% and <5 min with saturations below 90% []. A repeat blood gas after TTOT was not performed, as this would have required an indwelling arterial catheter to be representative of his true response to therapy while sleeping. Such maneuver was deemed too invasive for clinical therapy, considering his oximetry and overall clinical improvement. A daytime arterial blood gas, in a stable clinical state did demonstrate a decrease in PaCO2 to 48 while awake with TTOT. He had no complications of TTOT except for occasional mucous ball formation early in therapy and occasional tube dislodgment, which over time resolved with further patient education and the addition of guafenesin oral therapy. There were no problems related to air leaks or other pathology around the TTOT catheter site during CPAP therapy, and he markedly improved with decreased fatigue, dyspnea, and edema. He increased his activity level and lost 16 kg with diet and improved exercise tolerance. To determine if CPAP was still required, he was restudied without CPAP and with TTOT at 2 LPM. The overall AHI was 3.5/h, but with a supine AHI of 36/h. Saturations dropped to 87% with 17.2 min <89%. CPAP was reinstituted.\nOver the ensuing year he improved further clinically. He intentionally cancelled his disability payments and returned to work as a car salesman with TTOT at 2 LPM with SaO2>90% with ambulation.