Pulmonary hypertension (PH) is a challenging disease process to manage. Patients with significant PH have a difficult time tolerating the respiratory and hemodynamic changes that accompany general anesthesia. For patients with decompensated PH and associated right heart failure even a mild respiratory acidosis can lead to a catastrophic PH crisis. Simply intubating these patients during a period of decompensation carries a significant risk of cardiovascular collapse.1,2 Recently, use of extracorporeal membrane oxygenation (ECMO) in these patients for bridge to recovery (BTR) or lung transplantation (BTT) has been described.3,4 Additionally, the concept of “awake ECMO” has been described both in femoral cannulation and postcannulation.5–8 We have previously described our experience with subclavian artery cannulation for venoarterial (VA) ECMO in PH patients,9 and here we present three cases of subclavian artery cannulation while awake, in nonintubated PH patients.
This is a retrospective case series of three consecutive PH patients who underwent nonintubated, awake VA ECMO cannulation as BTR or BTT at the New York-Presbyterian Hospital/Columbia University Medical Center between 2013 and 2014. Demographic data, including medical therapies, ECMO configurations, ECMO course, and outcomes were gathered from the electronic medical record and are reported (Table 1).
Extracorporeal membrane oxygenation cannulation via right subclavian artery and internal jugular vein was performed by previously described techniques.10 The patients are brought to the operating room awake without mechanical ventilation, and the right subclavian artery is exposed through a subclavicular incision. Before surgery, lidocaine 1% without epinephrine is instilled into the subcutaneous tissue as well as around the brachial plexus to effect a nerve block to the area. A heparin bolus of 5,000 units is given after completing the dissection. A longitudinal arteriotomy is made to accommodate an end-to-side anastomosis between the vessel and a beveled 6 or 8 mm Hemashield vascular graft (Boston Scientific, Natick, MA). The graft is beveled to an angle of 45° to provide retrograde subclavian arterial flow and adequate antegrade upper body flow. After securing the graft to the artery, a counter-incision is made 5–6 cm inferolateral to the initial incision to tunnel the 18 or 24 Fr elongated one-piece arterial (EOPA) ECMO cannula (Medtronic, Brooklyn Park, MN). The cannula is brought through the tunnel, inserted into the graft in a sleeve-like fashion, and secured using silk ligatures around the graft. This reduces the risk of distal limb ischemia because the cannula is not inserted directly into the artery. Next, the right internal jugular vein is cannulated percutaneously using a 23 Fr Arterial Biomedicus cannula (Medtronic). The drainage and reinfusion cannulas are connected to the ECMO circuit and flow is commenced. Our ECMO circuit is a Cardiohelp system (Maquet Cardiovascular, Rastatt, Germany).
All patients had standard American Society of Anesthesiologists’ monitoring. In preparation for intraoperative right subclavian artery occlusion, pulse oximeter probes were placed on the left hand or lower extremities. Noninvasive blood pressure cuffs were placed on the left arm or lower extremities and left radial or femoral arterial pressure lines were inserted before surgery. Central venous lines were in situ in all patients.
The surgeon performed local anesthetic infiltration with 1% lidocaine. Patient 1 and Patient 2 required supplemental low dose intravenous anesthesia with a single bolus of midazolam (15–30 mcg/kg) and ketamine in intermittent boluses of 1–12 mg, with continuous subanesthetic ketamine infusions of 2–5 mcg/kg/min. Ketamine boluses were administered before the most intense periods of surgical stimulation: skin incision, dissection near the brachial plexus, arterial clamping, and arteriotomy. Patients remained responsive to voice throughout the procedures. Total ketamine doses ranged from 0.9 to 1.3 mg/kg.
Spontaneous ventilation was preserved in all patients. Supplemental oxygen was delivered via high flow nasal cannula (Patients 1 and 3) or bilevel positive airway pressure with face mask (Patient 2). Inhaled nitric oxide (Patients 1 and 2) was delivered and was weaned off in both patients after initiation of ECMO.
Three patients with PH underwent awake, nonintubated ECMO cannulation. Two patients had Group 1 pulmonary artery hypertension (PAH), one with idiopathic pulmonary arterial hypertension (IPAH) and a second patient with PAH following a ventricular septal defect repair; a third patient had pulmonary hypertension associated with severe emphysema.
This patient was a 58-year-old woman who was diagnosed with IPAH in 2009 after a syncopal episode. She was started on targeted PH therapy including sildenafil and ambrisentan and was listed for lung transplantation at our center. Her symptoms continued to worsen; she was unable to walk, gained 15 pounds with increasing abdominal girth from ascites, and had progressive right ventricular failure leading to admission to the medical intensive care unit (MICU). Her pulmonary artery systolic pressure was 90 mm Hg with a systemic systolic pressure of 120 mm Hg. Her symptoms were refractory to maximal medical therapy, and it was felt that she would not be a transplant candidate in her current state and would require ECMO support to allow for diuresis, exercise, and nutritional support. She was placed on upper body VA ECMO without being mechanically ventilated. Within one week of cannulation her B-Type Natriuretic Peptide (BNP) levels decreased from 558 to 182 pg/ml; she went from being bedbound to walking 400 feet with physical therapy; and her paO2 improved from 58 to 163 mm Hg (Table 2). After 44 days on extracorporeal support with no major adverse events and aggressive physical therapy, she received a double lung transplant.
This patient was a 20-year-old woman with pulmonary arterial hypertension associated with a repaired ventricular septal defect. She was managed on sildenafil, bosentan, and treprostinil at home with suprasystemic pulmonary arterial pressures. Just before hospital admission she developed pneumonia with 10 episodes of hemoptysis. Upon admission to the MICU, her oxygen saturation was 82% with an estimated pulmonary artery systolic pressure of 160 mm Hg. Since she had a reversible underlying cause for her acute exacerbation, she was considered a candidate for VA ECMO as a BTR. Without mechanical ventilation, and only using local anesthesia and monitored anesthesia care (MAC), she was cannulated with upper body VA ECMO. Within one week of cannulation her BNP levels decreased from 1,281 to 115 pg/ml; she went from being bedbound to ambulating 300 feet with physical therapy; and her paO2 improved from 51 to 107 mm Hg (Table 2). Following surgery she was treated for her pneumonia and ambulated daily with physical therapy. After 10 uneventful days on ECMO the patient had massive hemoptysis requiring bronchial artery embolization along with worsening sepsis and she ultimately died on ECMO day 15.
Patient 3 is a 34-year-old man with idiopathic bullous emphysema and vanishing lung syndrome who was listed for lung transplantation. He had secondary PH with a pulmonary artery systolic pressure of 94 mm Hg. After a rapid decline in his functional status he was admitted to the MICU. He was unable to eat or move from bed as his oxygenation worsened. He was placed on venovenous ECMO via 31 Fr Avalon Elite Bi-caval dual lumen cannula (Maquet Cardiovascular, Rastatt, Germany). He was adequately supported for 10 days but had progressive right ventricular failure leading to decompensation. The decision was made to place him on venovenous-arterial (VVA) ECMO using the Avalon cannula along with reinfusion through the right subclavian artery. The patient was never intubated for fear of positive pressure leading to bilateral pneumothoraces. He was maintained on VVA ECMO with adequate physiologic and symptomatic improvement for another 18 days until his right heart failure progressed. On day 28 of ECMO he was converted to straight VA ECMO after removing his Avalon Elite cannula and replacing it with a single drainage cannula, which was performed under MAC and local anesthesia. Though this patient had only modest improvements in his paO2 measurements, he was again able to work with physical therapy and went from being unable to lift his head to standing and walking in his room (Table 2).
Pulmonary hypertension is a challenging progressive disease process. With the advent of targeted PH drugs there are improved options for medical management. However, when medical management is insufficient or a secondary insult causes an acute PH exacerbation, ECMO can be used to bridge these patients to recovery or lung transplantation.3,4,9
A major operative risk for patients with severe PH is the potential for cardiovascular collapse with the induction of anesthesia and endotracheal intubation.1,2 There are reports of ECMO cannulation of awake patients, but these were percutaneous methods for venovenous or femoral cannulation for VA access.5–8 As demonstrated in Patient 3, venovenous ECMO is often insufficient in PH patients with concurrent right heart failure. Additionally, femoral VA ECMO provides inadequate perfusion because of the patients’ underlying lung disease, which limits upper body oxygenation. Although femoral VA ECMO partially unloads the right heart, the remaining intrinsic cardiac output relies upon pathologic lungs with poor diffusion capacity leading to poorly oxygenated blood supplied to the coronary and cerebral circulations. We contend that upper body VA ECMO is the most appropriate configuration in the PH patient with intrinsic lung disease and significant right ventricular dysfunction. Our team sought an approach to reduce the risk associated with general anesthesia in this particularly high risk group undergoing VA ECMO cannulation.
Upper body VA ECMO is well described and has been used at our institution routinely. Historically, it was done under general anesthesia with endotracheal intubation.10 We have modified our approach in patients with severe PH to avoid the pitfalls of endotracheal intubation and induction of general anesthesia and now utilize only local anesthesia with MAC. Local anesthetic infiltration with supplemental midazolam and ketamine, when necessary, is one approach to subclavian VA ECMO cannulation that maintains spontaneous ventilation and avoids airway instrumentation in patients at extremely high risk of perioperative pulmonary hypertensive crisis and hypoxemic cardiac arrest. The cannulation and subsequent weeks of awake ECMO support permitted a stable time period to correct end organ dysfunction and allow for recovery from the acute exacerbation or to BTT. While Patients 1 and 3 remained stable on upper body VA ECMO, Patient 2 did not fare as well. In hindsight, she may have benefitted from preventive angioembolization of the suspected bronchial artery collaterals despite not bleeding while on ECMO for 10 days. We do not consider hemoptysis a contraindication to ECMO because of our previous experience with patients who have had hemoptysis and the use of our low dose anticoagulation protocol with activated partial thromboplastin times maintained between 40 and 60 seconds.
We have demonstrated the feasibility and modest success in well-selected high-risk PH patients requiring complex ECMO cannulation. In the future, with appropriate monitoring, awake upper body VA ECMO might be performed at the bedside, which would obviate transport to the operating room.
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