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The Use of Transtracheal Oxygen Therapy in the Management of Severe Hepatopulmonary Syndrome After Liver Transplantation
The Use of Transtracheal Oxygen Therapy in the Management of Severe Hepatopulmonary Syndrome After Liver Transplantation T.N. Udoji, D.M. Berkowitz, R.I. Bechara, S. Hanish, and R.M. Subramanian ABSTRACT Hepatopulmonary syndrome (HPS) is a unique form of hypoxemia found in patients who have chronic liver disease. The definitive treatment for HPS is liver transplantation (LT), with resolution of hypoxemia occurring weeks to months after LT. Because there has been an increase in the use of LT to treat severe HPS (PaO2 50 mm Hg), alternatives to oxygen administration via nasal cannula (NC) or face mask must be examined to facilitate early postoperative mobilization and to minimize postoperative pulmonary complications. Transtracheal oxygen (TTO) therapy is a practical alternative that has been shown to improve oxygen requirements, facilitate patient mobility, and improve exercise tolerance in advanced lung disease. In this case series, we describe the use of TTO in the management of hypoxemia associated with severe HPS after LT. A transition from NC to TTO resulted in a significant reduction in oxygen requirements, early postoperative mobilization and discharge from the hospital, and a subsequent expedited liberation from supplemental oxygen. This case series emphasizes the potential utility of TTO therapy as an alternative to conventional oxygen delivery modalities in the management of severe HPS after LT.
H
EPATOPULMONARY syndrome (HPS) is a pulmonary vascular complication of chronic liver disease that results in an arterial oxygenation defect due to diffusion impaired transfer of oxygen from the alveolar space to a pathologically dilated pulmonary microvasculature.1 The prevalence of HPS in patients being evaluated for liver transplantation (LT) is 10% to 20%1 The severity of hypoxemia influences pretransplantation mortality and is the basis for the current practice of providing a higher priority on the transplantation wait list for patients with a room-air arterial oxygen tension (PaO2) 60 mm Hg. Specifically, patients with HPS with a room air PaO2 60 mm Hg are given a Model for End-stage Liver Disease (MELD) score of 22, irrespective of their intrinsic MELD score as determined by their serum bilirubin, international normalized ratio and creatinine values.2 Early in the disease process, the most sensitive measurement of arterial hypoxemia is an increase in the alveolar-arterial oxygen gradient.1,3 Patients experience worsening dyspnea related to a ventilation-perfusion mismatch in the upright position, resulting in platypnea and orthodeoxia. Diagnostic criteria for HPS include the presence of hypoxemia in the absence of parenchymal lung disease and the presence of “delayed” bubbles on echocardiography consistent with an intrapulmonary right-to-left
shunt. In addition, pulmonary function tests (PFTs) will show an isolated decreased diffusion capacity of carbon monoxide (DLCO). With respect to treatment, attempts using medical therapy3,4 or interventional therapy such as arterial coil embolization5e7 have shown very limited efficacy; therefore, the definitive treatment for HPS is LT.1,3 The reversible nature of hypoxemia after LT shows the reversibility of the pathologic pulmonary vasodilatation and supports the pathophysiology of a pulmonary vasodilator derived from the hepatic circulation.1 However, the duration of recovery after LT is variable and dependent on the degree of hypoxemia before transplantation.8 Prior studies have suggested that a preoperative PaO2 50 mm Hg in HPS patients is associated with increased mortality after LT.8,9 However, more recent studies have suggested From the Division of Pulmonary, Allergy, and Critical Care Medicine (T.N.U., D.M.B., R.I.B., R.M.S.), the Interventional Pulmonary Medicine (T.N.U., D.M.B., R.I.B.), the Division of Transplant Surgery (S.H.), and the Division of Gastroenterology and Hepatology (R.M.S.), Emory University School of Medicine, Atlanta, Georgia. Address reprint requests to Ram M. Subramanian, MD, 1365 Clifton Road NE, B6416, Atlanta, GA 30322. E-mail: rmsubra@ emory.edu
0041-1345/13/$esee front matter http://dx.doi.org/10.1016/j.transproceed.2013.05.007
ª 2013 by Elsevier Inc. All rights reserved. 360 Park Avenue South, New York, NY 10010-1710
3316
Transplantation Proceedings, 45, 3316e3319 (2013)
TRANSTRACHEAL OXYGEN THERAPY
3317
Table 1. Characteristics of Patients Before and After Liver Transplantation Characteristics
Patient 1
Patient 2
Patient 3
Age (y) Sex Race Etiology of ESLD Presence of intrapulmonary shunt on echocardiogram? Baseline pre-LT arterial oxygen tension (mm Hg) Baseline DLCO (% predicted) Baseline oxygen flow requirement Intrinsic MELD score Days between LT and TTO placement Duration (d) of TTO catheter use Time (d) to hospital discharge after TTO placement
51 Male Caucasian Hepatitis C Yes 41 57 8e10 L/min 13 3 88 20
56 Female Caucasian Hepatitis C Yes 45 Not available 60%e100% via facemask 12 8 15 8
42 Male Caucasian Hepatitis C Yes 52 42 7 L/min 20 10 32 15
Abbreviations: ESLD, end-stage liver disease; LT, liver transplantation; DLCO, diffusion capacity for carbon monoxide; MELD, model for end-stage liver disease, calculated on day before LT; TTO, transtracheal oxygen catheter.
that this degree of hypoxemia should not be a contraindication to transplantation, and that patients who have severe HPS can show postoperative survival rates similar to less severe cases of HPS.2,10 In light of this data, there is an increasing trend among liver transplantation centers to offer transplantation to patients with severe HPS. Given this evolving change in the acceptable degree of pretransplantation hypoxemia, practical alternatives to conventional oxygen delivery modalities (eg, nasal cannula [NC], face mask) must be examined before and especially after transplantation to facilitate early patient mobilization, reduce postoperative pulmonary complications, and to possibly reduce intensive care unit as well as hospital length of stay. Transtracheal oxygen therapy (TTO) is a practical oxygen delivery modality that is used for patients who have chronic irreversible hypoxemia in advanced lung disease in lieu of an NC or a facemask. This oxygen delivery method has improved supplemental oxygen flow requirements and facilitates patient mobility and exercise tolerance in patients with advanced lung disease. In this case series, we describe our experience showing a similar benefit of TTO in the treatment of three patients with severe HPS after LT. This study was approved by the Biomedical Committee of our institutional review board (IRB # 00064883). PATIENT 1
A 51-year-old white male with decompensated hepatitis C cirrhosis and HPS (as documented by hypoxemia, the presence of “late” bubbles on echocardiography, decreased DLCO on PFTs, and normal chest computed tomography) underwent evaluation for LT. The patient’s room-air oxygen saturation was 62%, which improved to 95% on 8e10 L/min of supplemental oxygen via NC. An arterial blood gas revealed a decreased PaO2 of 41 mm Hg on room-air. He underwent an uncomplicated LT, and was extubated to facemask with 50% oxygen on postoperative day (POD) 2. His postoperative hypoxemia necessitated a trial of multiple airway devices and oxygen flow of up to 15 L/min facemask. With a goal to facilitate mobilization and deliver oxygen more efficiently, a TTO catheter was placed on POD
3. After a period of 1 week to facilitate tract maturation of the TTO catheter, he was switched to TTO, with oxygen flows ranging from 6 to 10 L/min. The patient’s participation level in postoperative physical therapy and ambulation also improved, and he was discharged home on POD 23 with 5 L/min of oxygen. As an outpatient, he continued rehabilitation and weaning of oxygen, eventually transitioning to 2 L/min via NC 6 weeks after his TTO procedure. At this stage, the TTO catheter was removed. Five months after LT, the patient was liberated from oxygen therapy. He is currently 13 months post-LT with a normal functioning allograft and without the need for supplemental oxygen. PATIENT 2
A 56-year-old white female with hepatitis Ceinduced cirrhosis and severe HPS presented to our institution for evaluation for LT. The patient’s room-air oxygen saturation was 74% on pulse oximetry (PaO2 of 45 mm Hg). The patient underwent a LT without complications and was successfully extubated on POD 3. Her oxygen requirement varied between 10 and 15 L/min via a combination of NC and high-flow NC (HFNC). Because of persistent hypoxemia, the patient underwent a TTO catheter placement on POD 8. After a transition to oxygen delivery via the TTO catheter, her participation in physical therapy and mobilization progressively improved, which facilitated hospital discharge on POD 16 on 3 L/min of oxygen. Over time, the patient was transitioned to 2 L/min oxygen via NC and her TTO catheter was discontinued on POD 23. Her oxygen therapy was discontinued 3 months after LT, and she is currently 2 years post-transplantation with stable hepatic and pulmonary function. PATIENT 3
A 42-year-old white male with hepatitis C cirrhosis complicated by severe HPS was evaluated for LT. Pretransplantation evaluation revealed a room-air PaO2 of 52 mm Hg. He underwent an uncomplicated LT with
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successful extubation to a non-rebreather facemask with 100% oxygen on POD 2. Attempts to wean his oxygen were unsuccessful. On POD 5, he experienced episodes of oxygen desaturation while on 12 L/min oxygen via HFNC and his PaO2 was 59 mm Hg. Given his increasing oxygen flow requirement, he underwent TTO catheter placement on POD 10. With the subsequent use of the TTO catheter a week later, his oxygen flow requirements decreased and the patient was better able to participate in physical and occupational therapy. Discharge occurred on POD 25 with oxygen requirement of 8.5 L/min through his TTO catheter. Six weeks post-transplantation, he was successfully weaned to 2 L oxygen via NC, and his TTO catheter was removed. His oxygen was weaned off 2 weeks later, and he is currently 3 years post-LT without the need for oxygen therapy. Table 1 summarizes the characteristics of the three patients before and after LT, and outlines the timing of initiation and subsequent cessation of TTO therapy. DISCUSSION
We report our experience with TTO as an alternative to conventional oxygen delivery for three patients with severe HPS after LT which, to our knowledge, has not been reported previously. After LT, our patients had normal allograft function, but their postoperative pulmonary status was characterized by persistent hypoxemia despite the use of HFNC, facemask, or a combination of both devices. They were unable to participate optimally in physical and occupational therapy after surgery, and their mobility was impaired due to persistent dyspnea and hypoxemia. A transition to TTO decreased our patients’ oxygen flow requirement, improved their mobility and their ability to tolerate physical therapy, facilitated postoperative recovery, and expedited discharge from the hospital. Furthermore, subsequent liberation from oxygen was facilitated after removal of the TTO catheter and a short transition to NC. Patients with HPS with a pretransplantation room-air PaO2 of 50 mm Hg were reported to have increased posttransplantation mortality.8,9 However, recent studies have reported on the successful outcome and reversibility of hypoxemia after LT in these patients.2,10 However, because the duration for the reversibility of these pulmonary gas exchange abnormalities is variable, supplemental oxygen is usually required during the period of resolution of hypoxemia. The use of oxygen via HFNC, facemask, or a combination of both devices typically requires an intensive care unit stay that limits recovery of functional status, prolongs hospitalization, and could increase the incidence of postoperative pulmonary complications in these patients. TTO could represent an important treatment modality for persistent hypoxemia related to severe HPS in this post-transplantation period. Furthermore, the reversible nature of hypoxemia in HPS makes TTO a finite and practical option. Pleural effusions, pulmonary edema, pulmonary atelectasis, and pneumonia are examples of pulmonary complications observed after LT. These pulmonary complications can result
Fig 1. A Patient wearing a transtracheal oxygen catheter (white arrow) attached to oxygen tubing and secured with a necklace.
in significant hypoxemia with a high mortality rate. In the immediate post-LT period, patients with severe HPS can experience persistent dyspnea and hypoxemia that limits mobility and might increase the patients’ susceptibility to pulmonary atelectasis, which is an independent predictor of post-transplantation pneumonia.11 Also, these patients are administered immunosuppressants; therefore, they may be susceptible to hospital-acquired pulmonary infections. These potential additional pulmonary complications must be prevented to minimize post-transplantation morbidity and mortality. The use of TTO may provide a modality of efficient oxygen delivery that facilitates early mobilization and decreases or prevents postoperative pulmonary complications. TTO is used in the treatment of chronic irreversible hypoxemia in patients with end-stage lung diseases.12 Other indications for TTO include complications of chronic hypoxemia such as cor pulmonale and erythrocythemia,13 and to improve patients’ mobility and physical activity.12 Absolute contraindications include medical instability and coagulopathy.12 The oxygen catheter is placed using the Spofford Christopher Oxygen Optimizing Program (SCOOP) phases of care that includes patient selection, creation of a tracheocutaneous fistula, tract maturation management, and mature tract maintenance.12 Similar to NC oxygen delivery systems, transtracheal oxygen flow rates can be titrated to an acceptable level of oxygen saturation or
TRANSTRACHEAL OXYGEN THERAPY
arterial oxygen tension using either pulse oximetry or blood gas analysis, respectively.12 Patient and procedural complications are minor and depend on the phase of the SCOOP program and the proceduralist’s experience.12,14 The reported minor complications include displacement of the catheter and mucous plugging of the catheter tip due to incomplete maturation of the tracheocutaneous tract.12 Long-term complications are rare and the catheter can be removed when it is no longer needed. The physiological benefits of TTO have been attributed to the route of oxygen delivery. TTO delivery improves dyspnea15 and other complications of chronic irreversible hypoxemia.13,16,17 Couser and Make showed that inspired tidal volume, respiratory rate, and the work of breathing were significantly reduced when oxygen or air was delivered transtracheally compared to oral breathing. TTO therapy improves the effective FiO2 at a given oxygen flow rate,18 thereby reducing the oxygen requirements both at rest and with exertion compared to an NC oxygen delivery system. For example, a study of patients with end-stage lung disease showed that oxygen delivery via a TTO catheter resulted in a 45% less oxygen requirement at rest and 39% less oxygen requirement during exercise compared with an NC delivery system.19 Therefore, portable oxygen systems can last longer to accommodate the patients’ increased exercise tolerance.12,13 Psychological benefits of TTO include an improved self-image because the oxygen catheter can be hidden from view (Fig 1).12,14 Also, there is decreased ear and nose skin irritation compared with NC oxygen use which improves patient compliance with the prescribed oxygen therapy. In conclusion, TTO therapy should be considered as a practical alternative to NC and facemask oxygen delivery devices for the management of persistent hypoxemia in patients with severe HPS after LT. The benefits of TTO are well documented in patients who have severe irreversible hypoxemia associated with chronic lung disease, and this method of oxygen delivery could provide similar benefits in patients with reversible hypoxemia found in HPS. There are no long-term adverse effects associated with its use, and the reversibility of hypoxemia in HPS makes the finite duration of TTO an attractive option. In addition, it may reduce the frequency of immediate post LT pulmonary complications (i.e. atelectasis, pulmonary embolism and pneumonia) that may occur in these immunosuppressed patents, by facilitating improved mobility and physical therapy while receiving oxygen therapy for severe hypoxemia due to HPS.
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REFERENCES 1. Rodriguez-Roisin R, Krowka MJ. Hepatopulmonary syndromed a liver-induced lung vascular disorder. N Engl J Med. 2008;358: 2378e2387. 2. Iyer VN, Swanson KL, Cartin-Ceba R, et al. Hepatopulmonary syndrome: favorable outcomes in the MELD exception era [epub ahead of print]. Hepatology. 2012. 3. Rodriguez-Roisin R, Krowka MJ, Herve P, et al. Pulmonaryhepatic vascular disorders (PHD). Eur Respir J. 2004;24:861e880. 4. Krug S, Seyfarth HJ, Hagendorff A, et al. Inhaled iloprost for hepatopulmonary syndrome: improvement of hypoxemia. Eur J Gastroenterol Hepatol. 2007;19:1140e1143. 5. Saad NE, Lee DE, Waldman DL, et al. Pulmonary arterial coil embolization for the management of persistent type I hepatopulmonary syndrome after liver transplantation. J Vasc Interv Radiol. 2007;18:1576e1580. 6. Poterucha JJ, Krowka MJ, Dickson ER, et al. Failure of hepatopulmonary syndrome to resolve after liver transplantation and successful treatment with embolotherapy. Hepatology. 1995;21:96e100. 7. Lee HW, Suh KS, Kim J, et al. Pulmonary artery embolotherapy in a patient with type I hepatopulmonary syndrome after liver transplantation. Korean J Radiol. 2010;11:485e489. 8. Lange PA, Stoller JK. The hepatopulmonary syndrome. Effect of liver transplantation. Clin Chest Med. 1996;17:115e123. 9. Arguedas MR, Abrams GA, Krowka MJ, et al. Prospective evaluation of outcomes and predictors of mortality in patients with hepatopulmonary syndrome undergoing liver transplantation. Hepatology. 2003;37:192e197. 10. Gupta S, Castel H, Rao RV, et al. Improved survival after liver transplantation in patients with hepatopulmonary syndrome. Amer J Transplant. 2010;10:354e363. 11. Golfieri R, Giampalma E, Morselli Labate AM, et al. Pulmonary complications of liver transplantation: radiological appearance and statistical evaluation of risk factors in 300 cases. Eur Radiol. 2000;10:1169e1183. 12. Christopher KL, Schwartz MD. Transtracheal oxygen therapy. Chest. 2011;139:435e440. 13. Bloom BS, Daniel JM, Wiseman M, et al. Transtracheal oxygen delivery and patients with chronic obstructive pulmonary disease. Respir Med. 1989;83:281e288. 14. Kampelmacher MJ, Deenstra M, van Kesteren RG, et al. Transtracheal oxygen therapy: an effective and safe alternative to nasal oxygen administration. Eur Respir J. 1997;10:828e833. 15. Couser JI Jr, Make BJ. Transtracheal oxygen decreases inspired minute ventilation. Am Rev Respir Dis. 1989;139:627e631. 16. O’Donohue WJ Jr. Effect of oxygen therapy on increasing arterial oxygen tension in hypoxemic patients with stable chronic obstructive pulmonary disease while breathing ambient air. Chest. 1991;100:968e972. 17. Christopher KL, Spofford BT, Brannin PK, et al. Transtracheal oxygen therapy for refractory hypoxemia. JAMA. 1986;256:494e497. 18. Markovitz GH, Colthurst J, Storer TW, et al. Effective inspired oxygen concentration measured via transtracheal and oral gas analysis. Respir Care. 2010;55:453e459. 19. Hoffman LA, Wesmiller SW, Sciurba FC, et al. Nasal cannula and transtracheal oxygen delivery. A comparison of patient response after 6 months of each technique. Am Rev Respir Dis. 1992;145:827e831.
H
EPATOPULMONARY syndrome (HPS) is a pulmonary vascular complication of chronic liver disease that results in an arterial oxygenation defect due to diffusion impaired transfer of oxygen from the alveolar space to a pathologically dilated pulmonary microvasculature.1 The prevalence of HPS in patients being evaluated for liver transplantation (LT) is 10% to 20%1 The severity of hypoxemia influences pretransplantation mortality and is the basis for the current practice of providing a higher priority on the transplantation wait list for patients with a room-air arterial oxygen tension (PaO2) 60 mm Hg. Specifically, patients with HPS with a room air PaO2 60 mm Hg are given a Model for End-stage Liver Disease (MELD) score of 22, irrespective of their intrinsic MELD score as determined by their serum bilirubin, international normalized ratio and creatinine values.2 Early in the disease process, the most sensitive measurement of arterial hypoxemia is an increase in the alveolar-arterial oxygen gradient.1,3 Patients experience worsening dyspnea related to a ventilation-perfusion mismatch in the upright position, resulting in platypnea and orthodeoxia. Diagnostic criteria for HPS include the presence of hypoxemia in the absence of parenchymal lung disease and the presence of “delayed” bubbles on echocardiography consistent with an intrapulmonary right-to-left
shunt. In addition, pulmonary function tests (PFTs) will show an isolated decreased diffusion capacity of carbon monoxide (DLCO). With respect to treatment, attempts using medical therapy3,4 or interventional therapy such as arterial coil embolization5e7 have shown very limited efficacy; therefore, the definitive treatment for HPS is LT.1,3 The reversible nature of hypoxemia after LT shows the reversibility of the pathologic pulmonary vasodilatation and supports the pathophysiology of a pulmonary vasodilator derived from the hepatic circulation.1 However, the duration of recovery after LT is variable and dependent on the degree of hypoxemia before transplantation.8 Prior studies have suggested that a preoperative PaO2 50 mm Hg in HPS patients is associated with increased mortality after LT.8,9 However, more recent studies have suggested From the Division of Pulmonary, Allergy, and Critical Care Medicine (T.N.U., D.M.B., R.I.B., R.M.S.), the Interventional Pulmonary Medicine (T.N.U., D.M.B., R.I.B.), the Division of Transplant Surgery (S.H.), and the Division of Gastroenterology and Hepatology (R.M.S.), Emory University School of Medicine, Atlanta, Georgia. Address reprint requests to Ram M. Subramanian, MD, 1365 Clifton Road NE, B6416, Atlanta, GA 30322. E-mail: rmsubra@ emory.edu
0041-1345/13/$esee front matter http://dx.doi.org/10.1016/j.transproceed.2013.05.007
ª 2013 by Elsevier Inc. All rights reserved. 360 Park Avenue South, New York, NY 10010-1710
3316
Transplantation Proceedings, 45, 3316e3319 (2013)
TRANSTRACHEAL OXYGEN THERAPY
3317
Table 1. Characteristics of Patients Before and After Liver Transplantation Characteristics
Patient 1
Patient 2
Patient 3
Age (y) Sex Race Etiology of ESLD Presence of intrapulmonary shunt on echocardiogram? Baseline pre-LT arterial oxygen tension (mm Hg) Baseline DLCO (% predicted) Baseline oxygen flow requirement Intrinsic MELD score Days between LT and TTO placement Duration (d) of TTO catheter use Time (d) to hospital discharge after TTO placement
51 Male Caucasian Hepatitis C Yes 41 57 8e10 L/min 13 3 88 20
56 Female Caucasian Hepatitis C Yes 45 Not available 60%e100% via facemask 12 8 15 8
42 Male Caucasian Hepatitis C Yes 52 42 7 L/min 20 10 32 15
Abbreviations: ESLD, end-stage liver disease; LT, liver transplantation; DLCO, diffusion capacity for carbon monoxide; MELD, model for end-stage liver disease, calculated on day before LT; TTO, transtracheal oxygen catheter.
that this degree of hypoxemia should not be a contraindication to transplantation, and that patients who have severe HPS can show postoperative survival rates similar to less severe cases of HPS.2,10 In light of this data, there is an increasing trend among liver transplantation centers to offer transplantation to patients with severe HPS. Given this evolving change in the acceptable degree of pretransplantation hypoxemia, practical alternatives to conventional oxygen delivery modalities (eg, nasal cannula [NC], face mask) must be examined before and especially after transplantation to facilitate early patient mobilization, reduce postoperative pulmonary complications, and to possibly reduce intensive care unit as well as hospital length of stay. Transtracheal oxygen therapy (TTO) is a practical oxygen delivery modality that is used for patients who have chronic irreversible hypoxemia in advanced lung disease in lieu of an NC or a facemask. This oxygen delivery method has improved supplemental oxygen flow requirements and facilitates patient mobility and exercise tolerance in patients with advanced lung disease. In this case series, we describe our experience showing a similar benefit of TTO in the treatment of three patients with severe HPS after LT. This study was approved by the Biomedical Committee of our institutional review board (IRB # 00064883). PATIENT 1
A 51-year-old white male with decompensated hepatitis C cirrhosis and HPS (as documented by hypoxemia, the presence of “late” bubbles on echocardiography, decreased DLCO on PFTs, and normal chest computed tomography) underwent evaluation for LT. The patient’s room-air oxygen saturation was 62%, which improved to 95% on 8e10 L/min of supplemental oxygen via NC. An arterial blood gas revealed a decreased PaO2 of 41 mm Hg on room-air. He underwent an uncomplicated LT, and was extubated to facemask with 50% oxygen on postoperative day (POD) 2. His postoperative hypoxemia necessitated a trial of multiple airway devices and oxygen flow of up to 15 L/min facemask. With a goal to facilitate mobilization and deliver oxygen more efficiently, a TTO catheter was placed on POD
3. After a period of 1 week to facilitate tract maturation of the TTO catheter, he was switched to TTO, with oxygen flows ranging from 6 to 10 L/min. The patient’s participation level in postoperative physical therapy and ambulation also improved, and he was discharged home on POD 23 with 5 L/min of oxygen. As an outpatient, he continued rehabilitation and weaning of oxygen, eventually transitioning to 2 L/min via NC 6 weeks after his TTO procedure. At this stage, the TTO catheter was removed. Five months after LT, the patient was liberated from oxygen therapy. He is currently 13 months post-LT with a normal functioning allograft and without the need for supplemental oxygen. PATIENT 2
A 56-year-old white female with hepatitis Ceinduced cirrhosis and severe HPS presented to our institution for evaluation for LT. The patient’s room-air oxygen saturation was 74% on pulse oximetry (PaO2 of 45 mm Hg). The patient underwent a LT without complications and was successfully extubated on POD 3. Her oxygen requirement varied between 10 and 15 L/min via a combination of NC and high-flow NC (HFNC). Because of persistent hypoxemia, the patient underwent a TTO catheter placement on POD 8. After a transition to oxygen delivery via the TTO catheter, her participation in physical therapy and mobilization progressively improved, which facilitated hospital discharge on POD 16 on 3 L/min of oxygen. Over time, the patient was transitioned to 2 L/min oxygen via NC and her TTO catheter was discontinued on POD 23. Her oxygen therapy was discontinued 3 months after LT, and she is currently 2 years post-transplantation with stable hepatic and pulmonary function. PATIENT 3
A 42-year-old white male with hepatitis C cirrhosis complicated by severe HPS was evaluated for LT. Pretransplantation evaluation revealed a room-air PaO2 of 52 mm Hg. He underwent an uncomplicated LT with
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successful extubation to a non-rebreather facemask with 100% oxygen on POD 2. Attempts to wean his oxygen were unsuccessful. On POD 5, he experienced episodes of oxygen desaturation while on 12 L/min oxygen via HFNC and his PaO2 was 59 mm Hg. Given his increasing oxygen flow requirement, he underwent TTO catheter placement on POD 10. With the subsequent use of the TTO catheter a week later, his oxygen flow requirements decreased and the patient was better able to participate in physical and occupational therapy. Discharge occurred on POD 25 with oxygen requirement of 8.5 L/min through his TTO catheter. Six weeks post-transplantation, he was successfully weaned to 2 L oxygen via NC, and his TTO catheter was removed. His oxygen was weaned off 2 weeks later, and he is currently 3 years post-LT without the need for oxygen therapy. Table 1 summarizes the characteristics of the three patients before and after LT, and outlines the timing of initiation and subsequent cessation of TTO therapy. DISCUSSION
We report our experience with TTO as an alternative to conventional oxygen delivery for three patients with severe HPS after LT which, to our knowledge, has not been reported previously. After LT, our patients had normal allograft function, but their postoperative pulmonary status was characterized by persistent hypoxemia despite the use of HFNC, facemask, or a combination of both devices. They were unable to participate optimally in physical and occupational therapy after surgery, and their mobility was impaired due to persistent dyspnea and hypoxemia. A transition to TTO decreased our patients’ oxygen flow requirement, improved their mobility and their ability to tolerate physical therapy, facilitated postoperative recovery, and expedited discharge from the hospital. Furthermore, subsequent liberation from oxygen was facilitated after removal of the TTO catheter and a short transition to NC. Patients with HPS with a pretransplantation room-air PaO2 of 50 mm Hg were reported to have increased posttransplantation mortality.8,9 However, recent studies have reported on the successful outcome and reversibility of hypoxemia after LT in these patients.2,10 However, because the duration for the reversibility of these pulmonary gas exchange abnormalities is variable, supplemental oxygen is usually required during the period of resolution of hypoxemia. The use of oxygen via HFNC, facemask, or a combination of both devices typically requires an intensive care unit stay that limits recovery of functional status, prolongs hospitalization, and could increase the incidence of postoperative pulmonary complications in these patients. TTO could represent an important treatment modality for persistent hypoxemia related to severe HPS in this post-transplantation period. Furthermore, the reversible nature of hypoxemia in HPS makes TTO a finite and practical option. Pleural effusions, pulmonary edema, pulmonary atelectasis, and pneumonia are examples of pulmonary complications observed after LT. These pulmonary complications can result
Fig 1. A Patient wearing a transtracheal oxygen catheter (white arrow) attached to oxygen tubing and secured with a necklace.
in significant hypoxemia with a high mortality rate. In the immediate post-LT period, patients with severe HPS can experience persistent dyspnea and hypoxemia that limits mobility and might increase the patients’ susceptibility to pulmonary atelectasis, which is an independent predictor of post-transplantation pneumonia.11 Also, these patients are administered immunosuppressants; therefore, they may be susceptible to hospital-acquired pulmonary infections. These potential additional pulmonary complications must be prevented to minimize post-transplantation morbidity and mortality. The use of TTO may provide a modality of efficient oxygen delivery that facilitates early mobilization and decreases or prevents postoperative pulmonary complications. TTO is used in the treatment of chronic irreversible hypoxemia in patients with end-stage lung diseases.12 Other indications for TTO include complications of chronic hypoxemia such as cor pulmonale and erythrocythemia,13 and to improve patients’ mobility and physical activity.12 Absolute contraindications include medical instability and coagulopathy.12 The oxygen catheter is placed using the Spofford Christopher Oxygen Optimizing Program (SCOOP) phases of care that includes patient selection, creation of a tracheocutaneous fistula, tract maturation management, and mature tract maintenance.12 Similar to NC oxygen delivery systems, transtracheal oxygen flow rates can be titrated to an acceptable level of oxygen saturation or
TRANSTRACHEAL OXYGEN THERAPY
arterial oxygen tension using either pulse oximetry or blood gas analysis, respectively.12 Patient and procedural complications are minor and depend on the phase of the SCOOP program and the proceduralist’s experience.12,14 The reported minor complications include displacement of the catheter and mucous plugging of the catheter tip due to incomplete maturation of the tracheocutaneous tract.12 Long-term complications are rare and the catheter can be removed when it is no longer needed. The physiological benefits of TTO have been attributed to the route of oxygen delivery. TTO delivery improves dyspnea15 and other complications of chronic irreversible hypoxemia.13,16,17 Couser and Make showed that inspired tidal volume, respiratory rate, and the work of breathing were significantly reduced when oxygen or air was delivered transtracheally compared to oral breathing. TTO therapy improves the effective FiO2 at a given oxygen flow rate,18 thereby reducing the oxygen requirements both at rest and with exertion compared to an NC oxygen delivery system. For example, a study of patients with end-stage lung disease showed that oxygen delivery via a TTO catheter resulted in a 45% less oxygen requirement at rest and 39% less oxygen requirement during exercise compared with an NC delivery system.19 Therefore, portable oxygen systems can last longer to accommodate the patients’ increased exercise tolerance.12,13 Psychological benefits of TTO include an improved self-image because the oxygen catheter can be hidden from view (Fig 1).12,14 Also, there is decreased ear and nose skin irritation compared with NC oxygen use which improves patient compliance with the prescribed oxygen therapy. In conclusion, TTO therapy should be considered as a practical alternative to NC and facemask oxygen delivery devices for the management of persistent hypoxemia in patients with severe HPS after LT. The benefits of TTO are well documented in patients who have severe irreversible hypoxemia associated with chronic lung disease, and this method of oxygen delivery could provide similar benefits in patients with reversible hypoxemia found in HPS. There are no long-term adverse effects associated with its use, and the reversibility of hypoxemia in HPS makes the finite duration of TTO an attractive option. In addition, it may reduce the frequency of immediate post LT pulmonary complications (i.e. atelectasis, pulmonary embolism and pneumonia) that may occur in these immunosuppressed patents, by facilitating improved mobility and physical therapy while receiving oxygen therapy for severe hypoxemia due to HPS.
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REFERENCES 1. Rodriguez-Roisin R, Krowka MJ. Hepatopulmonary syndromed a liver-induced lung vascular disorder. N Engl J Med. 2008;358: 2378e2387. 2. Iyer VN, Swanson KL, Cartin-Ceba R, et al. Hepatopulmonary syndrome: favorable outcomes in the MELD exception era [epub ahead of print]. Hepatology. 2012. 3. Rodriguez-Roisin R, Krowka MJ, Herve P, et al. Pulmonaryhepatic vascular disorders (PHD). Eur Respir J. 2004;24:861e880. 4. Krug S, Seyfarth HJ, Hagendorff A, et al. Inhaled iloprost for hepatopulmonary syndrome: improvement of hypoxemia. Eur J Gastroenterol Hepatol. 2007;19:1140e1143. 5. Saad NE, Lee DE, Waldman DL, et al. Pulmonary arterial coil embolization for the management of persistent type I hepatopulmonary syndrome after liver transplantation. J Vasc Interv Radiol. 2007;18:1576e1580. 6. Poterucha JJ, Krowka MJ, Dickson ER, et al. Failure of hepatopulmonary syndrome to resolve after liver transplantation and successful treatment with embolotherapy. Hepatology. 1995;21:96e100. 7. Lee HW, Suh KS, Kim J, et al. Pulmonary artery embolotherapy in a patient with type I hepatopulmonary syndrome after liver transplantation. Korean J Radiol. 2010;11:485e489. 8. Lange PA, Stoller JK. The hepatopulmonary syndrome. Effect of liver transplantation. Clin Chest Med. 1996;17:115e123. 9. Arguedas MR, Abrams GA, Krowka MJ, et al. Prospective evaluation of outcomes and predictors of mortality in patients with hepatopulmonary syndrome undergoing liver transplantation. Hepatology. 2003;37:192e197. 10. Gupta S, Castel H, Rao RV, et al. Improved survival after liver transplantation in patients with hepatopulmonary syndrome. Amer J Transplant. 2010;10:354e363. 11. Golfieri R, Giampalma E, Morselli Labate AM, et al. Pulmonary complications of liver transplantation: radiological appearance and statistical evaluation of risk factors in 300 cases. Eur Radiol. 2000;10:1169e1183. 12. Christopher KL, Schwartz MD. Transtracheal oxygen therapy. Chest. 2011;139:435e440. 13. Bloom BS, Daniel JM, Wiseman M, et al. Transtracheal oxygen delivery and patients with chronic obstructive pulmonary disease. Respir Med. 1989;83:281e288. 14. Kampelmacher MJ, Deenstra M, van Kesteren RG, et al. Transtracheal oxygen therapy: an effective and safe alternative to nasal oxygen administration. Eur Respir J. 1997;10:828e833. 15. Couser JI Jr, Make BJ. Transtracheal oxygen decreases inspired minute ventilation. Am Rev Respir Dis. 1989;139:627e631. 16. O’Donohue WJ Jr. Effect of oxygen therapy on increasing arterial oxygen tension in hypoxemic patients with stable chronic obstructive pulmonary disease while breathing ambient air. Chest. 1991;100:968e972. 17. Christopher KL, Spofford BT, Brannin PK, et al. Transtracheal oxygen therapy for refractory hypoxemia. JAMA. 1986;256:494e497. 18. Markovitz GH, Colthurst J, Storer TW, et al. Effective inspired oxygen concentration measured via transtracheal and oral gas analysis. Respir Care. 2010;55:453e459. 19. Hoffman LA, Wesmiller SW, Sciurba FC, et al. Nasal cannula and transtracheal oxygen delivery. A comparison of patient response after 6 months of each technique. Am Rev Respir Dis. 1992;145:827e831.