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• W1601423963 abstract "The hepatopulmonary syndrome (HPS) is defined as the triad of liver disease, intrapulmonary vascular dilatation, and abnormal gas exchange, and is found in 10–32% of patients with liver disease. Liver transplantation is the only known cure for HPS, but patients can develop severe posttransplant hypoxemia, defined as a need for 100% inspired oxygen to maintain a saturation of ≥85%. This complication is seen in 6–21% of patients and carries a 45% mortality. Its management requires the application of specific strategies targeting the underlying physiologic abnormalities in HPS, but awareness of these strategies and knowledge on their optimal use is limited. We reviewed existing literature to identify strategies that can be used for this complication, and developed a clinical management algorithm based on best evidence and expert opinion. Evidence was limited to case reports and case series, and we determined which treatments to include in the algorithm and their recommended sequence based on their relative likelihood of success, invasiveness, and risk. Recommended therapies include: Trendelenburg positioning, inhaled epoprostenol or nitric oxide, methylene blue, embolization of abnormal pulmonary vessels, and extracorporeal life support. Availability and use of this pragmatic algorithm may improve management of this complication, and will benefit from prospective validation. The hepatopulmonary syndrome (HPS) is defined as the triad of liver disease, intrapulmonary vascular dilatation, and abnormal gas exchange, and is found in 10–32% of patients with liver disease. Liver transplantation is the only known cure for HPS, but patients can develop severe posttransplant hypoxemia, defined as a need for 100% inspired oxygen to maintain a saturation of ≥85%. This complication is seen in 6–21% of patients and carries a 45% mortality. Its management requires the application of specific strategies targeting the underlying physiologic abnormalities in HPS, but awareness of these strategies and knowledge on their optimal use is limited. We reviewed existing literature to identify strategies that can be used for this complication, and developed a clinical management algorithm based on best evidence and expert opinion. Evidence was limited to case reports and case series, and we determined which treatments to include in the algorithm and their recommended sequence based on their relative likelihood of success, invasiveness, and risk. Recommended therapies include: Trendelenburg positioning, inhaled epoprostenol or nitric oxide, methylene blue, embolization of abnormal pulmonary vessels, and extracorporeal life support. Availability and use of this pragmatic algorithm may improve management of this complication, and will benefit from prospective validation. The hepatopulmonary syndrome (HPS) is defined as a triad of liver disease, intrapulmonary vascular dilatation, and abnormal gas exchange, and is found in 10–32% of patients with cirrhosis (1.Arguedas MR Singh H Faulk DK Fallon MB. Utility of pulse oximetry screening for hepatopulmonary syndrome.Clin Gastroenterol Hepatol. 2007; 5: 749-754Abstract Full Text Full Text PDF PubMed Scopus (120) Google Scholar, 2.Lima BL Franca AV Pazin-Filho A Frequency, clinical characteristics, and respiratory parameters of hepatopulmonary syndrome.Mayo Clin Proc. 2004; 79 (et al): 42-48Abstract Full Text Full Text PDF PubMed Scopus (101) Google Scholar, 3.Schenk P Schoniger-Hekele M Fuhrmann V Madl C Silberhumer G Muller C. Prognostic significance of the hepatopulmonary syndrome in patients with cirrhosis.Gastroenterology. 2003; 125: 1042-1052Abstract Full Text Full Text PDF PubMed Scopus (297) Google Scholar, 4.Schiffer E Majno P Mentha G Hepatopulmonary syndrome increases the postoperative mortality rate following liver transplantation: A prospective study in 90 patients.Am J Transplant. 2006; 6 (et al): 1430-1437Abstract Full Text Full Text PDF PubMed Scopus (86) Google Scholar). This disease is associated with progressive hypoxemia and a high mortality (3.Schenk P Schoniger-Hekele M Fuhrmann V Madl C Silberhumer G Muller C. Prognostic significance of the hepatopulmonary syndrome in patients with cirrhosis.Gastroenterology. 2003; 125: 1042-1052Abstract Full Text Full Text PDF PubMed Scopus (297) Google Scholar,5.Fallon MB Krowka MJ Brown RS Impact of hepatopulmonary syndrome on quality of life and survival in liver transplant candidates.Gastroenterology. 2008; 135 (et al): 1168-1175Abstract Full Text Full Text PDF PubMed Scopus (196) Google Scholar). Although liver transplantation (LT) is curative in HPS, these patients have an elevated postoperative complication rate (6.Taille C Cadranel J Bellocq A Liver transplantation for hepatopulmonary syndrome: A ten-year experience in Paris.France Transplant. 2003; 75 (et al discussion 46–7 discussion 46–7): 1482-1489Crossref PubMed Scopus (138) Google Scholar, 7.Swanson KL Wiesner RH Krowka MJ. Natural history of hepatopulmonary syndrome: Impact of liver transplantation.Hepatology. 2005; 41: 1122-1129Crossref PubMed Scopus (352) Google Scholar, 8.Al-Hussaini A Taylor RM Samyn M Long-term outcome and management of hepatopulmonary syndrome in children.Pediatr Transplant. 2010; 14 (et al): 276-282Crossref PubMed Scopus (43) Google Scholar, 9.Gupta S Castel H Rao RV Improved survival after liver transplantation in patients with hepatopulmonary syndrome.Am J Transplant. 2010; 10 (et al): 354-363Abstract Full Text Full Text PDF PubMed Scopus (138) Google Scholar). In particular, “severe posttransplant hypoxemia,” defined as a need for 100% inspired oxygen (FiO2) to maintain a saturation of ≥85% (out of proportion to any other concurrent lung process) (10.Nayyar D Man HSJ Granton J Gupta S. Defining and characterizing severe hypoxemia after liver transplantation in hepatopulmonary syndrome.Liver Transpl. 2014; 20: 182-190Crossref PubMed Scopus (33) Google Scholar), has been identified as a major complication leading to prolonged ICU stay and death in this population (6.Taille C Cadranel J Bellocq A Liver transplantation for hepatopulmonary syndrome: A ten-year experience in Paris.France Transplant. 2003; 75 (et al discussion 46–7 discussion 46–7): 1482-1489Crossref PubMed Scopus (138) Google Scholar,9.Gupta S Castel H Rao RV Improved survival after liver transplantation in patients with hepatopulmonary syndrome.Am J Transplant. 2010; 10 (et al): 354-363Abstract Full Text Full Text PDF PubMed Scopus (138) Google Scholar, 10.Nayyar D Man HSJ Granton J Gupta S. Defining and characterizing severe hypoxemia after liver transplantation in hepatopulmonary syndrome.Liver Transpl. 2014; 20: 182-190Crossref PubMed Scopus (33) Google Scholar, 11.Arguedas MR Abrams GA Krowka MJ Fallon MB. Prospective evaluation of outcomes and predictors of mortality in patients with hepatopulmonary syndrome undergoing liver transplantation.Hepatology. 2003; 37: 192-197Crossref PubMed Scopus (308) Google Scholar, 12.Krowka MJ Porayko MK Plevak DJ Hepatopulmonary syndrome with progressive hypoxemia as an indication for liver transplantation: Case reports and literature review.Mayo Clin Proc. 1997; 72 (et al): 44-53Abstract Full Text Full Text PDF PubMed Scopus (186) Google Scholar). Although survivors have a complete normalization of gas exchange over time, severe posttransplant hypoxemia occurs in 6–21% of HPS patients, carries a mortality of 45%, and accounts for the majority of peri-operative deaths in this population (10.Nayyar D Man HSJ Granton J Gupta S. Defining and characterizing severe hypoxemia after liver transplantation in hepatopulmonary syndrome.Liver Transpl. 2014; 20: 182-190Crossref PubMed Scopus (33) Google Scholar). A variety of strategies to attempt to manage this complication have been described in the literature, but these have never been reviewed and summarized and are used inconsistently, which has led to calls for a systematic approach (6.Taille C Cadranel J Bellocq A Liver transplantation for hepatopulmonary syndrome: A ten-year experience in Paris.France Transplant. 2003; 75 (et al discussion 46–7 discussion 46–7): 1482-1489Crossref PubMed Scopus (138) Google Scholar,9.Gupta S Castel H Rao RV Improved survival after liver transplantation in patients with hepatopulmonary syndrome.Am J Transplant. 2010; 10 (et al): 354-363Abstract Full Text Full Text PDF PubMed Scopus (138) Google Scholar,10.Nayyar D Man HSJ Granton J Gupta S. Defining and characterizing severe hypoxemia after liver transplantation in hepatopulmonary syndrome.Liver Transpl. 2014; 20: 182-190Crossref PubMed Scopus (33) Google Scholar,13.Meyers C Low L Kaufman L Druger G Wong LL. Trendelenburg positioning and continuous lateral rotation improve oxygenation in hepatopulmonary syndrome after liver transplantation.Liver Transplant Surg. 1998; 4: 510-512Crossref PubMed Scopus (28) Google Scholar). We sought to review available evidence in order to develop a practical clinical management algorithm for severe posttransplant hypoxemia in HPS. We searched MEDLINE (from inception to October 20, 2014) for English language studies involving human subjects with “hepatopulmonary syndrome” as a medical subject heading or keyword. We supplemented this with a manual search of reference lists from all retrieved articles and by consulting experts in the field. We included studies which described outcomes of strategies expected to rapidly (<72 h) reverse hypoxemia either posttransplant, or in a nontransplant context which could be applied posttransplant (in patients with HPS). Two reviewers (DN, SG) screened all abstracts and categorized them as definitely, possibly, or definitely not meeting inclusion criteria. We retrieved and reviewed full manuscripts for abstracts categorized as definitely or possibly meeting inclusion criteria by one or both reviewers, review articles, and reports of LT outcomes in HPS (adults and children). The treatment algorithm was developed iteratively by a multidisciplinary team from two quaternary care LT centers (the University Health Network, University of Toronto and Hôpital St-Luc, Université de Montréal). Evidence suggests that protocol-driven care can improve ICU care-related outcomes (14.Wall RJ Dittus RS Ely EW. Protocol-driven care in the intensive care unit: A tool for quality.Crit Care. 2001; 5: 283-285Crossref PubMed Scopus (50) Google Scholar), and that early involvement of multidisciplinary teams in the protocol development can foster a sense of ownership, autonomy, and increased adherence (15.Chan PK Fischer S Stewart TE Practising evidence-based medicine: The design and implementation of a multidisciplinary team-driven extubation protocol.Crit Care. 2001; 5 (et al): 349-354Crossref PubMed Scopus (34) Google Scholar). Accordingly, we involved all relevant multidisciplinary stakeholders in the iterative development and approval of the algorithm. The team included five ICU physicians, one respirologist with an interest in HPS, two transplant hepatologists, and one ICU respiratory therapist. The algorithm was further reviewed and modified based on suggestions from ICU, transplant hepatology, liver transplant surgery, respiratory therapy, nursing, and extracorporeal life support (ECLS) team members. We determined which treatments to include in the algorithm and their recommended sequence of use based on their relative likelihood of success, invasiveness, and risk, based on available evidence from our literature search. Where evidence was not available, we relied on common sense and our practical experience in using these strategies at our specialized HPS center, where reported mortality from this complication was 28.6%, versus 75% in other reports (10.Nayyar D Man HSJ Granton J Gupta S. Defining and characterizing severe hypoxemia after liver transplantation in hepatopulmonary syndrome.Liver Transpl. 2014; 20: 182-190Crossref PubMed Scopus (33) Google Scholar). We retrieved 416 citations using the medical subject heading “hepatopulmonary syndrome,” and an additional 156 citations using the keyword “hepatopulmonary syndrome,” for a total of 572 citations. Of these, 18 definitely met, 149 possibly met, and 405 definitely did not meet inclusion criteria. Upon full manuscript review, of the 149 citations possibly meeting inclusion criteria, 15 met inclusion criteria. We identified an additional 23 citations of interest from the manual search of reference lists and from experts, nine of which met inclusion criteria upon full manuscript review, for a total of 42 manuscripts (7%) meeting inclusion criteria. Of these, 27 studies reported therapies that were included in the algorithm (Table 1). Given that this is an infrequent complication in a rare disease, evidence was limited to case reports and case series and could not be formally meta‐analyzed. A small number of patients have been reported for any one therapy, with inhaled nitric oxide (iNO) being the best studied (19 patients), followed by methylene blue (MB) (10 patients), inhaled epoprostenol (four patients), embolization of abnormal pulmonary vessels (four patients), combined iNO and MB (two patients), ECLS (three patients), and Trendelenburg positioning (one patient). Mechanisms and time‐courses of action for these agents are summarized in Table 2. Therapies that were not included in our algorithm, along with their mechanisms of action and reasons for exclusion are summarized in Supplemental Table S1.Table 1Summary of reports describing included strategies for management of severe posttransplant hypoxemia in HPSTreatment and studyNumber of patientsOutcome1FiO2 and time to initial improvement were included in brackets when available.Treatment durationPre- or post-LTPost-LT survival2Reports all deaths during transplant hospitalization/or and reported survivals > 30 days post liver transplant.Effect3Given variable reporting, a uniform criterion could not be used to determine effectiveness; accordingly, we report authors conclusions regarding effect.Trendelenburg positioningMeyers et al., 1998 (13.Meyers C Low L Kaufman L Druger G Wong LL. Trendelenburg positioning and continuous lateral rotation improve oxygenation in hepatopulmonary syndrome after liver transplantation.Liver Transplant Surg. 1998; 4: 510-512Crossref PubMed Scopus (28) Google Scholar)1SaO2 increase from 80% to 91% (FiO2 1.0) (immediate)3 daysPost-LTAlive 1 yr post-LTPositiveInhaled nitric oxideKarnatovskaia et al., 2014 (56.Karnatovskaia LV Matharu J Burger C Keller CA. Inhaled nitric oxide as a potential rescue therapy for persistent hepatopulmonary syndrome after liver transplantation.Transplantation. 2014; 98: e64-e66Crossref PubMed Scopus (1) Google Scholar)1PaO2 increase from 48 to 83 mmHg (30L/min O2) (1 h)2 weeksPost-LTAlive 1 yr post-LTPositiveNayyar et al., 2014 (10.Nayyar D Man HSJ Granton J Gupta S. Defining and characterizing severe hypoxemia after liver transplantation in hepatopulmonary syndrome.Liver Transpl. 2014; 20: 182-190Crossref PubMed Scopus (33) Google Scholar)43/4 improved gas exchange, 1/4 no effect1–29 daysPost-LT2/4 died (POD 77, 19), 2/4 alive > 4 yrs post-LTVariableSantos et al., 2014 (57.Santos J Young P Barjaktarevic I Lazar C Susanto I Wang T. The successful use of inhaled nitric oxide in the management of severe hepatopulmonary syndrome after orthotopic liver transplantation.Case Rep Hepatol. 2014; 2014: 1-4Crossref Google Scholar)4Case 1 from this report was excluded because hypoxemia did not develop until 13 days post liver transplant.1PaO2 increase from 50 to 154 mmHg (FiO2 1.0) (1 h)4 daysPost-LTAlive 2 months post-LTPositiveMonsel et al., 2011 (45.Monsel A Mal H Brisson H Extracorporeal membrane oxygenation as a bridge to liver transplantation for acute respiratory distress syndrome-induced life-threatening hypoxaemia aggravated by hepatopulmonary syndrome.Crit Care. 2011; 15 (et al): R234Crossref PubMed Scopus (35) Google Scholar)1No improvement in gas exchangeN/APre-LTN/ANo effectAl-Hussaini et al., 2010 (8.Al-Hussaini A Taylor RM Samyn M Long-term outcome and management of hepatopulmonary syndrome in children.Pediatr Transplant. 2010; 14 (et al): 276-282Crossref PubMed Scopus (43) Google Scholar)1SaO2 increase from 75–80% to >90% (FiO2 1.0)13 daysPost-LTN/APositiveSchiller et al., 2010 (29.Schiller O Avitzur Y Kadmon G Nitric oxide for post-liver-transplantation hypoxemia in pediatric hepatopulmonary syndrome: Case report and review.Pediatr Transplant. 2010; 15 (et al): E130-E134Crossref PubMed Scopus (14) Google Scholar)1SaO2 increase (immediate)5Quantitative details of improvement in gas exchange were not reported.9 daysPost-LTAlive 1 yr post-LTPositiveElias et al., 2008 (58.Elias N Scirica CV Hertl M. Liver transplantation for the Abernathy malformation.New Eng J Med. 2008; 358: 858Crossref PubMed Scopus (16) Google Scholar)1Gradual improvement in gas exchange5Quantitative details of improvement in gas exchange were not reported.N/APost-LTAlive >4 mo post-LTPositiveFleming et al., 2008 (59.Fleming GM Cornell TT Welling TH Magee JC Annich GM. Hepatopulmonary syndrome: Use of extracorporeal life support for life-threatening hypoxia following liver transplantation.Liver Transplant. 2008; 14: 966-970Crossref PubMed Scopus (42) Google Scholar)1No improvement in gas exchange6Acute hypoxemia occurred on postoperative day 8, at which time patient had ARDS; inhaled NO tried first, followed by ECMO.N/APost-LTAlive >1 yr post-LTNo effectTaille et al., 2003 (6.Taille C Cadranel J Bellocq A Liver transplantation for hepatopulmonary syndrome: A ten-year experience in Paris.France Transplant. 2003; 75 (et al discussion 46–7 discussion 46–7): 1482-1489Crossref PubMed Scopus (138) Google Scholar)33/3 improved gas exchangeN/APost-LTN/APositiveTaniai et al., 2002 (60.Taniai N Onda M Tajiri T Reversal of hypoxemia by inhaled nitric oxide in a child with hepatopulmonary syndrome after living-related liver transplantation.Transplant Proc. 2002; 34 (et al): 2791-2792Crossref PubMed Scopus (13) Google Scholar)1PaO2 increase from ∼70 to 110 mmHg (FiO2 1.0) (12 h)2 daysPost-LTN/APositiveDiaz et al., 2001 (61.Diaz S Garutti I Cruz P Galan A Fuentes J Fernandez-Quero L. [Improved oxygenation with nitric oxide treatment for hepatopulmonary syndrome after a liver transplant]. [Spanish].Rev Esp Anestesiol Reanim. 2001; 48: 340-343PubMed Google Scholar)1Improvement in gas exchange, allowing extubation5Quantitative details of improvement in gas exchange were not reported.N/APost-LTAlive 7 mo post-LTPositiveAlexander et al., 1997 (62.Alexander J Greenough A Baker A Rela M Heaton N Potter D. Nitric oxide treatment of severe hypoxemia after liver transplantation in hepatopulmonary syndrome: Case report.Liver Transplant Surg. 1997; 3: 54-55Crossref PubMed Scopus (34) Google Scholar)1SaO2 increase from ∼50% to 85% (2 h)15 daysPost-LTAlive 42 days post-LTPositiveDurand et al., 1997 (28.Durand P Baujard C Grosse AL Reversal of hypoxemia by inhaled nitric oxide in children with severe hepatopulmonary syndrome, type 1, during and after liver transplantation.Transplantation. 1997; 65 (et al): 437-439Crossref Scopus (43) Google Scholar)1PaO2 increase from 44 to 75 mmHg (FiO2 1.0)12 daysDuring and post-LTAlive 100 days post-LTPositiveOrii et al., 1997 (63.Orii T Ohkohchi N Kato H Liver transplantation for severe hypoxemia caused CNY by patent ductus venosus.J Pediatr Surg. 1997; 32 (et al): 1795-1797Abstract Full Text PDF PubMed Scopus (32) Google Scholar)1PaO2 increase from 44 to 54.3 mmHg (FIO2 not reported)14 daysPost-LTAlive 1 yr post-LTPositiveInhaled iloprost7This agent is not in the treatment algorithm, but may be considered in place of epoprostenol in centers where the latter is not available.Krug et al., 2007 (33.Krug S Seyfarth HJ Hagendorff A Wirtz H. Inhaled iloprost for hepatopulmonary syndrome: Improvement of hypoxemia.Eur J Gastroenterol Hepatol. 2007; 19: 1140-1143Crossref PubMed Scopus (31) Google Scholar)1PaO2 increase from 43 to 48 mmHg (R/A) (15 min)8 weeks pre-LT; 3 months post-LTPre- and Post-LTAlive 3 mo post-LTPositiveInhaled epoprostenolNayyar et al., 2014 (10.Nayyar D Man HSJ Granton J Gupta S. Defining and characterizing severe hypoxemia after liver transplantation in hepatopulmonary syndrome.Liver Transpl. 2014; 20: 182-190Crossref PubMed Scopus (33) Google Scholar)33/3 improved gas exchange1 – 4 daysPost-LT2/3 died (POD 77, 19), 1/3 alive > 4 yrs post-LTPositiveSaad et al., 2007 (39.Saad NE Lee DE Waldman DL Saad WE. Pulmonary arterial coil embolization for the management of persistent type I hepatopulmonary syndrome after liver transplantation.J Vasc Interv Radiol. 2007; 18: 1576-1580Abstract Full Text Full Text PDF PubMed Scopus (25) Google Scholar)1SaO2 increase from 76% (FiO2 1.0) to 90% (FiO2 0.5)N/APost-LTAlive 100 days post-LTPositiveMethylene blueRoma et al., 2010 (17.Roma J Balbi E Pacheco-Moreira L Methylene blue used as a bridge to liver transplantation postoperative recovery: A case report.Transplant Proc. 2010; 42 (et al): 601-604Crossref PubMed Scopus (21) Google Scholar)1PaO2 increase from 35 (FiO2 0.7) to 39 mmHg (FiO2 0.45) (4 h)Single dosePost-LTAlive 58 days post-LTPositiveAlmeida et al., 2007 (64.Almeida JA Riordan SM Liu J Deleterious effect of nitric oxide inhibition in chronic hepatopulmonary syndrome.Eur J Gastroenterol Hepatol. 2007; 19 (et al): 341-346Crossref PubMed Scopus (26) Google Scholar)1Reproducible, reversible decrease in PaO2 by 3–4 mmHgTwo dosesPre-LTN/ANegativeSchenk et al., 2000 (36.Schenk P Madl C Rezaie-Majd S Lehr S Muller C. Methylene blue improves the hepatopulmonary syndrome.[see comment].Ann Intern Med. 2000; 133: 701-706Crossref PubMed Scopus (178) Google Scholar)77/7 improved gas exchange (mean PaO2 increase from 58 to 74 mmHg) (5 h)Single dosePre-LTN/APositiveRolla et al., 1994 (65.Rolla G Bucca C Brussino L. Methylene blue in the hepatopulmonary syndrome.New Eng J Med. 1994; 331: 1098Crossref PubMed Scopus (105) Google Scholar)1PaO2 increase from 56 to 68 mmHg (RA) (20 min)Single dosePre-LTN/APositiveMethylene blue + inhaled nitric oxideNayyar et al., 2014 (10.Nayyar D Man HSJ Granton J Gupta S. Defining and characterizing severe hypoxemia after liver transplantation in hepatopulmonary syndrome.Liver Transpl. 2014; 20: 182-190Crossref PubMed Scopus (33) Google Scholar)1No improvement in gas exchange8A single dose of MB was given on postoperative day 17 in a patient on inhaled NO who had suffered from ventilator-associated pneumonia and had severe hypercapnia and acidemia.Single dosePost-LTDied POD 19No effectJounieaux et al., 2001 (66.Jounieaux V Leleu O Mayeux I. Cardiopulmonary effects of nitric oxide inhalation and methylene blue injection in hepatopulmonary syndrome.Intensive Care Med. 2001; 27: 1103-1104Crossref PubMed Scopus (17) Google Scholar)1No improvement in gas exchange; decrease in cardiac outputN/APre-LTN/ANegativeEmbolotherapy9Reports of embolotherapy were limited to those in patients with diffuse intrapulmonary vascular dilatation, as opposed to frank arteriovenous malformations.Lee et al., 2010 (38.Lee HW Suh KS Kim J Pulmonary artery embolotherapy in a patient with type I hepatopulmonary syndrome after liver transplantation.Korean J Radiol. 2010; 11 (et al): 485-489Crossref PubMed Scopus (10) Google Scholar)1SaO2 increase from 65% to 75% (5L O2) (immediate)–Post-LTAlive 2 yrs post-LTPositiveSaad et al., 2007 (39.Saad NE Lee DE Waldman DL Saad WE. Pulmonary arterial coil embolization for the management of persistent type I hepatopulmonary syndrome after liver transplantation.J Vasc Interv Radiol. 2007; 18: 1576-1580Abstract Full Text Full Text PDF PubMed Scopus (25) Google Scholar)1SaO2 increase from 76% (FiO2 1.0) to 95% (3L O2) 4 days after and 86% (R/A) 12 days after 2nd embolization–Post-LTAlive 100 days post-LTPositiveRyu et al., 2003 (40.Ryu JK Oh JH. Hepatopulmonary syndrome: Angiography and therapeutic embolization.Clin Imaging. 2003; 27: 97-100Abstract Full Text Full Text PDF PubMed Scopus (28) Google Scholar)1PaO2 increase from 65 to 72 mmHg (2L O2) (24 h)–Pre-LTN/APositiveFelt et al., 1987 (41.Felt RW Kozak BE Rosch J Duell BP Barker AF. Hepatogenic pulmonary angiodysplasia treated with coil-spring embolization.Chest. 1987; 91: 920-922Abstract Full Text Full Text PDF PubMed Scopus (33) Google Scholar)1PaO2 increase from 38 to 53 mmHg (R/A) (5 weeks)–Pre-LTN/APositiveExtracorporeal life supportAuzinger et al., 2014 (44.Auzinger G Willars C Loveridge R Extracorporeal membrane oxygenation for refractory hypoxemia after liver transplantation in severe hepatopulmonary syndrome: A solution with pitfalls.Liver Transplant. 2014; 20 (et al): 1141-1144Crossref PubMed Scopus (30) Google Scholar)1Successfully weaned off sedation, tolerated minimal respiratory support21 daysPost-LTN/APositiveMonsel et al., 2011 (45.Monsel A Mal H Brisson H Extracorporeal membrane oxygenation as a bridge to liver transplantation for acute respiratory distress syndrome-induced life-threatening hypoxaemia aggravated by hepatopulmonary syndrome.Crit Care. 2011; 15 (et al): R234Crossref PubMed Scopus (35) Google Scholar)1“Stabilized” gases (patient also had ARDS)5Quantitative details of improvement in gas exchange were not reported.5 daysPre-LTN/APositiveFleming et al., 2008 (59.Fleming GM Cornell TT Welling TH Magee JC Annich GM. Hepatopulmonary syndrome: Use of extracorporeal life support for life-threatening hypoxia following liver transplantation.Liver Transplant. 2008; 14: 966-970Crossref PubMed Scopus (42) Google Scholar)1“Stabilized” SaO2; decreased oxygen requirements (patient also had ARDS)5Quantitative details of improvement in gas exchange were not reported.,6Acute hypoxemia occurred on postoperative day 8, at which time patient had ARDS; inhaled NO tried first, followed by ECMO.18 daysPost-LTAlive >1 yr post-LTPositiveARDS, acute respiratory distress syndrome; FiO2, fraction of inspired oxygen; L, liters; min, minutes, LT, liver transplant; mo, month; N/A, data not available; O2, oxygen; PaO2, partial pressure of arterial oxygen; POD, postoperative day; R/A, room air; SaO2, arterial hemoglobin oxygen saturation; yr, year.1 FiO2 and time to initial improvement were included in brackets when available.2 Reports all deaths during transplant hospitalization/or and reported survivals > 30 days post liver transplant.3 Given variable reporting, a uniform criterion could not be used to determine effectiveness; accordingly, we report authors conclusions regarding effect.4 Case 1 from this report was excluded because hypoxemia did not develop until 13 days post liver transplant.5 Quantitative details of improvement in gas exchange were not reported.6 Acute hypoxemia occurred on postoperative day 8, at which time patient had ARDS; inhaled NO tried first, followed by ECMO.7 This agent is not in the treatment algorithm, but may be considered in place of epoprostenol in centers where the latter is not available.8 A single dose of MB was given on postoperative day 17 in a patient on inhaled NO who had suffered from ventilator-associated pneumonia and had severe hypercapnia and acidemia.9 Reports of embolotherapy were limited to those in patients with diffuse intrapulmonary vascular dilatation, as opposed to frank arteriovenous malformations. Open table in a new tab Table 2Time course and mechanisms of action for included therapiesTreatmentOnset of actionTiming of peak effectMechanism of actionTrendelenburg positioningMinutesMinutesIntrapulmonary vascular dilatations are predominantly basilar. Gravitational redistribution of blood flow to upper and mid lung zones decreases flow through intrapulmonary vascular dilatationsInhaled vasodilators (epoprostenol or nitric oxide)MinutesMinutesPreferentially vasodilates normal vessels, redirecting flow from (maximally vasodilated) intrapulmonary vascular dilatationsMethylene blue∼1 h5 hGuanylate cyclase inhibitor; blocks nitric oxide-induced vasodilation, which may vasoconstrict and reduce flow through intrapulmonary vascular dilatations (particularly in areas of impaired hypoxic vasoconstriction)Inhaled vasodilator + intravenous methylene blueMinutes5 hPreferentially vasodilates normal vessels in well-ventilated areas, and vasoconstricts intrapulmonary vascular dilatations in poorly ventilated areas with impaired hypoxic vasoconstrictionEmbolization of lower lobar pulmonary vesselsMinutes to 24 hUnclearRedistributes blood flow away from intrapulmonary vascular dilatations, to mid and upper lung zonesExtracorporeal life supportHoursSustainedSustains tissue oxygenation until intrapulmonary vascular dilatations begin to reverse and pulmonary gas exchange improves Open table in a new tab ARDS, acute respiratory distress syndrome; FiO2, fraction of inspired oxygen; L, liters; min, minutes, LT, liver transplant; mo, month; N/A, data not available; O2, oxygen; PaO2, partial pressure of arterial oxygen; POD, postoperative day; R/A, room air; SaO2, arterial hemoglobin oxygen saturation; yr, year. Using the existing definition of severe posttransplant hypoxemia in HPS (a need for 100% FiO2 to maintain a saturation ≥85%) (10.Nayyar D Man HSJ Granton J Gupta S. Defining and characterizing severe hypoxemia after liver transplantation in hepatopulmonary syndrome.Liver Transpl. 2014; 20: 182-190Crossref PubMed Scopus (33) Google Scholar), we designated the threshold for triggering the algorithm as a saturation <85% despite 100% FiO2. We further required these conditions for at least one hour, and with a PEEP of ≥10 mmHg, corresponding to existing standards for use of ECLS in acute respiratory distress syndrome (ARDS) (16.Hemmila MR Napolitano LM. Severe respiratory failure: Advanced treatment options.Crit Care Med. 2006; 34: S278-S290Crossref PubMed Scopus (11) Google Scholar). Given rapidly changing PaO2 (P) and FiO2 (F) in ICU patients, we chose PF ratio as the index f" @default.
• W1601423963 created "2016-06-24" @default.
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• W1601423963 date "2015-04-01" @default.
• W1601423963 modified "2023-09-26" @default.
• W1601423963 title "Proposed Management Algorithm for Severe Hypoxemia After Liver Transplantation in the Hepatopulmonary Syndrome" @default.
• W1601423963 cites W12184236 @default.
• W1601423963 cites W1507935366 @default.
• W1601423963 cites W1562659621 @default.
• W1601423963 cites W165010227 @default.
• W1601423963 cites W1851252178 @default.
• W1601423963 cites W1907054238 @default.
• W1601423963 cites W1957461957 @default.
• W1601423963 cites W1963994599 @default.
• W1601423963 cites W1966970386 @default.
• W1601423963 cites W1971638393 @default.
• W1601423963 cites W1979161727 @default.
• W1601423963 cites W1981141226 @default.
• W1601423963 cites W1981972882 @default.
• W1601423963 cites W1988534021 @default.
• W1601423963 cites W1992106406 @default.
• W1601423963 cites W1996096292 @default.
• W1601423963 cites W2015512789 @default.
• W1601423963 cites W2016930757 @default.
• W1601423963 cites W2020740200 @default.
• W1601423963 cites W2025883852 @default.
• W1601423963 cites W2026238033 @default.
• W1601423963 cites W2027869430 @default.
• W1601423963 cites W2029343919 @default.
• W1601423963 cites W2029421546 @default.
• W1601423963 cites W2029875994 @default.
• W1601423963 cites W2034848274 @default.
• W1601423963 cites W2036916867 @default.
• W1601423963 cites W2044777348 @default.
• W1601423963 cites W2047771803 @default.
• W1601423963 cites W2051516018 @default.
• W1601423963 cites W2051966447 @default.
• W1601423963 cites W2059365729 @default.
• W1601423963 cites W2060512234 @default.
• W1601423963 cites W2065306596 @default.
• W1601423963 cites W2067113337 @default.
• W1601423963 cites W2069068605 @default.
• W1601423963 cites W2070694153 @default.
• W1601423963 cites W2071529489 @default.
• W1601423963 cites W2072525890 @default.
• W1601423963 cites W2073782478 @default.
• W1601423963 cites W2074754069 @default.
• W1601423963 cites W2079788379 @default.
• W1601423963 cites W2084539273 @default.
• W1601423963 cites W2087169287 @default.
• W1601423963 cites W2088850345 @default.
• W1601423963 cites W2089143275 @default.
• W1601423963 cites W2089854019 @default.
• W1601423963 cites W2095098706 @default.
• W1601423963 cites W2095182002 @default.
• W1601423963 cites W2100970861 @default.
• W1601423963 cites W2104355052 @default.
• W1601423963 cites W2106923828 @default.
• W1601423963 cites W2109835681 @default.
• W1601423963 cites W2116973481 @default.
• W1601423963 cites W2130439372 @default.
• W1601423963 cites W2133681530 @default.
• W1601423963 cites W2158432078 @default.
• W1601423963 cites W2172232110 @default.
• W1601423963 cites W2221016545 @default.
• W1601423963 cites W2316052805 @default.
• W1601423963 cites W2318855670 @default.
• W1601423963 cites W2422848256 @default.
• W1601423963 cites W29392489 @default.
• W1601423963 cites W4242777265 @default.
• W1601423963 cites W2394900409 @default.
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