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Traditional One-Lung Ventilation & ALI; Have we been killing our Patients? Philip M. Hartigan, MD Brigham & Women’s Hospital Harvard Medical School. Case Report: 54 y/o male Smoking History COPD Persistent cough. Case Report: . CXR - Large RUL mass Cytology = NSCCA
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Traditional One-Lung Ventilation & ALI; Have we been killing our Patients? Philip M. Hartigan, MD Brigham & Women’s Hospital Harvard Medical School
Case Report: • 54 y/o male • Smoking History • COPD • Persistent cough
Case Report: • CXR - Large RUL mass • Cytology = NSCCA • Metastatic w/u Negative • Scheduled for a Right • Pneumonectomy
CASE REPORT: • General Anesthetic: • Thoracic Epidural • A-Line • TIVA • L-DLT • VT =10 ml/kg • PEEP = O
CASE REPORT: • Hospital Course – POD # 2: • Dyspnea • Hypoxemia • Pulmonary Edema
CASE REPORT: • Hospital Course (cont.): • Respiratory Failure • Reintubation • PCWP < 16 cmH2O • Diuretics • Fluid Restriction • ARDS • MSOF • Death
“Traditional” OLV“Protective” OLV VT = 10 ml/kg VT = 6 ml/kg PEEP = 0 PEEP = 5 cmH2O
Impact: Incidence: 2 - 9% Mortality: 35 – 72% “ALI/ARDS is emerging as the most prominent cause of perioperative mortality following pulmonary resection as other complications have become better controlled” Peter Slinger 2006
Known Causes of ALI / ARDS: Infection Aspiration BPF Cardiac Failure Pulmonary Embolic events TRALI Other (pancreatitis, trauma, CPB…)
Nomenclature Post-Pneumonectomy Pulmonary Edema ALI following Pulmonary Resection Primary ALI following Thoracic Surgery Idiopathic ALI following Pulm Resection
Hypothesis: • “Traditional OLV Causes ALI “ • Extrapolated Evidence • Retrospective Studies • Animal Studies • Clinical Studies
Extrapolated Evidence: ARDS Literature: Reduced ARDS Mortality with Protective Ventilation VILI Literature: Volutrauma Atelectrauma Inflammatory Response Alveolar Systemic
“The finding of small changes in cytokine concentrations is in no way indicative of a causal link with outcome” Dreyfuss Didier, 2003
Hypothesis: • “Traditional OLV Causes ALI “ • Extrapolated Evidence – (Weak) • Retrospective Studies • Animal Studies • Clinical Studies
Retrospective Studies; Factors Associated w/ ALI: • High Perioperative Fluid Balance • Extent of Surgery • Side of Surgery (R > L) • Duration of Surgery • Alcoholism / Chemotherapy • Increased Vent Pressures/Volumes
Retrospective Studies: Van der Werff ‘97 190 Pts PIPs > 40 assoc. w/ Pulm Edema Licker ‘03 879 PtsVentilatory Hyperpressure Index Fernandez - 170 Pts VT assoc with -Perez ‘06 Resp Failure 8.3 vs 6.7 ml/kg
Risk Factors for Primary ALI • Licker, et al: AnesthAnalg 2003;97:1558 • Pneumonectomy • Excessive Fluid • Alcoholism • VentilatoryHyperpressure Index
Risk Factors for Primary ALI • Licker, et al: AnesthAnalg 2003;97:1558 • Pneumonectomy • Excessive Fluid • Alcoholism • VentilatoryHyperpressure Index • (P-Plateau > 10 cmH20 x Duration OLV)
Hypothesis: • “Traditional OLV Causes ALI “ • Extrapolated Evidence - (weak) • Retrospective Studies – (weak) • Animal Studies • Clinical Studies
Animal Studies: De Abreu , et al. AnesthAnalg 2003 Control – 2LV @ 8 ml PEEP = 2 Protect - OLV @ 4 ml PEEP = 2 Tradit’l – OLV @ 8 ml PEEP = 0
OLV in the Rabbit Lung Model De Abreu, et al. AnesthAnalg 2003; 96:220 PIP MPAP WG TXB2 2-LV (CTRL) Protect OLV Traditional OLV
Hypothesis: • “Traditional OLV Causes ALI “ • Extrapolated Evidence – (weak) • Retrospective Studies – (weak) • Animal Studies – (suggestive) • Clinical Studies
Clinical Studies: • Schilling, et al 2005 • Schilling, et al 2007 • Schilling, et al 2011 • Traditional vs Protective OLV: • ProinflammatoryCytokines • Inhalational Agents are protective
I Protective OLV and Inflammatory Mediators Schilling T, et al. AnesthAnalg 2005;101:957 Design: 32 Pts for thoracotomy OLV @ 5 vs 10 ml/kg PEEP = 0 BAL at 3 time points Findings: Traditional OLV was associated with: Proinflammatory cytokines Antiinflammatory cytokines
IL-8 TNF-a IL-10 sICAM VT = 10 ml/kg VT = 5 ml/kg Schilling ‘05
III Effect of Volatile Anesthetics on Systemic and Alveolar Inflammatory Response Schilling T, et al. Anesthesiology 2011;115:65 Design: 63 Pts for thoracotomy 21 – Propofol (4mg/kg/hr) 21 – Desflurane (1 MAC) 21 – Sevoflurane (1 MAC) OLV @ 7 ml/kg PEEP = 5 BAL before & after OLV Findings: Desfl & Sevo attenuate proinflammatory changes even with protective OLV compared to Propofol.
Hypothesis: • “Traditional OLV Causes ALI “ • Extrapolated Evidence – (weak) • Retrospective Studies – (weak) • Animal Studies – (suggestive) • Clinical Studies – (suggestive)
OLV Inflammatory Response ALI / ARDS Death
OLV • Unbalance Drainage • Chemo / XRT • Extent of Surgery • Duration of Surg • Alcoholism • Genetic • Unrecognized: • Infection • Aspiration • Emboli • TRALI • Cardiac • Pneumonectomy • Impaired Lymphatics • Excessive Fluids Inflammatory Response ALI / ARDS Death
Low VT PEEP Sevoflurane Desflurane OLV • Unbalance Drainage • Chemo / XRT • Extent of Surgery • Duration of Surg • Alcoholism • Genetic • Unrecognized: • Infection • Aspiration • Emboli • TRALI • Cardiac • Pneumonectomy • Impaired Lymphatics • Excessive Fluids Inflammatory Response Low FiO2 ALI / ARDS Death
The Balancing Act of OLV O2 CO2 Injury
II OLV & Inflammatory Mediators: PropofolvsDesflurane Schilling T, et al. Br J Anaesth 2007;99:368 Design: 30 Pts for thoracotomy 15 – Propofol (4mg/kg/hr) 15 – Desflurane (1 MAC) OLV @ 10 ml/kg PEEP = 0 BAL at 3 time points Findings: Desflurane attenuates the proinflammatory changes of non-protective OLV
TNF-a IL-8 IL-10 sICAM-1 Propofol Desflurane Schilling ‘07
Postulated Causes • VILI from “Traditional” OLV • Oxygen Toxicity • Hyperperfusion Stress Injury • Inflammatory Response to Surgery • Postoperative Hyperexpansion • Unrecognized, Known Etiologies
Known Causes of ALI / ARDS: Infection Aspiration BPF Cardiac Failure Pulmonary Embolic events TRALI VILI Other (pancreatitis, trauma, CPB…)
Factors Associated with ALI • High Perioperative Fluid Balance • Extent of Surgery • Side of Surgery (R > L) • Duration of Surgery • Alcoholism / Chemotherapy
Idiopathic ALI following Pulm Resection • 2-9% following pneumonectomy • 35 – 50% Mortality • Clinical / Histology resembles ALI/ARDS • Low PCWP, high alveolar protein • Diagnosis of Exclusion