REVIEW ARTICLE - Stanford Medicinemed.stanford.edu/.../Periop_Mgt_Emphysema.pdfFig 1. A model of the...

REVIEW ARTICLEMartin J. London, MD

Section Editor

The Perioperative Management of Patients With Severe Emphysema

Katherine P. Grichnik, MD, and Steven E. Hill, MD

SEVERE EMPHYSEMA IS A frequent coexistent conditionin surgical patients. It is a chronic obstructive pulmonary

disease (COPD), part of a heterogenous group of diseases thatalso includes chronic bronchitis and asthma; COPD is charac-terized by airflow obstruction and hyperinflation.1 Specifically,emphysema is anatomically defined by “abnormal, permanentenlargement of airspaces distal to the terminal bronchiole,accompanied by the destruction of their walls, and withoutobvious fibrosis.”2 More than 2.9 million people in the UnitedStates are affected by emphysema, and 13,000 people die eachyear.3,4 Patients are more likely to be older, male, and at thetime of diagnosis have commonly lost 50% to 70% of their lungfunction.4-7 Optimal perioperative anesthetic care requires re-view of the anatomy and pathophysiology of emphysema,knowledge of the therapeutic options, understanding the reac-tions of emphysema patients to surgical and anesthetic proce-dures, and an awareness of common perioperative problems.

ANATOMY AND PHYSIOLOGY OF PULMONARYEMPHYSEMA

Definitions/Anatomy

Anatomically, the bronchiole is divided into the lobularbronchiolus, the terminal bronchiolus, and the respiratory bron-chiolus8 (Fig 1). Emphysema is limited to the gas exchangingacinus consisting of the respiratory bronchiolus, the alveolarduct, and the alveolus itself. Pathologically, there are 5 recog-nized types of emphysema (Table 1).1,8-10

Primary etiologies for emphysema include tobacco use and�-1 antitrypsin deficiency. However, industrial exposure totoxins, air pollution, and recurrent prior respiratory illnessesmay also lead to emphysema.11 Pathologically, lung tissue may

be injured by proteinases12 (elastases) released from neutro-phils and alveolar macrophages, which are normally neutral-ized by antielastase inhibitors such as �-1 antitrypsin. Animbalance of elastase release (stimulated by smoking, infec-tion, and industrial exposure) to antielastase inhibitor produc-tion (�-1 antitrypsin deficiency or oxidative damage to �-1antitrypsin from smoke inhalation) can lead to lung tissueinjury and subsequent emphysema. Animal studies support thistheory as the experimental inhalation of exogenous elastase andcollagenase result in acinar destruction, remarkably similar tohuman emphysema.13

Other evidence suggests that a more intricate process ofpulmonary remodeling also occurs.14 Pathologic loss of tissuetensile strength because of bioengineering or structural fatiguein repetitively stressed tissues is postulated.15 Chronic inflam-mation may also play a role, mediated by different pathwayscompared with asthma.16,17 Macrophages, cytotoxic T cells, andneutrophils are found in bronchial biopsies and bronchoalveo-lar lavage; they can release proteases to break down connectivetissue in lung parenchyma.18-20 Additionally, COPD patientshave increased hydrogen peroxide concentrations in exhaledbreath condensates and increased breath and urinary concen-trations of 8-isoprostane, a marker for oxidative stress,21-23

which can promote COPD through enhancement of inflamma-tion and proteolytic injury.24,25

Physiology

The pathophysiology of emphysema is based on airflowobstruction9,10,26 because of decreased elastic recoil from lossof elastin, collagen, and surfactant at the level of the alveolus.Loss of structural protein from small airways produces dy-namic airway collapse on expiration. Airway inflammation,bronchospasm, and increased secretions additionally increaseairway resistance. The end result is delayed lung emptyingleading to increased lung volumes, mechanical compromise ofthe diaphragm, and markedly increased work of breathing. Theclinical consequence is incomplete exhalation with resultingintrinsic positive end-expiratory pressure (auto-PEEP) or dy-namic pulmonary hyperinflation (DPH) caused by retained gasvolume in the lungs. These phenomena can happen in patientswith normal lungs when mechanically ventilated at high rates,but are especially characteristic of patients with emphysemaduring mechanical ventilation.27

Patients with emphysema have chest radiographs character-ized by hyperinflated lungs, a flattened diaphragm, an increasedanterior-to-posterior diameter, an elevated rib cage, and a small

From the Department of Anesthesiology, Division of CardiothoracicAnesthesia, Duke Heart Center, Duke University Health Care Systems,Durham, NC.

Presented in part at the 23rd Annual Society of CardiovascularAnesthesiologist Meeting, Vancouver, British Columbia, Canada, May5-8, 2001.

Address reprint requests to Katherine P. Grichnik MD, Departmentof Anesthesiology, Duke University Health Care Systems, Box 3094,Durham, NC 27710, 919-681-6893. E-mail: [email protected]

© 2003 Elsevier Inc. All rights reserved.1053-0770/03/1703-0001$30.00/0doi:10.1016/S1053-0770(03)00059-4Key words: emphysema, anesthesia, lung volume reduction surgery,

dynamic pulmonary hyperinflation, barotrauma, pulmonary edema

364 Journal of Cardiothoracic and Vascular Anesthesia, Vol 17, No 3 (June), 2003: pp 364-387

vertical heart (Fig 2).28 Emphysema is often heterogenouslydistributed with asymmetric bullae formation or lobar predom-inance of emphysematous tissue (Fig 3). Clinically, pulmonaryfunction tests are characterized by a ratio of forced expiratoryvolume in 1 second (FEV1) to forced vital capacity (FVC) of�70%, a decreased diffusion capacity for carbon monoxide

(DLCO), an increased residual volume (RV), an increased func-tional residual capacity (FRC), and an increased total lungcapacity (TLC).29,30 Gas exchange is typically impaired withdecreased arterial oxygen tension and increased arterial carbondioxide tension. Etiologies for abnormal gas exchange includeventilation-to-perfusion mismatch, increased physiologic dead-

Fig 1. A model of the lung illustrating the types of emphysema. A�centriacinar emphysema, B�paraseptal emphysema, C�panacinar

emphysema, D�irregular or scar emphysema. Reprinted with permission.8

Table 1. The Characteristics of the Types of Emphysema

Type ofEmphysema Airway Location

Upper VersusLower Lung Heterogeneity Miscellaneous

Centrilobular Proximal Upper Heterogenous Associated with tobaccoPanacinar Throughout Lower Uniform Associated with alpha-1 antitrypsin

deficiencyParaseptal Periphery Both Heterogenous Increased spontaneous pneumothoraxIrregular Periphery primarily arises

in scar tissueBoth Heterogenous Arises in scar tissue

Bullous Peripheral Both Heterogenous Abnormally large airspace enlargement(�1 cm) in focal areas

365SEVERE EMPHYSEMA

space, increased work of breathing, decreased diaphragmaticfunction, and diminished diffusion capacity between the alve-olus and the microvasculature. Physiologically, patients mayhave pulmonary hypertension, elevated right ventricular (RV)dimensions, elevated RV diastolic pressures, and depressed RVejection fractions.31

Expected declines in pulmonary function occur over timeincluding decreases in FEV1 (average of 15-30 mL/yr), DLCO,and arterial oxygen and carbon dioxide tensions.32-34 Determi-nants of survival include age, arterial oxygen tension, andpostbronchodilator FEV1 at the time of diagnosis.33-38 Longi-tudinal studies report a 60% 10-year mortality after the diag-nosis of emphysema (Fig 4).33,35,39

MEDICAL AND SURGICAL THERAPIES

Medical Treatment

The goals of medical therapy for emphysema are to retardchronic disease progression, treat acute exacerbations40 andcontrol symptoms to improve quality of life (QOL).20,41 Med-ical management includes patient education and risk factoridentification,42 avoidance of environmental toxins or causativeagents (tobacco),43 prevention of infection, graded exercise andpulmonary toilet instruction,44 and pharmacologic treatment.45

Effective medications include bronchodilators (�-adrenergicagonists and anticholinergics),46 but the role of methylxan-thines is unclear with conflicting evidence for efficacy.47-51

Corticosteroid therapy is commonly used to treat acute diseaseexacerbations;52 there is no role for chronic inhaled adminis-tration to reduce disease progression as initially postulated.53-56

Antibiotic therapy is also indicated for acute disease exacerba-tion with purulent sputum production,57,58 and vaccinationagainst pneumococcal disease and influenza is recommended.59

Psychoactive drugs such as bupropion hydrochloride may aidin smoking cessation.60 Intravenous �-1 antitrypsin supplemen-tation is used to replace intravascular levels in the �-1 anti-trypsin-deficient patient, but it is unclear if this therapy pre-vents disease progression.61-63 Low-flow oxygen can improveexercise tolerance and quality of life and is the only medicaltherapy shown to improve survival in hypoxemic patients.64

New agents include leukotriene-receptor antagonists, drugswith anti-inflammatory and bronchodilating properties.65 Theyare currently indicated for asthma but may become useful foremphysema as well. Potential future therapy includes the de-velopment of antagonists to postulated cellular mediators ofemphysema, increased types of protease inhibitor agents, andmore specific anti-inflammatory drugs.66,67

Surgical Treatment: Lung Volume Reduction Surgery

Because medical therapy has been relatively ineffective inhalting the progression of emphysema, others have turned tosurgical attempts to both palliate and treat this disease.68-72

Early maneuvers included costrochondrectomy and transversesternotomy to improve thoracic mobility.73 With the under-standing that thoracic distention was the result of and not thecause of emphysema, others attempted to limit lung expansionwith thoracoplasty and phrenectomy or elevate the diaphragmwith pneumoperitoneum and abdominal constrictive belts.74-77

Procedures such as tracheal stents to stabilize the posteriormembranous trachea in expiration and denervation to relievebronchospasm and mucus formation have also been tried.78-83

These procedures were associated with high morbidity andunpredictable results.

The concept of anatomic surgical resection of nonfunctionallung tissue was introduced in the 1940s70 but was not com-monly performed until 1957, when Brantigan and Mueller

Fig 3. Chest computed tomography of a patient with severe em-

physema demonstrating peripheral bullous disease, right greater

than left.

Fig 2. Chest radiograph of a patient with severe emphysema

demonstrating lung hyperinflation, flattened diaphragms and a small

vertical heart.

366 GRICHNIK AND HILL

advocated bullectomy to treat emphysema.84,85 Although 75%of patients derived a clinical benefit from the procedure, therewas also a high mortality (18%) and a lack of objective data,preventing wide acceptance. Thirty years later, Cooper, Wak-abayashi, and Eugene86-89 revitalized this procedure with anoperation now known as lung volume reduction surgery(LVRS). The operation involves resection of 20% to 30% ofhyperinflated lung that should be noncontributory to effectiveventilation. Proposed benefits are improvement in elastic recoil,lung compliance, and chest wall conformation to reduce hyper-inflation and allow the resumption of a more normal diaphrag-matic position. Additionally, enhanced ventilation-to-perfusionmatching should occur in the remaining lung tissue to result inclinical improvements in pulmonary function.87-97

Initial studies reported significantly positive clinical re-sults,87,98 which led to LVRS being performed by many sur-geons worldwide.99 Short-term results from many nonrandom-ized studies and case series have been reported, most showingreduced hyperinflation and improved pulmonary function, ven-tilatory mechanics and exercise tolerance at 3 to 6 months afterprocedure.91,100-105 (Outcomes from 180 studies [1995-1999]have been well reviewed by Flaherty and Martinez.106) How-ever, only 4 randomized trials of lung volume reduction surgeryversus medical management have been reported and are pre-sented in Table 2.107-110

Others reported less significant clinical benefit and consid-erable morbidity including prolonged postoperative air leaks(greater than 7 days with some requiring reoperation), subcu-taneous emphysema (Fig 5A and B), pneumonia, pneumotho-rax, prolonged mechanical ventilation because of respiratoryfailure (reintubation rate of 19%-33%), arrhythmias, and gas-trointestinal dysfunction.111-115 Cardiac and cerebrovascularcomplications have also been reported.116,117

Mortality from this procedure may also be high. Initial30-day mortalities were reported to be 0% to 15% and causes

Fig 4. Comparison of 10-year survival rates in three groups of

subjects with chronic airway obstruction. Group I subjects had asth-

matic bronchitis, Group II subjects had mixed features of various

disease states including chronic bronchitis, asthma and emphysema,

Group III subjects had the emphysematous form of COPD. Copyright

© 1987 Massachusetts Medical Society. All rights reserved. Repro-

duced with permission.33

Table 2. Selected Controlled Studies of LVRS Versus Medical Therapy

BaselineValues 30 Day 3 Months to 6 Months 12 Months 24 Months

36Months

Study Variable No. Age FEV1

WalkTest

Mortality%

No.F/U FEV1

WalkTest

Mortality%

No.F/U FEV1

WalkTest

Mortality%

No.F/U FEV1

WalkTest

Mortality%

Mortality%

Criner108 BilateralMS

19 59 0.69 260 6* 15/19 0.85 321 9.4*

Medical 18 58.8 0.72 273 N/R 15/18 0.82 303 N/R

Geddes107 BilateralMS

23 62 0.74 210 17/6† 19/23 0.91 260 21 13/23 0.84 290 N/R

Medical 24 60 0.75 220 N/R 23/24 0.7 230 12 19/24 0.74 205 N/R

Meyers109 BilateralMS

65 66 0.58 249 N/R 51/65 0.87 11 45/65 0.91 15 17

Medical 22 65 0.62 264 N/R 22/22 0.52 0 17/22 0.57 20 46

Pompeo110 Uni- orbilateralMS

30 61.9 0.86 380 3.3 30/30 1.32 473 6.6 28/30 13.3

Medical 30 64.1 0.83 376 0 30/30 0.84 407 3.3 27/30 14.8

Abbreviations: LVRS, lung volume reduction surgery; No., number of patients; FEV1, forced vital capacity in 1 second; Walk test, 6-minute walktest or shuttle-walk test in meters; No. F/U, number of patients followed up as a fraction of the number of patients at baseline; bilateral MS,bilateral median sternotomy lung volume reduction surgery; Uni, unilateral; medical, medical management; N/R, not reported.

*In this crossover study, 1 patient died before surgery, and 13 patients crossed over to surgery after completion of the medical arm†Initial high mortality noted (5/15) with patients with very low DLCO and walk distance. Inclusion criteria were subsequently modified to exclude

these patients. 17% includes these patients and 6% does not.Adapted with permission.104

367SEVERE EMPHYSEMA

included respiratory failure, cardiac failure, sepsis, multiorganfailure, pneumonia, acute respiratory distress syndrome, andaspiration.113 There are limited long-term mortality data, withthe few studies reporting 18% to 68% mortality at 3 to 5 years(Table 3); causes additionally include cancer, suicide, gastro-intestinal bleeding, and pulmonary embolus.118

A review of 711 Medicare claims in 1995 revealed LVRSpatients suffered from prolonged hospital length of stay, a highreadmission rate, and high use of rehabilitation services.119,120

Review of the published data and data requested from centersperforming the surgery determined that the reported results

were compromised by small patient numbers, inadequate con-trols with variability in patient selection, baseline assessments,perioperative care, the type of surgery performed, definitions ofadverse outcomes, and duration of follow-up.120 In 1 study,60% of LVRS patients did not return for follow-up after sur-gery; it was discovered that 27% of the nonreturn patients haddied as compared with 3% of the patients who returned.120,121

The cost of LVRS was also considered. At a reimbursementrate of $31,398 per procedure, it was estimated that if LVRSwere performed on every eligible Medicare beneficiary thatalmost 1 billion dollars would be spent.122 Thus, the role andexpenses of LVRS were questioned, and, in January 1996,Medicare stopped funding for this procedure, citing inadequateevidence for efficacy and long-term benefit.123

Subsequently, a multicenter randomized prospective clinicaltrial has been designed and supported by the National Heart,Lung and Blood Institute, the Health Care and Finance Orga-nization (now known as the Centers for Medicare and MedicaidServices), and the Agency for Health Care Policy and Re-search.120,124,125 The purpose of the National Emphysema Treat-ment Trial (NETT) is to determine (1) whether surgical ormedical therapy is more efficacious for patients with emphy-sema with respect to short- and long-term improvement ofpulmonary function and quality of life, (2) whether differentsurgical approaches (median sternotomy or thoracoscopy) areassociated with different outcomes, (3) the costs associatedwith this procedure over time.126 This trial was designed todefine who would and who would not benefit from LVRS.127-129

Similar studies are underway in Massachusetts (Overholt-BlueCross Emphysema Surgery Trial), Canada, and Great Brit-ain.104,130

Important concepts are emerging from the study of emphy-sema and the widely variable responses of patients to LVRS.The first NETT results examined 1033 patients and identified agroup of 69 patients at high risk of death compared withmedical management (relative risk [RR] � 3.9, 95%confidenceinterval [95%CI] � 1.9-9.0).131 They were patients with a lowpreoperative FEV1 and a uniform pattern of emphysema or alow DLCO. Others have also identified poor outcomes with ahomogenous distribution of emphysema,132,133 lower-lobeLVRS,118 a low DLCO, higher age, limited initial walk test,134

and pleural adhesions.107,114,116,135,136 In contrast, improved out-comes have been associated with emphysema heterogene-ity,133,137 upper- versus lower-lobe LVRS,118,137,138 bilateral ver-sus unilateral LVRS,103,139 and the use of buttressed staples forresection versus laser resection.140,141

Of concern is the finding that pulmonary function appears toimprove to maximal levels at 3 to 6 months and then re-gresses107,136,142,143 (Fig 6); in some, there was a correlationbetween the magnitude of short-term incremental improvementand the rate of deterioration in FEV1.144 When long-term datawere averaged, the rate of decline in FEV1 was 163 mL/y; itcould then be predicted that an average patient would return tobaseline FEV1 approximately 2 to 5 years postoperatively.These data suggest that surgery produced a one-time benefit butdid not modify the natural history of the disease. However, ithas been argued that the improved QOL with reduced dyspneais a long-lasting benefit of LVRS.103,145-148 QOL and dyspnea

Fig 5B. Subcutaneous emphysema after pulmonary surgery. Note

the prominent subcutaneous emphysema, especially on the right, in

the axillary tissue.

Fig 5A. Mechanism of soft-tissue emphysema following alveolar

disruption. Air from a torn alveolus (A) first enters perivascular in-

terstitium (B), dissection proximally within brochovascular sheath

toward the mediastinum (C). As mediastinal pressure rises, decom-

pression occurs in the cervical (D), subcutaneous and retroperitoneal

(E) soft-tissue spaces and may even cause pleural rupture producing

pneumothorax (F). Arrows indicate the direction of air movement.

Reprinted with permission.318


may be independent of FEV1 changes and more dependent onimprovements in other domains of the respiratory system.26,149

Other findings have included the development of pulmonaryhypertension in some patients,150 the observation that the con-tralateral lung function can improve after unilateral lung reduc-tion,151 the finding of variable arterial blood gas effects,152 anda lack of difference between a sternotomy versus video-assistedthoracoscopic approach.153,154 Still controversial is the amountof lung to resect.155 Severe hypercapnea may not be a contra-indication as initially determined.93,156

Independent of the NETT trial, others have sought reliablepredictors of who will benefit from LVRS. Preoperativeimaging techniques have been used for risk assessment butare variable among surgical centers.133,157,158 Highly quan-titative assessment of computed tomography scans can mea-sure volume and severity of emphysema versus normallung;136,159-162 scoring systems to assess the heterogeneityof emphysema distribution are proposed to correlate withLVRS outcome variables.163 The radiologic pattern of emphy-sema may also be prognostic as patients with centrilobular

Fig 6. Change in forced expiratory volume in one second (mL) over time. The median changes in FEV1 were obtained by comparing the

responses of each subject with his or her baseline values. Twenty-four patients underwent LVRS (surgical group) and 24 patients underwent

medical rehabilitation (medical group). P values are for comparison of the surgical group to the medical group at each point. The bars show 95

percent confidence intervals. Note the initial improvement in FEV1 at 3 months for the surgical group, which subsequently declines at

approximately the same rate as the medical group. Reprinted with permission.108

Table 3. Selected Studies of Long-Term Survival After LVRS

Study Population TechniquePerioperative

Survival % 2 Year % 3 Year % 4 Year % 5 Year %

Flaherty136 89 from 1994-1998 Bilateral MS 30 day � 94.4 89 82Gelb111 26 patients in 1995 Bilateral

VATS180 day � 96 81 69 54 42

Naunheim113 330, from 1993-1998 UnilateralVATS

30 day � 94.8 75 69

343, from 1993-1998 BilateralVATS

30 day � 93 81 74

Yusen118 200 patients, from1993-1998

Bilateral MS 90 day � 95.5 87 82 74 71

Abbreviations: MS, median sternotomy; VATS, video-assisted thoracic surgery.

369SEVERE EMPHYSEMA

emphysema may benefit more than patients with panacinaremphysema.164

Mechanical lung function may be prognostic. Dueck et al166

examined the improvement of preoperative flow limitation afterLVRS as an indicator of reduced dynamic pulmonary hyperin-flation (DPH) and correlated it to postoperative reductions inFRC and FRC/TLC.165 Similarly, preoperative auto-PEEP wasfound to correlate with postoperative FEV1.166 Improved post-operative workload was associated with reductions in pulmo-nary resistance, auto-PEEP, and WOB.167 However, Ingenito etal168 found that only preoperative inspiratory resistance corre-lated inversely with improved FEV1 after surgery.

The use of LVRS in patients with undiagnosed pulmonarynodules and/or isolated lung cancer is controversial.169 Inpathologic analysis of tissue from LVRS patients, a wide rangeof abnormal tissue including adenocarcinoma, bronchoalveolarmetaplasia, and carcinoid tumorlets has been found in tissuefrom LVRS patients.170,171 DeRose et al advocated LVRS com-bined with nodule resection and reported recurrent cancer inonly 1 of 14 patients at 1 year.172

Although the role of LVRS is not firmly established, it is alsobeing used in combination with other procedures to allowsurgery for patients deemed inoperable because of the severityof emphysema. LVRS has been performed in conjunction withcoronary artery bypass surgery, cardiac valvular surgery, andaortic aneurysm surgery.173-175

Future results from the NETT trial and similar trials in othercountries will clarify the questions of safety, efficacy, and costof LVRS surgery with emphasis on prognostic markers toidentify patients most able to benefit from the procedure.

Surgical Treatment: Lung Transplantation

The only other surgical alternative for treatment of severeemphysema is lung transplantation (LT), usually reserved forpatients not expected to live more than 2 years.13,176-178 Ingeneral, patients considered for LT have similar expiratory flowvolumes (FEV1 less than 30% predicted) to LVRS candidates;patients with relative contraindications to LVRS (such as ho-mogenous lung disease) may be considered for LT.178 Optimalcandidate selection criteria are presented in Table 4.

Thirty-nine percent of the total lung transplants performedfrom 1995 to 2001 were to treat COPD/emphysema using bothsingle and bilateral lung transplants (SLT, BLT).179-181 SLT isperformed most frequently to allocate the precious resource ofdonor lungs.176 However, BLT for emphysema may have anadvantage of preventing the remaining native emphysematouslung from “crowding out” the newly transplanted normal lungand may have better long-term outcomes.181

The major benefit of LT is that a patient can achieve near-normal lung function posttransplant, especially for BLT.181,182

Maximal gains in FVC and FEV1 occur 6-12 months afterLT181 in contrast to LVRS, at which time decline in lungfunction may be occurring. If lung function does decline, it isusually related to infection or rejection, not native diseaseprogression.183 BLT is characterized by normal spirometry,oxygenation, and ventilation with resolution of thoracic hyper-inflation; a mild restrictive defect may remain.184,185 SLT pul-monary function differs because of the physiologic interactionwith the native diseased lung; acutely, mediastinal shift mayoccur with hemodynamic compromise. Chronically, a biphasicexpiratory flow pattern is observed with high initial flow fromthe transplanted lung followed by slower terminal flow fromthe native diseased lung;178,186 hyperinflation of the thorax mayremain.187,188 Interestingly, the curvature of the diaphragm onthe transplanted side may return to normal with abnormalitiesremaining on the contralateral side.189 Despite these limitations,marked clinical and spirometric improvements (FEV1 im-proved from 0.49 L, 16% predicted to 1.6 L, 54% predicted) in1 study190 are seen; SLT recipients perform as well as BLTrecipients in some exercise testing.191

Potential complications of LT are multiple including acuteand chronic rejection, infection, primary organ dysfunction,development of bronchial strictures, gastroparesis, and thegradual development of obliterative bronchiolitis.192-195 Uniqueto SLT are (1) unchanged hyperinflation of the nativelung,196,197 (2) large ventilation-to-perfusion defect if severereperfusion injury of the transplanted lung occurs,198 and (3)lesions from the native lung (carcinoma, tuberculosis reactiva-tion, and infectious contamination) affecting the transplantedlung.178,179

Table 4. Selection Criteria for Lung Transplantation in Patients With Emphysema

Indications Contraindications Relative Contraindications

Severe emphysema, distribution less important Unresolved substance abuse Coronary artery diseaseFEV1 �30% predicted Severe coronary artery disease Mild renal insufficiencyRapid decline in oxygenation, ventilation Left ventricular dysfunction OsteoporosisDevelopment of secondary pulmonary hypertension Severe renal insufficiencySLT �65 years Hepatic dysfunctionBLT �60 years Active or recent cancer (except skin cancer)Ambulatory Viral infection with HIV, Hep B, Hep CBody weight 70-130% of ideal Acute illnessSix minute walk test �300 meters Mechanical ventilation*Global psychosocial risk assessment adequate

Abbreviations: FEV1, forced expiratory volume in 1 second; SLT, single-lung transplant; BLT, bilateral lung transplant; HIV, human immuno-deficiency virus; Hep B, hepatitis B virus; Hep C, hepatitis C virus; BiPAP, biphasic positive airway pressure. Data in table from Schulman.177

*Ambulatory patients with tracheotomy for nocturnal ventilation and patients using noninvasive ventilation such as BiPAP masks areacceptable candidates.


Perioperative mortality is 7% to 10%,178 and overall survivalfor lung transplantation in COPD/emphysema patients isgreater than 25% at 7 years with patients receiving bilaterallungs having a survival advantage (Fig 7).179 Early mortality isusually from infection or primary graft failure,179 and latemortality is usually from bronchiolitis obliterans or infec-tion.179,200 As with LVRS, the relative survival risk of LT foremphysema versus medical therapy has been questioned.Hosenpud et al201 compared survival after LT (65% at 3 years)versus survival of patients on the waiting list for LT (70% at 3years) and found that the relative risk of LT for emphysemanever dropped below the risk of waiting. However, the analysismay be confounded by the common practice of placing patientson a lung transplant waiting list in anticipation of needing atransplant after a long waiting period.178 The health-relatedQOL was also not examined; similar to LVRS, patients aftertransplant report significant improvements in wellbeing.202

Because organ supply is limited and waiting time for LTcandidates continues to increase, LVRS versus LT has beenexamined. In a comparison of SLT, BLT, and LVRS, superiorpulmonary function was found with LT: 79% improvement inFEV1 after LVRS versus 231% after SLT and 498% after BLT;similar results in exercise tests and oxygenation were reported.203

LVRS was performed on 20 patients awaiting LT; 95% sur-vived at 32 months and 75% improved enough not to need

LT.204 Similarly, Meyers et al performed LVRS on 99 patientspotentially eligible for LT; 59% of survivors did not need to belisted for LT.205 Cost must also be considered: LVRS costsapproximately $31,000 with few postprocedural expenses,whereas lung transplantation costs $108,000 with an estimated$1000/month medication cost.206 Other considerations forLVRS versus LT include the age of the patient, the risks ofimmunosuppression and comorbid conditions that could ex-clude a patient from transplantation but not from LVRS (eg,pulmonary nodule);204,207 LVRS has been performed before LTas a bridge to transplant208 or at the time of SLT to prevent/treathyperinflation of the remaining native lung.209,210 Salvage ofrespiratory function by LVRS has been attempted in patientswith SLT who are incapacitated by bronchiolitis obliterans.211

ANESTHETIC, HEMODYNAMIC AND VENTILATORYMANAGEMENT OF THE PATIENT WITH EMPHYSEMA

Preoperative Evaluation

Initial preoperative inspection should assess the adequacy ofprior medical management as determined by optimization ofmedications, pulmonary toilet, and pulmonary rehabilitation.Absence of concurrent infection will augment a limited abilityto clear secretions postoperatively. Review of prior steroid usemay determine the need for use of steroids intraoperatively.

Fig 7. Survival after lung transplantation for COPD/emphysema: Adapted from the International Society for Heart and Lung Transplantation

1994-2001 data.178

371SEVERE EMPHYSEMA

Preoperative arterial blood gas analysis and pulmonary func-tion testing with and without bronchodilators can both deter-mine the sufficiency of medical therapy and assist in riskassessment.

Patients with severe COPD are at higher risk of seriouspostoperative pulmonary complications compared to patientswith mild COPD or no COPD (relative risk from 2.7 to 4.7).212-216

Additionally, upper abdominal and thoracic surgery are inde-pendently associated with decline in pulmonary function with a10% to 40% risk of postoperative pulmonary complica-tions.212,217 The value of spirometry, split lung function testsand mimicry of postoperative conditions have also been used toassess perioperative respiratory risk, as promulgated in manyanesthesia textbooks (Table 5).218,219 It has been suggested thatincreased risk is associated with an FEV1 or FVC less than 50%to 70% of predicted value or a ratio of FEV1 to FVC of lessthan 65%.220,221 However, such risk tables were constructedfrom methodologically flawed studies,222 use data acquiredabout thoracic surgical outcomes before improvements in an-esthetic care and surgical technique,223 and do not address therole of exercise tolerance in risk assessment.

Spirometry has been found to have a variable predictivevalue (RR of an abnormal finding from 0.9 to 4.0)212 and is notbetter than clinical findings in the prediction of respiratorycomplications.213,224-226 The use of a “risk score” such as thecardiorespiratory risk index is also not reliable.227 However, thecalculation of a predicted postoperative (ppo) FEV1 based onthe amount of lung to be resected may correlate with pulmo-

nary complications.228 Some also found preoperative partialpressure of arterial carbon dioxide (PACO2) �45 mmHg to bea predictor of risk.229,230 Exercise tolerance has been advocatedas one of the best predictors of pulmonary outcomes aftersurgical procedures.231-235

Slinger and Johnston236 have addressed the above concernsin a novel approach to risk stratification. They propose evalu-ation in three domains: respiratory mechanical function, car-diopulmonary reserve, and lung parenchymal function, anddescribe the most valid test(s) for prediction of respiratory riskin each.

Respiratory mechanical function is most accurately evalu-ated by the predicted postoperative FEV1 (ppo FEV1 in L �preop FEV1 in L [% lung resected � preop FEV1 in L]).Nakahara et al228 found that a ppo FEV1 40% of the predictednormal for a particular patient resulted in no postoperativerespiratory complications, whereas a ppo FEV1 �30% of nor-mal resulted in all patients needing postoperative mechanicalventilatory support.228

Cardiopulmonary function can be assessed simply by a6-minute walk test with oximetry and more completely with anassessment of maximal oxygen consumption and ppo maximaloxygen consumption (calculated as for FEV1).237 In 1 study of25 thoracic patients, patients with complications had a ppomaximal oxygen consumption of 10.6 mL/kg/min comparedwith patients without complications who had 14.8 mL/kg/min(p � 0.1); all patients with a ppo maximal oxygen consumptionof less than 10 mL/kg/min died.238 A 6-minute walk test of lessthan 2,000 feet correlated with an oxygen consumption of lessthan 15 mL/kg/min239 and thus may be associated with in-creased perioperative morbidity.

Lung parenchymal function is best assessed by a ppo DLCO

(calculated as for ppo FEV1). In a multivariate analysis of 376thoracic surgical patients, a ppo DLCO of �40% was associatedwith increased respiratory complications (p � 0.004); DLCO andFEV1 were largely unrelated indicators of risk and should beassessed independently.236,240

Should a patient fall into a high-risk category based on ppoFEV1, surgery does not need to be cancelled but additionaltesting, precautions and perioperative care may be indicated asin Table 6.236

Table 5. Assessment of Operative Risk Using Pulmonary Function

Tests

Testing PhasePulmonary Function

TestIncreased Operative Risk

Result

Whole-lung tests Arterial blood gas(room air)

PaCO2 �45 mmHgPaO2 �60 mmHg

Spirometry FVC �1.5 mL/kgFEV1 �50% of FVC

Lung volume VC �2LMVV �50% predictedRV/TLC �50%

Single-lung tests Right and leftindividual lungfunction testsof perfusionand ventilationusingradioisotopes

Predicted postoperativeFEV1 �0.85 L or �70%blood flow todiseased lung

Mimicpostoperativeconditions

Unilateral balloonocclusion of aright or leftpulmonaryartery

Mean PAP �40 mmHg,PaCO2 �60 mmHg, orPaO2 �45 mmHg

Abbreviations: PaCO2, partial pressure of arterial carbon dioxide;PaO2, partial pressure of arterial oxygen; FVC, forced vital capacity;FEV1, forced expiratory volume in 1 second; VC, vital capacity; MVV,maximum voluntary ventilation; RV/TLC, residual volume to totallung capacity; PAP, pulmonary artery pressure.

Data from.217,218,220

Table 6. A Suggested Approach to Anesthetic Management Based

on Preoperative Assessment of Risk

Predicted Postoperative FEV1

�40% 30%-40% �30%

Extubate in the ORif clinicallyindicated

Consider extubationbased on:

Staged weaning frommechanicalventilation

1. Exercise tolerance2. Assess ppo DLCO

3. V/Q scan4. Associated diseases

Establish effectivethoracic epiduralanalgesia

Abbreviations: FEV1, forced expiratory volume in 1 second; OR,operating room; DLCO, diffusion capacity for carbon monoxide; ppo,predicted postoperative; V/Q, ventilation to perfusion.

Reprinted with permission.235


Monitoring and Sedation

Monitoring selected for the patient with severe emphysemashould be tailored to the type and extent of the procedure whileaccounting for the severity of the pulmonary disease. In addi-tion to the usual American Society of Anesthesiologists mon-itors, an arterial cannula should be considered for most patients.Frequent arterial blood gases and the ability to rapidly identifyhemodynamic compromise are crucial. Central venous accessshould be considered for procedures with significant potentialfor third-space volume shifting or blood loss. However, caremust be taken to avoid unintentional pneumothorax as a com-plication of line insertion (ipsilateral internal jugular vein can-nulation for thoracotomy is preferred). Foley catheterizationshould be used for any operation that may require significantfluid administration.

While placing catheters, sedation should be given cautiouslyas patients may be very susceptible to respiratory depressionfrom sedatives241 and residual effects may create difficulty withemergence from anesthesia. The relationship between CO2

retention and lung mechanics in 311 patients with COPD andvarying degrees of hypercapnea was examined.242 At rest,patients with more hypercapnea (PaCO2 �55) had greaterhyperinflation, airflow obstruction, and respiratory pump dys-function that resulted in a significantly lower minute ventilationthan normocapnic patients, mostly because of a reduction intidal volume. Gross et al examined the effect of midazolam onchanges in minute ventilation in response to hypercapnea inpatients with and without COPD (Fig 8).241 Although bothgroups had a diminished minute ventilation response to hyper-capnea with midazolam, the patients with COPD had a moreprofound decrease, which lasted for a longer period of time. Alow-dose infusion of the short-acting agent propofol may be

advantageous over bolus administration of benzodiazepines inthis setting.

Choices of Anesthesia and Analgesia

Although the type of anesthetic administered is probably notas important as the expertise with which it is administered,every plan must take into account the difficulties of ventilationin this patient population. Regional anesthesia can and shouldbe considered when appropriate. Avoidance of high spinal orepidural block levels is desirable for patients who rely onintercostal muscles for ventilation to prevent dyspnea and car-bon dioxide retention. A combined regional and light generalanesthetic approach can be effective. Regional techniques (eg,epidural, intercostal, paravertebral blocks) can facilitate re-duced intraoperative opioid use and minimization of inhalationagents to decrease prolonged anesthetic effects.243

In developing a strategy for postoperative analgesia, consid-eration should be given to the expected duration of chest tubedrainage and/or the intensity of the postsurgical pain. Theepidural route is especially effective for procedures expected torequire more than 1 day of analgesia and procedures in whichdelayed return of gastrointestinal function may prevent oralanalgesic administration. In general, placement of the epiduralclose to the dermatomal level of the surgical incision canincrease the efficacy of the analgesics administered.244-246 Localanesthetic use in the epidural can minimize the need for opioidsand their respiratory depressant effects; it has been suggestedthat the combination of local anesthetic and opioids for syner-gism is most effective.247,248 Adequate inspiratory and expira-tory muscle function must be assured with local anesthetic usein a regional analgesic technique.

Paravertebral blocks,249 intercostal blocks,250,251 and intrathe-cal opioids252-254 are alternative techniques, especially usefulfor short-stay procedures. Paravertebral blocks can provideunilateral analgesia with local anesthetic, to allow avoidance ofopioids, less hypotension, and less urinary retention than epi-dural analgesia.255,256 Single administration paravertebralblocks provide effective analgesia for only 9 to 12 hours, butcatheter techniques can be used to extend the duration of theblock.257,258 Similarly, single administration intercostal blocksmay last 6 to 12 hours, although intercostal catheters can beused for a longer duration of analgesia.259,260 Intrathecal opioidsmay provide analgesia for up to 24 hours and intrathecalcatheters for prolonged analgesia have been used.261,262 Theoptimal technique for postoperative analgesia in the patientwith severe emphysema is not known.

Should parenteral and/or epidural opioids be administered,care must be taken to meticulously monitor respiratory func-tion, as patients may be uniquely susceptible to carbon dioxideretention from the ventilatory depressant effects of the opi-oids.263-267 Supplemental analgesics devoid of respiratory de-pression such as nonsteroidal antiinflammatory agents shouldbe considered if not contraindicated to limit the respiratoryeffects of opioid administration.268

A theoretical concern about thoracic epidural analgesia is thepotential to cause increases in bronchial tone and reactivitythrough pulmonary sympathetic blockade and respiratory mus-cle weakness, with adverse effects on ventilation.269 To inves-

Fig 8. The slope of the fall in the minute ventilation response to

carbon dioxide after midazolam administration over time.

Slope�difference in minute ventilation between normocapnea and

hypercapnea divided by the difference in carbon dioxide tensions,

min�minutes. At time 0, midazolam was administered. Figure de-

rived from data from Gross et al, with permission.240

373SEVERE EMPHYSEMA

tigate these concerns, Gruber et al270 examined 12 patients withsevere emphysema presenting for LVRS. Preoperative thoracicepidural anesthesia with bupivacaine was found to improvetidal volume, peak inspiratory flow rates and decrease pulmo-nary resistance as compared with baseline values. Similarly,Groeben et al269 found no increase in airway obstruction in 20patients with severe COPD undergoing breast surgery withhigh thoracic epidural blockade as the sole anesthetic.

Two large analyses support the use of regional analgesia forpatients to preserve pulmonary function in the perioperativeperiod. Richardson et al271 examined 55 studies using epiduralanalgesia, paravertebral, or extrapleural analgesia (grouped to-gether); intercostal block, cryoablation; intrapleural analgesia;and transcutaneous nerve stimulation. Spirometric function wasreported as the percentage of preoperative pulmonary functionthat was preserved. Paravertebral blockade preserved spiromet-ric function to 75% of preoperative values, whereas intercostalblockade and epidural analgesia preserved spirometric functionto 52% and 47%, respectively, of preoperative values. Statis-tical analysis was not attempted because of variable studymethods, and no comparison to intravenous analgesia wasmade.

In a more rigorous analysis, Ballantyne et al272 examined 65studies using epidural analgesia, intercostal blockade, localwound infiltration, and interpleural and intravenous analgesiaas compared with systemic opioid analgesia. They examinedrelevant clinical outcomes of atelectasis incidence, pulmonaryinfections, pulmonary complications, and postoperative arterialpartial pressure of oxygen (PaO2). Secondarily, spirometricfunction was assessed. Epidural opioid analgesia comparedwith systemic opioids reduced the incidence of atelectasis(relative risk [RR] � 0.53, 95% confidence interval [CI] �0.33-0.85, p � 0.01). Epidural local anesthetic analgesia com-pared with systemic opioids decreased the incidence of pulmo-nary infections (RR � 0.36, 95% CI � 0.21-0.65, p � 0.001),pulmonary complications (RR � 0.58, 95% CI � 0.42-0.80,p � 0.001) and resulted in a greater postoperative PaO2 (dif-ference at 25% correlation � 4.56, 95% CI � �9.0757 to0.0585, p � 0.047). In contrast to the findings of Richardson etal, no differences in spirometric function were evident with anyof the therapies. It can be concluded that regional analgesictechniques can improve pulmonary outcomes perioperatively,as compared with conventional intravenous analgesia. It hasbeen suggested that the recent trend of improved outcome inhigh-risk thoracic patients after pulmonary resection seems tobe related to the use of epidural analgesia.273 Thoracic epiduraladministration of bupivacaine has also been shown to attenuatesupraventricular tachyarrhythmias after pulmonary resection ascompared with epidural morphine alone.274

Anesthetic Induction

Induction must be carefully undertaken when general anes-thesia with endotracheal intubation is necessary. Initially, anextended period of denitrogenation is required. COPD patientsmay need 9 to 10 minutes to achieve an end-tidal fractionaloxygen concentration of 90% after breathing 100% oxygen,whereas patients with normal lung function take only 2 to 3minutes (Fig 9).275 This is likely because of ventilation-to-

perfusion and diffusion abnormalities in patients with severeemphysema.

Hemodynamic instability is commonly observed in thesepatients during induction. Severe hypotension has been re-ported (and perhaps underreported) on induction of anesthe-sia.13,276-281 This may be because of the occurrence of DPH;institution of positive-pressure ventilation (PPV); the inadver-tent application of positive end-expiratory pressure (PEEP);pneumothorax; vasodilatation from anesthetic agents; and/orsympathetic blockade from regional anesthesia, hypovolemia,and myocardial ischemia. It is important to avoid excessiveventilation immediately after induction as can occur with maskventilation or when confirming endotracheal tube placement byauscultation as overventilation can lead to pulmonary gas trap-ping (Fig 10). Hypoventilation with ventilator timing set for aprolonged expiratory phase after induction may be advanta-geous until the degree of pulmonary dysfunction under anes-thesia is determined.

The properties of the ventilator used may influence theintraoperative course of the patient. A volume-controlled ven-tilator will deliver a preset volume without regard for thepressure necessary to deliver that volume. Use of a pressure-limited ventilator has been advocated in the literature.282 Ifauto-PEEP or breath stacking should occur, the pressure-lim-ited ventilator will sense the accumulating pressure and re-spond by reducing the volume of the next breath; an alarm forlow minute ventilation will alert the anesthesiologist if thisphenomenon compromises minute ventilation. In the absenceof a pressure-limited ventilator, use of an ICU ventilator withan intravenous anesthesia technique may be used. Close mon-itoring of peak and mean airway pressures is important becausethese are surrogate measures for retained volume in the lungs.Flow-volume loops available on selected ventilators can di-rectly display breath stacking by observation of continuedexpiratory flow at the point of starting the next inspiration(Fig 11).

The risk of bronchospasm during an anesthetic in a popula-tion with obstructive lung disease has been estimated to be7.7/1,000 as compared with the overall rate of 1.7/1,000 pa-tients based on a retrospective analysis of 156,064 patients.283

There was a lower incidence with regional versus generalanesthesia, but bronchoscopy and mediastinoscopy were asso-ciated with more bronchospasm. Although many have recom-mended intravenous lidocaine to prevent intraoperative bron-chospasm,284,285 its efficacy remains to be proven.286-288 Upperairway reactivity is also important to control; inhalation agentsat various minimum alveolar concentration levels and nebu-lized bronchodilators can facilitate this goal.289

The modes of ventilation used may be critically important.Maintenance of a short I:E ratio has been shown to reducepulmonary hyperinflation auto-PEEP.290,291 Slinger et al292

showed the importance of I:E time management as the appli-cation of external PEEP to patients with auto-PEEP duringone-lung ventilation (OLV) did not increase the total PEEP ifexpiratory flow time was increased. Further, use of an end-expiratory pause (as is common for many operating roomventilators) will shorten the expiratory time period; increasedauto-PEEP and decreased arterial oxygenation can occur.293 A


Fig 9. End-tidal oxygraphy over time in patients with and without chronic obstructive pulmonary disease (COPD). FEO2 tidal fractional

oxygen concentration, ��patients without COPD, o�patients with COPD. Reprinted with permission.274

Fig 10. The development of dynamic pulmonary hyperinflation during mechanical ventilation and a representation of lung deflation during

apnea. FRC�functional residual capacity. Adapted with permission.308

375SEVERE EMPHYSEMA

simple maneuver is to intermittently disconnect from the ven-tilator to allow expiration of trapped pulmonary gas.

Intraoperative anesthesia may be achieved with short-dura-tion drugs and inhalation agents to facilitate rapid emergenceand reduce the possibility of excessive sedation or inadequateventilation.294 Nitrous oxide should be avoided because of therisk of expansion of a closed gas space within diseased lungsand to allow for changing fraction of inspiratory oxygen (FIO2)without changing anesthetic depth.295 The use of short- tointermediate-duration nondepolarizing neuromuscular block-ade agents can avert ill-timed coughing during the surgicalprocedure, reducing the risk of barotrauma and yet allowing fora rapid recovery of neuromuscular function.

Treatment of intraoperative hypoxemia with OLV may needto be carefully considered. Application of continuous positiveairway pressure (CPAP) to the nondependent lung may lead tolung expansion because of increased compliance in emphy-sema.291 A useful first maneuver is to do fiberoptic bronchos-copy to confirm correct dual-lumen endotracheal tube positionand remove secretions. Careful application of CPAP and PEEPmay then be considered with attention to lung hyperinflation;nondependent lung re-expansion is the ultimate treatment.More common is intraoperative hypercarbia with increasedventilation-to-perfusion mismatch, significant deadspace venti-lation, and the need for caution with ventilatory patterns.296

Extrathoracic endoscopic procedures using insufflation of car-bon dioxide (CO2) may also result in impaired CO2 excre-tion.297 Hypercarbia in the absence of severe acidosis andhypoxia is usually well tolerated but may require inotropicsupport or lidocaine treatment.115,298,299

Prolonged emergence and return to adequate respiratoryfunction may occur. Volatile agents in concentrations as low as0.1 minimum alveolar concentration can depress the ventilatoryresponse to hypoxia in normal patients and may have a more

profound effect in the patient with emphysema.300,301 It hasbeen shown that patients with COPD have a higher volume ofdeadspace and that PaCO2 is higher for spontaneously breath-ing patients under anesthesia using volatile agents comparedwith patients without COPD.241 The importance of successfullyextubating the patient with severe emphysema should bestressed.87,302 Spontaneous ventilation improves preload, avoidsincreased afterload, minimizes DPH, and should decrease stresson pulmonary suture lines in the setting of lung surgery.

Parenchymal air leaks are a common perioperative prob-lem,303 first encountered with initial lung re-expansion; highgas flows may be required to adequately ventilate the patient.291

Excessive air leak can compromise the ability to extubate thepatient and may lead to the need for prolonged chest tubedrainage.141 Experience from care of the LVRS patient suggeststhat hypercarbia may be expected in the postoperative period,with elevations of PaCO2 noted to 48 hours after sur-gery.291,296,304 PaCO2 greater than 70 mmHg may be treatedwith a short period of CPAP.

A period of postoperative ICU care or intensive postanes-thetic care unit observation should be considered for the patientwith severe emphysema to assure adequate pulmonary functionpostoperatively, assess the chest X-ray, optimize analgesia, andassess any issues related to the operation. ICU care shouldalways be considered after any major surgery, especially tho-racic or upper abdominal procedures, because these procedurescan cause significant pulmonary dysfunction (reduction inFRC, depression of respiratory drive, impaired mechanics ofventilation, impaired gas exchange) even in the absence ofemphysema.305 A longer than usual hospital length of stay canbe anticipated with an increased need for postoperative oxygenadministration.296

COMMON PERIOPERATIVE PROBLEMS

Dynamic Pulmonary Hyperinflation and Intrinsic PEEP

DPH and auto-PEEP, which occur as more ventilation isinspired than is expired, may occur with increased expiratoryairflow resistance (Fig 10). Three factors determine DPH andauto-PEEP: (1) the patient’s intrinsic respiratory system resis-tance and compliance, (2) added external resistance (endotra-cheal tube diameter, ventilator tubing, and devices), and (3)ventilatory pattern (frequency, tidal volume, inspiration-to-ex-piration time ratios, inflation volume, and end-inspiratorypause).292,306,309 These conditions are particularly dangerouswith OLV for thoracic surgery as the entire ventilatory demandis placed on a single dependent diseased lung. Hemodynamicconsequences include impaired venous return, a tamponade-like effect on the RV from hyperinflated lungs, compression ofthe alveolar blood vessels by elevated intra-alveolar pressures,and septal shift causing left ventricle dysfunction.281,310 Exces-sive DPH or auto-PEEP may cause cardiac arrest characterizedby electromechanical dissociation.276-281

DPH or auto-PEEP can be particularly challenging to man-age because most standard anesthesia machines or ICU venti-lator monitors do not readily detect progressively increasingintrathoracic volume;278 use of a flowmeter may allow detec-tion of interrupted expiratory flow (Fig 11). Bardoczky et al311

have correlated interrupted expiratory flow with the develop-

Fig 11. A flow-volume loop from a mechanically ventilated pa-

tient with emphysema. Flow is in liters/minute and pulmonary vol-

ume is in liters. Note that expiratory flow does not return to baseline

prior to inspiration, creating a situation in which dynamic hyperin-

flation or auto-PEEP could occur.


ment of auto-PEEP (sensitivity 0.78, specificity 0.91, predictivevalue 0.92) facilitating monitoring for DPH.311 On recognitionof this problem, the patient should be immediately discon-nected from the ventilator and allowed to exhale. Depending onthe amount of accumulated air, this may take many seconds tominutes. Hemodynamic parameters should improve with exha-lation, but resuscitative medications may be required.

Ducros et al312 evaluated the incidence of auto-PEEP in thissetting (Fig 12). They found that lung transplant candidateswith severe emphysema had high levels of auto-PEEP imme-diately after induction of anesthesia, which increased withOLV; they also maintained high levels of trapped air. Con-versely, patients with restrictive lung disease did not developsignificant auto-PEEP or trapped air at any time.

Barotrauma

Pulmonary barotrauma is defined as extra-alveolar air inlocations in which it is not normally found and can occur as theresult of a sustained increase in intramural pulmonary pressure,secondary to alveolar overdistention.306 In patients with highlevels of DPH and auto-PEEP, conventional ventilatory settings(such as a tidal volume of 10-12 mL/kg) may shift ventilationto the upper, less-compliant portion of a volume-pressurecurve, thus risking alveolar rupture with overdistention.306 Therisk of barotrauma increases with high intrapleural pressure,increased expiratory resistance because of an endotrachealtube, coughing, or “bucking” against the ventilator and highlevels of extrinsic PEEP. The hemodynamic effects of baro-trauma are similar to hemodynamic effects of DPH and mayinclude mediastinal shift toward the nontraumatized lung. In-creased inflation pressures in the nontraumatized lung canoccur because it is compressed by the volume of gas in thecontralateral intrapleural space.

Avoidance of barotrauma may be aided by the use of musclerelaxants, intermittent disconnection from the ventilator, a longexpiratory time, and close monitoring. Minimization of peakinspiratory and plateau airway pressures have been recom-mended,27,313 although others have found no correlation ofthese pressures to the incidence of barotrauma in acute respi-ratory distress syndrome (ARDS) patients.314 Ventilation withsmaller tidal volumes than traditionally used (6 mL/kg v 10-12mL/kg) is beneficial.315 The addition of a small amount ofexternal PEEP to prevent distal airway collapse in a sheepmodel also resulted in less inflammation and histologic in-jury,316 factors thought to predispose to barotrauma. Improvedclinical outcomes have been shown in patients with ARDS

Table 7. Lung-Protective Strategy for Reduction of Barotrauma in

Patients With Acute Lung Injury

Maneuver Recommended Value

Limit inspiratory drivingpressure (PPLAT-PEEPTOTAL)

�20 cm H2O pressure

Limit peak airway pressure �40 cm H2O pressurePressure-limited or

pressure-supportventilation

Pressure-controlled inverseratio ventilation if FIO2 �

0.5Relatively high PEEP (If

PEEPAUTO occurs, thenPEEPTOTAL � PEEPEXT �

PEEPAUTO)

PEEPTOTAL 2 cm H2Opressure � PFLEX

Frequent lung recruitmentmeasures

Hold continuous positiveairway pressure at 30-40cm H2O pressure for 40sec

Respiratory rate �30

Abbreviations: cm H2O pressure, centimeters of water pressure;FIO2, fraction of inspired oxygen; PPLAT, plateau pressure after inspira-tory pause; PFLEX, the inflection point corresponding to the upwardshift in the slope of the pressure-volume curve; PEEPAUTO, the differ-ence between alveolar pressure at end-expiration and airway pres-sure; PEEPEXT, PEEP applied externally to the respiratory circuit,PEEPTOTAL, PEEPEXT � PEEPAUTO.

Data from.315

Fig 12. Auto-PEEP and trapped air volume in patients during

two-lung supine, two-lung lateral, and one-lung lateral ventilation.

Group 1 patients had mild obstructive airways disease; they only

developed auto-PEEP with OLV and had minimal air trapping. Group

2 had severe emphysema; they had high levels of auto-PEEP after

induction of anesthesia, which increased with OLV; they also main-

tained high levels of trapped air. Group 3 had severe restrictive lung

disease (pulmonary fibrosis); they generated minimal auto-PEEP and

trapped air. Patients with severe obstructive disease are prone to

pulmonary air trapping unlike those with restrictive disease. Re-

printed with permission.310

377SEVERE EMPHYSEMA

using such “lung-protective strategies” based on individualpatient lung mechanics (Table 7).317

Intraoperative pneumothorax in the dependent ventilatedlung may be difficult to detect and can quickly become atension pneumothorax with positive-pressure ventilation.318,319

Emergent treatment includes resuscitative vasoactive medica-tions and relief of intrapleural pressure can be accomplishedrapidly by chest tube thoracostomy or a large-gauge IV cath-eter. It may be necessary to turn the patient supine for adequateresuscitation. Barotrauma can also manifest as pneumomedia-stinum, pneumoperitoneum, and subcutaneous emphysema(Fig 5A and B).320,321

Post–Lung Resection Pulmonary Edema

Pulmonary edema is a perioperative problem of significanceto anesthesiologists.322,323 The syndrome of post–lung resectionpulmonary edema (PLRPE) has been reported after 2% to 4%of pneumonectomy procedures (right � left), after 1% oflobectomies and after 0.1% to 0.2% of thoracoscopic surger-ies.322-324 Radiologic signs may appear before symptoms, withsymptoms most commonly occurring on postoperative days 2to 4. The syndrome is resistant to treatment, with a 30% to 50%mortality. Histologically, PLRPE is similar to the ARDS.PLRPE can occur with normal pulmonary capillary wedgepressure (PCWP),322,325 although the measurement of PCWPmay be difficult postpneumonectomy326 or in mechanicallyventilated patients with COPD.327 The physiology of PLRPE isunclear. The volume of fluid given to the patient has beenimplicated, with most authors citing Zeldin et al.328 However,this study examined only 10 pneumonectomy patients withPLRPE, and adequate fluid data were available on only 40% ofthe patients. Two other studies support the concept that peri-operative fluid administration greater that 2 L is associated withthe syndrome.329,330

However, the pathophysiology may not entirely rest on thefluid balance because postpneumonectomy pulmonary edemaalso occurs in patients without high perioperative fluidload.324,331,332 A comprehensive review by Slinger322 suggeststhat fluid therapy is only one of the contributing factors to thissyndrome; other potential mechanisms are presented in Table8.322,324,325,333-336

Risk factors that predispose the patient to PLRPE include aright pneumonectomy (because of disruption of differentiallymphatic drainage with R�L),337 increased perioperative pul-monary arterial pressures (in part because of hypoxemia, hy-percarbia, pain),322,338 perioperative volotrauma (large tidal vol-ume during OLV, mediastinal shift, and lung hyperinflation

postsurgery),339,340-343 prior radiation therapy,330 and resectionof normally perfused lung (acutely shunting that blood flow toremaining lung tissue).330

Perioperative fluid loading could aggravate the above mech-anisms and patient risk factors. Increased cardiac output, in-creased pulmonary artery pressures, and increased net filtrationpressure across the pulmonary capillary bed can result in fluidtranslocation to the pulmonary interstitial space. These princi-ples may also be important in nonthoracic surgery.344 Pulmo-nary edema correlated with patients who received more than 67mL/kg/d for various surgical procedures,345 and a 10% inci-dence of respiratory failure was documented in a study ofperipheral vascular patients, in which patients received morethan 6 L of fluid in 24 hours.346

Debate also exists about the type of fluid, especially colloidversus crystalloid. Among the proposed benefits of colloids areslower and perhaps less translocation of the fluid from theintravascular (IVC) space to the extravascular space(EVC).347,348 Improved tissue microperfusion with less endo-thelial swelling, resulting in improved tissue oxygen tension,has been presented.349 However, conflicting data exist becausesome investigators have found increased long-term mortalitywith colloid use in sepsis patients.350,351 Ernest et al348 foundthat colloid agents, once translocated to the EVC space, actu-ally increased the volume of that space in excess of the amountof colloid given in septic patients. Others found that colloidadministration can promote lung water retention in burn pa-tients.352 A meta-analysis of randomized clinical trials of iso-tonic crystalloid versus colloid fluid therapy found no differ-ence in pulmonary edema or mortality.353

The total volume of fluid seems to be a critical contributoryfactor for PLRPE. In the absence of a leaky capillary syndrome(as in sepsis or burns), a combination of crystalloid and colloidis one strategy to attempt to prevent PLRPE. A minimal amountof crystalloid can be initially administered with the understand-ing that much of this fluid will translocate to the EVC space.Further fluids can be administered as colloids to replace intra-vascular volume because less total fluid volume is needed. Thetotal amount of intravenous fluid to be given can be guided byindices of adequate volume status, such as urine output andCVP. Mild hypotension may not need to be treated with fluidboluses as positional changes and vasoactive agents can beused to support hemodynamics if urine output and CVP areadequate.

Other Potential Problems

Perioperative supraventricular arrhythmias are common(18%-25%); increased age, increased intraoperative blood loss,and extent of resection are risk factors.354-356 Atrial fibrillationwas found to be the most common arrhythmia; 80% convertedto normal rhythm by 3 days.354 Postoperative SVT is associatedwith a higher rate of ICU admission, longer hospital LOS, anda higher 30-day mortality.356 Although infrequent, cardiac isch-emia or infarction can occur as well.117

Pulmonary hypertension or right ventricular dysfunctionmay also occur after pulmonary resection.150,356,358 Postulatedmechanisms include an increase in pulmonary vascular resis-tance with a decrease in lung cross-sectional area, reactivevasoconstriction, an alteration of vasodilatory to vasoconstric-

Table 8. Postulated Mechanisms for Post–Lung Resection

Pulmonary Edema

Lymphatic disruption and surgical traumaAcute inflammatory reaction to operative lung collapse and re-

expansionLung capillary endothelial damageRelative oxygen toxicityIschemia/reperfusion injury of operative lungMicroembolizationRestricted pulmonary capillary volume in emphysema patients


tive mediators, and kinking of the pulmonary blood vessels.150

Pulmonary infection remains a devastating complication andmay be related to ability to mobilize secretions postopera-tively.20,40 Malignant hyperinflation of a nondependent lung hasbeen reported during chest surgery, thought to be because ofairway secretions and a noncompliant dependent lung.359 Thiscondition may also occur postoperatively with mechanical ven-tilation. In contradistinction, mediastinal shift and cardiac her-niation have also been reported, usually after pneumonectomy,usually because of an imbalance of intrathoracic pressure be-tween the operative and nonoperative thoracic cavities.360,361

SUMMARY

Emphysema may be commonly encountered in many surgi-cal populations. The pathophysiology rests on airspace enlarge-ment and obstruction to airflow, especially expiratory airflow.Medical therapy can ameliorate symptoms and improve exer-cise tolerance but not cure the disease. Surgical attempts to treatemphysema with LVRS remain investigational and lung trans-plantation is limited by donor availability. Unique anestheticconsiderations include the potential for dynamic pulmonaryhyperinflation, barotrauma, and pulmonary edema.

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