The landscape of thoracic surgery is undergoing significant changes. The rate of surgical resection for nonsmall cell lung cancer has increased worldwide over the past decade owing to increased detection efforts and surgeries on high-risk patients who in the past would not have been deemed fit for surgery. Early detection and screening have effectively reduced the rate of pneumonectomy in favor of lesser resections, such as lobectomy and wedge resections. Lastly, improvements in surgical technique and technology in conjunction with improvements in perioperative care have reduced the early mortality rate [1–3].
The evolution of lung resection surgery reveals a track leading from open surgery to video-assisted thoracoscopic surgery and most recently to robotic lung resection. Disappointingly, despite this evolution in surgical technology, there have been no significant changes in regard to the mortality rate, length of hospital stay, or rate of pulmonary complications between the three approaches [4,5].
Pulmonary complications after lung resection remain a prime cause of mortality and present a spectrum of disease processes ranging from mild complications, such as atelactasis and pneumonia, to the more severe presentations of acute lung injury (ALI) and adult respiratory distress syndrome (ARDS). The incidence of ALI and ARDS varies according to the extent of resection with pneumonectomy carrying the highest incidence of 3–10% compared to 2–5% for lesser resections and a mortality rate of 25–60%. Multiple factors have been shown to be associated with pulmonary complications, of which the volume of intravenous fluids administered has attracted much attention [6–9].
Concern that intravenous fluids may exacerbate or even cause pulmonary complications has led to the widespread adoption of perioperative restriction of fluids for thoracic surgical patients. Restrictive fluid management incurs risks such as a hypovolemic state with impaired tissue perfusion which may result in organ dysfunction and in particular postoperative acute kidney injury (AKI). The risk of AKI has been underappreciated until recently. Data now show that the risk of AKI after lung resection surgery varies between 6 and 24% with a mortality rate from 0 to 19% [10▪,11,12,13▪].
The aim of this review is to highlight the impact of fluid management strategies on ALI and AKI in patients undergoing thoracic surgery.
THE CASE FOR RESTRICTIVE FLUID MANAGEMENT
The association between excessive fluid administration and development of ALI, ‘previously known as postpneumonectomy pulmonary edema (PPE)’, was first studied by Zeldin et al.  in their report of 10 patients who developed this complication following pneumonectomy. This was followed by an experimental dog model and was shown that after right pneumonectomy, PPE developed in six of 13 dogs following a Ringers lactate fluid bolus of 100 ml/kg followed by 100 ml/kg h−1 for 24 h. Of note, these dogs were ventilated with a tidal volume of 15 ml/kg. Clinical studies have subsequently corroborated these findings. Parquin et al.  reported that high intraoperative fluid load in excess of 2000 ml is an independent risk factor for PPE. Blank et al.  studied the incidence of all pulmonary complications including ALI/ARDS in 129 patients undergoing pneumonectomy and found perioperative administration of parenteral fluids of 2.7 liters followed by 1 ml/kg h−1 for 24 h to be an independent risk factor in a univariate analysis but not in a multivariable analysis and that 1 Unit of blood product increased the risk of pulmonary complication by 47%. In a multivariate analysis, Licker et al.  found two independent risk factors for ALI: the extent of lung resection with pneumonectomy carrying the highest risk and excessive fluid infusion consisting of 9.1 ml/kg h−1 intraoperatively followed by 1 ml/kg h−1 for 24 h. Although the authors attempted to limit the peak inspiratory pressure to less than 50 cmH20, they did not adopt a protective lung ventilation (PLV) strategy. Interestingly, when the authors compared this group of patients to a more recent group after implementation of PLV, they showed that the incidence of ALI/ARDS was markedly decreased despite no change in their fluid regimen between the earlier and later groups.
In patients who developed ALI/ARDS, excessive fluid volume administered was a common finding and has led to the widespread practice of perioperative restrictive fluids management. Recent literature, however, has further advanced our understanding of ALI and its relationship to fluid therapy. These findings have impacted current opinion that now views the optimal fluid regimen as more complex than simply restriction.
THE GENESIS OF PULMONARY EDEMA IN THORACIC SURGERY
The two main mechanisms for pulmonary edema development are an increase in pulmonary capillary hydrostatic pressure and/or an increase in capillary permeability. Addressing these mechanisms is critical to improve outcomes.
Hydrostatic edema and starling forces
The mechanism of fluid exchange between the microvascular and interstitial spaces remained poorly understood until 1896 when Ernest Starling presented the results of his experiment in an animal model. He concluded that fluid filtration and reabsorption between the capillaries and the interstitial space is determined by the difference between the capillary hydrostatic and osmotic pressures, and that, the capillary walls act as semipermeable membranes . Starling's forces are summarized in the following equation:
Equation (Uncited)Image Tools
Where Jv / A is the rate of fluid exchange per unit area of the vessel, Lp is the hydraulic permeability of the vessel wall, Pc – Pi is the difference in hydrostatic pressures between the capillary and interstitial fluid while
Equation (Uncited)Image Tools
is the difference in osmotic pressures between the capillary and interstitial fluid, σ is the reflection coefficient of the vessel wall to plasma proteins.
Conceptually, capillary hydrostatic pressure represents the chief filtration force, whereas capillary osmotic pressure represents the chief reabsorption force.
The pulmonary circulation is able to adapt substantial changes in cardiac output without an increase in pulmonary capillary pressure. This is achieved by several mechanisms including capillary recruitment and distention . In fact, until the left atrial pressure is doubled, the pulmonary capillary filtration does not markedly increase [19▪▪]. If adaptive mechanisms are overwhelmed, fluid starts to accumulate in the interstitium, in which the lymphatics then play an important role in fluid clearance. Lymph flow can increase five-fold to 10-fold in response to chronic elevations in interstitial pressure . Following an acute increase in hydrostatic edema, the rise in interstitial volume is limited by the low compliance of the interstitial compartment, limiting further accumulation of interstitial fluid. This protective mechanism is short-lived secondary to fragmentation of the proteoglycan skeleton of the interstitial matrix . The alveolar epithelial cells represent the last line of defense against pulmonary edema. Through the epithelial sodium channels (ENaCs), alveolar fluid clearance is enhanced and helps in the rapid resolution of alveolar edema. ENaCs are stimulated by β-adrenergic agonists with a potential future therapeutic role of these agents  and inhibited by endothelin-1 .
Pneumonectomy versus lesser resections
In a series of 1139 patients, ALI was diagnosed in 3.9%. The highest frequency was in patients who had extensive resections (12.9%) followed by pneumonectomy (6%), whereas in patients who had lobectomy, the risk was 3.7% .
It seems that the extent of the resection plays a very important role in the development of ALI after lung resection. In pneumonectomy, the whole cardiac output will be directed to the remaining lung. This volume in the presence of a decreased vital capacity may overwhelm the remaining lung's protective mechanisms resulting in a rise in the pulmonary capillary filtration pressure. And hence, a perioperative restrictive fluid management may be logical; this might not be the case following lesser resections. This was shown by the study by Waller et al. , in which pulmonary capillary pressure steadily declined after lobectomy compared to pneumonectomy (Table 1).
Nonpulmonary thoracotomy surgery
In surgeries like esophagectomy, the risk of pulmonary complications was related to the surgical approach with transthoracic carrying the highest risk and poor preoperative pulmonary status . In transthoracic approach for esophagectomy, an intraoperative and 5-day postoperative fluid regimen in excess of 8 liters was an independent risk factor for pulmonary complications .
Increased capillary permeability and acute lung injury
The American-European Consensus Conference on ARDS defined ALI and ARDS as a syndrome of inflammation and increased permeability that is acute in onset, associated with bilateral infiltrates on chest radiograph and hypoxemia [paO2 ≤300 mmHg for ALI and paO2 ≤200 for ALI regardless of positive end-expiratory pressure (PEEP)] with no evidence of left atrial hypertension or pulmonary capillary occlusion pressure of 18 mmHg or less . Therefore, pulmonary edema secondary to ALI is primarily the result of increased pulmonary capillary permeability and is associated with an increased ratio of edema to plasma protein content compared to cardiogenic pulmonary edema . Consequently, ALI can occur despite normovolemia and is exacerbated in states of fluid overload.
Fluid transport across capillary endothelium takes place through several pathways that include tight junctions, breaks in tight junctions, vesicular transport, and leaky junctions. The tight junctions allow transport of small water-soluble solutes (<2 nm in diameter) and are sealed by proteins linked to the cytoskeleton. Breaks in the tight junctions allow transport of larger water-soluble solutes up to 20 nm in diameter. Vesicular transport carries molecules up to 80 nm in diameter. Finally, leaky junctions associated with cell death allow transport of solutes up to 1330 nm in diameter. The luminal side of the capillary endothelium and the intercellular junction is lined by a complex network of glycosaminoglycans (GAGs) and proteins called the glycocalyx. The most prominent GAGs are heparan sulfate, chondroitin sulfate, and hyaluronic acid. The glycocalyx layer was recently found to play several important roles in capillary fluid dynamics. First, it acts as a molecular sieve for plasma proteins and hence, the difference in oncotic pressure between plasma proteins and interstitial space has been revised from the original Starling's equation with the glycocalyx now acting as the actual membrane. Second, it acts as a mechanosensor responsive to fluid shear stress (FSS) such that increases in capillary blood flow result in increases in capillary permeability. Heparan sulfate plays an important role in the transmission of this FSS through stimulation of endothelial nitric oxide synthesis (eNOs) [30,31].
VENTILATOR-INDUCED LUNG INJURY
The role of mechanical ventilation in precipitating increased capillary permeability and ALI has been the focus of interest for the last decade. The causative factors in ventilator-induced lung injury (VILI) involve both end-inspiratory and end-expiratory lung volumes.
End-inspiratory lung volumes
Gattinoni et al.  debated that high tidal volumes used during mechanical ventilation of normal lungs can increase the risk of VILI. They suggested that for stress rupture (barotraumas) to occur, the alveoli must be stretched beyond their maximal physiologic strain, that is, beyond total lung capacity. Importantly, Gattinoni et al. argue that such stress rupture can occur in ARDS patients mechanically ventilated at tidal volumes far below the 70 ml/kg total lung capacity. Gattinoni and Pesenti  publicized the concept of ‘baby lung’ based on computed tomography images, which showed that in adults with severe ARDS, the amount of lung that is actually aerated is only 200–500 g, which is equivalent to the lung tissue of a 5–6-year old. As the ‘baby lung’ is actually the lung that is at risk for VILI, tidal volumes needed to cause physical strain will be much lower than if calculated based on body weight. In fact, if this strain does not reach the level of physical rupture (barotrauma), it still causes stretch of the alveolar wall leading to upregulation of pulmonary cytokine production (biotrauma) and local inflammatory process of the lungs causing increased permeability and pulmonary edema as well as systemic inflammatory response and multiorgan system failure [34,35].
End-expiratory lung volume
Mead et al. found in a theoretical model that the pressure required to open a collapsed alveoli is far higher than those acting on an aerated alveoli and thus maintaining an open alveoli will cause far less stress (atelectrauma) on the alveolar walls. This concept led to the widespread adoption of PEEP, a ‘open up the lung and keep it open’ strategy ventilation [37,38].
Role of protective lung ventilation in mitigating ventilator-induced lung injury
The ARDS network study showed reduced mortality in ARDS patients who received PLV consisting of low tidal volumes, low inspiratory pressure, and PEEP . Instituting PLV into the intraoperative period as a prophylactic measure in patients requiring one-lung ventilation (OLV) was associated with a reduction in the incidence of ALI/ARDS from 3.7 to 0.9% together with a reduction in the incidence of atelactasis, fewer ICU admission, and shorter hospital stay . Large VT either alone or in conjunction with high intraoperative fluid load was an independent risk factor for postpneumonectomy respiratory failure in a retrospective study . This finding was also confirmed in a retrospective study on patients undergoing cardiac surgery in which VT more than 10 ml/kg of predicted body weight was associated with multiple organ failure and prolonged hospital stay . In a prospective study of cardiac and noncardiac surgical patients, large VT was not an independent risk factor for ALI, but a higher peak airway pressure was . Surfactant protein-D is an early marker for ALI/ARDS. Interestingly, application of PLV in ALI/ARDS patients was shown to attenuate the rise of this protein [43,44]. In an animal model, baseline capillary permeability increased by five-fold when PLa pressure increased from 7.5 to 15 cmH2O under PLV. Under standard ventilation (VT 6–8 ml/kg), the same rise of PLa resulted in an increase in capillary permeability by 15-fold [19▪▪]. These data show that although PLV may reduce the risk of permeability edema, it does not prevent it.
The case against restrictive fluid management in thoracic surgery
In concert with the current evidence questioning the value of restrictive fluid therapy as a prophylactic measure for ALI, recent literature brings in this debate the issue of AKI after lung resection surgery. Historically, the incidence of renal injury in thoracic surgical patients has been regarded as very low, with the Society of Thoracic Surgeons Database citing a rate of 1.4%. However, these data report only the incidence of patients requiring renal replacement therapy . As discussed below, the incidence of AKI as assessed by standardized criteria appears to be much higher.
In 2002, The Acute Dialysis Quality Initiative Group introduced a classification system of AKI termed RIFLE (risk, injury, failure, and loss and end-stage renal disease) . This classification system is based on increases in serum creatinine (SCr) and concomitant decreases in glomerular filtration rates (GFRs) and urinary output and has been validated in multiple studies . More recently, a new classification system of renal injury was described, namely the Acute Kidney Injury Network (AKIN) criteria  (Table 2). The difference between the two classification systems is that the AKIN introduced an absolute increase in SCr of 0.3 mg/dl as a diagnostic criterion for stage 1 disease. Using these criteria Ishikawa et al. recently reported an incidence of 5.9% in thoracic surgery patients [10▪]. Hobson examining a high-risk group of lung resection patients reported a 33% incidence of AKI .
Many clinicians question the clinical relevance of an apparently trivial increase in SCr (0.3 mg/dl). In a retrospective study, Basile showed worsened long-term outcomes in cardiothoracic patients developing postoperative AKI, even in stage 1, as compared to those patients with normal Scr values. In this study, the presence of post-thoracotomy AKI was associated with a hazard ratio of 1.6 for long-term survival. Of particular concern is the fact that even patients in whom the perioperative AKI resolved partially or completely still had a decreased long-term survival when compared to patients who maintained normal Scr values. This fact may be due to a progression of renal damage after normalization of the Scr, manifested by a decrease in the peritubular capillary density . In summary, it is important to recognize that mild perioperative rises in SCr represent an important outcome factor. To date, the cause of perioperative AKI remains elusive. It is likely that, similar to the lung injury, kidney injury is a multifactorial process. In general, it is currently accepted that anesthetics negatively impact the kidneys by decreasing GFR, urinary output, and sodium excretion . The operative procedure per se may unmask latent kidney disease caused by the patient's comorbidities such as hypertension, diabetes, or atherosclerosis. In addition, the general inflammatory state described after thoracic surgery may also impact the kidney. However, among all these causes, the perioperative fluid management is an important factor to consider in the cause of AKI. Both states of hypervolemia and hypovolemia may be associated with the development of AKI. In states of hypervolemia, the kidney's functional demands are increased. In the study of Hobson et al., the incidence of AKI after thoracic surgery was associated with an increased amount of crystalloid administration. However, those patients who received higher intraoperative fluid volumes had also longer surgical times. It remains unclear which factor had more negative impact on the kidney function. However, significant volume depletion with subsequent hypotension and decreased renal perfusion, in a high-risk patient and in the setting of a generalized inflammatory state (surgery), may promote the development of AKI such that it appears prudent to maintain adequate perioperative hemodynamics and avoid prolonged episodes of renal hypoperfusion [52,53].
THE CASE FOR ALTERNATIVE FLUID REGIMENS
Given the concerns with excess and inadequate fluid administration, alternative fluid practices are being explored.
One strategy to minimize both lung and kidney injuries during lung resection surgery is to apply PLV with a standardized fluid protocol targeting normovolemia. This approach resulted in no increase in the extravascular lung water (EVLW) compared to baseline and was associated with an improvement in cardiac index (CI)  and SCr. The fluid regimen consisted of maintenance fluids at 1.5 ml/kg h−1 in addition to replacement of deficit and blood losses. This maintenance rate continued in the postoperative period till patients are allowed to have oral intake . Although this approach was not goal-directed, it was able to maintain normal kidney function as shown by the stable SCr without an increase in EVLW.
The approach of goal-directed therapy (GDT) has been utilized in several types of surgeries to improve outcome with conflicting results. Recent meta-analyses on patients undergoing major abdominal and cardiovascular surgery showed decreased incidence of pneumonia, AKI, and other renal complications in patients who utilized GDT compared to those who received conventional or restrictive therapy [56–59]. In contrast, two recent randomized controlled studies on patients undergoing open abdominal aortic surgery and colorectal surgery failed to show benefit of GDT over conventional non-GDT on intensive care stay or length of hospital stay [60,61].
Although GDT showed controversial benefit in nonthoracic surgery, it is our opinion that it is a valuable approach in thoracic surgery, given the complexity of the problem of fluid resuscitation in this type of surgery.
CI has been the most common goal to achieve in GDT. Several methods were used to measure CI including thermodilution method using pulmonary artery catheter (PAC), transpulmonary thermodilution method (TTD) using PiCCO monitor (Fig. 1), transesophageal Doppler monitoring (TDM). GDT utilizing transpulmonary thermodilution was recently shown to be superior to thermodilution using PAC in a randomized controlled study on patients undergoing valve surgery . The utilization of TDM to achieve GDT in intubated patients undergoing abdominal surgery was shown to be associated with shorter hospital stay, faster return of gastrointestinal function, and fewer ICU admissions [63,64]. Diaper et al.  showed the utility of TDM in guiding fluid management in patients undergoing lung resection surgery.
EVLW was shown to be an independent predictor of survival in critically ill patients . Its application in thoracic surgery as an early monitor of ALI was performed in a prospective observational study and showed no change from baseline in patients who had PLV during OLV together with a non-GDT, normovolemic fluid regimen . The concern about the accuracy of single thermodilution measurement to estimate EVLW after lung resection was validated against double dye technique and found to be well correlated for up to 12 h .
Another approach to GDT is monitoring dynamic variables including stroke volume variation (SVV) and pulse pressure variation (PPV). These variables integrate the function of preload, respiratory variation, and conventional hemodynamics (blood pressure) in a dynamic form to assess fluid responsiveness. This approach was shown to be superior to conventional monitoring in major abdominal surgery in respect to hemodynamic stability, complication rate, and hospital stay . Two factors influence the use of these dynamic variables in thoracic surgery. First, its accuracy depends on the tidal volume given. In a recent study in cardiac surgery patients, tidal volume more than 7 ml/kg was found to be the most predictive of fluid responsiveness compared to lower tidal volumes . This will be hard to achieve in the era of PLV. Second, the benefit of dynamic variables in open chest surgeries tends to be controversial [70,71]. Encouragingly, a randomized controlled study on patients undergoing thoracotomy with OLV found that PPV was more predictive of fluid responsiveness in the group who received PLV with tidal volume less than 6 ml/kg compared to the group who received conventional therapy without PLV [72▪]. Recently, Haas et al. [73▪] showed that GDT utilizing SVV did not result in an increase in EVLW in patients undergoing thoracotomy for lung resection and esophagectomy with OLV under PLV.
CHOICE OF FLUIDS: CRYSTALLOIDS AND COLLOID SOLUTIONS
The debate on optimal perioperative fluid management in thoracic surgical patients is not complete without questioning the type of fluid used for maintenance as well as resuscitative purposes. However, the two main types of available fluids, crystalloid and colloids, have been considered as two different and opposing strategies employed to achieve this goal. The debate revolves around the issue of edema formation, including pulmonary edema, in situations in which large amounts of crystalloids are used versus the possibility of colloid-induced kidney dysfunction or coagulopathy in situations in which colloids are used as the main fluid regimen.
Colloids have also been classified based on their oncotic properties as hyperoncotic, and hypooncotic. The value of hyperoncotic colloids is that they are rapid plasma expanders, by their virtue of increasing the intravascular oncotic pressure and thus determining shifting of extravascular fluids into the bloodstream. As such, many researchers have considered hyperoncotic colloids as potentially having beneficial effects in patients with ARDS/ALI, by promoting the shift of lung water into the vascular compartment. In anesthetized animal models ventilated with high tidal volumes, infusion of hydroxyethyl starch (HES) solutions resulted in a decrease in the incidence of VILI and pulmonary edema as compared to infusion of crystalloid solutions [74,75]. In a surgical population, Verheij et al. compared the pulmonary effects of volume loading with 0.9% sodium chloride, gelatin 4%, HES 6%, or albumin 5% and found that HES decreased the pulmonary capillary permeability. Similar effects were demonstrated in a study on patients with early ARDS who were resuscitated with HES and were found to have a rapid improvement of their hemodynamics at no cost to the overall lung mechanics . However, other studies on surgical patients with ALI/ARDS have not suggested any pulmonary beneficial effects when using colloids versus crystalloids . Similarly, in patients with ALI after cardiac or major vascular surgery, loading with colloids or crystalloids had no impact on pulmonary mechanics, provided that fluid overload was prevented. More importantly, the recent Cochrane systematic review failed to prove any outcome benefit when fluid resuscitation was performed with colloids versus crystalloids [78▪▪]. However, it is important to underline that most of the randomized controlled trials included in the systematic review were performed on patients with sepsis or following nonthoracic surgeries, which limits the overall value for the thoracic anesthesiologist. In summary, colloid infusions appear to have a modest benefit on pulmonary mechanics but no overall survival benefit.
In this setting, the perioperative clinician is left with the question of the impact of colloids on kidney function. It has been suggested that hyperoncotic colloid use induces a hyperoncotic renal injury . This syndrome usually occurs when the high plasma oncotic pressure offsets the hydraulic pressure of glomerular filtration and thus suppresses urinary output . Another possible mechanism of colloid nephrotoxicity is the occurrence of kidney lesions such as osmotic nephrosis . In a prospective cohort study, Schortgen et al. found that resuscitation with hyperoncotic colloids was associated with a significantly higher rate of adverse renal events. These finding are in line with those of the VISEP trial. The study identified that HES therapy was associated with higher rates of AKI and requirement of renal replacement therapy as compared to Ringer's lactate . However, it must be emphasized that, in the above studies, large amounts of colloids were used (up to 34 ml/kg), thus potentially not providing enough free water at the glomerular level and potentiating the development of hyperoncotic syndrome. Similarly to the VISEP trial, another randomized, blinded trial, which included 798 ICU patients with severe sepsis, identified that fluid resuscitation with HES 130/0.42 is associated with a higher mortality at 90 days and an increased risk of requiring renal replacement therapy . In the recently published CHEST trial (The Crystalloid versus Hydroxyethyl Starch Trial) which included 7000 ICU patients randomized 1:1 to receive either 6% HES 130/0.4 or 0.9% sodium chloride, the investigators did not find any difference in 90-day mortality among the two groups but identified that the patients resuscitated with HES had a higher rate of renal replacement therapy . Ishikawa et al.[10▪] in their retrospective study in patients after lung surgery suggested a possible association between HES use and development of AKI. Few patients received HES in the study and, thus, this association should be regarded with caution.
In contrast to these studies, Sakr et al. demonstrated in a large multicenter observational study performed on critically ill patients that administration of HES had no impact on the renal function or the need for renal replacement therapy. However, in this study, the median use of HES was only 500 ml/day with a total maximal volume of 1000 ml over 2 days. Mahmood et al. demonstrated that volume expansion with 6% HES in combination with crystalloid, during openrepair of abdominal aortic aneurysm, had improved renal function and reduced renal injury as compared to volume expansion with 4% gelatin. Taking this approach further, Godet et al. evaluated the impact on renal function of 6% HES 130/0.4 in comparison to 3% gelatin in patients with baseline renal dysfunction undergoing open repair of abdominal aortic aneurysm. They concluded that resuscitation with HES had no adverse effects on renal function even in patients with baseline renal injury. It is important to emphasize that in all the studies showing no harmful renal effects of the modern 6% HES 130/0.4 molecule, colloids were used in combination with crystalloids and in total volumes not higher than the maximal manufacturer recommended dose of 20 ml/kg per day.
In conclusion, few studies address the issue of optimal fluid selection to be used in patients undergoing lung resection surgery. As such, most of the data are extrapolated from studies performed on septic, critically ill patients in ICUs or from patients undergoing cardiovascular surgeries. Evidence against reasonable use of the modern 6% HES 130/0.4, in a volume within the accepted limits, remains inconclusive. As such, it appears that HES is best used in combination with crystalloids, as part of a multimodal fluid resuscitation.
The current evidence shows strong support for PLV to reduce the incidence of ALI. In contrast, the widely used restrictive fluid therapy in lung resection surgery has limited supporting evidence and may pose risks on organ perfusion. Recent data suggest a significant incidence of kidney dysfunction after thoracic surgery. Alternative fluid strategies using euvolemia protocols or GDT as well as the use of colloidal solutions are being explored as opportunities to reduce the high morbidity following lung resection surgery.
Conflicts of interest
There are no conflicts of interest.
REFERENCES AND RECOMMENDED READING
Papers of particular interest, published within the annual period of review, have been highlighted as:
▪ of special interest
▪▪ of outstanding interest
Additional references related to this topic can also be found in the Current World Literature section in this issue (pp. 000–000).
1. Memtsoudis SG, Besculides MC, Zellos L, et al. Trends in lung surgery: United States 1988 to 2002. Chest 2006; 130:1462–1470.
2. Riaz SP, Luchtenborg M, Coupland VH, et al. Trends in incidence of small cell lung cancer and all lung cancer. Lung Cancer 2012; 75:280–284.
3. Strand TE, Bartnes K, Rostad H. National trends in lung cancer surgery. Eur J Cardiothorac Surg 2012; 42:355–358.
4. Gopaldas RR, Bakaeen FG, Dao TK, et al. Video-assisted thoracoscopic versus open thoracotomy lobectomy in a cohort of 13 619 patients. Ann Thorac Surg 2010; 89:1563–1570.
5. Louie BE, Farivar AS, Aye RW, Vallieres E. Early experience with robotic lung resection results in similar operative outcomes and morbidity when compared with matched video-assisted thoracoscopic surgery cases. Ann Thorac Surg 2012; 93:1598–1604.discussion 1604-1595.
6. Parquin F, Marchal M, Mehiri S, et al. Postpneumonectomy pulmonary edema: analysis and risk factors. Eur J Cardiothorac Surg 1996; 10:929–932.discussion 933.
7. Licker M, de Perrot M, Spiliopoulos A, et al. Risk factors for acute lung injury after thoracic surgery for lung cancer. Anesth Analg 2003; 97:1558–1565.
8. Alam N, Park BJ, Wilton A, et al. Incidence and risk factors for lung injury after lung cancer resection. Ann Thorac Surg 2007; 84:1085–1091.discussion 1091.
9. Marret E, Miled F, Bazelly B, et al. Risk and protective factors for major complications after pneumonectomy for lung cancer. Inter Cardiovasc Thorac Surg 2010; 10:936–939.
10▪. Ishikawa S, Griesdale DE, Lohser J. Acute kidney injury after lung resection surgery: incidence and perioperative risk factors. Anesth Analg 2012; 114:1256–1262.
A retrospective observational study of 1129 patients who underwent lung resection surgery. AKI was defined according to AKIN criteria. The incidence of AKI was 5.9%. This was associated with increased rates of reintubation, rates of mechanical ventilation, and longer hospital stay.
11. Golledge J, Goldstraw P. Renal impairment after thoracotomy: incidence, risk factors, and significance. Ann Thorac Surg 1994; 58:524–528.
12. Kushins S, Martin D, Phillips-Bute B, et al. The incidence of postpneumonectomy acute kidney injury is greater than/comparable to aortocoronary bypass surgery. Anesth Analg 2009; 108(SCA Suppl 78):1–104.
13▪. Licker M, Cartier V, Robert J, et al. Risk factors of acute kidney injury according to RIFLE criteria after lung cancer surgery. Ann Thorac Surg 2011; 91:844–850.
A retrospective analysis of 1345 patients who underwent lung resection surgery. AKI was defined according to RIFLE criteria. The incidence of AKI was 6.8% and that was associated with more frequent admission to the ICU, higher incidence of cardiopulmonary complication, and higher mortality rate.
14. Zeldin RA, Normandin D, Landtwing D, Peters RM. Postpneumonectomy pulmonary edema. J Thorac Cardiovasc Surg 1984; 87:359–365.
15. Blank RS, Hucklenbruch C, Gurka KK, et al. Intraoperative factors and the risk of respiratory complications after pneumonectomy. Ann Thorac Surg 2011; 92:1188–1194.
16. Licker M, Diaper J, Villiger Y, et al. Impact of intraoperative lung-protective interventions in patients undergoing lung cancer surgery. Crit Care 2009; 13:R41.
17. Starling EH. On the absorption of fluids from the connective tissue spaces. J Physiol 1896; 19:312–326.
18. West JB. Respiratory physiology: the essentials. Philadelphia:Wolters Kluwer/Lippincott Williams & Wilkins; 2008.
19▪▪. Dull RO, Cluff M, Kingston J, et al. Lung heparan sulfates modulate K(fc) during increased vascular pressure: evidence for glycocalyx-mediated mechanotransduction. Am J Physiol Lung Cell Mol Physiol 2012; 302:L816–828.
An elegant animal study of perfused rat lung preparations aiming to measure the effect of increasing capillary hydrostatic pressure on filtration coefficient. Various pressures were applied with standard and low tidal volume ventilation. The study highlights the safety margin for increases in capillary hydrostatic pressure, before filtration coefficient rises, and shows the role of tidal volume ventilation in capillary filtration and the role of heparan sulfate as a mediator of the capillary mechanotransduction.
20. Zarins CK, Rice CL, Peters RM, Virgilio RW. Lymph and pulmonary response to isobaric reduction in plasma oncotic pressure in baboons. Circ Res 1978; 43:925–930.
21. Miserocchi G, Negrini D, Passi A, De Luca G. Development of lung edema: interstitial fluid dynamics and molecular structure. News Physiol Sci 2001; 16:66–71.
22. Downs CA, Kriener LH, Yu L, et al. Beta-adrenergic agonists differentially regulate highly selective and nonselective epithelial sodium channels to promote alveolar fluid clearance in vivo. Am J Physiol Lung Cell Mol Physiol 2012; 302:L1167–1178.
23. Berger MM, Rozendal CS, Schieber C, et al. The effect of endothelin-1 on alveolar fluid clearance and pulmonary edema formation in the rat. Anesth Analg 2009; 108:225–231.
24. Kutlu CA, Williams EA, Evans TW, et al. Acute lung injury and acute respiratory distress syndrome after pulmonary resection. Ann Thorac Surg 2000; 69:376–380.
25. Waller DA, Keavey P, Woodfine L, Dark JH. Pulmonary endothelial permeability changes after major lung resection. Ann Thorac Surg 1996; 61:1435–1440.
26. Ferguson MK, Celauro AD, Prachand V. Prediction of major pulmonary complications after esophagectomy. Ann Thorac Surg 2011; 91:1494–1500.discussion 1500–1491.
27. Casado D, Lopez F, Marti R. Perioperative fluid management and major respiratory complications in patients undergoing esophagectomy. Dis Esophagus 2010; 23:523–528.
28. Bernard GR, Artigas A, Brigham KL, et al. The American-European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med 1994; 149:818–824.
29. Ware LB, Fremont RD, Bastarache JA, et al. Determining the aetiology of pulmonary oedema by the oedema fluid-to-plasma protein ratio. Eur Respir J 2010; 35:331–337.
30. Tarbell JM. Shear stress and the endothelial transport barrier. Cardiovasc Res 2010; 87:320–330.
31. Weinbaum S, Tarbell JM, Damiano ER. The structure and function of the endothelial glycocalyx layer. Annu Rev Biomed Eng 2007; 9:121–167.
32. Gattinoni L, Protti A, Caironi P, Carlesso E. Ventilator-induced lung injury: the anatomical and physiological framework. Crit Care Med 2010; 38:S539–548.
33. Gattinoni L, Pesenti A. The concept of ‘baby lung’. Intensive Care Med 2005; 31:776–784.
34. Halbertsma FJ, Vaneker M, Scheffer GJ, van der Hoeven JG. Cytokines and biotrauma in ventilator-induced lung injury: a critical review of the literature. Neth J Med 2005; 63:382–392.
35. Hegeman MA, Hennus MP, Heijnen CJ, et al. Ventilator-induced endothelial activation and inflammation in the lung and distal organs. Crit Care 2009; 13:R182.
36. Mead J, Takishima T, Leith D. Stress distribution in lungs: a model of pulmonary elasticity. J Appl Physiol 1970; 28:596–608.
37. Meade MO, Cook DJ, Guyatt GH, et al. Ventilation strategy using low tidal volumes, recruitment maneuvers, and high positive end-expiratory pressure for acute lung injury and acute respiratory distress syndrome: a randomized controlled trial. JAMA: J Am Med Assoc 2008; 299:637–645.
38. Briel M, Meade M, Mercat A, et al. Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: systematic review and meta-analysis. JAMA: J Am Med Assoc 2010; 303:865–873.
39. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med 2000; 342:1301–1308.
40. Fernandez-Perez ER, Keegan MT, Brown DR, et al. Intraoperative tidal volume as a risk factor for respiratory failure after pneumonectomy. Anesthesiology 2006; 105:14–18.
41. Lellouche F, Dionne S, Simard S, et al. High tidal volumes in mechanically ventilated patients increase organ dysfunction after cardiac surgery. Anesthesiology 2012; 116:1072–1082.
42. Fernandez-Perez ER, Sprung J, Afessa B, et al. Intraoperative ventilator settings and acute lung injury after elective surgery: a nested case control study. Thorax 2009; 64:121–127.
43. Eisner MD, Parsons P, Matthay MA, et al. Plasma surfactant protein levels and clinical outcomes in patients with acute lung injury. Thorax 2003; 58:983–988.
44. Determann RM, Royakkers AA, Haitsma JJ, et al. Plasma levels of surfactant protein D and KL-6 for evaluation of lung injury in critically ill mechanically ventilated patients. BMC Pulm Med 2010; 10:6.
45. Boffa DJ, Allen MS, Grab JD, et al. Data from The Society of Thoracic Surgeons General Thoracic Surgery database: the surgical management of primary lung tumors. J Thorac Cardiovasc Surg 2008; 135:247–254.
46. Bellomo R, Ronco C, Kellum JA, et al. Acute renal failure: definition, outcome measures, animal models, fluid therapy and information technology needs – the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care 2004; 8:R204–212.
47. Shaw A. Update on acute kidney injury after cardiac surgery. J Thorac Cardiovasc Surg 2012; 143:676–681.
48. Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care 2007; 11:R31.
49. Hobson CE, Yavas S, Segal MS, et al. Acute kidney injury is associated with increased long-term mortality after cardiothoracic surgery. Circulation 2009; 119:2444–2453.
50. Basile DP. Rarefaction of peritubular capillaries following ischemic acute renal failure: a potential factor predisposing to progressive nephropathy. Curr Opin Nephrol Hypertens 2004; 13:1–7.
51. Cousins MJ, Skowronski G, Plummer JL. Anaesthesia and the kidney. Anaesth Intensive Care 1983; 11:292–320.
52. Sanders G, Mercer SJ, Saeb-Parsey K, et al. Randomized clinical trial of intravenous fluid replacement during bowel preparation for surgery. Br J Surg 2001; 88:1363–1365.
53. Grocott MP, Mythen MG, Gan TJ. Perioperative fluid management and clinical outcomes in adults. Anesth Analg 2005; 100:1093–1106.
54. Assaad S, Perkal M, Kyriakides T, et al. Does liberalized fluid protocol increase lung water post lung resection surgery? Anesth Analg 2012; 114 (SCA Suppl):01–493.
55. Assaad S, Perkal M, Kyriakides T, et al. Liberalized fluid protocol and tissue perfusion biomarkers in lung resection surgery. Anesth Analg 2012; 114 (SCA Suppl):01–493.
56. Dalfino L, Giglio MT, Puntillo F, et al. Haemodynamic goal-directed therapy and postoperative infections: earlier is better. A systematic review and meta-analysis. Crit Care 2011; 15:R154.
57. Giglio M, Dalfino L, Puntillo F, et al. Haemodynamic goal-directed therapy in cardiac and vascular surgery. A systematic review and meta-analysis. Interact Cardiovasc Thorac Surg 2012; 15:878–887.
58. Corcoran T, Rhodes JE, Clarke S, et al. Perioperative fluid management strategies in major surgery: a stratified meta-analysis. Anesth Analg 2012; 114:640–651.
59. Prowle JR, Chua HR, Bagshaw SM, Bellomo R. Clinical review: volume of fluid resuscitation and the incidence of acute kidney injury – a systematic review. Crit Care 2012; 16:230.
60. Challand C, Struthers R, Sneyd JR, et al. Randomized controlled trial of intraoperative goal-directed fluid therapy in aerobically fit and unfit patients having major colorectal surgery. Br J Anaesth 2012; 108:53–62.
61. Bisgaard J, Gilsaa T, Ronholm E, Toft P. Optimising stroke volume and oxygen delivery in abdominal aortic surgery: a randomised controlled trial. Acta Anaesthesiol Scand 2012. [Epub ahead of print]
62. Lenkin AI, Kirov MY, Kuzkov VV, et al. Comparison of goal-directed hemodynamic optimization using pulmonary artery catheter and transpulmonary thermodilution in combined valve repair: a randomized clinical trial. Crit Care Res Pract 2012; 2012:821218.
63. Noblett SE, Snowden CP, Shenton BK, Horgan AF. Randomized clinical trial assessing the effect of Doppler-optimized fluid management on outcome after elective colorectal resection. Br J Surg 2006; 93:1069–1076.
64. Abbas SM, Hill AG. Systematic review of the literature for the use of oesophageal Doppler monitor for fluid replacement in major abdominal surgery. Anaesthesia 2008; 63:44–51.
65. Diaper J, Ellenberger C, Villiger Y, et al. Transoesophageal Doppler monitoring for fluid and hemodynamic treatment during lung surgery. J Clin Monit Comput 2008; 22:367–374.
66. Sakka SG, Klein M, Reinhart K, Meier-Hellmann A. Prognostic value of extravascular lung water in critically ill patients. Chest 2002; 122:2080–2086.
67. Naidu BV, Dronavalli VB, Rajesh PB. Measuring lung water following major lung resection. Interact Cardiovasc Thorac Surg 2009; 8:503–506.
68. Benes J, Chytra I, Altmann P, et al. Intraoperative fluid optimization using stroke volume variation in high risk surgical patients: results of prospective randomized study. Crit Care 2010; 14:R118.
69. Lansdorp B, Lemson J, van Putten MJ, et al. Dynamic indices do not predict volume responsiveness in routine clinical practice. Br J Anaesth 2012; 108:395–401.
70. Preisman S, Kogan S, Berkenstadt H, Perel A. Predicting fluid responsiveness in patients undergoing cardiac surgery: functional haemodynamic parameters including the Respiratory Systolic Variation Test and static preload indicators. Br J Anaesth 2005; 95:746–755.
71. Wyffels PA, Sergeant P, Wouters PF. The value of pulse pressure and stroke volume variation as predictors of fluid responsiveness during open chest surgery. Anaesthesia 2010; 65:704–709.
72▪. Lee JH, Jeon Y, Bahk JH, et al. Pulse pressure variation as a predictor of fluid responsiveness during one-lung ventilation for lung surgery using thoracotomy: randomised controlled study. Eur J Anaesthesiol 2011; 28:39–44.
A randomized controlled study of 49 patients undergoing lung resection surgery who were randomized into a PLV group or a conventional ventilation group. Both groups received fluid boluses and were monitored for PPV and cardiac output. PPV was more indicative of fluid responsiveness in the PLV group.
73▪. Haas S, Eichhorn V, Hasbach T, et al. Goal-directed fluid therapy using stroke volume variation does not result in pulmonary fluid overload in thoracic surgery requiring one-lung ventilation. Crit Care Res Pract 2012; 2012:687018.
A prospective study to evaluate the effect of goal-directed fluid therapy guided by SVV on the rate of accumulation of EVLW. The study included patients who require OLV for lung and esophageal surgery. It shows that SVV-guided GDT in thoracic surgery does not lead to fluid overload.
74. Huang CC, Kao KC, Hsu KH, et al. Effects of hydroxyethyl starch resuscitation on extravascular lung water and pulmonary permeability in sepsis-related acute respiratory distress syndrome. Crit Care Med 2009; 37:1948–1955.
75. Li LF, Huang CC, Liu YY, et al. Hydroxyethyl starch reduces high stretch ventilation-augmented lung injury via vascular endothelial growth factor. Transl Res 2011; 157:293–305.
76. Verheij J, van Lingen A, Raijmakers PG, et al. Effect of fluid loading with saline or colloids on pulmonary permeability, oedema and lung injury score after cardiac and major vascular surgery. Br J Anaesth 2006; 96:21–30.
77. van der Heijden M, Verheij J, van Nieuw Amerongen GP, Groeneveld AB. Crystalloid or colloid fluid loading and pulmonary permeability, edema, and injury in septic and nonseptic critically ill patients with hypovolemia. Crit Care Med 2009; 37:1275–1281.
78▪▪. Perel P, Roberts I. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev 2012:CD000567.
Systematic review of randomized clinical trials demonstrating no outcome benefit of colloid solutions used for resuscitation of septic and postoperative patients.
79. Honore PM, Joannes-Boyau O, Boer W. Hyperoncotic colloids in shock and risk of renal injury: enough evidence for a banning order? Intensive Care Med 2008; 34:2127–2129.
80. Baron J. Pharmacology of crystalloids and colloids. In: NATA, editor. Transfusion medicine and alternative to blood transfusion. R&J-Editions Médicales: Paris; 2000. pp. 123–137.
81. Cittanova ML, Leblanc I, Legendre C, et al. Effect of hydroxyethylstarch in brain-dead kidney donors on renal function in kidney-transplant recipients. Lancet 1996; 348:1620–1622.
82. Schortgen F, Girou E, Deye N, Brochard L. The risk associated with hyperoncotic colloids in patients with shock. Intensive Care Med 2008; 34:2157–2168.
83. Brunkhorst FM, Engel C, Bloos F, et al. Intensive insulin therapy and pentastarch resuscitation in severe sepsis. N Engl J Med 2008; 358:125–139.
84. Perner A, Haase N, Guttormsen AB, et al. Hydroxyethyl starch 130/0.42 versus Ringer's lactate in severe sepsis. N Engl J Med 2012; 367:124–134.
85. Myburgh JA, Finfer S, Bellomo R, et al. Hydroxyethyl starch or saline for fluid resuscitation in intensive carare. N Engl J Med 2012. [Epub ahead of print]
86. Sakr Y, Payen D, Reinhart K, et al. Effects of hydroxyethyl starch administration on renal function in critically ill patients. Br J Anaesth 2007; 98:216–224.
87. Mahmood A, Gosling P, Vohra RK. Randomized clinical trial comparing the effects on renal function of hydroxyethyl starch or gelatine during aortic aneurysm surgery. Br J Surg 2007; 94:427–433.
88. Godet G, Lehot JJ, Janvier G, et al. Safety of HES 130/0.4 (Voluven(R)) in patients with preoperative renal dysfunction undergoing abdominal aortic surgery: a prospective, randomized, controlled, parallel-group multicentre trial. Eur J Anaesthesiol 2008; 25:986–994.
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