REVIEW URRENT C OPINION

Fluid management in the cardiothoracic intensive care unit: diuresis – diuretics and hemofiltration Giovanni Mariscalco a and Francesco Musumeci b

Purpose of review The present review discusses the current concepts of fluid management in cardiothoracic surgery, and its clinical implications with special reference to organ-related complications and their prevention. Recent findings Current strategies in fluid management for cardiothoracic patients, various fluid formulation, and the preventive strategies for minimizing fluid-related complications are described, with particular reference to new discoveries and controversies that have arisen from recent literature. Summary The optimal fluid management in cardiothoracic patients has not been settled. Results of recent clinical published trials highlight the need for minimizing fluid administration and attempting to use diuretics to achieve a negative fluid, although hypovolemia and hypoperfusion should be carefully considered. An individualized optimization of fluid status, using goal-directed therapy, has emerged as a possible preferable approach. The old debate between crystalloid and colloid solutions has been partially solved, as some colloids have demonstrated deleterious effect on renal function and coagulation system. Various preventive strategies have also emerged for minimizing fluid-related complications. Keywords cardiac surgery, diuretics, fluid management, prevention, treatments

INTRODUCTION Fluid therapy has been demonstrated to significantly influence the postoperative outcomes of cardiothoracic surgery patients, impacting on cardiac, intestinal, pulmonary, and renal functions [1–13]. Therefore, the optimal fluid management is of utmost importance, especially in elderly patients with severe comorbidities who are now frequently undergoing complex surgeries [8]. Practitioners are always walking a fine line between hypovolemia with end-organ hypoperfusion and congestive heart failure with the negative effects of tissue edema. The type, amount, and timing of fluid administration remain the subject of extensive debates. However, only a handful of studies address the issue of optimal fluid management in the setting of cardiothoracic surgery [13,14]. Highlighting the current strategies in fluid management for cardiothoracic patients, various fluid formulations, and preventive strategies for minimizing fluid-related complications are the objectives of the present review.

CLINICAL IMPLICATIONS OF FLUID MANAGEMENT Perioperative fluid therapy aims to maintain an adequate circulating volume, ensuring end-organ perfusion and oxygen delivery to the tissues [5,6]. Inadequate oxygen delivery and higher oxygenation extraction in the immediate period after surgery, has been demonstrated to independently prolong ICU stay and to adversely impact the patient outcomes [1–13].

a

Department of Heart and Vessels, Cardiac Surgery Unit, Varese and Department of Cardiac Surgery and Transplantation, S. Camillo Hospital, Rome, Italy b

Correspondence to Giovanni Mariscalco, MD, PhD, Department of Heart and Vessels, Cardiac Surgery Unit, Varese University Hospital, Via Guicciardini, 7, 21100 Varese, Italy. Tel: +39 347 9689055; fax: +39 0332 264394; e-mail: [email protected] Curr Opin Anesthesiol 2014, 27:133–139 DOI:10.1097/ACO.0000000000000055

0952-7907 ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

www.co-anesthesiology.com

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Intensive care and resuscitation

KEY POINTS  Fluid management is of primary importance in ameliorating outcomes in patients undergoing cardiothoracic surgery.  Inadequate or excessive fluid administration may lead to insufficient cardiovascular function promoting organ dysfunction caused by inadequate peripheral perfusion/oxygen delivery.  Minimizing fluid administration and the use of diuretics to achieve a negative fluid balance seem to be associated with better outcomes, although hypovolemia and hypoperfusion are constant risks, which should be avoided.  Colloid solutions have not been shown to have a distinct advantage over crystalloids in volume replacement; however, they can negatively affect kidney function.  Ultrafiltration and other RRTs provide beneficial effects in critically ill patients.

dysfunction syndrome [15,20–22]. In addition, the surgical trauma causes an obligatory impairment in gastrointestinal motility, which may theoretically be amplified both by hypovolemia (decreased splanchnic circulation) and fluid overload (decreased motility caused by fluid accumulation in the gastrointestinal wall and surrounding tissue) [22–25]. Congestion and volume overload can also lead to acute cardiac decompensation, especially in cardiac surgical patient with a preoperative reduced left ventricular function or postoperative myocardial stunning [26]. Fluid overload may theoretically increase cardiac demands contributing to ischemia, arrhythmia, or cardiac failure [16]. Hypovolemia because of an inadequate hydration increases the risk of AKI, and the maintenance of renal perfusion remains the most important prophylactic measure to protect renal function [10,11,27 ]. &

FLUID LOADING AND TYPE

Adverse outcomes are strictly related with inadequate or excessive fluid administration, which can lead to a reduced effective circulating volume, diversion of blood toward vital organs (brain and heart) while diminishing perfusion to the nonvital organs (gut, skin, and kidneys) [15]. Both hypovolemia and fluid overload may lead to insufficient cardiovascular function promoting organ dysfunction caused by inadequate peripheral perfusion/oxygen delivery [15–17]. In addition, many cardiac surgical patients present with volume overload because of the cardiopulmonary bypass (CPB) use [5,10,11]. As a consequence, an optimal balance between inadequate and excessive fluid administration is difficult to obtain in this patient setting, and acute lung injury (ALI), acute kidney injury (AKI), acute heart decompensation, and impaired gastrointestinal function are frequent complications [1,2,15]. Excess fluid administration increases pressure in the venous circulation and results in fluid loss from the intravascular space into the interstitial one [15]. In the setting of increased capillary permeability, a hallmark of ALI, pulmonary edema worsens as intravascular hydrostatic pressure rises and oncotic pressure falls [15,18,19]. Fluid overload may also contribute to gut and cerebral edema. Intestinal edema leads to tissue hypoperfusion, which is associated with impaired gastrointestinal function intolerance to enteral nutrition, increased potential for the development of enteral bacterial translocation, and the development of multiple organ 134

www.co-anesthesiology.com

Amount and type of fluid administered are the key elements for an appropriate fluid management in cardiothoracic surgery. Liberal or restrictive strategies and crystalloid or colloid solutions are the unsolved controversies.

‘Liberal’ and ‘restrictive’ fluid management In the past, the outdated premise of patient hypotension and dehydration due to insensible perspiration, urinary output, and the unpredictable intraoperative ‘third space’ fluid loss, lead to a ‘liberal’ policy of routine infusion of a large volume of fluids [28,29]. However, subsequent evidence emerged, demonstrating the improved outcomes in patients who received ‘restrictive’ fluid administration [30–33]. Furthermore, fluid loading was observed to minimally affect the anaesthesia-related hypotension, which is more appropriately controlled by vasopressor therapy [34,35]. Brandstrup et al. [30] enrolled 141 colorectal surgery patients, randomly allocated to either a restricted or a standard intraoperative and postoperative intravenous fluid regimen. The restrictive group received a mean volume of 2.7 litres, whereas the liberal one 5.4 litres, and it was affected by a lower postoperative complication rate (33 vs. 51%, P ¼ 0.02). There was no observed increase in renal complications in the restrictive group . Other studies were not able to confirm a superiority of the restricted fluid regimen compared with the liberal one [32,33]. However, no common definitions of ‘liberal’ and ‘restricted’ fluid management exist. As a matter of fact, Volume 27  Number 2  April 2014

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Fluid management in the cardiothoracic intensive care unit Mariscalco and Musumeci

Bundgaard-Nielsen et al. [31] performing a review of restrictive vs. liberal fluid therapy, and investigating its effect on postoperative outcome, identified seven randomized trials. The range of fluids administered in the liberal group was from 2750 to 5388 ml and in the restricted one from 998 to 2740 ml. Advantages in patient outcomes were different among studies, with controversial results [31]. In the cardiothoracic setting, hemodilution and increase in capillary permeability occurring with CPB are other factors to consider in the amount of fluid administration [10,11]. Vretzakis et al. [36] randomly assigned 172 cardiac surgery patients to a restrictive or liberal fluid regimen. Fluid restriction conferred a lower risk of blood transfusion (62 vs. 82%, P < 0.04) [36]. Conversely, Toraman et al. [37] in 1280 consecutive patients undergoing isolated coronary artery bypass grafting (CABG), observed that intraoperative volume overload increased blood transfusion and length of hospital stay.

Goal-directed fluid therapy Because of the controversial results between liberal vs. restricted fluid regimen, an individualized optimization of fluid management using goaldirected therapy (GDT), has emerged as a possible approach [38–41,42 ,43–46]. GDT summarizes the guidance of intravenous fluid and vasopressors with or without drugs by using cardiac output or related parameters to optimize circulatory status in the perioperative period. Shoemaker et al. [38] first reported the positive effect of GDT on outcome in noncardiac high-risk patients undergoing surgery. The anesthetic management consisted of early fluid loading with or without dobutamine to increase patient output. GDT based on pulmonary artery catheter-derived hemodynamic goals lead to a significant reduction of mortality in their protocol group [38]. Consonant data were reported by other groups adopting different hemodynamic monitoring solutions [38–41,42 ,43–46]. In a randomized controlled trial, McKendry et al. [44] assessed the impact of a nurse-driven hemodynamic optimization protocol in 174 postoperative cardiothoracic patients allocated to conventional fluid management or to GDT protocol guided by esophageal Doppler flowmetry to maintain stroke index more than 35 ml/m2. The treatment group revealed a significant reduction in hospital stay, from a median of 9 to a median of 7 days [44]. In a recent metaanalysis of five randomized trials with 694 cardiac surgery patients, Giglio et al. [47] demonstrated that GDT significantly reduced the cardiac and noncardiac complications [odds ratio (OR) 0.35; 95% confidence interval (CI) 0.14–0.90 and OR 0.31; &&

&&

95% CI 0.16–0.63, respectively], although hospital mortality was not impacted by GDT regimen (OR 0.68; 95% CI 0.19–2.38) [47].

Crystalloid and colloid solutions Another area of debate is the type of fluid to administer especially with reference to the long-standing controversy between crystalloids and colloids. Crystalloid solutions are associated with the expansion of extracellular volume potentially leading to tissue edema, whereas colloids [especially hydroxyethyl starch (HES)] with a greater impairment of the coagulation system, predisposing patients to bleeding [48]. Recently, Magder et al. [49] recruited 262 patients undergoing cardiac surgery randomly allocated to receive 250 ml boluses of 0.9% physiological saline or a 250 molecular weight 10% solution of HES. A nurse-delivered algorithm using central venous pressure and cardiac index obtained from pulmonary artery catheter was adopted [49]. HES group compared with the physiological saline group revealed a lesser use of catecholamine (11 vs. 29%, P ¼ 0.001), a lower rate of pneumonia and mediastinal infections (2 vs. 8%, P ¼ 0.03), and less cardiac pacing (3 vs. 11%, P ¼ 0.02) [49]. Hospital mortality, renal function, and blood transfusions were not impacted by the two types of fluids [49]. However, although colloids better maintain or even expand intravascular volume and regional tissue perfusion than crystalloids, a reduced risk of death in patients with trauma, burns, or following surgery has never been clearly demonstrated by colloids in comparison with crystalloids [48]. Hypertonic crystalloid solutions have also been proposed for restoring hemodynamic balance and removing the excess extravascular fluid following cardiac surgery [50,51]. Ja¨rvela¨ et al. [50] randomly assigned 40 CABG patients to receive either hypertonic saline 7.5 or 0.9% physiological saline as a single dose of 4 ml/kg over 30 min in the postoperative rewarming phase in ICU. Hypertonic saline demonstrated a strong diuretic action without adverse effects [50]. The same authors subsequently compared the effects of hypertonic saline (7.5%) vs. normal saline (0.9%) and 6% HES on extracellular fluid volumes in the early postoperative period after CPB [51]. Again, hypertonic saline stimulated the excretion of excess body fluid, suggesting its usefulness in the situation in which water overload administration is to be avoided, but the intravascular volume needs correction [51]. Sirieix et al. [52] prospectively enrolled 24 patients undergoing mitral valve repair, investigating the acute hemodynamic effects of hypertonic or colloid infusion in the immediate postoperative period. They concluded that postoperative infusion

0952-7907 ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

www.co-anesthesiology.com

135

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Intensive care and resuscitation

of hypertonic saline increased left ventricular preload and left ventricular ejection fraction [52]. The effects of hypertonic colloids have also been investigated. Sirvinskas et al. [53] studied the hemodynamic effects of 250 ml of 7.2% hypertonic HES compared with 500 ml of Ringer’s acetate in 80 CABG patients. The study demonstrated that 7.5% hypertonic HES solution has a positive effect on hemodynamic parameters and microcirculation, with higher diuresis, lower need for the infusion therapy in the first 24 postoperative hours, and lower total fluid balance without adversely influencing blood loss [53]. In conclusion, studies suggest that pulmonary permeability and function do not seem affected by the choice of fluid solution, and colloids exhibit longer lasting hemodynamic effects compared with hypertonic and isotonic saline [13,54–59]. Conversely, coagulation seems to be less impacted by crystalloids compared with high-molecular-weight and highly substituted HES [13,48,52].

differences in the primary outcome of 60-day mortality were observed; however, the conservative strategy of fluid management improved lung function and shortened ICU stay with ventilator dependency, without increasing nonpulmonary organ failures [2]. On the contrary, recent evidence suggests that synthetic colloid solutions negatively impact renal function [65–67]. Recently, Bayer et al. [68 ] prospectively recruited 6474 cardiac surgery patients receiving HES, gelatin, and crystalloids in the operating room and during ICU stay. After a propensity score matching, authors observed that total fluid requirement was 163 ml/kg in the HES group, 207 ml/kg in the gelatin group, and 224 ml/kg in the crystalloid group. The fluid intake was higher in the crystalloid group during the first 20 h only. More importantly, a greater use of renal replacement therapy (RRT) was noted in the HES and gelatin patients compared with patients who received crystalloids (OR 1.46; 95% CI 1.08–1.97 and OR 1.72; 95% CI 1.33–2.24, respectively) [68 ]. On the basis of these studies, minimizing fluid administration and avoiding colloid administration seem to have beneficial effects, especially in cardiac surgery patients with acute respiratory distress syndrome (ARDS) and concomitant AKI. Furthermore, a study of patients with ARDS and AKI found that a positive fluid balance was associated with an increased risk of mortality, and that diuretic therapy after AKI improved mortality among patients with ARDS [1]. &&

&&

PREVENTION AND TREATMENT OF FLUID MANAGEMENT COMPLICATIONS In order to minimize the complications related to fluid administration, preventive strategies and prompt treatments are of utmost importance.

Hydration Adequate hydration reduces the risk to develop AKI following cardiac surgery and prevent contrastinduced nephropathy [10,11,60]. Hydration decreases the activity of the renin–angiotensin system, reduces the level of other vasoconstrictive hormones, increases sodium diuresis, decreases tubuloglomerular feedback, prevents tubular obstruction, protects against reactive oxygen species, and dilutes the contrast media in the tubule, thus decreasing any direct nephrotoxic effect of the contrast agent on the tubular epithelium [60,61]. Several studies suggest that hydration with physiological saline infusions for 12 h both before and after catheterization is beneficial in preventing AKI [60–62].

Fluid administration The optimal fluid management for ALI and AKI is not settled. In addition, diuresis or fluid restriction may improve lung function, but could worsen extrapulmonary-organ perfusion [2,63,64]. In a recent randomized study [2], a comparison was made between a conservative and liberal fluid management in 1000 ALI patients. No significant 136

www.co-anesthesiology.com

Diuretics and other drugs promoting diuresis Urine output is a nonspecific measure of renal function. Clearly, if no urine is produced, then no glomerular filtration occurs [69,70]. However, urine output is influenced by several factors [69,70]. Although intraoperative diuresis is increased in response to fluid administration, intraoperative diuresis per se does not seem to predict the postoperative AKI in elective surgical patients [69,70]. Congestion and volume retention are the hallmark of fluid overload in ALI and acute heart decompensation, and loop diuretic therapy plays a leading role in their treatment. Diuretics may reduce AKI, prevent tubule obstruction, and decrease oxygen consumption [71]. Data have suggested that diuretic infusion is associated with better outcomes than the intermittent one, and continuous infusion in the perioperative period seems to promote a gentle and sustained diuresis in cardiac surgery patients [72]. However, Zacharias et al. [27 ] recently performed a meta-analysis investigating &

Volume 27  Number 2  April 2014

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Fluid management in the cardiothoracic intensive care unit Mariscalco and Musumeci

the interventions for protecting renal function in the perioperative period. Patients treated with diuretics compared with those not receiving that did not reveal any benefit in terms of reduced mortality and AKI (OR 2.49; 95% CI 0.80–7.74 and OR 2.39; 95% CI 0.68–8.47, respectively) [27 ]. Lassnigg et al. [73] enrolled a total of 126 patients with preoperatively normal renal function undergoing elective cardiac surgery, randomly receiving a continuous infusion of either ‘renaldose’ dopamine, continuous furosemide infusion (0.5 micrograms/kg per min), or isotonic sodium chloride as placebo, starting at the beginning of surgery and continuing for 48 h or until discharge from the ICU. Renal function parameters and the maximal increase of serum creatinine above baseline value within 48 h were determined [73]. Renal-dose dopamine was ineffective, and furosemide was even detrimental in the protection of renal dysfunction after cardiac surgery in this study [73]. Other drugs have been tested in promoting diuresis and preventing AKI, possibly reducing the fluid overload-related complications [10]. Dopamine failed to demonstrate any renoprotective effect, and it may even exacerbate renal tubular injury in the early postoperative period [74,75]. On the contrary, fenoldopam, increases renal blood flow in a dose-dependent manner, has been repeatedly observed to reduce AKI after cardiac surgery [76,77]. Atrial and brain natriuretic peptide have been demonstrated to mitigate renal dysfunction, improving natriuresis by increasing glomerular filtration rate, and inhibiting sodium reabsorption by the medullary collecting duct [76,77]. &

Ultrafiltration Ultrafiltration has emerged as an additional approach to volume removal in the acute heart failure, especially in the case of diuretic resistance, in which diuretics fail to adequately control salt and water retention despite dose escalation [78]. Ultrafiltration permits precise selection of the hourly rate of net fluid removal, offering a mechanism for rapid and controlled treatment of volume overload [78]. In addition, ultrafiltration limits the significant fluctuations in intravascular volume.

Renal replacement therapy Once kidney failure occurs and management with diuretics is insufficient, RRT is necessary. However, optimal timing of RRT initiation is unclear, remaining a subjective clinical decision [79 ,80]. Continuous RRT [i.e., continuous venovenous &

hemofiltration-(CVVH)] has been demonstrated to provide less hemodynamic perturbation than intermittent techniques (i.e., intermittent hemodialysis), especially in critically ill patients in which continuous regulation of fluid avoids cycles of volume overload and depletion [80]. Vidal et al. [81] analyzed data from 141 cardiac surgery patients who underwent RRT to determine the impact of CVVH strategy in patients with AKI and cardiogenic shock. Obtained data suggested that CVVH that was promptly initiated and continued as long as possible for the first 72 h postoperatively improved the patients’ outcome [81]. CVVH has also been observed to be superior in heart transplant recipients with reduced kidney function in comparison with furosemide [82].

CONCLUSION The management of fluid therapy is of utmost importance as it has been demonstrated to significantly impact multiorgan functions and postoperative outcomes of cardiothoracic surgery patients. However, the type, amount, and timing of fluid administration are still being debated and the subject of extensive research. Only a minority of studies address the issue of optimal fluid management in the cardiothoracic surgery setting. Both hypovolemia and fluid overload may lead to depressed cardiovascular function, which causes inadequate peripheral perfusion/oxygen delivery leading to organ dysfunction. Because of volume overload associated with CPB use, the optimal balance between inadequate and excessive fluid administration is difficult to obtain in cardiac surgery patients. Minimizing fluid administration and attempting to use diuretics to achieve a negative fluid balance is an important objective, especially in patients with ALI, AKI, and acute heart decompensation. Colloids seem to impact on renal function, inducing hyperoncotic renal injury along with an osmotic nephrosis. Once kidney failure occurs and management with diuretics is insufficient, ultrafiltration and CVVH should be considered.

Acknowledgements We thank Fondazione Cesare Bartorelli (Milan, Italy) for his support. Relationship with industry and financial disclosure: None. Conflicts of interest There are no conflicts of interest.

0952-7907 ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

www.co-anesthesiology.com

137

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Intensive care and resuscitation

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 1. Grams ME, Estrella MM, Coresh J, et al. Fluid balance, diuretic use, and mortality in acute kidney injury. Clin J Am Soc Nephrol 2011; 6:966–973. 2. Wiedemann HP, Wheeler AP, Bernard GR, et al., National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network. Comparison of two fluid-management strategies in acute lung injury. N Engl J Med 2006; 354:2564–2575. 3. 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. 4. 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. 5. Okano N, Miyoshi S, Owada R, et al. Impairment of hepatosplanchnic oxygenation and increase of serum hyaluronate during normothermic and mild hypothermic cardiopulmonary bypass. Anesth Analg 2002; 95:278– 286. 6. Jakob SM, Ruokonen E, Takala J. Assessment of the adequacy of systemic and regional perfusion after cardiac surgery. Br J Anaesth 2000; 84:571– 577. 7. Mythen MG, Webb AR. Perioperative plasma volume expansion reduces the incidence of gut mucosal hypoperfusion during cardiac surgery. Arch Surg 1995; 130:423–429. 8. Grover FL. The Society of Thoracic Surgeons National Database: current status and future directions. Ann Thorac Surg 1999; 68:367–373. 9. Kollef MH, Wragge T, Pasque C. Determinants of mortality and multiorgan dysfunction in cardiac surgery patients requiring prolonged mechanical ventilation. Chest 1995; 107:1395–1401. 10. Mariscalco G, Lorusso R, Dominici C, et al. Acute kidney injury: a relevant complication after cardiac surgery. Ann Thorac Surg 2011; 92:1539–1547. 11. Shaw A. Update on acute kidney injury after cardiac surgery. J Thorac Cardiovasc Surg 2012; 143:676–681. 12. Stephens RS, Shah AS, Whitman GJR. Lung injury and acute respiratory distress syndrome after cardiac surgery. Ann Thorac Surg 2013; 95:1122– 1129. 13. Habicher M, Perrino A, Spies CD, et al. Contemporary fluid management in cardiac anesthesia. J Cardiothorac Vasc Anesth 2011; 25:1141–1153. 14. Assaad S, Popescu W, Perrino A. Fluid management in thoracic surgery. Curr Opin Anesthesiol 2013; 26:31–39. 15. Grocott MPW, Mythen MG, Gan TJ. Perioperative fluid management and clinical outcomes. Anesth Analg 2005; 100:1093–1106. 16. Holte K, Sharrock NE, Kehlet H. Pathophysiology and clinical implications of perioperative fluid excess. Br J Anaesth 2002; 89:622–632. 17. Boldt J. Fluid management of patients undergoing abdominal surgery: more questions than answers? Eur J Anaesthesiol 2006; 23:631–640. 18. Ware LB, Matthay MA. The acute respiratory distress syndrome. N Engl J Med 2000; 342:1334–1349. 19. Sibbald WJ, Short AK, Warshawski FJ, et al. Thermal dye measurements of extravascular lung water in critically ill patients: intravascular Starling forces and extravascular lung water in the adult respiratory distress syndrome. Chest 1985; 87:585–592. 20. Selewski DT, Cornell TT, Blatt NB, et al. Fluid overload and fluid removal in paediatric patients on extracorporeal membrane oxygenation requiring continuous renal replacement therapy. Crit Care Med 2012; 40:2694–2699. 21. Falk JL. Fluid resuscitation and colloid-crystalloid controversy: new thoughts on an old debate. Crit Care Med 1991; 19:451–453. 22. Wilmore DW, Smith RJ, O’Dwyer ST, et al. The gut: a central organ following surgical stress. Surgery 1988; 104:917–923. 23. Holte K, Kehlet H. Postoperative ileus: progress towards effective management. Drugs 2002; 62:2603–2615. 24. Mythen MG. Postoperative gastrointestinal tract dysfunction. Anesth Analg 2005; 100:196–204. 25. Lobo DN, Bostock KA, Neal KR, et al. Effect of salt and water balance on recovery of gastrointestinal function after elective colonic resection: a randomised controlled trial. Lancet 2002; 359:1812–1818. 26. Siribaddana S. Cardiac dysfunction in the CABG patient. Curr Opin Pharmacol 2012; 12:166–171. 27. Zacharias M, Mugawar M, Herbison GP, et al. Interventions for protecting & renal function in the perioperative period. Cochrane Database Syst Rev 2013; 9:CD003590. A systematic review with meta-analysis covering all the aspects (drugs and other measures) for preventing AKI. 28. Shires T, Williams J, Brown F. Acute change in extracellular fluids associated with major surgical procedures. Ann Surg 1961; 154:803–810. 29. Roberts JP, Roberts JD, Skinner C, et al. Extracellular fluid deficit following operation and its correction with Ringer’s lactate. A reassessment. Ann Surg 1985; 202:1–8.

138

www.co-anesthesiology.com

30. Brandstrup B, Tonnesen H, Beier-Holgersen R, et al. Effects of intravenous fluid restriction on postoperative complications: comparison of two perioperative fluid regimens: a randomized assessor-blinded multicenter trial. Ann Surg 2003; 238:641–648. 31. Bundgaard-Nielsen M, Secher NH, Kehlet H. ‘Liberal’ vs. ‘restrictive’ perioperative fluid therapy: a critical assessment of the evidence. Acta Anaesthesiol Scand 2009; 53:843–851. 32. Holte K, Foss NB, Anderson J, et al. Liberal or restrictive fluid administration in fast-track colonic surgery: a randomized, double blind study. Br J Anaesth 2007; 99:500–508. 33. Holte K, Kristensen BB, Valentiner L, et al. Liberal versus restrictive fluid management in knee arthroplasty: a randomized, double-blind study. Anesth Analg 2007; 105:465–474. 34. Jackson R, Reid JA, Thorburn J. Volume preloading is not essential to prevent spinal-induced hypotension at Caesarean section. Br J Anaesth 1995; 75:262–265. 35. Norberg A, Hahn RG, Li H, et al. Population volume kinetics predicts retention of 0.9% saline infused in awake and isoflurane anesthetized volunteers. Anesthesiology 2007; 107:24–32. 36. Vretzakis G, Kleitsaki A, Stamoulis K, et al. Intra-operative intravenous fluid restriction reduces perioperative red blood cell transfusion in elective cardiac surgery, especially in transfusion-prone patients: a prospective, randomized controlled trial. J Cardiothorac Surg 2010; 5:7. 37. Toraman F, Evrenkaya S, Yuce M, et al. Highly positive intraoperative fluid balance during cardiac surgery is associated with adverse outcome. Perfusion 2004; 19:85–91. 38. Shoemaker WC, Appel PL, Kram HB, et al. Prospective trial of supranormal values of survivors as therapeutic goals in high-risk surgical patients. Chest 1988; 94:1176–1186. 39. Polonen P, Ruokonen E, Hippelainen M, et al. A prospective, randomized study of goal-oriented hemodynamic therapy in cardiac surgical patients. Anesth Analg 2000; 90:1052–1059. 40. Goepfert MSG, Reuter DA, Akyol D, et al. Goal-directed fluid management reduces vasopressor and catecholamine use in cardiac surgery patients. Intensive Care Med 2007; 33:96–103. 41. Reuter DA, Felbinger TW, Kilger E, et al. Optimizing fluid therapy in mechanically ventilated patients after cardiac surgery by on-line monitoring of left ventricular stroke volume variations. Comparison with aortic systolic pressure variations. Br J Anaesth 2002; 88:124–126. 42. Aya HD, Cecconi M, Hamilton M, Rhodes A. Goal-directed therapy in cardiac && surgery: a systematic review and meta-analysis. Br J Anaesth 2013; 110:510–517. A systematic review and meta-analysis involving five studies (699 patients) to determine the effects of perioperative GDT in cardiac surgery. GDT reduced the postoperative complication rate and total length of stay. 43. Brock H, Gabriel C, Bibl D, et al. Monitoring intravascular volumes for postoperative volume therapy. Eur J Anaesthesiol 2002; 19:288–294. 44. McKendry M, McGloin H, Saberi D, et al. Randomised controlled trial assessing the impact of a nurse delivered, flow monitored protocol for optimisation of circulatory status after cardiac surgery. BMJ 2004; 329:258. 45. Kastrup M, Markewitz A, Spies C, et al. Current practice of hemodynamic monitoring and vasopressor and inotropic therapy in postoperative cardiac surgery patients in Germany: results from a postal survey. Acta Anaesthesiol Scand 2007; 51:347–358. 46. Kapoor PM, Kakani M, Chowdhury U, et al. Early goal-directed therapy in moderate to high-risk cardiac surgery patients. Ann Card Anaesth 2008; 11:27–34. 47. Giglio G, Dalfino L, Puntillo F, et al. Hemodynamic goal-directed therapy in cardiac and vascular surgery. A systematic review and meta-analysis. Interact Cardiovasc Thorac Surg 2012; 15:878–887. 48. Perel P, Roberts I, Ker K. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev 2013; 2:CD000567. 49. Magder S, Potter BJ, De Varennes B, et al. Fluids after cardiac surgery: a pilot study of the use of colloids versus crystalloid. Crit Care Med 2010; 38:2017– 2023. 50. Ja¨rvela¨ K, Kaukinen S. Hypertonic saline (7.5%) after coronary artery bypass grafting. Eur J Anaesthesiol 2001; 18:100–107. 51. Ja¨rvela¨ K, Koskinen M, Kaukinen S, Ko¨o¨bi T. Effects of hypertonic saline (7.5%) on extracellular fluid volumes compared with normal saline (0. 9%) and 6% hydroxyethyl starch after aortocoronary bypass graft surgery. J Cardiothorac Vasc Anesth 2001; 15:210–215. 52. Sirieix D, Hongnat JM, Delayance S, et al. Comparison of the acute hemodynamic effects of hypertonic or colloid infusions immediately after mitral valve repair. Crit Care Med 1999; 27:2159–2165. 53. Sirvinskas E, Sneider E, Svagzdiene M, et al. Hypertonic hydroxyethyl starch solution for hypovolemia correction following heart surgery. Perfusion 2007; 22:121–127. 54. Sivak ED, Starr NJ, Graves JW, et al. Extravascular lung water values in patients undergoing coronary artery bypass surgery. Crit Care Med 1982; 10:593–596. 55. Karanko MS, Klossner JA, Laaksonen VO. Restoration of volume by crystalloid versus colloid after coronary artery bypass: hemodynamics, lung water, oxygenation, and outcome. Crit Care Med 1987; 15:559–566.

Volume 27  Number 2  April 2014

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Fluid management in the cardiothoracic intensive care unit Mariscalco and Musumeci 56. Ernest D, Belzberg AS, Dodek PM. Distribution of normal saline and 5% albumin infusions in cardiac surgical patients. Crit Care Med 2001; 29:2299–2302. 57. Verheij J, van Lingen A, Raijmakers PGHM, 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. 58. 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. 59. Verheij J, van Lingen A, Beishuizen A, et al. Cardiac response is greater for colloid than saline fluid loading after cardiac or vascular surgery. Intensive Care Med 2006; 32:1030–1038. 60. Erley CM. Does hydration prevent radiocontrast-induced acute renal failure? Nephrol Dial Transplant 1999; 14:1064–1066. 61. Rudnick MR, Kesselheim A, Goldfarb S. Contrast-induced nephropathy: how it develops, how to prevent it. Cleve Clin J Med 2006; 73:75–87. 62. Trivedi HS, Moore H, Nasr H, et al. A randomized prospective trial to assess the role of saline hydration on the development of contrast nephrotoxicity. Nephron Clin Pract 2003; 93:C29–C34. 63. Simmons RS, Berndine GG, Seidenfeld JJ, et al. Fluid balance and the adult respiratory distress syndrome. Am Rev Respir Dis 1987; 135:924–929. 64. Humphrey H, Hall J, Sznajder I, et al. Improved survival in ARDS patients associated with a reduction in pulmonary capillary wedge pressure. Chest 1990; 97:1176–1180. 65. 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. 66. 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. 67. 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. 68. Bayer O, Schwarzkopf D, Doenst T, et al. Perioperative fluid therapy with && tetrastarch and gelatin in cardiac surgery: a prospective sequential analysis. Crit Care Med 2013; 41:2532–2542. A prospective observational cohort study of 6478 patients subjected to CPB. Different fluid therapy approaches were tested (colloid vs. crystalloid vs. gelatin). Perioperative administration of colloids was associated with a high risk of RRT, and was no more effective than crystalloid regimen.

69. Alpert RA, Roizen MF, Hamilton WK, et al. Intraoperative urinary output does not predict postoperative renal function in patients undergoing abdominal aortic revascularization. Surgery 1984; 95:707–711. 70. Priano LL, Smith JD, Cohen JI, Everts EE. Intravenous fluid administration and urine output during radical neck surgery. Head Neck 1993; 15:208–215. 71. Rosner MH, Okusa MD. Acute kidney injury associated with cardiac surgery. Clin J Am Soc Nephrol 2006; 1:19–32. 72. Gandhi A, Husain M, Salhiyyah K, Raja SG. Does perioperative furosemide usage reduce the need for renal replacement therapy in cardiac surgery patients? Interact Cardiovasc Thorac Surg 2012; 15:750–755. 73. Lassnigg A, Donner E, Grubhofer G, et al. Lack of renoprotective effects of dopamine and furosemide during cardiac surgery. J Am Soc Nephrol 2000; 11:97–104. 74. Park M, Coca SG, Nigwekar SU, et al. Prevention and treatment of acute kidney injury in patients undergoing cardiac surgery: a systematic review. Am J Nephrol 2010; 31:408–418. 75. Patel NN, Rogers CA, Angelini GD, Murphy GJ. Pharmacological therapies for the prevention of acute kidney injury following cardiac surgery: a systematic review. Heart Fail Rev 2011; 16:553–567. 76. Landoni G, Biondi-Zoccai GG, Marino G, et al. Fenoldopam reduces the need for renal replacement therapy and inhospital death in cardiovascular surgery: a meta-analysis. J Cardiothorac Vasc Anesth 2008; 22:27–33. 77. Nigwekar SU, Navaneethan SD, Parikh CR, Hox JK. Atrial natriuretic peptide for management of acute kidney injury: a systematic review and meta-analysis. Clin J Am Soc Nephrol 2009; 4:261–272. 78. Mun˜oz D, Felker GM. Approaches to decongestion in patients with acute decompensated heart failure. Curr Cardiol Rep 2013; 15:335. 79. Tolwani A. Continuous renal-replacement therapy for acute kidney injury. & N Engl J Med 2012; 367:2505–2514. A detailed review describing pathophysiology, effect, and clinical implications of continuous RRT with its current guidelines. 80. John S, Eckardt KU. Renal replacement strategies in the ICU. Chest 2007; 132:1379–1388. 81. Vidal S, Richebe´ P, Barandon L, et al. Evaluation of continuous veno-venous hemofiltration for the treatment of cardiogenic shock in conjunction with acute renal failure after cardiac surgery. Eur J Cardiothorac Surg 2009; 36:572– 579. 82. Mirhosseini SM, Fakhri M, Asadollahi S, et al. Continuous renal replacement therapy versus furosemide for management of kidney impairment in heart transplant recipients with volume overload. Interact Cardiovasc Thorac Surg 2013; 16:314–320.

0952-7907 ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

www.co-anesthesiology.com

139

Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

Fluid management in the cardiothoracic intensive care unit: diuresis--diuretics and hemofiltration.

The present review discusses the current concepts of fluid management in cardiothoracic surgery, and its clinical implications with special reference ...
228KB Sizes 1 Downloads 0 Views