Fluid Management as an Adjunct to Enhanced Recovery After Surgery

Fluid management is central to enhanced recovery after surgery (ERAS) pathways and aims to enhance mean systemic filling pressure and venous return and avoid hypervolemia.

Fluid Overload and Organ Dysfunction

ERAS is a bundle of evidence supporting best practices for perioperative interventions to maintain physiologic function and enhance recovery after major surgery. Fluid management is a major component of ERAS, as it has been shown to reduce postoperative complications by half.^1,2

Fluid overload induces tissue edema, which results in impaired oxygen and metabolite diffusion, and obstruction of capillary blood flow and lymphatic drainage. Therefore, fluid overload is considered one of the main causes for perioperative morbidity and mortality.³

In a multicenter trial, 172 patients scheduled for colorectal resection were randomly assigned to either restricted fluid management to maintain preoperative body weight (a zero-balance regimen) or a standard intra- and postoperative fluid regimen. Postoperative complications were 30% in the zero-balance group versus 56% in the standard one, and there were no deaths in the zero-balance group, whereas 4 deaths were recorded in the group receiving standard fluids.⁶Nisanevich et al randomly assigned 152 patients undergoing intraabdominal surgery to either a liberal group (bolus 10 mL/kg followed by 12 mL/kg/hour) or restricted patient group (4 mL/kg/hour). There were statistically fewer postoperative complications in the restricted group.⁷

Patients in VASST (Vasopressin in Septic Shock Trial) who received higher fluid intake had a significantly higher risk for death.⁸ Furthermore, patients with negative mean daily fluid balance in the RENAL (Randomized Evaluation of Normal vs. Augmented Level) trial for renal failure showed a reduced risk for death at 90 days and survival to either hospital discharge or 90 days.⁹In FACTT (Fluid and Catheter Treatment Trial), a conservative fluid management strategy was associated with better lung function and less demand for renal replacement therapy.¹⁰ The SOAP (Sepsis Occurrence in Acutely Ill Patients) study demonstrated that positive fluid balance was a risk factor for increased 60-day mortality and acute kidney injury (AKI).¹¹

In addition, restrictive fluid management during the perioperative period was associated with improved mortality and morbidity in patients with cancer.^12,13

The endothelial glycocalyx (EG) consists of a membrane-bound proteoglycans and glycoproteins network in which plasma or endothelial proteins are retained. The EG and bound fluids and plasma proteins form the endothelial surface layer (ESL), whose thickness is 1 mcm. The noncirculating part of plasma fixed within the ESL is 700 to 1,000 mL in humans. The EG serves as a mechanosensory complex of shear stress that stimulates the release of nitric oxide by endothelial cells.

The EG harbors several anticoagulant proteins, such as antithrombin III and thrombomodulin, which converts thrombin into activation of protein C and tissue pathway inhibitor for active factors VII and X. The EG decreases hematocrit in capillaries (the FåhrΔus effect), thereby enhancing blood flow in the capillaries by reducing blood viscosity. It also enhances laminar blood flow. The EG has anti-inflammatory and antioxidant functions. It prevents the adhesion of leukocytes and platelets to the endothelial cells and their migration to the interstitial tissues to initiate an adverse inflammatory response. Fluid overload leads to atrial natriuretic peptide (ANP). ANP sheds off the EG components into the circulation via activation of various metalloproteinases, which digest the EG (Figure 1).^14-20

Figure 1. The endothelial glycocalyx.

A: Physiologic functions of the endothelial glycocalyx: regulates nitric oxide synthetase activity, harbors superoxide dismutase, maintains vascular barrier, and decreases leukocytes and platelet adhesions.

B: Consequence of glycocalyx perturbation: increases vascular permeability, and activates coagulation and inflammation.

Figure used with permission. (Myburgh JA, Mythen MG. N Engl J Med.2013;369:1243-1245).

The zero-balance approach means the input fluid equals output fluid to maintain normovolemia, with no increase in body weight.² Zero balance is the term adopted by the American Society for Enhanced Recovery in its guidelines on perioperative fluid management.

Mean Systemic Filling Pressure and Fluid Therapy

Mean systemic filling pressure (MSFP) is the pressure of the pivot point of the circulation, where the pressure is independent of blood flow. The blood volume stretches the elastic walls of the vasculature structure and creates an elastic recoil force that is present when there is no flow, but it is also a key determinant of venous return. Therefore, venous return is dependent on the difference between MSFP and right atrial pressure (RAP) or central venous pressure (CVP).

The blood volume that stretches the walls is called stressed volume, and the alternative is called unstressed volume. In the circulation, 25% to 30% of total blood volume is stressed, and the remainder is unstressed. Thus, in someone with a total blood volume of 5.5 L, only 1.3 to 1.4 L of blood actually stretches the walls and produces recoil force, whereas the rest of the unstressed blood volume remains in the splanchnic capacitance vessels, specifically the splanchnic veins, which are the major site of capacitance activity.

During hypovolemia the sympathetic reflexes cause vasoconstriction, sending blood back to central circulation. Therefore, the splanchnic blood volume could be reduced by 500 mL after 1 L of hemorrhage in healthy male volunteers, while there were no changes in hemodynamic variables such as mean arterial pressure (MAP), heart rate, and cardiac output.²¹

The aim of fluid infusion or therapy is to enhance the MSFP and venous return. It was observed in 9 postoperative cardiac patients that 500 mL of hydroxyethyl starch increased MSFP from its baseline of 19.7 to 26.9 mm Hg.²²

The use of alpha-adrenergic agonists constricts the venous drainage of the splanchnic vasculature and enhances the MSFP, and thereby the venous return. Alpha-adrenergic agonists increase the precapillary resistance vessels and therefore reduce the capillary filtration. This could potentially reduce tissue edema formation. Of note, the use of an alpha-adrenergic agonist is very helpful in cases of vasodilation, for example, being under anesthesia and in the presence of sepsis, to maintain venous return and reduce tissue edema.

Collectively, the aim of fluid therapy is to enhance the MSFP and venous return while avoiding hypervolemia. Increases in RAP or CVP in hypervolemic states could impair venous return and cardiac output and result in tissue edema, and consequently impair tissue perfusion. Therefore, using increased CVP as a guide for preload enhancement and improvement of stroke volume (SV) should be discontinued, as increasing CVP with fluid therapy means the heart is unable to accommodate the infused fluid (ie, reduced cardiac compliance), thereby impairing venous return and SV instead of enhancing them.²³

Perioperative Fluid Management According To ERAS Protocol

Preoperative Hydration

American Society of Anesthesiologists’ guidelines recommend intake of clear fluids up to 2 hours before induction. Routine use of carbohydrate energy drinks containing high concentrations of complex carbohydrates will result in reducing thirst, hunger, anxiety, and postoperative insulin resistance through increasing insulin activity. These drinks can be taken safely 2 to 3 hours before surgery, depending on nutritional content.^24,25

Avoid routine mechanical bowel preparation, as this will result in increased dehydration, unpleasant sensation for the patient, and increased fluid overload during the intraoperative period. Routine bowel preparation does not reduce anastomotic leakage, wound infection, or mortality. Some surgeons prefer mechanical bowel preparation to make certain procedures easier, particularly laparoscopic cases, and some recent evidence has shown that mechanical bowel preparation may significantly improve 10-year survival data in elective colorectal cancer cases.²⁶ However, it increases incidence of spillage of bowel contents due to liquid bowel content.²⁷ Avoiding mechanical bowel preparation remains an essential part of the ERAS package because of the significant effects the preparation can have on preoperative hydration status, although it can be used in selected cases.²⁸

Intraoperative Fluid Management

According to the British Consensus Guidelines on Intravenous Fluid Therapy for Adult Surgical Patients, intraoperative fluid maintenance is best given in balanced crystalloid fluids (lactated Ringer’s solution, PlasmaLyte [Baxter], or Normosol-R [Hospira]) at the rate of 1 to 2 mL/kg per hour to meet the minimum daily requirements (1-2 mmol/kg of sodium, 1 mmol/kg of potassium, and 30 mL/kg of water).²⁹ The intraoperative fluid losses through blood loss or compartmental fluid shifts should be replaced by equivalent volumes of similar fluids, either colloidal or blood products. Of note, if there is no reason to suspect a volume deficit and the blood pressure is low, a judicious use of vasopressor is indicated.^2,28

Heart rate and MAP are rough indicators of patients’ fluid status, as healthy volunteers could tolerate the loss of up to 25% of their blood volume without change in heart rate and MAP. Urine output (UOP) is a crude marker of renal function and volume status. Perioperative oliguria (UOP <0.5 mL/kg/hour) is extremely common and occurs as a neurohormonal response to surgical stress. In an observational study of 65,043 patients undergoing noncardiac surgery, intraoperative oliguria was not associated with AKI.³⁰ The use of fluid in normovolemic patients to enhance UOP could lead to fluid overload. Raised intraabdominal pressure (IAP) induced by fluid overload increases renal venous pressure, reduces blood flow, and increases the pressure in Bowman’s space.

The kidney is an encapsulated organ, located in the retroperitoneal space of the abdominal compartment, which is especially vulnerable to the deleterious effects of increased IAP due to its anatomic position and blood supply. Fluid overload in encapsulated organs such as the kidneys will result in the development of renal compartment syndrome that impairs renal blood flow and from that the development of AKI. Increases in CVP above 12 mm Hg have been associated with impaired kidney function.^3,31,32 Therefore, in a retrospective study of 1,966 consecutive renal transplants, MAP of at least 93 mm Hg and perioperative fluid administration of less than 2,500 mL were associated with greater graft survival.³³

Collectively, the kidneys work as the canary in the coal mine to assess body perfusion and fluid status. The perfusions and consequent functions of other encapsulated organs, such as the heart and liver, also may be impaired in conditions of fluid overload.

The Use of Goal-Directed Fluid Therapy for Fluid Management

Use of SV optimization is preferable to guide fluid management throughout the perioperative period. An increase in SV by more than 10% by fluid challenge means the patient is a fluid responder and in the steep part of a Frank-Starling curve, and would benefit from further fluid challenge. Once the patient is euvolemic and has reached the plateau of the Frank-Starling curve, there is no further benefit from fluid bolus therapy. These can be harmful, however, as they may induce fluid overload. Dynamic indexes such as SV variation (SVV), pulse pressure variation (PPV), and systolic pressure variation are commonly used to predict fluid responsiveness. A PPV or SVV of more than 13% is highly predictive of fluid responsiveness. However, 9% to 13% is considered to be in a gray zone.

Systemic vascular resistance does not affect SVV; however, vascular resistance affects PPV. The PPV/SVV ratio is defined as dynamic arterial elastance (Ea_dyn). Elastance is the reciprocal to compliance. Ea_dyn can be used to predict the presence of tone or resistance in the vascular system and therefore the response of MAP after volume loading in hypotensive, preload-dependent patients. Patients with an Ea_dyn value less than 0.89 will not have increased MAP with volume administration vasodilation because they exhibit peripheral as with anesthesia or sepsis, which means that vasopressors should be added to the fluids to raise the MAP.

Nonetheless, an Ea_dyn value greater than 0.89 indicates that fluid loading alone will raise blood pressure, and the use of vasopressors can be delayed. An Ea_dyn value less than 0.94 was predictive of a decrease in arterial pressure in response to a reduced norepinephrine dose in resuscitated septic patients. In addition, in the same study, Ea_dyn was the only hemodynamic variable to predict the decrease of arterial pressure in response to norepinephrine dose reduction.³⁴ Therefore, the authors stated that Ea_dyn may constitute an easy-to-use functional approach to arterial tone assessment.³⁴

The use of dynamic parameters has its own limitations. PPV and SVV require normal sinus rhythm and normal pressures in the abdomen and chest; if these are not present, then their predictive value is reduced. PPV and SVV depend on heart/lung interactions during controlled ventilation. Therefore, a tidal volume less than 8 mL/kg decreases this interaction and results in low values for PPV and/or SVV.

The OPTIMISE (Optimization of Cardiovascular Management to Improve Surgical Outcome) trial was conducted in 17 acute care hospitals in the United Kingdom.³⁵ The trial included high-risk patients aged 50 years or older undergoing major abdominal surgery with an expected duration longer than 90 minutes. Patients were randomly assigned to cardiac output–guided hemodynamic therapy for IV fluid using LiDCOrapid and dopexamine infusion (0.5 mcg/kg/minute) during and 6 hours after surgery (n=368), or usual care (n=366). Both groups received dextrose 5% infusion at 1 mL/kg per hour. In both groups, MAP was kept between 60 and 100 mm Hg using an alpha-adrenergic agonist or vasodilator.

The primary outcome was a composite of predefined 30-day moderate and major complications and mortality. Secondary outcomes were morbidity on day 7; infection; critical care–free days; all-cause mortality at 180 days; and LOS. Primary outcome was met by 36.6% in the intervention group versus 43.4% in the usual care group with an absolute risk reduction of 6.8%. Following adjustment for baseline risk factors, the observed treatment effect remained insignificant.

Secondary outcomes were not significantly different between the two groups. The fluids used were almost the same in both groups: 4,190 mL in the intervention group versus 4,024 mL in the usual care group. However, when the results were included in an updated review and meta-analysis that included the results from OPTIMISE and 7 additional trials from 1966 to 2014, goal-directed fluid therapy (GDFT) significantly reduced the number of postoperative infections and LOS.³⁵ Those findings are consistent with the evidence summary reported in the Cochrane review by Grocott et al.³⁶

GDFT should be individualized according to the patient. GDFT is unlikely to cause harm or to add benefit in healthy patients undergoing uneventful surgery within an ERAS pathway. However, patients with preoperative bowel preparation who have significant comorbidities and prolonged surgery with blood loss will benefit from GDFT (Table and Figure 2).

Figure 2. Variables of surgical and patient risks.

GDFT, goal-directed fluid therapy

Adapted from reference 2.

Postoperative Period

Early oral intake reduces the risk for infection and reduces LOS with no increased risk foranastomotic dehiscence. In addition, it may lower the risk for pneumonia, intraabdominal abscess, and mortality, although these measures did not reach statistical significance in a meta-analysis.³⁷Continuing IV fluids into the postoperative period further increases the risk for developing postoperative ileus, as the ability to excrete and remove both sodium and chloride is reduced postoperatively.⁵

Intravenous fluids in the postoperative period should provide low-sodium, low-volume therapy and enable patients to return to zero fluid and sodium balance over the postoperative period.²⁹

Of note, hypotension in normovolemic patients who have had a thoracic epidural should not be treated with excess fluid but with either a reduction or modification of the epidural infusion and/or the use of vasopressors. Moreover, fluid management in high-risk patients in the postoperative period is better guided using the goal-directed technique.

What Fluid Should Be Used?

Intraoperative fluid maintenance should include a balanced crystalloid solution such as lactated Ringer’s solution, PlasmaLyte, or Normosol-R. Colloidal solution with albumin is the preferred choice for fluid replacement in cases of blood loss and objective hypovolemia. High-plasma chloride concentration has been shown to reduce renal blood flow and plasma clearance.³⁸

In a database study, the use of 0.9% saline versus a balanced crystalloid solution was associated with in-hospital mortality of 5.6% versus 2.9%, respectively. Patients who received 0.9% saline had significantly greater blood transfusion requirements and were 4.8 times more likely to require dialysis.³⁹ Furthermore, chloride restriction in ICU patients reduced the incidence of AKI and renal replacement therapy, but with no differences in hospital mortality or ICU LOS.⁴⁰

Meanwhile, in a recently published trial in patients undergoing cardiac surgery, a perioperative fluid strategy to restrict IV chloride administration was not associated with an altered incidence of AKI.⁴¹ Normal saline can be used in specific conditions, like hypochloremic metabolic alkalosis, as the result of high gastrointestinal losses.

If the blood loss is significant, blood loss should be replaced with blood products whenever possible, such as packed red blood cells, platelets, and other clotting factors. The use of colloidal solutions is preferred for replacing other volume losses because they are thought to increase SV and blood pressure more than same-volume crystalloid solutions, as colloids are less likely than crystalloid solutions to leak across the EG and out of the intravascular space.⁴²

The CRISTAL (Colloids Versus Crystalloids for the Resuscitation of the Critically Ill) trial, which was a large, multicenter, randomized controlled trial comparing crystalloid and colloidal solutions for resuscitation of hypovolemic shock, showed a significant reduction in 90-day mortality in the colloidal group, demonstrating benefit in using colloidal boluses in fluid-responsive patients to replace volume loss.⁴³ However, the use of hydroxyethyl starch solutions was associated with an increased risk for AKI or the need for renal replacement therapy in two large randomized studies.^44,45

Albumin is still the preferred colloid in the perioperative period. Albumin plays an essential role in maintaining the integrity of the vascular barrier. Albumin enhances the availability of sphingosine-1 phosphate (S1P), which is produced by red blood cells. S1P improves the vascular barrier and stabilizes the EG. S1P has been found to reduce metalloproteinase activation, thereby attenuating the loss of endothelial cell surface glycocalyx components. Both actions appear to involve signaling via the S1P receptor.⁴⁶

Albumin is the most important antioxidant of human plasma, and can protect the body from harmful effects from heavy metals, such as iron and copper, and reduce their ability to produce reactive oxygen radicals. Human serum albumin is the main depot for nitric oxide transport in the blood.⁴⁷

In a meta-analysis of 17 studies that included 1,977 randomly assigned participants, the use of albumin for resuscitation of patients with sepsis was associated with reduced mortality, with an odds ratio of 0.82% (95% CI, 0.67-1.0; P=0.047).⁴⁸ In patients with a subarachnoid hemorrhage, use of albumin at 1.25 g/kg per day for 7 days was associated with a lower rate of cerebral vasospasm, as measured by transcranial Doppler; delayed cerebral ischemia; and a reduced rate of cerebral infractions.49

The preemptive correction of a low preoperative albumin level by administration of albumin in patients undergoing off-pump coronary artery bypass (OPCAB) is associated with a significant reduction in the incidence of AKI: from 26% in the control group to 13.7% in the group receiving albumin.

The editorial that accompanied the study suggested that restoring the target level is associated with a reduction in AKI at an amplitude greater than that of any known intervention in patients undergoing OPCAB.50,51 Albumin is proposed for all patients with AKI and has benefits in spontaneous bacterial peritonitis, although this effect has not been seen in ot her septic etiologies.52 Moreover, albumin infusion seems to be a protective factor for greater graft survival after renal transplant.53

Conclusion

Fluid management is the heart of the ERAS pathway. GDFT should be individualized according to patients’ conditions to maintain tissue perfusion. Of note, the aim of perioperative fluid management is to maintain appropriate MAP for proper tissue perfusion using a zero-balance approach.

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