Version May 2024
INTRODUCTION — The management of fluid in the postoperative surgical patient can vary from simple to complex. Postoperative intravenous maintenance fluid therapy ensures adequate organ perfusion, prevents catabolism, ensures electrolyte- and pH-balance, and may be all that is required for patients who undergo surgical procedures that do not significantly alter the hemodynamic milieu. Typically, such procedures are associated with a small volume of blood loss (<250 mL), a short course of anesthesia and surgery (<3 hours), a small volume of intravenous fluid administration (<30 mL/kg), and little to no extravascular fluid shift in patients without significant organ dysfunction.
However, in many cases, postoperative patients with extensive traumatic or surgical tissue injury, burns, critical illness, or sepsis require more complex resuscitative fluid therapy in addition to maintenance therapy to compensate for preoperative and intraoperative losses, the stress response to surgery, the underlying disease state, ongoing fluid and blood loss. Such complex fluid management is often needed for patients who undergo surgical procedures that result in significant blood loss (>500 mL or 7 mL/kg) [1], fluid shifting out of the vascular space ("third-spacing"), large-volume intravenous fluid administration (>30 mL/kg), or hemodynamic instability [2,3].
The prescription of maintenance and resuscitative fluids in postoperative surgical patients is reviewed here. The management of electrolyte abnormalities and nutritional support in the perioperative period are reviewed separately. (See "Overview of postoperative electrolyte abnormalities" and "Overview of perioperative nutrition support" and "Postoperative parenteral nutrition in adults".)
Intraoperative fluid therapy is reviewed separately. (See "Intraoperative fluid management".)
PHYSIOLOGIC STRESS RESPONSE TO SURGERY — The stress response to traumatic or surgical tissue injury is a primal collection of biochemical pathways designed to facilitate survival following a major insult. The "fight or flight" response promotes expansion of the blood volume, glucose availability, perfusion of vital organs, and inflammation. This stress response is triggered by entry into a major body cavity (eg, chest, abdomen, joint, cranium), significant tissue disruption (eg, severe burn wounds, long bone fracture, penetrating gunshot wound, pancreatitis), significant blood loss (>500 mL or 7 mL/kg), hemodynamic instability, and sepsis.
Some devices and treatments used in surgery may also incite a massive inflammatory response. As an example, extracorporeal bypass uses an external circuit through which blood is forced for gas exchange and circulation while the patient undergoes cardiac surgery. Blood contact with artificial bypass tubing incites cytokine release, activation of the coagulation cascade, and the production of nitric oxide [4]. This inflammatory response may lead to vasodilation, deranged coagulation, systemic capillary leak, and systemic organ dysfunction. Another example is aggressive cancer treatment using heated intraperitoneal chemotherapy (HIPEC), which commonly results in an inflammatory response marked by supranormal fluid exudation, decreased systemic vascular resistance, and coagulopathy [5,6]. Derangements in physiology, intravascular volume, and coagulation associated with HIPEC commonly require aggressive fluid resuscitation. (See "Extracorporeal life support in adults in the intensive care unit: Overview" and "Anesthesia for cytoreductive surgery with heated intraperitoneal chemotherapy".)
Hormonal mediators — Hormonal mediators of the stress response include:
●Vasopressin – Vasopressin, also known as antidiuretic hormone (ADH), is secreted by the posterior pituitary gland in response to elevated plasma osmolality, low circulating blood volume, and stress. This results in water retention by the kidney, which expands the vascular volume.
●Aldosterone – The renin-angiotensin axis responds to volume contraction by stimulating aldosterone secretion in the adrenal gland. Aldosterone increases sodium and water retention by the kidney, thereby expanding the vascular volume.
●Cortisol – The hypothalamic-pituitary axis responds to stress by stimulating cortisol release from the adrenal gland. This promotes gluconeogenesis and muscle breakdown and results in hyperglycemia.
●Catecholamines – Epinephrine and norepinephrine are released from the adrenal gland in response to sympathetic nervous system stimulation, resulting in vasoconstriction, tachycardia, and catabolism. This combination leads to increased cardiac output, hypertension, and hyperglycemia.
●Cytokines – Acute phase reactants (eg, interleukins 1 and 6) generate a local inflammatory response at the site of injury, facilitating healing at sites of tissue disruption [7,8].
The stress response to tissue injury helps the body to compensate for hypovolemia. However, complications of the stress response can occur. As an example, aldosterone release leads to acute potassium wasting and secondary hypokalemia. If not appropriately treated, severe postoperative hypokalemia can result in arrhythmia. Similarly, cortisol and catecholamines contribute to hyperglycemia, which is associated with complications of wound healing in postoperative patients, including infection, dehiscence, and nonhealing. Furthermore, the systemic release of inflammatory mediators may result in local and/or systemic capillary leak, tissue injury, and systemic organ dysfunction (eg, acute renal failure, adult respiratory distress syndrome).
Distinguishing hypovolemia from the stress response in the postoperative patient can be challenging. In the past, manifestations of the stress response, including tachycardia, hypotension, and oliguria, were attributed to hypovolemia and inadequate fluid resuscitation. For this reason, postoperative fluid resuscitation was focused on resolving these physiologic derangements by administering large volumes of fluid. Such aggressive fluid resuscitation resulted in complications associated with volume overload, contributing to morbidity and mortality [9-11].
Our understanding of the stress response to surgery has evolved. In a 2016 statement on sepsis, the Society of Critical Care Medicine and the European Society of Intensive Care Medicine recognized that a stress response exists as a spectrum of organ dysfunction caused by a dysregulated host response to infection. In the absence of infection (eg, pancreatitis), an exaggerated stress response can result in a similar degree of organ dysfunction. As such, organ dysfunction (ie, acute kidney injury, transaminitis, or cardiomyopathy) in the postoperative patient may not reflect inadequate fluid resuscitation; rather, such dysfunction may be a manifestation of a pathologic stress response to the underlying disease or to surgery [12]. For this reason, new protocols, such as the Enhanced Recovery After Surgery (ERAS) protocol, are emerging to limit the fluid therapy in surgical patients and may include "permissive oliguria" in some cases [13].
FLUID LOSS AFTER SURGERY — Fluid loss in the postoperative period varies widely with the type of procedure performed, the condition of the patient at the time of surgery, the underlying disease for which the procedure was performed, and the severity of the stress response.
Bleeding — Bleeding should always be considered in postoperative patients with hypotension, tachycardia, dizziness, or pallor. However, these manifestations are late, occurring only after blood loss is in excess of 15 percent of the patient's blood volume (table 1). While fluid administration is appropriate to support the patient, blood products are often required to correct the acute blood loss anemia. In the 10th edition of the Advanced Trauma Life Support (ATLS) guidelines, 1 L of fluid is indicated for trauma patients requiring resuscitation to restore organ perfusion; thereafter, in cases of bleeding, balanced transfusional support is encouraged [14]. (See "Intraoperative transfusion and administration of clotting factors".)
In most cases, a return to the operating room is indicated for exploration and control of hemorrhage at the surgical site. In cases of occult bleeding, imaging may be needed to identify the bleeding source.
Drainage — Gastrointestinal drainage systems (eg, nasogastric tube) may evacuate large volumes of fluid during or following a surgical procedure (eg, small bowel obstruction) (table 2). Similarly, surgical entry into the chest (ie, pleural fluid from a chest tube), abdomen (ie, ascites from abdominal drains), or urinary system (ie, urine) may lead to the rapid evacuation of a large volume of fluid. For fluid evacuation in excess of one liter, hypovolemia and electrolyte derangement may result if the fluid is not sufficiently replaced to restore normal perfusion.
Third-spacing — Third-spacing refers to the process of capillary leak and extravasation of protein-rich serum into the interstitial spaces of the soft tissues (eg, skin, fat, muscle), organs, deep space cavities (eg, chest, abdomen), or retroperitoneum. It typically occurs during the first 72 hours following major surgery and is associated with a heightened stress response [15].
●Third-spacing into the soft tissue results in edema, whereas fluid that leaks from the peritoneal or pleural surfaces generates ascites or pleural effusion.
●Large nonanatomic cavities, such as those created from extensive subcutaneous dissection or following drainage of an infected pancreatic pseudocyst, can result in large-volume third-spacing into the newly created potential space.
●Spaces that are created during surgery (eg, the hernia cavity that remains following ventral hernia repair), in which the tissues are not approximated, can result in postoperative seroma.
●Reperfusion following an episode of ischemia, such as in cases of arterial occlusion, result in an intense local inflammatory response and extensive tissue edema, which can lead to compartment syndrome.
Hypoalbuminemia contributes to third-spacing; it is theorized that the resultant intravascular oncotic pressure, resulting from hypoalbuminemia, contributes to the fluid shifting. Some fluids contain higher concentrations of albumin, such as ascites, which may impact hemodynamics in a more impressive way. As an example, in a post hoc analysis of 31 patients involved in a trial to assess intravenous fluid administration following cytoreductive surgery, the evacuation of malignant ascites in excess of 500 mL caused greater hemodynamic instability and was associated with a larger fluid resuscitation compared with those in whom less than 500 mL ascites was drained [16]. (See "Etiology, clinical manifestations, and diagnosis of volume depletion in adults".)
Insensible losses — Insensible (evaporative) loss can be related to prolonged exposure during laparotomy or thoracotomy, or prolonged exposure of burn wounds during skin grafting. Older studies estimated that the losses from open abdominal exposure were 0.5 to 1 mL/kg/hour; however, the amount varies with the degree of organ exposure and the severity of the illness. Minimally invasive approaches are associated with less evaporative loss. Postoperatively, insensible losses can also occur through large open wounds, such as an open abdomen or burn wounds, and with persistent postoperative fever.
Insensible loss associated with ventilator support (intraoperative, postoperative) is limited.
FLUID RESUSCITATION — The goal of postoperative fluid resuscitation is to restore organ perfusion [17]. Through the administration of intravenous fluid, a deficit in intravascular volume is sufficiently replaced to restore organ perfusion. In some cases, blood transfusion is also necessary to achieve these goals.
Despite advances in critical care, there is no way to directly measure intravascular volume [17]. For this reason, we continue to rely on markers of inadequate perfusion to guide us in identifying hypovolemia. Any patient who demonstrates hemodynamic instability (ie, tachycardia, hypotension), end-organ dysfunction (eg, alteration in mental status, oliguria [<0.5 mL/kg]), lactic acidosis, or base deficit in the postoperative period should be considered for fluid resuscitation.
Postoperative fluid resuscitation begins with the identification of clinically impactful fluid loss resulting in hypovolemia, which may be due to any of the following:
●Preoperative fluid deficit (eg, bowel preparation-associated diarrhea) or fasting-associated deficit (eg, prolonged inanition prior to intestinal surgery).
●Intraoperative sensible and insensible fluid losses. (See 'Insensible losses' above.)
●Intraoperative blood loss, or ongoing postoperative blood loss. (See 'Bleeding' above.)
●Ongoing fluid loss related to the underlying condition (eg, septic shock, pancreatitis), which can be due to tissue (third-spacing) or external (eg, surgical drain, nasogastric tube) losses. (See 'Third-spacing' above and 'Drainage' above.)
Estimate the fluid deficit — Historically, fluid resuscitation was achieved by estimating and replacing the intravascular fluid deficit. However, the estimation of a patient's fluid deficit is an inexact science; by this method, many patients receive too much fluid. In simple cases, replacing some or all of the deficit is sufficient to complete resuscitation. In complex cases involving physiologic derangement (eg, hypotension, tachycardia), acute organ dysfunction (eg, acute kidney injury, sepsis-associated cardiomyopathy), or systemic illness (eg, vasodilation due to septic shock), resuscitation may be more complex. For this reason, resuscitation is focused on restoring normal perfusion rather than replacing an estimated volume deficit.
Blood collected from the operating field through closed suction evacuation is often readily apparent and measurable; however, some of this blood may have been collected and returned to the patient using autotransfusion technology. The estimate of the volume of blood lost on surgical sponges may also be difficult since the amount of estimated blood varies with the sponge size, sponge material, and degree of sponge saturation (ie, volumes range from a few mL to 100 mL per saturated sponge). In addition, the amount on a sponge may be overestimated as blood may be mixed with ascites or urine. Conversely, blood loss can be underestimated, as blood may also be lost on surgical gowns, drapes, and the operating room floor. Occult blood loss will not have been accounted for. As an example, a significant retroperitoneal hematoma due to arterial cannulation may not be apparent until much later, as the patient develops symptoms (eg, pain, ileus) or becomes hypotensive.
In hypovolemic patients, it may not be possible to reliably calculate the fluid deficit. Instead, it is a common practice to compare the physiologic parameters associated with hypovolemia to those associated with hemorrhage (table 1). As an example, with <15 percent circulating blood volume loss, the heart rate and blood pressure should be normal. If a patient demonstrates tachycardia or hypotension, it is likely that their volume deficit is greater than 15 percent. For a 70 kg individual, a 15 percent deficit would correspond to approximately 750 mL fluid deficit. While this method is not well supported with literature and is imprecise, it provides a good starting point. For this reason, the volume of intravenous fluid administered as a bolus (referred to as a fluid challenge) is often 500 mL to 1000 mL [17].
Measure ongoing fluid losses — In addition to replacing any postoperative fluid deficit, ongoing losses from drainage tubes must be accounted for. Provided the surgical drains are functioning properly, the volume of loss can be measured directly. We monitor drain output frequently; when it exceeds 400 mL in 8 hours (>50 mL/hour), fluid replacement is initiated to minimize fluid deficits and secondary hypovolemia, until the drain output subsides. Alternatively, we may begin replacing the output in a scheduled fashion (eg, 1 L every 12 hours), assuming the observed loss will continue at the same pace. These replacement protocols (hourly, every six hours, or intermittent bolus) can be revised several times a day, depending on the trend in output.
Volume of replacement fluid — Once the fluid deficit has been estimated and ongoing losses are measured, the total volume of replacement fluid can be determined. For hemodynamically stable patients, ongoing fluid losses should be evaluated and adjusted daily; fluid needs should be assessed two or three times daily in critically ill patients.
The postoperative patient can be expected to require a volume that is up to three times the estimated fluid deficit. As much as two-thirds of administered intravenous crystalloids are expected to shift out of the vascular space within hours of administration due to capillary leak, which correlates with the magnitude of the stress response to surgery. For patients with normal organ function, the fluid deficit is typically replaced in a ratio of 1:1, meaning that 1 L of fluid loss is replaced with 1 L of fluid replacement. Greater amounts with ratios as high as 3:1 may be necessary in those with a severe stress response to surgery (eg, after necrosectomy for necrotizing pancreatitis). Lower amounts (eg, 0.5 mL:1 mL) are used in those expected to receive a large volume of other fluids, such as medications or blood products, and in those who are not expected to tolerate excessive fluid volume (eg, recovery after kidney transplant). In the REstrictive versus LIbEral Fluid therapy (RELIEF) trial, 2983 patients with risk factors for complications (ie, >70 years of age, heart disease, diabetes, renal dysfunction, morbid obesity) were randomly assigned to restrictive (ie, zero balance) versus liberal fluid therapy during and after abdominal surgery [18]. There was no difference in the rate of pulmonary edema or duration of mechanical ventilation, but those assigned to a restrictive protocol had a higher rate of acute kidney injury (8.6 versus 5.0 percent; hazard ratio [HR] 1.71 95% CI 1.29-2.27) and need for replacement therapy (0.9 versus 0.3 percent; HR 3.27, 95% CI 1.01-13.8). The rate of surgical site infection was also increased (16.5 versus 13.6 percent; HR 1.22, 95% CI 1.03-1.45), but the incidences of other infectious complications (eg, sepsis, anastomotic leak, pneumonia) were no different. At one year, disability-free survival was no different between the groups (81.9 versus 82.3 percent). These findings suggest that a modestly liberal intraoperative and postoperative fluid regimen is needed to maintain renal perfusion in high-risk patients. For other subsets of patients, their postoperative physiology may be the reason that fluid replacement will be poorly tolerated. An example is the patient who undergoes pneumonectomy, whose remaining lung must acutely accommodate an entire blood volume. In such patients, smaller amounts of fluid are often used for replacement; permissive oliguria is often preferable to volume overload-associated pulmonary edema.
Ongoing gastrointestinal or other losses are generally replaced with a volume equal to the loss. These losses can be replaced periodically (eg, every six hours). Alternatively, a fluid replacement protocol can be employed to keep up with losses on an hourly basis once a goal vascular volume is achieved. As an example, during kidney transplantation, the patient is volume-loaded during surgery until the intravascular system is replete. Thereafter, each hour after surgery, the amount of fluid lost is measured and replaced using an equal volume of intravenous fluid during the following hour. In this way, the intravascular volume is maintained, and a fluid deficit is avoided. If large-volume losses are anticipated, the maintenance fluid goal rate can be increased temporarily. (See 'Maintenance fluid therapy' below.)
Replacement fluids — Crystalloids, colloids, and blood products are the replacement fluids typically administered to postoperative patients (table 3). It is important to consider the type and volume of fluid that was lost, which will help guide the choice of fluid, volume of fluid, and speed of fluid replacement.
Crystalloid solutions remain the fluid of choice for simple fluid replacement following surgery. Although used intraoperatively, starch solutions are not commonly used in postoperative surgical patients for volume expansion as they may result in abnormal coagulation, which can contribute to bleeding complications. (See "Intraoperative fluid management", section on 'Choosing fluid: Crystalloid, colloid, or blood'.)
Normal saline (ie, 0.9% sodium chloride; Na = 154 mEq/L), Lactated Ringer (Na = 130 mEq/L), and Plasma-Lyte (Na = 140 mEq/L) are widely used because their sodium content maintains serum osmolarity, which helps retain water in the vascular space and facilitates volume expansion. The pH of Lactated Ringer and normal saline is below physiologic pH, which also contributes to acid-base abnormalities. The lactate in Lactated Ringer is converted to bicarbonate, which serves as a buffer, but its metabolism and clearance depend on adequate liver and kidney function. Plasma-Lyte contains acetate, a buffer, which is quickly converted to bicarbonate, independent of the liver and kidneys [19]. Plasma-Lyte is more expensive than normal saline or Lactated Ringer, which limits its use.
●Normal saline (0.9%) is particularly useful in cases of chloride and volume loss as well as alkalosis (eg, vomiting). It contains the greatest concentration of sodium, repletes chloride loss, and will reverse contraction alkalosis.
●Normal saline (0.9%) is used in association with blood transfusion, particularly rapid transfusion, because it does not contain additives like calcium, potassium, or magnesium. Lactated Ringer and Plasma-Lyte contain these additives, which may not be compatible with all blood products and can result in red blood cell lysis, clot formation in the tubing, and electrolyte chelation [20].
●Normal saline (0.9%) is used for head-injured patients, in whom hypernatremia is preferable to hyponatremia or lowering the serum osmolarity. The brain does not tolerate edema well; maintaining a normal (or elevated) sodium ensures that cerebral edema is minimized.
●Lactated Ringer and Plasma-Lyte should be avoided in patients with hyperkalemia as they both contain potassium. Similarly, in patients with poor renal function, these choices may be used with caution to avoid hyperkalemia.
●Large volumes of normal saline are undesirable as they will result in hyperchloremic acidosis and renal vasoconstriction [18,21-25]. However, in some cases of renal and/or liver dysfunction, a provider may have no other choice but to use 0.9% saline. A chloride-restrictive approach may reduce the incidence of acute kidney injury [23].
●For patients with bicarbonate loss (eg, pancreatic fistula, bladder-drained pancreas transplant), bicarbonate replacement therapy may be administered intravenously in a continuous fashion. Sodium bicarbonate is commonly added to replacement fluids in increments of 50 mEq/L. The fluid vehicle is chosen to achieve the desired fluid sodium. For example, 150 mEq/L of sodium bicarbonate will provide 150 mEq of sodium per liter, which is nearly equivalent to 0.9% saline (154 mEq/L). As such, it is mixed in sterile water or 5% dextrose in water to avoid further sodium administration.
●Hypertonic saline (3% sodium chloride) is being used for the resuscitation of trauma and emergency general surgery patients whose abdomens are maintained open with a temporary abdominal closure device. In this highly selective population, volume overload results in delayed primary fascial abdominal closure and complications of open abdomen (eg, enteroatmospheric fistula). Inspired by a promising early report [26], similar encouraging reports have suggested that the complications associated with hypertonic saline resuscitation (hyperchloremia, hypernatremia, hyperosmolar acidosis) are well tolerated in this patient population [27]. Although this is not the standard of care, it remains a promising alternative to standard resuscitation and is supported by one systematic review [28].
Colloid solutions can also be used for volume expansion. The main colloid used in postoperative patients is albumin, most commonly in the setting of severe malnutrition or liver failure. It may maintain oncotic pressure better than crystalloid. However, the effects of albumin are short-lived since it remains in the vascular space only for hours. The critical care literature suggests that there is no benefit to using albumin. A systematic review and meta-analysis from 1998 reported that albumin did not reduce mortality when compared with crystalloid [15]. Later trials have also not demonstrated any benefit with respect to perioperative mortality with the use of albumin [29,30]. Caution is advised with the use of large volumes of albumin; hyperoncotic albumin resuscitation was associated with increased risk of death in an international prospective study [31]. Similarly, the use of albumin in neurologic injury is associated with increased mortality, likely due to the secondary increase in intracranial pressure that results [32]. A systematic review of albumin administration in decompensated cirrhosis did not demonstrate a short- or long-term mortality benefit, and the practice was associated with a higher incidence of pulmonary edema [33].
Other colloid solutions include gelatins, dextrans, and starches. The use of these agents in postoperative patients is very limited as their rheologic and anticoagulant effects are typically unwelcome. Similarly, they can incite anaphylactic reactions. In a Cochrane review of surgical and critically ill patients, no colloid was found to be superior in efficacy or safety [34].
Role of blood products — Blood product transfusion is generally limited to patients with accepted indications given the risk for transfusion-related complications, which include transfusion-associated infection, lung injury, multiorgan failure, and systemic inflammatory response syndrome (SIRS) [35]. Indications for blood product transfusion in postoperative patients include (see "Intraoperative transfusion and administration of clotting factors" and "Perioperative blood management: Strategies to minimize transfusions"):
●Resuscitation for bleeding – Active bleeding that is too rapid to be assessed by serial hemoglobin measurements in the postoperative period may be related to coagulopathy or traumatic vascular injury. For large-volume blood loss, the American College of Surgeon (ACS) Advanced Trauma Life Support (ATLS) protocol (10th edition) recommends an initial one-liter rapid infusion of warmed isotonic fluid followed by blood products [14]. Although massive transfusion protocols vary widely in the United States, most use a balanced transfusion strategy, whereby components of blood (ie, red blood cells, fresh frozen plasma, and platelets) are administered in equal amounts to equate to whole blood. (See "Massive blood transfusion".)
●Severe symptomatic anemia – For postoperative patients who are not actively bleeding, but with severe symptomatic anemia, specific thresholds for various patient populations and supporting randomized trials are discussed in detail separately. It is important to note that a numerical hemoglobin goal has not been established for postoperative patients who may have suffered acute blood loss intraoperatively. An individualized approach is needed. In our surgical practice, we aim for a hemoglobin goal of 7 to 8 g/dL in most patients; for those with coronary artery disease, we aim for a higher goal of 8 to 10 g/dL. (See "Intraoperative transfusion and administration of clotting factors", section on 'Indications and risks for specific blood components' and "Indications and hemoglobin thresholds for RBC transfusion in adults", section on 'Thresholds for specific patient populations'.)
●Reversal of coagulopathy, thrombocytopenia, or hypofibrinogenemia – Thresholds for platelet transfusion in postoperative patients who are actively bleeding or at risk for bleeding are individualized based on procedure. As an example, when bleeding into a confined operative field would be poorly tolerated (eg, spine, cranium), the desired minimum platelet level will be higher compared with a superficial operative field for which direct pressure can be applied, or for which a small amount of blood accumulation will not have dire consequences. Similarly, specialized treatments may result in focused consumption of elements in the clotting cascade and may require focused transfusion. As an example, during catheter directed thrombolysis for critical limb ischemia, fibrinogen is consumed and may require focused replacement with cryoprecipitate to prevent bleeding complications. (See "Intraoperative transfusion and administration of clotting factors", section on 'Platelets' and "Platelet transfusion: Indications, ordering, and associated risks".)
Fluid bolus administration — For most postoperative patients, replacement fluids (including blood) are administered through peripheral intravenous lines. For rapid fluid infusion, large bore (eg, 14-gauge, 16-gauge) peripheral intravenous (IV) lines are needed. A liter of fluid can be infused in under seven minutes through a 16 gauge IV by gravity infusion. For higher rates (300 to 500 mL/minute), a pressure bag or rapid infuser is needed (table 4) [36]. When such large volumes of fluid are needed, administration of room temperature fluid can lead to rapid-onset hypothermia. If this is anticipated, a rapid transfuser should be used since it warms the fluid as it infuses it.
●Resuscitative fluid is commonly administered as an intravenous bolus over 30 to 60 minutes for rapid volume expansion. For patients who are not in shock, fluid replacement is achieved using successive 3.5 to 14 mL/kg aliquots per hour. In general, for the average 70 kg adult, this corresponds to aliquots of 250 to 1000 mL for a total of 2 to 3 L until the desired response is observed (eg, improved urine output, improved mentation, normalizing base deficit). (See 'Endpoints of fluid resuscitation' below.)
●More volume-depleted patients will require larger aliquots. A patient in hypovolemic shock (40 percent or greater volume loss) will require rapid volume expansion with >2 L of fluid per hour to restore blood volume and tissue perfusion. In cases of anticipated aggressive third-spacing, additional ongoing fluid replacement is often needed.
●Patients who do not make urine due to chronic renal disease or who have poor heart/lung function require smaller aliquots (eg, 250 mL) and careful monitoring of responses to fluid challenges.
●When patients do not respond to the fluid challenge as expected, further evaluation in a closely monitored setting is warranted to identify bleeding or other complications of surgery (eg, acute renal dysfunction, myocardial infarction, sepsis). If a patient becomes unresponsive to fluid boluses, fluid replacement should be reconsidered to avoid complications of volume overload.
Blood products are typically transfused in a slow, monitored fashion (eg, one unit of red blood cells over three hours) to reduce the risk of transfusion-associated circulatory overload and enable early identification of transfusion reactions. In the setting of acute blood loss, more rapid transfusion may be needed to treat a patient in shock. Emergency rooms, trauma bays, intensive care units, and operating rooms have ready access to a rapid transfuser, which permits the rapid transfusion of warmed fluid and blood products at high rates (300 to 500 mL/minute). (See "Initial management of moderate to severe hemorrhage in the adult trauma patient".)
Endpoints of fluid resuscitation — The endpoint of fluid resuscitation is to restore normal organ perfusion to permit sufficient oxygen delivery, rather than simply the administration of a specific volume of fluid [37]. Normal perfusion is achieved when the end-diastolic volume of the left ventricle generates an adequate stroke volume. To achieve normal organ perfusion, blood volume must be restored to 80 to 85 percent of normal blood volume.
Although some clinical parameters and bedside examination may be helpful for assessing the adequacy of perfusion, laboratory measurements (ie, serum base deficit and serum lactic acid) and adequate intracardiac filling by echocardiography are better measures of adequate central volume. Approximately one-half of hemodynamically unstable patients will remain fluid responsive at the end of their initial resuscitation, further strengthening the argument to use endpoints of resuscitation rather than fluid responsiveness [38]. If a patient becomes unresponsive to fluid replacement, further fluid administration should be reconsidered to avoid complications of volume overload.
Since normal organ perfusion can be achieved without complete replacement of the estimated volume deficit for most patients, ongoing clinical assessment of the adequacy of organ perfusion is essential. In relatively healthy individuals who have not sustained large-volume blood or fluid loss, normalization of heart rate, blood pressure, urine output, and mental status mark the return of normal end-organ perfusion. A 45° passive leg raise in a recumbent patient can be helpful for evaluating fluid responsiveness, which is defined as an increase in stroke volume by more than 10 percent [39]. For the average adult monitored with a noninvasive cardiac output monitor, a passive leg raise is equivalent to a fluid bolus of approximately 300 mL (4 mL/kg). In one study of 72 elderly surgical patients, a passive leg raise correlated with a stroke volume rise of 10 percent in most patients who were fluid responsive. [40]
Serum lactic acid, base deficit, and central venous oxygen saturation (SvO2) are biochemical end-products of perfusion that are often used to confirm adequacy of end-organ perfusion in patients demonstrating complex physiology (eg, concurrent sepsis and vasodilatory shock). Trending values every four to eight hours is helpful. When a patient develops hypovolemia, impaired organ perfusion leads to anaerobic metabolism, which produces lactic acid. Lactic acid is buffered by base; it consumes the base, thereby creating a base deficit. Similarly, underperfused tissues will extract a greater percentage of oxygen than is normal, resulting in a decreased SvO2. As blood volume is restored, these parameters should trend toward normal. However, resolution of lactic acidosis is highly variable in its time course. Outcomes of surgical patients with lactic acidosis have not been as well studied as in the medical patient population [41]. However, lactic acidosis exceeding 4.0 mmol/L has been shown to be associated with increased mortality in emergency room patients with infection [42]. Serum lactic acid levels must be interpreted with caution in patients with liver dysfunction, who may not clear lactic acid as quickly compared with those who have normal liver function. Acute liver dysfunction can be observed in a variety of surgical settings (eg, sepsis, trauma, transplant). For patients with persistently elevated lactic acid and SvO2, in spite of adequate fluid resuscitation, further evaluation is warranted.
Estimates of central blood volume, including central venous pressure, the change in central venous pressure, and pulmonary artery wedge pressure are not good estimates of central blood volume [43]. Several meta-analyses have demonstrated the lack of evidence to support their use as endpoints of resuscitation [43-45]. These are being abandoned in favor of goal-directed therapy, using biochemical markers (discussed in the preceding paragraph) or functional estimates of central volume by echocardiography to establish real-time intracardiac hemodynamics [46,47]. (See "Hemodynamics derived from transesophageal echocardiography" and "Intraoperative fluid management", section on 'Goal-directed fluid therapy' and "Indications for bedside ultrasonography in the critically ill adult patient".)
Although a wide variety of measurable indices (eg, vena cava diameter, ejection fraction, arterial pulse pressure variation, jugular vein distensibility) continue to be popular study topics, these have not yet been widely adopted as measures for judging the adequacy of routine fluid resuscitation in postoperative surgical patients [48,49].
MAINTENANCE FLUID THERAPY — Once resuscitation is completed, maintenance fluid therapy is begun. Maintenance therapy is provided when the patient is not expected to tolerate oral or enteral feeding. The goal of maintenance therapy is to preserve blood volume and electrolyte balance and, if possible, to provide some calories to prevent muscle wasting. (See 'Fluid resuscitation' above.)
Daily fluid requirements — For most adult postoperative patients, approximately 30 mL/kg/day (1 to 1.5 mL/kg/hour) will meet their maintenance fluid requirements. For those with underlying organ dysfunction, daily maintenance volumes will need to be adjusted.
Restrictive fluid strategies may be helpful in avoiding overload in select patient populations. Literature in the trauma population supports a more restrictive maintenance fluid volume in normotensive patients, which has been associated with fewer ventilator days and a shorter intensive care unit course [50]. In such patients, the fluid goal is typically decreased by 50 to 75 percent, and, in some cases, permissive oliguria is accepted. Restrictive protocols have also been used after pneumonectomy, liver resection, and in Enhanced Recovery After Surgery (ERAS) settings with variable results. The most common downside to restrictive strategies used in the postoperative settings appears to be hypovolemia-associated hypotension and acute kidney injury. In a composite study of 1031 patients who underwent thoracotomy, a restrictive fluid strategy was associated with a higher incidence of composite complications (eg, acute respiratory distress syndrome, acute kidney injury, bronchopleural fistula) [51]. Similarly, in an randomized trial of 3000 patients undergoing abdominal surgery, a restrictive fluid strategy used during and after surgery did not improve survival and it was associated with a higher rate of acute kidney injury [18].
Fluid selection and rate — Hypotonic or isotonic saline solutions are the fluids most commonly used for maintenance fluid therapy in the postoperative period. The typical rate for maintenance fluid administration is 1 to 1.5 mL/kg/hour for patients with normal renal function who do not have significant ongoing fluid losses.
In the absence of shock and uncontrolled hyperglycemia (defined as glucose >180 mg/dL [52]), dextrose 5% may be added to half-normal saline (0.45%) or Lactated Ringer solution to stimulate basal insulin secretion and prevent muscle breakdown when the patient is unable to eat or drink, provided the patient has a normal serum sodium level. Other additives, including potassium, can also be added. For the average 70 kg adult, 400 to 500 calories per day is sufficient to stimulate basal insulin secretion for the prevention of catabolism. This amounts to approximately 100 to 150 grams per day of dextrose. However, this effect is short-lived, and after five days muscle breakdown will occur unless supplemental nutrition support is instituted. (See "Postoperative parenteral nutrition in adults".)
Patients with and without diabetes commonly develop transient hyperglycemia after surgery because of cortisol release with the stress response. Historically, insulin was administered to ameliorate this issue, whereas now it is common practice to simply exclude dextrose from maintenance fluids [53]. This is important to avoid uncontrolled hyperglycemia, which is associated with worse surgical outcomes. In a retrospective review of 7634 patients who underwent general, vascular, or gynecologic surgery, approximately half of patients without diabetes had hyperglycemia after surgery [54]. Patients without diabetes had worse outcomes compared with patients with diabetes for similar levels of hyperglycemia, which was defined as serum glucose >140 mg/dL. (See "Perioperative management of blood glucose in adults with diabetes mellitus".)
Many studies have driven the widespread practice of removal of dextrose from maintenance fluids for all patients, except for those with, or at risk for, hypoglycemia (eg, recent administration of insulin, decompensated cirrhosis, abrupt discontinuation of parenteral nutrition).
●For patients who cannot receive a large volume (eg, renal failure, heart failure, pneumonectomy), smaller volumes of dextrose 10% may be used instead of dextrose 5% (0.5 mL/kg/hour).
●For patients with hypernatremia, dextrose 5% in water can be used instead of saline. Close serum sodium monitoring is advised in this situation.
●For patients with shock, the standard of care is to remove dextrose from the fluid. Patients in shock will convert dextrose to lactate, thereby generating an acidosis.
●For patients who undergo neurosurgery or who suffer from traumatic and nontraumatic brain injury, hypotonic solutions are usually contraindicated because they may lower serum osmolarity, resulting in cerebral edema. Similarly, glucose-containing solutions are avoided due to possible exacerbation of neurologic injury [17].
Monitoring and adjustments — For patients receiving maintenance fluid therapy, a basic chemistry panel should be checked daily to ensure normal serum sodium is maintained without significant electrolyte derangement. In cases of large-volume administration (>4 L/day), consider checking the serum chemistry more than once daily to identify serum electrolyte derangements early. (See "Overview of postoperative electrolyte abnormalities".)
The volume and rate of maintenance fluid therapy may need to be adjusted to account for underlying physiologic conditions and other sources of fluid intake.
●As infection and inflammation subside, fluid in the "third-space" (ie, extravasated fluid) will return to the vascular space, a process referred to as "mobilization of the third-space fluid." As the patient's urine output increases (auto-diuresis), maintenance intravenous fluid rates can be safely reduced or discontinued.
●Most postoperative patients experience mild derangements in serum sodium balance due to intravenous fluid therapy, which can generally be managed by choosing an alternative fluid that provides more or less sodium. As an example, a general surgery patient with hypernatremia can receive dextrose 5% in water to lower the sodium or prevent it from rising further. Caution is advised in using the sodium to assess body water status in the setting of surgical fluid shifts as it may not be a reliable marker of total body water.
●Patients with cardiac, pulmonary, or renal disease often will not tolerate the standard amount of maintenance fluid therapy as they may be unable to tolerate excess volume expansion or eliminate excess fluid. Smaller maintenance fluid volumes (0.5 mL/kg/hour) can be administered to patients for whom volume overload may become a problem. Many of these patients also receive a significant volume of fluid associated with intravenous medications, which must be accounted for in the total daily fluid rate.
●Given that the transition to enteral intake may not go smoothly due to ileus, nausea secondary to pain medication, or poor appetite, oral intake should be established before maintenance fluids are discontinued. Patients who are able to quickly tolerate enteral intake usually tolerate a more rapid discontinuation of maintenance fluid therapy. Most other patients will typically continue to receive a modified amount of fluid, typically 25 to 50 percent of their daily goal, until improved enteral intake is demonstrated (ie, 1mL/kg/hour intake). Some providers will remove the dextrose from intravenous fluids once the patient tolerates enteral feeding.
●For patients who do not tolerate enteral intake and require parenteral nutrition, the parenteral nutrition rate is typically increased as maintenance fluid is decreased in equal volumes to maintain the goal fluid infusion per hour. Often, an order can be written as "total fluids = 1 mL/kg/hour"; this allows the nurse to make the appropriate changes in tandem over several hours.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Fluid and electrolyte disorders in adults".)
SUMMARY AND RECOMMENDATIONS
●Postoperative fluid therapy – Fluid management in the postoperative surgical patient can be simple or quite complex. Fluid therapy consists of replacement therapy and/or maintenance therapy. The volume of fluid needed is determined by the severity of the stress response to surgery, the underlying surgical disease, and the patient's overall medical condition. (See 'Introduction' above.)
•Replacement fluids – Replacement fluid therapy is indicated for many postoperative patients to compensate for deficits related to residual preoperative or intraoperative deficits, third-space losses related to the stress response to surgery, and to replace ongoing gastrointestinal or other bodily fluid losses. (See 'Fluid resuscitation' above.)
•Maintenance fluids – Maintenance fluids maintain hydration, electrolyte, and acid-base status and avoid catabolism in postoperative patients who cannot tolerate oral or enteral intake. (See 'Maintenance fluid therapy' above.)
●Stress response to surgery – The extent to which fluids administered intravenously in the postoperative period remain in the intravascular space depends on many factors, including the severity of the stress response to surgery. The stress response to surgery is triggered by (see 'Physiologic stress response to surgery' above):
•Entry into a major body cavity
•Significant tissue disruption
•Significant blood loss (>500 mL or 7 mL/kg)
•Hemodynamic instability
•Severe infection
●Estimating fluid losses – For fluid resuscitation, the type and volume of fluid that is lost guides the choice, volume, and rate of replacement. The fluid deficit is determined by estimating preoperative and intraoperative losses and subtracting the volume of fluid and blood given during the surgery. Ongoing gastrointestinal and other losses should be considered. (See 'Estimate the fluid deficit' above.)
●Endpoints of fluid resuscitation – The goal of fluid resuscitation is normal organ perfusion, which is achieved when the end-diastolic volume of the left ventricle generates an adequate stroke volume. To achieve normal organ perfusion, blood volume must be restored to 80 to 85 percent of normal blood volume. Physiologic markers of adequate perfusion include normalization of heart rate and blood pressure in healthy patients but may be unreliable in critically ill patients. (See 'Endpoints of fluid resuscitation' above.)
•Serum markers of adequate perfusion include lactic acid, base deficit, and central venous oxygen saturation (SvO2). Adequate intracardiac filling can be measured with echocardiography. As blood volume is restored, these parameters should trend toward normal.
•If a patient becomes unresponsive to fluid replacement, fluid therapy should be reconsidered to avoid complications of volume overload. For patients who do not respond appropriately to fluid challenge or have a persistently elevated lactic acid and SvO2, in spite of adequate fluid resuscitation, further evaluation in a closely monitored setting is warranted to identify bleeding or other complications of surgery (eg, acute renal dysfunction, myocardial infarction).
●Fluid selection – Crystalloid solutions remain the fluid of choice for replacement and maintenance fluid therapy following surgery. (See 'Fluid selection and rate' above.)
•Replacement fluids – For fluid replacement, isotonic or hypertonic fluids are used because their sodium content facilitates volume expansion (table 3), maintains serum osmolarity, and retains water in the vascular space. The choice is governed by the composition of the fluid that is lost. Resuscitative fluids are commonly administered as successive intravenous boluses (3.5 to 14 mL/kg aliquots) over 30 to 60 minutes until the desired response is observed (eg, improved urine output, improved mentation, normalizing base deficit). Rapid onset hypothermia can occur when large volumes of room-temperature fluid are administered. If this is anticipated, we suggest using a Level 1 rapid transfuser, which warms the fluid as it is infused.
•Maintenance fluids – For maintenance fluid therapy, isotonic or hypotonic solutions (table 3) with or without additives (eg, dextrose, potassium) are used to maintain normal acid-base status, electrolytes, and volume status. For postoperative patients with normal organ function, a volume of maintenance fluid between 1 and 1.5 mL/kg/hour will meet requirements. Adjustments may be required to account for organ dysfunction, intravenous medications, or nutritional therapies.
●Caloric support – In the absence of a shock state or hyperglycemia, dextrose can be added to maintenance fluid to provide a minimal number of calories (up to 500 calories per day) to stimulate basal insulin secretion and prevent catabolism. However, after five days muscle breakdown will occur unless nutritional support, preferably via enteral access, is instituted. (See 'Fluid selection and rate' above and 'Monitoring and adjustments' above.)
•Enteral intake should be established before maintenance fluids are titrated down or discontinued. Some patients may continue to require a modified amount of intravenous fluid until improved enteral intake is demonstrated.
•For those patients who do not tolerate enteral intake, parenteral nutrition may be indicated. The parenteral nutrition rate is increased as maintenance fluid is decreased in equal volumes to maintain the goal infusion rate per hour over several hours.
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