Perioperative Fluid Management

Abstract

Perioperative fluid management is a critical aspect of surgical care, containing the preoperative, intraoperative, and postoperative phases. Management of patients without individualisation, utilizing established standard protocols, may lead to undesirable events such as hypovolaemia and hypervolaemia during both intraoperative and postoperative periods. Insufficient fluid administration can result in peripheral vasoconstriction, leading to decreased oxygen delivery, impaired tissue perfusion, and dysfunction of vital peripheral organs. Conversely, excessive fluid administration may cause increased vascular permeability due to glycocalyx damage, tissue oedema, impaired tissue perfusion, local inflammation, delayed wound healing, wound infection, and anastomotic leaks. The pursuit of an optimal fluid regimen that prevents volume overload while maximizing tissue perfusion has led to the adoption of individualized, targeted fluid replacement therapies, supported by advancing technology. In this approach, basic physiological variables related to cardiac output or global oxygen distribution are measured. In optimized fluid management, fluid replacement is adjusted according to targeted physiological variables in a continuously re-evaluated process. These physiological variables can be assessed using different methods, from simple tests to complex devices that evaluate the patient’s tissue perfusion and cardiac output. Developments in recent years have drawn attention to the future of non-invasive or less invasive cardiac output measurement devices, as well as the utilization of ultrasonographic cardiac output measurements.

1. Introduction

Perioperative fluid management is a critical aspect of surgical care, which contains the preoperative, intraoperative, and postoperative phases.

Fluid therapy is essential for treating surgical patients, and it can be lifesaving. Insufficient fluid volume (hypovolemia) can lead to poor circulation, reducing oxygen delivery to organs and peripheral tissues, resulting in organ dysfunction and shock. Conversely, excessive fluid (fluid overload) can cause interstitial oedema, local inflammation, and hinder collagen regeneration, weakening tissue healing and increasing the risk of postoperative complications such as wound infections, wound rupture, and anastomotic leakage. Additionally, fluid overload can impair cardiopulmonary function. Therefore, administering fluid therapy on an individual basis, as needed, and in appropriate amounts is essential [1, 2, 3, 4, 5].

Perioperative fluid management strategies can be examined in three sections.

2. Preoperative fluid optimization

The body’s adaptive mechanisms in hypovolaemia attempt to maintain blood flow to critical organs such as the heart and brain. Peripheral vasoconstriction that develops through this mechanism may have harmful effects on organ function in the perioperative period. This can lead to ischemia in surgical tissues, which require adequate blood flow for tissue repair and healing.

Several factors contribute to reduced effective circulating blood volume in surgical patients. These include preoperative fasting, hypertonic bowel preparations, anesthetic agents, and positive pressure ventilation. Consequently, anesthetized patients often present with a functional intravascular volume deficit [1].

Preoperative hydration is an essential consideration for patient preparation. Studies demonstrate the benefits of preoperative oral carbohydrate solutions over traditional fasting rules, as well as the importance of personalized fluid plans tailored to the patient’s needs.

A meta-analysis of existing trials found that a shorter preoperative fasting period did not increase the risk of aspiration or result in larger volumes of gastric content [2].

The current guidelines in Europe and America suggest that clear fluids can be consumed up to 2 hours before elective surgery. A study has demonstrated that correcting intravascular volume deficits before surgery effectively reduces postoperative nausea and vomiting (PONV) as well as postoperative pain in high-risk patients [3].

A large retrospective review found that preoperative dehydration is linked to higher rates of postoperative acute renal failure (ARF), myocardial infarction (MI), and cardiac arrest. Additionally, hydrotherapy for dehydrated patients has been shown to decrease postoperative complications in colorectal surgery [4].

These approaches aim to prevent dehydration and maintain optimal physiological reserves before surgery, contributing to the acceleration of recovery and the reduction of perioperative complications. Individual treatments should be applied to the patient, and both hypovolemia and hypervolemia should be avoided. The main goal should be optimal tissue oxygenation and euvolemia.

3. Intraoperative fluid strategies

Calculating the fluid volume to administer per unit time based on a formula involving body weight, type of surgical trauma, and operation time is not supported by established physiological principles [5]. Studies have indicated that a strategy focusing on hemodynamic stabilization can reduce complications after major surgery [6]. Meta-analyses and reviews have further highlighted the effectiveness of this approach across different patient populations and types of surgeries [6, 7].

A patient’s physiological state and hemodynamic stability are complex. The main goals of the applied treatments, including fluid therapy and use of vasoactive drugs such as vasopressors, vasodilators, and inotropes, are to maintain adequate blood volume, perfusion pressure, cardiac output, tissue blood supply, and oxygen delivery.

Fluid therapy is often the first choice for hemodynamic support due to the decrease in circulating blood volume associated with anesthesia and surgery. However, its impact is indirect. Optimizing oxygen delivery and removing metabolic by-products may require a combination of fluid therapy, drugs, and mechanical support.

Both hypovolemia and hypervolemia increase postoperative morbidity. Hypovolemia can cause vasoconstriction, decreased oxygen delivery, reduced tissue perfusion, and dysfunction in peripheral organs. Conversely, hypervolemia can lead to tissue oedema, which can result in worsened tissue perfusion, pulmonary oedema, local inflammation, delayed wound healing, wound site infections, and anastomotic leaks [8]. Intestinal oedema, associated with hypervolemia, is known to increase bacterial translocation and the risk of multiple organ failure syndrome.

Hypervolemia can harm glycocalyx, an endovascular structure vital for endothelial integrity. This damage leads to fluid shifting into the interstitial space. Atrial natriuretic peptide (ANP) is also involved in this process and is secreted during hypervolemia [9]. When the glycocalyx is damaged, as in cases of ischemia, inflammation, surgery, or acute hypervolemia, colloids, and crystalloids leak from the vascular barrier into the interstitial space, resulting in tissue oedema [9, 10].

Fluid infusions directly increase vascular volume, improving perfusion and blood pressure, especially if the heart is responsive. However, these effects depend on the cardiac and peripheral vascular status, leading to varying effects. Therefore, blind fluid infusion or using vasopressors without understanding the patient’s cardiovascular status is not advised.

According to the Frank-Starling curve, there is a positive correlation between preload and stroke volume, and this relationship follows a curvilinear shape. A larger increase in stroke volume is observed for a given increase in preload in the steeply rising portion of the curve. This part can be considered as the preload-dependent area. The plateau portion of the curve can be defined as a preload-independent area where volume expansion will not create significant changes in stroke volume. Since left ventricular function reaches its maximum level near the plateau of the Frank-Starling curve, subsequent fluid load has little effect on cardiac output and only causes increased tissue oedema and tissue hypoxia. In daily practice, clinicians evaluate several hemodynamic variables to indicate whether the patient lies in the preload-dependent or preload-independent area of the Frank-Starling curve.

In the operating room, fluid management becomes a dynamic process, requiring careful consideration of fluid types and volumes. Balanced crystalloid solutions remain a cornerstone, but colloids may be indicated in specific cases such as major hemorrhage or hypoalbuminemia. The concept of goal-directed fluid therapy, guided by hemodynamic monitoring, allows for precise fluid administration, minimizing the risk of fluid overload or inadequate perfusion during surgery.

3.1 Goal-directed fluid therapy (GDFT)

The pursuit of an optimal fluid regimen that prevents volume overload while maximizing tissue perfusion has led to the adoption of individualized, targeted fluid replacement therapies, supported by advancing technology. In this approach, basic physiological variables related to cardiac output or global oxygen distribution are measured. The administration of crystalloids, colloids, blood products, or inotropic agents is then dynamically adjusted based on these targeted physiological variables.

Tissue and organ perfusion rely on both perfusion pressure and cardiac output (CO). It is crucial to accurately measure CO, or at least detect changes in CO. While invasive monitoring with a pulmonary artery catheter (PAC) was once the gold standard, many alternative and less invasive devices are now available. The term “Minimally Invasive CO Monitoring” encompasses all devices capable of calculating CO without requiring a PAC. Cardiac output monitor, used alongside protocols to optimize CO and oxygen delivery (DO₂), as well as direct intravenous fluid therapy and inotropic support, are fundamental to targeted fluid therapy. Studies have demonstrated that targeted fluid therapy, when combined with minimally invasive CO monitors, enhances perioperative outcomes in high-risk surgical patients [11].

The objective of intraoperative fluid management is to maintain central euvolemia. Therefore, it is recommended that patients undergoing surgery under the ERAS (Enhanced Recovery After Surgery) protocol have an individualized fluid management plan. Excessive crystalloid use should be avoided in all patients. A “zero balance” approach is encouraged for some patients undergoing low-risk surgery. Goal-directed fluid therapy (GDFT) is recommended for most patients undergoing surgeries involving large fluid shifts. Optimal perioperative fluid management is a critical component of the ERAS protocol. One study demonstrated that simply modifying fluid management on the day of surgery reduced perioperative complications by 50% [8].

Randomized controlled studies and meta-analyses have shown that GDFT reduces postoperative renal damage, postoperative complications, postoperative hospital stay, and mortality [12, 13, 14, 15]. Perioperative targeted fluid management algorithms have been shown to be beneficial in high-risk geriatric patients and may reduce the length of hospital stay [16].

Several dynamic parameters are used in GDFT to assess fluid responsiveness and guide fluid administration. By incorporating these dynamic parameters into fluid resuscitation protocols, clinicians can tailor fluid therapy to the individual patient’s needs, optimizing hemodynamic status and improving outcomes.

3.1.1 Dynamic methods in determining cardiac preload

Dynamic methods for assessing cardiac preload involve using physiological parameters that change in response to alterations in intrathoracic pressure or volume status. Dynamic parameters provide real-time information about the heart’s ability to respond to volume changes, which can help guide fluid therapy in critically ill patients or during surgery.

3.1.1.1 Pulse contour analysis

This is based on the principle that the area under the systolic portion of the arterial pressure waveform is proportional to the stroke volume (SV). It was first described by Erlanger and Hooker in 1904, who suggested that cardiac output (CO) was proportional to arterial pulse pressure [17]. In this method, the area under the curve is measured until the end of the post-diastolic ejection phase and divided by the aortic impedance measuring left ventricular (LV) function. It also measures stroke volume variation (SVV) and pulse pressure variation (PPV), which are useful in estimating fluid responsiveness.

3.1.1.1.1 Pulse pressure variation (PPV)

This dynamic parameter was established by demonstrating changes in stroke volume induced by positive pressure ventilation. Heart-lung interactions during mechanical ventilation and changes in hemodynamic signals with respiration have gained great popularity in recent years [18]. Arterial pulse pressure is calculated as the difference between systolic and diastolic blood pressure. PPV is calculated by dividing the peak pulse pressure (PP) (PPmax − PPmin) by the average PP [(PPmax + PPmin)/2] [19]. Arterial pulse pressure is directly proportional to stroke volume and inversely proportional to the compliance of large systemic arteries. Arterial compliance is assumed to remain constant throughout the respiratory cycle. Therefore, PPV should reflect the magnitude of respiratory-induced changes in stroke volume. Consequently, PPV should predict the degree of biventricular preload response and hence the hemodynamic response to fluid infusion. In conditions where there is no obstacle to the use of this parameter in the patient, if PPV is high and decreases with fluid infusion, the patient can be considered fluid-responsive [18]. Mechanically ventilated patients with normal tidal volume have been the subject of numerous studies in a variety of clinical settings (sepsis, intra-perioperative periods) and these studies have confirmed the excellent value of PPV in predicting fluid response in patients without spontaneous respiratory activity and cardiac arrhythmia [20, 21].

Most studies have also highlighted the clinical utility of PPV, showing that it is much better at predicting fluid response than static preload markers such as cardiac filling pressures. The threshold value of PPV varies between 10% and 15%. Hemodynamic monitors such as PiCCO, VolumeView, LiDCO, MostCare, and Pulsioflex allow automatic calculation of PPV and continuous display on their screens in real time. Therefore, PPV may be a helpful tool to guide volume expansion during surgery as a study done during perioperative phase demonstrated that its capacity to detect a change in cardiac output following volume expansion is better than changes in arterial pressure [22]. As a result, PPV can be used to track the hemodynamic response to fluid therapy in addition to predicting fluid response. to predict fluid response but also to monitor hemodynamic response to fluid therapy. The use of PPV for intraoperative GDFT has been shown to reduce the duration of mechanical ventilation, postoperative complications, and intensive care unit or hospital stay in patients undergoing high-risk surgery [23].

3.1.1.1.2 Stroke volume variation (SVV)

SVV is measured with continuous cardiac output monitoring devices such as FloTrac/Vigileo, PiCCO, LiDCO, MostCare, or esophageal Doppler. It is calculated by dividing the difference between maximum SV and minimum SV (SVmax − SVmin) by their average [(SVmax + SVmin)/2] over a 30-second time window [19]. SVV has been reported as a good predictor of fluid responsiveness in neurosurgical patients, general surgery patients, septic shock patients, and after cardiac surgery [24, 25, 26, 27]. In a study conducted on patients who underwent surgery for liver transplantation, a sensitivity and specificity of 94% and a threshold value of SVV of 10% were reported [28]. It has been shown that gastrointestinal complications are reduced in patients undergoing major abdominal surgery who undergo intraoperative SVV-guided GDFT [29].

3.1.1.2 Limitations of pulse contour analysis methods

The most significant limitation is the presence of spontaneous respiratory activity. In a patient with spontaneous respiratory effort, ventilation cannot be provided at regular intervals and with an equal volume of tidal volume. Accordingly, changes in intrathoracic pressure become irregular, and changes in stroke volume are not preload-dependent. The existence of cardiac arrhythmias is another restriction on the use of respiratory variability measures. In these situations, diastolic irregularity rather than heart-lung interactions is responsible for the variation in stroke volume. The final drawback is that the arterial pressure changes brought on by mechanical breathing are likewise minimal in patients with low tidal volume ventilation. Even in reaction to preload, there may not be a sufficient intrathoracic pressure change during low tidal volume breathing. For this reason, studies indicate that PPV is reliable when ventilation is provided with a tidal volume of at least 8 ml/kg [30, 31].

In cases of low lung compliance, changes in alveolar pressure are less effectively transmitted to intrathoracic structures. Consequently, intravascular pressure changes induced by mechanical ventilation may also be diminished. A clinical study demonstrated that PPV loses its ability to predict fluid responsiveness in patients with respiratory compliance less than 30 ml/cm/H₂O [32].

Another limitation is the patient’s high respiratory frequency. It has been reported that the reliability of SVV decreases if the ratio of heart rate to respiratory rate is lower than 3.6 or if the respiratory rate exceeds 40/min [33].

It is emphasized that operating room conditions are generally ideal for accurate interpretation of PPV and other respiratory variability indices. Its use has decreased in the intensive care environment where these limitations are common; alternative methods have been developed to estimate fluid response in critically ill patients [18].

1. End-expiratory occlusion test (EEOT): EEOT is a preload-dependent method that utilizes heart-lung interactions to estimate fluid response in ventilated patients. It can be used in patients with cardiac arrhythmia or spontaneous ventilator triggering, where parameters like PPV and SVV are not reliable. During a 15-second end-expiratory occlusion (EEO), a greater than 5% increase in arterial pulse pressure measured by the PiCCO device, or in the cardiac index derived from the pulse curve, provides a good prediction of fluid responsiveness [34]. This test is advantageous due to its simplicity. It is considered more reliable than PPV and SVV in patients with acute respiratory distress syndrome (ARDS) characterized by low tidal volume and low lung compliance [32, 35]. However, it cannot be used in patients in whom spontaneous triggering of the ventilator interrupts EEO and, of course, in patients who are not ventilated. Due to its brief duration, EEOT requires the use of a real-time hemodynamic monitor to assess hemodynamic response. Therefore, pulse contour analysis monitors or ultrasound techniques may be appropriate.

2. Mini fluid challenge test: Classic liquid loading typically involves infusing 300–500 ml of fluid [36], but its irreversibility can lead to fluid overload, especially with repeated daily administration. To reduce this risk, a ‘mini’ fluid challenge has been proposed, consisting of a rapid infusion of 100 ml over 1 minute. In clinical studies, an increase of more than 10% in the subaortic velocity time integral, measured using echocardiography, has been found to predict fluid responsiveness accurately [37]. However, a major limitation of this test is that even in cases of preload responsiveness, a very small volume infusion causes only minimal changes in cardiac output. Therefore, accurate measurement of cardiac output is crucial to minimize false-negative results.

3. Passive leg raise test (PLRT): PLRT is independent of heart-lung interactions when assessing preload. Therefore, it can be used in spontaneously breathing patients [38]. Raising the legs from the horizontal position induces a gravitational blood transfer from the lower extremities toward the intrathoracic area. This significantly increases right and left cardiac preload, allowing assessment of the position on the Frank-Starling curve of increased preload during testing [39]. PLRT remains a good indicator of fluid response in patients with acute circulatory failure, spontaneous respiratory activity, or cardiac arrhythmias [40, 41].

   A 10–12% increase in cardiac output or stroke volume during PLRT allows us to predict fluid responsiveness even in patients with cardiac arrhythmias and/or spontaneous ventilator triggering. However, since changes in arterial pressure may result in false-negative cases, cardiac output response should be monitored with real-time cardiac output monitoring technologies and devices to evaluate the hemodynamic response to PLR [38, 42].

   The complete reversibility of PLRT’s effects when the legs are returned to the supine position confirms its role as a safe, risk-free preload response test [38, 42]. However, despite its reliability and convenience, PLRT has limitations. It cannot be used in situations where patient mobilization is impossible or prohibited, such as in the operating room or in cases of head trauma [43]. Additionally, the reliability of PLRT is compromised in cases of increased intra-abdominal pressure [44].

4. Inferior vena cava collapsibility index (cIVC): The inferior vena cava (IVC) is a low-pressure and highly collapsible vein. Its diameter varies depending on intravascular volume status, right heart function, and respiration [45]. In each respiratory cycle, the IVC contracts and relaxes according to venous return, which changes due to negative pressure. Negative pressure during inspiration increases venous return to the heart, causing the IVC to collapse [46]. Conversely, during expiration, the IVC diameter increases again and returns to its baseline value. These changes in vessel diameter provide guidance in assessing the patient’s clinical status.

   In mechanically ventilated patients, the effect of respiration on intrathoracic pressure is completely reversed. Positive pressure applied during inspiration causes venous return to the heart to decrease and the diameter of the IVC to increase. The change in diameter on the IVC in mechanically ventilated patients can be calculated using the ‘distensibility index’ [47].

   It is believed that the collapse of the IVC during inspiration in spontaneously ventilated patients or the stretching of the IVC during inspiration in mechanically ventilated patients predicts fluid response [48].

   IVC ultrasound has several advantages over other fluid response assessment methods. It is non-invasive, inexpensive, widely available, can be obtained with minimal training, can be performed quickly, can be combined with heart and lung ultrasound, and can be repeated frequently [47].

   IVC ultrasound is performed with a low-frequency (2–5 MHz) convex probe using the subxiphoid view. The IVC should be viewed longitudinally in the long axis, keeping the connection between the IVC and the right atrium on the screen. The M-mode line should be placed perpendicular to the IVC and 2–3 cm before entering the right atrium. It should be measured at the widest (IVCd-max) and narrowest (IVCd-min) points by monitoring for 2 or 3 respiratory cycles [48].

   cIVC is calculated according to the formula:

   $$\text{cIVC}=\left(\text{IVCd-}\max –\text{IVCd-}\min \right)/\text{IVCd-}\max \times 100$$E1

   A cIVC value between 40% and 48% could predict fluid response with good specificity and sensitivity, according to studies assessing the usefulness of cIVC as an indicator of fluid response and a guide for fluid management in critically ill patients with acute circulatory failure and spontaneous breathing [31, 46, 49]. Given the circumstances, it seems that very high or very low cIVC values could be helpful in accurately indicating or ruling out fluid responsiveness, particularly in individuals suffering from acute circulatory failure brought on by sepsis. To guide fluid management, cIVC should be interpreted cautiously and considered in conjunction with other parameters, not as a stand-alone parameter [50].

   In spontaneously breathing patients undergoing elective non-cardiac surgery, cIVC-directed intravascular fluid therapy before spinal anesthesia has been shown to be an effective method to prevent hypotension after spinal anesthesia [51].

   In spontaneously breathing patients, IVC measurements estimate right atrial pressure (RAP), allowing rapid identification of hypovolemic patients [52, 53]. The American Society of Echocardiography states that in measurements with more than 50% collapsed IVC diameter (IVCd) less than 2.1 cm by incision, the right atrial pressure (RAP) is 3 mm Hg (0–5 mm Hg); it is stated that RAP is 15 mm Hg (10–20 mm Hg) in measurements with less than 50% collapse with inspiration and IVCd greater than 2.1 cm [54].

4. Postoperative fluid balance

Following surgery, patients face challenges related to fluid shifts, postoperative stress response, and potential complications such as dehydration or fluid overload. Postoperative patients with extensive traumatic or surgical tissue injury, prolonged surgeries and associated stress response, burns, critical illness, or sepsis require more complex resuscitative fluid therapy in addition to maintenance therapy.

The stress response to traumatic or surgical tissue damage is the “Fight or Flight” response designed to facilitate survival after a major injury. This stress response can occur when the integrity of large body cavities such as the chest, abdomen, joints, and skull is disrupted due to surgery or trauma. It can also be seen in cases of significant tissue damage such as burns, pancreatitis, and gunshot wounds. It may occur in postoperative patients in cases of significant blood loss, hemodynamic instability, and sepsis.

Vasopressin, aldosterone, catecholamines, cortisol, and inflammatory cytokines are secreted in response to stress. These substances affect the patient through various mechanisms, including hemodynamic response, cardiac output, glucose metabolism, and vascular permeability. These effects may occur more intensely in the postoperative period, and fluid management of the patient remains as important as in the intraoperative period.

Individualized postoperative fluid management, coupled with early mobilization, becomes crucial in restoring fluid balance and promoting recovery. Strategies focusing on personalized fluid replacement and monitoring contribute to better postoperative outcomes and reduced recovery times.

1. Assessment: assess the patient’s fluid status based on clinical signs, urine output, laboratory values (e.g., electrolytes, creatinine), and the type of surgery performed.

   Intravenous fluid administration will not improve tissue perfusion unless it increases stroke volume and, consequently, cardiac output.

   Studies show that almost half of unstable patients do not respond hemodynamically to fluid resuscitation [21, 55]. This indicates that fluid resuscitation may not always be the appropriate approach to ensure adequate tissue perfusion, especially in unstable patients. Therefore, assessing the patient’s response to fluid resuscitation should determine the need for additional volume.

2. Maintenance fluids: once the patient is stable, maintenance fluids should be provided to replace ongoing losses. The choice of fluids and rate of administration depends on the patient’s fluid status, comorbidities, and surgical considerations.

   There are generally two main types of fluids used during major surgery, and the choice of fluid can impact outcomes. The more commonly used type is crystalloid solutions, which remain the fluid of choice for simple postoperative fluid replacement. Crystalloid solutions increase intravascular volume, but their intravascular residence time is shorter than colloids. Prolonged administration of chloride-rich solutions can lead to hyperchloremic acidosis, kidney injury [56, 57, 58, 59, 60, 61, 62].

   Compared to crystalloid therapy, colloids require less volume to achieve the same hemodynamic effect. Therefore, the use of colloids can be considered an approach to limit total volumes and could potentially lead to better results. Studies comparing the results of surgical patients receiving colloid or crystalloid fluid replacement generally found no difference [63, 64]. A subgroup analysis of the postoperative population of a large, randomized trial in the intensive care unit found no difference in mortality between crystalloid and colloid-treated populations Although starch solutions can be used intraoperatively, they are not commonly used for volume expansion in postoperative surgical patients due to their potential to cause bleeding or abnormal clotting [65].

3. Avoiding overhydration: large volumes of intravenous fluid may cause complications due to the formation of tissue oedema. Liberal administration of fluid may impair pulmonary, cardiac, gastrointestinal, and renal function, contributing to postoperative complications and prolonged recovery [66, 67, 68, 69].

4. Electrolyte monitoring: monitor electrolyte levels regularly, especially in patients at risk of electrolyte imbalances (e.g., those with renal dysfunction or certain surgical procedures).

   Serum lactic acid, base deficiency, and central venous oxygen saturation (SvO2) are biochemical markers of perfusion frequently used to confirm the adequacy of end-organ perfusion in critically ill patients [70].

5. Considerations for specific surgeries: certain surgeries may require special considerations for fluid management. For example, patients undergoing major abdominal surgery may require different fluid strategies than those undergoing minor procedures, extensive traumatic or surgical tissue injury, burns, critical illness, or sepsis require more complex resuscitative fluid therapy.

6. Individualized approach: fluid management should be individualized based on the patient’s clinical condition, comorbidities, and surgical requirements. Collaborate with the surgical team and other healthcare providers to optimize fluid therapy.

7. Early mobilization and oral intake: encourage early mobilization and oral intake as tolerated, as this can help prevent fluid retention and promote recovery.

   Early mobilization is a key element of ERAS protocols for all postoperative patients capable of ambulation [71]. It is essential for reducing the risk of postoperative pneumonia and venous thromboembolism and hospital length of stay.

8. Monitoring and documentation: monitor the patient’s fluid status closely and document intake, output, and any fluid-related interventions to ensure continuity of care.

9. Multimodal approach: consider multimodal approaches to fluid management, including goal-directed therapy and dynamic methods in determining fluid response to optimize outcomes and minimize complications.

5. Future directions

In the future, the integration of emerging technologies and personalized approaches is poised to revolutionize perioperative fluid management. From advanced hemodynamic monitoring to individualized fluid optimization algorithms, the future holds promise for more precise and tailored strategies, ultimately enhancing patient safety and surgical outcomes. Areas for further research include the impact of fluid management on specific patient populations and the development of comprehensive perioperative fluid management guidelines.

6. Conclusion

In conclusion, perioperative fluid management stands as a cornerstone of surgical care, with far-reaching implications for patient recovery and outcomes. By embracing evidence-based practices, individualized approaches, and emerging technologies, healthcare providers can continue to refine perioperative fluid management, paving the way for safer surgeries and improved patient experiences.