Fluid management after hepatectomy: Pursuing precision recovery through balance

Abstract

Post-hepatectomy fluid management represents a critical determinant of patient outcomes, poised at the intersection of maintaining adequate organ perfusion and mitigating complications from fluid overload. The unique postoperative pathophysiology - characterized by systemic inflammation, transient hepatic insufficiency, and fluid redistribution - creates a clinical dilemma where both hypovolemia and hypervolemia carry significant risks. Contemporary practice has evolved from empirical, one-size-fits-all regimens toward a phased, goal-directed, and individualized strategy underpinned by dynamic hemodynamic monitoring. In the early postoperative phase (0-24 hours), a restrictive approach utilizing balanced crystalloids (initial target of 30 mL/kg/day to 35 mL/kg/day) is recommended. During the stable phase (> 24 hours), the focus shifts to achieving a negative fluid balance via diuretics, provided organ perfusion is secured. For special situations - including patients with cirrhosis, postoperative hemorrhage, or acute kidney injury - rigorous, real-time assessment of fluid responsiveness using dynamic parameters such as stroke volume variation and lactate trends is paramount. This opinion review synthesizes current evidence and controversies to present a modern, enhanced recovery after surgery-aligned framework for post-hepatectomy fluid management, arguing that meticulous, data-driven regulation is fundamental to reducing complications, promoting liver regeneration, and optimizing recovery.

Key Words: Hepatectomy; Postoperative care; Fluid therapy; Restrictive fluid resuscitation; Goal-directed therapy; Fluid balance; Postoperative complications

Core Tip: Post-hepatectomy fluid management is critical to postoperative recovery, with the core goal of balancing adequate organ perfusion and avoidance of fluid overload. A phased, goal-directed strategy is recommended: A restrictive 0-24 hours postoperative phase with restrictive fluid resuscitation using balanced crystalloids, followed by a stable phase (> 24 hours) targeting negative fluid balance via diuretics while preserving effective systemic perfusion. Guided by dynamic monitoring of key parameters, this enhanced recovery after surgery-aligned individualized approach prevents complications like pulmonary edema and intra-abdominal hypertension, promotes liver regeneration, and optimizes key clinical outcomes for patients undergoing hepatectomy.

INTRODUCTION

Hepatectomy is the primary treatment for space-occupying liver lesions. The quality of postoperative recovery depends not only on the surgical precision but also on the optimization of perioperative management[1,2]. Fluid management is a core component of perioperative care, which is fundamental to maintaining organ function, but one which often presents a significant clinical challenge[3,4]. Correctly managing patients’ fluid levels is not solely a decision about maintaining an optimal fluid volume, but rather the goal is to find and sustain an optimal balance between the dynamic states of hypovolemia and fluid overload[5]. Inappropriate fluid intervention can trigger serious complications: For example, fluid overload may lead to tissue edema, and in patients with cirrhosis, pre-existing portal hypertension, or limited cardiac reserve, it may also exacerbate portal hypertension and cause cardiopulmonary dysfunction, while hypovolemia can readily induce organ hypoperfusion injury and acute kidney injury (AKI). Both of these scenarios can significantly prolong hospital stays and increase postoperative mortality[6,7]. Following the widespread adoption of the enhanced recovery after surgery (ERAS) guidelines and the iterative advancement of hemodynamic monitoring technologies, post-hepatectomy fluid management has evolved from an empirical, standardized model toward a system of more personalized medicine. This new approach is based on pathophysiological mechanisms, implemented in stages, and guided by precise monitoring of patients[8,9].

CORE CHALLENGE: PRECISE NAVIGATION BETWEEN “SCYLLA AND CHARYBDIS”

The unique postoperative pathophysiological changes often observed in hepatectomy patients create a dilemma for planning fluid management. On one hand, systemic inflammatory response syndrome, which can be triggered by surgical trauma, increases capillary permeability, causing a significant fluid shift from the intravascular space to the third space (e.g., the intestinal wall, peritoneal cavity, or surgical site), resulting in a depletion of the relative effective circulatory volume. Moreover, insufficient or delayed fluid resuscitation at this stage can lead to the hypoperfusion of vital organs such as the kidneys and intestines, potentially inducing severe complications such as AKI and intestinal barrier dysfunction, thereby hindering postoperative recovery[10,11]. On the other hand, the liver, which is the core metabolic organ, can experience temporary postoperative functional impairment, leading to reduced albumin synthesis and a reduced capacity for endogenous aldosterone inactivation. In combination with inflammation-mediated changes to vascular permeability, this promotes fluid extravasation and tissue edema[12]. During this phase, excessive administration of fluids, particularly high crystalloid volumes, can significantly exacerbate tissue edema and increase intra-abdominal pressure. This not only impairs diaphragmatic movement and pulmonary ventilation, but it can also limit microcirculation at the plane of liver resection, thereby hindering hepatocyte regeneration. In severe cases, this can induce abdominal compartment syndrome[13]. Furthermore, tissue edema may impair wound healing and increase the risk of postoperative infection, particularly in patients undergoing combined organ resection or biliary/enteric reconstruction[14]. Therefore, the core challenge of post-hepatectomy fluid management is achieving a regulated balance between the risks of organ injury from hypovolemia and worsening complications due to fluid overload (Figure 1).

Figure 1 Summary of fluid management for patients after liver resection. AKI: Acute kidney injury. This figure was created with BioRender (Available from: BioRender.com).

MODERN MANAGEMENT STRATEGY: STAGED, GOAL-DIRECTED, AND INDIVIDUALIZED PROTOCOL

To address these clinical challenges, the current domestic and international guidelines, in addition to expert consensus, unanimously recommend abandoning a “one-size-fits-all” standardized fluid approach in favor of a staged, goal-directed, and individualized management strategy[8,15-17].

Early postoperative phase (0-24 hours): Restrictive fluid administration with defined resuscitation endpoints

The core principle of this phase is the administration of controlled fluid therapy, aiming to avoid unnecessary volume loading while ensuring basic organ perfusion. Recommendations suggest that a total fluid intake of approximately 30 mL/kg/day to 35 mL/kg/day (based on ideal body weight) can serve as a general starting framework for restrictive fluid therapy, with dosing requiring individualization based on the extent of liver resection, remnant liver function, intraoperative blood loss and transfusion status, the presence of cirrhosis or portal hypertension, and real-time perfusion and hemodynamic markers. The first choice of fluids should be balanced crystalloid solutions (e.g., Lactated Ringer’s solution, or acetate-balanced solutions), since their compositions are closer to physiological extracellular fluid and these confer a lesser impact on systemic acid-base balance. Notably, in patients with advanced cirrhosis, lactate interpretation can be challenging, and lactate trends should be interpreted with caution, with acetate-buffered balanced solutions serving as a preferred alternative in such cases. Colloids (e.g., hydroxyethyl starch) should be used cautiously due to the potential risks of renal injury and interference with coagulation[18,19]. In patients with severe edema and hypoalbuminemia, human albumin can be used, but its benefit for routine prophylactic use remains controversial[20,21].

During this phase, fluid administration endpoints are recommended to move beyond vague standards like “normal blood pressure” and instead rely on clear tissue perfusion indicators; for example, urine output maintained above 0.5 mL/kg/hour, normal or progressively decreasing blood lactate levels, a normal capillary refill time, and the patient should be conscious and with warm extremities. Notably, capillary refill time as a perfusion marker requires cautious interpretation due to its limitations, such as interference from vasopressor use and abnormal body temperature. These indicators allow for a more precise assessment of volume status, preventing unguided over-resuscitation or under-resuscitation[22,23].

Stable postoperative phase (> 24 hours): Transition to negative fluid balance and edema resolution

As the initial peak inflammatory response subsides and capillary permeability normalizes, the focus of fluid management shifts from a more restrictive input to an actively promoting output. Assuming that organ perfusion is adequate, diuretics (loop diuretics such as furosemide are preferred) can be used to achieve a daily negative fluid balance (whereby output is greater than input). This mobilizes and eliminates third-space fluid, reduces tissue edema, and subsequently promotes gastrointestinal function recovery, in addition to improved pulmonary ventilation[13]. Furthermore, the early resumption of oral intake should be encouraged during this phase to gradually reduce the patient’s dependence on intravenous (IV) fluids. IV fluid dosage should be dynamically adjusted based on oral intake, facilitating a smooth transition from IV support to enteral nutrition[24].

FOUNDATION FOR PRECISION REGULATION THROUGHOUT: DYNAMIC MONITORING SYSTEM

The effective implementation of a staged, individualized strategy relies on rigorous hemodynamic monitoring. Traditionally used indicators, such as heart rate, blood pressure, and central venous pressure (CVP), provide basic physiological information, but they have limitations. Static CVP values are influenced by various factors (thoracic pressure, ventricular compliance, position), limiting the value of absolute numbers. Maintaining a relatively low CVP (e.g., < 8 mmHg) may favor hepatic venous drainage and reduce postoperative bleeding risk. However, CVP should be interpreted as a trend and in the context of the overall clinical situation, rather than as a fixed postoperative target, and its value should be assessed comprehensively with other hemodynamic indicators[25-27].

However, dynamic indicators of volume responsiveness, such as stroke volume variation (SVV)[28], pulse pressure variation (PPV), and ultrasound-guided assessment of inferior vena cava respiratory variation, offer greater clinical value[29-32]. These indicators can be used to accurately predict a patient’s response to fluid challenges, helping clinicians decide whether to administer fluid, thereby avoiding unguided expansion of fluid administration or excessive restriction. Additionally, the continuous monitoring of blood lactate levels and mixed venous oxygen saturation can be used to effectively assess the balance between systemic oxygen delivery and consumption, enabling timely detection of occult organ hypoperfusion and providing precise guidance for making adjustments to fluid management[33]. A recent insightful study shows that arginine vasopressin elevation persists longer than aldosterone elevation after major liver resections, matching the period of early fluid accumulation. These findings indicate that targeting the V2 signaling pathway can optimize perioperative fluid management, especially for high-risk patients undergoing extensive liver resection[34].

INDIVIDUALIZED ADJUSTMENTS FOR SPECIFIC PATIENTS

Fluid management strategies must also be flexibly adjusted based on each patient’s underlying conditions and specific postoperative states. Special attention is required for hepatectomy patients with the following comorbidities.

Patients with cirrhosis

Post-hepatectomy fluid management in cirrhotic patients should avoid fixed fluid administration formulas. Instead, a feedback regulation system should be established based on objective data; essential patient measurements include SVV/PPV, lactate, urine output, daily weight, and electrolytes. Using these metrics, fluid management can transition from empirical to quantitative and precise management[35]. Using SVV or PPV as the primary dynamic indicators for assessing volume responsiveness is recommended to guide intraoperative and early postoperative fluid administration. These measurements are superior to static CVP; while CVP can serve as a trend for reference, it is not an absolute target[36]. Furthermore, the continuous monitoring of arterial lactate is crucial for assessing systemic perfusion: Levels should show a declining trend within the first 24 hours to 48 hours postoperatively, and persistent elevation should prompt an evaluation for hypoperfusion while also considering impaired hepatic lactate clearance, with close attention paid to lactate trends and the overall clinical context[37]. In addition, the following measurements should be assessed: Mean arterial pressure should be maintained (≥ 65 mmHg) to fundamentally support organ perfusion[38]; hourly urine output should be recorded, with a target of > 0.5 mL/kg/hour; and serum creatinine should be closely monitored to enable early recognition of AKI[39].

Beyond these measures, restrictive fluid management should be implemented for 24 hours to 72 hours postoperatively[40]. The total fluid intake (IV + oral/enteral) is typically controlled at 1.0-1.5 times the daily basal requirement (plus measurable losses). This can be validated using precise daily weighing; ideally, early postoperative weight gain should not exceed 5% of the patient’s preoperative weight, and 20% human albumin may be considered in the early phase for selected patients with marked hypoalbuminemia to maintain effective colloid osmotic pressure[41]. Sodium-containing crystalloid infusions are recommended, favoring balanced crystalloids; total daily sodium intake should be < 80-100 mmol. Hyperchloremic normal saline should be avoided to prevent aggravating fluid retention[42], and hourly/daily fluid balance should be recorded strictly. If a significant positive balance is observed (e.g., > 20 mL/kg/24 hours), the patient should be evaluated and diuretic administration taken into consideration[43].

Diuretic therapy (e.g., combination of furosemide and spironolactone at an initial ratio of approximately 1:2, a regimen primarily used for cirrhosis-related ascites management)[44] is recommended to be initiated in patients with progressive increase in abdominal girth, hypoalbuminemia, or deteriorating oxygenation when hemodynamic stability is maintained, and the dosage and ratio should be individualized for each patient rather than applied as a universal strategy for all post-hepatectomy cases. Furthermore, the dosage should be adjusted daily based on the patient’s urine output, weight, and electrolytes (K⁺, Na⁺). In addition to this, electrolytes should be monitored daily, focusing on preventing/treating dilutional hyponatremia, and if serum sodium falls below 130 mmol/L, water intake should be strictly limited (e.g., < 1000 mL/day) with a re-evaluation of the fluid plan[45,46].

Patients with post-hepatectomy hemorrhage

For these patients, a “permissive hypotensive resuscitation strategy” should be employed. Before surgical hemostasis is achieved, there must be a focus on reducing total blood loss by avoiding restoration of the normal blood pressure levels. Simultaneously, blood products (such as packed red blood cells and fresh frozen plasma) should be administered to maintain basic oxygen-carrying capacity and coagulation function[47]. Meanwhile, volume depletion should be addressed progressively after the hemorrhage is controlled. For young patients without traumatic brain injury, systolic blood pressure should be maintained at 80-90 mmHg or mean arterial pressure at 50-60 mmHg during active, uncontrolled bleeding until surgical hemostasis is obtained. In addition, baseline hemoglobin, hematocrit, and the coagulation profile should be monitored immediately, while the transfusion of packed red blood cells and fresh frozen plasma should be prioritized for resuscitation[48,49]. Where available, viscoelastic testing (e.g., Thromboelastography or Rotational Thromboelastometry) may be used to guide transfusion strategies and limit unnecessary volume administration. The rate and volume of crystalloids (e.g., balanced crystalloids) should be restricted, as they can dilute clotting factors, worsen acidosis and hypothermia, and increase the risk of abdominal compartment syndrome.

In the early period of hemorrhage, crystalloids should only be used to maintain IV access. In parallel, invasive arterial pressure, CVP, blood gas analysis, temperature, and coagulation should be monitored continuously to assess resuscitation effectiveness and coagulation status in real-time. Crucially, rapid and excessive fluid administration to achieve “normal” blood pressure must be avoided before the hemorrhage is controlled, as this worsens the “lethal triad” (hypothermia, acidosis, and coagulopathy) and increases mortality[50]. Permissive hypotension is a temporary measure to enable sufficient time for hemostasis. Once the patient’s clinical conditions permit, surgical or interventional hemostasis should be carried out immediately, followed by transition to tissue perfusion-guided adequate resuscitation.

Patients with post-hepatectomy AKI

Fluid management in post-hepatectomy patients with AKI requires a precise balance between maintaining renal perfusion and avoiding fluid overload[51]. The strategy should be dynamically adjusted based on AKI stage, hemodynamic status, and renal reserve function[10,52]. For pre-renal AKI or hypovolemia, a fluid challenge (e.g., rapid infusion of 200-500 mL crystalloid over 1-2 hours) should be performed, while monitoring the response using urine output, CVP, and SVV as key measurements. The goal is to rapidly correct effective circulatory volume depletion and restore renal perfusion[53].

For confirmed AKI or patients in the maintenance phase (especially when oliguric), once euvolemia is achieved, there should be an immediate switch to restrictive fluid management[54]. Total daily intake may be guided by a practical ICU approach of calculating as the previous day’s urine output + measurable losses + 500 mL, a strategy that is not a hepatectomy-validated standard; clinical reassessment using perfusion and congestion markers is therefore essential to individualize fluid intake. Where clinical expertise is available, bedside ultrasound-based assessment of venous congestion (e.g., the Venous Excess Ultrasound Score concept) or renal Doppler indices may be used as adjunctive tools to further guide fluid administration or de-resuscitation[55,56]. Following this, daily weight changes should be monitored, aiming for fluid balance or mild negative balance; balanced crystalloids are preferred over normal saline to reduce the risk of hyperchloremic acidosis[57].

In selected patients with marked hypoalbuminemia, clinically significant systemic edema, and an inadequate response to diuretics alone, the administration of 20% human albumin in combination with diuretics may be considered with close monitoring, for the purpose of increasing intravascular colloid osmotic pressure and promoting fluid elimination[58]. Adjunctive measures: Nephrotoxic drugs (e.g., non-steroidal anti-inflammatory drugs, aminoglycosides, and certain contrast agents) should be strictly avoided. If contrast is essential, adequate hydration and the use of iso-osmolar agents should be ensured. Diuretic use is only recommended in the case of volume overload or to reduce organ edema. Loop diuretics (e.g., furosemide) are first-line, but note that they increase urine output without altering AKI course, while high doses may worsen renal tubular injury and cause ototoxicity[59]. In these cases, diuretics should not be used to “force” diuresis in the absence of clear volume overload. Monitoring should include serum creatinine, blood urea nitrogen, electrolytes (especially hyperkalemia), acid-base balance, and urine output[60]. The ultimate goal of fluid management is to create the optimal internal environment for renal recovery, and not merely to achieve urine output targets[61]. In summary, for post-hepatectomy AKI patients, the basis of fluid management lies in a staged strategy based on precise volume assessment, which rapidly transitions from active resuscitative fluid to strict restrictive management, while remaining highly vigilant for fluid overload and nephrotoxic injury.

CONCLUSION

Post-hepatectomy fluid management is a task that depends on complex, multidisciplinary, and multidimensional system engineering. In the modern era, the refined implementation of fluid management has transitioned from extensive perioperative care models toward precision medicine. In the future, with the advancement of non-invasive/minimally invasive hemodynamic monitoring technologies, the clinical translation of biomarkers related to vascular endothelial injury, and the development of artificial intelligence-driven individualized predictive models, post-hepatectomy fluid management will achieve a higher level of precision and personalization. Fundamentally, while adhering to ERAS principles as the core, implementing staged, goal-directed management strategies, and relying on dynamic monitoring to shift from “experience-driven” to “data-driven” practice will further optimize patient outcomes, accelerate recovery, and provide a more solid foundation for the perioperative management of hepatectomy.