What are the fluid shifts that occur after a major burn injury in an adult?

Fluid Shifts After Major Burn Injury

Pathophysiology of Burn-Induced Fluid Shifts

After a major burn, massive fluid shifts occur from the intravascular space into the interstitial space, driven by increased capillary permeability, altered colloid osmotic gradients, and decreased interstitial hydrostatic pressure, resulting in hypovolemic shock and tissue edema that peaks in the first 24-48 hours. 1, 2

Mechanism of Vascular Hyperpermeability

• Capillary hyperpermeability is the primary driver, caused by release of inflammatory mediators including histamine, bradykinin, vascular endothelial growth factor (VEGF), and metabolic factors like adenosine triphosphate (ATP) 3, 4
• Endothelial barrier disruption occurs through breakdown of intracellular junctions, cell-matrix adhesion failure, and increased cytoskeleton contractile forces 4
• Activated neutrophils contribute to vascular permeability changes and perpetuate the inflammatory cascade 3
• This hyperpermeability affects both burned and non-burned tissue, though the effect is more pronounced in burned areas 2

Timeline and Extent of Fluid Shifts

• First 8-12 hours: Maximal capillary leak occurs, with rapid transcapillary shift of plasma into interstitial space 2
• First 24 hours: Capillary hyperpermeability remains severe enough that colloid infusions are largely ineffective at preventing fluid extravasation into burned areas 2
• After 24 hours: Vascular permeability begins to normalize, and interstitial edema starts to resorb back into the vascular space 2
• The extent of fluid shift correlates directly with total body surface area (TBSA) burned and injury severity 5

Clinical Consequences

• Intravascular volume depletion leads to decreased effective circulation volume and progressive hypovolemic shock 3
• Increased systemic vascular resistance and decreased cardiac output occur as compensatory mechanisms 3
• Peripheral tissue edema develops in both burned and non-burned areas, though more pronounced in injured tissue 2, 3
• Multiple organ failure can result from inadequate tissue perfusion if fluid shifts are not adequately managed 3
• Compartment syndrome risk increases, particularly with circumferential burns, due to tissue edema within fascial compartments 6, 7

Monitoring Fluid Shifts

• Bioimpedance spectroscopy (BIS) can objectively measure fluid shifts by detecting changes in resistance as edema develops and resolves 5
• Resistance variables decrease significantly with increasing net fluid shift and increased TBSA severity 5
• Urine output (target 0.5-1 mL/kg/hour) remains the primary clinical parameter for assessing adequacy of resuscitation 8, 6
• Hemoglobin/hematocrit measurements are confounded by resuscitation fluids and physiological fluid shifts from interstitial to vascular compartments 8
• Arterial lactate and base deficit reflect tissue hypoperfusion from inadequate intravascular volume 8

Resuscitation Strategy Based on Fluid Shift Physiology

• First 24 hours: Administer crystalloids (Ringer's Lactate) using the Parkland formula (2-4 mL/kg/%TBSA), with half given in the first 8 hours to replace ongoing intravascular losses 6, 7
• After 8-12 hours: Consider adding 5% albumin in patients with TBSA >30% to increase oncotic pressure and reduce further crystalloid requirements 8, 6
• Avoid "fluid creep": Excessive crystalloid administration worsens tissue edema and increases risk of abdominal compartment syndrome, acute respiratory distress syndrome, and acute kidney injury 8, 6
• After 24 hours: As capillary permeability normalizes, albumin administration becomes more effective at promoting edema resorption back into the vascular space 2