I. Epidemiology and Clinical Impact

Intravenous fluid administration is nearly universal in adult ICUs worldwide. Early resuscitation volumes, fluid composition, and cumulative balance are all linked to organ function and patient outcomes.

• Over 90% of ventilated or vasopressor-dependent ICU patients receive ≥2–3 L of crystalloids within the first 24 hours.
• Annual global usage reaches millions of liters, driving morbidity, resource utilization, and cost.
• Balanced crystalloids reduce major adverse kidney events at 30 days (MAKE30) compared to 0.9% saline (14.3% vs. 15.4%).
• Each additional liter of fluid infused in trauma correlates with a 5% increase in in-hospital morbidity.
• Restrictive versus liberal strategies in septic shock show no difference in 90-day mortality, underscoring the need for physiology-guided resuscitation.

II. Physiology of Fluid Compartments and Shifts

Total body water (TBW) distribution and membrane forces determine where administered fluid goes. Inflammation and endothelial injury profoundly alter these dynamics.

• TBW ≈60% of lean body mass: 40% is intracellular fluid (ICF); 20% is extracellular fluid (ECF), which is further divided into 5% intravascular and 15% interstitial space.
• Osmosis: Water moves toward higher solute concentration. The tonicity (effective osmolarity) of a fluid governs whether it expands the ECF or shifts into the ICF.
• Starling Forces: Capillary hydrostatic pressure pushes fluid out of vessels, while oncotic pressure (from proteins like albumin) pulls fluid back in. Glycocalyx degradation in sepsis flattens this gradient, promoting leaks.
• Capillary Leak: In severe inflammation, 20–30% of an isotonic crystalloid bolus can extravasate into the interstitium within hours, leading to “third spacing” and edema.

III. Influence of Chronic Diseases on Fluid Handling

Heart, kidney, and liver dysfunction each alter fluid tolerance and distribution, necessitating tailored strategies.

• Heart Failure: Elevated venous pressures blunt preload responsiveness, and diuretic resistance worsens congestion. Patients are highly susceptible to fluid overload.
• Chronic Kidney Disease (CKD): Reduced glomerular filtration rate (GFR) limits the body’s ability to excrete sodium and water. Small fluid loads can precipitate volume overload and hypertension.
• Cirrhosis/Hypoalbuminemia: Low oncotic pressure from decreased albumin production favors fluid shifts into the third space, causing ascites and peripheral edema.
• Composite Comorbidities: Patients with multiple organ dysfunctions require lower net fluid targets and frequent reassessment using dynamic tests (e.g., stroke volume variation, passive leg raise).

IV. Social Determinants and Risk Stratification

Socioeconomic and literacy barriers can influence a patient’s presentation, the timing of resuscitation, and their long-term recovery from critical illness.

• Lower-income patients may present later in the course of shock, often with higher lactate levels and more severe hypotension at ICU admission.
• Poor health literacy can impair adherence to outpatient diuretic regimens, leading to decompensation and emergent ICU admission for fluid overload.
• Early screening for social determinants of health (SDOH) and interprofessional interventions (e.g., transport vouchers, multilingual education) can help reduce readmission risk.
• Integrating a social vulnerability index into protocols can help identify high-risk patients who may require targeted support.

V. Clinical Presentation and Early Risk Identification

Differentiating hypovolemia from fluid overload is a critical first step that guides initial resuscitation and helps avoid iatrogenic harm.

Early warning scores (e.g., NEWS, qSOFA) and triage algorithms help identify patients needing urgent fluid assessment. Laboratory clues such as a rising BUN/creatinine ratio, hemoconcentration, and elevated lactate suggest under-resuscitation, while hyponatremia or a low hematocrit may reflect dilution from fluid overload.