• Insensible fluid losses are defined as losses of fluid secondary to evaporation into the environment. They are
  • Difficult to measure and ascertain
  • Involve estimates that are calculated from clinical experience
  • Replaced with either crystalloid or colloid; controversy exists as to the preferred fluid. Ultimately, the principal goal should be to optimize cardiac output.
• Common sources of insensible losses include
  • Open wounds, in particular abdominal incisions and exposure
  • Condensation in the breathing circuits
  • Sweating
  • Fever
  • Hyperventilation
• Insensible losses differ from "third spacing" (transcellular movement of fluids) or temporary sequestration (movement of fluid into functionless spaces). These can result from inflammation, trauma, or damage to the normal integrity of the vascular barrier

• The current practices of managing insensible losses are hypotheses; interestingly enough, there are no current studies that have proven that they are significant and need substantial replacement.
• Perioperative fluid therapy of insensible losses are guided by the following assumptions:
  • The preoperative patient is volume depleted as a result of fasting, continued physiologic insensible loss, and urine output.
  • Intraoperatively, insensible fluid loss to the environment increases with the size of the surgical incision, amount of tissue exposed, and duration of exposure.
  • Insensible fluid losses require replacement
    • Basal insensible loss. Mainly transdermal and estimated to be at most 0.5 mL/kg/hour and may increase to 10 mL/kg/hour with major abdominal surgery.
    • Size of incision. Insensible loss increases proportionally in relation to the surface area exposed to the environment.
    • Nonhumidified gases. Patients breathing nonhumidified gases have an increase in their insensible losses. This is further accentuated if the patient is hyperventilated.

• Abdomen
• Muscle
• Thorax

• Both hypovolemia and hypervolemia can have deleterious effects. In the perioperative period, anesthesia providers rely on physical examination, vital signs and monitors, as well as laboratory values to assess volume status and guide therapy.
• Hypovolemia. Decreases ventricular preload and hence stroke volume (Frank–Starling). Initially, the body may be able to compensate by increasing the heart rate and systemic vascular resistance. However, as hypovolemia progresses, the cardiac output can be impaired and organ hypoperfusion and dysfunction can result. Outcome studies have also shown that it can prolong hospital stay.
  • History. NPO status, fever, diarrhea, vomiting. Intraoperative blood loss, size of incision.
  • Physical exam. Dry mucus membranes, decreased skin turgor, decreased capillary refill, sunken fontanelles in newborns, increased heart rate, decreased BP, decreased urine output, and changes in mental status (awake patient)
  • Laboratory values. Hemoconcentration, hypernatremia, and an increased BUN:Cr ratio (>20:1)
  • Invasive monitors. Arterial line, central venous monitoring, pulmonary artery catheters, and transesophageal echocardiogram may be used in conjunction with, and to correlate, the overall clinical picture.
• Hypervolemia. Can lead to pulmonary edema and increased myocardial oxygen demand (increased preload and wall tension).
  • History. Ins and outs
  • Physical exam. Edema (likely pitting), wheezing, crackles on lung exam, increased urinary output, jugular venous distention. In the awake patient, cough and dyspnea.
  • Laboratory values. Hyponatremia, decreasing Hct levels (due to hemodilution), and increased A-a gradient or decreased a/A ratio.

• Much of current practice on fluid management is based on algorithms that propose replacement of
  • Preoperative deficits (e.g., NPO status and bowel prep)
  • Maintenance requirements
  • Surgical losses
  • Insensible fluid and third space losses
• Perioperative loss of fluid can be broken down into continuous loss (urine output and insensible perspiration) and losses exclusively from trauma (mainly blood loss). In the awake patient, continuous losses are replaced via the GI tract through the absorption of colloid-free fluid and electrolytes. However in the "fasted" patient this mechanism may fail and deficit replacement is performed by the anesthesia provider with crystalloid fluid.
• The principal goal of fluid management should be to optimize cardiac preload.
• Controversy and considerations
  • Outcomes. Fluid management can have effects on nausea and vomiting, tissue perfusion, pain, need for surgical revision, length of hospital stay and bowel motility, among other things.
  • Generous fluid resuscitation during laparoscopic procedures can decrease both postoperative pain and the incidence of nausea and vomiting in patients prone to PONV.
  • Errors with measurement. Insensible losses are difficult to accurately calculate, unlike blood loss that can be visibly ascertained. It is often largely overestimated in clinical practice, and many feel that it is negligible and should not be included in maintenance requirements.
  • Volume status. A clinical impression is based on several variables. At this time, direct blood volume measurements are not available to the anesthesia provider.
  • Colloid versus crystalloid. Many proponents still advocate that maintenance requirements and preoperative deficits should be replaced with crystalloid solution while blood loss should be replaced with colloid solution.
  • Fluid restriction. "Optimizing does not mean maximizing." Newer studies are challenging the current "standard" views of fluid therapy. In fact, some experts advocate not replacing perceived preoperative deficits, but instead fluid "restricted" strategies during the perioperative period (especially during major elective GI procedures). This theory is based on an increasing number of reports that demonstrate that excessive intravascular volume can lead to an increase in morbidity and mortality. Overhydration can lead to pulmonary edema, increased ICU duration, ileus, and abdominal compartment syndromes.
  • Anesthetic drugs commonly result in decreased systemic vascular resistance and vasodilation. This can unmask hypovolemia or relative hypovolemia (e.g., chronic hypertensives with increased vascular tone, but decreased intravascular volume).

• Crystalloids
• Colloids
• Extracellular Fluids

Ashley Greene , DO

Mary E. McAlevy , MD