Overview of Postoperative Fluid Therapy in Adults

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Official reprint from UpToDate®

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Overview of postoperative fluid therapy in adults

Author: Nicole Siparsky, MD, FACS, FCCM
Section Editors: Amalia Cochran, MD, FACS, FCCM, Richard H Sterns, MD
Deputy Editor: Kathryn A Collins, MD, PhD, FACS
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Feb 2023. | This topic last updated: Oct 14, 2021.
INTRODUCTION
The management of fluid in the postoperative surgical patient can vary from simple to complex.
Postoperative intravenous maintenance fluid therapy ensures adequate organ perfusion,
prevents catabolism, ensures electrolyte- and pH-balance, and may be all that is required for
patients who undergo surgical procedures that do not significantly alter the hemodynamic
milieu. Typically, such procedures are associated with a small volume of blood loss (<250 mL), a
short course of anesthesia and surgery (<3 hours), a small volume of intravenous fluid
administration (<30 mL/kg), and little to no extravascular fluid shift in patients without
significant organ dysfunction.
However, in many cases, postoperative patients with extensive traumatic or surgical tissue
injury, burns, critical illness, or sepsis require more complex resuscitative fluid therapy in
addition to maintenance therapy to compensate for preoperative and intraoperative losses, the
stress response to surgery, the underlying disease state, ongoing gastrointestinal fluid loss,
blood loss, and other bodily fluid loss. Such complex fluid management is often needed for
patients who undergo surgical procedures that result in significant blood loss (>500 mL or 7
mL/kg) [1], fluid shifting out of the vascular space ("third-spacing"), large-volume intravenous
fluid administration (>30 mL/kg), or hemodynamic instability [2,3].
The prescription of maintenance and resuscitative fluids in postoperative surgical patients is

reviewed here. The management of electrolyte abnormalities and nutritional support in the
perioperative period are reviewed separately. (See "Overview of postoperative electrolyte
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abnormalities" and "Overview of perioperative nutrition support" and "Postoperative parenteral

nutrition in adults".)
Intraoperative fluid therapy is reviewed separately. (See "Intraoperative fluid management".)
PHYSIOLOGIC STRESS RESPONSE TO SURGERY
The stress response to traumatic or surgical tissue injury is a primal collection of biochemical
pathways designed to facilitate survival following a major insult. The "fight or flight" response
promotes expansion of the blood volume, glucose availability, perfusion of vital organs, and
inflammation. This stress response is triggered by entry into a major body cavity (eg, chest,
abdomen, joint, cranium), significant tissue disruption (eg, severe burn wounds, long bone
fracture, penetrating gunshot wound, pancreatitis), significant blood loss (>500 mL or 7 mL/kg),
hemodynamic instability, and sepsis.
Some devices and treatments used in surgery may also incite a massive inflammatory response.
As an example, extracorporeal bypass uses an external circuit through which blood is forced for
gas exchange and circulation while the patient undergoes cardiac surgery. Blood contact with
artificial bypass tubing incites cytokine release, activation of the coagulation cascade, and the
production of nitric oxide [4]. This inflammatory response may lead to vasodilation, deranged
coagulation, systemic capillary leak, and systemic organ dysfunction. Another example is
aggressive cancer treatment using heated intraperitoneal chemotherapy (HIPEC), which
commonly results in an inflammatory response marked by supranormal fluid exudation,
decreased systemic vascular resistance, and coagulopathy [5,6]. Derangements in physiology,
intravascular volume, and coagulation associated with HIPEC commonly require aggressive
fluid resuscitation. (See "Extracorporeal membrane oxygenation (ECMO) in adults" and
"Anesthesia for cytoreductive surgery with heated intraperitoneal chemotherapy".)
Hormonal mediators — Hormonal mediators of the stress response include:
● Vasopressin – Vasopressin, also known as antidiuretic hormone (ADH), is secreted by the

posterior pituitary gland in response to elevated plasma osmolality, low circulating blood
volume, and stress. This results in water retention by the kidney, which expands the
vascular volume.
● Aldosterone – The renin-angiotensin axis responds to volume contraction by stimulating

aldosterone secretion in the adrenal gland. Aldosterone increases sodium and water
retention by the kidney, thereby expanding the vascular volume.
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● Cortisol – The hypothalamic-pituitary axis responds to stress by stimulating cortisol

release from the adrenal gland. This promotes gluconeogenesis and muscle breakdown
and results in hyperglycemia.
● Catecholamines – Epinephrine and norepinephrine are released from the adrenal gland in
response to sympathetic nervous system stimulation, resulting in vasoconstriction,
tachycardia, and catabolism. This combination leads to increased cardiac output,
hypertension, and hyperglycemia.
● Cytokines – Acute phase reactants (eg, interleukins 1 and 6) generate a local inflammatory
response at the site of injury, facilitating healing at sites of tissue disruption [7,8].
The stress response to tissue injury helps the body to compensate for hypovolemia. However,
complications of the stress response can occur. As an example, aldosterone release leads to
acute potassium wasting and secondary hypokalemia. If not appropriately treated, severe
postoperative hypokalemia can result in arrhythmia. Similarly, cortisol and catecholamines
contribute to hyperglycemia, which is associated with complications of wound healing in
postoperative patients, including infection, dehiscence, and nonhealing. Furthermore, the
systemic release of inflammatory mediators may result in local and/or systemic capillary leak,
tissue injury, and systemic organ dysfunction (eg, acute renal failure, adult respiratory distress
syndrome).
Distinguishing hypovolemia from the stress response in the postoperative patient can be
challenging. In the past, manifestations of the stress response, including tachycardia,
hypotension, and oliguria, were attributed to hypovolemia and inadequate fluid resuscitation.
For this reason, postoperative fluid resuscitation was focused on resolving these physiologic
derangements by administering large volumes of fluid. Such aggressive fluid resuscitation
resulted in complications associated with volume overload, contributing to morbidity and
mortality [9-11].
Our understanding of the stress response to surgery has evolved. In a 2016 statement on
sepsis, the Society of Critical Care Medicine and the European Society of Intensive Care
Medicine recognized that a stress response exists as a spectrum of organ dysfunction caused
by a dysregulated host response to infection. In the absence of infection (eg, pancreatitis), an
exaggerated stress response can result in a similar degree of organ dysfunction. As such, organ
dysfunction (ie, acute kidney injury, transaminitis, or cardiomyopathy) in the postoperative
patient may not reflect inadequate fluid resuscitation; rather, such dysfunction may be a
manifestation of a pathologic stress response to the underlying disease or to surgery [12]. For
this reason, new protocols, such as the Enhanced Recovery After Surgery (ERAS) protocol, are
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emerging to limit the fluid therapy in surgical patients and may include "permissive oliguria" in
some cases [13].
FLUID LOSS AFTER SURGERY
Fluid loss in the postoperative period varies widely with the type of procedure performed, the
condition of the patient at the time of surgery, the underlying disease for which the procedure
was performed, and the severity of the stress response.
Bleeding — Bleeding should always be considered in postoperative patients with hypotension,

tachycardia, dizziness, or pallor. However, these manifestations are late, occurring only after
blood loss is in excess of 15 percent of the patient's blood volume ( table 1). While fluid
administration is appropriate to support the patient, blood products are often required to
correct the acute blood loss anemia. In the 10th edition of the Advanced Trauma Life Support
(ATLS) guidelines, 1 L of fluid is indicated for trauma patients requiring resuscitation to restore
organ perfusion; thereafter, in cases of bleeding, blood transfusion is encouraged [14]. (see
"Intraoperative transfusion and administration of clotting factors")
In most cases, a return to the operating room is indicated for exploration and control of
hemorrhage at the surgical site. In cases of occult bleeding, imaging may be needed to identify
the bleeding source.
Drainage — Gastrointestinal drainage systems (eg, nasogastric tube) may evacuate large
volumes of fluid during or following a surgical procedure (eg, small bowel obstruction)
( table 2). Similarly, surgical entry into the chest (ie, pleural fluid from a chest tube), abdomen
(ie, ascites from abdominal drains), or urinary system (ie, urine) may lead to the rapid
evacuation of a large volume of fluid. For fluid evacuation in excess of one liter, hypovolemia
and electrolyte derangement may result if the fluid is not sufficiently replaced to restore normal
perfusion.
Third-spacing — Third-spacing refers to the process of capillary leak and extravasation of

protein-rich serum into the interstitial spaces of the soft tissues (eg, skin, fat, muscle), organs,
deep space cavities (eg, chest, abdomen), or retroperitoneum. It typically occurs during the first
72 hours following major surgery and is associated with a heightened stress response [15].
● Third-spacing into the soft tissue results in edema, whereas fluid that leaks from the
peritoneal or pleural surfaces generates ascites or pleural effusion.
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● Large nonanatomic cavities, such as those created from extensive subcutaneous

dissection or following drainage of an infected pancreatic pseudocyst, can result in large-
volume third-spacing into the newly created potential space.
● Spaces that are created during surgery (eg, the hernia cavity that remains following
ventral hernia repair), in which the tissues are not approximated, can result in
postoperative seroma.
● Reperfusion following an episode of ischemia, such as in cases of arterial occlusion, result

in an intense local inflammatory response and extensive tissue edema, which can lead to
compartment syndrome.
Hypoalbuminemia contributes to third-spacing; it is theorized that the resultant intravascular

oncotic pressure, resulting from hypoalbuminemia, contributes to the fluid shifting. Some fluids
contain higher concentrations of albumin, such as ascites, which may impact hemodynamics in
a more impressive way. As an example, in a post hoc analysis of 31 patients involved in a trial to
assess intravenous fluid administration following cytoreductive surgery, the evacuation of
malignant ascites in excess of 500 mL caused greater hemodynamic instability and was
associated with a larger fluid resuscitation compared with those in whom less than 500 mL
ascites was drained [16]. (See "Etiology, clinical manifestations, and diagnosis of volume
depletion in adults".)
Insensible losses — Insensible (evaporative) loss can be related to prolonged exposure during
laparotomy or thoracotomy, or prolonged exposure of burn wounds during skin grafting. Older
studies estimated that the losses from open abdominal exposure were 0.5 to 1 mL/kg/hour;
however, the amount varies with the degree of organ exposure and the severity of the illness.
Minimally invasive approaches are associated with less evaporative loss. Postoperatively,
insensible losses can also occur through large open wounds, such as an open abdomen or burn
wounds, and with persistent postoperative fever.
Insensible loss associated with ventilator support (intraoperative, postoperative) is limited.
FLUID RESUSCITATION
The goal of postoperative fluid resuscitation is to restore organ perfusion [17]. Through the
administration of intravenous fluid, a deficit in intravascular volume is sufficiently replaced to
restore organ perfusion. In some cases, blood transfusion is also necessary to achieve these
goals.
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Despite advances in critical care, there is no way to directly measure intravascular volume [17].
For this reasons, we continue to rely on markers of inadequate perfusion to guide us in
identifying hypovolemia. Any patient who demonstrates hemodynamic instability (ie,
tachycardia, hypotension), alteration in mental status, oliguria (<0.5 mL/kg), lactic acidosis, or
base deficit in the postoperative period should be considered for fluid resuscitation.
Postoperative fluid resuscitation begins with the identification of clinically impactful fluid loss
resulting in hypovolemia, which may be due to any of the following:
● Preoperative fluid deficit (eg, bowel preparation-associated diarrhea) or fasting-associated

deficit (eg, prolonged inanition prior to intestinal surgery).
● Intraoperative sensible and insensible fluid losses. (See 'Insensible losses' above.)
● Intraoperative blood loss, or ongoing postoperative blood loss. (See 'Bleeding' above.)
● Ongoing fluid loss related to the underlying condition (eg, septic shock, pancreatitis),
which can be due to tissue (third-spacing) or external (eg, surgical drain, nasogastric tube)
losses. (See 'Third-spacing' above and 'Drainage' above.)
Estimate the fluid deficit — Historically, fluid resuscitation was achieved by estimating and
replacing the intravascular fluid deficit. However, the estimation of a patient's fluid deficit is an
inexact science; by this method, many patients receive too much fluid. In simple cases,
replacing some or all of the deficit is sufficient to complete resuscitation. In complex cases
involving physiologic derangement (eg, hypotension, tachycardia), acute organ dysfunction (eg,
acute kidney injury, sepsis-associated cardiomyopathy), or systemic illness (eg, vasodilation due
to septic shock), resuscitation may be more complex. For this reason, resuscitation is focused
on restoring normal perfusion rather than replacing an estimated volume deficit.
Blood collected from the operating field through closed suction evacuation is often readily
apparent and measureable; however, some of this blood may have been collected and returned
to the patient using autotransfusion technology. The estimate of the volume of blood lost on
surgical sponges may also be difficult since the amount of estimated blood varies with the
sponge size, sponge material, and degree of sponge saturation (ie, volumes range from a few
mL to 100 mL per saturated sponge). In addition, the amount on a sponge may be
overestimated as blood may be mixed with ascites or urine. Conversely, blood loss can be
underestimated, as blood may also be lost on surgical gowns, drapes, and the operating room
floor. Occult blood loss will not have been accounted for. As an example, a significant
retroperitoneal hematoma due to arterial cannulation may not be apparent until much later, as
the patient develops symptoms (eg, pain, ileus) or becomes hypotensive.
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In hypovolemic patients, it may not be possible to reliably calculate the fluid deficit. Instead, it is
a common practice to compare the physiologic parameters associated with hypovolemia to
those associated with hemorrhage ( table 1). As an example, with <15 percent circulating
blood volume loss, the heart rate and blood pressure should be normal. If a patient
demonstrates tachycardia or hypotension, it is likely that their volume deficit is greater than 15
percent. For a 70 kg individual, a 15 percent deficit would correspond to approximately 750 mL
fluid deficit. While this method is not well supported with literature and is imprecise, it provides
a good starting point. For this reason, the volume of intravenous fluid administered as a bolus
(referred to as a fluid challenge) is often 500 mL to 1000 mL [17].
Measure ongoing fluid losses — In addition to replacing any postoperative fluid deficit,
ongoing losses from drainage tubes must be accounted for. Provided the surgical drains are
functioning properly, the volume of loss can be measured directly. We monitor drain output
frequently; when it exceeds 400 mL in 8 hours (>50 mL/hour), fluid replacement is initiated to
minimize fluid deficits and secondary hypovolemia, until the drain output subsides.
Alternatively, we may begin replacing the output in a scheduled fashion (eg, 1 L every 12 hours),
assuming the observed loss will continue at the same pace. These replacement protocols
(hourly, every six hours, or intermittent bolus) can be revised several times a day, depending on
the trend in output.
Volume of replacement fluid — Once the fluid deficit has been estimated and ongoing losses
are measured, the total volume of replacement fluid can be determined. For hemodynamically
stable patients, ongoing fluid losses should be evaluated and adjusted daily; fluid needs should
be assessed two or three times daily in critically ill patients.
The postoperative patient can be expected to require a volume that is up to three times the
estimated fluid deficit. As much as two-thirds of administered intravenous crystalloids are
expected to shift out of the vascular space within hours of administration due to capillary leak,
which correlates with the magnitude of the stress response to surgery. For patients with normal
organ function, the fluid deficit is typically replaced in a ratio of 1:1, meaning that 1 L of fluid
loss is replaced with 1 L of fluid replacement. Greater amounts with ratios as high as 3:1 may be
necessary in those with a severe stress response to surgery. Lower amounts (eg, 0.5 mL:1 mL)
are used in those expected to receive a large volume of other fluids, such as medications or
blood products, and in those who are not expected to tolerate excessive fluid volume, though
restricting fluid may lead to some complications. In the REstrictive versus LIbEral Fluid therapy
(RELIEF) trial, 2983 patients with risk factors for complications (ie, >70 years of age, heart
disease, diabetes, renal dysfunction, morbid obesity) were randomly assigned to restrictive (ie,
zero balance) versus liberal fluid therapy during and after abdominal surgery [18]. There was no
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difference in the rate of pulmonary edema or duration of mechanical ventilation, but those
assigned to a restrictive protocol had a higher rate of acute kidney injury (8.6 versus 5.0
percent; hazard ratio [HR] 1.71 95% CI 1.29-2.27) and need for replacement therapy (0.9 versus
0.3 percent; HR 3.27, 95% CI 1.01-13.8). The rate of surgical site infection was also increased
(16.5 versus 13.6 percent; HR 1.22, 95% CI 1.03-1.45), but the incidences of other infectious
complications (eg, sepsis, anastomotic leak, pneumonia) were no different. At one year,
disability-free survival was no different between the groups (81.9 versus 82.3 percent). These
findings suggest that a modestly liberal intraoperative and postoperative fluid regimen is
needed to maintain renal perfusion in high-risk patients. For other subsets of patients, their
postoperative physiology may be the reason that fluid replacement will be poorly tolerated. An
example is the patient who undergoes pneumonectomy, whose remaining lung must acutely
accommodate an entire blood volume. In such patients, smaller amounts of fluid are often used
for replacement; permissive oliguria is often preferable to volume overload-associated
pulmonary edema.
Ongoing gastrointestinal or other losses are generally replaced with a volume equal to the loss.
These losses can be replaced periodically (eg, every six hours). Alternatively, a fluid replacement
protocol can be employed to keep up with losses on an hourly basis once a goal vascular
volume is achieved. As an example, during kidney transplantation, the patient is volume-loaded
during surgery until the intravascular system is replete. Thereafter, each hour after surgery, the
amount of fluid lost is measured and replaced using an equal volume of intravenous fluid
during the following hour. In this way, the intravascular volume is maintained and a fluid deficit
is avoided. If large-volume losses are anticipated, the maintenance fluid goal rate can be
increased temporarily. (See 'Maintenance fluid therapy' below.)
Replacement fluids — Crystalloids, colloids, and blood products are the replacement fluids
typically administered to postoperative patients ( table 3). It is important to consider the type
and volume of fluid that was lost, which will help guide the choice of fluid, volume of fluid, and
speed of fluid replacement.
Crystalloid solutions remain the fluid of choice for simple fluid replacement following surgery.
Although used intraoperatively, starch solutions are not commonly used in postoperative
surgical patients for volume expansion as they may result in abnormal coagulation, which can
contribute to bleeding complications. (See "Intraoperative fluid management", section on
'Choosing fluid: Crystalloid, colloid, or blood'.)
Normal saline (ie, 0.9% sodium chloride; Na = 154 mEq/L), Lactated Ringer (Na = 130 mEq/L),
and Plasma-Lyte (Na = 140 mEq/L) are widely used because their sodium content maintains
serum osmolarity, which helps retain water in the vascular space and facilitates volume
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expansion. The pH of Lactated Ringer and normal saline is below physiologic pH, which also
contributes to acid-base abnormalities. The lactate in Lactated Ringer is converted to
bicarbonate, which serves as a buffer, but its metabolism and clearance depend on adequate
liver and kidney function. Plasma-Lyte contains acetate, a buffer, which is quickly converted to
bicarbonate in most tissues, independent of the liver and kidneys [19]. Plasma-Lyte is more
expensive than normal saline or Lactated Ringer, which limits its use.
● Normal saline (0.9%) is particularly useful in cases of chloride and volume loss as well as
alkalosis (eg, vomiting). It contains the greatest concentration of sodium, repletes chloride
loss, and will reverse contraction alkalosis.
● Normal saline (0.9%) is used in association with blood transfusion, particularly rapid
transfusion, because it does not contain additives like calcium, potassium, or magnesium.
Lactated Ringer and Plasma-Lyte contain these additives, which may not be compatible
with all blood products and can result in red blood cell lysis, clot formation in the tubing,
and electrolyte chelation [20].
● Normal saline (0.9%) is used for head-injured patients, in whom hypernatremia is

preferable to hyponatremia or lowering the serum osmolarity. The brain does not tolerate
edema well; maintaining a normal (or elevated) sodium ensures that cerebral edema is
minimized.
● Lactated Ringer and Plasma-Lyte should be avoided in patients with hyperkalemia as they
both contain potassium. Similarly, in patients with poor renal function, these choices are
typically avoided in order to avoid hyperkalemia.
● Large volumes of normal saline are undesirable as they will result in hyperchloremic
acidosis and renal vasoconstriction [18,21-25]. However, in some cases of renal and/or
liver dysfunction, a provider may have no other choice but to use 0.9% saline. A chloride-
restrictive approach may reduce the incidence of acute kidney injury [23].
● For patients with bicarbonate loss (eg, pancreatic fistula, bladder-drained pancreas
transplant), bicarbonate replacement therapy may be administered intravenously in a
continuous fashion. Sodium bicarbonate is commonly added to replacement fluids in
increments of 50 mEq/L. The fluid vehicle is chosen to achieve the desired fluid sodium.
For example, 150 mEq/L of sodium bicarbonate will provide 150 mEq of sodium per liter,
which is nearly equivalent to 0.9% saline (154 mEq/L). As such, it is mixed in sterile water
or 5% dextrose in water to avoid further sodium administration.
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● Hypertonic saline (3% sodium chloride) is being used for the resuscitation of trauma
patients whose abdomens are maintained open with a temporary abdominal closure
device. In this highly selective population, volume overload results in delayed primary
fascial abdominal closure and complications of open abdomen (eg, enteroatmospheric
fistula). Inspired by a promising early report [26], similar encouraging reports have
suggested that the complications associated with hypertonic saline resuscitation
(hyperchloremia, hypernatremia, hyperosmolar acidosis) are well tolerated in this patient
population [27]. Although this is not the standard of care, it remains a promising
alternative to standard resuscitation and is supported by one systematic review [28].
Colloid solutions can also be used for volume expansion. The main colloid used in postoperative
patients is albumin, most commonly in the setting of severe malnutrition or liver failure. It may
maintain oncotic pressure better than crystalloid. However, the effects of albumin are short-
lived since it remains in the vascular space only for hours. The critical care literature suggests
that there is no benefit to using albumin. A systematic review and meta-analysis from 1998
reported that albumin did not reduce mortality when compared with crystalloid [15]. Later trials
have also not demonstrated any benefit with respect to perioperative mortality with the use of
albumin [29,30]. Caution is advised with the use of large volumes of albumin; hyperoncotic
albumin resuscitation was associated with increased risk of death in an international
prospective study [31]. Similarly, the use of albumin in neurologic injury is associated with
increased mortality, likely due to the secondary increase in intracranial pressure that results
[32]. Other colloid solutions include gelatins, dextrans, and starches. The use of these agents in
postoperative patients is very limited as their rheologic and anticoagulant effects are typically
unwelcome. Similarly, they can incite anaphylactic reactions. In a Cochrane review of surgical
and critically-ill patients, no colloid was found to be superior in efficacy or safety [33].
Role of blood products — Blood product transfusion is generally limited to patients with
accepted indications given the risk for transfusion-related complications, which include
transfusion-associated infection, lung injury, multiorgan failure, and systemic inflammatory
response syndrome (SIRS) [34]. Indications for blood product transfusion in postoperative
patients include (see "Intraoperative transfusion and administration of clotting factors" and
"Perioperative blood management: Strategies to minimize transfusions"):
● Resuscitation for bleeding – Active bleeding that is too rapid to be assessed by serial
hemoglobin measurements in the postoperative period may be related to coagulopathy or
traumatic vascular injury. For large-volume blood loss, the American College of Surgeon
(ACS) Advanced Trauma Life Support (ATLS) protocol (10th edition) recommends an initial
one-liter rapid infusion of warmed isotonic fluid followed by blood products [14]. Although
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massive transfusion protocols vary widely in the United States, most use a balanced
transfusion strategy, whereby components of blood (ie, red blood cells, fresh frozen
plasma, and platelets) are administered in equal amounts to equate to whole blood. (See
"Massive blood transfusion".)
● Severe symptomatic anemia – For postoperative patients who are not actively bleeding,
but with severe symptomatic anemia, specific thresholds for various patient populations
and supporting randomized trials are discussed in detail separately. It is important to note
that a numerical hemoglobin goal has not been established for postoperative patients
who may have suffered acute blood loss intraoperatively. An individualized approach is
needed. (See "Intraoperative transfusion and administration of clotting factors", section
on 'Indications and risks for specific blood products' and "Indications and hemoglobin
thresholds for red blood cell transfusion in the adult", section on 'Thresholds for specific
patient populations'.)
● Reversal of coagulopathy or thrombocytopenia – Thresholds for platelet transfusion in

postoperative patients who are actively bleeding or at risk for bleeding are individualized
based on procedure. As an example, when bleeding into a confined operative field would
be poorly tolerated (eg, spine, cranium), the desired minimum platelet level will be higher
compared with a superficial operative field for which direct pressure can be applied, or for
which a small amount of blood accumulation will not have dire consequences. (See
"Intraoperative transfusion and administration of clotting factors", section on 'Platelets'
and "Platelet transfusion: Indications, ordering, and associated risks".)
Fluid bolus administration — For most postoperative patients, replacement fluids (including
blood) are administered through peripheral intravenous lines. For rapid fluid infusion, large
bore (ie, 16 gauge and larger) peripheral intravenous (IV) lines are needed. A liter of fluid can be
infused in under seven minutes through a 16 gauge IV by gravity infusion. For higher rates (300
to 500 mL/minute), a pressure bag or rapid infuser will be needed ( table 4) [35]. When such
large volumes of fluid are needed, administration of room temperature fluid can lead to rapid-
onset hypothermia. If this is anticipated, a Level 1 rapid transfuser should be used since it
warms the fluid as it infuses it.
● Resuscitative fluid is commonly administered as an intravenous bolus over 30 to 60

minutes for rapid volume expansion. For patients who are not in shock, fluid replacement
is achieved using successive 3.5 to 14 mL/kg aliquots per hour. In general, for the average
70 kg adult, this corresponds to aliquots of 250 to 1000 mL for a total of 2 to 3 L until the
desired response is observed (eg, improved urine output, improved mentation,
normalizing base deficit). (See 'Endpoints of fluid resuscitation' below.)
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● More volume-depleted patients will require larger aliquots. A patient in hypovolemic shock
(40 percent or greater volume loss) will require rapid volume expansion with >2 L of fluid
per hour to restore blood volume and tissue perfusion. In cases of anticipated aggressive
third-spacing, additional ongoing fluid replacement is often needed.
● Patients who do not make urine due to chronic renal disease or who have poor heart/lung
function require smaller aliquots (eg, 250 mL) and careful monitoring of responses to fluid
challenges.
● When patients do not respond to the fluid challenge as expected, further evaluation in a
closely monitored setting is warranted to identify bleeding or other complications of
surgery (eg, acute renal dysfunction, myocardial infarction, sepsis). If a patient becomes
unresponsive to fluid boluses, fluid replacement should be reconsidered to avoid
complications of volume overload.
Blood products are typically transfused in a slow, monitored fashion (eg, one unit of red blood
cells over three hours) to reduce the risk of transfusion-associated circulatory overload and
enable early identification of transfusion reactions. In the setting of acute blood loss, more
rapid transfusion may be needed to treat a patient in shock. Emergency rooms, trauma bays,
intensive care units, and operating rooms have ready access to a rapid transfuser, which
permits the rapid transfusion of warmed fluid and blood products at high rates (300 to 500
mL/minute). (See "Initial management of moderate to severe hemorrhage in the adult trauma
patient".)
Endpoints of fluid resuscitation — The endpoint of fluid resuscitation is to restore normal

organ perfusion to permit sufficient oxygen carrying capacity, rather than simply the
administration of a specific volume of fluid [36]. Normal perfusion is achieved when the end-
diastolic volume of the left ventricle generates an adequate stroke volume. To achieve normal
organ perfusion, blood volume must be restored to 80 to 85 percent of normal blood volume.
Although some clinical parameters and bedside examination may be helpful for assessing the
adequacy of perfusion, laboratory measurements (ie, serum base deficit and serum lactic acid)
and adequate intracardiac filling by echocardiography are better measures of adequate central
volume. Approximately one-half of hemodynamically unstable patients will remain fluid
responsive at the end of their initial resuscitation, further strengthening the argument to use
endpoints of resuscitation rather than only fluid responsiveness [37]. If a patient becomes
unresponsive to fluid replacement, further fluid administration should be reconsidered to avoid
complications of volume overload.
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Since normal organ perfusion can be achieved without complete replacement of the estimated
volume deficit for most patients, ongoing clinical assessment of the adequacy of organ
perfusion is essential. In relatively healthy individuals who have not sustained large-volume
blood or fluid loss, normalization of heart rate, blood pressure, urine output, and mental status
mark the return of normal end-organ perfusion. A 45° passive leg raise in a recumbent patient
can be helpful for evaluating fluid responsiveness, which is defined as an increase in stroke
volume by more than 10 percent [38]. For the average adult monitored with a noninvasive
cardiac output monitor, a passive leg raise is equivalent to a fluid bolus of approximately 300
mL (4 mL/kg).
Serum lactic acid, base deficit, and central venous oxygen saturation (SvO2) are biochemical
end-products of perfusion that are often used to confirm adequacy of end-organ perfusion in
patients demonstrating complex physiology (eg, concurrent sepsis and hypovolemic shock).
Trending values every six to eight hours is helpful. When a patient develops hypovolemia,
impaired organ perfusion leads to anaerobic metabolism, which produces lactic acid. Lactic acid
is buffered by base; it consumes the base, thereby creating a base deficit. Similarly,
underperfused tissues will extract a greater percentage of oxygen than is normal, resulting in a
decreased SvO2. As blood volume is restored, these parameters should trend toward normal.
However, resolution of lactic acidosis is highly variable in its time course. Outcomes of surgical
patients with lactic acidosis have not been as well studied as in the medical patient population
[39]. However, lactic acidosis exceeding 4.0 mmol/L has been shown to be associated with
increased mortality in emergency room patients with infection [40]. Serum lactic acid levels
must be interpreted with caution in patients with liver dysfunction, who may not clear lactic acid
as quickly compared with those who have normal liver function. Acute liver dysfunction can be
observed in a variety of surgical settings (eg, sepsis, trauma, transplant). For patients with
persistently elevated lactic acid and SvO2, in spite of adequate fluid resuscitation, further
evaluation is warranted.
Estimates of central blood volume, including central venous pressure, the change in central
venous pressure, and pulmonary artery wedge pressure are not good estimates of central
volume [41]. Several meta-analyses have demonstrated the lack of evidence to support their
use as endpoints of resuscitation [41-43]. These are being abandoned in favor of goal-directed
therapy, using biochemical markers (discussed in the preceding paragraph) or functional
estimates of central volume using echocardiography (ecophysiology) to establish intracardiac
hemodynamics [44,45]. (See "Hemodynamics derived from transesophageal echocardiography"
and "Intraoperative fluid management", section on 'Dynamic parameters to assess volume
responsiveness' and "Intraoperative fluid management", section on 'Goal-directed fluid
therapy'.)
3/30/23, 2:18 PM 15073
Although a wide variety of measurable indices (eg, vena cava diameter, ejection fraction,
arterial pulse pressure variation, jugular vein distensibility) continue to be popular study topics,
these have not yet been widely adopted as measures for judging the adequacy of routine fluid
resuscitation in postoperative surgical patients [46,47].
MAINTENANCE FLUID THERAPY
Maintenance intravenous fluid therapy is provided when the patient is not expected to tolerate
oral or enteral feeding. The goal of maintenance fluid therapy is to preserve blood volume and
electrolyte balance and to provide some calories to prevent muscle wasting. Once resuscitation
is completed, maintenance fluid therapy is begun. (See 'Fluid resuscitation' above.)
Daily fluid requirements — For most adult postoperative patients, approximately 30

mL/kg/day (1 to 1.5 mL/kg/hour) will meet their maintenance fluid requirements. For those with
underlying organ dysfunction, daily maintenance volumes will need to be adjusted.
Restrictive fluid strategies may be helpful in avoiding overload in select patient populations.
Emerging literature in the trauma population supports a more restrictive maintenance fluid
volume in normotensive patients, which has been associated with fewer ventilator days and a
shorter intensive care unit course, although this is not widely practiced [48]. In such patients,
the fluid goal is typically decreased by 50 to 75 percent, and, in some cases, permissive oliguria
is accepted. (See 'Endpoints of fluid resuscitation' above.)
Fluid selection and rate — Hypotonic or isotonic saline solutions are the fluids most
commonly used for maintenance fluid therapy in the postoperative period. The typical rate for
maintenance fluid administration is 1 to 1.5 mL/kg/hour for patients with normal renal function
who do not have significant ongoing fluid losses.
In the absence of shock, dextrose 5% is added to half-normal saline (0.45%) to stimulate basal
insulin secretion and prevent muscle breakdown when the patient is unable to eat or drink,
provided the patient has a normal serum sodium level. Other additives, including potassium,
can also be added. For the average 70 kg adult, 400 to 500 calories per day is sufficient to
stimulate basal insulin secretion for the prevention of catabolism; this amounts to
approximately 100 to 150 grams per day of dextrose. However, this effect is short-lived, and
after five days muscle breakdown will occur unless supplemental nutritional support is
instituted. (See "Postoperative parenteral nutrition in adults".)
● For patients who cannot receive a large volume (eg, renal failure, heart failure,
pneumonectomy), smaller volumes of dextrose 10% may be used instead of dextrose 5%
3/30/23, 2:18 PM 15073
(0.5 mL/kg/hour).
● For patients with hypernatremia, dextrose 5% in water can be used instead of saline.
● For patients with shock, the standard of care is to remove dextrose from the fluid. Patients
in shock will convert dextrose to lactate, thereby generating an acidosis.
● For patients who undergo neurosurgery or who suffer from traumatic and nontraumatic
brain injury, hypotonic solutions are usually contraindicated because they may lower
serum osmolarity, resulting in cerebral edema. Similarly, glucose-containing solutions are
avoided due to possible exacerbation of neurologic injury [17].
Patients with and without diabetes develop transient hyperglycemia after surgery as a result of
cortisol release during the stress response to surgery. A commonly observed practice is the
removal of dextrose from the fluid, which may ameliorate the issue of hyperglycemia but result
in catabolism. The better treatment for hyperglycemia is insulin therapy [49]. For patients with
poorly controlled hyperglycemia (>350 mg/dL), it is reasonable to hold the dextrose briefly until
the serum glucose is lowered to a safer level to avoid complications of hyperglycemia. (See
"Perioperative management of blood glucose in adults with diabetes mellitus".)
Monitoring and adjustments — For patients receiving maintenance fluid therapy, a basic
chemistry panel should be checked daily to ensure normal serum sodium is maintained without
significant electrolyte derangement. In cases of large-volume administration (>4 L/day),
consider checking the serum chemistry more than once daily to identify serum electrolyte
derangements early. (See "Overview of postoperative electrolyte abnormalities".)
The volume and rate of maintenance fluid therapy may need to be adjusted to account for
underlying physiologic conditions and other sources of fluid intake.
● As infection and inflammation subside, fluid in the "third-space" (ie, extravasated fluid) will
return to the vascular space, a process referred to as "mobilization of the third-space
fluid." As the patient's urine output increases (auto-diuresis), maintenance intravenous
fluid rates can be reduced.
● Most postoperative patients experience mild derangements in serum sodium balance due
to intravenous fluid therapy, which can generally be managed by choosing an alternative
fluid that provides more or less sodium. As an example, a general surgery patient with
hypernatremia can receive dextrose 5% in water to lower the sodium. Caution is advised in
using the sodium to assess body water status in the setting of surgical fluid shifts as it
may not be a reliable marker of total body water.
3/30/23, 2:18 PM 15073
● Patients with cardiac, pulmonary, or renal disease often will not tolerate the standard
amount of maintenance fluid therapy as they may be unable to tolerate excess volume
expansion or eliminate excess fluid. Smaller maintenance fluid volumes (0.5 mL/kg/hour)
can be administered to patients for whom volume overload may become a problem. Many
of these patients also receive a significant volume of fluid associated with intravenous
medications, which must be accounted for in the total daily fluid rate.
● Given that the transition to enteral intake may not go smoothly due to ileus, nausea
secondary to pain medication, or poor appetite, oral intake should be established before
maintenance fluids are discontinued. Patients who are able to quickly tolerate enteral
intake usually tolerate a more rapid discontinuation of maintenance fluid therapy. Most
other patients will typically continue to receive a modified amount of fluid, typically 25 to
50 percent of their daily goal, until improved enteral intake is demonstrated (ie,
1mL/kg/hour intake). Some providers will remove the dextrose from intravenous fluids
once the patient tolerates enteral feeding.
● For patients who do not tolerate enteral intake and require parenteral nutrition, the
parenteral nutrition rate is typically increased as maintenance fluid is decreased in equal
volumes to maintain the goal fluid infusion per hour. Often, an order can be written as
"total fluids = 1 mL/kg/hour"; this allows the nurse to make the appropriate changes in
tandem over several hours.
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions
around the world are provided separately. (See "Society guideline links: Fluid and electrolyte
disorders in adults".)
SUMMARY AND RECOMMENDATIONS
● Fluid management in the postoperative surgical patient can be simple or quite complex.
Fluid therapy consists of replacement therapy and/or maintenance therapy. The volume of
fluid needed is determined by the severity of the stress response to surgery, the
underlying surgical disease, and the patient's overall medical condition. (See 'Introduction'
above.)
• Replacement fluid therapy is indicated for many postoperative patients to compensate

for deficits related to residual preoperative or intraoperative deficits, third-space losses
3/30/23, 2:18 PM 15073
related to the stress response to surgery, and to replace ongoing gastrointestinal or

other bodily fluid losses. (See 'Fluid resuscitation' above.)
• Maintenance fluids maintain hydration, electrolyte, and acid-base status and avoid
catabolism in postoperative patients who cannot tolerate oral or enteral intake. (See
'Maintenance fluid therapy' above.)
● The extent to which fluids administered intravenously in the postoperative period remain
in the intravascular space depends on many factors, including the severity of the stress
response to surgery. The stress response to surgery is triggered by (see 'Physiologic stress
response to surgery' above):
• Entry into a major body cavity

• Significant tissue disruption
• Significant blood loss (>500 mL or 7 mL/kg)
• Hemodynamic instability
• Severe infection
● For fluid resuscitation, the type and volume of fluid that is lost guides the choice, volume,
and rate of replacement. The fluid deficit is determined by estimating preoperative and
intraoperative losses and subtracting the volume of fluid and blood given during the
surgery. Ongoing gastrointestinal and other losses also need to be taken into account.
• The goal of fluid resuscitation is normal organ perfusion, which is achieved when the
end-diastolic volume of the left ventricle generates an adequate stroke volume. To
achieve normal organ perfusion, blood volume must be restored to 80 to 85 percent of
normal blood volume. Physiologic markers of adequate perfusion include
normalization of heart rate and blood pressure in healthy patients but may be
unreliable in critically-ill patients.
• Serum markers of adequate perfusion include lactic acid, base deficit, and central
venous oxygen saturation (SvO2). Adequate intracardiac filling can be measured with
echocardiography. As blood volume is restored, these parameters should trend toward
normal.
• If a patient becomes unresponsive to fluid replacement, fluid therapy should be

reconsidered to avoid complications of volume overload. For patients who do not
respond appropriately to fluid challenge or have a persistently elevated lactic acid and
SvO2, in spite of adequate fluid resuscitation, further evaluation in a closely monitored
3/30/23, 2:18 PM 15073
setting is warranted to identify bleeding or other complications of surgery (eg, acute

renal dysfunction, myocardial infarction).
● Crystalloid solutions remain the fluid of choice for replacement and maintenance fluid
therapy following surgery.
• For fluid replacement, isotonic or hypertonic fluids are used because their sodium
content facilitates volume expansion ( table 3), maintains serum osmolarity, and
retains water in the vascular space. The choice is governed by the composition of the
fluid that is lost. Resuscitative fluids are commonly administered as successive
intravenous boluses (3.5 to 14 mL/kg aliquots) over 30 to 60 minutes until the desired
response is observed (eg, improved urine output, improved mentation, normalizing
base deficit). Rapid onset hypothermia can occur when large volumes of room-
temperature fluid are administered. If this is anticipated, we suggest using a Level 1
rapid transfuser, which warms the fluid as it is infused.
• For maintenance fluid therapy, isotonic or hypotonic solutions ( table 3) with or

without additives (eg, dextrose, potassium) are used to maintain normal acid-base
status, electrolytes, and volume status. For postoperative patients with normal organ
function, a volume of maintenance fluid between 1 and 1.5 mL/kg/hour will meet
requirements. Adjustments may be required to account for organ dysfunction,
intravenous medications, or nutritional therapies.
● In the absence of a shock state, dextrose can be added to maintenance fluid to stimulate
basal insulin secretion and prevent muscle breakdown. However, after five days muscle
breakdown will occur unless nutritional support, preferably via enteral access, is instituted.
• Enteral intake should be established before maintenance fluids are titrated down or
discontinued. Some patients may continue to require a modified amount of
intravenous fluid until improved enteral intake is demonstrated.
• For those patients who do not tolerate enteral intake, parenteral nutrition may be
indicated. The parenteral nutrition rate is increased as maintenance fluid is decreased
in equal volumes to maintain the goal infusion rate per hour over several hours.
Use of UpToDate is subject to the Terms of Use.
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simultaneous recordings of inferior and superior vena cavae diameters. Crit Care 2014;
18:473.
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responsiveness in septic patients. Crit Care 2014; 18:647.
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18:6195.
Topic 15073 Version 18.0
3/30/23, 2:18 PM 15073
GRAPHICS
Classes of hemorrhage in trauma
Class II Class III Class IV

Parameter Class I
(mild) (moderate) (severe)
Approximate <15% 15 to 30% 31 to 40% >40%

blood loss
Heart rate ↔ ↔/↑ ↑ ↑ / ↑↑

Blood pressure ↔ ↔ ↔/↓ ↓
Pulse pressure ↔ ↓ ↓ ↓
Respiratory rate ↔ ↔ ↔/↑ ↑
Urine output ↔ ↔ ↓ ↓↓
Glasgow Coma ↔ ↔ ↓ ↓
Scale score
Base deficit* 0 to –2 mEq/L –2 to –6 mEq/L –6 to –10 mEq/L –10 mEq/L or less
Need for blood Monitor Possible Yes Massive

products transfusion
protocol
* Base excess is the quantity of base (HCO3–, in mEq/L) that is above or below the normal range in
the body. A negative number is called a base deficit and indicates metabolic acidosis.
Reproduced with permission from: Advanced trauma life support student course manual (10th ed), chapter 3, page 49, Table
3.1; Signs and Symptoms of Hemorrhage by Class Table; Published by: American College of Surgeons (Corporate Author)
2018. Copyright © American College of Surgeons. All Rights Reserved.
Graphic 107655 Version 3.0
3/30/23, 2:18 PM 15073
Composition of body fluid
Electrolyte (mEq/L)
Secretion
Na + K+ Cl – … H+ Rate (mL/day)
Salivary 50 20 40 30 – 100 to 1000
Basal gastric 100 10 140 – 30 1000
Stimulated gastric 30 10 140 – 100 4200
Bile 140 5 100 – – 500 to 1000
Pancreatic 140 5 75 – – 1000
Duodenum 140 5 80 – – 100 to 2000
Ileum 140 5 70 – – 100 to 2000
Colon 60 70 15 – – –
Reproduced with permission from: Wait RB, Alouidor R. Fluids, electrolytes, and acid-base balance. In: Greenfield's Surgery
Scientific Principles and Practice, 5th ed, Mulholland MW, Doherty GM, Waier RW, et al (Eds), Lippincott Williams & Wilkins,
Philadelphia 2011. Copyright © 2011 Lippincott Williams & Wilkins. www.lww.com.
3/30/23, 2:18 PM 15073
Fluids for postoperative replacement and maintenance therapy
Solution
(US Sodium Potassium Chloride Lactate Acetate Osmolarity
pH
trade (mEq/L) (mEq/L) (mEq/L) (mEq/L) (mEq/L) (mOsm/L)
name)
0.9% 154 0 154 0 0 5.5 308

Sodium
Chloride
Lactated 130 4 109 28 0 6.5 273

Ringer's
5% 130 to ≤2 Varies 0 0 6.9 300

Albumin 160
(human)
Plasma- 140 5 98 0 27 7.4 294

Lyte
US: United States.
3/30/23, 2:18 PM 15073
Flow rates of various intravenous devices
Percentage Percentage
Rate of Rate of Rate of
increase decrease
Intravenous flow with flow with flow with
with with
catheter gravity pressure Bionector*
pressure Bionector*
(mL/min) (mL/min) (mL/min)
(%) (%)
14 G 50 mm cannula 236.1 384.2 138.3 62.7 –41.4
14 G 14 cm Abbocath 197 366 131.3 85.8 –33.4
16 G 50 mm cannula 154.7 334.4 109.6 116.2 –29.2
14 G 15 cm 117.3 211.1 101.1 80 –13.8

Leadercath
18 G 45 mm cannula 98.1 153.1 80.3 56 –18.1
16 G distal port triple 69.4 116.1 67.4 67.3 –2.88

lumen central line
20 G 33 mm cannula 64.4 105.1 58.5 63.2 –9.17
22 G 25 mm cannula 35.7 71.4 34.7 100 –2.80
18 G proximal port 29.7 79.3 28.7 167 –3.37

triple lumen central
line
In this experiment, flow rates from a standard 1 liter bag of saline were measured through various
intravenous catheters. For the gravity measurement, a height of 130 cm was chosen. For the
pressure measurement, an external pressure bag was inflated to 300 mmHg.
G: gauge.
* Needle-free intravenous access device attached to the cannula.
Reproduced with permission from: Reddick AD, Ronald J, Morrison WG. Intravenous fluid resuscitation: Was Poiseuille right?
Emerg Med J 2011; 28(3):201-2. Copyright © 2011 BMJ Publishing Group Ltd.
3/30/23, 2:18 PM 15073
Contributor Disclosures
Nicole Siparsky, MD, FACS, FCCM No relevant financial relationship(s) with ineligible companies to
disclose. Amalia Cochran, MD, FACS, FCCM Other Financial Interest: JAMA Surgery [Web and social media
editor]. All of the relevant financial relationships listed have been mitigated. Richard H Sterns, MD No
relevant financial relationship(s) with ineligible companies to disclose. Kathryn A Collins, MD, PhD,
FACS No relevant financial relationship(s) with ineligible companies to disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.
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Official reprint from UpToDate®

Overview of postoperative fluid therapy in adults

The prescription of maintenance and resuscitative fluids in postoperative surgical patients is

abnormalities" and "Overview of perioperative nutrition support" and "Postoperative parenteral

Intraoperative fluid therapy is reviewed separately. (See "Intraoperative fluid management".)

PHYSIOLOGIC STRESS RESPONSE TO SURGERY

Hormonal mediators — Hormonal mediators of the stress response include:

● Vasopressin – Vasopressin, also known as antidiuretic hormone (ADH), is secreted by the

● Aldosterone – The renin-angiotensin axis responds to volume contraction by stimulating

● Cortisol – The hypothalamic-pituitary axis responds to stress by stimulating cortisol

FLUID LOSS AFTER SURGERY

Bleeding — Bleeding should always be considered in postoperative patients with hypotension,

Third-spacing — Third-spacing refers to the process of capillary leak and extravasation of

● Large nonanatomic cavities, such as those created from extensive subcutaneous

● Reperfusion following an episode of ischemia, such as in cases of arterial occlusion, result

Hypoalbuminemia contributes to third-spacing; it is theorized that the resultant intravascular

Insensible loss associated with ventilator support (intraoperative, postoperative) is limited.

● Preoperative fluid deficit (eg, bowel preparation-associated diarrhea) or fasting-associated

● Normal saline (0.9%) is used for head-injured patients, in whom hypernatremia is

● Reversal of coagulopathy or thrombocytopenia – Thresholds for platelet transfusion in

● Resuscitative fluid is commonly administered as an intravenous bolus over 30 to 60

Endpoints of fluid resuscitation — The endpoint of fluid resuscitation is to restore normal

MAINTENANCE FLUID THERAPY

Daily fluid requirements — For most adult postoperative patients, approximately 30

SOCIETY GUIDELINE LINKS

SUMMARY AND RECOMMENDATIONS

• Replacement fluid therapy is indicated for many postoperative patients to compensate

related to the stress response to surgery, and to replace ongoing gastrointestinal or

• Entry into a major body cavity

• If a patient becomes unresponsive to fluid replacement, fluid therapy should be

setting is warranted to identify bleeding or other complications of surgery (eg, acute

• For maintenance fluid therapy, isotonic or hypotonic solutions ( table 3) with or

Use of UpToDate is subject to the Terms of Use.

1. Schulman S, Kearon C, Subcommittee on Control of Anticoagulation of the Scientific and

3. Myles PS, Andrews S, Nicholson J, et al. Contemporary Approaches to Perioperative IV Fluid

6. Schmidt C, Creutzenberg M, Piso P, et al. Peri-operative anaesthetic management of

24. Brandstrup B, Tonnesen H, Beier-Holgersen R, et al. Effects if intravenous fluid restruction

Vasc Anesth 2014; 18:352.

46. Charbonneau H, Riu B, Faron M, et al. Predicting preload responsiveness using

Classes of hemorrhage in trauma

Class II Class III Class IV

Approximate <15% 15 to 30% 31 to 40% >40%

Heart rate ↔ ↔/↑ ↑ ↑ / ↑↑

Base deficit* 0 to –2 mEq/L –2 to –6 mEq/L –6 to –10 mEq/L –10 mEq/L or less

Need for blood Monitor Possible Yes Massive

Graphic 107655 Version 3.0

Composition of body fluid

Salivary 50 20 40 30 – 100 to 1000

Basal gastric 100 10 140 – 30 1000

Stimulated gastric 30 10 140 – 100 4200

Bile 140 5 100 – – 500 to 1000

Pancreatic 140 5 75 – – 1000

Duodenum 140 5 80 – – 100 to 2000

Ileum 140 5 70 – – 100 to 2000

Graphic 107239 Version 3.0

Fluids for postoperative replacement and maintenance therapy

0.9% 154 0 154 0 0 5.5 308

Lactated 130 4 109 28 0 6.5 273

5% 130 to ≤2 Varies 0 0 6.9 300

Plasma- 140 5 98 0 27 7.4 294

US: United States.

Graphic 107900 Version 2.0