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Patients) demonstrated increased mortality in intensive care unit patients treated with colloids.22,23 As

mentioned above, albumin solutions are heat-treated to negate viral and bacterial contamination.

Allergic reactions are rare. The primary concern with albumin administration is cost; the infection risk is

negligible.

Hetastarch

Hydroxyethyl starches (HES) are synthetic colloids derived from hydrolyzed amylopectin. In the United

States, it is available as a 6% solution of high–molecular-weight (150 to 450 kD), highly hydroxyethyl

substituted HES in normal, isotonic saline. The average molecular weight of the starch molecules is

equivalent to that of albumin. However, HES is slightly more effective than 5% albumin as a colloid – it

has a higher colloid oncotic pressure than 5% albumin. The main advantage of hetastarch is its lower

cost compared to albumin.

Hetastarch has been used as a resuscitative solution in a variety of clinical settings with variable

results. Coagulopathy and bleeding complications have been widely reported after administration of

highly substituted, high–molecular-weight HES.24,25 This appears to be associated with reduced factor

VIII and von Willebrand factor levels, a prolonged partial thromboplastin time, and impaired platelet

function.26 It also has a long elimination half-life (17 days). Because of its long half-life, the

coagulopathy does not rapidly reverse after cessation of HES administration. Also, serum amylase

enzymes continually degrade HES molecules before renal clearance. It is common for serum amylase

levels to be elevated for the first few days after HES infusion. In order to differentiate this from

pancreatitis, serum lipase levels should be checked and are usually normal.

The above observations and reports of renal insufficiency after HES administration prompted a

prospective study, with results published in 2012.27,28 The results of these trials were so significant that

the FDA and the Pharmacovigilance Risk Assessment Committee, the European equivalent of the FDA,

recommended suspending marketing authorization of all HES products and issued warnings to its

use.29,30 The Surviving Sepsis Campaign recommends against HES administration in septic patients.31

Dextrans

First introduced in the 1940s, dextrans are glucose polymers synthesized by Leuconostoc mesenteroides

bacteria. These are available as synthetic plasma expanders in both 40 kD (dextran 40) and 70 kD

(dextran 70) solutions. Although neither is used frequently for volume expansion, dextran 70 has been

preferred because of its significantly longer half-life and better retention in plasma. It is degraded to

glucose and water by cells. The use of dextrans involves risks of anaphylaxis, hyperglycemia, renal

dysfunction and failure, coagulopathy (e.g., erythrocyte and platelet dysfunction), and increased

thrombosis rates. The use of dextran solutions is no longer favored given a higher relative risk of

mortality compared to HESs.32

Gelatins

Gelatin solutions produced from bovine collagen are effective as plasma volume expanders. These are

currently only available outside the United States in urea-linked (Gelofusin) and succinate-linked

(Haemaccel) formulations. Gelofusin has been used in similar clinical settings to HES, with similar

clinical results.33 Uniquely, coagulopathy does not appear to be an issue with gelatins. Renal

impairment has been reported with these colloids as having allergic reactions ranging in severity from

pruritus to anaphylaxis with both gelatin formulations.34

Artificial Oxygen Carriers

Recent clinical trials and subgroup analyses using temporary hemoglobin-based oxygen-carrying

solutions (e.g., PolyHeme, Northfield Laboratories, Inc.) have been encouraging albeit with some

controversy.35 PolyHeme is made from polymerized human hemoglobin. It originally began as a

military project following the Vietnam war. PolyHeme’s primary use is in trauma situations with

massive blood loss when fresh, whole blood is not readily available for transfusion. On May 9, 2009,

Northfield Laboratories, Inc. shut down operations after it failed to secure a biologic license application

for PolyHeme from the FDA. However, with further studies, solutions like PolyHeme may prove

beneficial in the future when volume expansion in conjunction with increased oxygen-carrying capacity

is required.

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GOALS OF FLUID AND ELECTROLYTE THERAPY

Maintaining homeostasis – body fluid and electrolyte concentrations – and normal hemodynamic

parameters are the goals of fluid and electrolyte therapy. This is accomplished by first understanding

the general maintenance fluid required by an idealized 70-kg male patient to account for normal daily

losses. Thereafter, it is imperative to correct existing volume and electrolyte abnormalities and any

ongoing losses associated with disease states and surgical treatments.

Table 11-5 Calculation of Maintenance Fluid Requirements

Maintenance Fluid Therapy

Maintenance fluid volume requirements can be calculated based on body weight taking into account a

larger per kilogram volume requirement of smaller body weight individuals (Table 11-5). A 10-kg child

requires 100 mL/kg/day or 1,000 mL/day. A 70-kg man requires 1,000 mL/day for the first 10 kg (100

mL/kg × 10 kg), plus 500 mL/day for the second 10 kg (50 mL/kg × 10 kg), plus 1,000 mL/day for

the last 50 kg (20 mL/kg × 50 kg), for a total daily water requirement of 2,500 mL/day. In patients

who may be intolerant of hypervolemia (i.e., cardiac disease, elderly patients), the requirement per

kilogram over 20 kg is decreased to 15 mL/kg/day.

Maintenance Electrolyte Therapy

One to 2 mEq/kg/day of sodium is required, with any administered excess managed by urinary sodium

excretion. Potassium requirements are approximately 0.5 to 1 mEq/kg/day. If sodium is replaced at 2

mEq/kg/day and potassium is replaced at 1 mEq/kg/day, a 70-kg patient requires 2,500 mL of water

containing 140 mEq of sodium and 70 mEq of potassium. Each liter of parenteral solution would contain

56 mEq of sodium and 28 mEq of potassium. The solution that best fits this patient’s daily maintenance

requirements is 0.33% saline solution (56 mEq/L Na+). Potassium chloride can be added to each liter of

solution (20 to 30 mEq/L), with appropriate adjustments for the patient’s electrolyte and renal

functional status.

Additional Electrolyte Therapy

Short-term maintenance therapy generally does not require addition of calcium, phosphate, or

magnesium. In patients with acute and/or chronic disorders, patients who experience significant volume

shifts, or patients who require long-term parenteral fluid therapy, these electrolytes should be measured

and corrected by the most practical, physiologically natural route. In general, the enteral route is

preferred given normal physiology. If the enteral route is unavailable, these additional electrolytes are

administered in parenteral nutrition solutions along with trace elements, vitamins, and appropriate

caloric sources. Corrections and allotment must be made for disease states that may alter the need or

absence of electrolytes (e.g., potassium in renal failure patients) in replacement solutions.

CORRECTION OF VOLUME ABNORMALITIES

Volume Deficits

States of subphysiologic volume (i.e., hypovolemia) are common among surgical and trauma patients.

This may be related to direct blood loss or other fluids. Large volumes of fluid can be sequestered in

extravascular spaces (third-space losses) as a consequence of inflammation, sepsis, or shock-related

endothelial injury and increased endothelial permeability.36 This situation is characterized by a

movement of proteins and fluid from the intravascular to the interstitial compartment. Examples of

disorders that cause third-space losses include bowel obstruction with edema of the bowel wall and

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transudation of fluid into the bowel lumen, pancreatitis (especially with retroperitoneal fluid

extravasation) and extensive tissue destruction in trauma. While the disease state exists, normal

homeostasis is altered and cannot be maintained. With the resolution of the pathologic condition and

normalization of microvascular permeability, these fluid losses abate. Sequestered extravascular fluid

returns – albeit at variable rates – to the intravascular space.

Volume deficits can manifest either acutely or over time. Chronic volume deficits may manifest with

decreased skin turgor, sunken eyes, oliguria, weight loss, hypothermia, tachycardia, and orthostatic

hypotension. In addition, serum BUN and creatinine values may be elevated, with a high

BUN/creatinine ratio (above 15:1). The absolute hematocrit level has been shown to be a poor predictor

of intravascular volume status. The hematocrit may be measured during dialysis as a way to indirectly

measure volume status.37 Optical measurements of absolute red cell mass and oxygen saturation are

measured as blood passes through the dialysis tubing while a patient is undergoing dialysis treatment.

The hematocrit is then determined by both the absorption properties of hemoglobin and the scattering

properties of red blood cells passing through the blood chamber.37

Acute volume losses usually manifest by changes in vital signs. In an attempt to provide sufficient

cardiac output for end-organ perfusion, the heart rate may increase. At the extreme, blood pressure will

drop resulting in hypotension. Urine output is usually low by this point.

Fluid resuscitation for hypovolemia is initiated with an isotonic solution such as normal saline or

lactated Ringer solution. Once routine laboratory values (e.g., chemistries) are measured, tailoring the

type of solution can be done. Urine flow in critically ill patients is monitored with an indwelling Foley

catheter with a goal of at least 0.5 mL/kg/hr output. In addition, a thorough history and physical

examination will help determine the origins of the volume deficits, specifically addressing underlying

causes and resultant losses.

Volume Excess

Volume excess may occur with significant resuscitative fluid, blood product administration, or excessive

parenteral volume administration. Volume overload will occur if adjustments to fluid therapy are not

made as the clinical status of the patient changes. Possible manifestations of volume overload are

weight gain, truncal and peripheral edema and pulmonary congestion (identified by rales on pulmonary

auscultation and/or radiographic chest imaging). Intravascular volume excess is treated by a

combination of volume restriction and diuresis. At the extreme, volume overload may be treated by

ultrafiltration of the blood (often done concurrently during hemodialysis).

REPLACEMENT OF ONGOING FLUID LOSSES

Ongoing losses from stomas, fistulae, open body compartments (e.g., abdomen, chest) and all tubes

(e.g., nasogastric) and drains – are recorded during the course of care. Once the net “ins and outs” have

been calculated, any existing volume deficits should be replaced with fluid replacement. The electrolyte

content of these fluids can be estimated or measured and used to guide the choice of replacement fluid

type (Table 11-6). As the disease state changes, the overall fluid balance of the patient can be estimated

and replaced beyond what is considered to be maintenance.

Table 11-6 Electrolyte Concentrations in Gastrointestinal Secretions

Intraoperative Fluid Therapy

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Fluid losses during operative procedures result from evaporative losses in open wounds, blood loss, and

extravascular, third-space sequestration. Relative operative blood loss can frequently be measured.

Evaporative losses as well as shifts of intravascular fluid to the extravascular space are difficult to

measure, but should be anticipated. Intraoperative replacement with crystalloid solutions is usually

accomplished at rates of 500 to 1,000 mL/hr as this is roughly equivalent to the hourly insensible loss

rate during open celiotomy cases. The choice of intraoperative fluid is dependent on many factors.

Administration of buffered solutions (e.g., Ringer lactate solution) is as efficacious and safe as

nonbuffered, saline-based fluids and may prevent postoperative hyperchloremia and metabolic acidosis.

Close monitoring of blood pressure, blood loss, urine output, and invasive monitoring techniques aids

the surgeon and anesthesiologist in gauging fluid shifts and potential problems associated with

intraoperative volume depletion.

Postoperative Fluid Therapy and Monitoring

Routine monitoring of intraoperative and postoperative fluid status consists of serial vital signs (e.g.,

blood pressure and heart rate), measurements of all tubes, lines, and drains (e.g., urine output) and

inclusive of all intravenous and enteral drips. These are recorded in the patient’s medical record and

used to plan ongoing fluid management. The net gains (all inputs) minus the losses allow daily and

length-of-stay volume assessments to be made. Daily weight should also be recorded and compared to

the patient’s starting or “dry” weight prior to their surgery, if possible. In the postsurgical patient, rapid

fluctuations in weight are generally related to changes in TBW. In the absence of any extenuating

circumstances (e.g., renal dialysis, kidney transplantation), adequate fluid is usually given to maintain a

urine output of greater than 0.5 mL/kg/hr in adult patients.

Urine specific gravity can also be measured and serves as an indicator of both volume status and renal

ability to concentrate and dilute the urine. A urine specific gravity of greater than 1.010 to 1.012

indicates that the urine is being concentrated (relative to plasma), and a urine specific gravity of less

than 1.010 indicates that dilute urine is being produced.

Renal failure in the postoperative period may be accompanied by low urine volume (oliguric renal

failure, <0.5 mL/kg/hr, or <500 mL/day). Additionally, normal or high urine volumes (nonoliguric or

high-output renal failure) may also indicate renal dysfunction. Measuring the fractional excretion of

sodium compared to creatinine (i.e., FeNa) can help delineate the potential etiology of renal dysfunction

by discerning prerenal states (FeNa usually <1%) from acute tubular necrosis (FeNa usually >2%).

FeNa = (UrineNa)(SerumCreat)/(UrineCreat)(SerumNa)

Central venous pressures (CVPs) have also been extensively used to gauge fluid status and

responsiveness. Normal CVP may range from 5 to 12 mm Hg. Higher pressures usually indicate volume

overload or cardiac failure, whereas pressures below this range indicate intravascular volume depletion.

However, the use of CVP measurements alone has been shown to be highly variable and inaccurate in

assessing intravascular volume and venous return. This is especially true in critically ill patients where

abnormalities of cardiac performance and vascular tone may confound interpretation of CVP

measurements.

More recently, assessments of fluid status, responsiveness, and overall tissue perfusion are being

accomplished by the use of (1) bedside echocardiography (e.g., transthoracic) to measure function

through ventricular filling and ejection, (2) ultrasound of the vena caval diameter, and (3) peripheral

arterial pulse-volume variability calculations. The latter measures the stroke volume variability (SVV)

during the ventilatory cycle via a peripherally placed arterial line. SVV is the calculated percentage of

the difference between the maximal and minimal stroke volumes (SVs) divided by the mean SV. This is

usually calculated over a time period between 20 to 30 seconds.38 Use of the SVV has been shown to be

a reliable indicator of fluid responsiveness.

It is important to note that the efficacy of these techniques may be altered in abnormal right and/or

left ventricular compliance, increased intrathoracic pressure (via elevated levels of positive end

expiratory pressure and intra-abdominal pressure), valvular heart disease (e.g., mitral stenosis) and

cardiac dysrhythmias (e.g., atrial fibrillation). In order to solve any serious questions of volume status,

the gold standard technique remains pulmonary artery catheterization in the critically ill patient.

ELECTROLYTES

8 An electrolyte is defined as a substance that ionizes when dissolved in an appropriate solvent, the

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