Colloid Osmotic Pressure in Health and Disease* - VetLearn.com

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896 V 

Vol. 23, No. 10 October 2001 

Article #4 (1.5 contact hours) 

Refereed Peer Review 

KEY FACTS 

■ COP is the main force retaining 

fluid within the vasculature and 

can be altered in different 

disease states. 

■ Albumin is the main 

determinant of COP. 

■ Use of formulas to calculate 

COP using total protein values 

is not as accurate as actual 

COP measurement, especially 

in critically ill animals. 

Colloid Osmotic 

Pressure in Health 

and Disease* 

Tufts University 

Daniel L. Chan, DVM 

Elizabeth A. Rozanski, DVM 

Lisa M. Freeman, DVM, PhD 

John E. Rush, DVM, MS 

Email comments/questions to 

compendium@medimedia.com 

or fax 800-556-3288 

ABSTRACT: The use of synthetic colloids has become commonplace in the treatment of critically 

ill animals. The theoretical benefits of colloid compared with crystalloid fluid therapy for 

increasing plasma volume include a more rapid and longer-lasting fluid resuscitation with colloids, 

a lesser fluid volume necessary to achieve the same level of resuscitation, and reduced 

risk of edema formation. These benefits are achieved, in part, by increasing or maintaining the 

patient’s colloid osmotic pressure (COP) to retain fluid within the vasculature and limit extravasation 

of fluid into the interstitium. COP, and ultimately fluid balance, are normally highly 

dependent on the concentration of albumin within the vasculature. Understanding how COP is 

affected in different conditions (e.g., hypovolemia, sepsis, systemic inflammatory response 

syndrome, acute and chronic hypoalbuminemia) can guide clinicians in the appropriate uses 

of colloid therapy. 

Maintenance of fluid homeostasis requires a delicate balance between 

hydrostatic and oncotic gradients. Of the forces involved, intravascular 

hydrostatic pressure and plasma COP are the most significant. Intravascular 

hydrostatic pressure is the main force promoting fluid extravasation 

from vessels, while plasma COP is the pressure that prevents fluid movement 

from the intravascular to the interstitial compartments. Starling’s equation (Figure 

1) relates these forces such that fluid flux is determined by the difference in 

hydrostatic and oncotic gradients found between the intravascular and interstitial 

compartments. The forces favoring filtration of fluid out of the intravascular 

space are capillary hydrostatic pressure and interstitial oncotic pressure. These 

forces are opposed by intravascular COP and interstitial hydrostatic pressure. In 

most biologic systems, there is always a net fluid flow out of the vascular system 

and into the interstitium. The excess interstitial fluid is eventually returned to 

*Dr. Chan’s residency program is funded by the Ralston-Purina Company. Hill’s Pet Nutrition 

has provided support for research on colloid osmotic pressure at Tufts University 

School of Veterinary Medicine.

Compendium October 2001 Small Animal/Exotics 897 

Figure 1—Starling’s Equation relates fluid flux (J v) as the difference 

between hydrostatic (P c – P i ) and oncotic (π c – π i ) gradients, 

where P c is the intravascular hydrostatic pressure, P i is the 

interstitial hydrostatic pressure, π c is the intravascular oncotic 

pressure, and π i is the interstitial oncotic pressure. K is the filtration 

coefficient representing the conductance or relative ease 

of fluids to cross the membrane, and σ is the reflection coefficient, 

which represents the permeability of the membrane or 

pore size. The arrows indicate the direction of each force. 

the intravascular fluid spaces via the lymphatic system. 

Two additional factors responsible for modulating 

the impact of Starling’s forces on fluid flux are the reflection 

coefficient and the filtration coefficient: 

• The reflection coefficient (σ) represents the permeability 

of the membrane to macromolecules. Mechanisms 

affecting macromolecular permeability include 

differences in size and charge of the molecules 

and route of transport. Macromolecules cross the 

microvascular membrane through large pores on the 

venous side of the capillary, and their transport is 

also influenced by the charge of endothelial cells and 

the composition of glycocalyx close to the endothelial 

membrane. 

• The filtration coefficient (Κ) represents conductance 

or the ease with which water and small molecules 

cross the membrane. In contrast to macromolecules, 

water and small molecules filter through both the 

small and large pores along the entire length of the 

capillary membrane. 1 

The interplay of Starling’s forces is dynamic and 

varies considerably among organ systems. For example, 

the permeability of capillary membranes to albumin is 

quite high in the lungs. As a result, an effective oncotic 

gradient cannot be maintained and therefore COP is 

less important in controlling fluid extravasation in this 

system. To compensate, lymphatic drainage is enhanced, 

preventing accumulation of filtered fluid. This 

π c 

π i 

J v = K [(P c – P i) – σ (π c – π i)] 

explains why pulmonary edema is more common in situations 

of high hydrostatic pressures, such as fluid overload 

and congestive heart failure (CHF), but relatively 

uncommon in hypoproteinemia. In contrast, the capillary 

permeability to albumin is low in the subcutaneous 

interstitium, which helps to account for the greater tendency 

to develop peripheral edema in hypo-oncotic 

states. This edema formation may be countered in clinical 

practice with support wraps, which increase the interstitial 

hydrostatic pressure. 

GENERATION AND MAINTENANCE 

OF COLLOID OSMOTIC PRESSURE 

Albumin is the principal contributor to COP, accounting 

for approximately 80% of plasma COP. 2 Other 

proteins (e.g., immunoglobulins, fibrinogen) also 

contribute to COP. These plasma proteins are marginally 

permeable through the capillary membranes and 

are therefore concentrated within the vasculature. Because 

of the poor permeability of these osmotically active 

proteins (i.e., albumin, immunoglobulins, fibrinogen), 

a concentration gradient is created across the 

membrane, generating most of the COP. 

Another property that is a significant contributor to 

COP is the Gibbs-Donnan effect. Most proteins, including 

albumin, are negatively charged molecules surrounded 

by noncovalently bound cations such as sodium. 

These sodium ions act independently from their 

own concentration gradients and further increase the 

water-retaining effect of COP within the vasculature. 

This effect is additive and increases disproportionately 

with increasing albumin concentration. Acidemia, 

which is common in critically ill patients, decreases the 

relative negative charge of albumin, limiting the Gibbs- 

Donnan effect and reducing the effective COP. 

Generation and maintenance of the COP (and albumin 

in particular) are important in healthy animals. 

The relationship between albumin synthesis and COP 

is incompletely understood. Albumin synthesis takes 

place exclusively in hepatocytes. In situations of adequate 

nutritional status and ample supply of amino 

acids, albumin synthesis is thought to be regulated by 

hepatic plasma COP. 3 However, other factors independent 

of COP may also be involved in albumin synthesis. 

4 For example, albumin is known as a negative 

acute-phase reactant, which means that its synthesis is 

suppressed in response to inflammation. Controversy 

exists as to whether the administration of natural or artificial 

colloids could, in fact, suppress albumin synthesis. 

3–5 A recent in vitro study demonstrated significant 

decreases in albumin synthesis by isolated hepatocytes 

when the cultures were incubated with solutions of albumin 

and hetastarch. 5

898 Small Animal/Exotics Compendium October 2001 

A low plasma COP has been associated with increased 

mortality in critically ill humans. 6 Critically ill 

veterinary patients have also been recognized as having 

abnormally low COP, but actual correlation to outcome 

has not been established. 7 Perhaps more important 

than the actual plasma COP is the ratio between 

plasma and interstitial COP. Conditions resulting in 

acute hypoalbuminemia dramatically decrease intravascular 

COP relative to interstitial COP and can result in 

hypovolemia, decreased tissue oxygenation, and systemic 

edema formation. 2,8 For example, in a case in 

which there is significant acute blood loss followed by 

massive crystalloid infusion, the decrease in intravascular 

COP promotes edema formation. Although peripheral 

edema may not have serious consequences in most 

patients, intestinal edema could be life-threatening in 

cases of intestinal surgery due to an increased risk for 

anastomotic dehiscence. 9 In cases of chronic hypoalbuminemia, 

as seen with protein-losing enteropathy and 

protein-losing nephropathy, COP is decreased in both 

the interstitium and the intravascular space, and therefore 

the ratio between these two compartments is preserved 

and fluid balance is maintained. These patients 

would have a low COP but no signs of edema unless 

crystalloids were administered. In the absence of peripheral 

edema, colloid therapy would offer little benefit 

in these chronic cases. 

OTHER MEASURES OF FLUID BALANCE 

As discussed, COP counterbalances hydrostatic pressure. 

Hydrostatic pressure is dependent on arterial 

blood pressure, precapillary and postcapillary resistance, 

and venous pressure. 10 Clinically, it is difficult to 

measure hydrostatic pressure, although pulmonary capillary 

wedge pressure (PCWP; measured via a Swan- 

Ganz catheter) and central venous pressure (CVP) 

might be useful as clinical correlates of hydrostatic pressure. 

A PCWP–COP gradient has also been shown to 

accurately predict the presence of pulmonary edema in 

critically ill humans, 11 although no such relationships 

have been demonstrated in veterinary medicine and 

PCWP is not routinely measured. In addition to hydrostatic 

and oncotic forces, increased vascular permeability 

has a major impact on fluid balance. 

MEASUREMENT OF 

COLLOID OSMOTIC PRESSURE 

Colloid osmotic pressure may be predicted or directly 

measured. Because the concentration of plasma proteins 

in part determines COP, predictive equations of 

COP based on total protein concentrations have been 

proposed. 12 Although these equations provide values 

that correlate well with COP in healthy humans, they 

are unreliable in critically ill patients. 13,14 This is due in 

part to changes in blood pH, particularly acidemia, 

which influence the Gibbs-Donnan effect. Attempts to 

apply these equations to dogs and cats have not produced 

reliable results. 15 Although new formulas have 

improved the ability to use total protein to predict 

COP, direct measurements remain the method of 

choice for determining COP in clinical patients. 14–16 A 

commercial colloid osmometer can be used to directly 

measure COP in the clinical setting, providing rapid 

and reliable results (e.g., Wescor ® 4420, Logan, UT; 

Figure 2). 

Some authors have cautioned that certain conditions 

can alter the reading of the COP by a colloid osmometer. 

Such artifacts as severely hemolyzed samples can reportedly 

falsely elevate COP readings through the addition 

of free hemoglobin, while the use of liquid 

anticoagulants in sample collection can cause a dilutional 

effect and falsely lower the COP measurement. 17 

Normally, immunoglobulins are only minor contributors 

to COP. In cases of severe hypergammaglobulinemia 

(e.g., multiple myeloma, feline infectious peritonitis), 

however, COP can be dramatically elevated. 15 The 

consequences of an abnormally elevated COP are unclear, 

although high COP could inhibit albumin synthesis 

and result in hypoalbuminemia. 4,5 Pathologic 

changes associated with hypergammaglobulinemia are 

usually attributed to increases in blood viscosity and 

the deposition of immunoglobulin complexes but apparently 

not to the altered COP. 

Figure 2—Schematic representation of a colloid osmometer. 

A sample (serum, plasma, or heparinized whole blood) from 

a patient is injected into Chamber A and allowed to equilibrate 

with the reference Chamber B (containing 0.9% 

saline). Chambers A and B are separated by a selectively permeable 

synthetic membrane. The COP of the sample causes 

water and small solute molecules to move from Chamber B 

to Chamber A with a fall in pressure in the lower chamber. 

This negative pressure is measured by the transducer and 

equals the COP of the sample in Chamber A.


Several studies have established normal values of 

COP in veterinary patients using colloid osmometry. 

Normal canine plasma COP values range from 14 to 

27 mm Hg, whereas normal feline plasma COP values 

can range from 21 to 34 mm Hg. 2,15,16 The reported 

mean COP in whole blood was 19.9 ± 2.1 mm Hg in 

dogs and 24.7 ± 3.7 mm Hg in cats. 18 However, just as 

with any laboratory test, a reference range should be established 

for the particular colloid osmometer and protocol 

used. 

FLUID BALANCE IN DISEASES 

The normal dynamics of various fluid compartments 

are altered during different disease states. Changes may 

include the following: 

• Increased vascular permeability 

• Acute or chronic decreases in albumin (and COP) 

• Increased intravascular hydrostatic pressure 

Increased vascular permeability is one of the more challenging 

conditions encountered in critically ill patients 

and one in which the use of synthetic colloids is perhaps 

most controversial. Diseases associated with increased 

vascular permeability include the systemic inflammatory 

response syndrome (SIRS), acute 

respiratory distress syndrome (ARDS), pneumonia, 

sepsis, vasculitis, reperfusion injury, pancreatitis, and 

anaphylaxis. 10,17,19,20 Additionally, envenomation (e.g., 

bees, wasps, rattlesnakes), trauma, burns, smoke inhalation, 

and multiple blood transfusions are also associated 

with increased vascular permeability. 19 Inflammatory 

cytokines can induce changes in endothelial cells that 

increase microvascular permeability and lead to capillary 

leakage. 21 For example, during reperfusion of hypoxic 

tissue, the endothelial junctions in capillary 

membranes separate, increasing the number and size of 

the pores in the capillary membranes. 22 In sepsis, it is 

thought that endothelial damage occurs as a result, in 

part, of the action of activated, degranulating neutrophils. 

23 Subsequently, the increased capillary permeability 

is responsible for albumin leakage and a decrease 

in plasma COP. With a decrease in plasma COP, fluid 

filtration from the intravascular compartment is enhanced 

and leads to edema formation and fluid loss 

into third spaces. The subsequent loss of plasma volume 

contributes to the cardiovascular dysfunction and 

tissue hypoperfusion in sepsis. 

In patients with ARDS, inflammatory cytokines are 

released in response to septic and inflammatory stimuli 

and cause deranged capillary permeability. These 

patients usually receive aggressive fluid therapy, result- 

ing in elevated pulmonary hydrostatic pressure. The 

combination of these effects favors filtration of fluid 

into the pulmonary interstitium and may impair pulmonary 

gas exchange. 19 With the increased permeability, 

the oncotic gradient between the pulmonary vasculature 

and interstitium is diminished, causing COP 

to become less significant in affecting fluid flux. This 

increase in permeability also presents a problem for 

patients receiving synthetic colloids. Although there 

are some data to suggest that medium-sized macromolecules 

could attenuate some of the increased permeability, 

most artificial colloids are heterogeneous 

solutions containing various-sized macromolecules. 

For example, hetastarch contains molecules ranging 

from 20 to 2500 kD (6% hetastarch in 0.9% sodium 

chloride, Abbott Laboratories, North Chicago, IL). 

The smaller particles may easily pass through capillary 

membranes and extravasate into the pulmonary interstitium. 

This could potentially lead to worsening of 

pulmonary edema. 24 

When hypoalbuminemia results from nephrotic syndrome, 

the exact mechanism of fluid retention and edema 

formation remains controversial. A pervasive theory 

states that renal sodium and water retention occur as a 

response to low intravascular volume caused by the 

transudation of fluid from the plasma to the interstitial 

compartment due to a low plasma COP. 25 However, 

some studies have cast doubt on this theory, and edema 

formation in nephrotic patients is now thought to occur 

as a result of primary renal mechanisms of sodium 

and water retention, independent of COP. 26 Therefore, 

the use of colloids to raise the COP in this patient population 

may not be warranted. Similarly, increases in 

pulmonary hydrostatic pressure are often seen in CHF. 

Colloid fluid therapy is usually avoided in animals with 

CHF due to concerns about intravascular volume overload 

and subsequent worsening of pulmonary edema or 

pleural effusion. 

COLLOID FLUID THERAPY 

Treatment of critically ill animals typically entails correction 

of dehydration and hypoperfusion via the administration 

of intravenous fluids to compensate for fluid 

losses and to maintain cardiovascular homeostasis. 

Intravenous fluids are categorized as either a crystalloid 

solution or a colloid solution based on their composition. 

A crystalloid is an aqueous solution with small particles 

that are normally osmotically active in body fluids 

and that can easily pass through the capillary membrane. 

Examples include 0.9% saline, lactated Ringer’s 

solution, and hypertonic saline. A colloid is an aqueous 

solution containing both small and large particles (larger 

than 30 kD), with the larger molecules being too large


to filter through capillary membranes. Colloids can be 

either natural (e.g., whole blood, plasma, albumin solutions) 

or synthetic (e.g., dextrans, hydroxyethyl starches, 

hemoglobin-glutamers [Oxyglobin ® , Biopure Corporation, 

Cambridge, MA]). Colloid therapy and products 

have been recently reviewed. 27 Parenteral nutrition components 

such as amino acid solutions, lipid emulsions, 

and dextrose solutions behave similarly to crystalloids 

and have COP measurements less than 1 mm Hg. 28 

Colloid therapy is employed based on the principle 

that the patient’s COP can be influenced by the administration 

of either natural or synthetic colloids. Properties 

of the different colloids may help predict their in 

vivo effects. For example, the inherent COP of synthetic 

colloids ranges from 29 to 65 mm Hg, and therefore the 

degree of COP change will depend on the type and volume 

of colloid used. 18,28–30 Other factors, such as the 

half-life of each particular colloid and the duration of 

effect, are thought to also influence the effect on COP. 

The expected increase in COP associated with particular 

dosages and types of colloids has not been established. 

While there are many benefits to colloid therapy 

(e.g., more rapid and longer-lasting resuscitation), there 

are potential side effects associated with synthetic colloid 

administration. 20 These rare side effects can be 

dose-dependent, such as fluid overload and changes in 

coagulation parameters, or the more unpredictable anaphylactic/anaphylactoid 

reactions and acute renal failure. 

2,16,18 To minimize the occurrence of some of these 

effects, general recommendations have been made, including 

dose recommendations for various colloids 

(e.g., 20 ml/kg/day for hetastarch) and monitoring 

COP during colloid therapy. Some authors have advocated 

using the COP to guide colloid administration 

(e.g., administering colloids until the patient’s COP is 

at least 15 mm Hg). 31 However, this therapeutic goal 

may not be optimal in all situations. In our experience, 

standard colloid therapy (20 to 40 ml/kg/day of hetastarch) 

results in only modest changes in COP of 4 to 

5 mm Hg posttreatment in most animals. Administration 

of synthetic colloids does not appear to increase 

COP in a predictable manner, although a general dosedependent 

effect is seen. The benefit of COP monitoring 

during colloid therapy may be clearer when observing 

trends rather than attempting to achieve a certain 

COP level. As with any laboratory test, the actual value 

is meaningless when taken out of context with respect 

to the clinical assessment of the patient. 

Increased transcapillary leakage of fluid and proteins 

is often seen in critically ill patients. 1 Continued use of 

crystalloids for fluid therapy in these patients could result 

in significant fluid losses from the intravascular 

space. Reducing vascular permeability may be of value 

to counteract the resultant tissue edema and hypovolemia. 

In some studies, the use of dextrans and hetastarch 

was shown to attenuate macromolecular leakage 

by presumably occluding some of the endothelial 

“gaps” associated with some conditions (e.g., ischemia, 

sepsis). 23,32,33 However, there are concerns over the use 

of heterogeneous colloid solutions in states of increased 

permeability because the smaller colloid particles will 

extravasate into the interstitium and potentially promote 

edema. 34 Furthermore, the clearance of these 

small, osmotically active particles from the pulmonary 

interstitium is particularly slow, and so colloids should 

be used with judicious care in cases of increased pulmonary 

vascular permeability. 35 

COLLOID OSMOTIC PRESSURE 

MEASUREMENTS IN CLINICAL CASES 

The three cases in Box 1 illustrate how measurement 

of COP could impact clinical decisions in both the diagnosis 

and treatment of veterinary patients. In Case 1, 

the acute decrease in COP associated with blood loss, 

coupled with increased hydrostatic pressure from aggressive 

fluid administration and possible increased vascular 

permeability from massive blood transfusions, 

favored edema formation. Restoration of the intravascular/interstitial 

COP gradient with synthetic colloids 

may have facilitated edema clearance. 

In Case 2, a similarly low COP was measured, yet no 

edema was noted. This was due to the chronicity of 

protein loss that allowed equilibration of protein distribution 

between the intravascular and interstitial compartments, 

thus preserving the normal gradient. This illustrates 

that edema cannot be predicted solely by the 

COP. 

In Case 3, the presence of generalized edema with a 

normal COP supports either an increase in vascular 

permeability or the inability to clear interstitial fluid, as 

may be seen with lymphatic obstruction associated with 

neoplasia as the cause for edema. Lymphatic obstruction 

was unlikely in this case because of the distribution 

of edema, leaving vasculitis as the main diagnostic 

differential. The normal COP also helped determine 

that colloid therapy was not indicated in this case. 

Knowledge of the COP can help in classifying and diagnosing 

diseases associated with edema as well as determining 

the appropriate situations in which synthetic 

colloids might be used. Colloid osmotic pressure is an 

important concept in understanding the pathophysiology 

of edema, fluid resuscitation, and colloid therapy. 

FUTURE RESEARCH 

As the intricacies of COP in both health and disease 

are further elucidated, an individual patient’s COP


Box 1. Clinical Cases 

Case 1 

A 10-year-old, intact male, 26-kg weimaraner was presented 

for acute weakness and hematemesis. Initial packed cell volume 

(PCV) was 32%, serum total solids (TS) were 4.2 g/dl, and 

initial COP was 16.4 mm Hg (reference range, 17 to 23 mm 

Hg). The dog was tachycardic and weak and had pale mucous 

membranes and poor pulse quality. Hypovolemic shock was 

aggressively treated over 3 hours with 5 L (200 ml/kg) of lactated 

Ringer’s solution, but severe hematemesis continued and PCV, 

TS, and COP continued to drop precipitously (PCV, 13%; TS, 

2.1 g/dl; COP, 10.3 mm Hg) with no improvement in 

hemodynamic signs. During resuscitation, multiple blood 

transfusions (7 units of packed erythrocytes) were administered. 

The dog became extremely edematous, especially on its limbs 

and face. At surgery, a large gastric ulcer was identified and 

attributed to NSAID therapy for arthritis. The peripheral edema 

began to resolve only after several days of supportive care, 

including colloid therapy with hetastarch and fresh-frozen 

plasma. Following colloid therapy, COP had increased to 14.6 

mm Hg, while TS were 4.3 g/dl. 

could potentially be used as a prognostic indicator. Although 

some studies have related low COP to an increased 

risk of developing pulmonary edema in humans, 

no such studies have been conducted in veterinary medicine. 

6 Measurement of COP can also be used as a guide 

for colloid therapy. However, an optimal level of COP 

achieved with colloid therapy in various clinical settings 

has yet to be determined. Because COP is so dependent 

on plasma albumin concentrations, the impact of nutri- 

Peripheral edema due to low COP. 

Case 2 

A 5-year-old, neutered, 24-kg Labrador retriever was presented for an 8-week history of small-bowel diarrhea and 

weight loss. The standard gastrointestinal workup included a complete blood cell count (CBC), biochemical profile, 

multiple fecal examinations, abdominal imaging studies, and endoscopy with biopsies. Based on clinical findings and 

histologic characteristics, the dog was diagnosed with severe lymphocytic-plasmacytic inflammatory bowel disease. 

Despite a low serum albumin of 1.4 g/dl (reference range, 3.0 to 4.2 g/dl) and a low COP of 10.6 mm Hg, no edema 

was detected. 

Case 3 

A 7-year-old, spayed, 31-kg Doberman pincher was presented for lethargy, inappetence, and edema extending 

from the face to all four limbs. A diagnostic workup was performed, and no abnormalities were noted on the CBC, 

urinalysis, thoracic radiography, or abdominal ultrasound. On a biochemical profile, the albumin concentration was 3.0 

g/dl (reference range, 3.0 to 4.2 g/dl) but was otherwise unremarkable. Systolic blood pressure (130 mm Hg), CVP (3 

cm H 2O), and COP (21.8 mm Hg) were within normal limits. Given the normal COP, the edema could not be 

explained by low oncotic pressure. Titers for ehrlichiosis, leptospirosis, and antinuclear antigen were negative. Skin 

biopsies demonstrated neutrophilic infiltration of vascular walls, consistent with vasculitis. Since no inciting cause was 

identified, prednisone (20 mg q12h PO) was initiated. After 2 weeks of therapy, the edema completely resolved and the 

dog showed no other signs of illness. Prednisone was gradually discontinued. 

tional support, either parenteral or enteral, on overall albumin 

synthesis needs to be evaluated. Development of 

newer synthetic colloids with decreased side effects and 

increased intravascular persistence holds much promise 

for the treatment of critically ill patients. As our understanding 

of COP in health and disease continues to develop, 

direct measurements of COP in clinical patients 

could become an indispensable tool in the monitoring 

and treatment of critically ill animals.


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ARTICLE 

CE 

#4 CE TEST 

The article you have read qualifies for 1.5 contact 

hours of Continuing Education Credit from 

the Auburn University College of Veterinary Med- 

icine. Choose the best answer to each of the follow- 

ing questions; then mark your answers on the 

postage-paid envelope inserted in Compendium. 

1. Intravascular COP 

a. is generated by interstitial albumin and other proteins. 

b. preserves fluid within the vasculature and opposes 

extravasation of fluid into the interstitium. 

c. is a negligible Starling force in biologic systems. 

d. is preserved despite losses of albumin encountered 

in many different diseases. 

2. Starling’s equation 

a. can be accurately calculated using CVP and plasma. 

b. relates fluid shifts in terms of reflection and filtration 

coefficients. 

c. relates fluid flux as a difference in hydrostatic and 

oncotic gradients found between the intravascular 

and interstitial compartments. 

d. is the relationship of forces regulating fluid homeostasis 

and is constant among all organ systems. 

3. Albumin 

a. is the main contributor to COP. 

b. synthesis is solely regulated by hepatic COP. 

c. is completely impermeable through capillary membranes. 

d. is an acute-phase protein, and its synthesis is increased 

in response to inflammation. 

4. One rationale for administering synthetic colloids is to 

increase 

a. endogenous albumin synthesis. 

b. lymphatic drainage. 

c. plasma COP. 

d. total protein. 

5. The Gibbs-Donnan effect 

a. refers to increased membrane permeability due to 

inflammation. 

b. contributes to COP by attracting immunoglobulins 

and other osmotically active proteins to albumin. 

c. increases COP by attracting sodium ions to albumin 

against their concentration gradient. 

d. is the difference between the oncotic and hydrostatic 

gradients. 

6. Increased vascular permeability 

a. is counteracted by increased protein synthesis. 

b. can be easily reduced by administering synthetic 

colloids. 

c. is usually transient and not significant in clinical 

cases. 

d. has been associated with conditions such as sepsis, 

SIRS, ARDS, vasculitis, and burns. 

7. Measurement of COP 

a. is inaccurate in acidemic patients; therefore, predictive 

formulas of COP based on total solids should 

be used. 

b. can be used to guide colloid therapy and help evaluate 

causes of edema. 

c. can be falsely reduced in hemolyzed samples. 

d. is useful in calculating the exact dose of colloid 

therapy. 

8. Plasma COP values above the reference range 

a. have significant implications for colloid therapy. 

b. can be seen with severe hypergammaglobulinemia 

associated with feline infectious peritonitis or multiple 

myeloma. 

c. can be used as a therapeutic endpoint of colloid 

therapy. 

d. predispose patients to pulmonary edema. 

9. Animals with chronic hypoproteinemia 

a. are best treated with natural rather than with synthetic 

colloids. 

b. should be treated with synthetic colloids until COP 

is restored to normal. 

c. do not require treatment because COP is maintained 

at normal levels by other molecules. 

d. may not require treatment if clinical signs (e.g., 

edema) are absent. 

10. Desirable characteristics of newly developed synthetic 

colloids include 

a. increased antigenic stimulation and uniform particle 

size. 

b. a shorter half-life than current synthetic colloids. 

c. decreased side effects and increased intravascular 

persistence. 

d. decreased intravascular persistence and the ability 

to increase vascular permeability.

Colloid Osmotic Pressure in Health and Disease* - VetLearn.com

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