Fluid Therapy in Hospital Patients (Trauma Model)
World Small Animal Veterinary Association World Congress Proceedings, 2006
Luis H. Tello, DVM, MS
Clinica Veterinaria Las Condes, Santiago, De Chile

Fluid therapy is one of the cornerstones in the trauma patients. Shock and hemorrhage, fluid shift from the vascular to the interstitial space, decreased blood pressure and the organic peripheral vasoconstriction are the main targets in the fluid therapy, because all of them are primarily cause of death in that patients.

Body Fluid Distribution

The total body water ranges from 55-70% of the lean body weight. In the average adult dog the total body water is about 60%. Thus in a 15 Kg dog the total body water will equal about 9 liters.

Total body water is distributed into 2 main compartments:

1.  The intracellular fluid space, and

2.  The extracellular fluid space.

About 66% of the total body water reside in the intracellular fluid space and 33% in the extracellular fluid space.

The extracellular fluid space is further subdivided into two fluid containing compartments:

1.  The interstitial space (containing 75% of the extracellular fluid space water) and

2.  The intravascular space (containing 25% of the extracellular fluid space water).

When water is added to one compartment, it distributes evenly across the total body water and the amount of volume added to any given compartment, is proportional to its fractional representation of the total body water. Thus, if one liter of free water is placed in the intravascular space, there will be a minimal increase in the intravascular volume after equilibrium takes place. In fact, approximately 30 minutes after rapid volume infusion of free water, only 1/10th of the volume infused remains in the intravascular space.

Trauma and Blood Loss

Blood loss is one the most common consequences in a trauma patients, therefore it is not well tolerated in the animal. Although loss of 80% of the adrenals and liver, 75% of the kidneys an red cell mass, and loss of several lobes of lung do not result in the demise of an animal, loss of 35% of the blood volume can be fatal. The dangers of hemorrhage are related to a cardiovascular system that operated whit a small volume and steep Frank-Starling curve, (volume sensitive ventricle) for which the purpose may be to limit cardiac work and conserve energy.

In a healthy animal, a 15% loss of blood volume does not require intervention with intravenous fluids. With a loss of this volume, there is a three phase compensatory response to mild hemorrhage:

Phase I

Within one hour of mild hemorrhage, interstitial fluid begins to move into the capillaries. This fluid shift continues for 36-40 hours. The egress of fluid from the interstitial space leaves an interstitial fluid deficit.

Phase II

The loss of blood volume activates the renin/angiotensin/aldosterone system, which promotes sodium conservation by the kidneys. Because sodium distributes primarily in the interstitial space (80% of sodium is extravascular), the retained sodium replenishes the fluid deficit in the interstitial space. About the PVC, when any plasma expander, including crystalloids, is infused. An immediate fall in PVC can be expected. As the intravenous resuscitation fluids redistribute, the PVC again rises.

Total serum protein shows similar changes to PVC. Endogenous restoration of depleted intravascular volume occurs through the movement of interstitial fluids into the intravascular space. Catecholamines mediate arteriolar vasoconstriction which diminishes capillary bed hydrostatic pressure favoring influx of interstitial fluid into the vascular tree distal to the arteriolar constriction. Subsequently, the lymphatic flow pattern returns the plasma proteins to the intravascular space. Increases in interstitial pressures caused by crystalloid distribution into the interstitial space may augment lymphatic flow thus the "protein-refill" mechanism. This process combined with increased albumin synthesis and spontaneous diuresis secondary to volume repletion explains the return of serum protein levels after crystalloid resuscitation.

Phase III

Within a few hours after mild hemorrhage, the bone marrow begins to increase production of erythrocytes. Unfortunately, their replacement is slow with only 15-20 ml of cell volume being produced daily and complete replacement requiring a couple of months.

Crystalloid Fluids for Resuscitation

Crystalloid fluids are mixtures of sodium chloride and other physiologically active solutes. They are generally isotonic with plasma and have sodium as their major osmotically active particle. The distribution of sodium determines the distribution of infused crystalloid fluids. Sodium is the major solute in the extravascular space and 75% of the extracellular space is extravascular. Therefore, infused sodium will reside primarily outside the vascular compartment.

During phase I there is an interstitial fluid deficit which needs to be replaced during early fluid therapy. In fact, the goal of fluid therapy for mild hemorrhage is to fill the interstitial space, not the vascular space. This is the rationale for using crystalloid (sodium-containing) fluids for the resuscitation of mild hemorrhage.

Sodium-containing fluids are well suited for the replacement of extracellular fluid losses (dehydration) and for replacement of blood volume. Their use is directed to replacement of the interstitial fluid deficits seen in hemorrhage. The significance of the deficit has been questioned. Nevertheless, crystalloid solutions have proven to be effective in the resuscitation of animals with acute hemorrhage and they continue to be popular resuscitation fluids for trauma victims.

Table I. Electrolyte concentrations of crystalloid solutions.



0.9% Saline

Ringer's Lactate

Normasol - R





















Buffer HCO3



Lactate (28)

Acetate (27)
Gluconate (23)











Hypertonic Crystalloids

The use of concentrate crystalloid solutions is appealing because of the reduced volumes of fluid required, decreasing the risks of pulmonary edema and the need for specialized equipment for delivery of very large volumes of fluids.

Hypertonic saline (1.7%, 3%, 5%, 7.5%) is used in hypovolemic and traumatic shock with or without hyperoncotic substances. Adding the hyperoncotic solutions, the duration of effect is prolonged over their very short action. These solutions are effective and provide prompt volume expansion with significantly less volume than necessary with conventional crystalloids. Additionally, a decrease in the intracranial pressure has been observed in trauma patients.

Experimental studies show hypertonic saline solutions will improve microcirculatory flow, possibly by reducing shock-induced endothelial swelling. With endotoxic shock models, hypertonic saline is more effective than isotonic crystalloids in proving cardiac output and oxygen transport but only very transiently. In another study no benefit was seen. Controlled trials in human beings nor veterinary medicine are not available.

The major drawback of hypertonic saline resuscitation is the very short duration of response. Combining hypertonic saline with something like 6% dexytran-70 will prolong the response. Other concerns regarding the use of hypertonic saline include producing a hypertonic state, the prompt movement of sodium to the interstitial space, the water shifts from the interstitium and intracellular space, and the potential for a rebound interstitial edema.

Colloid Fluids

Colloids are large molecular weight substances that do not readily pass across capillary walls. The particles retained in the vascular space will exert an osmotic force that keeps fluid in the blood vessels.

Hypovolemia represents the most life-threatening aspect of acute hemorrhage. Because colloids are more effective than crystalloids for increasing vascular volume, colloid resuscitation should be more useful with severe bleeding.

Colloid or Crystalloid

A recent review of 8 randomized (human) clinical trials comparing the effects of colloid versus crystalloid solutions on survival showed a 5.7% relative difference in mortality in favor of crystalloid therapy. However, a 12.3% difference in mortality rate was found in trauma patients in favor of colloids. The confidence intervals for these studies were large and one must question whether the studies were appropriately assigned to trauma or no trauma groups.

Head trauma with hemorrhage is one of the severe restrictions in the use of colloids by the risk to colloids leaving the vascular can draw additional fluid to the area, worsening the cerebral edema and total cerebral contain of water.

In a more recent analysis of these trials the pooled date demonstrated a 13.4% mortality rate for crystalloid-treated human patients and a 21-25% mortality rate for colloid-treated patients (not statistically significant at a p= 0.01 level). In this same study, when the trials were subdivided into the apparent severity of the underlying processes, again no statistically significant difference was noted between the two treatment groups, although there was a tendency to a higher mortality in colloid-treated patients with more severe illness.

Although mortality is but one factor in assessing colloids versus crystalloids, the following recommendations have been made:

 Prompt and adequate fluid therapy is the mainstay of treatment of septic shock.

 Colloid and crystalloid fluids lower hemoglobin concentration, oxygen carrying capacity and whole blood viscosity. The optimum hematocrit in septic shock has not been defined but a value of 30-35% seems acceptable.

 The choice of fluid should take into account its effect on plasma oncotic pressure (COP). Severe decreases in COP should be avoided.

 Volume treatment should be individualized and titrated to individual needs.

Hemodynamic Efficacy in Trauma Patients

There is no doubt that both, crystalloids and colloids will adequately resuscitate shock patients. With crystalloids the amount of fluid necessary to reach the same hemodynamic endpoint is usually 2-4 times higher with crystalloids than with colloids. This results in significant changes in body weight and induces the risk of systemic edema.

There is convincing evidence that colloid-containing fluids act more promptly than crystalloid solutions in restoring hemodynamic stability. In a study of 600 hypotensive human patients, the mean resuscitation time was shorter with colloids. A similar finding in traumatized humans showed for a given volume of fluids infused, colloid solutions expand the plasma volume to a greater extent than crystalloid solutions.

Hemodynamic and oxygen transport variables with colloids are more pronounced than with crystalloids. In a study of postoperative patients, plasma volumes before and after infusion of 1L of colloid, shows the advantage clearly to the colloids.

Pulmonary Function

One of the core issues in the colloid-crystalloid controversy is the potential difference of inducing pulmonary edema with these fluids. Infusion of crystalloids does result in a significant and prolonged decline in serum albumin concentration and colloid oncotic pressure (COP). Colloids maintain or even increase COP. A low COP can promote the development of pulmonary edema microvascular hydrostatic pressure increases above normal. However, increases in hydrostatic pressure are more likely to result in pulmonary edema than comparable decreases in COP. Therefore, hydrostatic pressure is more important in fluid exchange in the lung than COP.

Colloid advocates have long argued that crystalloids alone, dilute the plasma proteins, thereby reducing plasma COP, and thus sets the stage for development of pulmonary edema. On the other hand, colloids by maintaining plasma oncotic pressure, could aid in the retention of fluid in the intravascular compartment and limit the magnitude of edema formation, even in presence of permeability defect. Colloid infusion then could promote a transmicrovascular fluid composed of colloid resulting in an almost parallel increase in intra- and extravascular COP, thereby worsening the severity of edema. Experimental studies in models with increased pulmonary have yielded conflicting results.

The IV is the preferred way to deliver fluid in trauma patients. Short large catheter, 18-20 gauge for small dogs and cats and 14-16 g for dogs with 10 Kg or more.

The classic rate of 90 ml/Kg/hour, could be no good for many trauma patients due to the fact of endothelial damage, cardiovascular compromise and hemorrhage, so frequent small volumes looks work better in that patients.

Blood substitute call Oxyglobin® should provide advantages to animals with reduced oxygen carrying capacity, but not many trials has been evaluated.

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Luis H. Tello, DVM, MS
Clinica Veterinaria Las Condes
Santiago, Región Metropolitana, Chile

MAIN : Nursing : Fluid Therapy in Hospital Patients
Powered By VIN