Read the German translation: Lebensrettender Einsatz von Kristalloiden und Kolloiden Infusionen

Introduction

Normal perfusion and water balance is required for normal cell metabolism and life. Animals with acute or chronic diseases may present with various forms of fluid deficits. According to the history and clinical signs, the water deficit can be determined and fluid therapy with appropriate fluids can be instituted.

Physiology

The body consists of three fluid compartments. The intracellular compartment contains 2/3 or 66% of whole body water. The extracellular compartment (34%) is divided into the interstitial (25%) and intravascular (9%) compartment. Water can freely diffuse between all compartments, while electrolytes can only diffuse through the vessel membrane and macromolecules will not pass through membranes. The water is distributed over all compartments according to osmotic, oncotic and hydrostatic pressures within each compartment.

Clinically, fluid deficits can be divided into perfusion deficits (intravascular space) and dehydration (interstitium). Depending on the fluid loss, an animal may be over- or underperfused (shock), dehydrated or overhydrated (seen as edema), or combinations of these. Perfusion deficits are associated with decreased oxygen delivery and are therefore live-threatening. Based on the cause and physiologic processes that lead to hypoperfusion, shock can be classified into four forms: hypovolemic, distributive, obstructive and cardiogenic shock. All causes of shock--with exemption of cardiogenic shock--are treated with fluid therapy.

Shock

Clinical Signs

The clinical signs of shock depend on the state of shock / level of sympathetic stimulation as well as the cause of shock (Table 1). Compensated shock reflects the compensatory mechanisms associated with sympathetic stimulation without excessive arterial vasoconstriction. Compensatory mechanisms lead to tachycardia, pink or red MM and a short CRT. Blood pressure is normal or increased and pulse quality is strong or bounding. This compensatory stage may be missed in dogs and cats don't commonly show a compensated stage. As soon as peripheral arterial vasoconstriction occurs, this "centralization" of blood volume leads to underperfusion of other important organs of the body, and the shock state becomes "decompensated". Clinical signs of early-decompensated shock are tachycardia, pale MM with a prolonged CRT and eventually weak pulses and hypothermia. With late decompensated shock, MM may become white, CRT is not measurable, and patients show hypothermia and hypotension. Patients in terminal shock show grey-purple mucous membranes, bradycardia or arrhythmias followed immediately by cardiac arrest.

Patients with distributive shock do not show the same clear signs of vasoconstriction, making identification of the severity of shock difficult. Sepsis almost always presents with injected mucous membranes, rapid CRT, and fever.

Table 1. Clinical signs seen with different shock stages.

Shock Treatment

Establishment of a normal intravascular volume with fluid therapy (exception: cardiogenic shock), control of hemorrhage, oxygen supplementation and analgesia are the main objectives of shock treatment.

Fluid Therapy

Intravascular fluid deficits (hypovolemic, obstructive and distributive shock) can be replaced with isotonic crystalloid solutions, colloids, hypertonic saline or combinations of these. Isotonic crystalloid solutions such as lactated ringer's solution (LRS) or 0.9% NaCl will be distributed over the complete extracellular space and only ¼ of the administered fluid will remain intravascular. This may lead to edema formation, especially in patients susceptible for vasculitis (systemic inflammation, sepsis, toxic changes). Isotonic crystalloid solutions are the fluids of choice in patients with dehydration and shock (for example acute gastroenteritis or polyuric renal failure). In most other patients, use of colloid solutions in combination with a crystalloid are preferred, as colloids contain large molecules that will stay intravascular and will additionally exert an oncotic effect that keeps the crystalloid solution in the intravascular compartment.

Patients with late decompensated shock, terminal shock or concurrent head trauma may benefit from treatment with hypertonic saline (7-8% NaCl, 4 ml/kg slowly IV). The massive increase in intravascular osmolarity will lead to a substantial water shift from the interstitial space into the intravascular space. Unfortunately, the effect is only short-term (15-30 minutes). The effect may be prolonged with the addition of a colloid. Hypertonic saline is contraindicated in patients with dehydration.

Unfortunately, the amount of fluid lost in patients with signs of shock cannot be exactly determined. Historically, shock was treated with isotonic crystalloids at a dose of 90 ml/kg/h (50-60 ml/kg/h in cats). This dose would replace a 30% blood loss. Since volume loss may be more or less than 30% and because colloids are commonly used for treatment of shock, this dose should no longer be used. Since decreased perfusion leads to hypoxia and cell death, fluids administered in shock patients are given as a bolus over 5-15 minutes. Depending on the severity of shock (shock stage), a first bolus may be 10-30 ml/kg of an isotonic crystalloid combined with 5-10 ml/kg of a colloid. In cats, the lower dosages should be used. These boluses may be repeated as often as required, until perfusion parameters are normal (HR, MM color, CRT, blood pressure). It is important that these fluid boluses are given over a short period of time and not over several hours!

Exceptions of aggressive fluid therapy are patients with internal bleeding (hemoabdomen or lung contusions). The boli used are smaller (10 ml/kg of an isotonic crystalloid +/- 3-5 ml/kg of a colloid) and monitoring of mean arterial blood pressure (MAP) is essential. The goal of fluid therapy is a MAP of 60-70 mmHg in order to ensure perfusion of all organs without disruption of thrombus formation at the site of hemorrhage. This type of fluid therapy in shock patients with internal bleeding is called "limited fluid volume resuscitation". Another exception for aggressive fluid therapy are hypothermic cats. Hypothermia may lead to severe vasoconstriction so the clinical signs of hypothermia and decompensated shock may be similar and the risk of overinfusion is high. Cats should therefore be warmed and reassessed when the temperature has reached at least 36°C before large fluid boluses are administered.

Anemia may aggravate oxygen deficiency in shock states. Oxygen carried with hemoglobin is responsible for most of the oxygen delivered to tissues. If the PCV drops below 20%, the patient should be transfused with packed red blood cells, fresh whole blood or Oxyglobin®. 2 ml/kg of whole blood or 1-1.5 ml/kg of pRBC are needed to increase the hematocrit by 1%. Blood typing or a cross-match prior to transfusion are recommended in dog and requested in cats. Plasma (8-15 ml/kg IV as fast as required) may be indicated with coagulation abnormalities caused by severe bleeding, DIC, or dilution by excessive fluid therapy.

Dehydration

Clinical Signs

The degree of dehydration is estimated based on history of fluid loss, MM moisture and skin turgor (Table 2).

Table 2. Evaluation of dehydration.

Fluid Therapy

Based on the estimated dehydration, the fluid deficit can be calculated using the following formula: % dehydration x kg body weight x 10 = fluid deficit in ml. The fluid can be substituted IV or SC. Using the IV route, the calculated fluid deficit is given over 6-12 hours. Additionally, the maintenance rate (2-3 ml/kg/h) and estimated further fluid losses are administered. The fluid of choice for the interstitial fluid deficit is an isotonic crystalloid solution (lactated ringers).

Further Fluid Therapy

Further fluid therapy after normalization of perfusion and rehydration depends on ongoing losses through vomiting or diarrhea, polyuria or third-spacing. PCV, TS/Albumin and electrolytes should be monitored. Most animals will require at least maintenance fluid therapy with a low sodium crystalloid solution. Colloids should be continued as a CRI (1-2 ml/kg/h depending on the colloid used) in patients with an albumin < 20 g/l (2 g/dl) or total solids < 45 g/l (4.5 g/dl).

References

References are available upon request.