1. fluid volume to be administered.

2. type of fluids to be administered.

3. route of fluid administration.

4. rate of fluid administration.

• Fluids with a similar electrolyte composition to plasma are described as ‘balanced’.

• Crystalloids are solutions that contain both electrolyte and non-electrolyte solutes that can move freely between the extracellular and intracellular fluid compartments. Crystalloids may be isotonic, hypertonic, or hypotonic relative to plasma, and may be balanced or unbalanced. Examples of crystalloid fluids used commonly in equine medicine are shown in Table 26.2. Isotonic crystalloid fluids are administered primarily to restore and maintain hydration and correct electrolyte derangements. Hypertonic crystalloids are used to rapidly increase intravascular volume in patients with shock, but must be followed by an appropriate volume of isotonic fluids (see section on ‘Pathophysiology and management of shock’). Hypotonic fluids are used infrequently; they are used in patients with increased plasma osmolality (e.g. hypernatraemia).

• Colloids are solutions that contain high-molecular-weight solutes that cannot leave the vascular space, and thus serve to increase colloidal oncotic pressure. The most common colloids used in equine medicine are equine plasma or synthetic colloids such as dextrans and hydroxyethyl starch (hetastarch). Colloids are most often used in patients with shock or severe hypoproteinaemia (see section on ‘Pathophysiology and management of shock’).

• Oxygen-carrying fluids include whole blood, packed red blood cells, and purified bovine haemoglobin products (e.g. Oxyglobin®). Oxygen-carrying fluids are administered to patients with decreased oxygen-carrying capacity secondary to severe acute haemorrhage or anaemia. These products contain large macromolecules and are thus colloids, but as they do less to increase colloidal oncotic pressure, compared to plasma and synthetic colloids, they are not typically used in this manner. Administration of these products is covered in more detail below in the section on ‘Administration of blood products in equine critical care’.

 This route is used most often in equine critical care, as it permits rapid administration of large volumes of fluids.

 In horses and foals, intravenous access is most often achieved through catheterization of one or both jugular veins. In adult horses, the lateral thoracic veins may also be used, though fluids cannot be administered quite as rapidly (Figure 26.1).

 The cephalic veins are occasionally used if jugular or lateral thoracic vein access is limited, but cephalic catheters can be dangerous to place in some fractious horses and are typically difficult to maintain for long periods.

 This method is typically inexpensive and is appropriate for patients that can tolerate oral fluids (e.g. patients that are not refluxing and that do not have intestinal disease that would impair absorption of oral fluids) and for those that do not require rapid administration of large volumes of fluid (e.g. severely dehydrated patients or patients in shock).

 Enteral fluid therapy is typically administered to horses via a nasogastric tube; an indwelling nasogastric tube may be maintained for repeat administration or continuous infusions.

 Small amounts of pure water may be administered enterally, but if large volumes or prolonged enteral fluid therapy is required then an isotonic electrolyte solution should be used to prevent the development of hyponatraemia.

 Large volume enteral fluid therapy is rarely used in neonatal foals.

 In foals requiring fluid therapy in which the above routes are not usable, intraosseus fluids may be administered. However, it is difficult to maintain intraosseus catheters for long periods of time, and rapid or large volume fluid administration through this route can be challenging.

 Subcutaneous fluids are not well tolerated in horses and foals and should be avoided. Similarly, the risks associated with intraperitoneal fluid administration in horses (e.g. gastrointestinal puncture, peritonitis) almost always preclude the use of this method in horses or foals.

 Severely dehydrated patients showing signs of shock require rapid intravenous fluid administration, at 40–90 mL/kg/hour, to quickly restore intravascular volume.

 The patient should be closely monitored and the fluid rate modified accordingly as the hydration status improves.

 In adult horses, multiple large bore catheters and fluid pumps may be required to achieve such rapid rates (e.g. ~40 L/hour for a 450 kg horse).

 Therefore, hypertonic crystalloids and/or colloids followed by isotonic crystalloids may be alternatively or additionally used in these cases to more rapidly increase intravascular volume.

 In patients with less severe dehydration or in those receiving maintenance fluids only, the administration rate is determined by dividing the total volume of fluid required in 24 hours into intermittent boluses or a constant rate infusion (CRI). For instance, if the total 24-hour fluid volume required by a 40 kg foal with estimated 5% dehydration is 6 L (2 L hydration deficit and 4 L maintenance needs at 100 mL/kg/day), then the foal could receive a 1L bolus every 4 hours or a CRI of 250 mL/hour. Specialized IV sets that permit calculation of volume per hour based on drip rate or an electronic fluid pump are required for accurate administration of a CRI.

 No more than 6–8 L at one time or 2–4 L/hour of enteral fluids should be administered to an adult horse to avoid gastric distension and associated discomfort.

 Enteral fluid therapy rates should be slowed or discontinued if signs of colic or abdominal distension are observed during or after enteral fluid administration.

• Mildly to moderately dehydrated horses often exhibit a mild metabolic acidosis and hyperlactataemia associated with poor tissue perfusion that resolves without specific treatment when dehydration is corrected.

• However, in severely acidotic horses or foals, such as those with a blood pH < 7.1, serum bicarbonate concentration <15 mmol/L, or a base deficit >10–15 mEq/L, alkalinizing therapy with sodium bicarbonate is indicated.

• The bicarbonate deficit in adult horses is calculated as follows:

• Metabolic alkalosis is much less common in horses than metabolic acidosis, but may be seen in horses with excessive sweating or gastric outflow obstructions due to concurrent hypochloraemia.

• The alkalosis typically resolves without specific therapy when the hypochloraemia is corrected with administration of isotonic balanced crystalloids, though administration of acidifying fluids such as 0.9% NaCl can be helpful in severe cases.

 Q is the product of stroke volume (SV) and heart rate (HR). SV is affected by the preload and afterload to the heart as well as the heart’s contractility:

 C_aO₂ is the product of oxygen carried by haemoglobin and dissolved in the blood (P_aO₂). The amount of oxygen carried by haemoglobin is the product of the amount of haemoglobin in the blood ([Hb]) and the saturation of that haemoglobin with oxygen (S_aO₂). It is very important to recognize that most of the oxygen in the blood is carried by haemoglobin

• Blood volume can be lost as whole blood (haemorrhage) or free water (with or without electrolytes and/or proteins).

• The fluid can be lost outside of the body or sequestered within the body, but outside of the circulation (third space).

• Prolonged lack of fluid intake can also result in hypovolaemia.

• Examples of conditions that can be associated with hypovolaemic shock include:

• Cardiomyopathy – monensin toxicity, viral cardiomyopathy.

• Arrhythmias – third-degree AV block, ventricular tachycardia.

• Valvular dysfunction – cordae tendinae rupture.

• Circulating endotoxin interacts with a circulating host protein called LPS-binding protein (LBP) and a circulating or cell membrane receptor called CD14. This LPS–LBP-CD14 complex then binds and activates a cell surface receptor on leukocytes and endothelial cells called toll-like receptor 4 (TLR-4).

• Activated TLR4 initiates an intracellular signalling cascade that activates the transcription factor NFκB. NFκB enters the nucleus and stimulates the transcription of many proinflammatory mediators such as TNF-α, IL-1 and IL-6. These inflammatory mediators stimulate leukocyte adhesion and activation and endothelial cell activation, cause increased production of PGE2, ACTH, acute phase proteins, eicosanoids, and NO, and induce the release and activation of arachidonic acid metabolites, platelet-activating factor, reactive oxygen species, histamine, kinins and complement. Many of these substances have effects on vasomotor tone and vascular permeability, which can result in altered blood flow and distributive shock.

• Endotoxaemia can occur secondary to a variety of diseases in horses, including colitis, pleuropneumonia, and retained foetal membranes.

Sepsis: Sepsis is a condition that occurs in bacteraemic patients (those with bacteria in the bloodstream) when the body’s inflammatory response to the infection becomes systemic (resulting in the systemic inflammatory response syndrome – SIRS).

Anaphylaxis: This is a systemic hypersensitivity reaction that results in mast cell degranulation, and thus, the release of large amounts of histamine, prostaglandins, and leukotrienes. Severe vasodilation can occur as a result. Anaphylaxis is uncommon in horses but can occur with drug or blood product administration.

• Diseases that restrict the heart’s ability to expand such as pericardial effusion and restrictive pericarditis.

• Diseases that compress large vessels such as tension pneumothorax or large colon volvulus.

• Decreased oxygen carrying capacity or hypoxemia – anaemia, respiratory diseases resulting in poor oxygen exchange.

• Impaired tissue uptake of oxygen/blood release of oxygen – carbon monoxide toxicity.

• Impaired cell utilization of oxygen – cyanide toxicity.

• Increased cell demand for oxygen – sepsis.

 Fluid moves from the interstitial space into the vascular space causing an increase in blood volume.

 Decreased mean arterial pressure is sensed by baroreceptors (aorta and carotid), triggering catecholamine release, which leads to arterial and venous constriction, increased myocardial contractility, and increased heart rate. It also results in increased antidiuretic hormone (vasopressin) secretion, which stimulates an increase in water resorption in the kidney to increase blood volume.

 Decreased arterial pressure in the kidney results in activation of the renin-angiotensin-aldosterone pathway, which results in systemic vasoconstriction to increase blood pressure and increased sodium and thus water resorption to increase blood volume.

 Catecholamine and ACTH release leads to increased circulating cortisol, which stimulates gluconeogenesis and protein catabolism to meet increased cellular energy demands.

• Isotonic crystalloids, which are widely available and easy to use, can be administered at a shock dose of 90 mL/kg.

• Hypertonic saline solution (2–4 mL/kg IV bolus) can also be used to rapidly increase intravascular volume (2–4 L for every 1 L of hypertonic saline solution administered).

• Colloids (10–20 mL/kg) can also be used for fluid resuscitation for rapid volume expansion.

• Leakage of fluid into the interstitial space can occur with administration of crystalloids in diseases associated with hypoproteinaemia (colitis) or impaired vascular function (endotoxaemia, lung contusions, SIRS).

• In cases of uncontrolled haemorrhagic shock, rapid volume expansion can disrupt tenuous blood clots. In these cases, low-volume fluid resuscitation coupled with the administration of blood/plasma products to support coagulation is preferable to rapid, high-volume fluid resuscitation.

• In equine critical care, pressors and inotropes are most often used in neonatal foals at referral institutions, and are very rarely used in standing adult horses.

• However, as many of the disease conditions associated with shock in horses are associated with decreased vasomotor tone and may have effects on the myocardium, it is possible that some cases could benefit from such pharmacological support.

• Treatment with pressors and inotropes requires intensive monitoring and care, and detailed discussion of their use is beyond the scope of this text.

 In properly functioning kidneys, urine production is a crude estimate of blood flow to the kidney.

 Urine specific gravity can also be measured to provide information regarding hydration status and renal function.

 Tissues that are not receiving adequate oxygen turn to anaerobic metabolism to meet energy demands, resulting in hyperlactataemia and acidosis.

 Tissues that are not receiving adequate oxygen extract more of the oxygen carried in the blood as it passes through, resulting in a decrease in venous oxygen saturation.

 The primary determinants of CVP are venous return and cardiac function – volume depletion causes a low CVP, and poor cardiac function results in a high CVP. In standing horses CVP should be between 4 and 12 cm H₂O.

 CVP can be helpful in assessing whether adequate volume resuscitation has been performed and in preventing excessive volume expansion, especially in patients with heart disease.

• Provision of colloidal oncotic support to patients with hypoproteinaemia or shock.

• Provision of coagulation factors in coagulopathic patients.

• Provision of endogenous ‘anti-endotoxic’ factors such as anti-LPS antibodies and provision of immune support to patients at risk for, or with signs of, endotoxaemia or sepsis.

• Provision of immunoglobulins to neonatal foals at risk for, or with evidence of, failure of passive transfer or immunity.

• Fresh plasma, rather than frozen plasma or whole blood, is indicated when active functional platelets but not erythrocytes are required, such as in horses that are thrombocytopenic but not anaemic.

• Concentrated platelet preparations (platelet-rich-plasma) are often used in humans and small animals, and can be prepared with equine plasma, but are rarely used in horses due to the associated expense.

• Washed erythrocytes are most often administered to neonatal foals with neonatal isoerythrolysis (NI) (see Chapter 20). In these cases the dam’s blood is most often used. The dam’s plasma contains antibodies against the foal’s erythrocytes, so it must be removed by washing the cells prior to the transfusion.

• Purified bovine haemoglobin preparations (such as Oxyglobin®) can be used in horses requiring oxygen-carrying capacity for which a compatible blood donor is not available.

• Hyperimmune plasma or serum products consist of the plasma or pooled serum from horses that have been hyperimmunized against a particular substance to provide disease-specific antibodies in high concentrations.