Intensive care medicine

Chapter 23

Intensive care medicine

Chapter contents




Body water balance

Assessment of hydration status and effective circulating volume

Monitoring circulatory status and fluid therapy

Electrolyte balance

Assessment of electrolyte disorders

Acid–base balance

Principles of fluid therapy

Replacement therapy

Metabolic acidosis

Metabolic alkalosis

Maintenance fluid therapy


Technical considerations in fluid therapy

Inotropes and vasopressors






Critical care is an exciting area of equine practice that has undergone rapid advancement and increased specialization in recent years. The increasing pursuit of advanced critical care training and board certification has redefined equine critical care, providing a new focus in the understanding and management of horses requiring intensive care.

The provision of state-of-the-art emergency and critical care is facilitated through the use of an intensive care unit, or ICU, with provision of high level monitoring and nursing care, as well as advanced support. Such facilities should have fully trained nursing staff present at all times, with veterinary specialists available 24 h a day.

Critical care medicine is devoted to the comprehensive care of seriously ill horses, which are often suffering from multiorgan system failure. A successful outcome requires an interdisciplinary approach to the diagnosis, treatment and management of such cases. For example, the horse recovering from colic surgery that develops peritonitis, salmonellosis and renal compromise requires collaborative input from the surgeon, medical internist and critical care specialist. Selection of appropriate antibiotic therapy must address the cause of peritonitis and organisms involved, while balancing the effects of the chosen antimicrobial agents on the Salmonella strain, existing gut flora and patient’s renal function.

Principles of infectious disease control (q.v.) must be observed without disrupting primary patient care. The patient must be isolated from other susceptible horses, yet maintained in an environment suited to continuous IV fluid administration and frequent monitoring. Additional patient problems to anticipate include electrolyte disturbances associated with secretory diarrhea; catheter-related sepsis and venous thrombosis associated with systemic infection, endotoxemia, prolonged catheterization and rapid fluid administration; laminitis due to perfusion deficits and endotoxemia; and negative energy balance resulting from increased energy requirements due to fever, infection, wound healing and decreased feed intake. All aspects of such a case must be addressed concurrently and attention focused on monitoring patient trends. Potential complications that could arise while treating existing medical and/or surgical problems must be anticipated.

Excellence of nursing care is the mainstay of any ICU. Critically ill horses are inherently unstable and subtle changes in condition must be detected early to allow appropriate changes in therapy. The higher morbidity and mortality rates among critical care patients can become a demoralizing reality. Treatment of seriously ill animals often involves chronic intensive care, which is frequently plagued by the development of secondary complications associated with the patient’s debilitated state and the need for aggressive and often invasive diagnostic and therapeutic procedures. Nurses working in the ICU must have an understanding of the patient’s illness and an appreciation of intensive care therapy to maximize their surveillance capabilities and foster the development of innovative nursing care protocols. Support among co-workers is also vital and helps maintain a positive attitude in the ICU.

Creation of a critical care area within an equine hospital allows trained personnel to monitor and care for a number of seriously ill horses most efficiently. The establishment of a nursing station allows for supplies, drugs, delicate instrumentation and monitoring equipment to be centralized. Recumbency complicates the care of many horses suffering from neurologic disorders such as rhinopneumonitis and botulism (q.v.), or musculoskeletal problems such as long bone fractures and laminitis (q.v.). Stall modifications that facilitate care of critically ill patients include wall-mounted medical gases and suction, padded floors and walls, and ceiling hooks for fluid administration.

Prolonged recumbency is complicated by a variety of secondary problems including decubital sores, self-trauma, gut dysmotility, urine retention and dependent lung atelectasis (q.v.). A padded stall equipped with a 2-ton hoist and sling is an invaluable asset when treating such cases.

Deciding which horses to admit to the ICU is termed triage, the art of giving priority to the most critical cases. Patients should be admitted to the critical care facility based on the intensity of their treatments, the frequency of monitoring required, and the need for special bedding or ICU stall features.

Examples of patient problems that benefit from a critical care setting include the following: hepatoencephalopathy (q.v.), requiring continuous glucose and fluid infusion, sedation, a padded environment and protective head helmet; sepsis (q.v.), causing hypotension and organ dysfunction; renal failure (q.v.), requiring continuous fluid therapy, careful monitoring of fluid administration and urine output, controlled dopamine infusion and diuretic administration; severe corneal ulcers (q.v.), requiring hourly eye medication via a nasolacrimal or subpalpebral lavage system; botulism (q.v.), requiring a padded environment to minimize self-trauma associated with recumbency, frequent patient repositioning to prevent dependent lung atelectasis, continuous fluids and enteral nutrition via nasogastric intubation; severe laminitis (q.v.), requiring padded floors, deep bedding, and supportive care if recumbent; postoperative colic (q.v.), requiring frequent observation for recurrent pain, gastric decompression via nasogastric intubation, and continuous fluid therapy; impaction colic (q.v.), requiring continuous IV fluids and frequent administration of oral fluids and laxatives. Monitoring of any critical patient focuses on frequent evaluation of standard parameters such as those presented in Table 23.1.

This chapter focuses on guidelines for fluid and electrolyte replacement therapy, critical care protocols with emphasis on monitoring techniques and therapy, pharmacotherapeutics for critically ill patients, management of endotoxemia, and design principles for an intensive care facility. Resuscitation guidelines and principles of ventilatory and nutritional support are reviewed elsewhere, as are specific neonatal disease conditions (q.v.).



Fluid therapy is an integral part of critical care, and is the foundation of hemodynamic support in the ICU. In the emergency setting, horses exhibit a var-iety of fluid, electrolyte and acid-base disorders. These arise due to a number of factors, including anorexia (inadequate intake), excessive losses (sequestration, third-space losses) and hypoperfusion associated with distributive or cardiogenic shock.

The primary goals of fluid therapy are to replace and correct these imbalances, to restore effective circulating volume and blood pressure, to provide the body’s maintenance requirements for water and electrolytes, and to account for ongoing losses. Rational fluid therapy requires an understanding of the normal homeostatic mechanisms governing body water, electrolyte and acid-base balance, and the pathophysiologic processes that disrupt their homeostasis.


Total body water represents approximately 60–70% of body weight in adult horses and is comprised of the extracellular and intracellular spaces ( Table 23.2). The extracellular compartment includes the intravascular (plasma), interstitial and transcellular fluid (gastrointestinal tract water and lymph). The distribution of water between plasma and interstitial fluid is maintained by differences in colloidal osmotic and hydrostatic pressure, and also depends on the integrity of the endothelium.

Water balance is the difference between input and output. This is determined by the intake of water and fluid contained in food, and by the generation of water due to protein, fat and carbohydrate metabolism, versus water loss through urine and feces, respiratory tract and skin. The normal water intake for a 450 kg adult horse is approximately 20–30 L/day, although this can vary depending on the water content of the diet, ambient temperature and activity level. The largest component of water loss is through the urine.

Dehydration is defined as a reduction in total body water. In the critical care setting, this usually refers to losses in the interstitial fluid compartment. Dehydration occurs with water deprivation, either through lack of access to water or through the inability to swallow. It also follows excessive fluid loss, most commonly from the gastrointestinal tract, but also sweating or urinary losses. As opposed to hydration status, circulating volume refers to the intravascular fluid compartment. In dehydration, circulating volume may be decreased, but if the onset of dehydration is insidious, it may be maintained despite a reduction in total body water. The effective circulating volume is also reduced when fluid is sequestered in abnormal quantities within one part of the body (third-space accumulation), in hemorrhage and in hypovolemic shock.


Clinical examination

Clinical examination is the first, and most important, means of assessment of fluid disorders. The parameters used to evaluate both total body water (hydration status) and effective circulating volume are listed in Box 23.1. Clinical evaluation can be used to provide a rough estimate of the fluid deficit ( Box 23.1). However, these are only guidelines and replacement fluid therapy is best evaluated by serial monitoring of the clinical response. Body weight can be used to determine ongoing fluid losses, however in many clinical situations the initial weight is unknown so it is of little value at the initial evaluation. Fluid deficits will lead to a decrease in urine production, and so measurement of urine production in relation to water intake is useful to monitor fluid therapy.

Clinical markers of hydration status (interstitial volume) include skin turgor, mucous membrane texture and corneal quality (tear film). Intravascular volume is reflected in capillary refill time, heart rate, pulse quality, mentation, mucous membrane color, extremity temperature, jugular fill and urine production.


Packed cell volume and total plasma protein

Packed cell volume (PCV) and total plasma protein (TP) are invaluable for assessing fluid deficits and monitoring the response to fluid therapy. They are quickly performed, using a microhematometer and refractometer, respectively. Guidelines for their interpretation are given in Table 23.3. PCV and TP should always be interpreted together. Both rise with simple dehydration.

In horses there is a wide reference range for PCV. Splenic contraction, which occurs under the influence of epinephrine/adrenaline, in association with pain, excitement or other stresses, can increase the PCV markedly but generally does not influence TP. An increased PCV with a normal TP, a relative hypoproteinemia, is also seen in animals that are both dehydrated and hypoproteinemic, a common finding in horses with acute enterocolitis (q.v.).

Despite their usefulness, PCV and TP also have limitations. Anemia (q.v.) may mask dehydration as a PCV within the normal range. Similarly, a normal total protein concentration suggestive of euhydration can be misleading in a hypoproteinemic animal. At the opposite end of the spectrum, hyperproteinemia due to hyperglobulinemia (q.v.), rather than dehydration, can be misleading in a normally hydrated horse.

Serum urea and creatinine

Serum urea and creatinine concentrations ( Table 23.4) are increased in pre-renal, renal and post-renal dysfunctions (q.v.). Urea is produced in the liver as a result of breakdown of ammonia. In horses and other large animals, urea concentrations may be influenced greatly by dietary factors, and as a result creatinine concentration is considered to be a better guide to renal function.

Creatinine is produced at a relatively constant rate as a by-product of muscle metabolism (creatine phosphate). It is excreted by glomerular filtration. Decreases in renal blood flow caused by reduction in effective circulating volume produce an increase in serum creatinine concentrations, yielding pre-renal azotemia (q.v.). Restoration of circulating volume should produce a rapid response in serum creatinine in these horses, and if serum creatinine concentrations remain persistently increased after rehydration, the presence of primary renal dysfunction or post-renal causes should be evaluated further.

Arterial blood pressure

In many clinical situations, the initial goal of fluid therapy is to increase perfusion pressure by restoration of the effective circulating volume. Measurement of arterial blood pressure provides one objective means of determining and monitoring the response to fluid therapy. It is mandatory in cases in which inotrope or pressor support, in the form of pharmacologic agents to increase cardiac output or alter vascular tone, is being considered.

Arterial pressure is measured either directly via a manometer attached to an intra-arterial catheter, or indirectly using Doppler or oscillation techniques. Direct methods are more accurate and have the advantage that the pulse contour can also be assessed, providing information on the inotropic state and the afterload. Indirect methods are non-invasive, and thus are more readily performed in conscious horses ( Table 23.5).

In standing horses, catheters are maintained most easily over prolonged periods in the transverse facial artery, to measure direct arterial blood pressure. For indirect arterial blood pressure, cuffs are generally applied to the tail to measure from the middle coccygeal artery. The cuff bladder width to tail circumference ratio should be approximately 25% to obtain most accurate results, and measurements should be taken with the horse in the same position for comparison purposes. When using extremities, a ratio of 40–50% should be used.

While most indirect means of blood pressure measurement provide only systolic pressures, oscillometric techniques, such as the Dinamap Blood Pressure Monitor (Critikon, Tampa, FL, USA), provide systolic, diastolic and mean blood pressures. Correlation of the displayed pulse rate to the actual heart rate is one means of checking the accuracy of the indirect technique, as is averaging repeated measurements.

Blood lactate concentration

Venous or arterial blood lactate concentration can be utilized as a marker of peripheral perfusion. Blood or plasma lactate concentrations represent the balance between production (primarily from glycolysis) and clearance (hepatic, renal). During reduced oxygen delivery states glycolysis predominates and results in hyperlactatemia. Other causes of high blood lactate include proinflammatory states, catecholamine surges, thiamine deficiency and alkalosis. Patients with liver failure and lymphosarcoma may have reduced clearance of lactate, and fluids devoid of lactate should be used in these groups (e.g. Normosol R, Plasma-Lyte 148). Lactate concentrations are <2 mmol/L in healthy adult horses, while they can be as high as 4 mmol/L 1–2 h post partum in neonatal foals. By 24 h of age lactate concentrations should be <2 mmol/L in healthy foals. Serial measurement of lactate concentrations is most useful in assessing perfusion responses to fluid volume replacement.

Central venous pressure

Central venous pressure (CVP; see Table 23.5) is dependent on cardiac output and the venous return. It is the pressure within the intrathoracic vena cava and approximates right atrial pressure. It is influenced by blood volume, vascular tone, heart rate and ventricular contractility. CVP falls in association with hypovolemia and rises if there is an increase in circulating volume. Measurement of CVP is used to assess cardiac function and to monitor fluid therapy and, in particular, to avoid overzealous fluid administration. As such, it can be used as one end point to fluid therapy.

Hypotension (q.v.) can be treated with volume support until CVP approaches maximum. Exceeding normal CVP values has the potential to cause pulmonary and tissue edema. CVP is easy to measure, requiring only a simple water manometer, IV catheter and extension tubing. A procedure for the measurement of CVP is described in Box 23.2. It should be noted that the monitoring of trends in CVP over time is crucial, rather than focusing on one value. Pleural and pericardial diseases will also cause increases in CVP (q.v.).

Colloid osmotic pressure

Colloid osmotic pressure (COP), or oncotic pressure, is the osmotic force within the intravascular compartment exerted by albumin and other macromolecules, which counteract capillary and venule hydrostatic forces in determining net fluid flux across the endothelium. Plasma COP is primarily determined by albumin (65–80%) and is required to maintain proper circulating volume. Patients with hypoalbuminemia are therefore at risk for edema formation and relative hypovolemia, both of which lead to reduced tissue oxygen delivery.

Although total protein and albumin concentrations provide indirect information about COP, and are crucial in monitoring albumin dynamics, they are not as well correlated with oncotic pressure in the critically ill animal as compared to healthy horses. In ill patients, direct measurement of COP using a colloid osmometer (Wescor 4420 colloid osmometer, Wescor, Logan, UT, USA) is important. Additionally, total protein concentrations do not measure the oncotic contribution of synthetic colloids such as hetastarch or Hextend. Direct measurement of COP in horses receiving synthetic colloids is the only means of monitoring the oncotic effects of these products. Normal oncotic pressure in adult horses is 20–30 mmHg, and in neonatal foals is 15–23 mmHg.



Sodium is the most abundant cation in the extracellular fluid (ECF; see Table 23.4). Sodium is ingested with feed and water intake, and is lost in urine, feces and sweat. It can be regarded as the “skeleton” of the ECF, as it is the principal determinant of the ECF osmolarity, and consequently its volume. Osmolarity can be measured directly with an osmometer, or alternatively calculated using the following formula:


where sodium is in mEq/L and glucose and BUN are in mg/dL.

The excretion of sodium via the kidney is controlled by the renin–angiotensin–aldosterone system (q.v.). Hyponatremia (q.v.) occurs if there is a reduced intake of sodium, however deficits due to excessive losses are more common. These arise if sodium loss from the gastrointestinal or urinary tract is in excess of water loss, and thus hyponatremia indicates a relative water excess. Box 23.3 lists clinical conditions associated with hyponatremia.

Hypernatremia (q.v.) arises when water is lost in excess of electrolytes (see Box 23.3). Both hyponatremia and hypernatremia should be treated with caution; rapid correction of hyponatremia can result in demyelination and central pontine myelinolysis, while cerebral edema can result from overzealous treatment of hypernatremia. Plasma sodium concentrations should be altered slowly, not exceeding 0.5 mEq/h. Hyponatremia can be corrected using sodium-containing fluids such as 0.9% sodium chloride, lactated Ringer’s solution, Plasma-Lyte 148, or Normosol R. Varying formulations of hypertonic saline can also be used depending on the rate of rise. Hypernatremia can be treated with the provision of free water, as with maintenance fluids. These include Plasma-Lyte 56 or Normosol-M, but 5% dextrose in water can also be used.


Potassium is the primary intracellular cation. Potassium has a central role in the maintenance of cell membrane electrical potentials, and is important in muscle contraction. The normal intracellular potassium concentration is 145–150 mEq/L, whereas its extracellular concentration is 2.4–4.7 mEq/L. It is present in gastrointestinal secretions, sweat and urine. Its distribution between the intra- and extracellular compartments is influenced by the acid-base status; potassium leaves the cell in exchange for hydrogen ions so that in the presence of acidosis serum potassium concentrations increase.

In anorexic horses, potassium can quickly be depleted and diarrhea also frequently results in hypokalemia (see Box 23.3). Severe hypokalemia can be accompanied by muscle weakness and ileus. Management of hypokalemia should include supplementation of fluids with potassium chloride or potassium phosphate. The rate of supplementation should not exceed 0.5 mEq/kg/h. Empirical supplementation of fluids with 10–40 mEq/L of KCl is the usual range utilized to treat or prevent hypokalemia. As hypomagnesemia (q.v.) can be associated with refractory hypokalemia, magnesium concentrations should be monitored in these patients.

The causes of hyperkalemia are also listed in Box 23.3. Hyperkalemia must be regarded as an emergency as cardiac arrhythmias (q.v.) frequently occur as a result of the electrical instability of the myocardial cell membrane if serum potassium concentrations rise. Electrocardiographic changes associated with hyperkalemia include spiked T waves, prolonged PR interval, disappearance of P waves, prolongation of the QRS complex, shortening of QT or ST intervals and ventricular dysrhythmias (q.v.). Management of hyperkalemia includes the use of potassium-free fluids, dextrose, insulin and sodium bicarbonate. Dextrose can be added as a 5% solution. Insulin should be utilized only when plasma glucose concentrations can be monitored frequently and may be given as regular insulin (0.01–0.1 U/kg/h).

Sodium bicarbonate should be directed by blood gas analysis, but safe amounts can be administered at a dose of 0.5–1 mEq/kg over 30–60 min assuming the patient is not hypoventilating. Calcium supplementation can be used to antagonize the membrane effects of potassium, but will not lower potassium concentrations directly. Enhancement of potassium clearance can be accomplished with exchange resin enemas (polystyrene sulfonate or Kayexalate) and the use of loop or other potassium-excreting diuretics.


Chloride is present in high concentrations in the ECF (see Table 23.4). At most sites within the body, chloride tends to follow sodium passively by diffusion within the cell membrane, so that the regulation of chloride concentration in the ECF is directly related to the sodium concentration. In the ECF, chloride concentrations are inversely related to bicarbonate concentrations. Chloride is a strong anion, contributing to strong ion difference (SID).

With increases in chloride concentrations, the SID will decrease, resulting in an acidosis [SID = (Na + K) − (Cl + lactate)]. This is the reason that physiologic saline (0.9% NaCl) tends to be mildly acidifying. The chloride content of saline is relatively greater than sodium relative to normal serum concentrations. Chloride is present without sodium in gastric secretions, and there is a specialized transport system for chloride in the loop of Henle. Chloride is excreted in the urine in quantities dependent on the body’s need for bicarbonate.

In horses, chloride depletion occurs if there is loss of chloride-rich fluid from the proximal gastrointestinal tract, thus hypochloremia may be associated with esophageal obstruction (q.v.) or with nasogastric reflux due to ileus or proximal gastrointestinal obstruction (q.v.). Hypochloremia is usually accompanied by metabolic alkalosis (see Box 23.3) but may be seen in states of metabolic acidosis during attempts at metabolic compensation through enhanced excretion of urinary chloride.

Primary hyperchloremia due to excessive salt intake is uncommon, but may accompany renal dysfunction and dehydration due to water loss only. Hyperchloremia accompanies renal tubular acidosis.


Calcium is an abundant divalent cation throughout the body. Absorption of calcium is via the gastrointestinal tract. It has an integral role in multiple biological processes, including nervous, skeletal, smooth muscle and myocardial function, and blood clotting. It is excreted by the kidney, and bone represents a large calcium reservoir. Calcium homeostasis is regulated by the hormones parathormone and calcitonin (q.v.).

Hypocalcemia associated with lactation may produce signs of tetany, particularly in mares exposed to an additional stressor such as transport (see Box 23.3). Mild hypocalcemia is frequently observed with abdominal crises, and it may contribute to postoperative ileus (q.v.) and weakness in some of these horses.

Calcium supplementation should be performed slowly and diluted in fluids. Supplementation with 0.5–1 mEq/kg of calcium gluconate is indicated in horses with hypocalcemia or prolonged anorexia (250–500 mL of 23% calcium gluconate, diluted in fluids). Calcium-containing fluids should not be administered through the same lines as blood products or sodium bicarbonate, due to precipitation problems.

Hypercalcemia (see Box 23.3) is usually due to chronic renal failure (q.v.), a biochemical abnormality unique to the horse. Paraneoplastic syndromes (pseudohyperparathyroidism) and vitamin D excess are uncommon causes of hypercalcemia. Hypercalcemia is more difficult to treat, but as a minimum, calcium intake should be reduced by feeding a diet low in calcium; alfalfa should be avoided.

Monitoring of calcium in the ICU should include daily measurement of total calcium concentration, while ionized calcium concentrations should be checked more often in the patient receiving fluid therapy. Approximately 50% of calcium is bound to plasma proteins, while an additional 5–10% is chelated to plasma anions like phosphate. The remainder is free, ionized calcium, which is the physiologically active form.

Ionized hypocalcemia is the clinically significant form of hypocalcemia, while hypoalbuminemia causes a decrease in the amount of calcium in the protein-bound fraction and is not as physiologically important. Alkalosis causes a shift in calcium fractions and decreased ionized calcium concentration. This should be considered in patients being treated with sodium bicarbonate and in those with respiratory alkalosis. Patients receiving large volumes of blood products should also be monitored for ionized hypocalcemia because of calcium binding by citrate. Magnesium depletion is another risk factor for development of hypocalcemia in the ICU, by inhibiting parathyroid hormone secretion and target tissue responsiveness.


The assessment of electrolyte disorders must be based on laboratory evaluation of serum concentrations of electrolytes. Specific electrolyte disorders cannot be predicted simply from the clinical presentation or problem. Serum concentrations of sodium are accurate in assessing sodium deficits or relative excesses, as sodium is an extracellular ion. In contrast, measurement of serum potassium concentration does not reflect the whole body content of potassium, as this is primarily an intracellular ion. Acid-base status further complicates the interpretation of serum potassium concentrations. A decrease in pH of 0.1 units causes an increase in serum potassium concentration of 0.6 mEq/L. Thus, acidosis can mask potassium depletion by increasing the concentration of potassium in the ECF. This is seen commonly with bicarbonate and potassium losses associated with enterocolitis (q.v.).

Estimates of sodium and potassium deficits for the purposes of replacement therapy are made by considering the difference between the measured and desired serum concentrations, the horse’s body weight and the distribution of the ion within the body, as follows:



However, repeated laboratory evaluations are undoubtedly the most rational means by which to assess the response to replacement of electrolytes. Because potassium is primarily an intracellular ion, serum concentrations are poor indicators of whole body potassium balance. Urinary fractional excretion of potassium may improve understanding of body potassium stores. Fractional excretion is calculated as follows:


where Scr is serum creatinine concentration, Ucr is urine creatinine, Uk is urine concentration of potassium, and Sk is serum concentration of potassium.


The blood pH is dependent on the respiratory system and the function of a variety of buffering systems. The carbonic acid/bicarbonate buffer system is of most interest to the clinician, since it is amenable to clinical intervention. Hydrogen ions, carbon dioxide, water and bicarbonate are produced constantly by cellular metabolism. Carbon dioxide is transported in blood as dissolved or free carbon dioxide; in association with protein and hemoglobin; and as bicarbonate. In the lungs, bicarbonate dissociates to carbon dioxide and water, and carbon dioxide is exhaled. The regulation of serum bicarbonate concentration is achieved in large part by the kidneys.

Acid–base disorders may be classified as respiratory or metabolic in origin (see Box 23.3), and mixed acid-base disorders are common. Failure of ventilation results in the inability to remove carbon dioxide (respiratory acidosis), while hyperventilation decreases carbon dioxide and causes respiratory alkalosis. It is important to appreciate that acid-base disorders of respiratory origin cannot be alleviated by fluid therapy and require modification of respiratory function.

Metabolic acidosis can be the result of excessive production of organic acids (titration) or of loss of bicarbonate (secretion). The titration form of metabolic acidosis occurs when there is an increase in acid anions and bicarbonate is required for buffering. In the horse, lactic acidosis (q.v.) occurs commonly. It is usually associated with hypovolemic, cardiogenic or endotoxic shock (q.v.) and inadequate tissue perfusion. The secretion form of metabolic acidosis occurs when bicarbonate ions are actively lost from the body (see Box 23.3). In some conditions, both secretion and titration of bicarbonate will occur.

Mixed metabolic acidosis and alkalosis may be present in horses with gastrointestinal disease (q.v.). This occurs, for example, when fluid is sequestered in the proximal gastrointestinal tract leading to chloride and hydrogen ion loss and metabolic alkalosis, with a concurrent reduction in effective circulating volume, producing shock, poor tissue perfusion and lactic acidosis.

Assessment of acid–base balance

An arterial blood gas analysis is required for full evaluation of both the respiratory and metabolic components of acid–base balance. Normal values for arterial and venous blood gas analysis are given in Table 23.6. Interpretation of the respiratory component is based on the partial pressure of carbon dioxide in arterial blood ( Table 23.7). Metabolic disorders are manifested by alterations in bicarbonate concentrations and the base deficit. Both arterial and venous blood gas analysis are equally suitable for assessment of the metabolic component of acid–base disorders (see Table 23.6).

Respiratory and metabolic components of acid–base balance are interdependent so that a respiratory disorder may lead to compensation and concurrent alterations in bicarbonate concentrations. Equally, a metabolic disorder may induce changes in respiration pattern and alteration in the PCO2.

The anion gap (the difference between cations and measured anions) is used to distinguish titration and secretion forms of metabolic acidosis (see Table 23.7). The anion gap is a reflection of those ions that are not measured, organic acids, phosphates, sulfate and protein. Lactic acidosis increases the anion gap, whereas the anion gap is unchanged when the primary problem is loss of bicarbonate. In that situation, chloride concentrations increase as bicarbonate concentrations fall to maintain electrical equilibrium. An increase in the anion gap with a normal pH and bicarbonate are the hallmarks of mixed metabolic acidosis and alkalosis (see Table 23.6). Without assessment of the anion gap, this abnormality might otherwise go unnoticed as alterations in both pH and bicarbonate are counteracted by the conflicting processes.

Blood samples for blood gas analysis are collected in heparinized syringes, and tightly capped prior to analysis to prevent air contamination. Ideally, the sample should be processed as quickly as possible, but samples may be stored on ice for up to 4 h if necessary. Total carbon dioxide (TCO2) concentration can be used as an alternative to measurement of bicarbonate concentration for the assessment of metabolic acid-base disorders. Total carbon dioxide is slightly less accurate, but is usually adequate for clinical purposes. Various pieces of equipment are available for rapid “in practice” total carbon dioxide assays and this test is included in chemistry panels on many autoanalyzers. Base deficit can be estimated using the total carbon dioxide as well. Subtracting the TCO2 from the median normal bicarbonate (24 mmol/L) will provide an estimate of the base deficit.


In most clinical situations, the plan for fluid therapy includes three components: replacement of existing deficits; supplying of maintenance requirements; and matching ongoing losses.

Over-hydration, the administration of fluid in excess of the body’s requirements, is occasionally indicated. Colonic impactions (q.v.) represent clinical conditions that are treated with over-hydration. The selection of type of fluid and the rate of administration are dependent on the clinical problem and the specific deficits. The clinical and laboratory assessments described above are used to estimate deficits and evaluate ongoing losses.

In horses, fluids are administered either by oral or IV routes. In most clinical conditions in which replacement of fluid deficits or restoration of effective circulating volume is required, the IV route is mandatory because of the volumes required, and because many gastrointestinal diseases preclude oral administration. However, the oral route should be used whenever possible. It has the advantages that it is more physiological, it is considerably less expensive and the risk of iatrogenic or nosocomial infections is negligible.



The ideal crystalloid solution for volume replacement has a composition similar to that of plasma. These include lactated Ringer’s (Hartman’s) solution or similar balanced polyionic solutions such as Plasma-Lyte (Baxter Health Care Corp., Deerfield, IL, USA [available in 5L bags]), Multisol-R (Normosol-R, CEVA) and Isolec (IVEX Ltd, Larne, Northern Ireland, UK [available in 5L bags]) ( Table 23.8). Lactated Ringer’s solution (LRS) contains calcium, whereas Plasma-Lyte and Normosol contain magnesium.

Since blood products should not be administered through the same lines as calcium-containing fluids, the latter fluids should be used during blood or plasma transfusions. Another difference between LRS and Plasma-Lyte/Normosol is the type of alkalinizing agent present. LRS contains lactate and Plasma-Lyte/Normosol products contain acetate and gluconate. Lactate is cleared primarily by the liver, acetate is cleared primarily by muscle, and gluconate is metabolized by most cells.


Colloid solutions contain glycerin, glucose polymers, or dextrans of high molecular weight. They are effective because they remain in the intravascular compartment longer than crystalloid solutions, assuming normal vascular integrity. Anaphylactic or anaphylactoid reactions (q.v.) have been associated with the use of dextrans in horses, and hetastarch appears to be safer.

Plasma is a suitable alternative for rapid replacement of circulating volume (see Table 23.8). However, in the volumes required it is often prohibitively expensive to be used for colloid support alone. Under these circumstances, plasma should be used in combination with synthetic colloids such as hetastarch.

The rate of administration of replacement fluid depends on the severity of the clinical signs and the ongoing losses. There is no one correct way to replace volume; one half of the deficit may be given in the first 2–6 h, with the remainder being given over the following 6–12 h. However, in adult horses with cardiovascular collapse, fluids may be administered safely at rates of up to 30 L/h if necessary to restore perfusion. Such boluses are often required in horses with hypovolemic shock (q.v.). The clinical response is often the best guide to rate of fluid administration.

Fluid overload produces pulmonary edema, thus the respiratory rate and effort and the quality of the lung sounds should be evaluated frequently during the rapid IV administration of large volumes. CVP is the most objective guide to the rate of fluid administration, but examination of the height of the jugular pulse also gives a crude estimation of rising CVP. CVP can be easily measured in both horses and foals, through the use of central lines and a water manometer as described in Box 23.2. Optimization of the CVP can be used as a fluid administration end-point goal. Once near maximum CVP (10 cmH2O in a neonate; 12–15 cmH2O in an adult) is achieved using fluid loading, rates of administration should be decreased to avoid risks of edema formation.

Hypertonic saline (7%) is a valuable alternative for the emergency resuscitation of horses with hemorrhagic, hypovolemic or endotoxic shock (see Table 23.8). Administration of hypertonic solutions increases the effective circulating volume, cardiac output and blood pressure. The precise mechanisms by which it is effective are still unclear. A number of processes may be involved, including a vagally mediated reflex, redistribution of blood from peripheral to central vascular beds, increasing cardiac contractility, and relocation of fluid from the interstitium and ICF to the intravascular space.

Urine output is increased following administration of hypertonic solutions and this leads to a decrease in total body water. For that reason, it is imperative that hypertonic solutions are followed with isotonic solutions to maintain total body water. Hypertonic saline is administered at 4 mL/kg and is given as quickly as possible (in approximately 10 min). It is contraindicated in horses with renal failure. Some authors have expressed reservations about its use in hemorrhagic shock, as increasing the blood pressure may promote further bleeding. It should not be used in horses with uncontrolled bleeding.

Hyperosmolarity is another consideration. Because hypertonic solutions borrow water from the interstitium and intracellular spaces, they should not be utilized in maximally dehydrated horses. In these cases, concurrent or prior administration of isotonic crystalloid should be performed.


The approach to the correction of metabolic acidosis depends on the underlying cause. Acidosis due to depletion of bicarbonate by buffering acid anions in lactic acidosis (titration) is best addressed by the correction of the underlying cause. Hypoperfusion should be improved by volume replacement with a balanced polyionic solution. These solutions contain bicarbonate precursors such as lactate, acetate or gluconate. For horses with fluid-refractory hypotension, inotrope and vasopressor therapy should be considered. Hypoxemia or reduced oxygen carrying capacity should be addressed through oxygen supplementation or blood transfusions, respectively.

In horses with enterocolitis (q.v.) that are actively losing bicarbonate or sodium ions (secretion), administration of sodium bicarbonate may be warranted. Hyperchloremic metabolic acidosis may also benefit from sodium bicarbonate administration. Bicarbonate should only be supplemented when the serum base deficit is >6–8 mEq/L. The bicarbonate deficit may be estimated as follows:


or, if total carbon dioxide (TCO2) is measured, as on a serum biochemistry profile:


It is often suggested that one half of the calculated deficit be given over 1 h, the blood gas analysis then repeated, and the remainder of the deficit replaced over the next 6 h. However, in horses with diarrhea, considerable quantities of sodium bicarbonate may be required simply to meet ongoing losses, and more than the initial calculated deficit may be needed. Repeated blood gas or total carbon dioxide measurements are the most reliable guides to the administration of bicarbonate.

Sodium bicarbonate administration may have a number of adverse effects. It can constitute an excessive sodium load. Potentially, a paradoxical central nervous acidosis may develop because carbon dioxide is formed following bicarbonate administration, and this diffuses through the blood–brain barrier, decreasing pH in the cerebrospinal fluid, while bicarbonate cannot pass the blood–brain barrier to buffer the carbon dioxide. Intracellular acidosis may also be potentiated through the rapid administration of sodium bicarbonate for similar reasons. Bicarbonate should not be administered to horses with impaired ventilation as carbon dioxide excretion is limited, and bicarbonate administration can potentiate carbon dioxide production.

Bicarbonate administration may induce hypokalemia as potassium ions enter the cells in exchange for hydrogen ions. Potassium concentrations should be monitored and potassium chloride (20 mEq/L) should be added to bicarbonate solutions to avoid this. Sodium bicarbonate can also produce decreases in plasma ionized calcium.

Sodium bicarbonate is available as 5% and 8.4% solutions, both of which are hypertonic and should be diluted before use. An isotonic solution of bicarbonate can be made by dilution with sterile water to a concentration of 150 mEq/L of sodium and of bicarbonate (1.3% sodium bicarbonate) (see Table 23.8). Bicarbonate should not be added to calcium-containing solutions as precipitates are formed.


Metabolic alkalosis is uncommon in horses. It is seen as a result of loss of hydrogen and chloride ions in nasogastric reflux (q.v.), often accompanied by hypochloremia and hypokalemia. Horses with heavy sweating, such as those in endurance rides, can also develop alkalosis. Therapy is aimed at replacement of chloride, and promotion of excretion of bicarbonate via the kidney by restoration of body water. Normal saline, supplemented with potassium, is the fluid of choice for the treatment of metabolic alkalosis (see Table 23.8). Circulating volume deficits should be addressed. Supplementation with magnesium can also aid in treating refractory alkaloses.


Hyponatremia rarely requires specific therapy, however normal saline can be used to increase serum concentrations of sodium. Hyponatremia should be corrected slowly to prevent rapid dehydration of the central nervous system (CNS) thereby leading to central pontine dysmyelinolysis and demyelination (q.v.).

Hypernatremia indicates a water deficit. Replacement of water can be achieved using 5% dextrose, as at this concentration dextrose is metabolized to carbon dioxide and water. Once glucose is metabolized, 5% dextrose is essentially free water. Alternatively, an infusion of 0.45% saline in 2.5% dextrose may be used for delivery of lower rates of free water.

Extreme caution should be exercised in the treatment of hypernatremia as cerebral edema (q.v.) may develop if the plasma osmolarity is reduced too rapidly. A safe rule of thumb is that both hyponatremia and hypernatremia should be corrected slowly, without exceeding 0.5 mEq/h.


IV replacement of potassium deficits is difficult to achieve as cardiac arrhythmias can develop when excessive quantities of potassium are administered. No more than 0.5 mEq/kg/h should be given IV in horses with normal renal function, with lower amounts for those with kidney disease. Oral replacement of potassium is much safer, and larger quantities (up to 60 g at a time) can be administered. Potassium supplementation should be performed with extreme caution in horses with hyperkalemic periodic paralysis (HYPP) (q.v.) and those with acute anuria or oliguria.

Hyperkalemia is regarded as a medical emergency because of the risk of cardiac arrhythmias or dysrhythmias (q.v.), including diminished P wave amplitude, loss of P waves, spiked or tented T waves, increasing duration of the QRS complex and a variety of ventricular dysrhythmias.

The concentration of potassium in the ECF can be reduced by promoting cellular uptake by the administration of sodium bicarbonate, or insulin (0.1–0.5 units/kg), or enhancement of the secretion of insulin by dextrose infusion (4–6 mL/kg of 5% dextrose). Potassium-wasting diuretics, such as furosemide or carbon anhydrase inhibitors, may be used to remove potassium from the body. Calcium has been recommended for its cardioprotective effects in hyperkalemia because it raises threshold potential (0.2–0.4 mL/kg of a 23% calcium gluconate solution, administered very slowly and diluted, i.e. over no less than 20 min and preferably longer).

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Jul 8, 2016 | Posted by in EQUINE MEDICINE | Comments Off on Intensive care medicine
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