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EQUINE VETERINARY EDUCATION / AE / OCTOBER 2006 341

Tutorial Article disorders in horses with colic. Part 1: and magnesium K. E. BORER* AND K. T. T. C ORLEY† Royal Veterinary College, Equine Referral Hospital, Hawkshead Lane, North Mymms, Hatfield, Hertfordshire AL9 7TA, UK. Keywords: horse; colic; ; potassium; magnesium

Introduction concentrations might contribute to ileus. Garcia-Lopez et al. (2001) found lower concentrations of ionised Electrolyte disorders are common in horses with acute magnesium and calcium in horses that developed post abdominal disease, and are a significant cause of morbidity. operative ileus, than in those that did not. These decreased They are especially prevalent in horses treated surgically for electrolyte concentrations may be due to decreased intake and colic, and may be present before, during and after surgery. In increased loss of electrolytes in gastric reflux. one study, 54% of horses admitted for surgical colic had It is now possible to measure electrolytes using ‘patient- preoperative serum ionised magnesium concentrations below side’ portable analysers. The introduction of these cartridge- the reference range and 86% subnormal serum ionised based systems has enabled results to be obtained quickly and calcium concentrations (Garcia-Lopez et al. 2001). Electrolyte easily when laboratory techniques are unavailable abnormalities are particularly prevalent in horses with (Grosenbaugh et al. 1998). Different sensors are available to strangulating obstructions of the intestine. These horses have measure different combinations of electrolytes, blood lower preoperative serum concentrations of ionised biochemistry, PCV and blood gas tensions. The price of these magnesium and calcium than horses with nonstrangulating hand-held devices is rapidly decreasing and they are now lesions (Dart et al. 1992; Garcia-Lopez et al. 2001). Horses affordable for many private practices. The normal range for with decreased preoperative ionised magnesium were also any electrolyte may vary to some degree between analysers. more likely to be subjected to euthanasia during surgery. Therefore, horse specific normal ranges should be obtained The role of electrolyte derangements in contributing to from the manufacturers, if possible. adverse clinical events in horses with colic is still being In Part 1, we discuss the importance of potassium and investigated. The association between cardiac electrical magnesium and Part 2 covers calcium, , chloride disorders and blood calcium, magnesium and potassium and phosphorus. concentrations is well established in the horse (Harrington 1974; Glazier et al. 1979, 1982; Reef 1999) (Fig 1). Potassium Derangements in blood electrolyte concentration might also be associated with a longer hospital stay. Martin Potassium is primarily an intracellular , and uptake of et al. (1994) reported that dogs with low serum magnesium potassium into cells is stimulated by increased circulating concentrations were hospitalised for twice as long as those concentration and β-adrenergic stimulation (Gennari with a normal serum magnesium concentration. Conversely, 1998). The ratio of intracellular to extracellular potassium may Garcia-Lopez et al. (2001) did not find any correlation be affected by the acid-base status. Hydrogen moves into cells between serum ionised magnesium or calcium concentrations during acidosis; and from the intracellular to extracellular and length of hospitalisation, incidence of complications or fluid in alkalosis. In some acid-base conditions, potassium survival in horses treated surgically for colic. The association moves in the opposite direction to hydrogen to maintain between serum concentrations of potassium, calcium and electroneutrality (Corley and Marr 1998). Although erythrocyte magnesium with post operative ileus is still unknown in the potassium content has been used to estimate whole body horse. Dart et al. (1992) speculated that decreased serum potassium (Muylle et al. 1984), its accuracy has not been validated. Moreover, the extracellular potassium concentration (reflected in the plasma) is critical for neuromuscular *Author to whom correspondence should be addressed. †Present address: Anglesey Lodge Equine Hospital, The Curragh, Co. Kildare, transmission and therefore more relevant to clinical signs than Ireland. whole body potassium stores (Rose and Post 2001). 342 EQUINE VETERINARY EDUCATION / AE / OCTOBER 2006

Hypokalaemia potential to result in an (Schaer 1999). Symptoms of hypokalaemia can be mild and nonspecific, Fifty percent of horses are hypokalaemic after colic surgery including and reduced gastrointestinal motility. (Protopapas 2000). Clinical signs of hypokalaemia are chiefly The severity of symptoms is usually related to the speed of related to electrical conduction across the membrane. decrease in serum potassium. Severe hypokalaemia can result in Hypokalaemia results in hyperpolarisation of the cell membrane impairment of respiratory function, but cardiac abnormalities are (a more negative resting ) and therefore less rare in patients with no pre-existing cardiac disease (Gennari chance of a positive increase in charge reaching threshold 1998). Electrocardiogram changes that occur with hypokalaemia include increased P wave amplitude, reduced amplitude, prolongation of the P-R and Q-T interval and such as atrial tachycardia (Fig 1: Reef 1999; Schaer 1999). Hypokalaemia in horses with colic has been speculated to be associated with altered intake and absorption or excess loss from the caused by diarrhoea (Nappert and Johnson 2001). Several other causes could also be involved. Hypokalaemia can result from increased losses via the kidneys (Gennari 1998). Chronic fluid therapy with lactated Ringer’s solution, which contains a low potassium concentration and may result in sodium induced diuresis, can result in hypokalaemia Normal ECG (Atkins 1999). Horses that are producing large volumes of gastric reflux will lose chloride , resulting in metabolic alkalosis and subsequent hypokalaemia (Gennari 1998). Many drugs can induce hypokalaemia, including β-adrenergic agonists, glucocorticoids, insulin, and antibiotics. Both penicillin and gentamicin, antibiotics commonly used after colic surgery, may induce hypokalaemia. In the case of gentamicin, this is an indirect action, by causing hypomagnesaemia (Gennari 1998).

Hyperkalaemia

Hyperkalaemia has been reported to occur in association with Hypokalaemia , due to potassium exchange for hydrogen ions across cell membranes. However, this is chiefly a phenomenon of (inorganic) acidosis rather than (Perez 1981; Graber 1993). In horses with colic, the predominant cause of acidosis is lactic acid accumulation, associated with poor tissue perfusion and hypovolaemia (Corley and Marr 1998; Nappert and Johnson 2001). We found a moderate inverse correlation between plasma potassium concentration and pH, but no correlation between potassium and lactate concentration, in jugular venous blood from horses with surgically treated colic (C. Adams and K.T.T. Hyperkalaemia Stage 1 Corley, unpublished data). Hyperkalaemia is most commonly encountered in equine practice in foals that have a ruptured urinary bladder (Kablack et al. 2000). ECG signs of hyperkalaemia include , peaked T waves, small or absent P waves, widened QRS complexes and prolonged P-R intervals (Atkins 1999) as shown in Figure 1. These changes are indicative of reduced cardiac excitability, and may progress to or (Reef 1999). Muscle weakness can also be a feature of hyperkalaemia (Schaer 1999).

Magnesium Hyperkalaemia Stage 2

Fig 1: ECG abnormalities associated with electrolyte Magnesium plays a crucial role in many metabolic and cellular abnormalities. functions in the body, especially those involving adenosine 344 EQUINE VETERINARY EDUCATION / AE / OCTOBER 2006

triphosphate (ATP) and the production of energy (Page et al. prevalence rate varying between 20 and 65% (Olerich and 1998). It is an important coenzyme for the sodium-potassium Rude 1994; Hamill-Ruth and McGory 1996). ATPase pump (Tso and Barish 1992). Abnormalities of the In many studies, hypomagnesaemia appears to be normal resting membrane potential can result from associated with increased morbidity and mortality rates, interference with the normal function of this pump, causing although the underlying disease may be responsible for both membrane destabilisation and hyperexcitability (Tso and the lowered magnesium concentrations and the increased Barish 1992; Martin et al. 1994). Magnesium is an essential mortality (Olerich and Rude 1994). In one study, there was no cofactor in many enzymatic reactions in the body (Tso and relationship between ionised magnesium concentrations on Barish 1992). Magnesium also directly competes with calcium admission and survival in horses with gastrointestinal disease for some of its binding sites, allowing greater binding of (Garcia-Lopez et al. 2001). Relevant to the post operative colic calcium to enzymes in hypomagnesaemia. One such enzyme patient, hypomagnesaemic rats had greatly increased is phospholipase A2; increased calcium binding results in mortality from endotoxaemia, which could be reversed by greater activity of this enzyme, which leads to the increased magnesium chloride administration (Salem et al. 1995). formation of eicosanoids, particularly thromboxane A2 Magnesium intake is reduced in most horses after colic (Gunter 1991), which may play a role in thrombophlebitis surgery due to decreased food intake (Tso and Barish 1992). (Morris 1989). Renal and gastrointestinal losses constitute the most important Magnesium is absorbed from the intestine and filtered by causes of magnesium loss. Patients receiving large volumes of the . Only 5% of the magnesium filtered by the kidney fluids, especially sodium chloride, without magnesium is excreted, and the remainder is reabsorbed in the proximal supplementation, may become hypomagnesaemic. The high tubule and ascending loop of Henlé (Tso and Barish 1992; renal sodium load inhibits reabsorption of magnesium in Hamill-Ruth and McGory 1996). Ionised magnesium is the the loop of Henlé (Martin et al. 1994). Stress, and the biologically active form of the cation (Tso and Barish 1992), subsequent release of and , may cause and therefore is preferred to total magnesium for hypomagnesaemia (Tso and Barish 1992). Loop diuretics and measurement of magnesium status. However, only 1% of aminoglycoside antibiotics are also associated with total body magnesium is found in the , with hypomagnesaemia (Olerich and Rude 1994). Horses with 50% intracellular and the rest in bone. This means that diarrhoea or large volumes of gastric reflux may lose large extracellular (serum) magnesium concentrations may not be amounts of magnesium rich fluid (Tso and Barish 1992). representative of total body magnesium status (Fiaccadori et Parenteral nutrition solutions are also low in magnesium and al. 1988; Hamill-Ruth and McGory 1996). Methods for can result in a deficiency unless supplemented. Sweating also measuring intracellular magnesium have been developed in causes loss of magnesium from the body (Taylor 1996). man, using erythrocytes, mononuclear cells, bone or skeletal Hypomagnesaemia is often associated with other electrolyte muscle cells (Fiaccadori et al. 1988; Tso and Barish 1992), but abnormalities. Costa et al. (1999) found that 30% of are expensive and not widely available. Measurement of hypomagnesaemic horses with gastrointestinal disease were intracellular magnesium concentrations in intensive care also hypokalaemic, compared with 20% of normomagnesaemic patients usually reveals a higher prevalence of magnesium horses. Hypokalaemia occurs due to inhibition of renal depletion than measurement of serum concentrations alone potassium transport, and this form of hypokalaemia may be (Olerich and Rude 1994). For example, one study found that refractory to treatment with potassium supplementation 9.4% of humans in intensive care were hypomagnesaemic, without concurrent magnesium supplementation (Fiaccadori but 47% had subnormal magnesium concentrations in et al. 1988; Olerich and Rude 1994). quadriceps muscle cells (Fiaccadori et al. 1988). Hypochloraemia can occur in association with A recent study in horses suggested that the best method hypomagnesaemia (Hamill-Ruth and McGory 1996). Admission of determining magnesium status was to determine the data from horses with small intestinal volvulus demonstrated a fractional excretion of magnesium in the urine. Although a 37% prevalence of hypochloraemia in hypomagnesaemic 24 h urine collection provided the most accurate results, a horses compared with 14% prevalence in horses with normal ‘spot’ urine total magnesium fractional excretion was ionised magnesium concentrations (J.O. Stephen and K.T.T. sufficiently accurate for clinical use (Stewart et al. 2004). Corley, unpublished data). Hypocalcaemia can occur as a result of inhibition of parathyroid release by low Hypomagnesaemia magnesium concentrations (Olerich and Rude 1994). In the horse, severe hypomagnesaemia can result in Costa et al. (1999) surveyed 75 horses with gastrointestinal ventricular arrhythmias and also muscle tremors, ataxia, disease and found that 44% were hypomagnesaemic. Garcia- seizures and of elastic tissue (Harrington 1974). An Lopez et al. (2001) found decreased ionised magnesium in increased incidence of cardiac arrhythmias and myocardial 54% of colic patients on admission. Stephen et al. (2004) ischaemia is also found in human patients with found 73% of horses with a small intestinal volvulus had an hypomagnesaemia, especially if this is associated with ionised magnesium concentration below the reference range hypokalaemia (Olerich and Rude 1994; Hamill-Ruth and at admission. These findings are similar to those in human McGory 1996). These can vary from ectopic beats to atrial intensive care patients, where studies have documented a tachycardia and ventricular fibrillation (Fiaccadori et al. 1988; EQUINE VETERINARY EDUCATION / AE / OCTOBER 2006 345

Tso and Barish 1992). The frequency of ectopy was reduced in tachycardia, with a shortened Q-T interval on the ECG (Atkins human patients receiving supplemental magnesium, compared 1999; Schaer 1999). Severe hypermagnesaemia results in with a control population (Tso and Barish 1992; Hamill-Ruth respiratory paralysis and subsequent cardiac arrest (Bowen et al. and McGory 1996). This may be due to the action of 1970). Hypocalcaemia is common in horses with magnesium on the membrane potential and refractory period gastrointestinal disease (Dart et al. 1992; Garcia-Lopez et al. in the cardiac cells (Tso and Barish 1992). Hypertension can also 2001) and this may increase the severity of signs occur in hypomagnesaemic patients (Fiaccadori et al. 1988). of hypermagnesaemia. Platelet aggregation is increased in the face of (Olerich and Rude 1994). Hypomagnesaemic Prevention and treatment patients often have poor respiratory muscle strength and bronchospasm, which can be relieved by a bolus of magnesium Most commonly, horses hospitalised after colic surgery will (Tso and Barish 1992). Seizures and central nervous system receive electrolytes intravenously together with routine post manifestations, such as restlessness and disorientation, are also operative fluid therapy. However, these may not be in the reported (Tso and Barish 1992). Gastrointestinal motility is appropriate proportions for the horse, and may not include reduced, especially if hypomagnesaemia is associated with some important electrolytes. For example, lactated Ringers’ concurrent hypokalaemia (Schaer 1999). solution contains no magnesium or , and the amount of potassium is frequently inadequate to maintain Hypermagnesaemia plasma concentrations. Horses that have access to oral food and water can be Hypermagnesaemia is less common than magnesium deficiency given electrolytes orally. Horses are often unwilling to drink in intensive care patients. The prevalence reported in post electrolytes freely, when provided in a bucket of water. operative colic patients (11–14%) (Costa et al. 1999; Nasogastric intubation is a practical way to administer Protopapas 2000) is very similar to that reported in dogs electrolytes orally (McGinness et al. 1996). The horse must admitted to a critical care unit (13%) (Martin et al. 1994). have a functional gastrointestinal tract and must be checked Mortality rates were more than twice as high in these regularly for the presence of gastric reflux, indicating ileus. Up hypermagnesaemic dogs compared to normomagnesaemic to 8 l of fluid can be given by nasogastric tube every 30 min patients. This may be related to the severity of the underlying to a 500 kg horse (McGinness et al. 1996). However, in the illness or a direct pathological effect of the magnesium (Martin et al. 1994). Hypochloraemia was present in 75% TABLE 2: Replacement guidelines of hypermagnesaemic horses, compared with 18% of normomagnesaemic horses. Amount to add to 5 l bag of Iatrogenic hypermagnesaemia can occur in horses that have Measured value balanced electrolyte solution received magnesium sulphate (Epsom salts) orally for the Hypokalaemia K <2.5 mmol/l Add 40 mmol/l treatment of large colon impactions. The recommended dosage (77 ml of 13 mEq/5 ml KCl) of magnesium sulphate is 0.5–1.0 g/kg bwt, and toxicity has and 0.1–0.2 g/kg bwt per os been reported when twice the normal dosage has been (if appropriate) K <2.9 mmol/l Add 30 mmol/l administered. Any conditions that reduce renal excretion of (58 ml of 13 mEq/5 ml KCl) magnesium, such as hypovolaemia, or allow increased intestinal and 0.1–0.2 g/kg bwt per os absorption of magnesium, such as delayed intestinal transit due (if appropriate) to colic, drug therapy or increased permeability of the intestinal K <3.2 mmol/l Add 20 mmol/l wall, may allow toxicity to develop (Henninger and Horst 1997). (39 ml of 13 mEq/5 ml KCl) K <3.5 mmol/l Add 10 mmol/l Magnesium antagonises the effects of calcium at the (19 ml of 13 mEq/5 ml KCl) neuromuscular junction, and signs of hypermagnesaemia include sweating, flaccid paralysis, coma and recumbency due Hyperkalaemia K >7.0 mmol/l 1) Ca gluconate 40% to a blockade of peripheral neuromuscular transmission (Bowen 0.5 ml/kg bwt over 10 min 2) Dextrose 50% 2ml/kg bwt et al. 1970). Magnesium has a negative inotropic effect (Tso and over 5 min ± Barish 1992; Atkins 1999), resulting in hypotension and reflex 0.1u/kg bolus 3) Bicarbonate 1–2mEq/kg bwt TABLE 1: Approximate normal ranges and interference levels over 15 min for electrolytes in post surgical colics K <7.0 mmol/l Diuresis with Hartmann’s (and, if clinically appropriate, Normal range Treat if falls below Treat if rises above 1mg/kg bwt frusemide) (mmol/l) (mmol/l) (mmol/l) Hypomagnesaemia Mg sulphate 4–16mg/kg bwt Potassium 3.2–5.2 3.5 7.0 per 5 l bag, and remeasure Magnesium within 12 h. (ionised) 0.45–0.65 0.35 1.3 or symptomatic Magnesium Hypermagnesaemia Ca gluconate 40% 125– (total) 0.66–0.95 0.4 1.6 or symptomatic 250ml over 15 min 346 EQUINE VETERINARY EDUCATION / AE / OCTOBER 2006

authors’ experience, this volume can result in mild discomfort are given in Table 2. Horses that are also hypomagnesaemic in some horses, even those with normal gastrointestinal may be refractory to potassium replacement therapy, unless motility. These solutions are easy to make and inexpensive. the magnesium deficit is simultaneously corrected (Hamill- Ideally, slightly hypotonic or isotonic solutions should be Ruth and McGory 1996). provided to avoid drawing further fluid from the extracellular space into the intestinal lumen. Adding 30 ml of table salt Hyperkalaemia crystals per 4 l of water results in an approximately isotonic solution. Treatment of hyperkalaemia can be accomplished in several Sosa León et al. (1998) reported the use of a concentrated ways (Table 2). Fluid therapy with sodium chloride should be paste of electrolytes to replace fluid and electrolyte deficits instituted to promote kalliuresis. A combination of insulin and induced by frusemide administration. The paste was made up dextrose saline will promote cellular uptake of potassium. from sodium and (table salt and ‘Lo-salt’) will negate the cardiac effects of and administered using feeding syringes. All horses were hyperkalaemia (Reef 1999). has the least allowed ad libitum access to water after paste administration. effect on potassium concentrations, but acts to alkalinise the The concentrated paste stimulated water consumption and plasma and drive potassium intracellularly. improved the overall balance of sodium, potassium and chloride, compared to administration of water alone (Sosa Hypomagnesaemia León et al. 1998). Our subjective experience is that oral electrolyte pastes do not increase water consumption in post Magnesium sulphate can be added to intravenous polyionic operative colic patients. replacement fluids at rates up to 64 mg/kg bwt depending on The approximate normal ranges for the electrolytes the degree of hypomagnesaemia. After 4–8 h, serum discussed are given in Table 1. However, it is not necessary, or concentrations should be remeasured. indeed desirable, to maintain all the electrolytes within their normal ranges in post operative colic patients. Therefore, as a Hypermagnesaemia guide, we have produced electrolyte concentrations at which therapeutic intervention is likely to be necessary (‘interference The treatment for hypermagnesaemia should include levels’), for use in our own hospital. These are also presented intravenous calcium, fluid therapy and loop diuretics, such as in Table 1. However, it is important to note that these may frusemide, to increase renal excretion of magnesium (Tso and vary slightly with different analysers, and should always be Barish 1992; Henninger and Horst 1997). used in context of the whole clinical scenario. Guidelines for correction of these electrolyte References abnormalities are given in Table 2. For all electrolyte abnormalities, it is important to realise that losses may be Atkins, C.E. (1999) Cardiac manifestations of systemic and metabolic disease. In: Textbook of Canine and Feline Cardiology, 2nd edn., ongoing. Furthermore, there may be intracellular shifts, or Eds: P.R. Fox, D. Sisson, and N.S. Moïse, W.B. Saunders, accelerated excretion of exogenously administered Philadephia. pp 768-770. electrolytes. For this reason, it is not appropriate to calculate Bowen, J.M., Blackmon, D.M. and Heavner, J.E. (1970) Effect of a theoretical deficit and replace the calculated deficit. Such magnesium ions on neuromuscular transmission in the horse, calculations assume that the horse is a chemistry flask, and do steer, and dog. J. Am. vet. med. Ass. 157, 164-173. not acknowledge dynamic changes in absorption and Corley, K.T.T. and Marr, C.M. (1998) Pathophysiology, assessment and excretion. 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(1988) Muscle and serum magnesium in at a maximum rate of 0.5–1 mEq/kg bwt/h. Potassium pulmonary intensive care unit patients. Crit. Care Med. 16, 751-760. chloride is the ideal replacement salt, especially in horses that Garcia-Lopez, J.M., Provost, P.J., Rush, J.E., Zicker, S.C., Burmaster, H. and Freeman, L.M. (2001) Prevalence and prognostic importance are refluxing and concurrently hypochloraemic (Gennari of hypomagesemia and in horses that have colic 1998). High crystalloid flow rates result in increased urine surgery. Am. J. vet. Res. 62, 7-12. production and kalliuresis, and therefore can make it harder Gennari, F.J. (1998) Hypokalaemia. New Eng. J. Med. 339, 451-458. to replace potassium intravenously. For this reason, oral Glazier, D.B., Littledike, E.T. and Evans, R.D. (1979) supplementation is preferred for severe hypokalaemia, in Electrocardiographic changes in induced hypocalcemia and horses in which the oral route is available. Suggested doses hypercalcemia in horses. 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ERRATUM

The article ‘Cor pulmonale in a horse with granulomatous pneumonia’ by Schwarzwald et al. was published in Equine Veterinary Education, Volume 18, pp 182-187. There was a typographic error on page 182: the final sentence of the Haematology and serum biochemistry section should have read “Serum cardiac Troponin I concentration was <0.15 ng/ml (reported reference value <0.3 ng/ml [Cornelisse et al. 2000]).” The editor wishes to apologise for any inconvenience that this may have caused.