History and presenting complaint

The exhausted horse syndrome is a term used to describe a multisystem disorder that can develop in horses participating in athletic activity over an extended period (e.g. three-day events, endurance racing, and other long-distance rides), particularly when exercise is performed in hot ambient conditions.1–3 The clinical presentation is variable and dependent upon the severity and speed of onset of fatigue as well as the individual horse’s tolerance to physiological strain. In general, clinical signs are reflective of dehydration, electrolyte and acid–base disturbances, depletion of energy reserves, hyperthermia and muscle pain.^2,3

Physical examination

Initially, there are subtle signs of fatigue with mild alterations in mental state (alertness and attitude) and inconsistencies in gait that may be due to muscle soreness. Clinical evidence of exhaustion becomes more pronounced if exercise is continued; muscles start to show localized hardening and pain on palpation, the gait becomes stiff and stilted, and muscle spasms and cramps may occur, as may synchronous diaphragmatic flutter (SDF).2,3 Severely affected horses are often unwilling to continue to exercise, are depressed and are unwilling to eat or drink. They may show incoordination (ataxia), become recumbent, and show other neurologic signs such as head pressing and seizures.

Temperature, heart and respiratory rates are elevated and after cessation of exercise show a delayed return to resting values. Although the heart and respiratory rates of an exhausted and a non-exhausted horse may be similar immediately following exercise, these rates return to normal (heart rate <60 bpm, respiratory rate <25 breaths/min) within 10 to 20 minutes of exercise cessation in the non-exhausted horse but not in the exhausted one. Rectal temperature may be 42°C or higher. However, measured rectal temperature may be lower than true body temperature if the horse has diminished anal sphincter tone. Respiratory rate is elevated in an attempt to increase respiratory heat loss; heart rate is elevated to maintain cardiac output. Auscultation of the heart may reveal cardiac irregularities, capillary refill time is increased and both pulse pressure and jugular distensibility are decreased.

Dehydration is expressed clinically as decreased skin turgor, sunken eyes, dry mucous membranes, firm, dry feces and decreased urine output. Mild signs of dehydration usually become apparent at a body water deficit of 4–5%. Subjectively, the sweating response may appear inappropriate relative to the level of hyperthermia (e.g. a patchy appearance or, in severe cases, a hot and dry coat). Despite significant dehydration, affected horses often are not interested in water or feed. Intestinal stasis commonly occurs with decreased or absent borborygmi, poor anal tone and, occasionally, colic.2,3

In severely affected horses, a number of serious complications may develop immediately or over the following 1–4 days. These complications include exertional rhabdomyolysis, renal failure secondary to muscle necrosis and myoglobinuria, hepatic dysfunction, gastrointestinal dysfunction, laminitis and central nervous system disorders. Despite intensive supportive care, the horse may die.

Laboratory examination

In an exhausted horse, early clinicopathologic findings include increased packed cell volume (PCV) and plasma protein concentration due to dehydration, normo- or slight hyponatremia, hypokalemia, hypocalcemia (ionized), hypochloremia, and azotemia.1–3 The PCV of endurance horses eliminated from races due to metabolic problems may be as high as 55–65%, while plasma protein concentration may exceed 10 g/dl (typical reference range, 5.9 to 7.5 g/dl). As a result of muscle exertion or damage, increases in muscle enzyme activity (e.g. creatine kinase, CK; and aspartate amino transferase, AST) and plasma phosphorus concentration may be evident. Plasma creatinine values may be elevated, suggesting a reduction in glomerular filtration rate because of dehydration. Urine samples appear dark due to myoglobinuria, hematuria, proteinuria and glycosuria.^4,5 Serum electrolyte concentrations may be decreased (especially, K⁺, Cl⁻, Ca²⁺ and Mg²⁺). Metabolic alkalosis is the most common acid–base disturbance although metabolic acidosis may develop in horses with profound hypovolaemia and circulatory shock.⁶ Metabolic alkalosis along with hypocalcemia and hypokalemia contribute to the development of SDF. Profound neutropenia with a left shift is sometimes observed within 24 h of the onset of exhaustion.³

It should be noted that laboratory evidence of muscle damage as well as disturbances in electrolyte and acid–base balance also may be present in horses that successfully complete endurance races. Conversely, some exhausted horses may not show substantial alterations in clinicopathological variables at the time of diagnosis. During endurance races, muscle enzyme activities and serum creatinine concentration increase as a function of distance covered and in one study were not useful for the early diagnosis of metabolic stress.⁷

Necropsy examination

Necropsy findings include skeletal and myocardial muscle damage, gastrointestinal ulceration, renal necrosis and sometimes renal infarction as well as laminitis.⁸

Diagnosis

Diagnosis is based on history, clinical signs and laboratory findings. Although diagnosis is straightforward in severe cases, early recognition of the exhausted horse is difficult due to the subtlety of clinical signs and lack of objective clinical and/or clinicopathological diagnostic criteria. Careful observation during rest stops is essential to identify horses at risk of severe exhaustion. A lack of interest in feed or water in the face of dehydration indicates the need for aggressive intervention, including elimination from the race and prompt initiation of fluid therapy.

Therapeutic aims

Cooling the overheated horse and fluid therapy to replace fluid and electrolyte losses and to assist in restoration of circulating blood volume are essential components of therapy.

Therapy

Exercise must cease to minimize further damage and a horse with marked hyperthermia (rectal temperature 41°C or greater) should be cooled down as quickly as possible. Repeated application of cool or cold water by sponges or by hosing down and ventilation via a natural breeze or a fan will enhance heat loss via convection and evaporation. Ice-water enemas can be effective in a severely compromised patient. Cooling should continue until the body temperature is reduced to nearly normal (<39°C).

For mildly affected horses, rest together with cooling out and access to water, salt and feed may be sufficient. However, fluid therapy is required if the horse does not drink or eat within 15–30 minutes. In severe cases, fluid therapy should be started immediately. Under most circumstances, it is better to treat a horse in the field and not to attempt a trailer ride until it has been rehydrated. Oral fluid therapy may be considered in mildly affected horses that have adequate gut sounds and no evidence of colic. Oral fluid administration offers the advantages of speed and convenience and can be used if the horse has normal gut sounds. Between 4–8 L of fluid can be given via nasogastric tube every 30–60 min until the horse shows signs of improvement. Oral administration can be started immediately after exercise, because consumption of 10–15 L of cool (~16°C) water within 3–5 min of completing exercise is not harmful.9,10 Isotonic solutions containing sodium, potassium, calcium, chloride and glucose are often well tolerated and fairly rapidly absorbed. Commercial electrolyte powders should be those formulated for horses. For example, electrolyte formulations designed for use in calves with diarrhea usually contain bicarbonate, lactate or citrate. Therefore, these preparations are not the best choice for the treatment of horses with exercise-induced dehydration because of their alkalinizing effects. The oral administration of hypertonic solutions should also be avoided because they may cause a transient reduction in plasma volume due to movement of water into the bowel lumen.^9,11 Oral administration should be halted if any discomfort or gastric reflux becomes apparent.

Many exhausted horses are severely dehydrated (fluid deficits in the range of 30 to 60 L) and/or have evidence of compromised gut function (absent gut sounds, gastric reflux), thus necessitating use of the intravenous (i.v.) route. The rate of fluid administration will depend on the extent of hypovolemia and dehydration. In general, a 14-gauge jugular catheter is adequate for delivery of i.v. fluids; however, a larger-bore catheter (10- or 12-gauge) and/or the insertion of a second catheter may be indicated in severely affected horses to facilitate a rapid rate of fluid administration during the first hour of therapy. The initial rate of fluid administration should be in the range of 15 to 20 ml/kg/h (7.5 to 10 L/h for a 500 kg horse). The subsequent rate of fluid administration should be based on ongoing clinical assessment. Some horses will require as much as 60–80 L of fluid over a 6–12 h period, while others will show marked clinical improvement after receiving 20–25 L (e.g. restoration of gut sounds, initiation of eating and drinking) and may not require further i.v. fluid therapy. Preferred fluids are isotonic or only slightly hypertonic solutions containing sodium, potassium, chloride, calcium and glucose (e.g. Normosol-R or Ringer’s solution with 5% glucose). An alternative is 0.9% saline with glucose and potassium added: 1–3 g of potassium chloride/L and 5 to 10 g of glucose/L. The added glucose will also assist in the replacement of energy deficits. In horses with SDF, a 23% calcium borogluconate solution (100 to 300 ml) should be administered by slow i.v. infusion. Calcium should be added to the fluids of horses with evidence of hypocalcemia (ionized calcium <1.25 mmol/L); correction of hypocalcemia may help to improve gastrointestinal motility.

Lactated Ringer’s solution (LRS) is not the ideal fluid choice because exhausted horses often have metabolic alkalosis; however, the volume of administered fluid rather than its composition is of primary importance for correction of hypovolemia and cardiovascular compromise, i.e. LRS should be used if it is the only sterile i.v. fluid available.

The use of hypertonic solutions (e.g. 1–2 L of a 7.5% NaCl solution) for resuscitation of severely dehydrated, hypovolemic horses is controversial due to concern that the administration of a hyperosmotic solution will exacerbate intracellular dehydration. In one study of endurance horses disqualified from a race for metabolic conditions, the administration of 2 L 7.2% NaCl in combination with 5 L of LRS solution resulted in greater decreases in PCV, total plasma protein, and albumin concentration and earlier onset of urine production when compared to treatment with LRS alone.¹² It was concluded that the i.v. administration of hypertonic solutions appears to be safe in the treatment of dehydrated endurance horses but this treatment must always be accompanied by the administration of isotonic fluids for correction of fluid deficits.¹²

The administration of non-steroidal anti-inflammatory drugs (NSAIDs) and phenothiazine agents such as acepromazine should be avoided during the initial phase of treatment of the exhausted horse. Renal perfusion during hypovolemia is in part dependent on the local production and action of prostaglandins I₂ and E₂. As such, the administration of NSAIDs that block prostaglandin synthesis may compromise renal blood flow in dehydrated or hypovolemic horses and increase risk for NSAID toxicity. The administration of acepromazine may potentiate hypotension in exhausted horses due to its peripheral vasodilatory effects. Treatment with NSAIDs – flunixin meglumine (0.5–1.0 mg/kg), phenylbutazone (2.2–4.4 mg/kg) or ketoprofen (0.5–1.0 mg/kg) – for control of pain and inflammation can be initiated once the horse has received sufficient fluids to induce diuresis. The lower end of the recommended dosage range should initially be used.

A thorough physical examination, including evaluation for gastric reflux, palpation per rectum, and abdominal ultrasonography, should be performed in horses with colic. Ileus appears to be primary cause of colic pain in exhausted horses and the colic often resolves with fluid therapy and an improvement in intestinal motility. Pain should be managed with xylazine (0.33 to 0.55 mg/kg i.v.), butorphanol (0.01 to 0.02 mg/kg i.v.), or a combination of the two. Surgical lesions (e.g. small intestinal volvulus) have been reported in endurance horses after racing;³ repeated examinations are therefore imperative for horses that show persistent colic in the face of medical treatment.

Close clinical monitoring is indicated during and after initial treatment for exhaustion, including the frequency and volume of urination, serum BUN, creatinine and electrolyte concentrations, gastrointestinal function (gastric reflux, gut sounds, fecal characteristics), and clinical signs of laminitis (foot pain, increased digital pulse amplitude and hoof wall temperature). Intravenous fluid therapy should be continued in horses with evidence of compromised renal function (i.e. persistent azotemia and/or oliguria). Treatment with furosemide (loading dose of 0.15 mg/kg i.v., followed by a constant-rate infusion [CRI] of 0.12 mg/kg bwt per hour) should be considered if ongoing fluid therapy fails to induce an increase in urine production. In hypoproteinemic horses (e.g. secondary to diarrhea or renal disease), colloids and/or plasma may be necessary to limit development of pulmonary or peripheral edema. The initiation of laminitis prophylactic treatments (e.g. digital cryotherapy, aspirin 15 mg/kg per os every 24 or 48 hours) should be considered although the efficacy of these measures for prevention of laminitis in exhausted horses is not known.

Some clinicians advocate the administration of broad-spectrum antibiotics (e.g. a combination of procaine penicillin and gentamicin) and anti-endotoxin medications (e.g. polymyxin B, 3000 iu/kg, i.v., every 12 hours) to counter sepsis and/or endotoxemia, particularly for exhausted horses with profound leukopenia.

Prognosis

Prognosis is good for mildly and moderately affected horses; these horses generally respond to conservative treatment and can be returned to training after 1–2 weeks of rest. The prognosis for more severely affected horses is guarded; some exhausted develop serious sequelae that lead to death or necessitate euthanasia.