Common Medical Disorders That Can Affect Performance


Peak performance in the canine athlete requires a level of health that is quite different from the sedate dog. For there to be success, many physiologic parameters have to be normal and well integrated with an overwhelming number of interacting organ systems. Changes in the body’s ability to carry nourishment, supply energy, and remove waste efficiently are a miraculous integration of thousands of biochemical reactions. Many substances respond to disease states by increasing or decreasing their quantity per unit volume, which in turn can have profound effects on performance. Too much serum insulin or too little, poor intestinal absorption, and dehydration can all play a role in affecting serum glucose levels, raising or lowering it out of the normal range and yet, in each case, decreased performance might be the only clinical sign. Some diagnoses are harder to make and the signs themselves may be subtle. Patients with hypoadrenocorticism often have an atypical form of this disease, and both sodium and potassium values may be normal. Many of these patients are treated for gastrointestinal maladies, which then are blamed for the athlete’s poor performance. Electrolyte imbalances, endocrinopathies, failure to maintain adequate tissue oxygen, vascular abnormalities, inadequate nutrition, and nerve and muscle disorders are just some of the pathologies that can mildly to severely affect performance. A thorough and complete examination as well as appropriate preventive medicine and diagnostic testing are exceptionally important to guarantee that an athlete is going to perform at their best.

Electrolyte Imbalances


Hypoadrenocorticism, commonly called Addison’s disease is a failure of the two outer zones of the adrenal cortex to produce adequate amounts of either mineralocorticoids or glucocorticoids or both. In classic hypoadrenocorticism the mineralocorticoid and glucocorticoids are deficient, producing deficiencies of potassium and sodium exchange. Sodium is lost while potassium is retained producing an abnormal sodium : potassium ratio. Sodium and potassium are critical for maintaining an electrical differential across cell membranes. The concentrations of these two electrolytes are the basis for nerve conduction and muscle contraction. Atypical forms of this disease are becoming more frequently recognized.

Diagnostic tests commonly recommended:

  • Serum sodium
  • Serum potassium
  • Serum calcium
  • Serum glucose
  • Blood urea nitrogen BUN
  • Resting cortisol level
  • Adrenocorticotropic hormone (ACTH) stimulation test.

Common clinical signs:

  • Lethargy
  • Weakness
  • Bradycardia
  • Radiographic evidence of microcardia
  • Dehydration, vomiting, and diarrhea.

Clinical signs of hypoadrenocorticism are often vague and may be inconsistent. Gastrointestinal (GI) disease and overall weakness are common. In most cases replacement hormone therapy is successful and usually lifelong. There is a genetic predisposition in the Bearded Collie, Standard Poodle, Portuguese Water Dog, and Nova Scotia Duck Tolling Retriever.

Case Study 17.1 Athlete with progressive lethargy and GI upset


9 year-old M/N Labrador × Poodle mixed breed.


Rapid decline in activity. Had been an active disc dog showing no signs of slowing down 1 year before presentation. Owner describes patient becoming lethargic rapidly, starting ∼1 year prior to presentation. When moving quickly, he stumbled and showed very little interest in play. Difficult GI upset, R/O food allergies. Diets and medications had not helped.


Grades II/VI systolic murmur, point of maximum intensity: L 4th intercostal space, heart sounds bounding, pulses extremely thready and weak. No neurologic deficits.

Pertinent Laboratory Findings: 

Six months previous

  • Sodium 144 mEq/L
  • Potassium 5.0 mEq/L
  • Sodium/potassium ratio 29 (normal >30)
  • Normal abdominal ultrasound examination.

Three months previous

  • Sodium 149 mEq/L
  • Potassium 4.7 mEq/L
  • Urine specific gravity 1.048.


Any case requires the clinician to first ask whether all of the clinical signs and laboratory findings can be explained by a single coherent diagnosis. The cardiovascular changes, GI disease, and generalized nonspecific weakness could occur with numerous conditions but with borderline sodium and potassium values, it is reasonable to consider hypoadrenocorticism. ACTH stimulation test is an easy way to confirm this, and with a 24-hour turnaround time, it was decided to start there.

Resting cortisol was <0.7 µg/dL and poststimulation was <0.7 µg/dL, confirming a diagnosis of hypoadrenocorticism. Prestimulation resting cortisol should be 1–5 µg/dL. The patient’s cortisol levels did not change with ACTH administration. Patient had not been on any corticosteroids that might make the test results invalid. This is usually a very treatable disease although treatment is lifelong. It is rather common to have this condition with sodium and potassium that are not out of the normal ranges, as was the case here.

Hypocalcemia and Hypercalcemia

Calcium is critical for muscle contraction to occur. Abnormal calcium levels have profound effects upon muscle function. Total calcium concentrations are the sum of the ionized and nonionized fractions. To determine the actual physiologic calcium level, one must know the ionized value specifically.

Calcium availability is extremely complicated. Sources of calcium, phosphorus, and Vitamin D are in a constant state of flux. Parathormone oversees the absorption of calcium from the bone to maintain normal serum calcium levels, and is controlled through a feedback loop determined by the calcium levels in the serum. Vitamin D is critical in promoting calcium absorption in the intestines, but it is also involved in maintaining normal calcium and serum phosphorous levels for bone production.


Hypocalcemia is actually quite uncommon, though hypocalcemia secondary to birthing and nursing is well documented. The most common cause of hypocalcemia is iatrogenic, secondary to thyroid or parathyroid surgery. Hypocalcemia can be caused by a lack of Vitamin D in the diet, leading to nutritional secondary hypoparathyroidism or rickets.

Naturally occurring hypocalcemia secondary to primary hypoparathyroidism is quite uncommon. Hypocalcemia is quite devastating as so many neuromuscular functions depend critically upon calcium.

Diagnostic tests commonly recommended:

  • Total calcium
  • Ionized calcium
  • Parathyroid hormone
  • Vitamin D level.

Common clinical signs:

  • Seizures
  • Muscle tremors
  • Cramping
  • Aggression
  • Facial rubbing.

The diagnosis of hypocalcemia is critical as the clinical signs are serious and can progress quite quickly. Calcium replacement therapy is usually very successful.


Hypercalcemia in dogs is most commonly the sequela of a neoplastic process. In several cancers, parathyroid hormone (PTH), parathyroid hormone-related protein (PTHrP), cacitrol, and other tumor-produced hormonal factors will raise serum calcium levels. Parathyroid neoplasm(s) can pro­duce excess parathormone. Chronic renal disease has also been associated with hypercalcemia. Some home-cooked diets and some commercial pet foods may have excessive levels of Vitamin D leading to hypercalcemia (Dr. Tina Conway, pers. comm.).

Diagnostic tests commonly recommended:

  • Routine hemogram
  • Routine serum chemistries
  • Routine urinalysis
  • Serum calcium
  • Ionized calcium
  • Parathyroid hormone
  • Parathyroid hormone-related protein
  • Radiographs
  • Abdominal ultrasound.

Common clinical signs:

  • Polydypsia, polyuria
  • Reluctance to exercise
  • Depression
  • Inappetance
  • Weakness
  • Stilted gait.


Hypokalemia is common with excessive body fluid loss. Vomiting and/or diarrhea are the most common causes of hypokalemia as potassium in the GI fluid is lost. At the same time, animals frequently have a decreased intake during GI maladies. Any condition causing polyuria, such as renal disease or hyperadrenocorticism, can decrease the serum potassium level.

As potassium is a critical ion in maintaining healthy cell membranes, weakness and cardiac arrhythmias are commonly associated with its deficiency.

Diagnostic tests commonly recommended:

  • Routine hemogram
  • Routine serum chemistries, including electrolytes
  • Routine urinalysis
  • Serum potassium
  • EKG
  • Radiography
  • Abdominal ultrasound.

Common clinical signs:

  • Weakness
  • Cardiac arrhythmias.


Increases in serum sodium are usually from excessive loss of fluid (water) or excessive salt intake. Because dogs control temperature through respiration, increased panting without adequate replacement of fluid losses can also deplete total body water leading to dehydration. Diabetes insipidus caused by CNS-driven excessive thirst is rare, but also has been associated with hypernatremia.

As sodium is extremely important for healthy cell membranes, intracranial signs including seizures and disorientation can occur.

Diagnostic tests commonly recommended:

  • Routine hemogram
  • Routine serum chemistries
  • Routine urinalysis
  • Serum sodium.

Common clinical signs:

  • Abnormal mentation
  • Seizures
  • Weakness.

Hormone Imbalances

Diabetes Mellitus

The most common cause of canine diabetes mellitus is a lack of insulin secretion from the pancreatic beta cells. Insulin is necessary for effective man­agement of glucose, the main source of energy throughout the body. The neurologic component of long-standing or poorly controlled diabetes mellitus is of potential importance to the canine athlete. People commonly develop peripheral, particularly sensory, neuropathies in association with their diagnosis of diabetes mellitus. Although the nervous system does not require insulin to the same degree that other organs do to maintain normal health, the neuropathies are hard to avoid. Some motor neuron neuropathies are seen in dogs with uncontrolled diabetes mellitus.

Diagnostic tests commonly recommended:

  • Fasting glucose
  • Routine urinalysis
  • Glucose curve (while developing a treatment plan).

Common clinical signs:

  • Hind limb weakness


Hyperadrenocorticism in dogs has a large number of associated clinical signs, the severity of which varies widely. The condition is designated Canine Cushing’s Syndrome to distinguish it from the human disorder. All of the clinical signs of Canine Cushing’s Syndrome are the result of an excess of circulating corticosteroids. The adrenal glands that produce corticosteroids are under a feedback loop mechanism with a stimulating hormone, ACTH, produced in the pituitary gland. Pituitary-dependent hyperadrenocorticism occurs when too much ACTH is produced. Excess ACTH production can occur from a large neoplasm of the pituitary gland called a macroadenoma or a microscopic group of cells called a microadenoma. In some necropsies, neither can be found. A much less common cause of Canine Cushing’s Syndrome is an adrenal tumor. Dogs are placed on corticosteroids orally or by injection for a large number of conditions. If these doses exceed normal physiologic limits, iatrogenic hyperadrenocorticism can occur. Canine Cushing’s Syndrome has a propensity for smaller dogs but all breeds are at risk.

Diagnostic tests commonly recommended:

  • Routine serum chemistries
  • Urinalysis
  • ACTH stimulation test
  • Low-dose dexamethasone suppression test
  • Urine cortisol : creatinine ratio
  • High-dose dexamethasone suppression test
  • Endogenous ACTH concentrations
  • Radiography
  • Abdominal ultrasonography
  • Magnetic resonance imaging.

Common clinical signs:

  • Increased appetite
  • Polydypsia, polyuria
  • Hair loss
  • Pendulous abdomen
  • Enlarged liver
  • Polyphagia
  • Muscle weakness.

Hyperadrenocorticism is a very common disease, and the clinical signs usually occur gradually and are slowly progressive. It can be difficult to diagnose as many of the tests in common usage have an incidence of false negatives and false positives. Medical management, radiation therapy, and surgery are all possible treatments depending upon an accurate diagnosis.


Hypothyroidism is very common in dogs and is the result of idiopathic atrophy or immune-mediated thyroiditis. Dermal manifestations, such as alopecia, dry scaly skin, and hyperpigmentation are most commonly recognized. Although there has been a long-standing concern that hypothyroidism is associated with neuropathies, these findings have been very inconsistent, and replacement therapy often does not resolve the neurologic problems (Jaggy et al., 1994). One specific peripheral neuropathy, degeneration of the recurrent laryngeal nerves, causes decreased size and insufficient opening of the glottis. This condition is called laryngeal paralysis. The association between laryngeal paralysis and hypothyroidism is not straightforward, but there are quite a few references to it (Braund et al., 1989; MacPhail & Monnet, 2001).

Diagnostic tests commonly recommended:

  • Basal thyroid hormone concentration
  • Free thyroxine concentration
  • Serum endogenous canine thyroid-stimulating hormone concentration
  • Thyroid-stimulating hormone stimulation test
  • Thyrotropin-releasing hormone stimulation test
  • Antithyroglobulin antibodies
  • Thyroid hormone autoantibodies.

Common clinical signs:

  • Dermatopathies
  • Lethargy
  • Weight gain
  • Polyneuropathy including laryngeal paralysis.

Diagnosis of hypothyroidism is usually not a challenge as long as suspicion is raised. The diagnosis cannot be made on a single T4 value as this is not an accurate reflection of the patient’s thyroid status. Replacement therapy is generally successful although it can take months for the clinical signs to resolve.

Insufficient Oxygenation


Anemia refers to the lack of adequate red blood cells in the peripheral blood. Anemia is usually the result of one of three occurrences:

Jul 9, 2017 | Posted by in EQUINE MEDICINE | Comments Off on Common Medical Disorders That Can Affect Performance

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