Clinical Vignette
History
Hank is a 6-year-old male intact Walker coonhound used for hunting trials. Six months ago, Hank developed progressive loss of stamina. He seems to improve after rest, but becomes very weak and tired with exercise.
During the past 7 days, Hank has developed copious salivation (see Chapter 25), difficulty swallowing food and water (see Chapter 26), and gagging and throwing up nondigested food (see Chapter 27). During the past 3 days, Hank has become very depressed and he has developed a moist cough (see Chapter 20). His vaccinations are current and he is given heartworm preventative.
Physical Examination
The temperature was 103.7°F, heart rate was 110 bpm, and the capillary refill time was less than 3 seconds. The oral mucous membranes were inflamed, oral ulcers were present, and the saliva was thick and foul smelling.
Hank is thin (body condition score 2.0/5.0) and depressed. Thoracic auscultation revealed fine crackles in the ventral lung fields (see Chapter 23). Hank gags when trying to swallow saliva. He shows generalized weakness after walking a short distance and his strength improves with rest.
Identify the problems in Hank and develop an initial plan complete with rule-outs and diagnostic procedures for each rule-out. Study this chapter to understand the causes of episodic weakness that might be affecting Hank and perhaps responsible for the other problems.
Problem Definition and Recognition
Weakness that occurs with exercise and dissipates with rest is termed episodic. It is recognized as early fatigue with mild exercise, although in some cases, more vigorous or prolonged exercise may be needed to induce the problem. Signs of weakness may include a short strided gait with or without ataxia, panting, reluctance to walk or run, lying down, and collapse. The animal may be alert or depressed. Following rest, muscle strength improves.
Pathophysiology
The correct approach to diagnosis of this problem is based on knowledge of the normal physiology of muscle function during exercise and at rest. In addition, the function of other organs that support muscle metabolism (i.e., by supplying oxygen, calories) during exercise must be considered. Diagnosis is based on knowledge of the neuromuscular events that control muscle fiber contraction and cardiopulmonary events that support exercising muscle fibers.
Muscle and nerves are tissues that generate electrical activity, called action potentials, along the cell membranes. Action potentials are generated by the movement of sodium and potassium ions through the cell membrane. The movement of these ions is controlled by calcium. Therefore, diseases that cause electrolyte imbalances may produce episodic weakness as their primary clinical manifestation. Table 4-1 describes the effects of various electrolyte disturbances on the production of action potentials and the resultant clinical signs or problems.
In the normal animal, skeletal muscle fibers are stimulated to contract by the lower motor neurons. The muscle fibers are connected to the nervous system via neuromuscular junctions (also called motor endplates). The motor endplate transmits electrical activity (action potentials) from the axon to the muscle fiber. Acetylcholine is the neurotransmitting agent released in the motor endplate that stimulates action potential production on the muscle fiber membrane. The release of acetylcholine is modulated by the calcium ion (see Table 4-1) and is inactivated by acetylcholine esterase enzyme. Thus, disturbances of calcium homeostasis or disorders that affect the activity of acetylcholine esterase may adversely affect neuromuscular transmission and can produce episodic weakness.
Table 4-1. Effects of electrolyte imbalance on the production of action potentials, motor endplate function, and muscle function
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