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Myopathy is a disease that affects either muscles, or muscle tissues, whether it be cardiac, skeletal or smooth muscle tissue (Harari 2019). Muscular myopathies may present in for several reasons. This could be due to electrolyte imbalances caused by nutritional deficiencies or superfluities, such as hypokalemia and hyperkalemia respectively (Chawla 2011). Myopathies can also present due to other reasons such as cancer, inflammation, poisons, muscular injury as well as other metabolic disorders.
Hypokalemic polymyopathy is a disorder commonly defined and characterized as generalized muscle weakness (Harari 2019). This muscle weakness is usually painless (Chawla 2011). Another clinical sign that usually presents in felines is ventroflexion of the head (Phillips & Polzin 1998). Ventroflexion of the head is described as the flexion of the neck or cervical spine towards the ventral surface. Additional clinical signs include a stilt gait that is stiff (Phillips & Polzin 1998). Physiologically, cardiac arrhythmias may be present, and increase in severity with regards to the progression and severity of the disease (Phillips & Polzin 1998).
It arises as a secondary disorder to hypokalemia (Harari 2019). The results of having hypokalemia extracellularly, causes the cell membrane of muscles to hyperpolarize, which then cause “secondary excessive permeability to sodium” (Harari 2019). The end result is the hypopolarization of muscle cells ensuing in eventual muscle weakness (Harari 2019).
For all intents and purposes hypokalemia with regards to myopathy in felines will be discussed. Within the body there exists a potassium balance. This is dictated by the total intake and absorption of potassium within the gastrointestinal tract (which goes unregulated) of the animal and the total excretion of the ion by the urogenital system of the animal, more specifically, the renal system (Constable 2019). Potassium is transported both actively and passively in gastrointestinal tract. It moves passively through the small intestine and actively in the colon by way of the hormone aldosterone (Constable 2019). Aldosterone is an instrumental hormone with regards to the excretion of potassium (Constable 2019). It is released by the adrenal gland, to combat the presence of hyperkalemia within the body (Constable 2019).
Potassium is regulated and determined by a simple balanced relationship between the amount of potassium consumed and the amount of potassium excreted by the body, which is typically balanced (the same amount of potassium ingested equals the amount of potassium excreted) (Phillips & Polzin 1998).
The majority of potassium in the body (~95%) is found to be intracellular, while skeletal muscle contains the bulk of the intracellular potassium (anywhere between 60%-75%) (Constable 2019). Any change in extracellular potassium concentration will result however, in a change of cellular resting membrane potential (Manning 2001). This is not achieved by potassium alone. Potassium also works in combination with sodium and ATPase, in which potassium is kept at high concentrations intracellularly versus extracellularly (Manning 2001). This is the primary reason for the negative electric potential throughout cell membranes (Constable 2019). The normal membrane resting potential found in skeletal muscle is -90mV, a cell reaches the threshold for membrane potential as sodium ions diffuse into the cell and potassium ions exit the cell, this is when both depolarization and action potential transpire (Phillips & Polzin 1998). Skeletal muscle has a normal threshold membrane potential of -60mV (Phillips & Polzin 1998). This causes nerve excitation, nerve impulse conduction, and muscle contraction, more specifically, skeletal and cardiac muscle (Phillips & Polzin 1998). There is a direct correlation between cell excitability and the difference between resting and threshold membrane potential, which causes the cell to become more excitable when there is a smaller difference between resting membrane potential and threshold membrane potential (Phillips & Polzin 1998).
It is with the reduced extracellular potassium levels wherein lies the problem. This causes the charge of the resting membrane potential to become more negative (increasing negativity), therefore increasing the difference between both resting membrane potential and threshold membrane potential resulting in an increased time for repolarization and decreasing overall excitability (Phillips & Polzin 1998).
If the concentration of potassium increases extracellularly however, it disturbs the membrane potential of the cell, and causes instabilities within the neuromuscular junction (Manning 2001). The potassium that is found extracellularly, affects the propensity of cells to release action potentials, affecting muscle contraction (Gandolfi et al. 2012). This misfiring or lack of firing of action potentials by the cells can be moderately or severely incapacitating, in many cases, it can even become life-threatening if affecting say for instance cardiac muscle (Gandolfi et al. 2012).
With regards to blood chemistry analyses, the results are what would be expected from a patient with hypokalemic myopathy. On average, extracellular potassium levels are decreased anywhere less than 3.5mEq/L (Harari 2019). Blood serum analysis also reveals increased levels of creatinine, denoting kidney damage, or diminished renal function (Harari 2019). This is mainly due to the fact that the kidneys cannot filter or clear the creatinine from the blood, therefore it remains circulating throughout the body (Harari 2019). The analysis of blood serum also reveals obvious signs of muscle damage, more specifically cardiac muscle or skeletal muscle (Harari 2019). For all intents and purpose, we are interested in skeletal muscle damage with regards to hypokalemic polymyopathy. Creatine Kinase is an enzyme needed by muscle to function. The fact that this enzyme is found in blood serum, suggests that there is muscle damage and the enzyme has been release into the extracellular fluid for filtration and removal. The presence of this enzyme in blood serum coupled with the presence of creatinine and low extracellular potassium ion levels, leads us to believe that renal failure is the primary culprit, causing the hypokalemia, therefore resulting in polymyopathy. It has also been found that cats having hypokalemic polymyopathy, also present with low urine specific gravity (Harari 2019).
Hypokalemic myopathy is usually caused by one of two things, an increased urination and excretion of potassium, or a decrease of alimentary intake of potassium (Taylor 2000). This disease is commonly found in felines that have chronic renal failure (CRF), and cats that have a high acidifying diet (Taylor 2000). This disease has been documented in felines of any breed, sex or age, although Burmese cats seem to have a predisposition to the disease (Gandolfi et al. 2012; Taylor 2000). It is interesting to note that felines with either “polyuria, polydipsia, secondary to hyperthyroidism or anorexia” due to any cause are at a higher risk for developing hypokalemic polymyopathy (Taylor 2000). Polyuria and or polydipsia in patients seem to be a result “impairment of normal thirst
and urine-concentrating mechanisms “ (Phillips & Polzin 1998). Within the central nervous system, there seems to be an increase of the synthesis of the hormone, angiotensinogen II (Phillips & Polzin 1998). This hormone is responsible for the stimulation of the thirst center of the central nervous system. The more of this hormone that is synthesized, the thirstier the patient becomes (Phillips & Polzin 1998). This ultimately increases fluid intake and excretion of potassium ions from the body, resulting in low potassium ion concentration within the body (Phillips & Polzin 1998). This disease may also occur in patients whom are being administered a large amount of IV fluids, and those with anorexia, in turn causing metabolic alkalosis (Constable 2019). Cats may also develop hypokalemic myopathy when fed vegetarian based protein diets (LEON et al. 1992). These diets are usually potassium deficient and result in clinical signs of developing polymyopathy within about two weeks (LEON et al. 1992).
There are also other non-specific clinical signs that go hand in hand with hypokalemia, some more obvious than others. Physiologically, potassium is used for cell growth, overall volume, DNA, protein, and glycogen synthesis (Phillips & Polzin 1998). Knowing this, we can surmise that clinically, patients would present with growth retardation, decreased muscle mass, as is with the case of myopathy and polymyopathy (Phillips & Polzin 1998). We would similarly also observe weight loss, especially if anorexia is present, and very poor hair coat (Phillips & Polzin 1998).
As previously stated, hyperkalemia has been found to be a predisposition in Burmese cats (Gandolfi et al. 2012). This disease in known as Burmese hypokalemic periodic
polymyopathy (BHP) otherwise known as Feline hypokalemic periodic paralysis (Gandolfi et al. 2012). This disease as it relates to Burmese cats is a genetic abnormality, thought to be an autosomal recessive trait in the Burmese cat breed (Gandolfi et al. 2012). Interestingly, the condition has been described in Burmese cats from the UK, New Zealand, Australia, the Netherlands, and throughout Europe (Gandolfi et al. 2012). The disease however, has not been identified in the Burmese cat population within the United States (Gandolfi et al. 2012). The clinical signs for Burmese hypokalemic periodic polymyopathy vary slightly, from episodic to unremitting (Gandolfi et al. 2012). Unlike in hypokalemic myopathy, myalgia from the result of palpation is a common sign, but much like the aforementioned disease, patients present with generalized muscle weakness and have a crouching gait, which is more prominent in the hind limbs (Gandolfi et al. 2012). Burmese hypokalemic periodic polymyopathy usually becomes apparent anywhere between two to six months of age, and up to two years in some cases (Gandolfi et al. 2012). Clinically, the disease may be prompted by stress or exercise (Gandolfi et al. 2012).
There are ways to diagnose hypokalemia if clinical signs are not very well apparent or defined. Firstly, a history must be taken, as well as a physical exam, secondly, blood chemistry analyses should be performed, paired with blood-gas analyses if needed for acid/base determinations, and finally a urinalysis to determine the loss of potassium via excretion by the urogenital system (Phillips & Polzin 1998).
In many instances hypokalemic myopathy and polymyopathy can be reversed or even managed successfully as long as there is either no renal disease present, or is acute (Gandolfi et al. 2012). The treatment for hypokalemic induced myopathy/polymyopathy is the supplementation of potassium (preferably orally, which is the safest and easiest way for owners), this can be either done in pill, powder, gel or liquid form, as with most calculated dosages, it must be adjusted accordingly depending on the response of the patient (Phillips & Polzin 1998). If the disease is severe, potassium fluid therapy may be warranted, cats with renal failure may however require higher dosages of potassium supplementation (Phillips & Polzin 1998).
- Chawla, J 2011, “Stepwise Approach to Myopathy in Systemic Disease”, Frontiers in Neurology, vol. 2.
- Constable, P 2019, Overview of Disorders of Potassium Metabolism – Metabolic Disorders – Veterinary Manual, Merck Veterinary Manual. viewed <https://www.merckvetmanual.com/metabolic-disorders/disorders-of-potassium-metabolism/overview-of-disorders-of-potassium-metabolism?query=feline%20myopathy%20hypokalemia>.
- Gandolfi, B, Gruffydd-Jones, T, Malik, R, Cortes, A, Jones, B, Helps, C, Prinzenberg, E, Erhardt, G & Lyons, L 2012, “First WNK4-Hypokalemia Animal Model Identified by Genome-Wide Association in Burmese Cats”, PLoS ONE, vol. 7, no. 12, p. e53173.
- Harari, J 2019, Muscle Disorders in Cats – Cat Owners – Veterinary Manual, Merck Veterinary Manual. viewed <https://www.merckvetmanual.com/cat-owners/bone,-joint,-and-muscle-disorders-of-cats/muscle-disorders-in-cats?query=feline%20myopathy>.
- Harari, J 2019, Feline Hypokalemic Polymyopathy – Musculoskeletal System – Veterinary Manual, Merck Veterinary Manual. viewed <https://www.merckvetmanual.com/musculoskeletal-system/myopathies-in-small-animals/feline-hypokalemic-polymyopathy>.
- LEON, A, BAIN, S & LEVICK, W 1992, “Hypokalaemic episodic polymyopathy in cats fed a vegetarian diet”, Australian Veterinary Journal, vol. 69, no. 10, pp. 249-254.
- Manning, A 2001, “ELECTROLYTE DISORDERS”, VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE, vol. 31, no. 6, pp. 1294-1300.
- Phillips, S & Polzin, D 1998, “CLINICAL DISORDERS OF POTASSIUM HOMEOSTASIS Hyperkalemia and Hypokalemia”, VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE, vol. 28, no. 3, pp. 545-564.
- Taylor, S 2000, “Selected Disorders of Muscle and the Neuromuscular Junction”, Veterinary Clinics of North America: Small Animal Practice, vol. 30, no. 1, pp. 59-75.
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