Muscle Cramps in Two Standard Poodles With Hypoadrenocorticism
Two standard poodles were evaluated for painful, episodic muscle cramps affecting their thoracic and pelvic limbs. Both dogs had been diagnosed with hypoadrenocorticism and were being treated with fludrocortisone acetate and prednisone when evaluated for muscle cramps. However, the muscle cramping started approximately 1 month prior to the diagnosis of hypoadrenocorticism. Findings on general physical examination included lethargy and dehydration. Neurological examination was normal between episodes. Serum biochemical abnormalities included hyperalbuminemia, azotemia, hyponatremia, hypochloremia, and hyperkalemia. Altering treatment to desoxycorticosterone pivalate resolved the electrolyte abnormalities and the episodes of muscle cramping in both dogs. The authors conclude that hypoadrenocorticism can be associated with episodes of painful muscle cramping in standard poodles.
Introduction
Muscle cramps are prolonged, involuntary, painful muscle contractions.1 They are a common condition in humans, frequently occurring in apparently normal individuals (i.e., physiological cramps),2–4 but they are also induced by neurological, muscular, and metabolic disorders.34 The terminology for muscle cramps is confusing. The terms muscle spasms and muscle cramps are frequently used interchangeably. Involuntary muscle contractions can be subdivided according to a classification system developed by McGee into true cramps, contractures, tetany, and dystonia.3
True cramps are the result of motor neuron hyperactivity, as demonstrated by repetitive motor unit potentials on electromyography (EMG). The muscle contractions are focal and painful and are usually associated with muscle fasciculations.3 Causes of true cramps include diseases of the motor neuron itself (e.g., peripheral neuropathies, nerve root compression), electrolyte and fluid abnormalities (including those caused by high ambient temperatures, hepatic cirrhosis, and hemodialysis), exercise, certain drugs (e.g., alcohol, nifedipine, salbutamol, terbutaline), hypo- and hyperthyroidism, and diabetes mellitus.34 Physiological cramps are an example of true cramps for which the cause is unknown.134
Contractures are electrically silent on EMG. They occur when muscle energy supply is exhausted, resulting in cytosolic accumulation of calcium that prevents muscle relaxation. Metabolic muscle disease is the most common cause of contractures, and the signs are often seen following exertion.3 Tetany results from generalized nerve hyperexcitability, resulting in both motor unit and sensory nerve hyperactivity throughout the body. Humans with tetany report paresthesias at the onset of clinical signs, reflecting the involvement of sensory nerves. The paresthesias progress to sustained muscle contractions throughout the body, and generalized seizures may occur.3 The classic cause of tetany is hypocalcemia, but other electrolyte disorders (e.g., hypomagnesemia, hypokalemia) and respiratory alkalosis have also been implicated.3 Dystonia describes simultaneous contraction of agonist and antagonist muscles producing contortions, and it is caused by antipsychotic medications and repeated fine-motor tasks (e.g., occupational cramp).3 This classification system does not encompass all types of involuntary muscle contractions. For example, myotonia and structural muscle diseases are also important causes of muscle cramping.56 Myotonia is a failure of muscle relaxation associated with characteristic spontaneous discharges on EMG and prolonged contractures following percussion of a muscle (i.e., dimpling).5
In veterinary medicine, muscle cramps have rarely been documented as a presenting clinical sign.7–16 In this report, two standard poodles that were evaluated for episodes of involuntary muscle contractions that resembled true muscle cramps are presented. Both dogs were diagnosed with hypoadrenocorticism. The aim of this report is to describe the clinical characteristics of the muscle cramps exhibited by these dogs and the possible relationship between these muscle cramps and hypoadrenocorticism.
Case Reports
Case No. 1
An 18-month-old, 24-kg, castrated male standard poodle presented to North Carolina State University, Veterinary Teaching Hospital (NCSU-VTH) for evaluation of a 3-month history of episodic muscle cramps. The owner described sudden onset of rigid extension of a thoracic limb (either limb could be affected) that lasted for a few seconds. The muscle cramps occurred when the dog was moving or at rest. If moving when an episode occurred, the dog would protract the rigid limb by abducting it and swinging it forward. When he attempted to bear weight on the limb, it would frequently slide from under him, causing him to fall. The dog always maintained consciousness and was not lame between episodes. The frequency and severity of the episodes worsened over a period of 6 weeks, and the dog became progressively more lethargic. When vomiting and regurgitation developed, the dog was referred to NCSU-VTH. Serum biochemical abnormalities at the time included hyponatremia (130 mmol/L; reference range, 144 to 150 mmol/L), hyperkalemia (6.2 mmol/L; reference range, 3.5 to 4.7 mmol/L), and hypochloremia (101 mmol/L; reference range, 109 to 118 mmol/L). Hypoadrenocorticism was diagnosed based on absent serum cortisol response to exogenous adrenocorticotrophic hormonea (ACTH; 0.25 mg intramuscularly [IM]; cortisol preACTH, <0.45 μg/dL; reference range preACTH, 0.1 to 6.6 μg/dL; 1-hour postACTH, <0.45 μg/dL; reference range postACTH, 6.5 to 15 μg/dL).17
Treatment with fludrocortisone acetateb (0.4 mg per os [PO] q 24 hours) and prednisone (10 mg PO q 24 hours for 7 days, then 5 mg PO q 24 hours) was initiated, and the owners reported resolution of the lethargy, vomiting, and regurgitation. The muscle cramps also resolved initially; however, 1 month later they recurred and worsened in severity. The duration of the episodes increased up to 1 minute, and the contractions spread to involve two legs simultaneously (all combinations of thoracic and pelvic limbs occurred). Lethargy, vomiting, and regurgitation did not recur, and the dog appeared normal between episodes. Serum biochemical analysis revealed persistent hyponatremia (130 mmol/L) and hyperkalemia (5.8 mmol/L). Creatine kinase concentration was within reference range. The dose of fludrocortisone acetate was increased to 0.5 mg q 24 hours, and prednisone was continued at a dose rate of 2 mg q 24 hours, but the episodes did not resolve. Four days after increasing the fludrocortisone acetate dose, the dog developed muscle spasms in all four legs and appeared extremely agitated (interpreted by the owner as a response to pain). He was presented to NCSU-VTH the following day.
On physical examination, the dog was bright and alert, and all vital signs were within normal limits except for tacky mucous membranes and a capillary refill time of 2 seconds. Several episodes of muscle spasms were observed in the examination room. These involved both thoracic limbs (only one at any given time). The entire limb (shoulder to digits) would become rigidly extended for a few seconds at a time and could not be flexed manually by the clinician. During the episodes, the muscles felt hard and fasciculations were palpable. Percussion of the muscles with a plexor did not induce further contractions (i.e., “dimpling”). Cranial nerve examination during an episode was normal, but the dog appeared anxious and had an elevated respiratory rate. Neurological and orthopedic examinations between episodes were unremarkable. Hematological abnormalities included neutrophilia (22.7 × 103/μL; reference range, 3 to 11.5 × 103/μL), with 0.284 × 103 bands/μL (reference range, 0 to 3 × 103/μL) and monocytosis (1.7 × 103/μL; reference range, 0.15 to 1.35 × 103/μL). Serum biochemical analysis revealed hyperalbuminemia (4.1 g/dL; reference range, 2.8 to 3.8 g/dL), azotemia (blood urea nitrogen [BUN], 25 mg/dL; reference range, 6 to 23 mg/dL), hyponatremia (127 mmol/L), mild hyperkalemia (4.8 mmol/L), and hypochloremia (95 mmol/L). Calculated serum osmolality was low (270 mosm/kg; reference range, 285 to 310 mosm/kg). The calcium concentration was elevated (11.3 mg/dL; reference range, 8.8 to 10.7 mg/dL) but was within the reference range when corrected for elevated albumin (corrected calcium [measured calcium–albumin +3.5], 9.9 mg/dL). Serum ionized calcium was also within the reference range (1.28 mmol/L; reference range, 1.15 to 1.39 mmol/L). Urinalysis revealed minimally concentrated urine (urine specific gravity [USG], 1.018) with no other abnormalities. A thyroid profilec was unremarkable.
The dog was treated with a continuous intravenous (IV) infusion of 0.9% sodium chloride (2 mL/kg per hour for 24 hours), and the doses of fludrocortisone acetate and prednisone were increased (0.6 mg and 5 mg PO q 24 hours, respectively). Intravenous fluids were continued for 24 hours, and no episodes of muscle cramps were observed during this period. A serum biochemical analysis was repeated 12 hours after fluid therapy was discontinued. The azotemia had resolved (BUN, 19 mg/dL), and the electrolyte concentrations had improved but were not normal (sodium, 132 mmol/L; potassium, 4.9 mmol/L; chloride, 98 mmol/L). The USG was 1.024. Serum creatinine kinase was within reference range (46 IU/L; reference range, 28 to 97 IU/L). The dose of fludrocortisone acetate was again increased to 0.7 mg q 24 hours to address the electrolyte abnormalities. Neurological examination was repeated 48 hours after fluid therapy was discontinued. During the examination, the dog had another episode of muscle cramping in one thoracic limb; EMG was performed immediately after this episode, and no abnormalities were detected. The dog was hospitalized for an additional 24 hours (total 4 days’ hospitalization) without another episode and was discharged with owner instructions to administer 0.7 mg fludrocortisone acetate and 5 mg of prednisone PO q 24 hours. At the time of discharge, the dog was still hyponatremic (131 mmol/L), hyperkalemic (5.4 mmol/L), and hypochloremic (98 mmol/L).
After discharge, the owner reported that the dog continued to have intermittent episodes of muscle spasms when he was walking, and he was returned to the NCSU-VTH on the following day. Physical examination was unremarkable. Serum electrolyte analysis revealed persistent hyponatremia (130 mmol/L), hyperkalemia (5.4 mmol/L), and hypochloremia (94 mmol/L). Serum creatinine kinase concentration was slightly elevated (115 IU/L). Treatment with desoxycorticosterone pivalate (DOCP)d (60 mg IM, q 25 days) was initiated, and the fludrocortisone acetate was tapered over 5 days and discontinued. Treatment with prednisone was continued at a dose of 5 mg q 24 hours.
One week after DOCP administration, the dog was reevaluated. There had been no further episodes of muscle spasms since treatment with DOCP was initiated. The serum electrolyte concentrations were within the reference range (sodium, 146 mmol/L; potassium, 4.5 mmol/L; chloride, 117 mmol/L). Electrolyte concentrations were checked every 10 days over the following month and remained within the reference range. Over the past 3 years, the dog has received DOCP (50 mg IM, every calendar month) and prednisone (5 mg PO, q 24 to 48 hours). Electrolyte concentrations have remained within the reference range, and no further episodes of muscle cramps have been reported.
Case No. 2
A 30-month-old, 19-kg, intact female standard poodle was presented to NCSU-VTH with a 4-month history of painful muscle cramps affecting her thoracic limbs. The cramps were acute in onset. During each episode, one or both of her thoracic limbs became rigidly extended for a few seconds, the dog sat back on her haunches to avoid bearing weight on the affected limb or limbs, and vocalized loudly in apparent pain. Initially, the right thoracic limb was affected, but the episodes progressed to involve the left thoracic limb as well. Episodes occurred when the dog was at rest or moving, and the duration of the episodes increased from several seconds to a couple of minutes. The dog’s gait was normal between episodes. Approximately 1 month after onset of these signs, the dog was evaluated by her regular veterinarian for lethargy and intermittent vomiting. A thyroid profilec suggested a euthyroidsick response (free thyroxine, 5 pmol/L; reference range, 9 to 40 pmol/L; thyroid stimulating hormone, 21 mU/L; reference range, 0 to 30 mU/L), and no treatment was initiated. The lethargy and vomiting persisted, and the dog was reevaluated by her regular veterinarian 1 month later. An ACTH stimulation test was consistent with a diagnosis of hypoadrenocorticism (cortisol level, preACTH, 0.3 μg/dL; 1-hour postACTH, 0.5 μg/dL). Serum biochemical abnormalities noted at that time included hyperkalemia (6.0 mmol/L; reference range, 3.6 to 5.5 mmol/L) and mild hypochloremia (99 mmol/L; reference range, 102 to 120 mmol/L). Sodium concentration was low normal (140 mmol/L; reference range, 139 to 154 mmol/L).
Treatment with fludrocortisone acetate (0.3 mg PO, q 24 hours) and prednisone (5 mg PO q 24 hours) was initiated. Over 7 weeks prior to presentation to NCSU-VTH, the lethargy and painful episodes did not resolve, and the serum electrolyte levels fluctuated (sodium, 136 to 149 mmol/L; potassium, 5.0 to 6.3 mmol/L; chloride, 99 to 110 mmol/L) despite multiple adjustments in fludrocortisone and prednisone dose. During this period, the frequency of the painful muscle cramps increased from once every few days to twice a day. Radiographs of the thoracic limbs, including the shoulders, were unremarkable. The dog presented to NCSU-VTH 7 weeks after diagnosis with hypoadrenocorticism for evaluation of these episodes of painful muscle cramps and persistent lethargy.
On presentation, the dog was being treated with fludrocortisone acetate (0.5 mg PO q 24 hours) and prednisone (10 mg PO q 12 hours). In addition to the other problems, the owner reported that the dog had been polyuric and poly-dipsic (PU/PD) since starting treatment with fludrocortisone and prednisone. On physical examination, the dog appeared to be lethargic. Vital signs were normal, and physical examination was otherwise unremarkable. Neurological and orthopedic examinations were within normal limits apart from the lethargy. Percussion of the muscles of the thoracic limbs with a plexor did not induce muscle contractions (i.e., “dimpling”). Hematological and serum biochemical abnormalities included mature neutrophilia (21.4 × 103/μL), hyperalbuminemia (5 g/dL), and hypoglobulinemia (1.6 g/dL; reference range, 2.7 to 3.0 g/dL). Serum electrolyte abnormalities included hyponatremia (137 mmol/L), a potassium concentration at the high end of normal (4.7 mmol/L), and hypochloremia (98 mmol/L). Calculated serum osmolality was low (278 mosm/kg). Serum calcium concentration was high (11.4 mg/dL) but was normal when corrected for elevated albumin. Urine specific gravity was 1.007, and other results of the urinalysis were unremarkable. Serum creatinine kinase concentration was within the reference range (42 IU/L). Abdominal ultrasound was performed. The adrenal glands were bilaterally small, measuring 4 mm in diameter, and no abnormalities were noted with the other abdominal organs. Poorly controlled hypoadrenocorticism was suspected, and the dog was discharged with owner instructions to increase the dose of fludrocortisone acetate (0.3 mg PO, q 12 hours) and decrease the dose of prednisone (5 mg PO, q 12 hours).
Ten days later, the dog presented to NCSU-VTH for routine reevaluation. The owner reported continued lethargy and PU/PD, but no further episodes of muscle cramping had been observed since the medication was changed. Repeated blood work indicated mature neutrophilia (20.4 × 103/μL) and hyperalbuminemia (4.4 g/dL) with normal globulin levels. There was persistent mild hyperkalemia (5.0 mmol/L), and USG was 1.005. Urine culture was performed to rule out urinary tract infection as a cause of the low USG, and it was negative. Baseline total thyroxine was low (0.95 μg/L; reference range, 1.5 to 3.5 μg/L), but because the dog was being treated with corticosteroids at the time, treatment with thyroxine supplementation was not instituted. The continued PU/PD and lethargy were suggestive of glucocorticoid excess, and it was therefore decided to change her mineralocorticoid source from fludrocortisone acetate to DOCP (44 mg IM, q 25 days). The fludrocortisone acetate was tapered over 5 days and discontinued, and the prednisone was gradually decreased to 2.5 mg per day. The PU/PD resolved with these changes in medications. Treatment with thyroxine (0.5 mg PO, q 24 hours) was initiated empirically by the referring veterinarian 1 month later because of continued lethargy. Further thyroid testing was not performed.
Follow-up was obtained by telephone communication with the referring veterinarian and the owner of the dog. The dog has been treated with DOCP (44 mg IM, q 25 days) and prednisone (2.5 mg PO, q 24 hours) for the last year. The electrolyte concentrations have been checked every 3 to 6 months and have remained within reference range. The dog’s lethargy has improved, although it has not entirely resolved, and there have been no more episodes of muscle cramping. Polyuria and polydipsia have not recurred.
Discussion
This paper describes two standard poodles diagnosed with hypoadrenocorticism that presented with episodes of painful muscle cramping involving the thoracic and pelvic limbs. The characteristics of these episodes were almost identical in both dogs, although case no. 2 showed more pronounced signs of pain than case no. 1. The episodes appeared to be associated with electrolyte abnormalities (e.g., hyponatremia, hyperkalemia, hypochloremia) and fluid volume depletion secondary to hypoadrenocorticism. Correction of the electrolyte and fluid abnormalities was associated with resolution of muscle cramping in both dogs. The episodes of muscle cramping seen in these two dogs clinically most resembled true cramps in that they were focal, painful, self-limiting, accompanied by muscle fasciculations, and they could occur at rest or with exercise. Electromyography performed in case no. 1 between episodes was not consistent with a diagnosis of myotonia, and percussion of the muscles in both dogs did not elicit muscle contraction. As it was never possible to perform an EMG during an episode (the episodes were too brief), it was not possible to describe the electrophysiological characteristics of the muscle cramps.
There are few reports of true muscle cramps in the veterinary literature. Spastic syndrome in cattle is a progressive disorder in which movement initiates spasms of the muscles of the pelvic limbs and back.7–9 One description, which included morphological examination of muscles and peripheral nerves, did not report any histopathological abnormalities and concluded that the syndrome is a type of idiopathic or true muscle cramps.8 The authors were unable to find any report of “true muscle cramps” in dogs. Scottish terriers suffer from a disorder called “Scotty cramp,” in which exercise or excitement induces dramatic changes in gait and muscle hypertonicity that is not painful.9–11 Scotty cramp is believed to be caused by decreased levels of central nervous system serotonin11 and is more accurately described as hyperkinesis.9 Other similar disorders have been reported sporadically in other breeds of dog.12–14 Muscle cramps have also been reported in association with inherited phosphofructokinase deficiency in dogs.1516 As this disease is a metabolic disorder, these cramps are most likely properly classified as contractures.3
The pathophysiological basis of true muscle cramps is a controversial subject. It is now accepted that muscle cramps originate in the motor neuron rather than the muscle itself, because EMG during cramps shows repetitive potentials similar to motor unit potentials.1 Some groups theorize that motor unit hyperactivity results from abnormal feedback from peripheral afferents to the alpha motor neuron.118–20 However, others believe that the increased motor neuron activity originates distally, in the peripheral termination of the nerve close to the muscle fibers.232122 Many conditions are known to induce motor unit hyperactivity in humans. These include diseases of the motor neuron itself, such as amyotrophic lateral sclerosis, peripheral neuropathies, and nerve root compression.34 The dogs described in this report did not have any muscular weakness; neurological examination was normal; there was no muscle atrophy or hypertrophy; and EMG in case no. 1 did not show any spontaneous electrical activity. Their clinical presentations and subsequent resolution of signs were therefore not consistent with neuropathic disease, although a full electrophysiological and histopathological evaluation of their peripheral nervous system was not performed.
Fluid and electrolyte abnormalities are common causes of muscle cramps in humans and are the most likely causes of the cramps observed in these dogs. Total body salt depletion, with or without hyponatremia, can cause cramps (e.g., cramps associated with heat, dialysis, severe diarrhea).3423 Hyponatremia with normal or expanded total body sodium (e.g., water intoxication, congestive heart failure) does not cause cramps.3 Hypoadrenocorticism causes chronic salt depletion because of mineralocorticoid deficiency, and has been associated with muscle cramps in humans, although it is a rare finding.2425 Both dogs in this report were hyponatremic throughout the period of muscle cramping, presumably as a result of mineralocorticoid deficiency. Total body salt depletion in these dogs was suggested by signs of intravascular volume contraction, including prolonged capillary refill time, hyperalbuminemia, prerenal azotemia (i.e., increased BUN), and inability to concentrate urine in the face of dehydration.1726 The hypochloremia noted in these dogs may also have played a role in causing muscle cramps. Mutations in chloride channels that reduce chloride conductance cause myotonia in goats and in humans.2728 A decrease in chloride conductance causes an increase in sarcolemmal resistance, because chloride conductance accounts for about 70% of total membrane conductance at resting membrane potentials. At higher membrane resistance, less current is needed to trigger an action potential, and the membrane becomes more excitable.28 Decreases in chloride conductance also cause potassium accumulation in the T-tubules, leading to persistent depolarization of the membrane.28 The hypochloremia noted in both dogs of this report may have caused a decrease in chloride conductance and hence predisposed the dogs toward muscle cramping.
Hypovolemia and hypo-osmolality have also been incriminated as possible causes of muscle cramps in humans.29–31 Unfortunately, it can be difficult to separate hypovolemia, hyponatremia, and hypo-osmolality because these conditions are often concurrent, as illustrated by the dogs described in this report. Hyperkalemia is listed as a cause of muscle cramps432 and can be associated with muscular rigidity and fasciculations known as hyperkalemic periodic paralysis (HPP) in individuals with an underlying sodium channel defect.2833–35 However, HPP typically causes a combination of myotonia and paralysis not consistent with the signs displayed by the dogs in this report. The association of hyperkalemia with both extremes of muscular activity (i.e., myotonia and flaccid paralysis) in animals with sodium channel defects results from the effect of potassium concentrations on sarcolemmal resting potential. A mild increase in serum potassium concentrations causes a reduction in resting potential (i.e., partial depolarization) and so increases sarcolemmal excitability. However, further increases in potassium concentration reduce the resting potential such that it is less than the threshold potential. In this scenario, membranes cannot repolarize following depolarization, and flaccid paralysis ensues.28 The episodes of muscle cramping resolved in these dogs after correction of the electrolyte abnormalities and hypovolemia associated with their hypoadrenocorticism.
The response of the dogs in this report to treatment for hypoadrenocorticism suggests that electrolyte and fluid abnormalities triggered the muscle cramps. The authors were unable to find any other reports of severe muscle cramps in canine hypoadrenocorticism, although muscular weakness is a common finding.36–38 It is possible that other factors contributed to the generation of muscle cramps in these dogs. There was no evidence that the dogs had received drugs that can cause muscle cramping, and they did not appear to have other systemic diseases. Both hyper-and hypothyroidism have been associated with muscle cramps in humans,3940 and concurrent hypothyroidism and hypoadrenocorticism are not uncommon in dogs41 and have been reported in a standard poodle.42 Case no. 1 had a normal thyroid profile, and his signs resolved with treatment of the hypoadrenocorticism alone. Case no. 2 was eventually supplemented with thyroxine to address her persistent lethargy, but her muscle cramps had resolved with treatment of hypoadrenocorticism alone prior to initiation of thyroxine supplementation. Hyperadrenocorticism has been associated with the development of a myotonic myopathy in dogs.4344 Such dogs develop a stiff gait, and muscle dimpling can be induced by percussion of a muscle. Both dogs reported in this paper did exhibit signs consistent with increased glucocorticoid levels when being treated with fludrocortisone acetate. However, in both cases, the muscle cramping developed prior to initiation of treatment with fludrocortisone, and the episodes were therefore unlikely to be associated with glucocorticoid excess. Muscle biopsies would be useful in future cases in order to identify myopathic changes consistent with endocrine disease.
Both dogs were standard poodles, suggesting that they could have a genetic predisposition to muscle cramps. This could purely reflect the known predisposition of standard poodles to hypoadrenocorticism.3637 However, inherited muscle and nerve diseases can manifest primarily as muscle cramping.64546 Although the clinical presentation of these dogs makes such disorders unlikely, it is possible that inherited motor neuron dysfunction46 or ion-channel disease5 could predispose an animal to cramps in the face of electrolyte and fluid abnormalities. As poodles are also the breed that is most commonly affected with myotonia in association with hyperadrenocorticism,43 it is possible that poodles may have a genetic predisposition to disorders of muscle contraction triggered by endocrinopathies.
Hypoadrenocorticism causes both mineralocorticoid (i.e., aldosterone) and glucocorticoid (i.e., cortisol) deficiency in dogs.17 It is therefore possible that glucocorticoid deficiency caused the muscle cramps, although this has never been reported. Treatment of hypoadrenocorticism is aimed at supplementing mineralocorticoid and glucocorticoid hormones in proportions that are titrated to each individual’s needs. The most commonly used drugs are fludrocortisone acetate (mineralocorticoid and glucocorticoid activity), prednisone (glucocorticoid activity), and DOCP (mineralocorticoid activity). In both dogs described in this report, treatment with oral fludrocortisone acetate and prednisone was unsuccessful despite dose adjustment, whereas treatment with DOCP normalized electrolyte concentrations rapidly and was associated with resolution of the muscle cramps. This suggests that mineralocorticoid, rather than glucocorticoid deficiency, played an important role in causing the muscle cramps. It has been reported previously that DOCP is a more effective treatment for hypoadrenocorticism than fludrocortisone acetate in some dogs.1747 The reason for this is not clearly documented but may be related to the glucocorticoid action of fludrocortisone acetate that complicates dose titration.47
Conclusion
The painful muscle spasms exhibited by the two standard poodles described in this report were most consistent with true muscle cramps. These episodes of muscle cramps appeared to be associated with undiagnosed or inadequately controlled hypoadrenocorticism, and they resolved after serum electrolyte concentrations were normalized and hypovolemia was corrected. To the authors’ knowledge, painful muscle cramps associated with hypoadrenocorticism have not been reported previously in dogs. Hypoadrenocorticism should be considered in dogs with a history of painful episodes of rigid limb extension.
Cortrosyn; Organon, Bedford, OH
Florinef; Apothecon, Princeton, NJ
Michigan State University endocrine diagnostic laboratory; Michigan State University, MI
Percorten-V; Novartis, Greensboro, NC
Contributor Notes
