Hypokalemia-Induced Polymyopathy in an African Cheetah (Acinonyx jubatus jubatus)
IAAAM 2000
Douglas P. Whiteside1, DVM; Graham J. Crawshaw1, BVetMed, MS, MRCVS, DACZM; Tristan K. Weinkle2, DVM
1Toronto Zoo, Scarborough, ON, Canada; 2Angell Memorial Animal Hospital, Boston, MA, USA


A 2.5-yr-old male hand-reared captive African cheetah (Acinonyx j. jubatus) was examined for an acute onset of marked ventroflexion of the neck, hypermetria of the forelimbs, reluctance to walk, and ataxia. At the onset of clinical signs, the cheetah was still aware of its surroundings and responded to vocal commands. The previous day it had been observed roughhousing with another cheetah and had been chased into a perimeter fence. With the exception of some minor abrasions, no injuries were incurred.

After induction of anesthesia, initial diagnostics included physical examination, cervical radiographs, electrocardiogram (EKG), arterial oxygen saturation, end-tidal CO2 and indirect blood pressure measurements. Blood was collected for a complete blood count (CBC) and serum biochemical analysis. Cerebrospinal fluid (CSF) was obtained for analysis. A complete urine analysis was also performed.

The most significant abnormal laboratory finding was a marked hypokalemia (2.60 mmol/L, ISIS values = 3.9-4.7 mmol/L). Other abnormalities included a moderate increase in creatine phosphokinase (CPK, 1000 U/L, ISIS values = 0-451 U/L), a very mild increase in hematocrit (47%, ISIS values = 37-45%), mild hyperproteinemia (7.7 g/dl, ISIS values = 6.1-7.3 g/dl), mild hyponatremia (143 mmol/L, ISIS values = 154-162 mmol/L) and mild hypochloremia (106 mmol/L, ISIS values = 120-126 mmol/L). The EKG revealed T waves that were large and bizarre. The urinalysis, arterial oxygen saturation, end tidal CO2, and blood pressure were all within normal limits. No significant abnormalities were noted on cervical radiographs or CSF analysis, which greatly reduced the likelihood of a traumatic, infectious or inflammatory associated myelopathy as the cause of the clinical signs.

The clinicopathologic findings were consistent with a diagnosis of hypokalemic polymyopathy. Sedation was maintained in the cheetah for several hours with diazepam (0.12 mg/kg i.v., Diazepam, Sabex Inc., Boucherville, Quebec, Canada). Intravenous fluids containing 80 mEq/L of potassium chloride (KCl) were administered over a 3-hr period. An additional 25 mEq of KCl was administered rectally, late in the day, when the cheetah had recovered from anesthesia. Oral potassium supplementation (K-Lyte*/Cl, Roberts Pharmaceutical Canada Inc., Oakville, Ontario, Canada) was initiated at 25 mEq in food b.i.d.

Within 24 hrs of initiation of therapy, the cheetah was normokalemic (4.5 mmol/L). Oral supplementation was tapered down to 25 mEq KCl s.i.d for one more treatment, and then discontinued. Potassium levels remained normal over the next 5 days and no further episodes were noted. However, within 2 wk of discontinuation of therapy, hypokalemia (3.0 mmol/L) returned with concurrent normal serum sodium and chloride levels. The cheetah was noted to vomit on occasion during this time period. Urinary fractional electrolyte excretion values (FE) were determined to assess renal loss of electrolytes. While FEsodium and FEchloride were considered within normal limits, the FEpotassium was abnormal (26.8%, normal = 0-11.7%).3 When the cheetah had another episode of emesis that was followed by a brief period of spastic behavior, blood was collected, and serum biochemistry evaluation revealed that serum potassium had fallen to 2.9 mmol/L. Daily oral potassium supplementation was initiated at 26.6 mEq KCl (Kaochlor-20, Pharmacia Inc., Mississauga, Ontario, Canada). This dose was adjusted based on serum potassium levels. Currently the cheetah receives 20 mEq KCl s.i.d., and no further episodes of ventral cervical flexion, weakness or ataxia have been observed.

Based on the abnormal FEpotassium and the association of renal disease in cheetahs with, adrenocortical hyperplasia,2 further diagnostics are currently in progress to rule out hyperaldosteronism as a cause of the electrolyte abnormality. These diagnostics include comparative plasma aldosterone levels and urinary fractional electrolyte excretion in our captive cheetah population. Emetic losses must also be considered, due to the history of intermittent vomiting in this cat, and a predisposition of cheetahs in general to gastritis.8 Hyponatremia and hypochloremia can stimulate aldosterone release as a response to sodium depletion, causing renal retention and gastrointestinal uptake of sodium, with resulting excretion of potassium. However these stimulatory effects are considered minimal, thus with a moderate or marked hypokalemia, other causes should be considered.4,5

Although reported relatively frequently in domestic animals,5-7 hypokalemic polymyopathy is an infrequent finding in zoo species. Hypokalemia can arise from insufficient intake, increased gastrointestinal or renal loss of the electrolyte, or transcellular shifts.6,7 A genetic condition, hypokalemic periodic paralysis, has been documented in Burmese cats and humans.1,6 Clinical signs of hypokalemia often manifest in the neuromuscular and cardiovascular systems, due to an increased cell membrane potential with resulting hyperpolarization of membranes, leading to decreased excitability of the myocytes.1 Treatment of hypokalemia centers around eliminating the primary disease to minimize hypokalemic episodes. When clinical signs are present, parenteral or oral supplementation is indicated. Long-term oral replacement may be necessary while dealing with the inciting primary disease, and serum potassium levels should be regularly monitored.4,6,7


The authors acknowledge the assistance of C. Shilton, DVM, J. Taylor, DVM, DVSc, Dipl ACVP, and the animal care and animal health center staffs of the Toronto Zoo in the management of this case.


1.  Ahn A. 1994. Hyperaldosteronism in cats. Semin. Vet. Med. Surg. (Small Anim.) 9: 153-157.

2.  Bolton LA, L Munson. 1999. Glomerulosclerosis in captive cheetahs (Acinonyx jubatus). Vet. Pathol. 36: 14-22.

3.  Citino SB, EM Rush. 1999. Clinical challenge. J. Zoo Wildl. Med. 30: 314-317.

4.  Flood SM, JF Randolph, ARM Gelzer, K Refsal. 1999. Primary hyperaldosteronism in two cats. J. Am. Anim. Hosp. Assoc. 35: 411-416.

5.  Kaneko JJ, JW Harvey, ML Bruss (eds). 1997. Clinical Biochemistry of Domestic Animals. 5th ed. Academic Press, San Diego, California.

6.  Peres Y. 2000. Hyponatremia and hypokalemia. In: Ettinger S.J. and E.C. Feldman (eds.). Textbook of Veterinary Internal Medicine 5th ed. W.B. Saunders Company, Philadelphia, Pennsylvania. Pp. 222-227.

7.  Phillips SL, DJ Polzin. 1998. Clinical disorders of potassium homeostasis: hyperkalemia and hypokalemia. Vet. Clin. North Am. Small Anim. Pract. 28: 545-564.

8.  Wack RF, KA Eaton, LW Kramer. 1997. Treatment of gastritis in cheetahs (Acinonyx jubatus). J. Zoo Wildl. Med. 28: 260-266.

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Douglas P. Whiteside, DVM

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