This consult concerns a 7-year-old female spayed Pit-bull. Her last veterinary examination was over 5 years ago. She presented today with the main complain of chronic diarrhea of 3-weeks duration. On exam, the dog was very lethargic, weak, and 7-8% dehydrated.

On her in-house screening blood tests, primary abnormalities included severe hyponatremia (113 mEq/L; reference range, 139-154 mEq/L) and hyperkalemia (6.5 mEq/L; reference range, 3.5-5.5 mEq/L). The sodium:potassium ratio was low at 17.

On her fecal examination, I found a large number of whipworm eggs on a very poorly formed, mainly liquid sample, so I suspect she is loaded with these parasites.

Based on the finding of whipworms, I suspect that she does not have true hypoadrenocorticism (Addison’s disease) but rather pseudo-Addison’s disease. Do you agree? Do I need to do an ACTH stimulation test on this dog?

Do these dogs need IV fluids and other supportive treatment or is just treating them for the whipworms going to resolve the electrolyte disturbances without further treatment? Do we need mineralocorticoid replacement (e.g., Florinef or Percorten)?

My Response:

These are severe electrolyte derangements and definitely should be addressed as an emergency. Therefore, I would definitely hospitalize the dog and very slowly correct the low serum sodium concentrations. If hyponatremia is corrected too rapidly, central nervous system dysfunction and death can result.

During the chronic hyponatremia, the brain adapts to prevent cerebral edema. With rapid correction of serum sodium concentration, osmotic shifts and cerebral dehydration can occur. This may result in CNS changes including central pontine myelinosis. This can lead to severe neurological signs, including generalized weakness, ataxia, mental depression, and head pressing several days following correction of severe hyponatremia (1,2). Thus, we are faced with a conflict between the need to rapidly correct the dog’s hypovolemia while ensuring the serum sodium concentration does not increase too rapidly.

In dogs whose sodium depletion has been chronic or is severe (Na < 120 mEq/L), sodium replacement must be cautiously and slowly corrected, such that serum sodium rises by no more than 0.5 mEq/liter/hour or 15 mEq/liter in a 24 hour period (1,2). Overzealous and too rapid correction of serum sodium to normal levels must be avoided.

If serum sodium is < 120 mEq/L, it may be better to avoid normal saline because of the high sodium content (154 mEq/L), and instead administer either Lactated Ringer's (130 mEq/L sodium) or Normosol-R (140 mEq/L sodium). Although these two fluids also contain a small amount of potassium, intravascular volume correction will offset the potential risk of exacerbating hyperkalemia. Hypertonic saline administration (strengths of 513 or 858 mEq/L sodium) is contraindicated in initial treatment of severe hyponatremia.

As far as the definitive diagnosis, whipworm (Trichuris) infestation is a well-known cause of pseudo-Addison’s disease and those parasites should be treated (3). I would also do either an ACTH stimulation test or at least a resting serum cortisol concentration to rule out true Addison’s disease. If the basal cortisol is normal (>2.0 µg/dl) and/or the cortisol response to ACTH stimulation is normal, then we can be more certain that the serum electrolyte imbalances are due to the whipworms (3,4).

As long as fluid therapy is being administered, mineralocorticoid supplementation should not be necessary. Hopefully, the serum cortisol results will be back within the next day or so and then we can decide if other treatment for Addison’s disease is required.

Follow-up Report:

A basal serum cortisol concentration on this dog was normal at 3.3 µg/dl (reference range, 1-4 µg/dl). She responded very well to the initial fluid therapy and deworming, with normalization of the serum electrolytes and resolution of all of her diarrhea and other clinical signs.

The final diagnosis was indeed pseudo-Addison’s disease secondary to severe Trichuris (whipworm) infestation.

References:

- Brady CA, Vite CH, Drobatz KJ. Severe neurologic sequelae in a dog after treatment of hypoadrenal crisis. Journal of the American Veterinary - Medical Association1999;215:222-225, 210.
- MacMillan KL. Neurologic complications following treatment of canine hypoadrenocorticism. Canadian Veterinary Journal 2003;44:490-492.
- Graves TK, Schall WD, Refsal K, et al. Basal and ACTH-stimulated plasma aldosterone concentrations are normal or increased in dogs with trichuriasis-associated pseudohypoadrenocorticism. Journal of Veterinary Internal Medicine 1994;8:287-289.
- Lennon EM, Boyle TE, Hutchins RG, et al. Use of basal serum or plasma cortisol concentrations to rule out a diagnosis of hypoadrenocorticism in dogs: 123 cases (2000-2005). Journal of the American Veterinary Medical Association 2007;231:413-416.


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