Q.  A 4-year-old FS Portuguese water dog presented to the emergency clinic in the evening for evaluation of weakness and lethargy.  The dog is hypotensive at 60mmHg with poor perfusion parameters.  The following abnormalities were found in laboratory testing:

BUN                 140

Creat                5.6

Phos                 10.4

Glu                  89

K+                   6.1

Na+                  118

Cl-                   84

Lipase             1487

Urine specific gravity was 1.058 and all other parameters were normal.  Addisonian crisis was suspected and an ACTH stimulation test submitted.  An IV catheter was placed for fluid therapy with normal saline and 0.1mg/kg of dexamethasone SP was also administered.  In the next 2 hours, the dog’s attitude and general strength dramatically improved.  Electrolytes were rechecked and produced the following values:

BUN    42

Glu      110

K+       5.2

Na+      129

Cl-       100

The dog was released the following morning for follow up with the rDVM the next day.  40 hours after initial presentation, the dog was rechecked by the rDVM.  The owner complained that the dog had started pacing overnight and was becoming increasingly fervent.  She also wasn’t responding normally to being called and had started showing a head tremor and stumbling in the last few hours.  Examination revealed compulsive pacing and wandering in the room with occasional stumbling.  She appeared to have mild to moderate dementia and mild obtundation with poor menace OU, cerebellar-like head tremor, and slow conscious proprioception in all four limbs.  Recheck electrolytes were:

BUN    18

Glu      126

K+       4.2

Na+      146

Cl-       128

The veterinarian calls you for a consultation.  What do you tell her based on this history and examination findings?

A.  It does appear correct that the dog’s initial presenting signs and laboratory values are consistent with hypoadrenocorticism.  This may be confirmed when the ACTH stimulation test results are available.  This disease does not specifically cause neurologic signs in otherwise stable dogs.  However, I am concerned that the treatment for her crisis may have contributed.  The sodium level changed 11mEq in 2 hours.  This is more rapid than the recommended limit of 0.5mEq/hour.  Dogs who have such a rapid shift in sodium can cause fluid shifts from the brain parenchyma into the blood stream to try to help achieve better osmotic balance.  These fluid shifts can lead to parenchymal dehydration significant enough to result in a delayed myelinolysis.  In dogs this can be pontine (as in humans), but more often thalamic in nature.  This can help to explain the changes in mentation, cerebellar-type movement, and compulsive pacing.  Unfortunately, at this stage the only treatment is supportive care.  This dog may continue to worsen and has the potential to progress to coma and death, so it is a good idea to monitor for serial neuro exams in the hospital.  If she remains stable, she can improve over time.  Some dogs may be able to return to normal.  Others may have permanent deficits like tremor and ataxia.  I like to tell people that dogs who are more severely affected are more likely to have permanent deficits.  In all cases, the rate and degree of improvement over the first couple of weeks will help to dictate expectations for the rate and degree of improvements overall.  For example, a dog who improves dramatically has a better chance of regaining normal or close to normal function over a shorter time period.  Dogs who show only small improvements have a better chance of incomplete recovery and overall slow recovery before plateauing. 

J Vet Intern Med. 1994 Jan-Feb;8(1):40-8.

Myelinolysis after correction of hyponatremia in two dogs.

J Am Anim Hosp Assoc. 1999 Nov-Dec;35(6):493-7.

Suspected myelinolysis following rapid correction of hyponatremia in a dog.

Can Vet J. 2003 Jun;44(6):490-2.

Neurologic complications following treatment of canine hypoadrenocorticism.