‘Hamburger thyrotoxicosis’ in a dog?
Ludo, an eight year old female entire Leonberger, was first referred to Southern Counties Veterinary Specialists in July 2016 due to idiopathic bilateral laryngeal paralysis. A unilateral arytenoid lateralisation procedure (laryngeal tie-back) was performed and Ludo made an excellent recovery, returning to completing hour-long daily walks with no difficulty. In March 2017 her owner noticed the recurrence of a rasping noise associated with Ludo’s breathing and a marked reduction in exercise tolerance. A therapeutic trial of prednisolone per os resulted in no improvement and so Ludo was referred back to Southern Counties Veterinary Specialists.
On presentation Ludo was bright, panting constantly with audible stridor and seemed anxious. On examination bilateral mild hind limb muscle atrophy was apparent and hind limb proprioception was slightly reduced.
A CBC and serum biochemistry panel revealed elevated hepatic parameters considered most likely to be related to the recent steroid administration. Failure of the sutures previously placed to abduct the left arytenoid, or fracture of the left arytenoid, were considered the most likely differential for Ludo’s recurrence of clinical signs. A small proportion of dogs with laryngeal paralysis are reported to require bilateral arytenoid lateralisation surgery to adequately address their upper respiratory tract obstruction however it seems logical to presume that if this were the case for Ludo, it would have been apparent soon after the surgery in July, rather than becoming the case eight months later.
Laryngeal examination performed under a light plane of anaesthesia revealed the expected degree of left arytenoid abduction following a tie-back procedure, and despite the persistent paralysis of the right arytenoid, there was subjectively plenty of room for air flow through the larynx. It was my impression that the rima glottidis was adequate in size, if irregular in shape, leading me to suspect that Ludo’s primary problem was excessive panting, and that this in the face of an atypically shaped rima glottidis was producing ‘incidental’ stridor.
Ludo was subsequently intubated and maintained on inhalant anaesthesia to facilitate additional investigations. Thoracic radiographs were acquired to assess for lower airway disease including aspiration pneumonia which is a life-long risk for dogs that have had a tie-back procedure. No abnormalities were detected.
Interestingly even when Ludo was intubated and at a surgical plane of anaesthesia, her breathing remained fast and shallow, further reducing suspicion for upper airway obstruction being the primary problem.
Ludo’s rectal temperature was 39.5C on admission and despite no active warming this steadily increased to 40C under anaesthesia, perhaps as a result of intense respiratory muscle activity. Following discussion with the neurology team regarding the possibility of a polyneuropathy underlying Ludo’s laryngeal paralysis, reduced hind limb proprioception and respiratory abnormalities, they recommended electromyography. This revealed no abnormalities. Unfortunately nerve conduction velocity testing produced uninterpretable results, possibly due to Ludo’s elevated temperature. Further serum was acquired to check her T4/TSH levels and Ludo was recovered from anaesthesia. Her temperature normalised and she was discharged home whilst we awaited the outstanding laboratory results.
Ludo’s serum total T4 returned an unusually high result of 106nmol/L (range 13-50) and cTSH was undetectable (<0.030ng/ml, range 0.0-0.6) so serum free T4 was requested. The free T4 was also elevated (58.6 pmol/L (range 7.0-40.0)), consistent with hyperthyroidism.
Hyperthyroidism is exceedingly rare in dogs and usually occurs as a result of thyroid carcinoma, though only occurs in 10-20% of thyroid carcinoma cases. Exogenous sources of thyroxine were considered and given that Ludo was fed a raw diet we particularly focussed on this. The raw diet was purchased frozen and Ludo’s owner mixed a few different items together each day. Most items were of known origin (e.g. tripe) but Ludo was also fed ‘economy mince’. A dietary change was made and the client reported resolution of the clinical signs. Total and free T4 and cTSH were rechecked four weeks later and were all within normal limits. The response is consistent with a dietary-induced hyperthyroidism. This has previously been described in dogs and also in humans in which it has been termed ‘hamburger thyrotoxicosis’ due to contamination of minced beef with thyroid tissue! Frustratingly we were unable to find a UK laboratory offering thyroxine testing in food so causality could not be proven. Nevertheless we are delighted that Ludo has returned to excellent health.
Karen would like to express her gratitude for the support of Ludo’s referring vet and practice, Alice McLeish of Forest Veterinary Clinic, to Ludo’s owner for her permission to share Ludo’s case details, and to her colleagues across multiple departments of the hospital for their support.