Weight Loss, Polyphagia, & Ataxia in a Cat

A 15-year-old, spayed female domestic shorthair cat presents with a 2-month history of weight loss and polyphagia and a 1-day history of ataxia.

The owners had noticed that the cat was becoming thin over the past 2 months, despite an increase in appetite. This morning the cat collapsed acutely and then appeared to be unable to move its hindlimbs. This indoor-only cat lives in southern Ontario, Canada, and has no history of travel outside of this area.

The cat is quiet and alert upon examination. Tachycardia is noted (heart rate, 220 beats/min), but respiratory rate and temperature are normal. A mass (approximately 1.5 cm diameter) is palpable in the ventral midcervical region. The body condition score is 2.5 of 5. The cat can stand with support, has voluntary movement in all 4 limbs, but has delayed placing and hopping reflexes in the hindlimbs that are worse on the left than the right. The remainder of the neurologic examination is normal, and no pain is elicited along the spine. The systolic blood pressure, measured via Doppler on the right mid antebrachium, is 195 mm Hg.

A complete blood count, serum biochemical profile, total T4 level, and urinalysis are performed. The only abnormality is a marked elevation in total T4 (12.35 mcg/dL; reference range, 1–4.3 mcg/dL or 159 nmol/L; reference range, 13–55 nmol/L).

1. What are the differential diagnoses in this case?
2. Where is the lesion localized?
3. What is the significance of the blood pressure measurement?
4. What are possible consequences of hypertension in this cat?

Hyperthyroidism is a common feline endocrinopathy, affecting up to 1 in 300 cats. The median age at diagnosis is 13 years, and the condition can result in multisystemic clinical signs. More than 98% of cases are due to nonmalignant changes of the thyroid, such as adenomas or hyperplasia.

1. Hyperthyroidism is the most likely differential diagnosis in light of the clinical description. Other differential diagnoses for cats with weight loss and polyphagia include diabetes mellitus, gastrointestinal disease, or malnutrition.
2. The neurologic deficits localize the lesion to the thoracolumbar spinal cord. Differential diagnoses include a vascular event (hemorrhage or infarct), disk disease, neoplasia, and aortic thromboembolism. Aortic thromboembolism was considered unlikely because of the presence of palpable femoral pulses bilaterally. In addition, the hindlimbs were not painful or swollen on palpation and had a palpably normal temperature.
3. A systolic blood pressure that is persistently ≥ 160 to 170 mm Hg in an awake, unstressed cat is consistent with hypertension. It can be difficult to accurately measure blood pressure in cats and dogs because stress will falsely elevate the readings.
4. Hypertension can occur in hyperthyroid cats and may damage vascular organs, such as the eyes, kidneys, heart, and nervous system.

Survey spinal radiographs in this case were normal. Spinal magnetic resonance imaging was declined by the owner. The cat was hospitalized for monitoring and received IV fluids for 24 hours. Treatment with amlodipine and methimazole was initiated.

The cat began ambulating with support over the next 24 hours, and began walking unassisted within the next 3 weeks. Mild ataxia persisted at a recheck 3 months after initial diagnosis. A vascular event was considered the most likely differential diagnosis in this case because of the im­­prove­­ment noted in response to supportive care.

Increased levels of circulating thyroid hormones affect almost all organ systems. Along with typical signs of hyperthyroidism—weight loss, polyphagia, restlessness, poor hair coat, polyuria, and polydipsia—hyperthyroid cats can show evidence of associated organ damage, such as cardiovascular abnormalities (eg, systolic murmur detected on physical examination or, less commonly, dyspnea secondary to congestive heart failure) and occasionally gastrointestinal signs (eg, intermittent vomiting).

The exact mechanism of hypertension developing secondary to hyperthyroidism in cats is unknown. Thyroid hormone excess is thought to cause beta-cell upregulation, leading to increased heart rate and cardiac output and resulting in an increase in blood pressure. In addition, increased stimulation of the renin–
angiotensin–aldosterone system may contribute to hypertension in hyperthyroidism.^1,2

Hyperthyroidism can be treated medically or surgically, or can be cured with radioactive iodine. Before treatment, the patient should be fully assessed to identify concurrent disease. Occult chronic renal insufficiency or heart disease may coexist with hyperthyroidism and will influence treatment plans.

Medical management of hypertension includes calcium-channel blockers, such as amlodipine (total dose, 0.625–1.25 mg PO Q 12–24 H, titrated as needed); ACE inhibitors, such as benazepril (0.25–0.5 mg/kg PO Q 12–24 H); or beta-blockers, such as atenolol (total dose, 6.25–12.5 mg Q 12 H). Beta-blockers may prove especially useful in hyperthyroid cats because of the effects of thyroid hormone on beta-receptors. Single-agent antihypertensive therapy may not be sufficient in controlling blood pressure in hypertensive cats, and it is common to combine medications for optimal therapy. ACE inhibitors are the least effective therapy for hypertension in cats.

Specific therapy for CNS vascular events in hyperthyroid cats has not been described. Because hypertension may be a causative factor in these events, control of hypertension is indicated. With proper nursing care, anecdotal experience suggests that neurologic deficits may begin to resolve within 3 to 4 weeks or more.

Hyperthyroidism is reported to be associated with the development of secondary hypertension. Hypertension was once thought to be common in cats with hyperthyroidism, with one report showing hypertension in 87% of hyperthyroid cats.² However, more recent reports suggest that a smaller proportion of hyperthyroid cats (up to 25%) are hypertensive.^1,3

Hypertension may resolve with control of the hyperthyroid state. However, because hypertension can lead to end-organ damage, antihypertensive treatment is indicated in cats that show evidence of ocular or CNS deficits or those with moderate to severe persistent hypertension (ie, systolic blood pressure ≥ 160–170 mm Hg on 2 or more occasions).⁴ In cats without evidence of end-organ damage, hypertension should be treated medically if it does not resolve once euthyroidism is achieved. Be aware that hypertension may first occur in cats whose T4 is controlled even if they did not have hypertension while hyperthyroid. In addition, one study reported that incidence of hypertension was greater in hyperthyroid cats after treatment than before treatment.³

Persistent hypertension may result in end-organ damage, including CNS vascular events. Head tilt, paresis, and paralysis have been associated with CNS vascular events in hyperthyroid cats.¹ Overall, neurologic clinical signs associated with feline hyperthyroidism are uncommon but should be considered in cats displaying neurologic abnormalities, especially those with concurrent hypertension.

For more information on hyperthyroidism, see the following articles:

Thyroid Hormone Concentration After Methimazole
Cardiac Biomarkers in Cats
Feline Hypertension