Parathyroid Surgery
The major reason for parathyroid gland surgery is a condition called primary hyperparathyroidism. The parathyroid glands are a series of usually four tiny glands that lie in close proximity to the thyroid glands. In dogs, two of the glands (the caudal or internal parathyroid glands) actually come to reside within the actual thyroid gland on either side, while the remaining two (cranial or external parathyroid glands) lie near the top or front end of the thyroid gland, sharing a common capsule and blood supply with the respective thyroid gland. The parathyroid glands are important for the regulation of blood calcium levels. Calcium is important for many cellular functions, and blood levels are maintained by the body within a fairly narrow range. This regulation is complex, and involves such things as control of calcium absorption from the intestinal tract, excretion of calcium in the urine, and deposition or extraction of calcium from the bones. Several hormones are involved in this regulatory system, including Vitamin D, calcitonin (derived from special cells in the thyroid glands), and the hormone produced by the parathyroid glands, logically called parathyroid hormone or parathormone (PTH). These hormones and calcium itself work in an intertwined fashion to raise or lower blood calcium as required to maintain homeostasis, or normal balance.
Primary hyperparathyroidism occurs when (usually just) one of the parathyroid glands develops a tumor, and begins secreting excessive amounts of PTH. Normally, the secretion of PTH is controlled by a “negative feedback loop”. This means that the parathyroid gland cells can detect the level of calcium in the blood. If the calcium drops too low, the cells are stimulated to secrete PTH. Parathyroid hormone, in turn, and working in concert with vitamin D, acts to increase calcium absorption from the intestinal tract, decrease excretion of calcium in the urine, and mobilize calcium from the bones. All of these actions serve to raise the level of blood calcium. Once the calcium is restored to the normal range PTH secretion is turned off and the process ceases. In primary hyperparathyroidism the PTH secretion is not turned off, even as the calcium returns to the normal range, and therefore the body tends to have more calcium in the blood than needed or normal (hypercalcemia). Although there are other mechanisms by which the body responds to hypercalcemia to try and excrete the excess, these eventually become overwhelmed. The result is not only an increase in blood calcium (and urine calcium), but a gradual leeching of calcium out of the bones (very similar to osteoporosis).
Hypercalcemia may not produce obvious symptoms in the patient for some time. However, chronic hypercalcemia can cause decreased nerve function, decreased muscle function, and increased urination. Signs that might be seen in an affected dog therefore might include fatigue, weakness, excessive thirst and frequent urination, and in some cases calcium kidney stones. Bone pain is also possible. In addition, calcium itself can be toxic to the kidneys and cause progressive kidney failure. Finally, if for some reason the animal’s phosphorous level in the blood is also elevated, the combination of high calcium and high phosphorous can lead to mineralization (calcium phosphate) of various soft tissues in the body.
Some animals with hypercalcemia may be detected because of the signs above, but many are found during routine blood screening. Besides primary hyperparathyroidism, there are other causes for hypercalcemia. So, if your doctor detects hypercalcemia, he or she will usually order a battery of tests to determine the cause. Unfortunately, the most common cause for hypercalcemia is not a primary parathyroid gland problem, but other forms of cancer. Some tumors produce substances that are chemically similar to PTH. So even though the parathyroid glands are responding appropriately to the elevated blood calcium (i.e., they are “turned off”), these cancer-derived substances have effects on the target organs normally stimulated by true PTH. These conditions are called “pseudohyperparathyroidsm.” Treatment for this form of hypercalcemia depends on identifying and treating the underlying cancer.
One of the tests your doctor may order is a measurement of ionized calcium, along with actual determinations of PTH levels. In addition, some of the substances responsible for pseudohyperparathyroidism can be detected and measured as well (called PTH-related hormone, or PTH-rp). Ionized calcium refers to calcium in the blood not bound to proteins or other molecules. It is the active form of calcium that affects cell function and which the parathyroid gland “sees”. It is a more accurate way of determining if the patient is truly hypercalcemic. In simple terms, if a dog is hypercalcemic and has elevated (even normal) levels of PTH, the PTH-rp is negative, and no other cancer is found on blood tests, x-rays, ultrasound, etc., then the diagnosis of primary hyperparathyroidism is much likelier.
Once the tentative diagnosis of primary hyperparathyroidism is made, the next step is to identify the abnormal gland and stop its secretion of PTH. Because the parathyroid glands are tiny, even tumors of these glands are small (often less than an inch in diameter), and are not detectable by simply feeling in the neck. One method for examining the glands is to use ultrasound imaging. Ultrasound can also be used to guide non-surgical treatment of a parathyroid gland tumor. A needle can be placed into the abnormal gland and an alcohol solution injected that acts to kill the cells and destroy the gland. This treatment method avoids the risks and costs of surgery, but is not uniformly successful, and is not done by many veterinarians, even skilled and experienced ultrasonographers. Moreover, there is some risk for the alcohol to come into contact with other important structures (such as nerves that control larynx or voice box function), causing serious side effects. Another, similar method for percutaneous (non-surgical) ablation (destruction) is to use special probes that overheat the abnormal gland.
Most dogs with primary hyperparathyroidism will be treated with conventional surgery. This entails an incision in the bottom of the neck, identification of the abnormal gland, and removal of the gland without harming the adjacent thyroid gland (although sometimes it is necessary to remove the thyroid gland on that side as well) or other important structures. In rare instances a dog or cat might have ectopic (out of normal position) parathyroid glands lower in the neck, or even the upper part of the chest cavity, and surgery can allow for detection and treatment of these as well. Surgery itself is usually very well tolerated and not very painful.
Prior to surgery the surgeon will try to bring the calcium level closer to normal, so as to avoid any risks from anesthesia (since nerve and muscle function, including cardiac muscle, can be affected by the hypercalcemia). This might require the patient to be treated with intravenous saline solution for a while before surgery to try and promote excretion of calcium in the urine. Other drugs are also sometimes used to lower the calcium level.
The most common problem associated with surgical or non-surgical ablation of a parathyroid gland tumor is rebound hypoparathyroidism and hypocalcemia. Because the remaining glands are normal, they have been appropriately “turned off” and not producing PTH during all the time that the dog has been hypercalemic (often months, and sometimes years). Once the abnormal gland is removed, the stimulus for elevating blood calcium stops, and calcium is no longer leeched from the bones, or absorbed from the intestinal tract. The blood calcium level therefore begins to fall, as it should. However, if the remaining parathyroid glands have lost their sensitivity to low calcium, the blood calcium will continue to drop, even below the low end of the normal range. Some dogs never recover function of the surviving glands, while others do, but take weeks to months to do so. Many, fortunately, have no problem with the remaining glands, and so no complications ensue. One of the predictors for rebound hypoparathyroidism is the pre-operative level of calcium. Those dogs with calciums in the higher range (usually above 14 mg/dl) seem to be more likely to have this problem than dogs with levels less than this. Your doctor may discuss some strategies for trying to prevent this problem by treating the dog just before surgery with a synthetic vitamin D product.
If a dog develops hypocalcemia after surgery it may not do so for several days. For this reason, your surgeon may recommend that your dog be kept in the hospital for monitoring for 3-5 days after surgery. It is far better to detect hypocalcemia on a blood test than to wait until symptoms develop, since the symptoms are much worse than the hypercalcemia the dog had before surgery. Symptoms of hypocalcemia include restlessness, nervousness, rapid heart rate, muscle twitching, and facial itching. In severe cases that are not treated quickly enough the animal can have convulsions. Treatment depends on the severity of the hypocalcemia. Sometimes it can be managed with oral medications alone (usually using a calcium supplement and a vitamin D product), while some cases will require intravenous calcium treatments. Once controlled in the hospital, dogs will usually require oral calcium and vitamin D therapy for some weeks to months afterwards (or permanently if the other parathyroid glands never recover their function).
Most parathyroid gland tumors are benign, and even those that are malignant are usually cured with surgery. Most dogs with primary hyperparathyroidism are older (often >10 years of age), but this does not usually present a hindrance to successful treatment.