Endocrine System

Introduction

Adrenalectomy is most often performed for treatment of primary adrenal tumors (adrenal cortical adenoma, carcinoma, and pheochromocytoma). Rarely, adrenal resection may be used for treatment of metastatic tumors, sex hormone imbalances, and treatment of pituitary-dependent hyperadrenocorticism refractory to medical therapy. Adrenal tumors are often biologically active resulting in adverse physiologic alterations, and may invade the adjacent great vessels (vena cava, aorta, renal vein or artery). Clinical management and resection can be challenging. Surgeons must have a thorough understanding of the pathophysiology associated with adrenal diseases, be suitably familiar with the regional anatomy and make appropriate perioperative preparations to minimize complications and maximize treatment success.

Preoperative Management 

Routine diagnostic and staging tests recommended for adrenal masses include: complete blood count and serum biochemistry profile, thoracic radiographs, and abdominal ultrasound (including Doppler flow evaluation of great vessels for presence of tumor thrombus). For the majority of patients this collection of diagnostic tests is adequate for preoperative assessment. In selected patients, further imaging evaluation may be deemed necessary and abdominal CT (with contrast) and MR imaging provide excellent assessment of the adrenal glands and surrounding tissues.

Adrenal cortical tumors may produce excess cortisol and symptoms of Cushing’s disease. Where indicated by clinical findings, patients are evaluated by low dose dexamethasone suppression test (or similar assessment) prior to surgery. Hyperadrenocorticism can predispose patients to complications resulting from hypertension, delayed wound healing, immune suppression, and thrombosis. If testing confirms hyperadrenocorticism, preoperative adrenal suppression may reduce the risk of complications. Ketoconazole therapy (10 mg/kg q 12hours) is a rapid and safe method for suppression. The optimal duration of preoperative therapy to reverse adverse effects remains unknown, and further study would be valuable. Empirically, the authors find a 10 day course of treatment is effective. When significant hypertension is present, concurrent use of vasodilator therapy is also indicated (Table 37-1).

Pheochromocytomas can produce excess catecholamines resulting in hypertension, tachycardia, arrhythmias, and chronic myocardial changes. Patients should have blood pressure measured, and where indicated by relevant clinical signs, echocardiographic evaluation. For cases where definitive diagnosis remains difficult, catecholamine by-products can be measured in the urine (vanillylmandelic acid, metanephrine and normetanephrine).¹ When hypercatecholaminemia is present preoperative treatment with phenoxybenzamine and atenolol or propranolol can reduce anesthetic complications (Table 37-1). The optimal duration of preoperative catecholamine suppression is also unknown, however empirically the authors have found a 10-day course of treatment to be effective. When significant hypertension is present concurrent use of vasodilator therapy is also indicated (Table 37-1).
 

Surgical Anatomy

The adrenal glands are located craniomedial to the pole of each kidney in the retroperitoneal space. The left adrenal gland lies in loose collagenous connective tissue, is generally well localized, and easily visualized with retraction of the mesocolon. The right adrenal is less well localized from the adjacent structures and the capsule is often continuous with the outer tunic of the vena cava. In some animals the gland lies dorsal to the vena cava. Deep chested animals require substantial retraction of the mesoduodenum for adequate visualization. The adrenals have a rich blood supply and it is often significantly enhanced by tumor neovascularization. The renal artery and vein run along the caudal boundary of each adrenal gland and these vessels can be encroached upon and invaded as tumors enlarge. The phrenicoabdominal veins course dorsoventrally across the center of each gland and are frequently invaded by a tumor thrombus. The right adrenal vein empties into the caudal vena cava, and the left adrenal vein enters the left renal vein. Clinically relevant arterial supply is by multiple short branches located on the dorsomedial side of the glands arising from the aorta, renal, lumbar, and phrenicoabdominal arteries. Innervation is by preganglionic sympathetic nerve fibers from the splanchnic supply, and medullary cells are the postganglionic neurons (Figure 37-1).²
 

Surgical Approach

Adrenalectomy is best performed via ventral midline laparotomy. Though a paracostal retroperitoneal approach is described, the field of view is small making resection of larger tumors difficult or impossible. The ventral approach allows exposure to both adrenal glands, permits complete exploration of the abdominal cavity for identification and biopsy of suspected metastatic lesions, and provides exposure for intravascular thrombus resection or nephrectomy if necessary. Disadvantages are minimal but include risk of iatrogenic pancreatic injury and more severe consequences of wound dehiscence. On rare occasions in deep chested dogs, a right paracostal extension is needed. The laparotomy incision is continued dorsolaterally from the xiphoid cartilage, following 1cm caudal to the last rib. The rectus abdominis, external and internal abdominal oblique, and transverses abdominis muscles are incised respectively. Care is taken to avoid inadvertent incision of the diaphragm and creation of a pneumothorax. The formed abdominal muscle flap is retracted caudodorsally, exposing the craniolateral abdomen. Closure is by approximation of the abdominal wall at the junction of the combined ventral and paracostal incisions near the xiphoid cartilage followed by routine closure of the linea alba and each muscle layer of the paracostal incision.³

Patient preparation for caudal median sternotomy and anesthesia provisions for ventilatory support are readied if a tumor thrombus extends cranial to the diaphragm and access to the thoracic vena cava is needed. The neck may also be prepared to harvest a jugular venograft if significant caval involvement is suspected.⁴ Intraoperative complications should be anticipated and prepared for (Table 37-2).
 

Surgical Technique

Abdominal viscera are covered and padded with laparotomy sponges and retracted by hand or with malleable retractors. Retraction must be gentle in animals with hyperadrenocorticism as tissues are often friable and easily torn. The adrenal gland and retroperitoneal tissues are inspected for extent of local invasion, and the abdomen inspected for metastasis to the liver, regional lymph nodes, and along the sympathetic chain (pheochromocytoma). Biopsy specimens are procured from any suspected metastases.^5,6 The phrenicoabdominal vein, vena cava, ipsilateral renal artery and vein, and aorta are palpated for evidence of tumor thrombus. In the authors’ experience thrombus formation is by far most common in the phrenicoabdominal vein and vena cava. Renal vein thrombi are uncommon and aortic or renal artery thrombus formation is rare. After surgical staging is complete a resection plan is made and initiated.

Wide incision is made in the peritoneum around the mass and a combination of blunt and sharp dissection of surrounding fatty tissue and ventral paralumbar muscle fascia are utilized to isolate the mass in an envelope of normal tissue (Figure 37-2). It is generally easiest to work from the periphery of the mass towards the great vessels. If a tumor thrombus is present the authors prefer to completely dissect the adrenal tumor first, and then perform venotomy while using the tumor to tether the thrombus for manipulation. Attention to hemostasis is paramount to visualize fine anatomy, and keeping the tissues under constant tension allows delicate layer-by-layer dissection. The phrenicoabdominal vein is ligated, and hemostatic clips and electrocautery are used for occlusion of smaller perforating arteries (Figure 37-3). Though difficult, an attempt is made to isolate and ligate tumor blood supply as much as possible prior to extensive tumor manipulation to minimize iatrogenic hormone release. Careful technique and barrier sponges/material are utilized to avoid seeding the abdominal cavity with neoplastic cells.

When a tumor thrombus is present, additional preparation is made. If the thrombus is confined to the phrenicoabdominal vein a standard adrenalectomy is performed and the thrombus removed by ligation and en bloc removal of the phrenicoabdominal vein. Intracaval or aortic thrombi are removed by isolating the affected segment of vessel (and renal vessels if thrombus proximity requires occlusion more caudally) with Rumel tourniquets (Figure 37-4). Following complete tumor dissection, occlusion of blood flow is quickly implemented and the vessel wall at the site of tumor penetration is circumferentially incised with a #11 scalpel blade. The thrombus is removed by exerting traction on the tumor base and tethered thrombus with one hand, while the other hand is used to “milk” the thrombus out by extramural manipulation.⁵ The incision is extended as needed to allow thrombus removal without tearing the vessel wall. The lumen is lavaged and a partial occlusion clamp (Satinski or similar) is placed to permit vascular flow during suturing. The vessel wall is closed with a continuous suture pattern using 4-0 or 5-0 polypropylene. Air is displaced from the lumen by releasing the caudal Rumel tourniquet prior to tightening the final suture. The cranial tourniquet is released and the suture line checked for bleeding. Minor leakage is controlled with gentle pressure, and more significant leakage with placement of additional interrupted sutures. Vessel occlusion must be as brief as possible to avoid visceral injury.
 

Special Surgical Considerations

If the tumor thrombus extends cranial to the diaphragm, a caudal median sternotomy is performed to allow placement of a Rumel tourniquet cranial to the thrombus; removal is as described above.

En bloc nephrectomy is occasionally required because of tumor invasion into the renal vessels or parenchyma. The tumor and kidney are isolated en bloc before great vessel incision to minimize occlusion time and facilitate rapid thrombus removal.

When pheochromocytoma is suspected but tumor location is not evident, identification can be aided by a palpation induced increase in arterial blood pressure of a suspected mass, and subsequent decrease in pressure following removal (even if preoperative adrenergic blocking agents have been used). If blood pressure fails to decline, unidentified metastases are likely.

Nonresectable tumors are debulked if possible to decrease circulating cortisol or catecholamines and improve the efficacy of long-term medical management.⁶

Consider jejunostomy tube placement before closure when iatrogenic pancreatitis is of concern.

Complications and Postoperative Management

Adrenalectomy (particularly with thrombusectomy) is a demanding surgery. Minor complications are almost always expected, and provisions always made in preparation for major complications.

Intraoperative complications include bleeding, arrhythmias, hypotension, hypertension, and air embolism. Bleeding can arise from the adrenal (usually from dorsomedial short perforating arteries), or from retraction injury to the liver and pancreas. Adrenal artery hemostasis is best controlled with vascular clips or electrocautery. Organ parenchymal injuries are prevented by gentle retraction and padded covering with thick laparotomy sponges. Parenchymal bleeding is generally mild and easily stopped with pressure or application of topical hemostatic sponges. Cardiovascular complications mostly arise from catecholamine secretion and are largely preventable (Table 37-1). Use of crystalloid and colloid fluid supplementation will adequately manage most abnormalities; for more severe fluctuations in pressure or rhythm, drug therapy is indicated (Table 37-2). Air embolism occurs if the vascular lumen is not purged before final closure of vessel wall sutures.

Postoperative complications include adrenal insufficiency, pulmonary thromboembolism, infection, and delayed wound healing for adrenal cortical tumors; and arrhythmia, hypotension, and hypertension for medullary tumors.⁷ General complications include persistent organ parenchymal bleeding and pancreatitis from iatrogenic trauma.

Following unilateral adrenalectomy for cortisol producing tumors, glucocorticoid supplementation is required during and for a short period after surgery. Dexamethasone is administered parenterally until the animal is eating, and then oral prednisone is used for ongoing management. Glucocorticoid supplementation can generally be tapered by 6 to 8 weeks. Permanent glucocorticoid and mineralocorticoid replacement therapy is necessary in patients undergoing bilateral adrenalectomy (Table 37-3).^6,8,9 Risk of thromboembolic disease is reduced with heparin and low dose aspirin therapy and treatment is generally tapered as the patient stabilizes over 2 to 5 days. Supplementation with Vitamin A is used to offset cortisol induced delayed wound healing; treatment is generally discontinued at the time of suture removal. Infection is prevented by routine use of perioperative antibiotics; prolonged therapy is avoided except in cases where infection is documented or risk is significant.
 

Paradoxically, following adrenalectomy for catecholamine producing tumors, persistent or episodic hypertension or hypotension can occur. The cause remains unknown, but in people the fluctuations can be severe. Though arrhythmias can occur, incidence generally decreases after tumor removal since peptide hormones have a short half life. Adjustments to crystalloid and colloid fluid supplementation are adequate for management of most abnormalities; for more severe fluctuations drug therapy is indicated (Table 37-2).

Management of persistent parenchymal bleeding is by transfusion and conservative treatment such as abdominal pressure wrap. In severe cases reexploration may have to be considered. Pancreatitis is managed by traditional supportive therapy.

Prognostic factors remain incompletely defined for adrenal tumors, and even histologic grading and determination of malignancy can be difficult. In one study neurologic signs, abdominal distension, and weight loss were more frequently associated with advanced disease and a poorer prognosis.¹⁰ Prognostic factors in humans with pheochromocytomas that indicate malignancy are large tumor size, local tumor extension at surgery and DNA ploidy.¹¹ In dogs as in humans, clinical evidence of metastasis defines malignancy and the sites reported in the dog are lung, liver, spleen, kidney, bone, heart, pancreas and lymph nodes. About 50% of reported pheochromocytomas are considered malignant and long-term prognosis is undoubtedly poorer with metastatic or invasive disease. However reported survival times following successful resection, even with the presence of metastasis, range from 18 months to 2 years.^5,10,12 The frequency of caval invasion with pheochromocytomas in one report was 54%, and 11% with adrenocortical tumors. The right side was affected in 35% of cases and the left side in 20%. This study also determined that adrenalectomy with thrombusectomy did not significantly increase morbidity and mortality, provided appropriate surgical technique was used.¹³ The long term prognosis is generally favorable for cure of adrenal adenoma, and for adrenal carcinoma reported median survival time in one study was 778 days.¹⁴

References

1. Maher ER, McNiel EA. Pheochromocytoma in dogs and cats. Vet Clin North Am Small Anim Pract 1999; 27:359-380.
2. Evans HE, Christensen GC. Miller’s anatomy of the dog. 2nd ed. Philadelphia: WB Saunders, 1993: 578-579.
3. Smith MM, Waldron DR. Atlas of Approaches for General Surgery of the Dog and Cat. Philadelphia: WB Saunders, 1993: 171.
4. Axlund TW, Winkler JT. Surgical Treatment of Canine Hyperadrenocorticism. Compend Contin Educ Pract Vet 2003; 25(5):334-346.
5. Gilson SD, Withrow SJ, Orton C. Surgical Treatment of Pheochromocytoma: Technique, Complications, and Results in Six Dogs. Vet Surg 1994; 23:195-200.
6. Locke-Bohannon LG, Mauldin GE. Canine pheochromocytoma: Diagnosis and management. Compend Contin Educ Pract Vet 2001; 23(9); 807-814.
7. Scavelli TD, Peterson ME, Matthiesen DT. Results of surgical treatment for hyperadrenocorticism caused by adrenocortical neoplasia in the dog: 25 cases (1980-1984). J Am Vet Med Assoc 1986; 189:1360-1364.
8. Feldman EC, Nelson RW. Canine hyperadrenocorticism (Cushing’s syndrome). In: Feldman EC, Nelson RW. Canine and Feline Endocrinology and Reproduction, Third Edition. Philadelphia: WB Saunders Co., 2004: 252-357.
9. Kirk RW: Current Veterinary Therapy IX. Philadelphia, W. B. Saunders Co, 1986: 972-981.
10. Gilson SD, Withrow SJ, Wheeler SL, et al: Pheochromocytoma in 50 dogs. J Vet Intern Med. 1994: 8; 228-232.
11. Werbel SS, Ober KP: Pheochromocytoma: Update on diagnosis, localization and management. Med Clin North Am. 1995: 79; 131-153.
12. Twedt DC, Wheeler SC: Pheochromocytoma in the dog. Vet Clin North Am Small Anim Pract. 1984: 14; 767-782.
13. Kyles AE, Feldman EC, De Cock HE, et al. Surgical management of adrenal gland tumors with and without associated tumor thrombi in dogs: 40 cases (1994-2001). J Am Vet Med Assoc 2003; 223;654-662.
14. Anderson CR, Birchard SJ, Powers BE, et al. Surgical Treatment of Adrenocortical Tumors: 21 Cases (1990-1996). J Am Anim Hosp Assoc 2001; 37:93-97.
     

Introduction

Thyroid neoplasia is the primary indication for thyroidectomy in dogs and cats. Thyroid tumors in dogs are usually malignant and non-functional, whereas in cats they are usually benign and functional. Thyroidectomy can range from a straightforward to complex surgical procedure, depending on the invasiveness and size of the tumor. A working knowledge of the regional anatomy, pathophysiology of thyroid and parathyroidectomy disorders, and the principles of pre and postoperative care is necessary for successful patient management. Animals with thyroid tumors tend to be geriatric and frequently have disorders of other organ systems that should be recognized and treated appropriately. This is particularly true for cats with hyperthyroidism, a potentially severe multi-system disorder that can increase the risks associated with anesthesia and surgery.

The purpose of this chapter is to provide an overview of the pathophysiology of thyroid neoplasia, to review the anatomy of the thyroid and parathyroid glands, and to describe the surgical technique for thyroidectomy. Postoperative care and complications are also covered.

Surgical Anatomy

The thyroid gland in the dog and cat is divided into two lobes which are located adjacent to the trachea and just caudal to the larynx. The left lobe is slightly caudal to the right.¹ The normal gland is pale tan. The principle blood supply to each lobe is the cranial thyroid artery, a branch of the common carotid artery¹ (Figure 37-5). The caudal thyroid artery in the dog arises from the brachiocephalic trunk or common carotid artery. The caudal thyroid artery is absent in the cat.² Venous drainage of the thyroid is through the cranial and caudal thyroid veins.¹ The thyroid has a distinct capsule that can be bluntly separated from glandular tissue. Small blood vessels may be located on the capsule surface and between the capsule and the parenchyma of the gland. Two parathyroid glands are usually associated with each thyroid lobe. The external parathryoid gland usually lies in the loose fascia at the cranial pole of the thryoid lobe.² The internal parathyroid gland is usually embedded in the thyroid parenchyma and is variable in location. The external parathyroid glands are much smaller than the thyroid lobe and can be distinguished from the thyroid tissue by their lighter color and spherical shape. The blood supply to the parathyroid glands also arises from the cranial thyroid artery.¹
 

Thyroid Tumors in Dogs

Pathophysiology

Thyroid tumors in dogs account for 1.2% of all canine tumors.³ The majority of the tumors are malignant, and adenocarcinoma is the most common tissue type reported.⁴ Less than 20% of dogs with thyroid tumors have hyperthyroidism.⁵ Boxers, beagles, and golden retrievers appear to have a greater risk of developing thyroid carcinoma.³

The most common presenting signs in dogs with thyroid tumors are the presence of a palpable neck mass and coughing or respiratory distress.⁴ Other reported clinical signs are vomiting, dysphagia, anorexia, and weight loss.⁵ Signs of hyperthyroidism are usually not present because elevation of thyroid hormone level is infrequent in dogs with thyroid neoplasia. However, the author has seen 2 dogs with functional thyroid adenocarcinomas that had elevated triiodothyronine (T₃) and thyroxine (T₄) levels but did not have signs of hyperthyroidism. Most thyroid tumors in dogs are malignant and are carcinomas. Thyroid carcinomas in dogs most frequently metastasize to the lungs.⁴ Studies have indicated that over 50% of all thyroid carcinomas produce lung metastases.^3,6 The larger the primary tumor, the greater the chance for lung metastasis.⁶ The second most common site of metastasis is the cervical lymph nodes.

A key factor in the preoperative evaluation of a dog with suspected thyroid neoplasia is determining whether or not the affected gland or mass is movable. Thyroid masses that are freely movable on palpation tend to be less invasive into surrounding tissues, are surgically resectable, and have a better long-term prognosis than those masses that are invasive and non-movable. One study found that, of 82 dogs with thyroid carcinoma, 20 had movable tumors.⁷ These tumors were resected and median survival of the group was 20.5 months. A more recent study evaluated dogs with bilateral thyroid tumors that underwent thyroidectomy. As with unilateral tumors, long-term postoperative survival was good but many dogs required treatment for hypoparathyroidism.⁸

Diagnosis

Diagnosis of thyroid neoplasia in dogs is by physical examination (palpation of a neck mass), and biopsy of the tumor. Fine needle aspiration of the mass should yield cells characteristic of a carcinoma but may be inconclusive due to hemorrhage. A Tru-cut needle biopsy of the tumor may be considered if cytology is inconclusive but may cause hemorrhage due to the extensive neovascularization of the tumor and therefore is not recommended. Thoracic radiographs are mandatory to rule out pulmonary metastases. Thyroid function should be evaluated with a thyroid- stimulating-hormone stimulation test or free T₄ assay if the dog is showing signs of hyperthyroidism or hypothyroidism. Routine preoperative tests, such as complete blood count, serum chemistry profile, and urinalysis are also recommended.

Preoperative Considerations

Surgical thyroidectomy is indicated for those dogs with small, movable thyroid masses that are not invasive. Treatment options other than surgery should be considered for dogs with large, fixed neoplasms. Radiation therapy has recently been shown to be effective in several dogs with infiltrative thyroid carcinoma.⁹ Chemotherapy can also be used and may benefit dogs with nonresectable tumors, or with tumors that have been incompletely excised. Consultation with an oncologist is recommended in such cases.

Surgical Technique

The dog is placed in dorsal recumbency with the front legs tied caudally and the neck slightly hyper extended over a rolled towel or other cushion. The ventral cervical region from the caudal mandible to the manubrium is prepared for aseptic surgery. A ventral midline cervical skin incision is made from the caudal aspect of the larynx to 2 to 3 cm cranial to the manubrium. The paired sternohyoideus and sternothyroideus muscles are separated on the midline and retracted with self-retaining retractors. The trachea is gently retracted and both thyroid lobes are carefully examined.

An attempt should be made to identify the parathyroid glands, although visualization of the glands may be impaired by larger neoplasms (Figure 37-6). The tumor is carefully dissected from surrounding tissues (Figure 37-7). The author usually starts at the caudal aspect of the lobe and works cranially. Care is taken to avoid injury to the esophagus, carotid artery, jugular vein, vagosympathetic trunk, and recurrent laryngeal nerves.
 

If involved with the mass, the carotid artery, jugular vein, vagosympathetic trunk, and recurrent laryngeal nerve may be removed unilaterally. These tumors are extremely vascular and strict hemostasis is important to prevent serious blood loss. The Ligasure^® vessel sealing device is a very useful tool for hemostasis of the highly vascular thryroid tumors in dogs. Even small vessels should be ligated or cauterized since surgery is hampered by a bloody field. Removal of large tumors results in dead space in the tissues; a closed suction drain (e.g. Jackson-Pratt) should be placed in the area of resected tumor to prevent hematoma or seroma formation. The sternohyoideus and sternothyroideus muscles are closed with absorbable suture, such as, (3-0 poliglecaprone 25 (Monocryl) or polydioxanone (PDS)) in a simple continuous pattern. The subcutaneous tissues are closed in the same fashion. Skin is closed with non-absorbable suture (4-0 nylon) in a simple interrupted pattern or with 4-0 absorbable intradermal suture in a simple continuous pattern.

The thyroid tissue should always be submitted for histologic examination. Results of histologic examination help to determine the need for adjunctive therapy, such as chemotherapy, and to evaluate the patient’s long-term prognosis. One study found that surgery and chemotherapy did not improve survival in dogs compared to surgery alone.¹⁰

Postoperative Care

Post-operatively, the animal should be closely observed during recovery for bleeding at the surgical site. Serum calcium levels should be monitored daily for 2 to 4 days post-operatively if a bilateral tumor is resected. Hypocalcemia due to hypoparathyroidism is treated according to the protocol in Table 37-4.¹¹

The animal should be reevaluated at 2 weeks, 3 months, 6 months, and 1 year and radiographs of the thorax should be obtained at these rechecks to monitor for metastasis. Prognosis for the individual patient depends upon tumor type and completeness of surgical excision. As previously mentioned, even thyroid carcinoma can be associated with a good prognosis if the tumor is mobile and is completely excised.
 

Thyroid Tumors in Cats

Pathophysiology

Thyroid masses in the cat are usually benign and functional. The disease can be unilateral or bilateral and histologically the tumors are usually adenomatous hyperplasia. Rarely, (in 1 to 2% of cases), the tumors are carcinomas.⁶ Thyroid tumors in cats produce excessive amounts of thyroxine and cats develop the clinical syndrome of hyperthyroidism. Classic clinical signs of hyperthyroidism include tachycardia, hyperactivity, weight loss, polyphagia, and polyuria/polydipsia.⁵ In addition to tachycardia a gallop rhythm, systolic murmurs, and arrhythmias can occur due to the catecholamine like effects of the excessive thyroxine on the myocardium. Some cats have apathetic hyperthyroidism, a syndrome characterized by signs opposite to the classic presentation for hyperthyroidism, such as depression, lethargy, and anorexia.⁵

Diagnosis

Diagnosis of feline hyperthyroidism is based on the history and clinical signs, palpation of a neck mass, and elevated serum triiodothyronine and thyroxine concentrations.⁵ One or more thyroid nodules are palpable in approximately 85 to 90% of affected cats. The cats may also have leukocytosis, higher than normal packed cell volume, and high alkaline phosphatase.⁵ Hyperthyroid cats may also have hypertrophic cardiomyopathy with hypertrophy of the left ventricular free wall and ventricular septum.⁵ Renal function should be carefully evaluated prior to treatment of hyperthyroidism in cats. Hyperthyroidism may mask chronic renal failure by increasing renal blood flow.¹² Treatment of the hyperthyroidism can result in exacerbation of the renal dysfunction when renal blood flow returns to normal. Some clinicians recommend a thirty-day therapeutic trial course of methimazole to assess the effect of decreased renal blood flow on kidney function.

Radionuclide scan of the thyroid gland in cats with hyperthyroidism reveals increased uptake and size of the affected lobes. Nuclear scan can be a useful diagnostic tool in cats that do not have a palpable thyroid nodule or that have had relapse of hyperthyroidism after thyroidectomy.⁵ However, nuclear scans have limited practicality because of the specialized equipment and expertise needed to perform the studies.

Treatment options for hyperthyroidism in cats include use of methimazole, which lowers thyroxine by blocking uptake of iodine by the thyroid, radioactive iodine treatment, or surgical removal of the gland (s).⁵ Reported success rates are high with all of these treatment methods. Medical treatment with methimazole is the least invasive and least expensive method and may be a reasonable option in high-risk anesthetic patients or where radioactive iodine is not available. However, side effects to methimazole have been reported and problems with owner adminstration may complicate long-term use of the drug.¹³ Radioactive iodine therapy has been repeatedly shown to be safe and effective. Anesthetic and surgical complications (e.g. hypoparathyroidism) are avoided with this therapy, however, specialized facilities and expertise limit this to a referral procedure. Thus, availability may be a limiting factor. When this treatment option is not possible, and assuming the cat is a good anesthetic and surgical candidate, surgical thyroidectomy may be an option for long-term resolution of the condition.

Perioperative Considerations

There are several aspects of feline thyroidectomy that should be considered prior to performing surgery. Preoperatively, affected cats are treated with methimazole to establish euthyroidism which makes the animal a better candidate for anesthesia and surgery. Methimazole (Tapazole^®, 5 mg orally twice a day) is administered for 7 to 10 days before surgery. The patients thyroxine levels are rechecked and, if normal or significantly reduced, surgery is scheduled. Cats that are only mildly affected by hyperthyroidism (i.e., only mildly elevated thyroxine, normal weight, not severely tachycardic) are operated without pretreatment with methimazole.

In an attempt to prevent postoperative hypocalcemia in dogs or cats undergoing bilateral thyroidectomy, some clinicians administer oral calcitriol (20ng/kg q12h) for 3 to 4 days preoperatively. Calcitriol administration is continued at 5-10ng/kg q12h for 1 week or more postoperatively depending on results of repeated serum ionized calcium assays.

Anesthesia in hyperthyroid cats can be challenging. Anesthetic facilities should allow for adequate monitoring of the cat, particularly since intraoperative electrocardiographic abnormalities are common. If premature ventricular contractions occur during anesthesia and do not resolve by increasing oxygenation, propanolol (0.1 mg IV) can be given to control the arrhythmia.

The surgeon should be comfortable with the regional anatomy, and with performing fine dissection of very small anatomic structures. Surgical instruments that are helpful include tenotomy scissors, DeBakey or Simkin thumb forceps, sterile cotton tipped applicators, and bipolar electrocautery.

Adequate postoperative monitoring is mandatory for recognizing and managing potential complications, such as hypocalcemia.¹¹ It is recommended that facilities and personnel be suitable for providing intensive postoperative care that is occasionally required.

Surgical Techniques

Thyroidectomy in the cat is performed by a ventral midline cervical approach.¹⁴ Even if only one thyroid lobe appears grossly abnormal bilateral thyroidectomy is recommended since most cats have or will develop disease in both glands. Several techniques for thyroidectomy in cats have been described, some allowing for resection of the capsule (extracapsular dissection) and others preserving the capsule (intracapsular dissection).^14,15 The author typically performs the extracapsular technique because of the reduced incidence of recurrence of hyperthyroidism due to remnants of thyroid tissue left behind that can occur with the intracapsular technique. However, in cats where the parathyroid glands are not visible, the modified intracapsular technique is performed in order to be sure of preserving at least one of the parathyroid glands. Both techniques are described here.

An alternative surgical approach is staged bilateral thyroidectomy.¹⁶ In order to reduce the incidence of postoperative hypocalcemia, one affected thyroid lobe is removed, then the remaining affected lobe removed several weeks later. This technique has been shown to be associated with a reduced incidence of postoperative hypoparathyroidism. However, considering the low risk of this complication in the hands of an experienced surgeon, and the increased cost and morbidity of a second operation, the author prefers to perform bilateral thyroidectomy in one procedure.

Extracapsular Technique

The thyroid lobes are exposed through a ventral midline cervical approach as described in the dog. The affected thyroid lobe is dissected free from surrounding fascia, working from caudally to cranially. The external parathyroid gland is identified at the cranial aspect of the thyroid gland. The thyroid gland capsule is incised adjacent to the parathyroid gland (Figure 37-8). Pinpoint electrocautery is used on any vessels encountered during this dissection with care taken to avoid damage to the parathyroid gland or its blood supply. The parathyroid gland is then carefully separated from the thyroid using sterile cotton-tipped applicators. Once the parathyroid gland is completely separated from the thyroid, the thyroid gland is completely removed using blunt and sharp dissection and pinpoint electrocautery on all vessels. Minor hemorrhage adjacent to the parathyroid glands can be controlled using small amounts of hemostatic gelatin sponge. Closure of the incision is by simple continuous suture pattern in the sternohyoideus muscle using absorbable suture, simple continuous pattern in the subcutaneous tissues with absorbable suture, and interrupted sutures in the skin with non-absorbable sutures. As an alternative to skin sutures, a continuous absorbable intradermal suture layer may be placed.
 

Modified Intracapsular Technique

A small nick incision is made in an avascular area of the thyroid capsule (Figure 37-9). This incision is extended with small scissors. The thyroid tissue is then gently separated from the capsule with sterile cotton tipped applicators. Meticulous hemostasis is critical to maintain good visualization of the surgical field. Hemorrhage from small capsular vessels is controlled using pinpoint electrocautery. Extreme care is required during manipulation of the cranial pole of the thyroid to avoid injury to the blood supply of the extracapsular parathyroid gland. If the thyroid gland becomes fragmented during dissection, the surgical field is carefully examined for remnants of thyroid tissue that were not removed. These remnants and associated capsule are removed. Remaining remnants of capsule are also removed since microscopic thyroid tissue may be attached to them. The incision is closed as described under the extracapsular technique. All resected tissue is submitted for histologic evaluation.
 

Postoperative Care

Postoperatively, the cat is closely monitored for evidence of hemorrhage from the surgical site. Serum calcium levels are monitored for at least 2 days postoperatively. If hypocalcemia develops due to removal or damage to the parathyroid glands, the cat is treated with calcium (parenteral and/or oral administration) and vitamin D as described in Table 37-4. Calcium supplementation potentiates the effect of calcitriol, but calcium supplements alone are not effective for control of hypocalcemia. Early signs of hypocalcemia are muscle soreness or spasm, anorexia, and depression. Later signs are collapse and tetany. Thyroid replacement therapy (L-thyroxine, 0.1 mg orally once daily) is not given routinely but it may be indicated for cats that have had bilateral thyroidectomy and show clinical signs of hypothyroidism (e.g. lethargy, weight gain, skin problems).

Renal function should be monitored closely in cats after thyroidectomy, especially if they have evidence of chronic renal failure preoperatively. As previously described, renal function in some cats worsens after thyroidectomy, presumably due to a decrease in renal blood flow after lowering the thyroxine levels.¹²

The prognosis for hyperthyroid cats after thyroidectomy is good. Treated cats show improved behavior and significant weight gain. Histologic examination of the thyroid tissue usually reveals adenomatous hyperplasia. Rarely, histologic exam of the excised mass reveals thyroid carcinoma.¹⁷ These tumors are much larger and more vascular than the more common benign adenomatous hyperplasia.

Rarely, relapse of hyperthyroidism can occur 1 to 2 years postoperatively due to regrowth of the adenoma.¹⁸ This may be due to incomplete removal of the adenomatous tissue during the first surgery. Postoperative hypocalcemia is more common after reoperation for thyroidectomy.

References

1. Evans HE, Christensen GC: Miller’s Anatomy of the Dog, The Endocrine System, WB Saunders, Philadelphia, 1979, pp. 611-618.
2. Nicholas JS, Swingle WW: An experimental and morphological study of the parathyroid glands of the cat. Am J Anat 34:469-508, 1925.
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