Web Chapter 17 Hyperadrenocorticism in Ferrets Karen L. Rosenthal, Philadelphia, Pennsylvania Mark E. Peterson, New York, New York Hyperadrenocorticism is a common problem in pet ferrets (3 years of age or older) in the United States and many other countries around the world. The most frequently observed clinical signs include alopecia in both sexes and a large vulva in females. Characteristic of the disease are unilaterally or, less commonly, bilaterally enlarged adrenal glands that produce abnormally high quantities of various androgens or estrogens, which are responsible for the observed clinical signs. Clinicians must understand that this disease is not Cushing’s disease and that affected ferrets do not have consistently high concentrations of plasma cortisol. Treatment is aimed at reducing the secretion of androgens or estrogens produced by the abnormal adrenal gland or glands. Clinical Signs Alopecia is seen in most ferrets with hyperadrenocorticism. Hair loss typically begins on the rump, the tail, or the flanks and spreads to the sides, dorsum, and ventrum. Most spayed female ferrets develop an enlarged vulva, sometimes accompanied by a localized vaginitis with a seromucoid discharge. More than one third of affected ferrets are pruritic. Owners may also report that their ferret acts sexually aggressive toward other ferrets and has a musky odor. Infrequently, male ferrets develop dysuria because of urethral blockage, which occurs when prostatic tissue surrounding the proximal urethra becomes hyperplastic or cystic and narrows the urinary conduit. Hematology and Biochemistry Typically, results of a complete blood count are within normal limits. Rarely, adrenal gland disease in ferrets results in anemia (always nonregenerative) and, even more rarely, pancytopenia. The results of plasma biochemical analysis are usually within reference interval limits. Hypoglycemia caused by a pancreatic β cell tumor also may be found because this disease is also common in older ferrets. Diagnosis The diagnosis of hyperadrenocorticism in ferrets is made through a combination of history, clinical signs, detection of adrenal gland enlargement by means of abdominal ultrasonography, and demonstration of high plasma concentrations of adrenal androgens or estrogens. Few other diseases in ferrets cause similar clinical signs. Radiographs are almost never diagnostic. Large adrenal glands can be detected only with ultrasonography performed by an experienced sonographer. Determination of baseline or adrenocorticotropic hormone (ACTH)–stimulated plasma cortisol concentration does not aid in the diagnosis of adrenocortical disease in ferrets because excessive cortisol secretion is not part of the disease in this species. Similarly, the dexamethasone suppression test is not helpful in the diagnosis of adrenal gland disease in ferrets. If by using the above criteria the diagnosis of adrenal gland disease is still equivocal, the most useful assay measures the concentrations of basal plasma androgens and estrogens. In ferrets with adrenal gland disease, some adrenal androgens and estrogens are produced in abnormally large quantities. The four hormones that are most commonly elevated include dehydroepiandrosterone sulfate (DHEAS), androstenedione, estradiol, and 17-hydroxyprogesterone (Rosenthal and Peterson, 1996b). In practice, the diagnosis of hyperadrenocorticism in ferrets is usually unambiguous. However, there are two uncommon instances in which ferrets may have signs similar to those of a ferret with adrenal gland disease. Young, intact female ferrets or ferrets with a functional ovarian remnant may have a large vulva and minimal alopecia. If the ferret is intact or an ovarian remnant is suspected, injection of 1000 U of human chorionic gonadotropin (hCG) once and repeated in 2 weeks results in a reduction in the size of the vulva. The adrenal androgen assay usually helps differentiate between functional ovarian tissue and hyperadrenocorticism unless only the estrogen concentration is elevated in a ferret with adrenal gland disease. Additionally, a skilled ultrasonographer should be able to discern adrenal enlargement from ovarian and uterine tissue. Treatment Although medical treatment can be used, surgery is preferred because it can be curative and because ferrets commonly become refractory to medical treatment. Thus adrenalectomy should be recommended unless the ferret has concurrent disease (e.g., heart disease) that makes it a poor surgical candidate. Other factors to be considered include age, cost of treatment, and health status. In older ferrets with insulinoma, the pancreatic tumor or tumors can be removed at the same time that adrenalectomy is performed. Most ferrets with hyperadrenocorticism are not seriously ill and do not need surgery immediately. Two life-threatening conditions associated with adrenal gland disease in ferrets that necessitate immediate attention include profound anemia (rarely observed) and urethral blockage. Surgery In most ferrets, surgery is curative because adrenal gland cortical tumors rarely metastasize, and signs of the disease resolve after surgery. Signs recur if the contralateral adrenal gland becomes diseased or if the diseased gland is not entirely removed. Typically, removal of the left adrenal gland is a simple task, but right adrenalectomy is technically challenging. Before surgery, the ferret should not be fed for at least 4 hours. A ferret with an insulinoma requires intravenous administration of fluids with dextrose during this time. If the ferret is severely anemic, a transfusion may be required. During surgery, the abdomen should be explored fully. One should monitor the heart rate and rhythm, blood pressure, and fluid administration. At the time of surgery, both adrenal glands should be visualized, palpated for size and firmness, and compared with each other, since disease can be bilateral. The clinician should examine other organs, including the liver, lymph nodes, pancreas, kidneys, and spleen, and should take appropriate biopsy specimens. The technique of adrenalectomy in ferrets has been described (Ludwig and Aiken, 2004). The left adrenal gland is found cranial to the left kidney in fatty tissue. The clinician should dissect the left adrenal gland free from the fatty tissue while ligating one or more small vessels attached to the gland. Right adrenalectomy is more difficult, inasmuch as the right adrenal gland lies between the kidney and a liver lobe and is bound to the vena cava by fascial tissue. Removal of the entire right adrenal gland usually produces vena caval damage, resulting in severe hemorrhage. Alternatively, one can debulk as much tissue as possible from the right adrenal gland, leaving the vena cava intact, but this method leaves diseased tissue in the ferret. If both glands are diseased, one option is to perform a complete adrenalectomy on one adrenal gland and a subtotal adrenalectomy on the other gland. One should completely remove the larger of the two glands or should remove the entire left adrenal gland, since it is more accessible, and as much of the right as possible. In any case, debulking of the adrenal gland is less than ideal in that disease will still be present, and further treatment, either medical treatment or a second surgery, will be necessary. After surgery, the ferret should be given maintenance and replacement fluids, if needed, until it can be fed. Cortisol hypersecretion does not play a role in this syndrome; thus postoperative glucocorticoid replacement is not usually necessary in a ferret that has had unilateral adrenalectomy. However, if the ferret appears lethargic after surgery for no apparent reason, or if parts of both adrenal glands have been removed, one can administer dexamethasone sodium phosphate (2 to 4 mg/kg IV). The prognosis with surgical treatment is excellent. Complications include recurrence of the adrenal tumor (metastasis is very rare), contralateral adrenal gland enlargement, and life-threatening vena caval bleeding.< div class='tao-gold-member'> Only gold members can continue reading. Log In or Register to continue You may also needChapter 23: Treatment of Insulinoma in Dogs, Cats, and FerretsCanine Hyperadrenocorticism TherapyChapter 16: Differential Diagnosis of Hyperkalemia and Hyponatremia in Dogs and CatsAlopecia XToxoplasmosisCanine HypoadrenocorticismChapter 81: American LeishmaniasisFeline Diabetes Mellitus Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window)Click to share on Google+ (Opens in new window) Related Tags: Kirks Current Veterinary Therapy XV Jul 18, 2016 | Posted by admin in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Chapter 17: Hyperadrenocorticism in Ferrets Full access? Get Clinical Tree
Web Chapter 17 Hyperadrenocorticism in Ferrets Karen L. Rosenthal, Philadelphia, Pennsylvania Mark E. Peterson, New York, New York Hyperadrenocorticism is a common problem in pet ferrets (3 years of age or older) in the United States and many other countries around the world. The most frequently observed clinical signs include alopecia in both sexes and a large vulva in females. Characteristic of the disease are unilaterally or, less commonly, bilaterally enlarged adrenal glands that produce abnormally high quantities of various androgens or estrogens, which are responsible for the observed clinical signs. Clinicians must understand that this disease is not Cushing’s disease and that affected ferrets do not have consistently high concentrations of plasma cortisol. Treatment is aimed at reducing the secretion of androgens or estrogens produced by the abnormal adrenal gland or glands. Clinical Signs Alopecia is seen in most ferrets with hyperadrenocorticism. Hair loss typically begins on the rump, the tail, or the flanks and spreads to the sides, dorsum, and ventrum. Most spayed female ferrets develop an enlarged vulva, sometimes accompanied by a localized vaginitis with a seromucoid discharge. More than one third of affected ferrets are pruritic. Owners may also report that their ferret acts sexually aggressive toward other ferrets and has a musky odor. Infrequently, male ferrets develop dysuria because of urethral blockage, which occurs when prostatic tissue surrounding the proximal urethra becomes hyperplastic or cystic and narrows the urinary conduit. Hematology and Biochemistry Typically, results of a complete blood count are within normal limits. Rarely, adrenal gland disease in ferrets results in anemia (always nonregenerative) and, even more rarely, pancytopenia. The results of plasma biochemical analysis are usually within reference interval limits. Hypoglycemia caused by a pancreatic β cell tumor also may be found because this disease is also common in older ferrets. Diagnosis The diagnosis of hyperadrenocorticism in ferrets is made through a combination of history, clinical signs, detection of adrenal gland enlargement by means of abdominal ultrasonography, and demonstration of high plasma concentrations of adrenal androgens or estrogens. Few other diseases in ferrets cause similar clinical signs. Radiographs are almost never diagnostic. Large adrenal glands can be detected only with ultrasonography performed by an experienced sonographer. Determination of baseline or adrenocorticotropic hormone (ACTH)–stimulated plasma cortisol concentration does not aid in the diagnosis of adrenocortical disease in ferrets because excessive cortisol secretion is not part of the disease in this species. Similarly, the dexamethasone suppression test is not helpful in the diagnosis of adrenal gland disease in ferrets. If by using the above criteria the diagnosis of adrenal gland disease is still equivocal, the most useful assay measures the concentrations of basal plasma androgens and estrogens. In ferrets with adrenal gland disease, some adrenal androgens and estrogens are produced in abnormally large quantities. The four hormones that are most commonly elevated include dehydroepiandrosterone sulfate (DHEAS), androstenedione, estradiol, and 17-hydroxyprogesterone (Rosenthal and Peterson, 1996b). In practice, the diagnosis of hyperadrenocorticism in ferrets is usually unambiguous. However, there are two uncommon instances in which ferrets may have signs similar to those of a ferret with adrenal gland disease. Young, intact female ferrets or ferrets with a functional ovarian remnant may have a large vulva and minimal alopecia. If the ferret is intact or an ovarian remnant is suspected, injection of 1000 U of human chorionic gonadotropin (hCG) once and repeated in 2 weeks results in a reduction in the size of the vulva. The adrenal androgen assay usually helps differentiate between functional ovarian tissue and hyperadrenocorticism unless only the estrogen concentration is elevated in a ferret with adrenal gland disease. Additionally, a skilled ultrasonographer should be able to discern adrenal enlargement from ovarian and uterine tissue. Treatment Although medical treatment can be used, surgery is preferred because it can be curative and because ferrets commonly become refractory to medical treatment. Thus adrenalectomy should be recommended unless the ferret has concurrent disease (e.g., heart disease) that makes it a poor surgical candidate. Other factors to be considered include age, cost of treatment, and health status. In older ferrets with insulinoma, the pancreatic tumor or tumors can be removed at the same time that adrenalectomy is performed. Most ferrets with hyperadrenocorticism are not seriously ill and do not need surgery immediately. Two life-threatening conditions associated with adrenal gland disease in ferrets that necessitate immediate attention include profound anemia (rarely observed) and urethral blockage. Surgery In most ferrets, surgery is curative because adrenal gland cortical tumors rarely metastasize, and signs of the disease resolve after surgery. Signs recur if the contralateral adrenal gland becomes diseased or if the diseased gland is not entirely removed. Typically, removal of the left adrenal gland is a simple task, but right adrenalectomy is technically challenging. Before surgery, the ferret should not be fed for at least 4 hours. A ferret with an insulinoma requires intravenous administration of fluids with dextrose during this time. If the ferret is severely anemic, a transfusion may be required. During surgery, the abdomen should be explored fully. One should monitor the heart rate and rhythm, blood pressure, and fluid administration. At the time of surgery, both adrenal glands should be visualized, palpated for size and firmness, and compared with each other, since disease can be bilateral. The clinician should examine other organs, including the liver, lymph nodes, pancreas, kidneys, and spleen, and should take appropriate biopsy specimens. The technique of adrenalectomy in ferrets has been described (Ludwig and Aiken, 2004). The left adrenal gland is found cranial to the left kidney in fatty tissue. The clinician should dissect the left adrenal gland free from the fatty tissue while ligating one or more small vessels attached to the gland. Right adrenalectomy is more difficult, inasmuch as the right adrenal gland lies between the kidney and a liver lobe and is bound to the vena cava by fascial tissue. Removal of the entire right adrenal gland usually produces vena caval damage, resulting in severe hemorrhage. Alternatively, one can debulk as much tissue as possible from the right adrenal gland, leaving the vena cava intact, but this method leaves diseased tissue in the ferret. If both glands are diseased, one option is to perform a complete adrenalectomy on one adrenal gland and a subtotal adrenalectomy on the other gland. One should completely remove the larger of the two glands or should remove the entire left adrenal gland, since it is more accessible, and as much of the right as possible. In any case, debulking of the adrenal gland is less than ideal in that disease will still be present, and further treatment, either medical treatment or a second surgery, will be necessary. After surgery, the ferret should be given maintenance and replacement fluids, if needed, until it can be fed. Cortisol hypersecretion does not play a role in this syndrome; thus postoperative glucocorticoid replacement is not usually necessary in a ferret that has had unilateral adrenalectomy. However, if the ferret appears lethargic after surgery for no apparent reason, or if parts of both adrenal glands have been removed, one can administer dexamethasone sodium phosphate (2 to 4 mg/kg IV). The prognosis with surgical treatment is excellent. Complications include recurrence of the adrenal tumor (metastasis is very rare), contralateral adrenal gland enlargement, and life-threatening vena caval bleeding.< div class='tao-gold-member'> Only gold members can continue reading. Log In or Register to continue You may also needChapter 23: Treatment of Insulinoma in Dogs, Cats, and FerretsCanine Hyperadrenocorticism TherapyChapter 16: Differential Diagnosis of Hyperkalemia and Hyponatremia in Dogs and CatsAlopecia XToxoplasmosisCanine HypoadrenocorticismChapter 81: American LeishmaniasisFeline Diabetes Mellitus Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window)Click to share on Google+ (Opens in new window) Related
