See the Full Issue
June 2023
2023 AAHA Selected Endocrinopathies of Dogs and Cats Guidelines
Executive summary of the latest from AAHA, the 2023 AAHA Selected Endocrinopathies of Dogs and Cats Guidelines.
Executive Summary
These guidelines were prepared by a task force of experts convened by the American Animal Hospital Association. This document is intended as a guideline only, not an AAHA standard of care. These guidelines and recommendations should not be construed as dictating an exclusive protocol, course of treatment, or procedure. Variations in practice may be warranted based on the needs of the individual patient, resources, and limitations unique to each individual practice setting. Evidence-guided support for specific recommendations has been cited whenever possible and appropriate. Other recommendations are based on practical clinical experience and a consensus of expert opinion. Further research is needed to document some of these recommendations. Drug approvals and labeling are current at the time of writing but may change over time. Because each case is different, veterinarians must base their decisions on the best available scientific evidence in conjunction with their own knowledge and experience.
This executive summary is not a substitute for reading the guidelines in their entirety. The full guidelines are published in the Journal of the American Animal Hospital Association (J Am Anim Hosp Assoc 2023; 59:113–135. DOI 10.5326/JAAHA-MS-7368) or visit aaha.org/endocrine-disease.
Overview
These guidelines discuss four endocrinopathies that practitioners will inevitably encounter: canine hypothyroidism, canine hypercortisolism (Cushing syndrome), canine hypoadrenocorticism (Addison’s disease), and feline hyperthyroidism (FHT). Three less common feline endocrinopathies are briefly discussed: feline hyperaldosteronism, feline hypothyroidism, and feline hyperadrenocorticism. Canine and feline diabetes mellitus are not discussed in these guidelines but are addressed in the 2018 AAHA Diabetes Management Guidelines for Dogs and Cats.
The clinical signs of endocrinopathies are typically nonspecific and highly variable; in some cases, they can be iatrogenic. Early-stage disease can be subclinical. Complicating factors are possible comorbidities, some of which can be secondary to advancing age. Early intervention avoids the severe syndromes that can impact quality of life and cause secondary organ damage and mortality.
Diagnosis involves recognizing clinical signs or physical examination abnormalities, compiling the patient’s history, interpreting hormone concentration assays, and excluding comorbidities. Monitoring and treatment involves noting the presence or resolution of clinical signs, trends in endogenous hormone levels, and therapeutic dose adjustments.
It is important to engage the owner in managing the pet’s health. Dialogue with the client should involve the entire practice team. Accordingly, these guidelines include a section on practice team and client considerations to promote better adherence to treatment recommendations and improved outcomes.
How the Guidelines Are Organized
The guidelines provide a practical, stepwise approach to diagnosis and treatment. Each endocrinopathy is introduced with a definition and clinical profile. The discussion of each endocrinopathy uses an innovative, categorical approach to diagnosis based on clinical presentation and medical history, previously described in the 2016 AAFP Guidelines for the Management of Feline Hyperthyroidism. The clinical presentation of each disease is summarized in a table, which also includes the next steps for diagnosis and treatment. Accompanying each table is a more detailed narrative specific to each disease. The table is a prescriptive, quick-reference tool, whereas the narrative provides contextual background for making clinical decisions.
A decision tree for feline hypothyroidism depicts options for diagnosis and treatment.
Feline hyperthyroidism is extremely common and, if untreated, is fatal. Radioactive iodine provides a cure in more than 95% of cases.
This executive summary highlights the guidelines’ categorical approach to endocrinopathies. To use it properly, practitioners must read the guidelines in their entirety. In addition, practitioners will benefit from consulting the abundant literature to gain additional clinical perspectives on each disease.
Canine Hypothyroidism
Hypothyroidism is one of the most common endocrinopathies of the dog, and a clear-cut diagnosis can be made when the signalment and presentation of symptoms are classic and are supported by appropriate test results. However, hypothyroidism is commonly overdiagnosed because of the nonspecific nature of the signs and the challenges of interpreting thyroid function tests.
The guidelines identify three categories of canine hypothyroidism:
Group 1: Dogs with classic signs of hypothyroidism and a low total thyroxine concentration (TT4). Signalment includes middle-aged dogs and breed predisposition, including beagles, golden retrievers, Doberman pinschers, and Great Danes.
Group 2: Dogs with no clinical signs of hypothyroidism and a low TT4. It is critical to consider the dog’s signalment, such as age and breed, before proceeding with additional testing for hypothyroidism. The guidelines task force recommends using breed-specific reference ranges when interpreting hormone levels in predisposed breeds, especially if no clinical signs are present.
Group 3: Dogs with clinical signs of hypothyroidism and a normal TT4. These dogs have a similar clinical presentation to Group 1 dogs, but the TT4 does not confirm hypothyroidism. The guidelines advise investigating other causes by reviewing the patient’s medical history with the client and pursuing additional diagnostics.
Table 1 summarizes the clinical presentation and next steps for each group.
Low-stress visits encourage reliable diagnostic results because stress can influence many endocrine-related diagnostics.
Canine Hypercortisolism (Cushing Syndrome)
The guidelines discuss naturally occurring adrenocorticotropic hormone (ACTH)–dependent Cushing syndrome (CS) and ACTH-independent CS. They do not discuss ectopic ACTH secretion and food-dependent hypercortisolism.
All diagnostic tests for CS have limitations and can yield false-positive results in patients with concurrent nonadrenal illness or stress. Practitioners should test only those patients who present two or more clinical or biochemical abnormalities that suggest CS. There are many published monitoring and testing protocols; there is no universal consensus on one protocol. Measurement of cortisol concentrations (before pill or following ACTH stimulation technique, or ACTHST) is recommended to help determine whether to adjust the dose. Because CS is a highly variable disease, clinician judgment and discretion are important in determining the monitoring protocol.
Table 2 lists clinicopathologic findings that can occur with CS, and Table 3 lists clinical signs associated with naturally occurring CS.
The guidelines identify four categories of canine hypercortisolism (CS):
Group 1: Dogs with clinical signs and clinicopathologic findings consistent with CS (Tables 2 and 3). Specific endocrine testing should be performed. The guidelines panel recommends a low-dose dexamethasone suppression test (LDDST) as a routine first step.
Group 2: Dogs with no clinical signs but with clinicopathologic abnormalities suggestive of CS (Table 2). Probe the patient’s history with specific questions about water intake, urination habits, worsened incontinence, or nocturia. Also rule out glucocorticoids, including ophthalmic or otic preparations. Specific endocrine testing is not necessary unless or until clinical signs of CS are present.
Group 3: Dogs with clinical signs suggestive of CS (Table 3) without clinicopathologic abnormalities. Question the owner to rule out administration of glucocorticoids that could cause CS.
Group 4: Sick patients presenting with signs and/or clinicopathologic findings consistent with CS. Presenting signs must be addressed before pursuing diagnostics. Hypercortisolism does not cause anorexia, vomiting, or diarrhea. Presenting signs may be due to a disease process unrelated to CS or a comorbidity associated with CS.
Table 4 summarizes the clinical presentation and next steps for each category of dog.
Canine Hypoadrenocorticism (Addison’s Disease)
Addison’s disease describes a spectrum of conditions resulting in deficiencies of important adrenal hormones (i.e., cortisol and aldosterone). The clinical signs can occur in dogs of any age or breed. Most, however, are diagnosed in middle age, with a female predisposition inconsistently reported. Commonly affected breeds are listed.
Table 5 lists diseases with a clinical presentation similar to HA, Table 6 lists conditions that biochemically resemble hypoadrenocorticism (pseudo-Addisonian conditions), and Table 7 lists laboratory changes that can occur with hypoadrenocorticism.
The patient history is essential to case management. The guidelines offer advice for taking a quality patient history.
The guidelines identify four categories of canine hypoadrenocorticism:
Group 1: Dogs with classic clinical disease. Patients present with chronic or episodic clinical signs and laboratory abnormalities consistent with hypoadrenocorticism. Options for diagnostic testing depend on whether suspicion of disease is high or low and whether resting cortisol is greater or less than 0.2 mcg/dL.
Group 2: Dogs with no clinical signs but with classic laboratory abnormalities, including hyperkalemia and/or hyponatremia. Additional laboratory abnormalities may be present (Table 7). If deeper analysis reveals no clinical signs, other causes of laboratory changes, such as spurious causes (Table 6), should be ruled out.
Group 3: Addisonian crisis. Group 3 dogs present in hypovolemic shock with or without historic episodic signs consistent with hypoadrenocorticism. This is the most serious and life-threatening manifestation of hypoadrenocorticism and typically presents as hypovolemic shock accompanied by severe hyperkalemia and hyponatremia. Other laboratory abnormalities may also be present (Table 7). Next steps for immediate and follow-up treatment are provided.
Group 4: Dogs with clinical signs with nonspecific laboratory abnormalities (atypical presentation). These dogs present with chronic or episodic clinical signs without the characteristic findings associated with classic hypoadrenocorticism. Because signs of canine hypoadrenocorticism can mimic many other diseases, patients may present with episodic clinical signs that could be consistent with Addison’s disease without the hallmarks of hyperkalemia or hyponatremia (Table 6).
Table 8 summarizes the categorical approach to diagnosing suspected canine hypoadrenocorticism.
The guidelines note that clients can learn to administer subcutaneous injections. Once the dose and dosing interval are established, someone other than the veterinarian may administer desoxycorticosterone pivalate (DOCP) injections.
Feline Hyperthyroidism
The management of feline hyperthyroidism (FHT) has been covered extensively in other publications, notably the 2016 AAFP Guidelines for the Management of Feline Hyperthyroidism. Much of the information in those guidelines remains applicable. This discussion highlights certain key points from the AAFP Guidelines and presents recent findings.
FHT is an extremely common endocrinopathy in cats and, left untreated, will eventually be fatal. The treatment of choice is radioactive iodine (131I), which will provide a cure in more than 95% of cases.
The AAFP Guidelines identify six categories of cats with FHT:
Group 1: Classic clinical disease. This includes cats with one or more clinical signs consistent with FHT that have an elevated T4 and no identifiable concurrent disease. The AAFP Guidelines recommend that reference laboratory testing be used for diagnosis and monitoring of FHT so that precise serum hormone levels can be followed throughout treatment and to avoid quality control discrepancies.
Group 2: Possible FHT with probable nonthyroidal disease. Cats in this category have clinical signs suggestive of FHT along with T4 within the laboratory reference interval.
Certain classic signs of hyperthyroidism (e.g., polydipsia, polyuria, and weight loss in the face of a good appetite) have similarities with the following morbidities that are plausible differential diagnoses: diabetes mellitus; gastrointestinal malabsorption and maldigestion; and gastrointestinal neoplasia, especially lymphosarcoma.
Group 3: Enlarged thyroid gland without clinical FHT. These are cats without clinical FHT, T4 within the reference interval, but with enlarged thyroid gland(s). Monitor clinical signs in these cats and repeat a serum T4 assay in six months.
Group 4: Subclinical FHT. Cats without overt clinical hyperthyroidism but with an elevated T4 and with some physical examination findings suggestive of hyperthyroidism. Repeat the T4 test in one to two weeks. If serum T4 is still elevated, treat the cat for FHT. While no data exists for the best way to manage Group 4 cats, the consensus of the AAFP Guidelines panel is to treat these cats for hyperthyroidism.
Group 5: Clinical FHT and with confirmed nonthyroidal disease. Cats with clinical hyperthyroidism confirmed by elevated T4, and one or more concurrent diseases. Hyperthyroid cats are commonly middle-aged or older and often have concurrent diseases. Because FHT is a serious disease that can result in rapid deterioration, the AAFP Guidelines panel recommends the treatment of all diagnosed cats, including animals with comorbidities. Common comorbidities associated with FHT are listed in the guidelines.
Group 6: Clinically normal cats. These cats have no clinical signs of hyperthyroidism and no palpable thyroid nodule but have an elevated T4 on screening laboratory test. Because falsely elevated T4 values may occur, repeat the T4 test preferably using radioimmunoassay or chemiluminescent enzyme assay. If the T4 is elevated, treat for FHT.
Important Note
The AAHA Guidelines task force recommends that for AAFP Guidelines Groups 4 and 6, the practitioner should consider checking TSH before 131I treatment and postponing if measurable (>0.03 ng/mL) to help avoid creating iatrogenic hypothyroidism.
Table 9 summarizes the clinical presentation and next steps for the six categories of FHT. This table is reprinted with permission from the 2016 AAFP Guidelines for the Management of Feline Hyperthyroidism.
Less Common Feline Endocrinopathies
Three feline endocrinopathies that are encountered less often than FHT are feline hyperaldosteronism, feline hypothyroidism, and feline hyperadrenocorticism. The guidelines provide general overviews of these important diseases, including some clinical tips.
In addition to the narrative discussion, Table 10 lists key factors in managing feline primary hyperaldosteronism, and Table 11 lists clinical signs of feline hypothyroidism, both congenital and iatrogenic or adult-onset disease. Figure 1 is a decision tree that helps practitioners progress through diagnosis and treatment of feline hypothyroidism.
Team Approach
Printable Handout for
|
From initial patient presentation to long-term management, the pet owner interacts with every veterinary healthcare team member. Developing communication resources and telephone triage skills will help nonclinical staff determine appropriate scheduling for ill patients and those requiring ongoing monitoring with timed testing or even potentially life-threatening situations. Because the patient history plays an essential role in case management, the guidelines discuss how to take a quality patient history, including several specific and helpful tips.
Low-stress visits reinforce pet owner compliance for timely follow-up and encourage more reliable diagnostic results because stress can influence many endocrine-related diagnostics.
Client communication is important for the successful management of these diseases. The client should have a basic understanding of the disease, the clinical signs, adverse events, long-term goals, and recommendations regarding treatment and ongoing care.
Constance Hardesty is a freelance writer living in Colorado. She is former editor-in-chief of AAHA. |
Photo credits: Pekic/E+ via Getty Images, ilkermetinkursova/E+ via Getty Images, shironosov/iStock via Getty Images Plus, Supitnan Pimpisarn/iStock via Getty Images Plus