Clinical techniques in small animal practice最新文献

The most common cause of primary hyperparathyroidism in dogs and cats is a solitary adenoma involving an extracapsular parathyroid gland. The prognosis is excellent if the affected parathyroid gland is removed. Nonsurgical methods are discussed, although there are no current data to support any benefit over conventional surgery. The common postoperative complication to consider is hypocalcemia. Hypocalcemia can be successfully managed in these animals if it is anticipated and treated promptly.

There are numerous conditions that may result in defects of the hard and soft palate. Reconstruction of these defects may be difficult due to anatomical limitations and limited tissue availability. The majority of palate defects, even when large, may be closed using local and/or axial pattern flaps, while other more advanced techniques such as free tissue transfer and prosthetic implants are required in a smaller number of cases. This article describes the use of local and axial pattern flaps in the reconstruction of the hard and soft palate.

Pituitary-dependent hyperadrenocorticism is a common endocrine disorder in dogs in the United States. Once a diagnosis is established, a decision must be made whether or not to pursue treatment, and if so, which medication to use. Historically, mitotane (Lysodren, o,p’-DDD, Bristol-Myers Squibb, New York) has been the most commonly used treatment for medical management. Its use is complicated and comes with many potential side effects, making many practitioners wary of its use. Recently, trilostane has been proven to be an effective treatment of pituitary-dependent hyperadrenocorticism and is approved for use in other countries. Treatment with trilostane is somewhat simpler and the incidence of side effects seems to be less when compared with mitotane therapy. Either treatment can be a safe and effective method of treatment for pituitary-dependent hyperadrenocorticism when the practitioner and client are well educated regarding their use and an appropriate monitoring protocol is used.

The diagnosis and treatment of hypoadrenocorticism can be one of the greatest challenges faced by veterinary practitioners, as Addison’s disease may have many faces and many presentations. Although the disease is most often diagnosed in dogs, cats may also suffer from Addison’s disease. The practitioner must have a high index of suspicion to make a diagnosis of hypoadrenocorticism. This index of suspicion is based on knowledge of the common signalment, history, physical examination, and laboratory findings. Diagnosis of hypoadrenocorticism is supported by appropriate choice of diagnostic endocrine tests that are described in detail in this article. Once a diagnosis of hypoadrenocorticism has been made, expedient treatment is of foremost concern. Timely treatment using fluids, corticosteroids, and supportive care will ensure a successful outcome; the emergency treatment of Addison’s is covered briefly in this article and fully in another article in this issue. The purpose of this review was to describe the clinical diagnosis and chronic treatment of hypoadrenocorticism in dogs and cats.

Hypoadrenocorticism is caused by a lack of endogenous glucocorticoid and mineralocorticoid. These deficiencies can cause a myriad of clinical signs. This disease is uncommon and its clinical presentation is similar to many much more commonly recognized diseases such as renal failure and various gastrointestinal disorders. Severely affected patients may present in a life-threatening adrenocortical crisis, which is characterized by variable degrees of volume depletion and electrolyte abnormalities. The emergency clinician should maintain a high clinical suspicion for hypoadrenocorticism, as early recognition and rapid treatment of hypovolemia and electrolyte abnormalities can be lifesaving. The approach to emergency treatment of hypoadrenocorticism should be to recognize and treat life-threatening arrhythmias, replace intravascular volume and normalize perfusion, correct electrolyte abnormalities and hypoglycemia, administer glucocorticoids, and perform the adrenocorticotrophic hormone stimulation test for definitive diagnosis. Patients with this condition should have a favorable outcome when treated appropriately.

Diagnosis of sex steroid excess or hyperadrenocorticism in dogs may be challenging. Unlike Cushing’s disease, sex steroid excess may have a multitude of manifestations that differ from standard hyperadrenocorticism. In particular, the clinical scenario of a dog with sex steroid imbalance involves one of three systems: dermatologic, reproductive, or hepatic. The history of a dog with hyperadrenocorticism manifesting as sex steroid imbalance often lacks the classical clinical signs of polydipsia and polyuria. Dogs with sex steroid imbalance will often be of specific breeds such as miniature poodles and exhibit trunkal hair loss as the only sign. There is often involvement of the reproductive system, manifested as the growth of perianal adenomas in neutered male or female dogs. The most common laboratory findings consist of elevations in serum alkaline phosphatase and serum alanine transferase. The following article reviews the etiology, common signalment, clinical signs, and laboratory findings associated with atypical hyperadrenocorticism caused by sex steroid imbalance and then explores the medical, surgical, and radiation treatment options.

Although only recently discovered, feline adrenal disorders are becoming increasingly more recognized. Feline adrenal disorders include diseases such as hyperadrenocorticism (Cushing’s syndrome) and hyperaldosteronism (Conn’s syndrome). The clinical signs of feline hyperadrenocorticism, which include unregulated diabetes mellitus and severe skin atrophy, are unique to the cat. Other signs of feline hyperadrenocorticism, such as potbellied appearance, polydipsia, polyuria, and susceptibility to infections are also seen in dogs with hyperadrenocorticism. Conn’s syndrome has only recently been described in the cat and is in fact more common in cats than in dogs. Characterized by severe hypokalemia, hypertension, and muscle weakness, Conn’s syndrome may be misdiagnosed as renal failure. The clinician should become familiar with the clinical signs of adrenal disorders in cats and the common diagnostic tests used to diagnose these syndromes in cats as they differ from those in the dog. Treatment of feline adrenal disorders may be challenging; the clinician should become familiar with common drugs used to treat adrenal disorders in cats.

A presumptive diagnosis of hyperadrenocorticism in dogs can be made from clinical signs, physical examination, routine laboratory tests, and diagnostic imaging findings, but the diagnosis must be confirmed by use of pituitary-adrenal function tests. Screening tests designed to diagnose hyperadrenocorticism include the corticotropin (adrenocorticotropic hormone; ACTH) stimulation test, low-dose dexamethasone suppression test, and the urinary cortisol:creatinine ratio. None of these screening tests are perfect, and all are capable of giving false-negative and false-positive test results. Because of the limitation of these diagnostic tests, screening for hyperadrenocorticism must be reserved for dogs in which the disease is strongly suspected on the basis of historical and clinical findings. Once a diagnosis has been confirmed, the next step in the workup is to use one or more tests and procedures to distinguish pituitary-dependent from adrenal-dependent hyperadrenocorticism. Endocrine tests in this category include the high-dose dexamethasone suppression test and endogenous plasma ACTH measurements. Imaging techniques such as abdominal radiography, ultrasonography, computed tomography, and magnetic resonance imaging can also be extremely helpful in determining the cause.

Unfortunately, fires are common events both in urban and rural portions of the United States. Smoke inhalation is the leading fire-related cause of death. The elemental combustion products of fire are light, heat, and smoke. Smoke is a very complex mixture of potentially harmful substances. Although a relatively rare presenting event to small animal hospitals, when animal fire victims do appear, clinicians must know how to recognize the signs of smoke inhalation and how to successfully deal with them. This discussion will investigate the toxic nature of fire smoke, its mechanism of action upon respiratory tissues, the clinical signs displayed, and its diagnosis and treatment. Differential diagnoses of smoke inhalation and prevention and prognosis will also be explored. Veterinary hospitals should have set protocols in place for managing animal victims of smoke inhalation in order to ensure a successful outcome.

A truly astonishing variety of “over-the-counter” drugs not taken under the auspices of a physician or veterinarian and not regulated by the Federal Drug Administration (FDA) are currently available to the American public. Many of these are widely advertised, readily available, remarkably inexpensive, and universally taken. Although most of the over-the-counter medications are fairly safe, the potential for toxic episodes exists due in large part simply on account of the amounts curious unsupervised animals may ingest. Another part of the problem is that since they are over the counter a large proportion of the public perceives them as totally harmless. In this article, we will investigate the most frequently seen non-prescription intoxications, their mechanism of action, clinical signs, diagnosis management, and prevention.