Canis lupus familiaris or Canis familiaris popularly known as the domestic dog is one of the most common and loved domestic animals reared all over the world. It has a long snout, an acute sense of smell and can bark, howl and whine. Apart from being a good pet, it is also reared for work such as being a guard or sniffer or used in filed sports. A common endocrine disorder that is quite difficult to diagnose in dogs is the Cushing's syndrome (CS). CS is a collection of symptoms that occur when the dog’s body creates and releases too much cortisol, a hormone that assists a dog respond to stress, deal with excess weight, fight infections and regulate blood sugar ( Foster & Smith, 2016 ). Between 80 % and 90 % of the diagnosed cases fall under the categorization Cushing’s disease while the 15 % to 20% are adrenal dependent (Roberts, 2015) .
Pathophysiology & Common Sequela
Cortisone hormone is controlled by the endocrine system and is responsible for the metabolism of proteins and carbohydrates in the body. Due to a tumor in the enlargement of, or the growth of a tumor in the pituitary glands, too much Cortisone is produced and this hinders the body’s metabolic process thus leading to hypertension or gastrointestinal disorders. This disorder results into a condition referred to as hyperadrenocorticism, which is among the most common hormonal related disorders in dogs (Roberts, 2015). The formation of Cortisone is triggered by the Adrenocorticotropic hormone (ACTH). When there is enough Cortisone in the system, it hinders the production of ACTH thus forming a hormonal imbalance between the two (Watson & Heeren, 2014). The formation of tumors in the pituitary glands, or the existence of Congenital Adrenal Hyperplasia (CAH) will cause abnormal production of ACTH which will lead to hyperadrenocorticism. However, this may also occur if too much glucocorticoid is administered to a dog.
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Possible secondary DS and complications
The endocrine system works on a sequence of checks and balances. Once an imbalance occurs as in the case of CS and is not addressed, it triggers an indefinite hormonal chain reaction, which with time may trigger, encourage or cause one or several of the following conditions.
Hypothyroidism also referred to as Law Thyroid or underactive thyroid is a hormonal disorder where the thyroid doesn’t enough hormones lead to cold intolerance, fatigue, depression and obesity (Watson & Heeren, 2014) .
Pancreatitis : this refers to the inflammation of the pancreas and can be triggered by CS related imbalances.
Diabetes mellitus: CS hinders metabolism thus increasing the possibility of Diabetes Mellitus, an inability to produce sugar, and therefore energy, despite the consumption of food.
Seizures : The low energy levels created by the hampered metabolism will if not checked create the inability to supply enough oxygen to the brain leading to seizures.
Hypertension : This is the long term consequences of too much pressure in the pumped blood leading to damage in the arteries. Blood pressure is partially hormonally controlled and an untreated hormonal defect will almost always lead to hypertension (“Cushing’s Syndrome” 2010).
Congestive Heart Failure : This is among the extreme consequences of undiagnosed and untreated CS defined as the weakening of the heart leading to a fluid build-up in the lungs as well as other vital body organs and is almost always fatal (“Cushing’s Syndrome” 2010) .
Thromboembolism : Hormones such as estrogen and progesterone affect the clotting of blood. A hormonal imbalance will in time cause clotting within the blood circulation system. A blood clot may loosen and get caught in a more dangerous part of the circulatory system causing Deep Venous Thrombosis (DVT) and Pulmonary Embolism (PE).
Liver failure : CS’s effect on metabolism and its kindred consequences will overtime overload the liver leading to chronic liver failure, a situation that is potentially fatal unless treated immediately (“Cushing’s Syndrome” 2010).
Kidney failure : This is closely related to liver failure and results from the long term effect of CS to the metabolic system leading to kidney overuse and eventual failure.
Equine
A related condition in horses referred to as the Equine Metabolic Syndrome (EMS) occurs when adipose tissue releases increased adipokines, a protein hormone which in turn occasions the increased production of cortisol leading to the disruption of the horse’s reaction to insulin (Getty, 2014). This results in high insulin and glucose blood concentrations. As the horse can no longer properly metabolize carbohydrates including starches and sugars, this may lead to the onset of laminitis, a debilitating inflammatory condition that occasions the bonding of the hoof with the pedal bone (Malazdrewich, 2012).
Clinical Symptoms and diagnosis
One of the clinical signs is Polydipsia and Polyuria. This refers to an extra ordinary increase in both thirsts (Polydipsia) and urinations (Polyuria). This is common in 85% of cases and the consumption of water with the resultant increase in urination will increase between 2 to 10 times (Watson & Heeren, 2014). The second sign is Polyphagia. Due to the hindered metabolism, the dog may be continuously and extremely hungry leading to constant overfeeding. The good and constant appetite may be misconstrued for a sign of good health and blanket the realization that the dog is sick (Roberts, 2015). The dog also shows a tendency to pant abnormally and exceedingly with an abnormally huge belly (Potbelly). This results from the shifting of fat to the abdominal area while the muscle mass in the stomach wastes away encouraging protrusion.
Becoming overweight and obese will also cause the dog to have a thin and fragile skin making it susceptible to contract bruising (Summers, 2013; Watson & Heeren, 2014). Other signs include development of fat pads on the neck and shoulders, general but abnormal hair loss, the dog being lethargic, inert and weak, insomnia, anestrus among females, testicles shrinking, and darkening of the skin and formation of hard white scaly patches on the skin elbows.
Common Difficulties in the Detection of CS
CS increases the appetite of the dog as opposed to other ailments that inhibit appetite. This creates the assumption of good health leading to the dog’s custodian not seeking medical attention in time (Watson & Heeren, 2014). CS mostly happens to mid-aged to older dogs and apes the common signs of aging like lethargy and obesity leading to it being ignored or assumed.
Prevention
The only avoidable form of CS is that occasioned by external glucocorticoid via steroid drugs which can be avoided through proper use. However, proper vigilance would prevent extreme symptoms and development of CS through early treatment and introduction of control measures. Any likely symptoms such as combination of seemingly normal circumstances ought not to be ignored as the earlier CS is diagnosed, the better for its control (Watson & Heeren, 2014).
Prognosis
The prognosis of CS is dependent of several factors with the most important being its cause, the point at which diagnosis has been done, the treatment regimen effected, and the age of the dog. Vigilance ought to be exhibited by the caretaker as symptoms will appear and disappear quickly. In the case of early diagnosis, pituitary surgery to excise the tumor causing the overproduction of cortisol will cause remission in 85% to 90% of the rimes (Roberts, 2015). When this is done in good time, it will occasion remission of hormonal imbalance in time to avoid neurological disorders. Surgery may also have a curative effect in adrenal tumors caused by CS. It is, however, worth noting that surgery in either adrenal or pituitary glands does not prevent onset of CS occasioned by the alternate glands as treatment of pituitary caused CS does not prevent adrenal caused CS and vice versa (Watson & Heeren, 2014). The cessation of symptoms is also relative with symptoms like Insomnia, Polydipsia, Polyuria and Polyphagia ceasing within a few weeks of treatment but others like hair-loss take quite some time to cease (“Cushing’s Syndrome” 2010).
Factors affecting the nature of prognosis include the vigilance of the caretaker, duration between onset and diagnosis, the cause of the CS, correct diagnosis, treatment regiment, if cause by tumors, the nature, size, operability and location of the tumors, whether the said tumors are benignant or malignant and if malignant to what level, level of success of the treatment regimen effected, age of the dog and nature of care during convalescence (Roberts, 2015). CS is incurable in horses; early diagnosis however will stop the onset of laminitis and its kindred consequences.
Diagnosis
Accurate and timely diagnosis of CS is critical for treatment and recovery. Since the symptoms of CS mirror many other or even signs of old age, it is important for the medical and conduct history of the dog to be properly and accurately reported to the medical attendant to enable the vital proper and early detection (Watson & Heeren, 2014). The physical tests follow the evaluation of the dog’s history. Signs of probable CS should lead to blood tests, which involves a complete blood count (CBC), blood chemistry panel, and urinalysis for proper diagnosis. These tests are aimed at checking increase in alkaline phosphatase and Liver enzymes referred to as ALT, abnormal increase in cholesterol, a kidney function test to check decrease in BUN and a urine low specific test (Watson & Heeren, 2014). This is the routine and initial test. The hormonal tests should also be conducted to test levels of cortisone in the bloodstream and may be conducted in three steps.
The first step is the urine cortisol creatinine ratio test followed by low-dose dexamethasone suppression test and finally an adrenocorticotropin hormone (ACTH) simulation test. If cumulative levels of cortisone are found, the dog is positive for CS. The third round of tests involves establishing the cause of the CS and if tumors; their position, nature and size. Commonly, most CS is pituitary based and will require tests to confirm if it is a Pituitary Dependent Hyperadrenocorticism (PDH) related tumor or an overgrowth of the pituitary gland itself and is conducted through radiography (Roberts, 2015).
A blood test will first either confirm or rule out adrenal tumors leaving the more prevalent and if an adrenal tumor is confirmed, radiographic tests will determine the nature, size, and form of the tumors. A chest ultra sound test will also confirm or rule out metastasizing to indicate if the tumor is malignant or not.
Treatment and nursing care
Lifestyle changes needed once DS
The first lifestyle change required is diet. CS creates a risk for Diabetes Mellitus and required a special diet to avoid the same. A proper diet prescription should be obtained to balance with the nature of illness and form of treatment and followed to the letter. Preferably a low fat, salt, sugar, artificial flavor, coloring, preservatives, and similar chemicals should be observed (Roberts, 2015). Secondly, there is need for more exercise for a CS affected dog. Exercise can also be creatively incorporated in the treatment for example by walking instead of driving to the clinic during the pre and post diagnosis visits (U.S. Food and Drug Administration, 2013). Comfort is also an essential change since DS can be triggered and exacerbated by stress. All measures should be undertaken to ensure that the affected dog is comfortable and stress free at all times.
Treatment
There are different treatment regiments depending on the age of the dog, cause, and duration of CS. These treatment options include oral medication, which is usually prescribed for the incurable pituitary dependent CS and is meant to help in the control symptoms. It includes Trilostane and Mitotane or Lysodren. This regiment may have serious side effects and must be given under close supervision and with strict adherence to prescription and instructions (Roberts, 2015).
Radiation is another treatment option that is most helpful in the case of timey pituitary tumors as it shrinks them thus reducing symptoms of kindred CS. surgery is mainly done in case of adrenal dependent CS and involves removal of the affected adrenal gland. Trilostane may also be effective in controlling adrenal dependent CS to control symptoms but it’s not curative. Transsphenoidal surgery is an advance procedure, for the removal of a pituitary tumor (U.S. Food and Drug Administration, 2011). Albeit complex and expensive, its success saves the dog from lifelong medication for CS as its curative in nature
Nursing Care
Client education
Extra care with regard to steroid medication is important. Close scrutiny is necessary for any adverse side effects. In case of extreme side effects, a change of medical regiment is advisable. The dog should also get consistent veterinary check-ups upon diagnosis, during treatment and incase of curative treatment, even after successful treatment. Expert advice should be sought before breeding decisions as some CS triggers are congenital. As earlier indicated treatment of one kind of CS does not stop the onset of another type, complete vigilance and alertness to symptoms is always important. Finally, healthy dos practices including proper diet, exercise, medical check-ups and examinations should be maintained.
Conclusion
Having been consistently labeled as man’s best friend, the good health of our dogs is vital for our own well-being. CS by its very nature and complexity is a big challenge to any person who cares for a dog and it is important to learn how to detect it, refer the dog for veterinary attention within good time, and follow veterinary advice to the latter. Most of the causes of CS are beyond the scope of the care giver and all that can be done is catch it in good time for a cure or proper control of symptoms for a better and longer life for the dog as most of the CS traits are incurable. The same applies for the Equine related CS that albeit having no cure, can also be controlled symptomatically for a dog’s better life. In all circumstances, it is better to err on the side of caution than of speed as far as seeking veterinary advice is concerned.
References
Cushing’s disease. (2010). Retrieved from <https://www.vetmed.wsu.edu/outreach/Pet-Health-Topics/categories/diseases/cushing’s-disease/>
Foster & Smith. (2016). Cushing’s disease (Hyperadrenocorticism) in dogs . Retrieved from <http://www.peteducation.com/article.cfm?c=2+2114&aid=416/>
Getty, J. M. (2014). Equine Cushing's disease: Nutritional management .
Jack, C. M., Watson, P. M., & Heeren, V. (2014). Veterinary Technician's Daily Reference Guide: Canine and Feline, 3rd Editi . John Wiley & Sons.
Malazdrewich, DVM, C. (2012). American Association of Equine Practitioners . Retrieved from <http://www.aaep.org/info/horse-health?publication=748/>
Reeder, D., & American Association of Equine Veterinary Technicians and Assistants. (2009). AAEVT's equine manual for veterinary technicians . Ames, IA: Wiley-Blackwell.
Roberts, G. (2015). Cushing's Disease in Dogs: A comprehensive guide to Cushing's Disease in dogs written by veterinary expert Dr. Gordon Roberts . Author.
Summers, A. (2013). Common diseases of Companion animals (3rd ed.). Elsevier.
U.S. Food and Drug Administration. (2011). FDA Approves First Drug to Treat Cushing’s Disease in Horses. Retrieved from <http://www.fda.gov/AnimalVeterinary/NewsEvents/CVMUpdates/ucm280401.htm/>
U.S. Food and Drug Administration. (2013). Treating Cushing's Disease in Dogs . Retrieved from <http://www.fda.gov/ForConsumers/ConsumerUpdates/ucm151209.htm/>
