Adrienne is a certified dog trainer, behavior consultant, former veterinarian assistant, and author of "Brain Training for Dogs."
Addison’s disease in dogs, otherwise known as hypoadrenocorticism, is a condition that occurs when a dog's adrenal glands no longer work as they should. In a healthy dog, well-functioning adrenal glands are responsible for producing the important hormones cortisol (a hormone that plays a role in a dog's ability to manage stress and regulate glucose) and aldosterone (a hormone responsible for maintaining proper hydration and correct electrolyte/mineral balance.)
When the adrenal glands no longer work as they should, these hormones aren't secreted at normal levels. In many cases, the glands fail to work properly as a result of damage caused by the immune system. While the immune system is responsible for keeping dogs and people healthy, a time may come where for unknown reasons, it ends up attacking and damaging its own tissues.
Addison's disease is often nicknamed "the great pretender." This condition is known for causing vague, intermittent symptoms that may come and go, vary in intensity, and may mimic several other conditions. This condition is frequently misdiagnosed and causes loss of time, frustration, and general risks. Left untreated, the disease may progress to what is known as an Addisonian crisis, which may quickly turn life-threatening if not treated promptly.
When it comes to statistics, this condition has a strong preference for female dogs. It is estimated that 70% of dogs diagnosed with Addison's disease are female. Although it may affect dogs of any sex or age, there is a high prevalence in young to middle-aged dogs, generally between the ages of 4 to 7 years old.
Although any dog breed may get Addison's, some dog breeds appear to be more predisposed:
Although the disease can turn life-threatening, the good news is that once discovered, it can be managed fairly easily. Treatment of Addison's disease in dogs varies based on whether you are dealing with typical or atypical Addison's disease in dogs.
In dogs suffering from typical Addison's disease (also known as primary Addison's disease), the middle and outer layers of the dog's adrenal glands are typically damaged, which leads to both cortisol (glucocorticoids) and aldosterone hormones (mineralocorticoids) not being produced in sufficient amounts.
When dogs with undiagnosed typical Addison's disease undergo blood tests that include checking the dog's electrolyte levels, their sodium and potassium levels are generally off the charts. They will have elevated BUN and creatinine levels and mild to moderate anemia, which often prompts veterinarians to consider testing for a definite diagnosis through what's called an ACTH test.
Dogs with typical Addison's disease do not produce sufficient amounts of cortisol and aldosterone, so treatment consists of replacing these hormones with corticosteroid drugs and electrolyte replacement drugs, such as Florinef.
In most cases, canine Addison's disease, or primary hypoadrenocorticism, is likely caused by immune-mediated destruction of adrenal tissue in response to an unknown trigger, resulting in primary adrenocortical failure with glucocorticoid (cortisol) and mineralocorticoid (aldosterone) insufficiency.
— Dr. David S. Bruyette, board-certified veterinarian specializin in internal medicine.
Sometimes, only the middle layer of the dog's adrenal glands is damaged, which allows the dog's adrenal glands to produce the electrolyte balancing hormone aldosterone, but not cortisone. If only the middle layer fails, meaning the adrenals are still producing electrolyte balancing hormones, the condition is known as atypical Addison's disease.
Atypical Addison's disease in dogs is challenging at times to diagnose. The fact is, affected dogs' routine blood work doesn't provide any hints such as the abnormalities often detected in the typical type. There are no abnormal levels of sodium, chloride, and potassium levels or other significant abnormalities.
Since dogs with the atypical type are glucocorticoid deficient, their main treatment consists of prednisone. Once therapy is implemented, affected dogs should quickly recover, feel better, return to eating and drinking, and gain back weight. Dog owners must consider providing larger doses of prednisone as needed when their dogs are likely to encounter periods of physical or medical stress.
Most patients with atypical Addison's disease are not mineralocorticoid-deficient and maintain normal sodium/potassium ratios throughout their lives.
— Jennifer E. Waldrop, Diplomate” of the American College of Veterinary Emergency and Critical Care
Resting cortisol concentration is a great way to rule OUT Addison's disease. If the resting cortisol concentration is > 2 µg/dl, then the patient is not likely to be addisonian. In cases with a resting cortisol < 2 µg/dl, you must perform an ACTH stimulation test to confirm the disease.
Adrienne Farricelli (author) on April 10, 2018:
Thanks Larry, one of my dogs has some of these symptoms so I am passing along some info as I prepare for possibly scheduling soon an ACTH TEST.
Larry W Fish from Raleigh on April 10, 2018:
A great and informative article, Adrienne. Thank you for pointing out things about dogs that I never knew.
I read your recent post regarding Addison's disease and I'm writing to see if you could clear up (or add to the debate) a discussion that we are having at our hospital. I am a second-year medicine resident and our medical staff is having a debate about what is considered a normal vs. an abnormal cortisol response to ACTH stimulation and what exactly is "atypical" Addison's disease.
For example, what about dogs that have chronic gastrointestinal (GI) signs that have not yet been been diagnosed but a flat cortisol response to ACTH stimulation is found? If we perform an ACTH stimulation test on these dogs, many will have a basal cortisol level well within reference range limits (e.g., 2 to 4 μg/dl) but the post-ACTH stimulated cortisol concentration will not rise to levels 3-5 times higher than the basal cortisol concentration. Some of these dogs will have ACTH-stimulated cortisol concentrations that are below the post-ACTH reference range (e.g., in the range of only 3-6 μg/dl). Is this atypical Addison's disease?
What do you do in these cases? Look for other causes of the GI signs? And if no other cause found supplement with steroids? Should we just repeat the ACTH stimulation test down the line?
First of all, you must remember that the blog post on Addison's disease you are referring to was written primarily for dog owners, not veterinarians. I was trying to be clear, which is difficult when we are discussing a topic that could include typical, atypical, or secondary adrenal insufficiency.
Almost all dogs with primary hypoadrenocorticism (typical Addison's disease) and near complete destruction of the adrenal cortex will have subnormal basal and ACTH-stimulated serum cortisol concentrations ( 250 pg/ml) with a severely blunted serum cortisol response to ACTH stimulation, that would be diagnostic for primary hypoadrenocorticism (1-4). If the serum electrolytes are normal, that could be called "atypical" Addison's disease. Some of these dogs will certainly go on to develop serum electrolyte changes, whereas others never seem to do so. I suspect that these latter dogs do not actually have adrenal destruction, but may have an ACTH receptor defect where circulating ACTH values are high but the adrenal gland doesn't bind the ACTH so it cannot act to stimulate cortisol secretion. Again, the best way to distinguish secondary from primary hypoadrenocorticism in these dogs is to measure plasma ACTH before any glucocorticoids are administered (or off all glucocorticoids for at least 1-2 weeks).
But let me get back to your original question about the dogs that have chronic GI signs and whose ACTH stimulation test results reveal a normal (or low) basal cortisol with a post-ACTH cortisol values that is blunted, rising to only 3-6 μg/dl. This is certainly not a "normal" response, abut it's very difficult for me to explain why these dogs would have any signs when these circulating cortisol values are within or slightly above the normal basal range. If this was a dog on mitotane or trilotane, for example, we would be very pleased with those serum cortisol results and would not be worried about hypoadrenocorticism (5-7).
In my experience, most of these dogs have a history of being treated with glucocorticoids, which could lead to secondary (iatrogenic) hypoadrenocorticism. Again, if you would measure a plasma ACTH concentration in these dogs, the values should be low-normal if they do indeed have secondary ACTH deficiency. If there is now history of glucocorticoid use, I would certainly repeat basal or ACTH-stimulated cortisol values in 2-4 weeks, but most of these dogs do not end up having primary adrenal disease.
Now that's not to say that they don't need steroid supplementation, but not for "atypical" adrenal disease.
I have a somewhat related follow-up question, if I may.
I have a dog that is presenting with low resting cortisol (1.3 on his ACTH Stim Test, normal range 2-5), but stimmed in the high normal range (16.7, normal range 6-18). A full vial of Cortosyn was used, IV this is an 80 pound German Shepherd.
His electrolytes are within normal ranges, with Na:K ratio 35:1.
Unfortunately, at the time of the stim test, the resting ACTH level was not run, so we don't have that value steroids were started shortly after. The low resting cortisol was confirmed on a later test also.
He also presents with hypovolemia (He was brought in for severe exercise intolerance and panting). His xrays are said to look just like an Addison's dog (under-sized heart with corresponding vascular changes), and this was confirmed by the cardiologist, that he does not have heart disease, but the left-side of his heart is not being supplied with enough blood and has become smaller. He is hypotensive.
On ultrasounds, his adrenals could not be visualized, they are assumed small. His spleen is slightly enlarged, but within breed standards.
An MRI or CT scan is not financially possible.
It appears that he became less responsive to his thyroid medication (Soloxine, .7mg BID) once he was on prolonged ketoconazole therapy. He has been off this drug since December 2010.
I do not know if this is related, but this GSD typically has a lipase value in the 50's (normal range 100-750), and a normal amylase. Since the end of November 2010, over the last 4 blood panels, the lipase has been steadily increasing, while the amylase is decreasing.
His bloodwork that was run several days after the ACTH Stim Test also showed a low normal calcium value of 8.5 (normal 8.2-12.4), as compared to his normal of about 10.0.
While this dog is not an Addison's dog, does it make sense to assume that there is a problem in the ACTH feedback loop somewhere? Perhaps the pituitary?
My understanding about hypovolemia in Addison's patients, is that it is caused by fluid imbalance and that would show up in the electrolyte values. This does not appear to be the case here. Do you know of any other possible cause for the hypovolemia?
Do you have a recommendation on prednisolone dosing for a dog in this situation? He is currently on 5mg in the morning, and 2.5 mg later in the day/early evening. We would like to keep the dose as low as possible, without putting him into a crisis.
Would there be any advantage to using methylprednisolone over prednisolone in this case?
Would it be recommended to monitor this dog's resting cortisol to check for response to treatment? Any other recommendations?
As you noted, the results of the ACTH stimulation test showed a low-normal basal cortisol value but the adrenal glands did respond normally when tested. This completely excludes Addison's disease (both atypical or typical).
The fact that the adrenal glands could not be seen on ultrasound is confusing, but that doesn't mean Addison's because the ACTH stimulation test revealed a normal adrenal cortex. Sometimes the adrenal glands can be difficult to visualize but ultrasound cannot be used as a diagnostic tests for hypoadrenocorticism.
I do not know why the dog is hypovolemic, but again, you have proven it's not related to the adrenal gland. The dog could have a pituitary gland problem but that is not very likely, and it is clearly is not related to ACTH deficiency.
At the moment, you have the dog of higher-than-maintenance doses of prednisone. The dose of prednisone for an average human patient is only 5 mg per day, so an 80 pound dog with Addison's should do well on 5 mg per day too.
But again, this dog shouldn't need ANY prednisone because you have already excluded Addison's disease. I would consider stopping the drug.
When we administer synthetic steroids such as prednisone, you cannot use cortisol measurements to monitor the circulating glucocorticoid values. In fact, these drugs may feedback to the pituitary gland to inhibit pituitary ACTH secretion and make the whole situation worse.
In summary, I don't know what is wrong with your patient — it could be a number of different disorders — but I do now that the dog does not have Addison's disease or any other form of under-active adrenal disease. I'd stop the prednisone and continue the workup if the problems persist to get to the definitive diagnosis.
i have a 5 month old french mastiff that is having a really hard time eating. he went into either an addisons crisis or hypoglycemic. my vet sent a cortisol out and we got a reading of 2.0 and a retest the next day of 1.8, we are going to do the ACTH test but we are waiting for the drug, do you think that is low enough to even be considered addisonian? some vets i spoke to said no way and others said maybe.
It's certainly possible, but unlikely that your dog has Addison's disease.
The age of 5 months is younger than we generally see (most dogs are much older), and the French mastiff isn't a breed that is predisposed to developing Addison's disease.
So his ACTH was 2.7 pre ACTH and 8.5 after the injection..normal?
Both the resting cortisol value (2.7 μg/dl) and the ACTH-stimulated cortisol value(8.5 μg/dl) are completely normal. This completely excludes a diagnosis of hypoadrenocorticism (or Addison's disease - both typical or atypical).
So now that we have ruled out Addison's disease, you can continue the workup for other problems.
Could you expand on the causes of a dog with a low resting cortisol but a normal ACTH stim?
I ran routine bloodwork on a 7yr SF lab that came back with Na:K ratio of 21, high K+ 6.9(N=4-5.6), low normal Na 145(N=141-156) high Cl+ 117(N=105-115.
Other bloodwork was WNL, including T4=2(N=1=4).
We did an ACTH stim which revealed low baseline Cortisol 0.5(N=2-6) and a normal post ACTH 7.7(N=6-18).
This dog has multiple limb lameness (bilateral TPLO's as well as elbow and metacarpal arthritis) treated with monthly injections on Adequan 1.5ml SQ, Legend 1.0 ml IM (off label)and Rimadyl 75mg BID as needed. The dog, is very active (mountain hiking multiple times a week), has normal energy, good weight and appetite.
The only other abnornalities are occassional vomiting (Bile and grass approx 1x/week) and loose stool during and after heavy exercise which resolves the following day.
Having ruled out Addison's with the ACTH stim, I am wondering if the drugs this dog gets for arthritis pain could cause the low cortisol?
To my knowledge, none of these drugs have an impact on serum cortisol concentrations by directly affecting the cortisol synthetic pathways in the adrenal gland or indirectly by suppressing ACTH levels.
Remember that serum cortisol is secreted episodically, with peaks and valleys throughout the day. So you might have sampled at a low point.
We also have to consider lab error, both with the pre- or post-ACTH cortisol values AND the serum electrolytes. That is especially true is the labs were done "in-house." If there is any doubt, don't hesitate to repeat some of this labwork in the future.
My veterinarian has diagnosed my dog Leopold as an Atypical Addison. I am having trouble understanding this diagnosis, and do not want to keep him on the 2.5mg of daily prednisone if it is not needed (he is a 37 pound, 1 year old Standard Poodle. He has normal lytes, and normal sodium. His basal cortisol level before any prednisone treatment was December 2, 2015 at 3:09 AM Dr. Mark E. Peterson said.
Obviously, your dog is a complicated case and I cannot confirm the diagnosis based on what you have told me here. However, the ACTH stimulation test is certainly consistent with adrenal insufficiency or hypoadrenocorticism. If the prednisone is helping, it cannot hurt anything and I would recommend you continue it.
To follow up on your original comments regarding the original diagnosis and need to perform an ACTH level, I have a question. I currently have a 16 year old Chihuahua that was referred to me as an "atypical" Addisonian. He has been treated for years (I believe at least 8-10)with an appropriate prednisone dose. He has done really well. Recently he has been presenting with intermittent elevations in his amylase and lipase. On ultrasound his pancreas has been prominent intermittently and a PLI submitted was in the questionable range (217 ug/L, December 7, 2015 at 3:59 PM Dr. Mark E. Peterson said.
You could do another ACTH stimulation test and measure aldosterone to help rule out mineralocorticoid deficiency, However, I've never seen a dog have atypical Addison's for 6-8 years and only then develop mineralocorticoid deficiency. But, as you know, anything is possible!
I am not sure if this thread is still open, but I have a 1 year old GSD who has gastrointestinal problems and severe allergies. I am getting conflicting information from all the vets he see's. Some think he has atypical addison's and some say definitely not. His baseline cortisol results from Idexx were very low below 1.0. His ACTH stim test came back high at 11.7 (range was 1.0-5.0). Can an adrenal glad disease be ruled out? Thank you!
That ACTH stim test DEFINITELY, POSITIVELY rules out any form of Addison's disease. I would fire anyone that wanted to call this Addison's!
I was wondering if you could provide an opinion: I have a 2ish terrier mix with intermittent GI problems. Based on her vet's suspicion, she had a Cortsyn ACTH test done with a resting cortisol of 1.1 (range 1.0-5.0) and stimulated cortisol of 4.2 (range of 8.0-17.0). Would this be considered definitely Addison's? (She took no steroids or any other medication prior to the ACTH test. Her electrolyte bloodwork has only just been sent out.)
No, this rules out Addison's disease.
Thanks for the quick response! I just wanted to follow up: Does this rule out all types of Addison's, even though her stimulated cortisol levels are so low? (Primary, atypical, and secondary) Do you have any recommendations for what other tests to run to diagnose the low cortisol levels and GI problems? She's never had an Addisonian crisis so is it possible she's pre-Addisonian? Thanks again!
This rules out all types of Addison's disease. Most of these dogs have received some type of steroids in the recent past, which has partially suppressed the cortisol response. A pre-Addison's dog would not have any GI signs.
If you are worried, you can always repeat the test in the future (3-6 months from now).
As with many health conditions, Addison’s disease dog treatment cost can vary between cases. That means that there will most likely be a variance in the cost of treatment depending on what drugs your dog needs, the veterinary surgeon treating it, and the veterinary practice or specialist clinic involved.
Addison’s is a somewhat uncommon disease and can be hard to detect in many cases, especially as symptoms may only become pronounced once the disease has progressed significantly. Additionally, there are three presentations or subtypes of the illness.
Detection and treatment costs will depend on the timeline of the investigation, as well as the subtype of the disease.
Primary Addison’s is caused by adrenal dysfunction where the adrenal gland deteriorates through an autoimmune response.
Atypical Addison’s is a situation in which the adrenal cortex only stops production of cortisol but not other hormones. These cases are not as severe for the animal. However, it will eventually progress into typical or primary Addison’s after a few months which makes diagnosis challenging.
Secondary Addison’s also only affects cortisol production but it will not progress to the typical form of the disease and electrolyte imbalance does not occur.
All three types still require medication but the types of medication differ based on what hormones are needed to be boosted or outright replaced.
The indicators of Addison’s are somewhat broad as described above, so diagnosing it specifically can be a challenge. Of course, at the sign of any abnormal behavior or health with your animals, one should take them in to see the vet.
Standard exams run around $50 and will include heart and pulse checks, as a low pulse or irregular heartbeat can indicate Addison’s.
Bloodwork can help in diagnosis as dogs with the disease tend to have low sodium and high potassium levels, among other abnormalities. Urinalysis is also helpful for detecting Addison’s as the urine is usually diluted with it in dogs. This will run $70 to $250 depending on how extensive the bloodworm and urinalysis is.
The definitive test for addison’s is a blood test called an ACTH stimulation test. The ability of the adrenal gland to produce cortisol in response to ACTH is measured.
First your dog will have his blood drawn. ACTH will be administered. Your dog will need to remain at the veterinarian for two hours and his blood will be drawn again. This will run around $200 as it is a highly specialized test.
Lastly, an EKG can be used to examine changes in the heart that would occur due to high levels of potassium. This test costs around $50 to $100.
Sometimes, imaging may be needed to rule out other causes of your dogs symptoms. It will also give your veterinarian information about how addison’s has affected your dog.
Radiographs – If radiographs are required, the average cost of these ranges from $60 to $180, depending on how many images are needed.
Abdominal ultrasound – The vet may carry out an abdominal ultrasound scan at the cost of between $250 and $500.
As mentioned, Addison’s is usually only detected once the dog is severely ill and so, short-term hospitalization may be required to help with recovery. IV drugs are administered to remedy dehydration and cortisol-like drugs are given to regulate hormone levels.
Most dogs will recover within a few hours from this. These drugs will run between $100 and $200.
If your dog has suffered an Addisonian crisis, admission to a veterinary hospital is necessary. Hospitalization, although largely dependent on your location and specific clinic, may be in the ballpark of around $150 to $300 per day.
Following hospitalization, long-term treatment involves life-long drug therapy, which replaces the hormones that can no longer be produced. The hormone supplements can range in cost somewhat drastically, depending on the specific ones needed to be replaced, as well as your dog’s response to the treatment.
Larger dogs will need larger doses of medication and so may end up costing more. Generally speaking, these meds will run for about $50 to $200 a month.
Dogs with Addison’s on appropriate drug therapy regimens have great prognoses and their life expectancies are not expected to be affected unless other health problems arise. Most vets recommend the dog be brought in every 3 months to continue monitoring its bloodwork.
Patty Khuly, VMD, MBA is a prolific pet health writer, occasional media personality, and a practicing veterinary clinician (for almost 23 years!).
Many of the functional disturbances of chronic adrenal insufficiency are not highly specific they include recurrent episodes of gastroenteritis, a slowly progressive loss of body condition, and failure to respond appropriately to stress. Although hypoadrenocorticism is seen in dogs of any breed, sex, or age, idiopathic adrenocortical insufficiency is most common in young, female adult dogs. This may be related to its suspected immune-mediated pathogenesis.
A reduction in secretion of aldosterone, the principal mineralocorticoid, results in marked alterations of serum levels of potassium, sodium, and chloride. Potassium excretion by the kidneys is reduced and results in a progressive increase in serum potassium levels. Hyponatremia and hypochloremia result from renal tubular loss. Severe hyperkalemia may result in bradycardia and an irregular heart rate with changes in the ECG. Some dogs develop a pronounced bradycardia (heart rate ≤50 bpm) that predisposes to weakness or circulatory collapse after minimal exertion.
Although the development of clinical signs is often unnoticed, acute circulatory collapse and evidence of renal failure frequently occur. A progressive decrease in blood volume contributes to hypotension, weakness, and microcardia. Increased excretion of water by the kidneys, because of decreased reabsorption of sodium and chloride, results in progressive dehydration and hemoconcentration. Emesis, diarrhea, and anorexia are common and contribute to the animal’s deterioration. Weight loss is frequently severe. Similar clinical signs are seen in cats with hypoadrenocorticism.
Decreased production of glucocorticoids results in several characteristic functional disturbances. Decreased gluconeogenesis and increased sensitivity to insulin contribute to the development of moderate hypoglycemia. In some dogs, hyperpigmentation of the skin is seen because of the lack of negative feedback on the pituitary gland and increased ACTH release. Atypical Addison disease has been reported in dogs and is associated with hypocortisolemia with normal electrolytes. Clinical signs are similar to those seen in dogs with both glucocorticoid and mineralocorticoid insufficiency.
The most common abnormality in dogs is bilateral idiopathic adrenocortical atrophy, in which all layers of the cortex are markedly reduced in thickness. The adrenal cortex is reduced to one-tenth or less of its normal thickness and consists primarily of the adrenal capsule. The adrenal medulla is relatively more prominent and, with the capsule, makes up the bulk of the remaining adrenal glands.
All three zones of the adrenal cortex are involved, including the zona glomerulosa, which is not under ACTH control however, no obvious pituitary lesions have been seen in dogs with idiopathic adrenal cortical atrophy.
A destructive pituitary lesion that decreases ACTH secretion is characterized by severe atrophy of the inner two cortical zones of the adrenal gland the zona glomerulosa remains intact.
Addison’s disease (hypoadrenocorticism) is caused by a lower than normal production of hormones, such as cortisol, by the adrenal glands. The adrenals are small glands that are located near the kidneys. Adrenal hormones are necessary to control salt, sugar and water balance in the body.
Addison’s disease occurs less commonly than the opposite condition, Cushing’s disease (overproduction of cortisol) in dogs, and is rare in cats.
Addison’s disease occurs most commonly in young to middle-aged female dogs. The average age at diagnosis is about 4 years old. The signs of Addison’s disease may be severe and appear suddenly, or may occur intermittently and vary in severity. Signs may include weakness, depression, lack of appetite, vomiting, diarrhea, and occasionally increased thirst (polydipsia) and increased urine production (polyuria).
When a pet is stressed, their adrenal glands produce more cortisol, which helps them deal with the stress. Because dogs with Addison’s disease cannot make enough cortisol, they cannot deal with stress, so the signs may occur or worsen when stressed. What a dog finds stressful depends upon his/her temperament. For many dogs, any change in their day-to-day routine, such as being boarded or having house guests, is stressful and may precipitate or worsen signs of Addison’s disease.
On examination of dogs with Addison’s disease one may see depression, weakness, dehydration, weak pulses and sometimes a slow, irregular heart rate. Routine laboratory tests often show a low blood sodium and high blood potassium. Loss of water, in vomit and diarrhea, can lead to dehydration. Severe dehydration increases waste products in the blood (creatinine and blood urea nitrogen = BUN) that are normally eliminated by the kidneys. Addison’s disease can be confused with primary kidney disease. Some dogs with Addison’s disease have low blood sugar. See What Do Those Lab Tests Mean? for additional information about laboratory tests.
Sick dogs often show a pattern of changes in their white blood cells (WBCs) called a stress leukogram. This pattern of changes in the WBCs is caused by cortisol. The absence of a stress leukogram in a sick dog may be a clue to consider Addison’s disease. The urine is often dilute.
Increased blood potassium can cause life-threatening abnormalities in the heart rhythm. These abnormalities can cause the heart rate to be slow and irregular and can be seen on an electrocardiogram (ECG).
X-rays of dogs with Addison’s disease do not show any specific abnormalities. The heart may appear smaller than normal and rarely the esophagus (tube from mouth to stomach) can be enlarged.
The history, physical examination, and initial laboratory tests provide suspicion for Addison’s disease, but a more specific test, an ACTH challenge, should be performed to confirm the disease .
There are two stages of treatment for Addison’s disease in-hospital treatment and long term treatment. Very sick dogs with Addison’s disease require intravenous fluids, cortisol-like drugs and drugs to neutralize the effects of potassium on the heart.
Long-term treatment involves the administration of hormones in one of two forms either a daily pill or a shot that is given about every 25 days. Because dogs with Addison’s disease cannot produce more cortisol in response to stress, stress should be minimized whenever possible. It may be necessary to increase the amount of hormones given during periods of stress (e.g. boarding, surgery, travel, etc.).
With appropriate treatment for Addison’s disease, dogs can live a long and happy life.
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