Seizures

Those who own a pet that has suffered from seizures know firsthand how scary these episodes can be. A seizure is defined as uncontrollable behavior or muscle activity caused by an abnormal increase in the brain’s nervous activities. Epilepsy is a term used to describe recurring seizures.

Seizural activity in dogs and cats can be quite obvious or quite subtle. In essence, seizures should be suspected anytime that a pet undergoes sporadic, unexplained behavioral changes.

What causes seizures in dogs and cats? Potential causes are numerous and include viral infections (e.g., distemper, FIP), toxoplasmosis, fungal infections (e.g., cryptococcosis), epilepsy, hydrocephalus, brain tumor, intestinal parasites, low blood sugar, low blood calcium, insecticide poisoning, and heat stroke. Sometimes the cause cannot be determined; if so, seizure episodes are termed “idiopathic.”

Because causes of seizures are so numerous, a thorough examination and blood workup by a veterinarian is warranted whenever a pet exhibits seizures. In some cases, managing or eliminating an underlying cause will eliminate the seizures. In others, such as with idiopathic epilepsy, there is no known cause, yet by ruling out the other potential causes and establishing a pattern of occurrence, most cases can be effectively managed with anticonvulsant medications. With idiopathic epilepsy, seizures can begin at any stage in life, yet, for the most part, they begin around 1 to 3 years of age. While the cause of idiopathic epilepsy is unknown, it has been shown to be inheritable in some dog breeds, including beagles and dachshunds.

Seizures themselves are rarely life-threatening, unless some physical harm comes to the pet as a result of the fit. The typical seizure or epileptic fit has three stages, or phases. The first of these, the preictal phase, is marked by anxiety and restlessness on the part of the pet. The actual period of the seizure activity, ictus, follows next. Its duration might be for only a few seconds or it might be minutes. Certainly the longer the seizure lasts, the more dangerous it is to the health of the pet. The postictal phase following the seizure is characterized by an overall depression or confusion. Postictal pets can appear to be blind, running into walls and objects, or they might just sleep a lot. This phase can last for a few hours or for days, with the pet returning to its normal state after its conclusion.

There is one seizural presentation called status epilepticus that can prove fatal to a pet. This condition is characterized by a cluster of seizure events occurring in quick succession. Unless appropriate emergency medication is administered intravenously to stop the seizures, these dogs and cats can lapse into a coma and die. As a result, prompt recognition and action on the part of the pet owner is essential.

When attempting to diagnose the cause of seizural activity, veterinarians will first look at the age and the type of pet involved. For example, seizures occurring in pets under 1 year of age commonly result from birth defects or from infectious diseases, such as canine distemper or intestinal parasites, whereas seizures occurring in a very old dog or cat often indicate kidney failure or cancer. In smaller, toy puppies and in active hunting dogs, low blood sugar brought on by illness, stress, or overexertion can be an important inciting cause.

Seizures occurring in a pregnant dog or cat or one that has just given birth are usually caused by “milk fever,” or low blood calcium. Finally, as mentioned above, certain breeds are prone to idiopathic epilepsy. A good history is also vital to help determine the cause of the seizures. Does the pet have access to any type of poison? Has the pet ever suffered any type of physical trauma, such as being hit by a car? Has the intensity of the seizures gradually been getting worse or increasing in frequency? The answers to these and other questions can help a veterinarian narrow the choices.

A complete blood profile and urinalysis should be performed to help rule out the metabolic and infectious causes of seizures. Radiographs and ultrasound can prove to be helpful in certain instances as well. If no underlying cause can be found, and the history supports it, a diagnosis of idiopathic epilepsy is made and treatment is started on this premise.

For cases other than idiopathic epilepsy, treatment is geared toward correcting or managing the underlying problem, whether it is kidney failure, poisoning, low blood sugar, or another condition. Ininstances in which idiopathic epilepsy is suspect, anticonvulsant medications can be used to control or even eliminate the seizural activity.

Determining the exact dosages of anticonvulsant medications might require frequent adjustments at the start in order to accommodate the pet’s individual needs. Pets on anticonvulsant medication may need liver function tests performed annually, since some of these medications can damage the liver over the long term.

Paralysis

Paralysis can be defined as a disruption of the nervous system leading to an impairment of motor function and/or feeling to a particular region or regions of the body. This impairment can be in the form of a spasticity of the muscles in the involved region, or these muscles may become completely limp. In either case, the muscles involved are unable to function in the manner in which they were intended.

Paralysis involving the sensory portion of the nervous system can result in an increased sensitivity to pain or in a complete absence of it. Finally, paralysis resulting in the inefficient function of certain internal organs can occur as well if the nerves supplying these structures are disrupted in any way.

Any disease or disorder that traumatizes the brain, spinal cord, and nerves has the potential to cause paralysis. In dogs and cats, some of the more common causes seen by veterinarians include infectious diseases and parasites, being hit by a car, ruptured disks, and in the case of facial muscle paralysis, ear infections.

Treatment of paralysis is geared toward identifying and treating the underlying cause. If it has been caused by trauma, anti-inflammatory agents combined with drugs designed to draw fluid out of the central nervous system might help reverse signs of paralysis, yet their usefulness is dependent on the extent of the nervous injury and how quickly therapy is instituted.

Pets that have sensory paralysis in a limb might require limb amputation to prevent self-mutilation of the leg. In instances where an irreversible paralysis involves more than one limb, or involves the malfunction of internal organs, pet owners must seriously consider not only their pet’s quality of life as a paralytic but their own as well, before prolonged therapeutic or rehabilitative measures are undertaken.

Degenerative Disk Disease (DDD)

Coursing along the length of the back, the spinal cord travels protected within the bony vertebral column. Separating each vertebra, and located beneath the spinal cord itself, are structures called intervertebral disks, which serve as cushions between each individual vertebra, absorbing shock and forming joints that allow the vertebral column to bend. Each circular disk is composed of an outer band of tough, fibrous tissue called the annulus fibrosus surrounding an inner gelatinous center called the nucleus pulposus. This latter structure is responsible for absorbing any shock placed on the disk.

Degenerative disk disease (DDD) is characterized by the slow degeneration of the nucleus pulposus within one or more intervertebral disks. As these continue to degenerate, they become less resilient and can even calcify, leaving the intervertebral disk without its shock-absorbing unit. As a result, the disks so affected become very susceptible to compression damage, even from normal day-to-day activity. In pets so affected, continued stress or sudden trauma to the disk or vertebral column can lead to an overt tearing or rupture of the annulus fibrosus, and extrusion of the degenerating nucleus pulposus. Unfortunately, since the top portion of the annulus is much narrower than the bottom portion, this extrusion usually occurs upward directly into the spinal canal, damaging the spinal cord and associated nerves.

Overt disk ruptures may be classified as partial or complete. In partial ruptures, the annulus can either be stretched or displaced into the spinal canal, or it can partially rupture, allowing a small amount of the nucleus within to escape and pressure the spinal cord. With complete ruptures, the entire nucleus content is allowed to escape into the spinal canal. Obviously, the consequences of such a rupture versus a partial one are much more severe.

The region of the vertebral column most susceptible to rupture is that portion extending from the last rib to the pelvis. The neck region is another area that can be affected. In a pet suffering from DDD, even the slightest wrong move, such as jumping off the couch or running too fast, can cause an affected disk to rupture.

Dogs are the species primarily afflicted with DDD. Although any dog can suffer from DDD, there do seem to be some breed dispositions. The dachshund breed certainly leads the list in the number of cases reported. Other breeds commonly afflicted with degenerative disk disease include poodles, Pekingese, and Lhasa apsos. Beagles and cocker spaniels also have a notable incidence of DDD in their neck region.

Problems with DDD can show up in smaller breeds as early as 3 years of age. In larger dogs, the onset of signs might not occur until they are 6 to 7 years old. Overweight dogs are at an especially high risk of developing complications associated with intervertebral disk disease.

The clinical signs seen with degenerative disk disease and/or disk rupture depend on the location of the lesion and the amount, if any, of the rupture that has taken place. In fact, the extent of pressure or damage to the spinal cord can be estimated according to the signs seen.

Dogs with early or mild cases of disk disease causing slight pressure upon the cord will be quite painful and reluctant to move. Many will cry or yelp when picked up. If the neck is involved, any manipulations attempted will be met with vigorous protests. These pets often prefer not to be bothered, and have the tendency to isolate themselves.

Appetites are usually reduced as well. Since nerve fibers responsible for coordinated muscle movement run within the outer layers of the spinal cord, owners may also notice weakness and/or incoordination when their pet attempts to walk. With more severe disk ruptures, damage to the deeper portions of the spinal cord can become a serious factor. When this occurs, partial or complete paralysis of one or more limbs might result, depending on the location of the rupture. If the entire depth of the spinal cord is involved, these animals will also lose all pain sensation to one or all four limbs, again depending on the areas of the spinal cord involved.

Such severe cases carry a very grave prognosis, since treatment at this stage is rarely successful. In most cases, confirmation of a ruptured disk is made via a thorough examination, clinical signs, and with radiographs of the vertebral column. If the exact location of the spinal lesion cannot be pinpointed with regular radiographs, a special test, called a myelogram, is performed. This test involves injecting a dye directly into the spinal canal. The dye, which can be identified on a radiograph, helps outline the cord lesion and demonstrate the extent of the disk rupture.

The type of treatment instituted for disk disease and/or rupture depends on the extent of the damage done by the disk to the spinal cord. For those dogs showing only pain with some mild incoordination, a strict 2-week confinement period, either at home or in a hospital setting, is a must! After-ward, short 10- to 15-minute physical therapy sessions, including swimming, can be performed twice daily to help speed recovery and return to normal function.

For cases in which the affected dog is having great difficulty walking, strict cage confinement combined with anti-inflammatory therapy and other specific treatment is indicated. If the disease is such that the dog is unable to support weight on the limbs at all, even after medical therapy, then surgery is required to reduce the pressure placed on the spinal cord by the ruptured disk.

This surgery, called a laminectomy or hemilaminectomy, works best if performed within the first 24 hours of the injury. It involves the removal of part of the vertebra over the affected cord segment. By eliminating the enclosed space through which the spinal cord runs, the pressure on the cord caused by the inflammation is allowed to dissipate. At the same time, surgeons often elect to perform intervertebral disk fenestrations, aimed at removing the offending nucleus pulposus from the disk in question and from adjacent disks as well.

The prognosis is poor for those pets that are unable to walk and have lost deep pain sensation in their legs as a result of a ruptured disk. The loss of deep pain indicates that the entire depth of the spinal cord is invariably involved, and surgical salvage procedures are rarely successful.

In those instances where surgery is unsuccessful, or in which paralysis is permanent, euthanasia is not always the only option left to the owner. Special “wheelchairs” for dogs have been developed for dogs paralyzed by a ruptured disk or other neurological accidents. Although not suitable for every patient, these carts can help afford mobility to select patients willing to wear the apparatus and an alternative for those owners willing to devote much time and care to their paralyzed pet. If you think that such a device could be applicable to your own pet’s situation, ask your veterinarian for more details regarding this and other management options available.

There are specific measures that pet owners can take to help protect their dog from a ruptured disk. The first and most important is to prevent obesity. Overweight dogs are prime candidates for such complications; hence, they should be placed on a strict diet to reduce this risk factor.

Jumping should be discouraged in dogs predisposed to intervertebral disk disease. Many ruptured disks result from pets jumping off and on furniture. Pets so inclined should be assisted up or down whenever possible. Even better, a small chair or ramp can be placed in front of the dog’s favorite piece of furniture to allow easier access.

Whenever lifting a dog with back problems, be sure to firmly support both the front and hind ends, keeping the back as straight as possible. This stabilizes the position of the spine and affords the handler with better and safer control should the pet struggle. Surgical intervertebral disk fenestration is often used as a preventive measure in dogs that have previously suffered from bouts of intervertebral disk disease. As mentioned before, this involves the penetration and removal of the nucleus pulposus from one or more intervertebral disks suspected of causing current or future problems. If this is done, the danger associated with later disk rupture is removed with the nucleus.

Vertebral Instability (Canine Wobbler Syndrome)

Seen primarily in Great Danes and Doberman pinschers, vertebral instability is characterized by instability and deformities in the vertebra of the neck region, leading to pressure on the spinal cord in that region. The condition in these breeds is hereditary in nature; however, trauma can predispose any dog to canine wobbler syndrome. Signs associated with vertebral instability include incoordination, weakness, and paralysis. Pain is rarely a feature of this disease. Diagnosis of vertebral instability is made with radiographic X rays. Treatment involves the use of anti-inflammatory medication to reduce the spinal cord inflammation. Surgical decompression of the spinal cord is also warranted in severe cases.

Myelopathies

Myelopathies are degenerative diseases that strike the spinal cord and nerve fibers coursing throughout the body. These diseases involve the gradual loss of the outer, conductive coating that surrounds certain nerve fibers, called myelin. This loss impairs the fiber’s ability to transmit nerve impulses. Seen primarily in older, larger breeds of dogs, especially German shepherds, myelopathies are characterized by muscular incoordination, weakness, and atrophy. As the nerves innervating the hindlegs are affected, a turning under or dragging of the hind feet may result. In fact, the hind limb weakness exhibited by some dogs with degenerative myelopathy is often mistaken for arthritis of the hips or spondylosis deformans of the spine. However, pain is rarely a factor in this disease. A myelopathy is tentatively diagnosed using historical findings, clinical signs, and reflex testing. Dogs afflicted with this condition will exhibit weak to absent reflex activity in their limbs. Electromyograms (EMGs) may be performed as well to evaluate electrical activity associated with the muscle tissue of the body.

Unfortunately, because an exact cause of most myelopathies, other than genetics, remains a mystery, there is no effective treatment to date. Vitamin therapy has been used in some instances to slow the progression of the disease, yet motor incapacitation is inevitable.

Feline Hyperesthesia Syndrome

Feline hyperesthesia syndrome (“twitchy skin syndrome”) is a condition characterized by some unique clinical signs. Affected cats exhibit a rippling of the skin on their backs, especially when petted in the lower back region. They might chew or lick at their tail incessantly, and appear to be “spaced out,” spontaneously darting throughout a room or house and attacking objects and owners without provocation. The exact cause of this condition remains unknown. Some researchers feel that it is a form of epilepsy. Because “emotional” breeds such as Siamese, Persians, and Himalayans seem to be most often affected, other researchers believe that it is actually a behavioral disorder brought about by an upsetting experience or circumstance. Even food preservatives used in cat foods have been accused of causing feline hyperesthesia syndrome.

Medical therapy for this disorder consists of the use of antianxiety medications or sedatives in an attempt to modify the cat’s behavior. Identifying and correcting any environmental upsets (including any dietary changes) that might have a possible link to the problem are needed as well.

Ischemic Encephalopathy (Cats)

Feline ischemic encephalopathy (FIE) is a neurologic condition that has been known to strike cats. FIE is caused by a sudden disruption of blood supply to the brain, similar to a stroke in humans. Although a definitive cause has yet to be determined, cardiomyopathy, neoplasia metastasis, and even feline heartworms are suspect. Affected cats exhibit marked depression, incoordination, circling behavior, and/or seizure activity. The pupils of the eyes may become dilated, and blindness may be apparent. Acute clinical signs usually resolve within 7 to 10 days; however, residual neurologic deficits of varying degrees often remain indefinitely.

Diagnosis of feline ischemic encephalopathy is based on history and clinical signs seen, as well as ruling out other causes of similar symptoms, such as vestibular disease, feline leukemia, and poisonings. Treatment of this neurologic disorder involves the administration of high doses of anti-inflammatory medications. In addition, medications designed to dilate the brain’s blood vessels and thin the blood may be employed in an effort to improve overall circulation to the affected regions of the brain. The prognosis for survival in cats with FIE is guarded during the first 48 hours following onset of clinical signs. After 48 hours, the prognosis for survival is good, since FIE is a nonprogressive disorder.

Hypothyroidism (Dogs)

The thyroid gland, through production of thyroid hormones, functions to influence nutrient and oxygen utilization within the body, hence affecting overall metabolism. As a result, deficiencies in thyroid hormone or interference with its function can have profound effects on the body. In dogs, immune system malfunctions, iodine deficiencies, incomplete thyroid gland development, and pituitary gland malfunctions can all lead to a condition of hypothyroidism. Predisposed breeds include cocker spaniels, Dobermans, dachshunds, beagles, and golden retrievers.

Clinical signs associated with this disorder are varied, owing to the tremendous scope of thyroid hormone function. Dogs with hypothyroidism tend to be lethargic, sleeping a lot and tiring easily after exercise. Some exhibit a profound intolerance to cold floors or cool environmental temperatures. Puppies so affected might seem to be slow learners when it comes to training. As the skin around the face of these dogs often thickens as a result of the disease, a dog’s voice might change to a lower pitch, and facial features might appear droopy or sad.

In addition, hypothyroid dogs may also have poor appetites, yet still gain weight. Over 50 percent of dogs afflicted with hypothyroidism will exhibit changes to the skin and haircoat. A loss of the undercoat occurs, resulting in a thinned, poor-looking coat. Skin thickening occurs, and secondary seborrhea is not uncommon. Finally, eye problems, neurologic disorders, reproductive infertility, arthritis, and aggressive behavior could all have their roots in a thyroid disorder.

A veterinarian can evaluate your pet’s thyroid function right at the office. A simple blood test can be used to screen thyroid hormone levels within the body. If a problem is found, then more extensive thyroid function tests may be ordered to help determine the extent of the problem. If a dog is taking corticosteroid hormones for other problems at the time of the testing, the results could come back falsely low. As a rule, however, if clinical signs correlate with blood test results, then it is safe to assume that a condition of true hypothyroidism exists.

Regardless of the underlying cause, treatment of hypothyroidism in dogs involves daily supplementation with synthetic thyroid hormone tablets. Thyroid hormone levels will need to be monitored during the initial stages of treatment to ensure that the proper dosage is being met. For the most part, this is a medication that affected dogs will need to stay on for the rest of their lives. Clinical response to medicating is usually seen within 2 weeks after initiation, with resolution of signs occurring soon after.

Hyperthyroidism (Cats)

A condition of hyperthyroidism in cats is caused by an increase in circulating levels of thyroid hormones, namely, thyroxine (T3) and triiodothyronine (T4). When it occurs, hyperthyroidism is most commonly seen in cats greater than 8 years of age, usually as a result of a tumor involving the thyroid gland. Because thyroid hormone helps regulate the body’s metabolism, the clinical signs seen with hyperthyroidism can be directly related to the exaggerated increase in the cat’s metabolic rate. These symptoms may be mild to severe depending on the amount of excess hormone being secreted. Signs typically include noticeable weight loss in the presence of a voracious appetite, nervousness and hyperactive behavior, and a rough, unkempt haircoat. Other less common signs seen include increased water consumption, regurgitation (due to rapid overeating), panting, and breathing difficulties, especially if the thyroid glands are grossly enlarged. In addition, many cats with elevated thyroid levels also suffer from inflammatory bowel disease (IBD). As a result, vomiting and/or diarrhea related to this may be seen in the hyperthyroid feline as well.

Diagnosis of hyperthyroidism is made through the evaluation of clinical signs, physical exam findings, and special laboratory tests. On physical examination, nodules can usually be palpated in the neck region because of glandular enlargement. In addition, a rapid heart rate and pulse are often detected because of the effects of the thyroid hormones on the heart.

This cardiac affect can be especially dangerous in cats suffering from concurrent cardiomyopathy. A diagnosis of hyperthyroidism can also be verified through the use of special tests designed to detect levels of thyroid hormone in the blood. If this condition is definitively diagnosed, a number of treatment options exist. The type of treatment chosen will depend on the severity of the thyroid hormone elevation and other underlying disease factors (such as the presence of heart disease or kidney disease). Medical treatment for hyperthyroidism involves the administration of special drugs designed to inhibit production of thyroid hormone by the thyroid gland, thereby controlling clinical signs. Side effects from giving such drugs can include anemia, immune cell suppression, decreased appetite, vomiting, weakness, and itching. Since most cats must stay on this medication for the remainder of their lives, close monitoring by and periodic communication with a veterinarian is essential.

Yet another form of medical therapy that yields successive results in hyperthyroid felines is called radioactive iodine therapy. This type of therapy selectively destroys malfunctioning thyroid cells using radiation. Most cats suffering from hyperthyroidism will respond favorably to medical therapy. However, if drug therapy fails to resolve the disorder and radioactive iodine therapy is unavailable, surgical removal of the thyroid gland (partial or complete thyroidectomy) must be performed.

If extensive tumor involvement necessitates the removal of the thyroid, then daily thyroid hormone supplementation will be required for the remainder of the cat’s life. Felines placed on such supplementation should have blood thyroid levels checked every 6 to 8 months to ensure that adequate levels are being given.

An inherent risk associated with the surgical removal of the thyroid gland in cats is a complication known as hypoparathyroidism. This condition, characterized by low blood calcium levels, is caused by the inadvertent removal of the parathyroid gland (tightly adhered to the thyroid gland) when the thyroid tissue is removed. Signs of low blood calcium, which normally arise within 3 days of parathyroid gland removal, include profound weakness, muscle tremors and spasms, and in some cases, seizures. Felines suffering from this postsurgical complication require prompt treatment with calcium supplements. These supplements, as well as vitamin D tablets, will be required for life to help maintain proper calcium levels within the body.

Hyperadrenocorticism (Cushing’s Disease)

Steroid hormones, specifically the class known as glucocorticosteroids produced by the adrenal glands, serve over 50 vital functions within the body. Some of the more important ones have to deal with carbohydrate, protein, and fat utilization and with maintaining water and electrolyte balance within the body. Veterinarians fighting allergic reactions or inflammation in dogs and cats rely on glucocorticosteroids for their anti-inflammatory effects when given at low dosages. Similarly, since high doses of glucocorticosteroids can suppress the immune system, they are quite useful in treatment against autoimmune diseases in pets, including pemphigus, a disease that causes severe skin lesions in affected dogs.

Unfortunately, since steroid hormones help maintain a delicate balance within the body, an overproduction of these hormones within the body can upset this balance. This is precisely what happens in Cushing’s disease. An overproduction of glucocorticosteroids from the adrenal glands occurs within the body, usually as the result of a tumor affecting one or both glands, or, more commonly, a tumor affecting the pituitary gland. The disease is most common in dogs over 8 years of age. Furthermore, poodles, boxers, and dachshunds seem to be afflicted with a greater frequency than other breeds. Fortunately, the condition is rarely seen in cats.

Some of the clinical signs seen in dogs with Cushing’s disease include a marked increase in water and food consumption, an increase in elimination activity, lethargy and exercise intolerance, and a generalized reduction in muscle size and tone, which, when it affects the muscles of the abdominal wall, leads to a characteristic pot-bellied appearance.

The skin and coat changes that occur in a dog with Cushing’s disease might be the first clues as to the existence of the problem. A generalized thinning of the haircoat and skin will be seen, with flakiness, pigmentation, and secondary infections. Eye problems are common in these dogs, too, with recurring ulcers affecting the cornea. Because high levels of steroids have a suppressing influence on the immune system, secondary infections, especially bladder infections, are often seen in these dogs as well. Finally, if a tumor is present in the pituitary gland at the base of the brain, neurological problems might occur as pressure is increased on the brain.

These signs can lead a clinician to suspect Cushing’s disease, but more extensive blood testing and radiographic X rays are usually required to confirm a diagnosis. Measuring actual blood levels of steroids within the bloodstream is one way to test for Cushing’s disease; other methods include injecting small amounts of special synthetic hormones, designed to alter the production of steroids within the body, into the dog and measuring the body’s response to them. If these hormones cannot alter the steroid production, then a diagnosis can be made.

Once a dog is diagnosed with Cushing’s disease, therapy may be instituted in a number of ways. Surgical removal of the tumor in either the adrenal glands and/or pituitary gland can be attempted, but this is a very difficult procedure associated with many postoperative complications.

Chemotherapy can be employed to target the adrenal glands and reduce the amount of steroids being produced by them. Used correctly, this treatment can reduce or eliminate the clinical signs seen and greatly improve a dog’s quality of life. Close veterinary monitoring for the appearance of side effects during the initial treatment stage is recommended. Therapy is usually required for life. Because of the intense management required with these modes of therapy, some pet owners prefer to stick to conservative treatment when dealing with this disease in their dogs. In these cases, dogs should be placed on high-protein diets to counteract protein loss caused by the disease. In addition, treating secondary problems as they arise—such as skin infections, bladder infections, and corneal ulceration—is necessary. Because the tumors responsible for Cushing’s disease are usually slow-growing, most dogs can live for up to 2 years with this treatment approach alone.

Hypoadrenocorticism (Addison’s Disease)

While Cushing’s disease is caused by too many corticosteroids circulating within the body, Addison’s disease is caused by the exact opposite: inadequate amounts of circulating corticosteroids. This includes not only the glucocorticosteroids produced by the adrenal glands but the mineralocorticoids as well. Because the latter are so vital at maintaining a fluid and electrolyte balance within the body, Addison’s disease can be acutely life-threatening in the affected individual. Like Cushing’s disease, Addison’s disease is primarily a disease of dogs; it is rare in cats. Causes of this disease in dogs can include tumors, infections, autoimmune diseases, and toxins. It can also occur secondarily to overtreatment with corticosteroids.

The clinical signs seen resemble those exhibited by pets afflicted with viral or parasitic gastroenteritis—namely vomiting, diarrhea, and dehydration. Loss of appetite and weight loss accompany these signs as well, yet there might be an increase in water consumption. Because the levels of sodium and potassium, two electrolytes vital to proper muscle contraction, are disrupted, profound muscle weakness, including a slowing of the rate at which the heart muscle contracts, are also observed. In severe cases, collapse of the entire circulatory system, with shock and then death, has been documented.

Diagnosis of Addison’s disease can made based on the history (i.e., long-term corticosteroid therapy), clinical signs seen, and determining the ratio of sodium to potassium in the bloodstream. Marked increases in potassium and decreases in sodium are indicative of primary Addison’s disease. Physical examination and electrocardiograms will reveal abnormal heart activity in these patients as well. If Addison’s disease is diagnosed or suspected, treatment should be instituted immediately. Dehydration is combated with intravenous fluids, and injections of mineralocorticoids are administered to stabilize fluid and electrolyte levels. For cases of primary Addison’s disease, periodic injections with mineralocorticoids will be required throughout the dog’s life to prevent relapses from occurring. If the condition was caused by the sudden cessation of glucocorticosteroid therapy, such therapy is reinstituted and then gradually tapered off over weeks to months.

Date: 2014-12-21; view: 1018