Category: Canine

Acral lick dermatitis, acral lick furunculosis.
Lick granuloma.

Affected Animals:
Acral lick granuloma may affect dogs of both sexes and all breeds; however, males or dogs that are older than five years are more often affected. Breeds disposed to this condition include the Great Dane, Doberman pinscher, Labrador retriever, golden retriever, German shepherd, and Irish setter.

Overview:
A commonly seen skin disorder of dogs, acral lick granulomas are skin wounds that are worsened by a dog’s constant licking of the affected area. Because the repeated licking hinders resolution of the lesion, dogs must be prevented from licking the acral granuloma until the wound has healed completely.

Acral lick granulomas have a variety of possible causes. The disease is often bothersome to owners as well as their dogs. A veterinarian can implement appropriate medical therapies to treat the lick granuloma and to prevent recurrence.

Clinical Signs:
Lick granulomas are skin wounds typically located on the distal area of the front leg or hind leg of a dog. Some dogs may have more than one lick granuloma at a time. These lesions usually appear as firm, raised, hairless areas of skin that may be hyperpigmented, or darkened with pigment, due to the dog’s chronic licking of the area. The center of the lesion is usually ulcerated, red, and moist, or may be covered by a scab.

Symptoms:
See Clinical Signs.

Description:
An acral lick granuloma is a lesion, usually located on the distal part of one of the limbs of dogs, which is caused or worsened by the animal’s obsessive licking of it. Damaged cells are believed to release pain-relieving endorphins that addict the dog to the licking and mutilation of the lesion.

The possible causes of the itching and licking behavior include boredom, trauma, arthritis or other joint problems, allergies, and skin infection. Often it is difficult to ascertain whether the cause of the lick granuloma is due to an underlying condition or the dog’s obsessive licking.

Treatment is usually lengthy and often only minimally effective. Early interventions have the best chance of success. Some animals will respond to medical therapy by maintaining a milder form of the lesion.

Diagnosis:
Diagnosis of acral lick granuloma and its cause requires a thorough history and physical exam. The following tests may be performed in order to determine the underlying cause of skin lesions: cellular evaluation using a slide impression of the mass, biopsy, allergy testing, and x-rays. Underlying conditions of the lesions include joint disease, cancer, bacterial or fungal infection, demodex mite infection, previous trauma, allergy, and psychogenic licking.

Prognosis:
Because acral lick granuloma is difficult to cure, veterinarians usually give it a guarded prognosis. Dogs that receive early treatment have a better prospect of recovery than dogs with chronic conditions.

Transmission or Cause:
The causes of acral lick granulomas include infections caused by bacteria, fungi, or mites; allergies, cancer, joint disease, or previous trauma; and an obsessive-compulsive disorder caused in some dogs by boredom. Dogs are incited by their condition to lick an area until they cause hair loss and erosion of the superficial skin layers. The consequence is further itching, which in turn results in more licking. This itch-lick cycle is exacerbated by the fact that damaged cells release endorphins, or brain chemicals, that are powerful analgesics. The licking may with time cause secondary infections, thickening of the skin, and changes in pigmentation.

Treatment:
Treatment of acral lick granuloma requires addressing the suspected cause of the lesions. Bacterial infections, for example, are treated with antibiotics. Arthritis is treated with pain management and joint therapy.

The obsessive-compulsive component of the disease is more difficult to treat. The dog may be prevented from licking the area by using some type of mechanical blocking device such as a collar, muzzle, or bandage. A topical product may be used for a period of weeks to decrease the itchiness of the area and aid in the healing process. Severe cases may call for the injection of a corticosteroid into the lesion. If the lesion is small, it may be surgically removed. Radiation therapy has been tried in some cases, but its rate of success is poor.

Prevention:
There are few recommended measures for prevention. Dogs suffering from boredom or from the stress of being left alone for too long should be given a more stimulating and socially interactive environment.

Category: Canine

Canine hypoadrenocorticism
Addison’s disease

Affected Animals:
Female dogs are more likely to develop Addison’s disease. Younger dogs of an average age of four to five years are more commonly affected than older dogs. Any breed of dog can develop Addison’s disease, although in some studies, the majority of affected dogs were of mixed breeding. Veterinarians have observed that Labrador retrievers, Rottweilers, and West Highland white terriers seem to be diagnosed with Addison’s disease at a higher frequency than other breeds.

Overview:
Clinically known as canine hypoadrenocorticism, Addison’s disease results from the decreased production of steroid hormones by the adrenal glands. The common symptoms of Addison’s disease are not very specific, and can include lethargy, weakness, gastrointestinal upset, and poor appetite. Often these symptoms appear intermittently during an extended period of time.

Although some dogs may be diagnosed while in a relatively stable condition, most are diagnosed when an Addisonian crisis develops—a severe stage of the disease in which shock and collapse can occur. If a dog is treated successfully for an Addisonian crisis, however, the long-term outlook is excellent, as most dogs can be controlled with oral or injectable medications to replace the deficient hormones.

Clinical Signs:
Clinical signs include anorexia, or an absent appetite, a thin body condition, depression, vomiting, diarrhea, weakness, collapse, polyuria, or increased thirst, signs that come and go over time, trembling or shaking, and abdominal pain.

Symptoms:
See Clinical Signs.

Description:
Addison’s disease refers to the syndrome that results from failure of the adrenal glands to produce the hormones that they normally make. The adrenal glands are two small structures located alongside each kidney. The main hormones produced by the adrenal gland are steroids. There are two major classes of these steroids: mineralocorticoids and glucocorticoids. Aldosterone, the main hormone in the mineralocorticoids class, plays a major role in regulating sodium, potassium, and water balance. Cortisol, the main hormone in the glucocorticoids class, acts on almost every major tissue in the body, helping to regulate glucose production and metabolism, influencing fat and protein breakdown, stimulating red blood cell formation, helping to regulate blood pressure, counteracting stress, and suppressing inflammation.

Despite their different control mechanisms, both classes of steroids usually are affected by primary adrenal gland failure in Addison’s disease. However, some animals will have symptoms primarily related to mineralocorticoid deficiency, while others will experience problems primarily from glucocorticoid deficiency. Although sex hormones such as estrogens and androgens also are produced by the adrenal glands, signs due to deficiencies of these hormones do not occur in dogs with Addison’s disease.

Destruction of 85 to 90 percent of the steroid-producing cells in the adrenal gland appears necessary for signs to develop secondary to deficiencies of mineralocorticoids and glucocorticoids. This destruction is most commonly due to immune system-mediated destruction of the adrenal glands. Less frequently, infections, inflammation, cancer, drug therapy, or abnormalities in blood supply to the adrenal gland can contribute to the development of Addison’s disease. Secondary adrenal gland failure due to problems that affect the hypothalamus or pituitary gland may also occur, resulting in the signs seen with Addison’s disease.

Symptoms of Addison’s disease may follow an intermittent course, often coming and going over a long period of time before the illness is suspected. Occasionally, Addison’s disease can be diagnosed in dogs with relatively mild symptoms. However, it is common for dogs not to be diagnosed until a life-threatening crisis due to Addison’s disease develops. Severe signs of illness including shock and collapse characterize these crises. Usually, the animal can be stabilized successfully if it receives immediate treatment with fluid resuscitation and medications to improve electrolyte and acid-base system abnormalities and to replace deficient glucocorticoids. Once the initial crisis passes, maintenance treatment with either oral or injectable mineralocorticoids, and for many dogs, oral glucocorticoids will be necessary for life. Despite the serious nature of Addison’s disease, the vast majority of dogs can be well controlled with medication. However, supplementing some dogs with glucocorticoid insufficiency will be necessary during any stressful period.

Atypical Addison’s disease refers to primary or secondary adrenal gland failure in dogs that do not exhibit the classic symptoms or electrolyte abnormalities usually seen in Addison’s disease. Animals diagnosed with this condition may have more subtle changes on blood tests and other diagnostic procedures. Although these dogs will not have the classic findings with Addison’s disease, they will exhibit abnormally low responses to ACTH on the ACTH stimulation test, and generally they will respond to treatment with glucocorticoids alone, since the sodium and potassium regulation will remain normal.

Diagnosis:
In many cases, changes on routine screening tests, including the complete blood count, biochemistry profile, and urinalysis, will trigger the suspicion of Addison’s disease. Chest x-rays may reveal a reduced heart size and esophageal enlargement. An electrocardiogram may show changes if the potassium concentration is elevated.

A definitive diagnosis depends on the results of a test of adrenal gland function called the ACTH stimulation test. Serum concentrations of cortisol, one of the main hormones produced by the adrenal gland, are measured before and after the administration of either synthetic or natural ACTH. Measurements of another hormone called aldosterone, which helps regulate the sodium and potassium balance, also can be checked, although this procedure is fairly uncommon. Measurement of aldosterone may be helpful in distinguishing primary failure of the adrenal glands from secondary adrenal gland failure due to abnormalities in the hypothalamus or the pituitary gland. Similarly, measurement of yet another hormone, called adrenocorticotropic hormone, also may be used to distinguish between primary and secondary adrenal failure.

Prognosis:
With appropriate medical treatment, the long-term outlook for dogs with Addison’s disease is excellent. Effective communication between the owner and veterinarian is vital in managing dogs with Addison’s disease, and owners should always have prednisone on hand in case it is needed in a crisis situation.

Transmission or Cause:
Addison’s disease most commonly is caused by primary failure of the adrenal gland to secrete adequate amounts of mineralocorticoids, glucocorticoids, or both. It is thought that immune system-mediated destruction of the adrenal gland is the most common cause of primary adrenal gland failure. Other causes can include infection or inflammation in the adrenal gland; abnormalities in blood supply to the adrenal gland or bleeding within the gland; infiltration of cancer cells within the adrenal gland; the deposition of abnormal proteins within the adrenal gland; and physical trauma to the glands. Rapid withdrawal of drugs such as prednisone after chronic administration and overdoses of drugs used to treat Cushing’s disease can result in adrenal gland failure. Secondary adrenal gland failure can occur due to primary problems in either the hypothalamus or the pituitary gland.

Treatment:
The treatment of dogs with Addison’s disease depends on the severity of the presenting signs. Many dogs diagnosed with Addison’s disease are severely ill at the time of presentation, often with potentially life-threatening fluid deficits and abnormal serum electrolyte concentrations. These animals must receive immediate medical attention, since rapid treatment is extremely important to stabilize dogs experiencing an Addisonian crisis. The main goals of treatment are to correct fluid volume deficits, to improve blood vessel integrity, to provide a source of glucocorticoids, to correct electrolyte and acid base abnormalities, and to confirm the diagnosis. Fluid volume deficits are addressed most appropriately with intravenous fluid administration; usually, saline is used. If low blood sugar concentrations are known or suspected, then the fluids should be supplemented with dextrose. Glucocorticoids usually are given via injection. Glucocorticoids that will not affect ACTH stimulation test results are better used than those that might make it difficult to confirm a diagnosis of Addison’s disease if they are given prior to the ACTH stimulation test.

Electrolyte imbalances are corrected with the intravenous fluids and with administration of mineralocorticoid replacement drugs. These drugs generally are not used until the diagnosis is confirmed, since the other measures used to treat a dog in crisis are usually successful in stabilizing a dog in an Addisonian crisis. Sometimes it will be necessary to take specific measures to lower dangerously high serum potassium concentrations, such as the administration of glucose and insulin, calcium, and sodium bicarbonate. Bicarbonate also can be used to treat animals with extreme acid-base system disturbances. Most dogs in crisis will improve within one to two hours with appropriate treatment. Intravenous fluids often are maintained for 24 to 48 hours, until the dog is eating and drinking on its own without vomiting. Injectable medications can then be switched to oral medications

Once the crisis period has passed, dogs are given either oral or injectable mineralocorticoids. The oral medications need to be given on a daily basis, usually twice a day, and sometimes very high doses are needed to control the disease. The injectable mineralocorticoid used most commonly is called DOCP. It is given via injection approximately every 25 days, and is almost always effective. For many dogs, especially large breed dogs, the injectable drug is much less expensive than the oral form. Most dogs with Addison’s disease do well clinically with mineralocorticoid replacement alone, but others will require glucocorticoid supplementation with prednisone as well. As many as 50 percent of dogs on injectable DOCP also will require prednisone administration. For any dog with Addison’s disease that may be undergoing stress, surgery, or that develops a non-adrenal gland dependent disease, prednisone should be considered on a short-term basis. Dogs that are used as working dogs also should take prednisone on a short-term basis.

Prevention:
There is no known way to prevent the development of Addison’s disease, except for cases in which it is caused by rapid withdrawal of prednisone or other steroids that have been used for long periods of time. Slowly tapering the doses of such drugs before discontinuing them is almost always effective in preventing the development of Addison’s disease in these patients.

Category: Exotic

Adrenal gland disease, Hyperadrenocorticism
Cushing’s disease of ferrets

Affected Animals:
The majority of ferrets develop signs of this disease in young middle age, when they are between three to four years old. Most ferrets with adrenal gland disease are neutered before the age of six weeks, but almost all ferrets in the United States are neutered by the time the disease presents. Both male and female ferrets develop this disease.

Overview:
Adrenal gland disease is a common problem in middle-aged to older ferrets. The disease results in one or both of the adrenal glands producing abnormal amounts of the androgens and/or estrogens, which are the male and female sex hormones. This disease can cause hair loss, itching, vulvar enlargement in females, and in rare cases, severe anemia and urinary blockage.

Because adrenal gland disease can be difficult to diagnose through routine bloodwork, it is often necessary to do specialized blood tests and ultrasound examination of the abdomen to diagnose adrenal disease. Physical exam findings and clinical signs often will lead to a suspicion of adrenal gland disease. Although clinical signs such as itching and hair loss are not life threatening, a ferret’s quality of life is impacted and, on rare occasions, the disease can lead to more serious complications. Treatment is best accomplished by surgery, although medical treatment is also possible.

Clinical Signs:
Alopecia is usually the first and sometimes the only sign of adrenal gland disease in ferrets. It can be present on the tail, rump, ventrum, and dorsum. The hair will epilate easily and the skin can appear flaky, inflamed, and erythematous. In unusual cases, the skin may become thin. It is not uncommon for alopecia to begin in the late winter and early spring. In younger ferrets with this disease, the hair will regrow in the late summer, but then alopecia will return the next winter or spring. Pruritus can accompany the alopecia although a number of ferrets may develop just pruritus with no other signs.

The vulva is enlarged in over 90 percent of females with this disease. Vulvar enlargement may be accompanied by vulvar discharge and vaginitis. Approximately one-third of the ferrets with adrenal gland enlargement have a palpable mass that can be felt next to the kidney. Some male ferrets will exhibit stranguria and dysuria. Older neutered ferrets may also begin to act intact and show signs of sexual aggressiveness towards other ferrets.

Symptoms:
Typically, ferrets will begin to lose their hair around their tail base. Hair loss usually progresses to involve the sides and belly of the ferret. Some ferrets with adrenal gland disease will scratch incessantly. A few male ferrets will develop a urinary tract blockage with this disease and will have difficulty urinating. In many cases, female ferrets develop a large vulva.

Description:
There are two adrenal glands that are each located next to a kidney. The gland has two major layers that function as two different endocrine organs. The outer layer is called the adrenal cortex and it makes steroid hormones such as sex hormones, glucocorticoids, and mineralocorticoids. The inner layer is called the adrenal medulla and it makes catecholamines such as epinephrine.

In ferrets, adrenal gland disease occurs when one or both of the adrenal glands produce abnormal amounts of the sex hormones called androgens and/or estrogens. Very rarely, the overproduction of androgens can cause the development of two serious complications: bone marrow suppression resulting in anemia, a decrease in red blood cell formation, prostate enlargement in male ferrets, a condition which blocks the flow of urine.

Adrenal gland disease mainly affects middle age to older ferrets. Although not usually a serious health concern, ferrets may have no relief from the itching that is associated with this disease if it is not treated.

It is important to realize that adrenal gland disease is not the same condition as Cushing’s disease, which affects dogs. Dogs can also develop adrenal problems, but their dysfunction does not involve the overproduction of sex hormones. Serum cortisol concentrations are normal in most affected ferrets and they also have a normal response to the ACTH stimulation test. A more appropriate term is hyperadrenocorticism or adrenal gland disease.

Diagnosis:
Physical examination is an important part of diagnosing adrenal gland disease. Diagnosis typically is suspected based on clinical signs because there are few other diseases in ferrets that exhibit the same group of symptoms. In clinical cases, the urine cortisol:creatinine ratio has not been shown to be useful to diagnose this disease. Since cortisol concentrations rarely are elevated due to this disease, blood tests such as an ACTH stimulation test and low or high dose dexamethasone tests will not diagnose this disease either.

At present, the best way to diagnose this disease definitively, short of doing exploratory surgery, is with a specialized blood test called an adrenal androgen panel offered by the University of Tennessee. Ferrets with adrenal gland disease have elevated plasma concentrations of androgens and/or estrogens. A baseline plasma sample should be taken to measure androgen and estrogen concentrations. Elevations of these hormones may indicate the presence of adrenal gland disease. An ultrasound of the abdomen may show an enlarged adrenal gland—also confirming the presence of this disease.

Prognosis:
Uncomplicated cases with surgical removal of the adrenal gland usually carry an excellent prognosis. If the ferret is not treated for this disease, the lasting problems may only be cosmetic, such as hair loss and an enlarged vulva. Serious health concerns that can arise due to untreated adrenal gland disease include urinary blockage in male ferrets, which is rare, and anemia, which is even less common.

Transmission or Cause:
The cause of adrenal gland disease is unknown. The affects of this disease are caused by the over-production of androgens and sex steroids by the adrenal gland.

Treatment:
Until medical treatments are well studied, surgery is still the best treatment. The abdomen is examined for any abnormalities and the abnormal adrenal gland is removed. If both adrenal glands are abnormal, either the larger gland is removed and the other gland is partially removed, or both glands are removed. When both glands are removed, life-long supplementation may be necessary.

The right adrenal gland is more difficult to remove because it is attached by a ligament to the vena cava and may even invade the vena cava. Laceration of this large vessel, one of the major veins that returns blood to the heart, may occur if great care is not used in the right adrenal gland removal.

A number of drugs have been proposed to treat adrenal gland disease including mitotane, Lupron®, Flutamide®, and Arimidex®. Mitotane shows equivocal results in ferrets. Lupron® is a GNRH analog that may have some use in controlling adrenal gland disease. Flutamide® is an androgen blocker that may be most useful in ferrets with prostatic enlargement. Arimidex® is an aromatase inhibitor and should decrease the effects caused by androgens in the ferret.

Prevention:
There is no known way to prevent this disease or to predict which ferrets will develop this disease.

Category: Canine

Anal sac impaction, anal sacculitis, anal sac abscess
Impacted anal sacs, infection of the anal sac, abscessed anal sac

Affected Animals:
Although any dog can be affected, smaller breeds such as chihuahuas, dachshunds, and miniature or toy poodles are more commonly seen by veterinarians for anal gland problems. Cats suffer from the disease less commonly.

Overview:
Anal sacs are the reservoirs for the secretions of anal glands which are located on either side of a dog’s anus, at approximately four and eight o’clock. These sacs contain liquid secretions from the anal gland, which, in healthy animals, are normally pale yellow-brown to grayish in color. The contents are usually emptied during normal bowel movements, or when a dog is nervous or scared. In most animals, these sacs empty easily. However, some dogs, especially small breed dogs, are not able to empty the sacs properly and become susceptible to anal sac disease.

A dog with anal sac disease may scoot across the ground in an attempt to relieve the sensation of pressure and irritation around its rectum. Dogs with this illness will also chase their tails and bite or lick their rear ends to alleviate the discomfort.

1. Normal anal sac
2. Inflamed and ruptured anal sac

There are three progressive stages of anal sac disease. The three stages include anal sac impaction, anal sacculitis, and anal sac abscess. Anal sac impaction occurs when the liquid accumulates and thickens, causing the anal sacs to become distended and difficult to empty. A veterinarian can usually relieve the impaction by rectally squeezing the grape-like sacs individually until the thickened substance is expressed.

The second stage of the disease is known as anal sacculitis, or inflammation of the anal sac. In this stage the anal sac material continues to accumulate and may become infected by bacteria. The third, and final, stage is abscess formation. This stage is the most severe and the most painful of the anal sac diseases. It may require surgical treatment. Sometimes the abscess can rupture through the skin, leaving an oozing red hole that is visible next to the anus. All stages of anal sac disease are treatable by a veterinarian.

Clinical Signs:
Signs of anal sac disease include scooting across the floor; licking the area around the anus; tenesmus, or straining to defecate; biting or chasing the tail; discharge, swelling, or pain around the anal area; and behavioral change. When an abscess ruptures, a purulent discharge may be seen draining from the lesion. The area surrounding the abscess may appear red, swollen, and painful.

Symptoms:
See Clinical Signs.

Description:
Anal sac disease occurs in progressive stages: impaction, inflammation, and abscess formation. Impaction of the anal sacs occurs when the anal gland secretions contained in the anal sac thicken so that the sac is unable to empty during a bowel movement. Inflammation of the anal sac, or anal sacculitis, is an infection usually resulting from impaction; it may also be caused by bacterial growth within the anal sac.

During the sacculitis stage, the impacted fluid may become thinner and fill with pus. Abscess occurs when the inflammation of the anal sac has reached an extreme stage; at this point, a red-brown substance will be seen coming from the sac, which will be enlarged, hot, red, and very painful. Usually, the abscessed sac will rupture, leaving a hole near the side of the rectum that oozes a foul-smelling liquid. The tissues surrounding the abscess will swell up, and this will worsen the dog’s inflammation and pain.

Diagnosis:
Diagnosis and staging of anal sac disease is made clinically with a rectal examination. Impacted or swollen anal sacs are often quite painful and some dogs may need sedation before a thorough examination can be done. Normal anal sac fluid is clear or pale yellow-brown; thick, brown or yellowish-green secretions are typical of animals with anal sac disease.

If the inflammation of the anal sacs has led to an abscess, a large, red, and swollen area may be visible on the side of the anus. A rupture of the abscessed sac can result in the oozing of a foul-smelling liquid material.

Prognosis:
Expression, or applying pressure to the anal sac, is a successful method for removing impacted secretions from the anal glands, but in many cases, this procedure must be performed on a regular basis to prevent recurrence. Antibiotics most often eliminate the infection. If abscess has occurred, the abscessed anal sacs usually heal. However, all animals with anal sac disease usually have to have their anal sacs expressed on a regular basis to prevent further problems.

Transmission or Cause:
The cause of anal sac disease is unknown. Smaller dog breeds, such as Chihuahuas and poodles, are most often affected. Excessive anal gland production, soft feces or diarrhea, poor muscle tone, and obesity also contribute to higher risk of developing anal sac disease. Anal sac abscess tends to occur after an impacted anal gland has become so severely swollen and infected that the anal sac forms an abscess and ruptures.

Treatment:
When the anal sac disease is at the impaction stage, the most common treatment is an outpatient procedure called expression in which the veterinarian applies pressure to the anal glands until the thickened secretions are expelled from the sacs. Sedation may be needed if the dog is nervous or is in great pain.

For the anal sacculitis stage of the disease, the same expression procedure is performed; afterwards, an antibiotic-steroid combination ointment is applied directly to the anal sac. In addition, the examining veterinarian may prescribe oral antibiotics to help fight infection. To help determine the appropriate antibiotic, the veterinarian may also need to take cultures to identify what type of bacteria caused the sacculitis.

When anal sac disease is at the abscess stage, a surgical procedure is required if the abscess has not already ruptured. The veterinarian, after sedating the dog or placing it under general anesthesia, will surgically open the infected anal sac to clean out the infected material and drain the remaining liquid.

Following surgery for ruptured abscesses, an antibiotic-steroid combination ointment will be applied directly to the anal sac to fight infection and inflammation. An oral antibiotic probably will be prescribed as well. As in the treatment of sacculitis, culture of the abscess may be necessary to help determine the best antibiotic medication. If infection continues after the surgery, surgical removal of the anal sac may be required.

Prevention:
Expression of the anal sacs every few weeks or months often will help prevent anal gland fluid from accumulating and becoming thickened again. High fiber diets have been shown to help prevent anal sac disease in at-risk dogs, especially those that are obese.

Category: Canine,Feline

Anemia
Anemia, low red blood cell count

Affected Animals:
All animals. Kittens and puppies are at increased risk of blood loss anemia from severe parasitic infestations.

Overview:
Anemia, the condition of having lower than normal numbers of red blood cells called erythrocytes, can have many clinical manifestations. Affected animals often suffer from decreased energy levels, pale or yellowed gums, an increased heart rate, and an intolerance to exercise. Anemia itself is not a primary disease, but the result of an underlying disease process.

The function of red blood cells is to carry oxygen to all the cells of the body. Erythrocytes are crucial to all animals, and a severe decrease in their number causes the body cells to go through the trauma of oxygen deprivation. Owners of an anemic animal may notice that their companion’s gums are pale or white in color instead of the normal pink or red.

Because the heart must work harder to provide oxygen to the starving body cells, dogs and cats with anemia have an increased heart rate. Having deprived the body cells of oxygen, anemia makes animals feel very tired and sick, and they will often show signs of depression.

Puppies and kittens can become anemic from blood-sucking pests such as fleas and intestinal parasites. The disease also is caused by blood loss from trauma, feline leukemia virus, feline immunodeficiency virus, and cancer. Treatment involves correcting the underlying disease or problem, and giving a blood transfusion if needed.

Clinical Signs:
Pale or icteric mucous membranes; lethargy; depression; weakness; anorexia; heart murmur; tachypnea; tachycardia.

Symptoms:
Pale gums or mucous membranes are seen when the lip is pushed up, and the eyes and ears may be pale as well. Anemic animals often become weak, depressed, sleep more than normal, stop grooming themselves, have a decreased appetite, and have increased breathing and heart rates.

Description:
An animal becomes anemic when it has an insufficient number of red blood cells carrying oxygen to its body. Without oxygen, the cells of the body become damaged and may die. The hearts of anemic animals beat faster, pumping the blood at an increased rate, in an attempt to direct more oxygen to the cells. Because animals with anemia have fewer red blood cells, their blood is thinner. As a result, anemic animals can develop heart murmurs; the noise a heart murmur makes comes from the turbulent sound thinner blood makes as it flows through the heart.

The clinical signs of the disease depend on the severity of the anemia and how quickly the anemia occurred. Those animals that become anemic gradually have a much greater chance of recovery than animals whose anemia is more sudden. With gradual anemia, the body has the time to adjust to the decreased red blood cell count; animals that become anemic very quickly, however, may die because their bodies cannot handle the sudden loss in red blood cells and oxygen.

The many possible causes of anemia can be divided into three categories. Blood loss anemia is caused by the leaking of blood out of the vascular system. Hemolytic anemia is the result of the destruction of red blood cells circulating within the blood stream. Nonregenerative anemia refers to a decrease in erythrocyte production.

Diagnosis:
The examining veterinarian will perform a blood test to determine the number of erythrocytes present in the animal’s bloodstream. An in-hospital test called a “packed cell volume,” or PCV, will approximate closely the percentage of red blood cells present. However, the veterinarian will typically opt to perform a complete blood count or CBC, which not only provides a more exact count of the red blood cells, but also measures the white blood cells and the platelets.

A CBC will tell the veterinarian whether the anemia is regenerative or nonregenerative. A regenerative anemia is one in which the bone marrow has released new red blood cells into the circulation in an attempt to replace the ones that were missing. If the initial CBC results suggest a nonregenerative anemia, it is possible either that the bone marrow has not had adequate time to react to the anemia or that the bone marrow is not able to produce the new red blood cells for some other reason. CBCs are usually run periodically until the patient’s red blood count is stable and has returned to normal. If an animal has a true nonregenerative anemia, it will be necessary to determine the cause by means of further diagnostics. These may include fecal examination for blood parasites, urinalysis, serum chemistry, or bone marrow aspiration and evaluation.

Prognosis:
Animals who get immediate medical attention have the best chance of surviving. The more severe the disease, of course, the more severe the anemia. After making a diagnosis of the underlying cause of the anemia, the veterinarian should be able to estimate the animal’s likelihood of recovery.

Transmission or Cause:
Animals get anemia for many different reasons. The most common ones are drug or toxin reaction, disease, and blood loss. Many common household products pose a serious toxic threat; acetaminophen, the active ingredient in Tylenol, is among the deadliest. Onions, whether cooked, raw, or dehydrated, are also especially dangerous. Other anemia-inducing substances include anti-inflammatory medications like aspirin, zinc, and propylene glycol, which is sometimes found in canned food.

Certain infectious diseases that animals contract are immune-mediated—that is, the body begins killing its own red blood cells, resulting in hemolytic anemia. These diseases are more common among dogs. Other infectious diseases that can lead to anemia include the feline leukemia virus, feline immunodeficiency virus and blood parasites such as Haemobartonella and Babesia. Cancer and kidney failure, as well, can make a cat or dog anemic.

Blood loss, of course, means fewer red blood cells, so animals that have lost blood through trauma often become anemic. Fleas are literally bloodsuckers and are especially threatening to kittens and puppies, which are smaller and have less blood than adult animals.

Treatment:
Treatment varies according to the underlying cause of the anemia. With severe anemia, a blood transfusion is needed to replace the lost blood. In order to treat the underlying disease that is causing the anemia, intravenous fluids and certain medications may also be necessary.

Prevention:
Some diseases that cause anemia are preventable. Newly introduced products that repel or kill fleas and ticks are both easy to apply and very effective. Diseases like the feline leukemia virus are preventable through limiting a cat’s contact with other cats or by vaccination; cats at high risk for this virus, such as outdoor cats, should be vaccinated. Cats and dogs should not be given any drugs unless instructed to do so by a veterinarian; Tylenol, especially, can be fatal.

Category: Feline

Urolithiasis
Urinary bladder calculi, bladder stones

Affected Animals:
Dogs and cats. Cats of any age, sex, or breed can develop bladder stones. Struvites, the most common stone type, usually are found among younger adult cats. Calcium oxalate stones occur most often in male cats aged four to nine years old.

Overview:
Bladder stones are rock-hard collections of minerals, clinically known as uroliths, which can rub and irritate the bladder wall, causing it to bleed. As a result of the irritation, the cat may feel like it needs to urinate frequently, even if it has only a small amount of urine to release. Bladder stones may also obstruct urinary flow. A cat that meows or cries while in the litter box may be experiencing bladder stone-related pain.

A variety of minerals can develop into different stone types. Cats will get each of the different stone types for different reasons. The various stones, which are named based on their mineral components, include the following: struvite, calcium oxalate, urate, calcium phosphate, xanthine, and cystine. In cats, struvite is the most frequently encountered stone, accounting for 50 to 65 percent of the stones analyzed. Calcium oxalate, seen in about 20 percent of bladder stone cases, is the second most common type of stone. The other types are uncommon in the cat.

Bladder stones come in many different sizes and shapes. Smaller stones often pose the greatest health risk because they are more likely to obstruct a cat’s ability to urinate. Small stones sometimes can escape from the bladder into the exiting canal called the urethra, only to get stuck as the urethra becomes narrower. As a stone becomes wedged, it will block the flow of urine partially or completely, making it difficult or impossible for the cat to urinate. This is the most serious problem associated with bladder stones, because an obstruction of the bladder, if untreated, can lead to irreversible damage to the kidneys, and in turn, death.

The method of treatment and prevention of bladder stones is based on the stone type. A stone usually is collected from the cat and analyzed for its mineral content in order to determine what method should be followed.

Clinical Signs:
Clinical signs associated with urolithiasis are influenced by the location of the stone or stones. Common findings include pollakiuria, hematuria, and dysuria or stranguria. Some cats can become obstructed by stones lodged in the urethra. Symptoms of obstruction can include frequent, unsuccessful attempts to urinate; vocalization and pacing; hiding; vomiting; depression; weakness; and excessive grooming of the urogenital area.

Symptoms:
Symptoms will depend on the type, size and location of the stone. The disease becomes serious or life threatening when the stones obstruct a cat’s ability to urinate. Thus, “red flags” to watch for include urinating outside of the litter box, frequent urination, meowing or crying during urination, and the presence of blood in the urine. Cats unable to urinate as a consequence of bladder stone obstruction still may attempt to urinate even if nothing is produced. They also may hide, vomit, cry or howl, or show signs of depression and weakness.

Description:
A bladder stone, or urolith, is comprised of minerals held together in an organic matrix. There are many different types of bladder stones—they vary according to which minerals they contain. Of all the different kinds of bladder stones, though, struvite is the most commonly encountered in cats. In a certain urinary environment, the amount of struvite stone minerals present in the urine becomes so significantly high that they are unable to remain in the dissolved state. Instead, the magnesium and phosphorus minerals will precipitate, or fall out of solution, into crystals that in turn will conglomerate into stones. The incidence of the struvite stone has decreased in the last 10 or so years due to the development of preventive diets.

Among felines, calcium oxalate is the second most commonly diagnosed stone type. The mode of formation of these stones is not completely understood. It is believed that the struvite prevention diets are inadvisable for cats prone to forming calcium oxalate stones, since the magnesium restriction and urine acidification may influence calcium oxalate stone formation.

With all types of bladder stones, frequent urination, blood in the urine, and difficulty urinating may result. Irritation of the bladder generally is the cause of blood in the urine and frequent urination. When a stone obstructs the bladder outflow—a much more threatening condition—a severely decreased ability or inability to urinate results.

Diagnosis:
The examining veterinarian may be able to feel the bladder stones while palpating the cat’s bladder. X-rays and ultrasound techniques also may be used to detect the stone’s presence, number, size, and location. Other common diagnostic tests include a complete urinalysis, a complete blood cell count, a blood chemistry panel, and a urine culture to check for bacterial infection.

In addition, it is very likely that the veterinarian will order a quantitative urolith analysis. This test will determine which type of bladder stone the cat has; this is important since different types may require different treatment protocols. Knowing the type of stone involved is also important in attempting to prevent stone formation in the future. Some cats may pass very small stones in their urine, which if collected, allow urolith analysis to be performed without surgical retrieval. However, in most cases, the stone, or stones, must be removed surgically for this test to be performed.

Prognosis:
The prospect of recovering from bladder stones is likely if the cause of the stone formation can be diagnosed and corrected. Bladder stones that result in an obstruction of the cat’s ability to release urine carry a more serious prognosis. Recurrence of stone formation is not uncommon.

Transmission or Cause:
Bladder stones form when the amount of mineral present in the urine is high enough that the mineral is unable to remain dissolved. Instead, the minerals fall out of solution and become crystals, which, in turn, will coalesce into a stone. Different characteristics of the urine—such as how acidic or basic the pH level is —can make certain minerals more likely to precipitate into bladder stones. Some diseases can cause increased amounts of minerals to accumulate in the urine. Diet can also play a role. In addition, urinary tract infections can lead to struvite stone formation, as can different abnormalities in a cat’s anatomy and metabolism.

Each bladder stone type has predisposing factors that cause certain cats to form that type repeatedly. Cats who develop cystine bladder stones, for example, usually have a genetic inability to absorb the cystine mineral within the kidney.

Treatment:
Treatment is based on the results of the diagnostic tests and determination of the stone type. The veterinarian will prescribe an antibiotic if an infection is present.

A special stone-dissolving diet may be prescribed to eliminate struvite stones. This food must be fed exclusively in order for it to be effective. The veterinarian will monitor the cat’s response to the diet by follow-up exams and repeated bladder x-rays. If the diet fails to dissolve the stones, surgical removal will have to be considered.

Most of the other bladder stones do not respond to medications; thus, alternative methods of removal will be required. If the stones are very small, a procedure called urohydropropulsion can be performed to flush the stones out of the bladder. However, larger stones will need to be removed surgically through an operation called a cystotomy. This is done after the cat is put under general anesthesia; it involves incisions into the abdomen and the bladder.

Prevention:
There are different methods for preventing some types of bladder stones. Stone prevention diets are appropriate for struvites; for others, medications to control the urine pH may be used. The animal’s owner should follow the veterinarian’s recommendations for bladder stone prevention, and continue regular follow-up visits for early detection and treatment of any recurrences.

Category: Canine,Equine,Feline

Blastomycosis, Blastomyces dermatidis infection
Blasto, Blastomycosis

Affected Animals:
Dogs, humans, cats, horses, and occasionally other animals may be affected. Most dogs with the infection are between one and five years of age. Males have a higher risk than females, and may be less responsive to treatment. Immunosuppressed animals are more at risk; animals that become infected may have an underlying immune-system defect, or may be on immunosuppressive medications.

Overview:
Blastomycosis is an infection caused by the fungal organism Blastomyces dermatidis. The disease usually results in respiratory infection; however, the organism can cause disease in many body tissues including the eyes, skin, reproductive tract, and bones. Blastomycosis is a serious disease that can be fatal.

Blastomyces dermatidis is found in the environment predominantly in the Missouri, Ohio, Tennessee, and Mississippi river valleys. Although all animals in these regions are exposed to the organism, only some animals will develop infections. A compromised immune system is the primary risk factor.

Symptoms depend upon the tissues infected by the organism. Treatment requires the use of antifungal medications, often for several weeks to months. In some instances, a cure is not possible and death may result. However, constant medication may keep the disease under control.

Clinical Signs:
Clinical signs of blastomycosis infection include coughing; dyspnea, or difficulty breathing; fever; uveitis, or eye inflammation; depression; weight loss; lymphadenopathy, or enlarged lymph nodes; draining skin lesions; and lameness.

Symptoms:
See Clinical Signs.

Description:
Blastomycosis is a severe systemic infection caused by the fungal organism Blastomyces dermatidis. The organism grows in the soil in specific regions of the country, including the Missouri, Ohio, Tennessee, and Mississippi River valleys. Dogs and humans are most at risk for infection; however, cats, horses, and other animals are occasionally affected.

Because many tissues can be infected by the organism, the signs of the disease will vary. Signs such as difficulty breathing, exercise intolerance, weight loss, and coughing will be seen when pneumonia, a common manifestation of respiratory infection, is present. With bone infections, lameness may be the only sign. A third of the cases involve the eyes, resulting in pain, redness, glaucoma, retinal detachment, and blindness. In addition, about one-fourth of affected animals will have skin disease that may manifest as nodular areas or draining wounds. The prostate and testes can also be affected. Prostatic involvement may result in abdominal pain, a stiff gait, and difficulty urinating. Testicular infections may result in swelling, pain, and sterility.

Systemic fungal infections are always serious, and can be difficult to treat. Many times affected animals are immunocompromised, or have weakened immune systems, making the disease harder to eradicate. If untreated, most infections are eventually fatal.

Diagnosis:
A presumptive diagnosis can be made based on the animal’s clinical signs, history, geographical region of the country, and serologic tests. A CBC, or complete blood count, and chemistry panel are usually performed. Many animals will have an elevated white blood cell count, and elevated calcium levels are sometimes seen. Because respiratory disease is the most common manifestation of infection, chest x-rays are usually taken. X-rays of the abdomen, limbs, or other parts of the body may be indicated if the animal is showing signs in these areas.

A definitive diagnosis is made by identification of the Blastomyces dermatidis organism through biopsy, fine-needle aspiration, or culture. Occasionally, imaging tests, such as a CT scan or nuclear scintigraphy, may be performed to better identify which tissues are infected and to monitor treatment. This equipment is typically available only at universities or large referral institutions.

Prognosis:
The prognosis for treatment is guarded. Animals with severe respiratory or central nervous system signs have the poorest prognoses. With severe disease, animals often succumb during the first week of treatment, due to the inflammatory response that occurs as the organism is killed. If the animal does respond to treatment, the prognosis is more favorable; however, recurrence is seen in about 20 percent of cases, generally occurring within the first six months. A full course of therapy must be reinitiated in cases of relapse. Rarely, animals require lifelong treatment to control the disease.

Transmission or Cause:
The causative agent of the disease is Blastomyces dermatidis, a fungus. Most cases of infection occur by inhalation of the infective spores present in the environment. The organism can then disseminate or spread to other tissues such as eyes, skin, bone, lymph nodes and other tissues. At body temperature, the fungus exists as a single-celled yeast, while at environmental temperature it exists as the infectious mycelial form. Animals infected with the disease can not pass it on to others, unless there is drainage from skin lesions.

Treatment:
Antifungal drugs including ketoconazole, itraconazole, fluconazole, and amphotericin B are the mainstay of treatment. Amphotericin B was one of the first drugs found to be effective in the treatment of blastomycosis. It can cause kidney damage, and requires intravenous administration.

Ketoconazole, itraconazole, and fluconazole belong to the same drug family. Each has been used effectively in the treatment of Blastomycosis. Ketoconazole and itraconazole can cause liver damage, and are available as oral medications. Itraconazole is generally more effective than ketoconazole, but it is also more expensive. Fluconazole is often used for treating infections of the central nervous system and eye because of its better penetration into these tissues.

Prevention:
Other than avoiding endemic regions, there are no preventive measures.

Category: Equine

Gasterophilus intestinalis, Gasterophilus hemorrhoidalis, Gasterophilus nasalis
Bots

Affected Animals:
Horses.

Overview:
During warm weather, bot flies swarm around horses. These parasites, of the species Gasterophilus, lay numerous tiny white eggs on the haircoats of horses. Bot eggs are not only aesthetically unpleasing, but once they have hatched into larvae, they also may cause the horse pain and irritation in the mouth. Adult flies that have developed from larvae may also cause various gastrointestinal problems.

Horses infected by bots often develop no clinical signs of disease. There must usually be a large number of bot eggs present before the animal becomes sick from the infection. Deworming treatments are very successful in treating severe cases of infection, and there are several effective tools for removing the eggs from the hair.

Clinical Signs:
Clinical signs include the presence of tiny, white-colored eggs measuring roughly one to two millimeters. Bot eggs can be found on any part of the body covered in hair, but are usually located along the forelegs, shoulders, and face. Horses with bots may suffer mild gastritis and stomatitis, resulting in pain or discomfort during eating. However, most horses with bots remain asymptomatic, aside from the visible eggs on their haircoats.

Symptoms:
See Clinical Signs.

Description:
In the warm summer months, flies of the species Gasterophilus lay eggs on the haircoats of horses. These eggs, and the flies they produce, are called bots. There are three primary species of Gasterophilus. Flies of the G. intestinalis species lay their eggs anywhere on the horse’s body, but most commonly on the shoulders and front legs. G. hemorrhoidalis usually glue their eggs to the mouths of horses. G. nasalis deposit eggs on the bottom part of the lower jaw and throat. G. intestinalis are the most common form of bot flies.

After the eggs have been laid, they will hatch within a few days. The larvae migrate into a horse’s mouth, and bury themselves between the molars and in the tongue. The bots will stay there for approximately one month, causing the horse pain and irritation. Eventually, the bots are swallowed and move to the stomach, where they continue to develop for nine to 12 months. From the stomach, the larvae move throughout the rest of the intestines and are passed into the feces. Over the course of the next month, the larvae mature into adult flies. The adult fly’s remaining life span is typically about two weeks.

Larvae affect a horse most dramatically when they are living in its stomach, where they hook onto its lining and cause the formation of ulcers. While many horses with bots have no clinical signs, some severely infected horses will manifest symptoms that include gastritis and stomatitis.

Diagnosis:
In order to diagnose an infection of Gasterophilus, immature worms or larvae must be located and identified in the feces of the horse. A tentative diagnosis may also be made when white eggs are seen attached to the haircoat of the horse.

Prognosis:
Excellent.

Transmission or Cause:
Transmission occurs primarily in the summer months, when the Gasterophilus flies lay their eggs on the haircoat. Within a few days, the eggs hatch and the larvae migrate into the horse’s mouth. When a horse licks or chews its haircoat, it stimulates some species of Gasterophilus to hatch. Other species of bots are able to hatch on their own, without stimulation from the horse. After hatching, the bot larvae move into the mouth and are swallowed. Eventually, the bots will travel through the intestinal system and be ejected in a horse’s feces.

Treatment:
Horses infested with bot eggs should be dewormed with an effective medication, such as ivermectin. Treatment can be performed during any season, but optimally should take place during autumn or early winter, after the first frosts have killed adult flies.

Prevention:
Prevention relies on keeping the horse’s haircoat free of bot eggs. Dull blades, fine-toothed combs, and special pumice stones are effective devices. These objects help to scrape and remove the eggs from the haircoat of the infected horse. The use of fly repellents may be helpful in preventing flies from landing on the horse and depositing eggs. Also an effective tool, a fly mask is made from a mesh-like material, and fits around a horse’s face and ears while leaving its mouth free.

Category: Bovine

Bovine postparturient paresis, parturient paresis, hypocalcemia
Milk fever

Affected Animals:
Cows, especially older, higher producing dairy cows are most often affected.

Overview:
Milk fever is a condition of older, third to sixth lactation, high-producing dairy cows. It is associated with parturition, usually within 72 hours of giving birth. Because of the high volume of milk produced during this time, and subsequent demand for calcium, these cows often develop hypocalcemia, or abnormally low levels of calcium in the blood. Since calcium is required for the release of acetylcholine at the neuromuscular junction, affected animals will begin to experience muscle weakness. As this hypocalcemia worsens, the cow will become too weak to stand and will eventually become comatose over a matter of hours.
The hypocalcemia of bovine postparturient paresis is treated intravenously with calcium gluconate. Affected cows have an excellent prognosis if treated early and properly. However, the worse the symptoms, the worse the prognosis tends to be. Milk fever may be prevented with appropriate feeding or calcium or vitamin D supplementation during the weeks preceding parturition.

Clinical Signs:
Initial signs include excitability, hypersensitivity and restlessness. Tachycardia and mild hyperthermia are commonly associated with tetany in the early stages. Subsequently gradual, worsening muscular weakness begins that progresses into sternal then lateral recumbency. Gastrointestinal atony predisposes to constipation and mild bloating. As calcium levels decrease other signs may include weak pulses, poor pupillary light response, flaccid paralysis, severe bloating, and coma.

Symptoms:
A weak, trembling cow is first seen. Localized spasmodic muscle contractions may cause a mild increase in body temperature. The heart rate is often elevated. The heart rate remains elevated but the temperature declines with progression. In advanced stages the most common symptom is a “downer” cow that is usually unable to rise when stimulated. An affected cow will often have its head turned into its flank. If left untreated the cow will lie down on her side and stretch out, thus predisposing her to bloat. The cow will become progressively more depressed until she is unresponsive and comatose, with dilated, unresponsive pupils.

Description:
Postparturient paresis, or severe muscle weakness in cows resulting from hypocalcemia, occurs in older, third to sixth lactation, high-producing dairy cows that are near calving or have recently calved. It is characterized by progressive muscle weakness and depression that progresses into coma if not treated promptly.

Calving causes a high volume of milk production, and with it, a high demand for calcium from the cow’s body. If the body is unable to respond quickly to this demand, the cow develops hypocalcemia, or an abnormally low blood-calcium level. Calcium is critically important to normal nerve and muscle function. Acetylcholine, a neurotransmitter substance acting at the neuromuscular junction, requires calcium to properly stimulate muscle movement. Hypocalcemic cows will begin trembling, and as the calcium level continues to plummet, will no longer be able to stand. Subsequently the cow becomes recumbent, first in the sternal position, and then laterally. Milk fever is one of a number of conditions that leads to a “downer” cow.

Postparturient paresis is favorable to early treatment with intravenous calcium supplementation. Delayed treatment may result in a comatose animal with a much poorer prognosis. Left untreated most patients will die.
As with most illnesses prevention is the key. Dietary calcium levels should be lowered in the weeks leading up to calving. This stimulates the cow to produce parathyroid hormone, which is necessary for quickly increasing blood calcium from calcium stored in the bones.

Diagnosis:
An older dairy cow near calving or that has recently calved that shows clinical signs and symptoms is highly diagnostic. Serum calcium levels will reveal hypocalcemia, or low blood calcium. However, because of the rapid nature of this illness and the often slow return of laboratory results, treatment is usually initiated based on clinical signs only.

Prognosis:
The prognosis is excellent if cows are treated early and properly. As the symptoms worsen so does the prognosis. Cows down for more than 48 hours may develop muscle inflammation and never be able to stand. Relapse is relatively common unless longer acting supplements are added to the treatment plan. Older cows and cows displaying signs prior to calving have the highest risk for relapse.

Transmission or Cause:
Postparturient paresis, or severe muscle weakness in cows resulting from hypocalcemia, occurs in older, third to sixth lactation, high-producing dairy cows that are near calving or have recently calved. It is characterized by progressive muscle weakness and depression that progresses into coma if not treated promptly.
Calving causes a high volume of milk production, and with it, a high demand for calcium from the cow’s body. If the body is unable to respond quickly to this demand, the cow develops hypocalcemia, or an abnormally low blood-calcium level. Calcium is critically important to normal nerve and muscle function. Acetylcholine, a neurotransmitter substance acting at the neuromuscular junction, requires calcium to properly stimulate muscle movement. Hypocalcemic cows will begin trembling, and as the calcium level continues to plummet, will no longer be able to stand. Subsequently the cow becomes recumbent, first in the sternal position, and then laterally. Milk fever is one of a number of conditions that leads to a “downer” cow.

Postparturient paresis is favorable to early treatment with intravenous calcium supplementation. Delayed treatment may result in a comatose animal with a much poorer prognosis. Left untreated most patients will die.
As with most illnesses prevention is the key. Dietary calcium levels should be lowered in the weeks leading up to calving. This stimulates the cow to produce parathyroid hormone, which is necessary for quickly increasing blood calcium from calcium stored in the bones.

Treatment:
Early intravenous calcium gluconate is the treatment of choice for severely affected patients. The solution must be given slowly because rapid calcium infusion may result in cardiac arrest. Concurrent use of subcutaneous calcium gluconate may prevent recurrence, by slow release of biologically available calcium from the tissues into the bloodstream. Patients with mild signs are appropriately treated with subcutaneous, intraperitoneal, and/or oral calcium products.
The response to properly administered calcium therapy is quite characteristic. The cow’s symptoms will appear to reverse themselves as they had previously progressed. The laterally recumbent cow will sit up to sternal position, then it will often begin to have tremors over its body. As all bodily functions affected by hypocalcemia begin to reverse, the affected animal may urinate, belch, and then begin the wobbly effort to rise. Cows generally rise within one hour. Repeat treatment may be necessary in 12 hours if the cow is still unable to rise.

Prevention:
Milk fever may be prevented with appropriate feeding during the weeks leading up to parturition. During this “dry-off” period, the cow’s dietary intake of calcium should be lower than when the cow is producing milk. The resulting lower blood calcium level stimulates production of parathyroid hormone, or PTH. PTH stimulates the cow’s body to quickly increase blood-calcium levels from calcium stored in the bones. However, PTH is slow to synthesize in the face of a rapid calcium decline. Essentially, lower dietary calcium during the dry-off period keeps the cow’s PTH at a level that will meet any sudden calcium demand.
Another important preventive measure is dietary acidification through reduction of the dietary cation-anion difference (DCAD). Diets can be adjusted for the portion of the herd that is near parturition, using urine pH to monitor the cows’ acid-base status. Prophylactic calcium treatment of cows near to or immediately after, calving may lower the incidence of milk fever in a herd. Vitamin D supplementation before calving will increase calcium absorption through the intestines, and is sometimes recommended to prevent milk fever.

Category: Canine,Feline

Bronchoscopy
Bronchoscopy, airway scoping

Affected Animals:
Animals with respiratory tract diseases that cannot be diagnosed with x-rays or ultrasound, or those that do not respond to symptomatic treatment for their problems, are potential candidates for bronchoscopy.

Overview:
Bronchoscopy is a diagnostic procedure for patients with respiratory tract disease. It can be used to identify structural abnormalities, abnormal airway secretions, foreign bodies, and mass lesions including certain tumors. Additional procedures combined with bronchoscopy can allow for identification of inflammation or infection in the respiratory tract. Specialized equipment and expertise is required for performing bronchoscopy and for monitoring the patients during the procedure.

Bronchoscopy does not always identify the cause of an individual animal’s problem, but at least it can rule out many potential explanations for it.

Description:
Very heavy sedation or general anesthesia is necessary for bronchoscopy in small animal patients. Injectable anesthetic drugs are used so that it is not necessary to use an endotracheal tube for the inhalation of gas anesthesia during the procedure. Without such a tube, there is more room for the bronchoscope to be inserted into the trachea and the bronchi. Oxygen can be delivered during the procedure through a small catheter inserted down into the trachea or through the bronchoscope itself. In larger patients, gas anesthesia may be used, as the bronchoscope can pass through larger endotracheal tubes while still allowing for the delivery of oxygen and gas anesthetic agents to the patient. Patients are monitored with an electrocardiogram and with pulse oximetry during the procedure.

Once the patient is anesthetized, the bronchoscope is passed into the trachea from the oral cavity. In most cases, bronchoscopy is done with flexible fiberoptic endoscopes. Many times, these are attached to a small camera that can record findings during the procedure. Rigid bronchoscopes are also available, but they are not commonly used in small animal patients.

Bronchoscopy is used to visually inspect the airway for any evidence of collapse, compression, or dilation. Mass lesions can be seen if present within the lining of the trachea or bronchi. Abnormal discharges such as excessive mucus, blood, or pus may also be seen. If a foreign object has been inhaled, it may be seen if the scope can reach the point where it is lodged.

The procedure is useful not only for visualization of abnormalities, but also for obtaining samples. With bronchoscopy, biopsies can be taken if lesions requiring biopsy are seen, and samples of abnormal discharges can be collected and submitted for microscopic analysis and culture. Flushing sterile saline through the endoscope often facilitates sample collection. Special brushes may be passed through the endoscope for collecting samples as well. If airway foreign bodies are seen, special grasping forceps may allow for their removal without surgical intervention.

Prognosis:
The prognosis depends primarily on the diagnosis and on the presence of other factors affecting the patient. Since complications due to the procedure are rare, the prognosis for an animal undergoing bronchoscopy is usually good with respect to the procedure itself.

Potential problems that can arise during the procedure include anesthesia-related complications, including death. Heart arrhythmia and bleeding may occur. Oxygen levels may drop temporarily but can usually be corrected quickly by supplying additional oxygen. Fever, infection, and abnormalities in the lungs that can be seen on chest x-rays can develop, but these complications occur infrequently.

Preprocedure Care:
Prior to bronchoscopy, animals need to be prohibited from eating because the procedure is performed under anesthesia. In emergency situations this may not be possible, particularly when bronchoscopy is needed to attempt removal of an airway foreign body. Since it is not usually a first-line diagnostic tool, prior evaluation almost always includes chest x-rays.

Postprocedure Care:
Following bronchoscopy, animals are usually given oxygen to breathe until they are awake. Because the procedure is usually short in duration, and since the injectable or gas anesthetic agents also tend to be short acting, most patients that are stable at the time the procedure is performed can be released the same day. For those that are seriously ill, hospitalization is usually required for ongoing treatment of their illness, not because of the procedure itself.

Prevention:
Many complications can be avoided by careful patient selection. Critically ill patients with serious heart disease or metabolic conditions that need to be stabilized first are not good candidates for anesthesia; bronchoscopy is therefore not recommended for them. Animals in severe respiratory distress are not good candidates; however bronchoscopy may be indicated in these patients when an airway foreign body or some other type of structural airway disease is suspected that absolutely requires bronchoscopy for an accurate diagnosis or prompt therapeutic intervention. Patients with severe bleeding disorders, or with very low oxygen levels in their blood that do not respond to oxygen supplementation, should not undergo bronchoscopy.