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DEMODEX MANGE or DEMODECOSIS
What is Demodex? Canine demodecosis is an inflammatory parasitic disease of dogs characterized by the presence of a high number of mites in the hair follicles which often leads to secondary bacterial infection. The mite, Demodex canis, is part of the normal fauna of canine skin and is normally present in small numbers. The mite resides in the hair follicles and oil glands of the skin. Pathologic changes develop from mite infestation when numbers exceed that tolerated by the immune system. The initial proliferation of mites may be due to a genetic or immunologic disorder.
What are the Signs of Demodex?
Localized Demodecosis: Most cases occur in young dogs with a median age of 3-6 months. There are no recognized breed or sex predilections. Clinical lesions are usually mild and consist of redness and a light dandruff. One to several patches may be present, and the most common site is the face, especially around the mouth and eyes. Patches may also be seen on the body and legs. Most cases heal spontaneously with less than 10% progressing to generalized demodecosis.
Generalized Demodecosis: The generalized form of the disease can occur in both the young and old. Adult onset demodecosis is often a severe canine skin disease that responds poorly to treatment. The disease can be widespread from the onset with multiple, poorly circumscribed patches of redness, hair loss, and dandruff. As hair follicles become distended with large numbers of mites, secondary bacterial infections are common, often with rupturing of the follicle. As the condition progresses, the skin can become severely inflamed, with pus and swelling present. The sudden occurrence of adult onset demodecosis is often associated with internal disease, cancers, or immunosuppressive disease.
How is it Diagnosed? Skin scrapings are diagnostic—large numbers of mites will be seen in the majority of cases. Occasionally getting a diagnosis may necessitate a skin biopsy.
How is it Treated? Localized Demodecosis: Treatment of the localized form of the disease can be conservative. Most cases (90%) resolve spontaneously with no treatment or simple topical medicine. Generalized Demodecosis: Demodecosis in the adult dog is often a management problem for the owner. Expense and frustration with the chronicity of the disease are at issue. Many of these patients are medically controlled rather than cured. The prognosis for canine demodecosis depends heavily on genetic, immunologic, and underlying diseases.
The general health status of dogs with the localized or the generalized form of the disease should be evaluated. The treatment consists of: 1. Apply a benzoyl peroxide shampoo prior to the application of the dip as a bactericidal therapy and to increase exposure of the mites to the miticide through its follicular opening activity. Protect your pet’s eyes prior to bathing with a drop or two of mineral oil (available at any drug store). 2. Amitraz (Mitaban-Upjohn) is the most commonly used treatment. It is used weekly (the label reads every other week) and MUST BE diluted 1/2 vial (5.3mls) per gallon of water (or 1.3ml [or cc] per quart of water) until the resolution of clinical signs and no mites are found on skin scrapings (do not rinse off the dip, let the dog air dry). Cover every square inch of skin with the dip solution.
Studies show that 11-30% of patients will not be cured with Amitraz, so we may need to choose an alternate therapy if no response is seen or control the case with maintenance amitraz dips every 2-8 weeks. If you have any questions about it’s usage, please call us.
The most common side effects of amitraz including sleepiness, inactivity, depression, and loss of appetite are seen in 30% of patients for 12-36 hours post treatment. The incidence and severity of the side effects do not appear to be proportional to the dosage or frequency of use. Humans can develop dermatitis, headaches, and respiratory difficulty after exposure to amitraz, so use it in a well ventilated area and wear rubber gloves. Allow your dog to air dry outside.
FOLLOW-UP Periodic examination of multiple skin scrapings and evidence of clinical resolution are used to monitor progress.Nort
DIABETES MELLITUS (Sugar Diabetes)
What is Diabetes Mellitus? Commonly called “sugar diabetes,” it is a disorder of carbohydrate, fat, and protein metabolism caused by an absolute or relative insulin deficiency. There are two types of diabetes mellitus. Type I (insulin-dependent diabetes mellitus [DM]) is characterized by very low to absent insulin secretory ability. These patients die if not treated with insulin and are prone to develop a toxicity called ketoacidosis. Type II (noninsulin- dependent DM) is characterized by inadequate or delayed insulin secretion relative to the needs of the patient. Many of these patients can live without additional insulin and are less prone to ketoacidosis. Type II diabetes is often associated with underlying diseases or obesity.
What Happens in Diabetes Mellitus? The pancreas gland produces insulin. With continued damage to the beta cells that secrete insulin, a deficiency of insulin in the blood causes an impaired ability of tissues, especially muscle cells, fat tissue, and liver cells, to utilize carbohydrates, fats, and proteins. Impaired glucose (sugar) utilization and ongoing glucose production cause hyperglycemia (excess blood sugar levels). Glucosuria (glucose in the urine) develops, causing copious dilute urine (osmotic diuresis), increased thirst and drinking, and compensatory weight loss. Mobilization of fats to the liver causes both hepatic lipidosis (“fatty liver”) and ketogenesis (production of blood ketones).
Systems affected include: Endocrine/metabolic (blood salts depletion and blood shift toward acidity); Liver (hepatic lipidosis, liver failure may develop—particularly in cats); Eyes (cataracts in dogs); Kidney (urinary tract infection and osmotic diuresis); and Nervous (peripheral neuropathy in cats’ rear legs). The prevalence in both dogs and cats varies between one in 400 to 500 animals. There is a higher risk in some breeds of dogs than others (especially the keeshond, puli, miniature pinscher, and Cairn terrier) and possible higher risk in poodle, dachshund, miniature schnauzer, and beagle. No breed differences in cats have been reported. Mean age in dogs is about 8 years; range, 4-14 years (excluding rare juvenile form), and in cats about 75% are 8- 13 years; range, 1-19 years. Oddly there is a predominance according to sex. In dogs, the female is more likely to develop diabetes, while in cats it is the male more likely.
What Symptoms are Typical of Diabetes Mellitus? Dogs show signs are more often in the early stages of the disease than in cats. Early signs include: increased thirst and urine production, more frequent eating, and weight loss. Later on, the pet may show loss of appetite, lethargy, depression, and vomiting. An overweight pet with recent weight loss is typical. Back muscle wasting and an oily coat with dandruff is common in cats. Enlarged livers may be present in both dogs and cats, but jaundice is more prevalent in cats. Less commonly cataracts may be seen in dogs and a weakness in the rear legs in cats (diabetic neuropathy).
What Causes this Disease? This is open to conjecture but a number of factors have an influence. Genetic susceptibility sets the stage in some dog breeds. Infectious (viral) diseases have been implicated as is immune-mediated beta cell destruction. Pancreatitis (infection or inflammation of the pancreas), predisposing diseases (e.g., hyperadrenocorticism and acromegaly), and certain drugs (e.g., glucocorticoids and progestagens) have been implicated.
How is It Diagnosed? The combination of sugar in the urine, increased thirst and urine production, and loss of weight is very suggestive of diabetes mellitus. Blood glucose levels greater than 200 mg% in dogs and greater than 250 mg% in cats are typical. Other tests may show liver pathology, ketones in the urine, blood pH moving toward acidity, and electrolytes (blood salts) may be deficient. Radiography (x-rays) may be useful to evaluate for concurrent or underlying disease (e.g., urinary stones, liver pathology, and pancreatitis). Ultrasonography (ultrasound) is indicated in selected patients, particularly those with jaundice, to evaluate for liver pathology and pancreatitis. Liver biopsy may be indicated in some jaundiced patients.
How is Diabetes Mellitus Treated?
INPATIENT vs. OUTPATIENT: Dogs and cats that are alert, hydrated, and eating and drinking without vomiting can be managed as outpatients.
ACTIVITY: Strenuous activity may lower the daily insulin requirement. So, a consistent amount of activity each day is helpful.
DIET: Avoid soft, moist foods because they cause severe hyperglycemia after eating. Normal weight dogs and cats should be fed a consistent diet that the pet will reliably eat. Keep daily calorie intake constant. Obese dogs and cats need a gradual weight reduction to improve insulin sensitivity (and reverses diabetes in some cats with type II DM). Techniques to aid in weight loss under your veterinarians supervision: Technique 1: Reduce the calorie intake to 70% (cats) or 60% (dogs) of the caloric requirement for the animal’s ideal body weight. Technique 2: Feed a high-fiber, low-calorie food in a quantity similar to which the pet is accustomed. Try to achieve the target weight over 2-4 months. Rapid weight loss is inadvisable, especially in obese cats with diabetes because they are prone to hepatic lipidosis (“fatty liver”). With thin dogs and cats, you should avoid a reduced calorie diet. Starvation exacerbates a toxic condition called ketoacidosis and leads to poor immune function. The role of fiber in the diet is mainly in weight loss and obesity prevention. Another beneficial effect may be improved sugar control. The recommended diet is high in fiber, low in fat, and high in complex carbohydrates (Canine or Feline W/d are good examples). In cats a diet with moderately high protein and fat and decreased carbohydrates has proven helpful in decreasing insulin requirements and stabilizing the blood sugar levels (Feline M/d). When feeding the diabetic patient, feed the pet half its daily food every 12 hours to coincide with twice-daily insulin injections or orally administered hypoglycemic agent. For animals on once-daily insulin injections, half the food is given with the injection and the remainder in 8-10 hours or at the time of peak insulin activity, if that has been determined. For nibblers, dry food can be fed ad libitum, and two small meals of canned food given as described.
SURGICAL CONSIDERATIONS: Intact females should have an ovariohysterectomy (“spay”) when stable. Progesterone secreted between heat periods makes management of diabetes difficult.
MEDICATIONS: Insulin is the treatment of choice for all dogs and most cats. Beef, pork, beef/pork, and human recombinant insulin are options, but animal-origin insulins are being phased out. Keep your pet on the same type and species of insulin if possible. Oral administration of a hypoglycemic agent (eg. glipizide) is useful with dietary therapy in some cats with type II DM. The cat should have uncomplicated DM and no history of ketoacidosis. Potential side effects are hypoglycemia (low blood sugar), hepatic enzyme alterations, icterus, and vomiting.
How Can I Tell if the Insulin is Working?
PATIENT MONITORING The glucose curve test is the best method of monitoring the response to insulin. Here’s how the test works: You feed your pet, inject the insulin, and then bring the patient to the hospital for serial blood glucose testing every 1-2 hours, beginning about an hour after the injection. The goal is to maintain blood glucose between 100 and 200 mg% for at least 20-22 hours per day in dogs, and between 100 and 300 mg% in cats. The curve is performed every few weeks until the disease is regulated, and then every few months or whenever a problem arises. Urine glucose monitoring: There are a number of methods of monitoring the diabetic patient. Urine can be tested for glucose and ketones before the meal and insulin injection. To use this as a regulatory method, the pet must be allowed to have trace to 1/4% glucosuria to avoid hypoglycemia. Animals regulated by urine alone may be more hyperglycemic than ideal, and insulin overdose with rebound hyperglycemia is an inherent risk with this method. It is most useful to combine urine monitoring with intermittent glucose curves. Owners should seek veterinary attention if ketonuria is detected. The fructosamine test may be helpful in deterimining the long-term level of regulation. Clinical signs are an excellent way an owner can assess degree regulation, by monitoring water consumption and urine production, appetite, and body weight. If these are normal, the disease is well regulated.
POSSIBLE COMPLICATIONS • Cataracts (dogs) and diabetic neuropathy (cats) with poor glycemic control. • Seizure or coma with insulin overdose. • Anemia and red blood cell breakdown with severe low levels of blood phosphorus, which can occur after initial insulin therapy.
EXPECTED COURSE AND PROGNOSIS Some cats recover to become non-diabetic, but may relapse at a later time. Dogs have permanent disease. Prognosis with treatment is good. Most animals have a normal life span when regulated correctly.
PREGNANCY Diabetes mellitus can develop during pregnancy, in which case the pregnancy is difficult to maintain. Exogenous insulin administration may cause fetal oversize and difficult birth. Insulin resistance may develop, making hyperglycemia difficult to control. The pregnant dog is prone to ketoacidosis. An emergency ovariohysterectomy may be necessary. Dogs with DM should not be used for breeding.
Notify the Doctor if Any of the Following Occur: • You cannot give the insulin as directed, or urine-sugar levels increase. • Your pet’s thirst and urination increase. • Your pet has diarrhea, loss of appetite, or vomits frequently. • Your pet acts weak or depressed
DIABETES INSIPIDUS (Water Diabetes)
It is a disorder of the body’s water balance characterized by increased urine production, urine of low concentration, and increased water consumption. It is considered rare. Dogs and cats can both be affected. There are two types of diabetes insipidus: • Central diabetes insipidus— due to a deficiency in the secretion of antidiuretic hormone (ADH). • Nephrogenic diabetes insipidus—the kidneys are nonresponsive to ADH.
What are the Signs of Diabetes Insipidus? The congenital forms of central and nephrogenic diabetes insipidus, will show up in pets younger than one year. The acquired forms of central diabetes insipidus can occur at any age. The common signs are increased urine production and increased thirst. Some pets will show incontinence too (leaking urine during sleep).
What Causes Diabetes Insipidus? The most common causes are associated with inadequate secretion of ADH by the pituitary. This can be due to a congenital defect, idiopathic (unknown) cause, trauma, or pituitary gland tumor. The renal insensitivity to ADH form may be caused by a congenital defect, or secondary to drugs (e.g., lithium, demeclocycline, and methoxy-fluorane), or secondary to endocrine and metabolic disorders (e.g., hyperadrenocorticism, low potassium, pyometra (pus filled uterus), and high calcium.
How is Diabetes Insipidus Diagnosed? The history and physical examination findings will suggest diabetes as a possible problem, but a urinalysis is needed to get a presumptive diagnosis. The urine specific gravity (concentration) will be very low. A water deprivation test will show urine that remains dilute in spite of gradual body water loss. An ADH stimulation test is diagnostic for central diabetes insipidus (an injection of ADH is given and the concentration of the urine is measured over the next several hours).
Can It be Treated? Yes, it is treated with medicines for the rest of the pet’s life. • Central diabetes insipidus—DDAVP: (1-2 drops of the intranasal preparation are placed on the eye under the eyelid once or twice daily to control the disease). The dose and frequency is based on water consumption. • Nephrogenic diabetes insipidus—chlorothiazide is given by mouth twice daily.
Water should always be kept available. Pets with untreated diabetes insipidus can become dehydrated very rapidly without water. It is wise to monitor the volume of water used each day.
Call Us If… • Your pet’s drinking or urinating habits appear to be getting worse. • You notice any degradation in your pet’s general health. • You have trouble giving the prescribed medicine.
How is Darrhea Treated?
DO NOT GIVE YOUR PET MILK! Many pets cannot digest the sugar in cow’s milk (lactose). It passes through their digestive tract, providing a medium in which bacteria will bloom. This can cause or exaggerate diarrhea. If there is only diarrhea and no vomiting, you do not need to withhold water or food.
Food Intake: You may offer a bland diet in small amounts. Don’t overburden the digestive tract with food that may pass through incompletely digested. Small meals three to six times daily is best for the next three days.
Here are some bland diets:
Mix one carbohydrate with one protein at a ratio of 3/4 carbohydrate and 1/4 protein. Feed approx-imately one cup of cooked carbohydrate and four ounces of protein per 20 pounds of body weight daily. After three days on a bland diet, if your pet is responding well, gradually switch your pet to its regular diet over the next three or four days by slowly adding more of the regular food to the bland diet each day.
Medicine: Use as directed and on the label. Unless otherwise directed, give it until it is used up. It is often advisable to give yogurt (or Acidophilus capsules) after using enteric antibiotics to “replant” the good bacteria. The amount of yogurt is not critical but a tablespoon twice daily is adequate for a cat and four ounces twice daily is fine for a large dog. Adjust for your pet’s weight accordingly.
Call Us If… • Diarrhea is not controlled within three days. • Your pet refuses to eat the bland diet. • You are unsure if the response you are seeing is as expected. • You have trouble giving the medicine. • Vomiting occurs.
What is meant by Intervertebral Disk Disease? The spine is made up of bone segments called vertebrae. The spinal disks, more properly called intervertebral disks, are located between the vertebrae and serve as shock absorbers and flexors for the spinal column. Each disk is made up of a fibrous outer ring called the annulus and an inner section called the nucleus, which is soft and jellylike in consistency. When a disk becomes diseased, either through gradual degeneration or injury, the weakened annulus gives way and bulges into the spinal canal. It may also rupture completely and force the contents of the nucleus into the canal. Resulting pressure on the spinal cord causes the signs of pain, weakness, incoordination, or paralysis. Thora-columbar intervertebral disk disease is an age-related change within the intervertebral disk which can result in disk protrusion or extrusion in the spine of the thorax or lumbar part of the back. Intervertebral disk disease is classified as either Hansen type I or Hansen type II. Hansen type I disease involves cartilage degeneration of the disk, disk mineralization, and acute extrusion (3-6 years of age). Hansen type II disease involves gradual fibrous changes of the disk, with an insidious bulging or protrusion of the dorsal annulus (8-10 years of age). There is no known genetic basis for this disease, but breeds such as dachshund, shih tzu, Pekingese, Welsh corgi, beagle are predisposed to Hansen type I disease, while large breeds are predisposed to Hansen type II disease.
What are the Symptoms Associated with This? The clinical signs of disk disease are variable depending on the type of disk disease and the severity of disk extrusion. Signs may include back pain only, back pain with hindleg poor control, on to complete rear leg paralysis. The onset of signs may follow jumping; often there is no history of trauma. Small-breed dogs with Hansen type I disease usually have acute onset of clinical signs, while large-breed dogs with Hansen type II disease usually have a slow onset. On physical examination back pain is a common finding elicited by deep palpation of the back muscles. Varying degress of paraparesis may be present. Hindlimb placing and fine control may be diminished or absent.Pain perception in the hindlimbs may be diminished or absent.
How is It Diagnosed? The history, symptoms, and physical examination would make it suspect. Radiographs (x-rays) of the back often reveal a narrowed, wedged-shaped disk space and other changes. With Hansen type I disease, mineralized disk material may be seen within the spinal canal. Contrast radiographs or myelography can be helpful in localizing which disc is protruding into the spinal canal. Likewise MRIs and CAT scans can be diagnostic in difficult cases. Cerebral fluid examination (“spinal tap”) may be indicated in some cases.
How is It Treated? Medical treatment for intervertebral disk disease may relieve pain and inflammation, but surgery may be necessary to relieve cord pressure and prevent paralysis. Physical examination, x-rays, and nerve tests will help to determine the best course of treatment for your pet. Dogs with thoracolumbar disk disease can be broken down into four categories:
Dogs in the first category are usually treated as outpatients with medications to relieve the pain and inflammation. Muscle relaxants may also be indicated. Dogs in the third and fourth categories require hospital care and imediate medical attention, including intravenous medications.
ACTIVITY: All dogs with disk disease should have reduced activity levels. In cases with an initial episode of back pain only, cage confinement for 2-4 weeks may alleviate signs and should be tried prior to surgical treatment.
DIET: All obese dogs should be placed on a reducing diet.
SURGICAL CONSIDERATIONS: Surgery is indicated for animals with repeated episodes of back pain and most animals with neurologic deficits. In animals with loss of deep pain perception, the prognosis is unknown but generally considered guarded to poor. Animals with acute loss of deep pain perception may benefit from emergency decompressive surgery.
What is the Long-term Prognosis?
POSSIBLE COMPLICATIONS: Recurrence of back pain with or without neurologic deficits is possible. Animals treated surgically may be less likely to have recurrences though. Catastrophic spinal cord compression may occur with thoracolumbar disk disease.
EXPECTED COURSE AND PROGNOSIS: Some animals treated medically have recurrence and ultimately require surgery, while most animals treated surgically do not have recurrent episodes unless other disks become involved.
What do I Need to Do?
At home, follow the instructions from your Veterinarian in regards to Medication, Diet, & Exercise. Observe for regular bowel movements and urination. Provide a firm padded sleeping surface. Lift small dogs carefully so their back remains straight without excess tension on it (support them evenly from front to back). Urinary bladder function should be closely monitored. Manual expression (3-4 times daily) often is necessary in dogs unable to ambulate.
Confinement is very important. The spine will require approximately one month to heal, so restrict activity for that long — no jumping up or down off furniture or stairs. When they start feeling better they have the tendency to act normally. It is up to us to be sure they don’t get too active early in the healing period.
Notify Us if Any of the Following Occurs: 1. Your pet seems increasingly uncomfortable. 2. Your pet cannot lie down or continually braces himself/herself with front legs. 3. Your pet loses control of his/her bowel movements. 4. Your pet has difficulty with or is unable to have bowel movements or to urinate. 5. Your pet is limping or refusing to use a leg.
DISK DISEASE, INTERVERTEBRAL
Cervical or neck, intervertebral disk disease is an agerelated change within the intervertebral disk which can result in disk protrusion or extrusion. Intervertebral disk disease is classified as either Hansen type I or Hansen type II. Hansen type I disease involves cartilage degeneration of the disk, disk mineralization, and acute extrusion (3-6 years of age). Hansen type II disease involves gradual fibrous changes of the disk, with an insidious bulging or protrusion of the dorsal annulus (8-10 years of age). There is no known genetic basis for this disease, but breeds such as dachshund, beagle and Pekingese are predisposed to Hansen type I disease, while large breeds, especially the Doberman pinscher, are predisposed to Hansen type II disease.
What are the Symptoms Associated with This? The clinical signs of cervical disk disease are variable depending on the type of disk disease and the severity of disk extrusion. Based on the degree of disk extrusion, signs may include pain when the dog is picked up or when its neck is manipulated, failure to flex the neck to eat or drink, and failure to turn the head and neck to the right or left. Spasms of the neck and shoulder muscles may occur. If the disk extrusion impinges on a nerve root, the dog may hold one front limb off the ground or limp. Paresis or paralysis of all four limbs may rarely occur, but is much less common than neck pain only.
How is It Diagnosed? The history, symptoms, and physical examination would make it suspect. Radiographs (x-rays) of the neck often reveal a narrowed, wedged-shaped disk space and other changes. With Hansen type I disease, mineralized disk material may be seen within the spinal canal. Contrast radiographs or myelography can be helpful in localizing which disc is protruding into the spinal canal. Likewise MRIs and CAT scans can be diagnostic in difficult cases. Cerebral fluid examination (“spinal tap”) may be indicated in some cases.
How is It Treated? Medical treatment for intervertebral disk disease may relieve pain and inflammation, but surgery may be necessary to relieve cord pressure and prevent paralysis. Physical examination, x-rays, and nerve tests will help to determine the best course of treatment for your pet. Dogs with cervical disk disease can be broken down into three categories:
Dogs in the first category are usually treated as outpatients with medications to relieve the pain and inflammation. Muscle relaxants may also be indicated.
ACTIVITY: All dogs with disk disease should have reduced activity levels. Harnesses rather than collars should be used for leash walking and animals should be discouraged from any form of jumping. In cases with an initial episode of neck pain only, cage confinement for 2-4 weeks may alleviate signs and should be tried prior to surgical treatment.
DIET: All obese dogs should be placed on a reducing diet.
SURGICAL CONSIDERATIONS: Surgery is indicated for most animals with repeated episodes of neck pain and all animals with neurologic deficits.
What is the Long-term Prognosis? POSSIBLE COMPLICATIONS: Recurrence of neck pain with or without neurologic deficits is possible. Animals treated surgically may be less likely to have recurrences though. Catastrophic spinal cord compression almost never occurs with cervical disk disease. EXPECTED COURSE AND PROGNOSIS: Some animals treated medically have recurrence and ultimately require surgery, while most animals treated surgically do not have recurrent episodes unless other disks become involved.
What do I Need to Do?
At home, follow the instructions from your Veterinarian in regards to Medication, Diet, & Exercise. Observe for regular bowel movements and urination. Provide a firm padded sleeping surface. Lift small dogs carefully so their back and neck remains straight without excess tension on it (support them evenly from front to back). Urinary bladder function should be closely monitored. Manual expression (3-4 times daily) often is necessary in dogs unable to ambulate.
Confinement is very important. The spine will require approximately one month to heal, so restrict activity for that long — no jumping up or down off furniture or stairs. When they start feeling better they have the tendency to act normally. It is up to us to be sure they don’t get too active early in the healing period.
Notify Us if Any of the Following Occurs: 1. Your pet seems increasingly uncomfortable. 2. Your pet cannot lie down or continually braces himself/herself with front legs. 3. Your pet loses control of his/her bowel movements. 4. Your pet has difficulty with or is unable to have bowelmovements or to urinate. 5. Your pet is limping on or refusing to use a front leg.
Why is My Pet’s Eye Red? A “red eye” is usually inflamed. Eye inflammation can be the result of many different abnormalities. One type of eye inflammation is conjunctivitis, which is an inflammation of the mucous membrane that covers the front portion of the eyeball and lines the third eyelid at the inside corner of the eye and underside of the upper & lower lids. One cause of conjunctivitis is insufficient lubrication of the eye with tears. Keratoconjunctivitis sicca is a condition where the surface of the eyeball is inflamed because of insufficient tear production. Specifically it is defined as: “A deficiency of aqueous tear film resulting in drying and inflammation of the cornea and conjunctiva.” In other words, the clear window in the front of the eyeball, the white of the eye, and the underside of the eyelids are inflamed. This is very common in dogs, but much rarer in cats.Many breeds of dogs are predisposed, including the cocker spaniel, bulldog, West Highland white terrier, Lhasa apso, and shih tzu.
What Symptoms are Typical of This Disease? Some of the signs we may see in a pet with this condition include: Tight, painful eyelids that are squeezed against the eye; Eye redness due to enlarged blood vessels; Swelling of the eye and surrounding tissues; Prominent third eyelids; Mucus or pus discharge; Corneal changes, including superficial blood vessels, patches of black pigment-ation, and ulceration; Impaired or loss of vision if superficial corneal inflammation and pigmentation become severe.
What Causes it? There are a number of possible causes, including: • Immunologic—the most common cause is immunemediated inflammation of the tear glands. • Congenital—pug and Yorkshire terrier. • Neurogenic—occasionally seen after traumatic eye prolapsed or neurologic disease that interrupts the nerves to the tear gland. • Drug-induced—general anesthesia and atropine cause transient reduction in tear production. • Drug toxicity—some sulfa-containing drugs can cause transient or permanent KCS in some animals. • Removal of the nictitans gland (third eyelid) may predispose some animals to KCS. • X-ray therapy for cancer—when the eye area is treated. • Whole-body diseases—canine distemper virus or any debilitating disease. • Chronic conjunctivitis—occasionally seen in cats with chronic viral conjunctivitis or forms of chronic eyelidrelated conjunctivitis in dogs. • Breed-related predisposition
KCS is easily confused with bacterial conjunctivitis, since most dogs with chronic KCS have secondary bacterial infection. It may be differentiated by use of the Schirmer tear test, which measures tear production. Fluorescein staining may be performed to evaluate for the possibility of corneal ulceration as well. Cell or discharge examination in the microscope may indicate the nature and degree of bacterial overgrowth.
How is It Treated? It is typically treated on an outpatient basis, unless secondary disease and complications are noted. The treatment consists of: • Clean the eyes gently with moistened Kleenex tissues before instilling medication. • Keep your pet’s eyes and eyelids clean and free of dried discharge. • If your pet experiences an increase in eye pain, you should call at once, because animals with KCS are predisposed to severe corneal ulceration.
The medications used include: • Cyclosporine A is the drug of choice for treating KCS in dogs. It is most effective in the immune-mediated type of KCS, and one study showed it to be effective in promoting tear production in 80% of animals. • A new medication called Tacrolimus may be even more effective than Cyclosporine A (up to 92% effective). It is only available through “compounding” pharmacies. • Occasionally pilocarpine is effective in improving tear production by direct stimulation of the gland. • Artificial tears and lubricant ointments help moisten the cornea but must be used frequently, and they only provide transient relief from drying. • Eye antibiotics (drops or ointments) are often used in the initial treatment of a pet with chronic KCS due to secondary bacterial overgrowth. • Topically applied corticosteroids (“cortisone”) were frequently used in animals with KCS before cyclosporine use. They minimize inflammation and are effective in reducing corneal vascularization and pigmentation. In some situations we will still use them. • Rarely mucolytic agents are also used to help break up tenacious mucous discharge.
Are There Side-effects to the Treatments? There can be. Topically applied cyclosporine is irritating in some animals. Topically applied pilocarpine is initially irritating; however, animals seem to develop a tolerance. Orally administered pilocarpine causes vomiting and diarrhea in some animals. Topically applied corticosteroids are best avoided in animals with a corneal ulcer as it will slow the healing.
What is the Long-term Prognosis and Care? Some pets will respond very well and once they are making tears again, the medicines may be tapered off. Others will require medicine for the rest of their lives. Because of this variation, patients should be rechecked at regular intervals to monitor the response and progress, and to determine if continued treatment is mandatory. Most animals with the immune-mediated form of KCS will need lifelong treatment. Other types of KCS may be transient, and treatment need only continue until tear production returns.
Call Us If… • Your pet’s eye(s) appears to be getting worse. • You notice any degradation in your pet’s general health. • You have trouble giving the prescribed medicine.
DYSTOCIA (Difficult Birth)
Normal Birthing Labor has three stages: Stage 1 begins with onset of uterine contractions and ends when the cervix is fully dilated. It averages from 6-12 hours. Dogs may appear restless, nervous, lose their appetite, and may shiver, pant, vomit, or pace. Most will seek a place to “nest” near the end of this stage. Cats tend to vocalize initially, then purr as delivery approaches. Stage 2 begins with full dilation of the cervix and entry of the first offspring into the cervical canal; it ends with delivery of the last offspring. The dog shows obvious abdominal contractions in her attempt to deliver the puppies. The time between initiation of stage 2 and delivery of the first offspring varies (usually less than 4 hours). The time between delivery of subsequent young also varies (usually 20-60 minutes), but can be as long as 2-3 hours in the dog. Stage 3 begins after delivery of the offspring and ends with passage of all placentas. If the dog has multiple puppies, she may alternate between stage 2 and stage 3.
What Causes Difficult Birthing? Dystocia centers around three factors: a small or deformed birth canal, infant oversize, or uterine weakness (insufficient uterine force to propel the young through the birth canal). Infant causes: Oversized (a one-pup litter or abnormally shaped infant) or poor position in birth canal. Maternal causes: Abnormal pelvic canal from previous pelvic fracture; Congenitally small pelvis (Welsh corgi and brachycephalic breeds like English bulldog); Pelvic immaturity; Abnormalities of the vagina; Insufficient cervical dilation; Lack of adequate lubrication; Uterine torsion; Poor uterine contractions caused by muscle defect, biochemical imbalance, psychogenic disturbance, or exhaustion; Ineffective abdominal press due to pain, exhaustion, diaphragmatic hernia, or age. Risk factors: Age; Brachycephalic and toy breeds; Persian and Himalayan cats; Obesity; Abrupt change in environment; Previous history of dystocia.
What are the Signs of Dystocia? It is common in brachycephalic, miniature, and small dog breeds, and occasionally seen in large dog breeds with an extremely large litter. It is frequently seen in the
Persian and Himalayan cats. The prevalence increases with age.
Signs include: The mother has had 30 minutes of persistent, strong, abdominal contractions without expulsion of an offspring. Or more than 4 hours from the onset of stage 2 to delivery of the first young. Or more than 2 hours between delivery of offspring. Or failure to deliver a puppy or kitten 24 hours after rectal temperature falls below 99° F. Or the mother cries and displays signs of pain and constantly licks the vulvar area when delivering. Or prolonged gestation, i.e., over 70 days from day of first mating or over 59 days from the first day of end of estrus (dogs).
How is it Diagnosed? The history and physical examination make dystocia fairly obvious. The cause is not always so obvious. Some blood tests are helpful and may show low blood sugar, dehydration, and low blood calcium level depending on the length of dystocia. X-rays of the abdomen and pelvic area are paramount to determine the presence or absence of pregnancy, pelvic structure, number, size, and malposition of offspring. Ultrasound is recommended to monitor fetal viability.
How is Dystocia Treated? Dystocia is treated as an inpatient until delivery of all young and stabilization of the mother is accomplished. Manual treatment is used to deliver an infant lodged in vaginal vault. Failure to deliver the infant within 25-30 minutes is an indication for cesarean section. Intravenous fluid therapy, glucose, and calcium may be indicated. The uterine stimulant oxytocin is often used too. A Cesarean section is indicated with uterine inertia unresponsive to oxytocin, pelvic or vaginal obstruction, uncorrectable infant malposition, infant oversize, infant stress, or dead infants in the uterus. Elective Cesarean section is indicated in breeds highly prone to dystocia and animals with a history of dystocia.
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Desert Hills Animal Clinic 1039 East Carefree Hwy, Suite A, Phoenix, AZ 85085 Phone: 623-581-1558 Email: DesertHillsAnimalClinic@hotmail.com |