Saturday, 15 March 2014
Friday, 14 March 2014
Liver Failure in Cats
The liver is the largest internal organ of the body and it is responsible for a number of metabolic, functional and detoxification processes. It is located in the abdomen, under the diaphragm. The liver is the only organ in the body that is capable of rejuvenating itself.
Functions of the liver include:
Cleans the blood, removing medications and toxins.
Regulating chemicals in the blood.
Produces and secretes bile, which aids digestion and absorption of fats. Bile is a greenish-yellow fluid which consists of bile acids and waste products such as bilirubin. It is made by the liver and stored in the gall bladder.
Breaks down haemoglobin creating metabolites that are added to bile as pigment (bilirubin).
Produces specific enzymes which aid digestion of food.
Converts most sugars into glycerine which it stores up as glycogen until required.
Fat soluble vitamins A, D, E and K need bile in order to be absorbed by the body, these vitamins are stored in the liver.
Production of blood clotting factors.
Manufacture of certain hormones.
The liver changes ammonia, a toxic by product of protein metabolism into urea, which is excreted in the urine.
The liver is divided into sections (known as lobes), each of which is composed of thousands of structural and functional units (hepatic lobules).
Two blood vessels enter the liver. The hepatic portal vein contains de-oxygenated blood from the spleen, pancreas and digestive system and the hepatic artery contains oxygen rich blood from the lungs.
Liver Disease:
Liver disease occurs when the liver is damaged, resulting in loss of function. It can be acute (sudden onset) or chronic (slow and progressive). There are several causes of liver disease in cats, which include:
Hepatic Lipidosis (also known as Idiopathic Hepatic Lipidosis or Fatty Liver Disease). Hepatic Lipidosis is the most common type of liver disease in the cat and occurs when your cat becomes anorexic (stops or reduces the amount of food he is eating), the body begins to use fat stores as fuel. These fat stores are sent to the liver, to be broken down to supply nutrients. Unfortunately, the liver sometimes becomes overwhelmed and is unable to process this fat as quickly as necessary, leading to a build up of fat in the liver, which interferes with normal liver function.
Cholangitis/cholangiohepatitis complex: This is a number of related inflammatory and or infectious disorders of the liver and/or the biliary tract. Cholangitis relates to infection or inflammation of the bile duct and cholangiohepatitis is inflammation of the biliary system and by extension the liver. Causes of infection may often include FIP, Pancreatitis, inflammatory bowel disease (IBD), bacterial infection, parasitic infection (including toxoplasmosis).
Damage by toxins (Toxic Hepatopathy): This is caused by exposure to drugs, toxins or lack of blood to the liver.
Cancer: There are many different types of tumour which affect the liver. Primary liver cancer (beginning in the liver) is uncommon in cats. Most cancers of the liver originate from some other site and spread to the liver.
Portosystemic shunt (also known as liver shunt): Portosystemic shunts are abnormal communications between the portal and systemic venous system which allows intestinal blood to be delivered to the systemic circulation prior to hepatic detoxification. A shunt means that blood bypasses the liver, resulting in blood not being detoxified by the liver and a rise in toxins. Portosystemic shunts may be congenital or acquired, most shunts in cats are congenital (known as CPSS) and cats demonstrate clinical signs within 12 months of age.
Liver disease can occur in cats of any age although in younger cats it's most commonly caused by a portosystemic shunt or toxic hepatopathy.
What are the signs of liver disease in cats?
Symptoms may vary depending on what has caused liver disease, and symptoms can often be vague and non specific. Early symptoms you may notice include:
Loss of appetite (anorexia): One of the early signs of liver disease in cats.
Weight loss: Another early sign of liver disease.
As the liver becomes more damaged, further symptoms develop, such as:
Jaundice (icterus): Signs of jaundice are yellowing of the eyes, skin and mucous membranes. This is caused by hyperbilirubinemia, high levels of bilirubin in the blood. Bilirubin is a yellow bile pigment that is produced by the breakdown of red blood cells.
Ascites (abdominal effusion) - Build up of fluid in the peritoneal cavity caused by portal hypertension (high blood pressure) in the portal vein of the liver.
Polyuria (increased urination)/polydipsia (increased thirst).
Hepatomegaly (enlargement of the liver) or microhepatica (small liver).
Lethargy.
Diarrhea.
Vomiting.
Seizures.
Dark coloured but clear urine caused by the presence of bilirubin.
Bad breath.
How is liver disease diagnosed?
Your veterinarian will perform a physical examination of your cat and will want to run several tests, including a biochemical profile to look at:
Changes to the liver enzymes ALT (alanine aminotransferase) and AST (aspartate aminotransferase). The ALT test determines the level of this enzyme in the blood, which increases when damage to the liver cells has occurred. AST is an enzyme also found in skeletal and cardiac muscle cells, the brain and red blood cells. Elevated AST in the blood is also an indicator of liver disease, although as it is found in other organs, it is not as specific for liver cell injury as elevations in ALT.
Bilirubin: This is a major breakdown product of red blood cells. When red blood cells wear out they are trapped in the spleen and destroyed, releasing bilirubin into the blood. This type of bilirubin is called unconjugated. This bilirubin is transported in the blood to the liver, where it is taken up and conjugated (joined with glycuronic acid). This conjugated form may either be stored in the liver cells or excreted into the bile. Bilirubin levels are increased in cats with liver disease, gallbladder disease or have excessive destruction of red blood cells (known as hemolysis).
Low blood urea nitrogen (BUN), albumin, glucose, cholesterol which reflect the liver's inability to metabolise urea and glucose or produce albumin or cholesterol.
Other tests he may perform include:
Complete blood count: May reveal the presence of poikilocytes, which are abnormally shaped red blood cells. Anemia may also be present. Reduced white blood cells or platelets may indicate portal hypertension.
Urinalysis may reveal ammonium biurite crystals and/or bilirubin in the urine.
Thyroid testing.
Bile acids tolerance test. This involves taking a blood sample from your cat and then feeding him a fatty meal. Two hours later, a second blood sample is taken. When a cat eats, bile is released into the small intestine to assist with the digestion of fats (lipids). The bile is then absorbed by the intestine and returned back to the liver where it is removed from the bloodstream. In a cat with liver disease, this process doesn't occur as efficiently and levels of bile remain high in the blood.
Ultrasound: An ultrasound can give your veterinarian an idea of the size and shape of your cat's liver and gallbladder, and detect gallstones and biliary obstruction (blockage of the flow of bile from the liver). Abnormal vessels may be seen on ultrasound. Intrahepatic (inside the liver) are more easy to see on ultrasound than exgtrahepatic (outside the liver) vessels.
X-Ray: An x-ray may be taken to give your veterinarian an idea of the size and shape of your cat's liver. X-ray may also detect the presence of tumours.
Biopsy: A liver biopsy is taken to determine the exact type of liver disease. This may be done at the same time as the ultrasound.
Serologic Testing: Testing for diseases such as FeLV, FIV, FIP and toxoplasmosis may be taken as these diseases are associated with some liver disorders in cats.
How is liver disease treated?
Treatment depends on the cause of liver disease.
Hepatic Lipidosis:
Intensive nutritional support. Most frequently this involves feeding a calorie dense, high protein food via a feeding tube either directly into the stomach or esophagus. This type of feeding will usually be required for 6 - 8 weeks.
Fluid and electrolyte therapy if the cat is dehydrated.
Cholangitis/cholangiohepatitis complex:
Supportive care with IV or subcutaneous fluids and nutritional support.
If the cause is bacterial, antibiotics will be prescribed.
Medication to control vomiting if necessary.
Corticosteroids may also be helpful in cats.
Damage by toxins:
Immediately stopping the toxins (such as medications) where possible.
Removal of toxins from the body with activated charcoal.
Surgical ligation if physically and financially possible.
A prescription diet which is restricted in protein may be recommended.
Supportive care, where necessary.
Functions of the liver include:
Cleans the blood, removing medications and toxins.
Regulating chemicals in the blood.
Produces and secretes bile, which aids digestion and absorption of fats. Bile is a greenish-yellow fluid which consists of bile acids and waste products such as bilirubin. It is made by the liver and stored in the gall bladder.
Breaks down haemoglobin creating metabolites that are added to bile as pigment (bilirubin).
Produces specific enzymes which aid digestion of food.
Converts most sugars into glycerine which it stores up as glycogen until required.
Blood Diarrhea |
Production of blood clotting factors.
Manufacture of certain hormones.
The liver changes ammonia, a toxic by product of protein metabolism into urea, which is excreted in the urine.
The liver is divided into sections (known as lobes), each of which is composed of thousands of structural and functional units (hepatic lobules).
Two blood vessels enter the liver. The hepatic portal vein contains de-oxygenated blood from the spleen, pancreas and digestive system and the hepatic artery contains oxygen rich blood from the lungs.
Liver Disease:
Liver disease occurs when the liver is damaged, resulting in loss of function. It can be acute (sudden onset) or chronic (slow and progressive). There are several causes of liver disease in cats, which include:
Hepatic Lipidosis (also known as Idiopathic Hepatic Lipidosis or Fatty Liver Disease). Hepatic Lipidosis is the most common type of liver disease in the cat and occurs when your cat becomes anorexic (stops or reduces the amount of food he is eating), the body begins to use fat stores as fuel. These fat stores are sent to the liver, to be broken down to supply nutrients. Unfortunately, the liver sometimes becomes overwhelmed and is unable to process this fat as quickly as necessary, leading to a build up of fat in the liver, which interferes with normal liver function.
Cholangitis/cholangiohepatitis complex: This is a number of related inflammatory and or infectious disorders of the liver and/or the biliary tract. Cholangitis relates to infection or inflammation of the bile duct and cholangiohepatitis is inflammation of the biliary system and by extension the liver. Causes of infection may often include FIP, Pancreatitis, inflammatory bowel disease (IBD), bacterial infection, parasitic infection (including toxoplasmosis).
Damage by toxins (Toxic Hepatopathy): This is caused by exposure to drugs, toxins or lack of blood to the liver.
Cancer: There are many different types of tumour which affect the liver. Primary liver cancer (beginning in the liver) is uncommon in cats. Most cancers of the liver originate from some other site and spread to the liver.
Portosystemic shunt (also known as liver shunt): Portosystemic shunts are abnormal communications between the portal and systemic venous system which allows intestinal blood to be delivered to the systemic circulation prior to hepatic detoxification. A shunt means that blood bypasses the liver, resulting in blood not being detoxified by the liver and a rise in toxins. Portosystemic shunts may be congenital or acquired, most shunts in cats are congenital (known as CPSS) and cats demonstrate clinical signs within 12 months of age.
Liver disease can occur in cats of any age although in younger cats it's most commonly caused by a portosystemic shunt or toxic hepatopathy.
What are the signs of liver disease in cats?
Symptoms may vary depending on what has caused liver disease, and symptoms can often be vague and non specific. Early symptoms you may notice include:
Loss of appetite (anorexia): One of the early signs of liver disease in cats.
Weight loss: Another early sign of liver disease.
As the liver becomes more damaged, further symptoms develop, such as:
Jaundice (icterus): Signs of jaundice are yellowing of the eyes, skin and mucous membranes. This is caused by hyperbilirubinemia, high levels of bilirubin in the blood. Bilirubin is a yellow bile pigment that is produced by the breakdown of red blood cells.
Ascites (abdominal effusion) - Build up of fluid in the peritoneal cavity caused by portal hypertension (high blood pressure) in the portal vein of the liver.
Polyuria (increased urination)/polydipsia (increased thirst).
Hepatomegaly (enlargement of the liver) or microhepatica (small liver).
Lethargy.
Diarrhea.
Vomiting.
Seizures.
Dark coloured but clear urine caused by the presence of bilirubin.
Bad breath.
How is liver disease diagnosed?
Your veterinarian will perform a physical examination of your cat and will want to run several tests, including a biochemical profile to look at:
Changes to the liver enzymes ALT (alanine aminotransferase) and AST (aspartate aminotransferase). The ALT test determines the level of this enzyme in the blood, which increases when damage to the liver cells has occurred. AST is an enzyme also found in skeletal and cardiac muscle cells, the brain and red blood cells. Elevated AST in the blood is also an indicator of liver disease, although as it is found in other organs, it is not as specific for liver cell injury as elevations in ALT.
Bilirubin: This is a major breakdown product of red blood cells. When red blood cells wear out they are trapped in the spleen and destroyed, releasing bilirubin into the blood. This type of bilirubin is called unconjugated. This bilirubin is transported in the blood to the liver, where it is taken up and conjugated (joined with glycuronic acid). This conjugated form may either be stored in the liver cells or excreted into the bile. Bilirubin levels are increased in cats with liver disease, gallbladder disease or have excessive destruction of red blood cells (known as hemolysis).
Low blood urea nitrogen (BUN), albumin, glucose, cholesterol which reflect the liver's inability to metabolise urea and glucose or produce albumin or cholesterol.
Other tests he may perform include:
Complete blood count: May reveal the presence of poikilocytes, which are abnormally shaped red blood cells. Anemia may also be present. Reduced white blood cells or platelets may indicate portal hypertension.
Urinalysis may reveal ammonium biurite crystals and/or bilirubin in the urine.
Thyroid testing.
Bile acids tolerance test. This involves taking a blood sample from your cat and then feeding him a fatty meal. Two hours later, a second blood sample is taken. When a cat eats, bile is released into the small intestine to assist with the digestion of fats (lipids). The bile is then absorbed by the intestine and returned back to the liver where it is removed from the bloodstream. In a cat with liver disease, this process doesn't occur as efficiently and levels of bile remain high in the blood.
Ultrasound: An ultrasound can give your veterinarian an idea of the size and shape of your cat's liver and gallbladder, and detect gallstones and biliary obstruction (blockage of the flow of bile from the liver). Abnormal vessels may be seen on ultrasound. Intrahepatic (inside the liver) are more easy to see on ultrasound than exgtrahepatic (outside the liver) vessels.
X-Ray: An x-ray may be taken to give your veterinarian an idea of the size and shape of your cat's liver. X-ray may also detect the presence of tumours.
Biopsy: A liver biopsy is taken to determine the exact type of liver disease. This may be done at the same time as the ultrasound.
Serologic Testing: Testing for diseases such as FeLV, FIV, FIP and toxoplasmosis may be taken as these diseases are associated with some liver disorders in cats.
How is liver disease treated?
Treatment depends on the cause of liver disease.
Hepatic Lipidosis:
Intensive nutritional support. Most frequently this involves feeding a calorie dense, high protein food via a feeding tube either directly into the stomach or esophagus. This type of feeding will usually be required for 6 - 8 weeks.
Fluid and electrolyte therapy if the cat is dehydrated.
Cholangitis/cholangiohepatitis complex:
Supportive care with IV or subcutaneous fluids and nutritional support.
If the cause is bacterial, antibiotics will be prescribed.
Medication to control vomiting if necessary.
Corticosteroids may also be helpful in cats.
Damage by toxins:
Immediately stopping the toxins (such as medications) where possible.
Removal of toxins from the body with activated charcoal.
Surgical ligation if physically and financially possible.
A prescription diet which is restricted in protein may be recommended.
Supportive care, where necessary.
Thursday, 13 March 2014
Saturday, 8 March 2014
Pelvic fracture
The pelvis is a ring like structure of bones located at the lower end of the trunk. It consists of two halves, each one containing three bones, the ilium, ischium, and pubis.
A broken pelvis is the second most common bone breakage to occur in cats. They are typically the result of a motor vehicle accident or a fall from a building. Despite the severity of a broken pelvis, the chance of recovery, if there is no other internal damage is very good.
What are the symptoms of a broken pelvis in cats?
If you suspect your cat has been hit by a car, he should be taken to a veterinarian immediately. Common symptoms you may see include:
Your cat may or may not be able to walk. When our cat broke his pelvis, he was able to run away, despite being in a great amount of pain and with a severely damaged pelvis (see x-ray).
He may also have torn/ripped claws, from gripping at the ground (if hit by a car)
There may be external injuries such as cuts and abrasions.
If you suspect your cat has been injured and may have a broken pelvis, take extreme care when handling him. He will need to be kept as still as possible to avoid further injury. He will need to be put in a cat carrier and taken to the vet immediately.
Your veterinarian may be able to feel the break during the physical examination, however diagnosis is made by x-ray.
How is a broken pelvis treated?
Treatment of a broken pelvis depends on the severity of the injury. A minor break may be left to heal itself, however a major breakage will require surgery and possibly pins, plates, screws or wires to realign the pelvis. Your vet may choose to wait a day or so to allow any swelling to go down prior to the surgery.
Painkillers may be administered before and after surgery to help with discomfort.
Your cat will not be discharged from the vet until he can go to the toilet on his own. Our cat was released from hospital one week after his accident, and then placed on cage rest for a further six weeks.
Treatment for any other injuries such as soft tissue, damaged organs etc may also be necessary.
Home care:
Regardless of the outcome, your cat will most likely need to be on cage rest for 6 weeks to allow the pelvis to heal and the bones to fuse. Obviously this also has the benefit of preventing your cat from moving around and especially jumping up and down. A largish dog crate is perfect for this as it can accommodate the litter tray, food and water bowls and a cat bed. Make sure you have a low sided litter tray as moving around may be difficult in the early days. We used the lid from a cardboard box and cut out one side, lined it with a litter tray liner and filled it with litter. I have a very active cat who had to be put on cage rest for 6 weeks and he coped remarkably well.
It is important to keep a close watch on your cat's toileting habits while he is recovering and ensure he is having frequent bowel movements and urinating. If he stops going to the toilet, veterinary attention must be sought.
Long term outcome:
The outcome for cats with a broken pelvis is generally very good. Long term problems may include persistent lameness and arthritis of the hip joint in later years. Our cat has made an almost full recovery, he is a little wobbly at the back end, but it doesn't appear to have affected him a great deal.
If the injured cat is an entire female, it may be in her best interests to have her spayed as pelvic fractures can lead to a narrowing of the birth canal.
Fracture distal femoral
Fractures involving the distal femoral physis are relatively common in immature dogs and cats with the greatest incidence occurring between the ages of 5 and 8 months. Physel fractures have been classified by Salter and Harris into 5 categories: Type 1 traverse the physeal plate through the zone of hypertrophying cartilage; Type 2 involves the physis and continues through the mtaphysis; Type 3 involves the physis and continues through the epiphysis to involve the articular surface; Type 4 involves the articular surface, crosses the physis and continues into the metaphysis; and Type 5 a compression injury to the zone of resting cartilage of the physis.
Distal femoral physeal fractures are commonly Types 1 and 2; most physeal fractures in the dog are Type 2 while those in the cat are Type 1. This is due in part to the fact that the distal femoral metaphysis has four projections that correspond to four similar deep depressions in the epiphysis in the dog while in the cat, the projections are flatter and do not interdigitate as deeply with the corresponding epiphyseal depressions. Physeal fractures usually occur through the zone of hypertrophying cartilage, because this zone is characterized by large, vacuolated cells with minimal intercellular matrix. Therefore, this zone is the weakest.
A variety of treatment methods have been described for repair of distal femoral physeal fractures including closed reduction and external fixation, normograde or retrograde placement of a single intramedullary pin with or without an anti-rotational Kirshner wire, multiple intramedullary pins, paired Rush pins, Steinman pins, or Kirshner wires employed in Rush pin technique, cross pins, bone plates, and lag screws. The ultimate goal of treatment should be accurate reduction and rigid stabilization of these fractures with as little iatrogenic damage to the germinal cells of the physis and their blood supply as possible.
While closed reduction and external fixation may be successful in selected cases, every attempt should be made to satisfactorily stabilize the fracture internally so that early return to function is achieved and restricted joint movement is avoided. When closed reduction and external fixation is used, a good result is the most that one can expect.
Surgical exposure for open reduction and internal fixation is achieved via a lateral parapatella approach with reflection of the patella medially. Interference with growth is a consideration in the selection of the method of repair; however, recent studies have suggested that premature closure of the physis occurs more commonly as a result of the initial trauma than the method of treatment employed. Distal femoral physeal closure normally occurs between six and eight months of age; as the majority of physeal fractures occur in dogs and cats greater than five months of age, over 90 percent of their skeletal growth has already been achieved by the time of injury. Therefore, in animals over five months of age, while some degree of femoral shortening may occur, the overwhelming majority of animals clinically accommodate shortening by a change in stifle or hock angulation. In dogs and cats under five months of age with substantial growth potential, the method of fixation chosen should provide adequate stabilization but should not mechanically bridge the physis. Early implant removal may minimize premature physeal closure. Any implant, which traverses the growth plate, will result in some degree of permanent damage to the growth plate. The least damage occurs when round, smooth, non-threaded implants are placed perpendicularly to the long axis of the growth plate.
Single intramedullary pin fixation, Rush pinning and modified Rush pin technique, and cross pinning are the most commonly employed techniques used to treat Salter Type 1 and 2 fractures. A single intramedullary pin should provide excellent alignment and stability if the opposing surfaces of the fracture interlock following anatomic reduction. However, in large dogs, single pin fixation may be inadequate to allow early use of the limb. In addition, femoral intramedullary pins existing the trochanteric fossa have been associated with sciatic nerve injury. Normograde pinning of distal femoral physeal fractures is less likely to induce sciatic nerve injury then retrograde pinning. Implant migration may also result in damage to the intra-articular surface of the stifle joint.http://adf.ly/fBkJ8
Although cross pin fixation works well, it is associated with more complications than other techniques including caudal malalignment and/or displacement of the distal fragment and quadriceps tie-down. In very immature animals, cross pin fixation may interfere with physeal growth because of the excessive pin angulation necessary for adequate stabilization.
Rush pins provide excellent fixation for distal femoral physeal fractures. Their disadvantage is the need for special instrumentation and the cost of the implants. Rush pins provide three point fixation, thereby increasing stabilization and making their application especially indicated in large dogs. If Rush pins are used in very immature animals, great care must be taken when driving the pins to prevent excessive compression of the germinal cell layer, which may result in growth arrest.
Steinman pins or Kirshner wires may be used in exactly the same way as Rush pins. Once the fracture is reduced, the pins are inserted laterally just cranial to the tendon of origin of the long digital extensor muscle, and medially on the distal medial bondyle symmetric to the later pin placement. The pins are alternately advanced in the medullary cavity. I prefer that the pins do not exit the trochanteric fossa so as to minimize the potential complication of sciatic nerve injury. Pre-bending the pins accentuates a three point fixation and results in rigid internal fixation and rotational stability. This technique can be used in very immature animals when fear of Rush pin compression of the germinal layer may be a factor. Such pins may be placed with relative minor trauma to the physis, and most animals continue to lengthen their femurs despite the pins through the growth plate. With proper alignment and internal fixation, an excellent result should be expected
Distal femoral physeal fractures are commonly Types 1 and 2; most physeal fractures in the dog are Type 2 while those in the cat are Type 1. This is due in part to the fact that the distal femoral metaphysis has four projections that correspond to four similar deep depressions in the epiphysis in the dog while in the cat, the projections are flatter and do not interdigitate as deeply with the corresponding epiphyseal depressions. Physeal fractures usually occur through the zone of hypertrophying cartilage, because this zone is characterized by large, vacuolated cells with minimal intercellular matrix. Therefore, this zone is the weakest.
A variety of treatment methods have been described for repair of distal femoral physeal fractures including closed reduction and external fixation, normograde or retrograde placement of a single intramedullary pin with or without an anti-rotational Kirshner wire, multiple intramedullary pins, paired Rush pins, Steinman pins, or Kirshner wires employed in Rush pin technique, cross pins, bone plates, and lag screws. The ultimate goal of treatment should be accurate reduction and rigid stabilization of these fractures with as little iatrogenic damage to the germinal cells of the physis and their blood supply as possible.
While closed reduction and external fixation may be successful in selected cases, every attempt should be made to satisfactorily stabilize the fracture internally so that early return to function is achieved and restricted joint movement is avoided. When closed reduction and external fixation is used, a good result is the most that one can expect.
Surgical exposure for open reduction and internal fixation is achieved via a lateral parapatella approach with reflection of the patella medially. Interference with growth is a consideration in the selection of the method of repair; however, recent studies have suggested that premature closure of the physis occurs more commonly as a result of the initial trauma than the method of treatment employed. Distal femoral physeal closure normally occurs between six and eight months of age; as the majority of physeal fractures occur in dogs and cats greater than five months of age, over 90 percent of their skeletal growth has already been achieved by the time of injury. Therefore, in animals over five months of age, while some degree of femoral shortening may occur, the overwhelming majority of animals clinically accommodate shortening by a change in stifle or hock angulation. In dogs and cats under five months of age with substantial growth potential, the method of fixation chosen should provide adequate stabilization but should not mechanically bridge the physis. Early implant removal may minimize premature physeal closure. Any implant, which traverses the growth plate, will result in some degree of permanent damage to the growth plate. The least damage occurs when round, smooth, non-threaded implants are placed perpendicularly to the long axis of the growth plate.
Single intramedullary pin fixation, Rush pinning and modified Rush pin technique, and cross pinning are the most commonly employed techniques used to treat Salter Type 1 and 2 fractures. A single intramedullary pin should provide excellent alignment and stability if the opposing surfaces of the fracture interlock following anatomic reduction. However, in large dogs, single pin fixation may be inadequate to allow early use of the limb. In addition, femoral intramedullary pins existing the trochanteric fossa have been associated with sciatic nerve injury. Normograde pinning of distal femoral physeal fractures is less likely to induce sciatic nerve injury then retrograde pinning. Implant migration may also result in damage to the intra-articular surface of the stifle joint.http://adf.ly/fBkJ8
Although cross pin fixation works well, it is associated with more complications than other techniques including caudal malalignment and/or displacement of the distal fragment and quadriceps tie-down. In very immature animals, cross pin fixation may interfere with physeal growth because of the excessive pin angulation necessary for adequate stabilization.
Rush pins provide excellent fixation for distal femoral physeal fractures. Their disadvantage is the need for special instrumentation and the cost of the implants. Rush pins provide three point fixation, thereby increasing stabilization and making their application especially indicated in large dogs. If Rush pins are used in very immature animals, great care must be taken when driving the pins to prevent excessive compression of the germinal cell layer, which may result in growth arrest.
Steinman pins or Kirshner wires may be used in exactly the same way as Rush pins. Once the fracture is reduced, the pins are inserted laterally just cranial to the tendon of origin of the long digital extensor muscle, and medially on the distal medial bondyle symmetric to the later pin placement. The pins are alternately advanced in the medullary cavity. I prefer that the pins do not exit the trochanteric fossa so as to minimize the potential complication of sciatic nerve injury. Pre-bending the pins accentuates a three point fixation and results in rigid internal fixation and rotational stability. This technique can be used in very immature animals when fear of Rush pin compression of the germinal layer may be a factor. Such pins may be placed with relative minor trauma to the physis, and most animals continue to lengthen their femurs despite the pins through the growth plate. With proper alignment and internal fixation, an excellent result should be expected
Reference
http://www.animalmedcenter.com/faqs/category/surgical-repair-of-distal-femoral-physeal-fractures
Friday, 7 March 2014
Allergies
Just like people, dogs can show allergic symptoms when their immune systems begin to recognize certain everyday substances—or allergens— as dangerous. Even though these allergens are common in most environments and harmless to most animals, a dog with allergies will have an extreme reaction to them. Allergens can be problematic when inhaled, ingested or contact a dog’s skin. As his body tries to rid itself of these substances, a variety of skin, digestive and respiratory symptoms may appear.
What Are the General Symptoms of Allergies in Dogs?
Itchy, red, moist or scabbed skin
Increased scratching
Itchy, runny eyes
Itchy back or base of tail (most commonly flea allergy)
Itchy ears and ear infections
Sneezing
Vomiting
Diarrhea
Snoring caused by an inflamed throat
Paw chewing/swollen paws
Constant licking
Allergic dogs may also suffer from secondary bacterial or
yeast skin infections, which may cause hair loss, scabs or crusts on the skin.
after : condition 10 day treatment and dietary |
What Substances Can Dogs Be Allergic To?
A few common allergens include:
Tree, grass and weed pollens
Mold spores
Dust and house dust mites
Dander
Cigarette smoke
Food ingredients (e.g. beef, chicken, pork, corn, wheat or
soy)
Prescription drugs
Fleas and flea-control products
Perfumes
Cleaning products
Fabrics
Insecticidal shampoo
Rubber and plastic materials
Can Dogs Be Allergic to Food?
Yes, but it often takes some detective work to find out what
substance is causing the allergic reaction. Dogs with a food allergy will
commonly have itchy skin, breathing difficulties or gastrointestinal problems
like diarrhea and vomiting, and an elimination diet will most probably be used
to determine what food he is allergic to. If your dog is specifically allergic
to chicken, for example, you should avoid feeding him any products containing
chicken protein or fat.
Please note that food allergies may show up in dogs at any
age.
What Should I Do If I Think My Dog Has Allergies?
Visit your veterinarian. After taking a complete history and
conducting a physical examination, he or she may be able to determine the
source of your dog’s allergic reaction. If not, your vet will most probably
recommend skin or blood tests, or a special elimination diet, to find out
what's causing the allergic reaction.
How Are Dog Allergies Diagnosed?
If your dog’s itchy, red or irritated skin persists beyond
initial treatment by a veterinarian, allergy testing, most often performed by a
veterinary dermatologist, is likely warranted. The diagnostic test of choice is
an intradermal skin test similar to the one performed on humans.
The only way to diagnose a food allergy is to feed your dog
a prescription or hydrolyzed protein diet exclusively for 12 weeks. The
importance of not feeding your dog anything but the diet cannot be emphasized
enough—that means no treats, table food or flavored medication. This diet will
be free of potential allergy-causing ingredients and will ideally have
ingredients your dog has never been exposed to. He’ll remain on the diet until
his symptoms go away, at which time you’ll begin to reintroduce old foods to
see which ones might be causing the allergic reaction.
Please note, many dogs diagnosed with a food allergy will
require home-cooked meals—but this must be done in conjunction with your
veterinarian, as it requires careful food balancing.
How Can Dog Allergies Be Treated?
The best way to treat allergies is to remove the offending
allergens from the environment.
Prevention is the best treatment for allergies caused by
fleas. Start a flea control program for all of your pets before the season
starts. Remember, outdoor pets can carry fleas inside to indoor pets. See your
veterinarian for advice about the best flea control products for your dog and
the environment.
If dust is the problem, clean your pet's bedding once a week
and vacuum at least twice weekly—this includes rugs, curtains and any other materials
that gather dust.
Weekly bathing may help relieve itching and remove
environmental allergens and pollens from your dog’s skin. Discuss with your vet
what prescription shampoos are best, as frequent bathing with the wrong product
can dry out skin.
If you suspect your dog has a food allergy, she’ll need to
be put on an exclusive prescription or hydrolyzed protein diet. Once the
allergy is determined, your vet will recommend specific foods or a home-cooked
diet.
Are There Allergy Medications for Dogs?
Since certain substances cannot be removed from the
environment, your vet may recommend medications to control the allergic
reaction:
In the case of airborne allergens, your dog may benefit from
allergy injections. These will help your pet develop resistance to the
offending agent, instead of just masking the itch.
Antihistamines such as Benadryl can be used, but may only
benefit a small percentage of dogs with allergies. Ask your vet first.
Fatty acid supplements might help relieve your dog’s itchy
skin. There are also shampoos that may help prevent skin infection, which
occurs commonly in dogs with allergies. Sprays containing oatmeal, aloe and
other natural products are also available.
An immune modulating drug may also be helpful.
There are several flea-prevention products that can be
applied monthly to your dog’s skin.
If the problem is severe, you may have to resort to
cortisone to control the allergy. However these drugs are strong and should be
used with caution and only under the guidance of your veterinarian.
Are Allergies and Bronchitis Related?
Chronic exposure to inhaled irritants (including cigarette
smoke) may be a cause of bronchitis in the dog. Bronchitis is characterized by
a persistent cough due to inflammation of the airway and excessive mucus
production. Treatment may include medication to open breathing passages,
antibiotics and anti-inflammatory agents. Please remember, your pets should not
be exposed to cigarette smoke.
Reference
http://www.aspca.org/pet-care/dog-care/allergies
Thursday, 6 March 2014
Bleeding Disorder in Dogs
Von Willebrand's Disease in Dogs
Bleeding from the vagina |
Von Willebrand’s disease (vWD) is a blood disease caused by a deficiency of
von Willebrand Factor (vWF), an adhesive glycoprotein in the blood required for
normal platelet binding (i.e., clotting) at the sites of
small blood vessel injuries. In addition, vWF is a carrier protein for
coagulation Factor VIII (necessary for blood to clot). A lack of vWF impairs
platelet stickiness and clumping. Similar to hemophilia in humans, this condition can lead to excessive bleeding following an
injury, due to the lack of clotting.
VWF is an autosomal (non-sex-linked) trait, which both males and females
express and transmit genetically and with equal frequency. The expression
pattern of the severe forms (Types 2 and 3 vWD) is recessive while the milder
form (Type 1 vWD) appears to be recessive or incompletely dominant. This is the
most common hereditary blood clotting disorder in dogs, occurring with more
frequency in some breeds, including German shepherds, Doberman pinchers and
golden retrievers. In our clinic even ever seen with dog kintamani (indonesia
domestic breed dog) with vWD sign
Symptoms and Types
Spontaneous hemorrhage
Nosebleeds
Blood in the feces
(black or bright red blood)
Bloody urine
Bleeding from the gums
Bleeding from the
vagina (excessively)
Bruising of skin
Prolonged bleeding after surgery or trauma
Blood loss anemia if there is prolonged bleeding
Bleeding from the gums |
Bleeding from the vagina |
Causes
·
Hereditary vWD is caused by mutations that impair vWF synthesis, release,
or stability.
Diagnosis
Your veterinarian will perform a thorough physical exam on your dog, taking
into account the background history of your dog's health and onset of symptoms.
A blood chemical profile will be performed, with a complete blood count, a
urinalysis, and an electrolyte panel. If there has been blood loss, a
regenerative anemia will be seen on the complete blood count. Typically, the
platelet count will be normal (unless your dog has experienced recent, massive
bleeding), and coagulation tests will show normal results.
A clinical diagnosis of von Willebrand disease is based on a specific
measurement of plasma vWF concentration bound to the antigen (vWF:Ag). The length of time that it takes for platelets to plug a small
injury will be measured, with a test called the buccal mucosa bleeding time
(BMBT). The BMBT test, along with the platelet function analyzer (PFA 100), are
point-of-care screening tests where the endpoints are prolonged in patients
with platelet clumping defects and vWF deficiency. Prolongation is nonspecific,
and may accompany numerous severe disorders of the blood.
Treatment
Transfusion
of fresh whole blood, fresh plasma, fresh frozen plasma, and cryoprecipitate
will supply vWF to the blood. Component therapy (fresh frozen plasma or
cryoprecipitate) is best for surgical prophylaxis (prevention) and nonanemic patients,
to prevent red cell sensitization and
volume overload. Patients with severe vWD may require repeated transfusion to
control or prevent hemorrhage. If a dog lacking vWF requires surgery, a
pre-operative transfusion should be given just before the procedure.
Living
and Management
Most
dogs with mild to moderate vWD will continue to have a good quality of life,
requiring minimal or no special treatment. Dogs with more severe forms will
require transfusion for surgery, and should be transfused if supportive care
fails to control a spontaneous bleeding episode. Most of these dogs can be
maintained comfortably, but their activities will need to be monitored and
limited. If your dog has von Willebrand Disease and it has an episode of
prolonged bleeding, call your veterinarian and take it to a veterinary clinic
immediately for emergency treatment.
Reference
http://www.petmd.com/dog/conditions/cardiovascular/c_dg_von_willebrand_disease?page=2
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