SECTION 9 Hemolymphatic System

Section Editor: Kristi S. Lively, DVM, DABVP

Acute Lymphocytic Leukemia

Anemia in Dogs and Cats

Anticoagulant Rodenticide Toxicity

Aplastic Anemia

Babesia Infection in Dogs

Chronic Lymphocytic Leukemia

Coagulopathy Associated with Liver Disease

Disseminated Intravascular Coagulation

Fever of Unknown Origin

Hemobartonellosis in Cats

Hemophilia A

Hemophilia B

Hypercalcemia Associated with Cancer

Immune-Mediated Hemolytic Anemia

Immune-Mediated Thrombocytopenia

Primary and Secondary Polycythemia

Splenic Hemangiosarcoma

Splenic Torsion

Splenomegaly

Thrombocytopenia: Other Causes

Thrombosis

Von Willebrand Disease

Acute Lymphocytic Leukemia

Kristi S. Lively, DVM, DABVP

BASIC INFORMATION

TREATMENT AND FOLLOW-UP

Treatment Options

Dogs and cats with ALL are generally quite sick at the time of diagnosis, and treatment should be started early and done aggressively. Chemotherapy is the treatment of choice. Protocols may include drugs such as vincristine, L-asparaginase, cyclophosphamide, doxorubicin, and prednisone. Other supportive care may be needed, such as intravenous fluids, nutritional support, antibiotics, and transfusions.

Follow-up Care

Blood counts and other laboratory tests are repeated periodically to assess response to treatment and to monitor for side effects from the chemotherapeutic medications. Drug doses are adjusted if the neutrophil counts become excessively low, because low neutrophil counts predispose the patient to infections. Antibiotics may be prescribed to help prevent infection if the neutrophil counts are low.

Prognosis

Prognosis is grave, and survival time depends largely on the response to chemotherapy. With aggressive chemotherapy, only about 30% of patients achieve remission (disappearance of the cancerous cells from the blood). Without chemotherapy, most patients die within a few weeks of diagnosis. Even with chemotherapy, most animals survive only a few months.

SPECIAL INSTRUCTIONS:

Anemia in Dogs and Cats

Kristi S. Lively, DVM, DABVP

BASIC INFORMATION

Description

Anemia is an abnormally low red blood cell (RBC) count. The primary function of the RBC is to transport oxygen to tissues, so inadequate RBC numbers cause decreased oxygenation of tissues. Anemia is not a specific disease but reflects an underlying disease process.

Causes

Anemia may be caused by decreased production of RBCs, increased destruction of RBCs (hemolysis), or loss of RBCs. Decreased RBC production arises secondary to chronic metabolic diseases, such as kidney disease, cancer, or malnutrition. RBCs are produced in the bone marrow, and infections or cancer of the marrow may also affect production.

Excessive RBC destruction is commonly immune mediated, although toxins, infections, blood parasites, cancer, drug reactions, and inherited RBC membrane defects can also cause hemolysis. Anemia secondary to blood loss may be overtly noted with trauma, but it may be hidden with other conditions, such as gastrointestinal tract bleeding, certain parasites (fleas, ticks, hookworms), and clotting disorders.

Clinical Signs

Clinical signs of anemia depend on both the severity of the anemia and the underlying cause. Clinical anemia typically causes weakness, lethargy, increased heart rate, poor appetite, and pale gums. Signs of the underlying cause may include fever, jaundice, enlarged spleen, pica (eating abnormal objects such as dirt), enlarged lymph nodes (glands), vomiting, diarrhea, weight loss, or depression.

Diagnostic Tests

Anemia is reasonably easy to diagnose, but diagnosing the underlying cause may be more difficult. Packed cell volume (PCV) is one measurement of the RBC count. Normal PCV values vary depending on the species of animal and the laboratory being used. An abnormally low PCV value confirms the diagnosis of anemia.

If anemia is diagnosed, other laboratory tests may be recommended to further characterize the cause of the anemia:

• Evaluation of a blood smear to identify potential blood parasites

• Biochemistry profile and urinalysis to evaluate organ function

• Fecal examination to identify internal parasites

• Reticulocyte count to determine whether the bone marrow is trying to replace lost RBCs

• Bone marrow aspiration and evaluation if there is no evidence that the RBCs are regenerating (low reticulocyte count)

• X-rays to evaluate for the presence of tumors, size of various organs, or evidence of trauma

• Clotting tests if excessive or persistent bleeding is present

• Other tests to screen for potential immune-mediated destruction of RBCs

TREATMENT AND FOLLOW-UP

Treatment Options

If the anemia is severe and life-threatening, hospitalization and blood transfusions may be recommended to stabilize the patient while the underlying disease is identified and potentially treated. Patients with severe anemia may also require oxygen therapy to compensate for decreased oxygen delivery to tissues. The treatment plan is then directed at the underlying cause and may include immunosuppressive drugs, antibiotics, parasite control, chemotherapy, or hormone injections. Not all underlying causes of anemia are treatable.

Follow-up Care

Follow-up depends on the underlying cause. Isolated events such as trauma may require monitoring of the PCV for a few days, whereas chronic conditions such as cancer or renal disease may require long-term monitoring. Immune-mediated anemia usually requires several months of therapy and monitoring.

Prognosis

The prognosis for anemia alone can be good with early intervention in reversible cases. Long-term prognosis depends on the severity of the underlying disease and whether the underlying disease can be treated.

SPECIAL INSTRUCTIONS:

Anticoagulant Rodenticide Toxicity

Kristi S. Lively, DVM, DABVP

BASIC INFORMATION

Description

Ingestion (eating) of certain rodent poisons (rodenticides) by dogs and cats can cause bleeding problems because they act as anticoagulants (prevent blood clotting). The pet may directly ingest rodent bait, may ingest food contaminated with the poison, or may even ingest a rodent that has died from the poison (especially cats).

Active ingredients in these rodenticides fall into two categories, coumarin-based products (warfarin, coumafuryl, brodifacoum, and bromadiolone) and indanedione-based products (diphacinone, pindone, yalone, and chlorophacinone). Coumarin-based products have a shorter duration of action.

Agents in these categories also fall into two generations, depending on when they were first developed.

• First-generation anticoagulants (warfarin, pindone, coumafuryl, coumachlor, isovaleryl-indanedione) are less toxic and often require ingestion of a larger amount to be problematic.

• Second-generation anticoagulants (brodifacoum, bromadiolone) are highly toxic after a single exposure.

Most of these poisons are bright blue-green pellets, and dogs and cats often confuse them for tasty kibble.

Causes and Toxicity

These products interfere with vitamin K activity in the body, which is required for blood to clot normally. When vitamin K–related clotting proteins are inactive, signs of bleeding occur. Coumarin-based products affect vitamin K for days, whereas the effects of indanedione-based products may last for weeks.

Clinical Signs

Signs can take several days to develop, because vitamin K stores must first be depleted. Signs are related to anemia or bleeding tendencies. External signs of bleeding are not always present if the bleeding is internal, so weakness and depression may be the only signs noted. Pale gums; bruising; nose bleeds; blood in the urine, feces, or eyes; or difficulty breathing may occur. Bleeding may be sudden and life-threatening.

Diagnostic Tests

If ingestion of the rodenticide is seen by the owner, the diagnosis is straightforward. Not all rat poisons are anticoagulants, so it is important to inform your veterinarian which product was ingested. If ingestion or exposure was not witnessed, other causes of bleeding must be ruled out through a series of laboratory tests that assess platelets, various aspects of blood clotting, and effects on other organs. A test to detect abnormally high levels of inactive vitamin K–dependent proteins (PIVKA test) may be submitted. Additional tests, such as x-rays and an ultrasound, may be recommended.

TREATMENT AND FOLLOW-UP

Treatment Options

If ingestion has just occurred, vomiting may be induced to minimize absorption of the toxin. Treatment involves providing adequate vitamin K1 so that blood clotting remains normal. Even if the poison is vomited and there is no external evidence of bleeding, treatment with vitamin K1 is usually instituted to ensure patient safety. Contact your veterinarian immediately if you suspect possible ingestion of rat poison, even if your pet seems fine, so that blood clotting can be assessed and preventive treatment can be started.

The duration and dosage of vitamin K1 required depend on the type of toxin ingested. Coumarin products are active for days, whereas indanedione products are active for weeks. First-generation products require lower doses of vitamin K1 than second-generation products. If the exact type of toxin is not known, treatment is often given at high doses for 4-6 weeks. Initially, vitamin K1 may be given by injection for 1-2 days, and then pills may be started. Oral vitamin K1 is given with food to maximize its absorption.

If bleeding and anemia are severe, hospitalization is often necessary. Whole blood or plasma transfusions and intensive supportive care needed to stabilize the patient.

Follow-up Care

Certain clotting and other laboratory tests are often repeated during therapy and 48 hours after stopping vitamin K to ensure that there is no more active toxin in the system. If clotting tests are abnormal after the drug is stopped, vitamin K treatment is usually continued for 2 more weeks. If the vitamin K is stopped for longer than 48 hours and the toxin is still active, bleeding may recur, so it is very important to precisely follow your veterinarian’s instructions. Notify your veterinarian if any signs recur or any changes occur in the medication schedule.

Prognosis

Because vitamin K1 is the antidote for anticoagulant rodenticide toxicosis, prognosis is excellent if treatment is started in a timely manner and is carried out for an appropriate duration with adequate patient monitoring. In cases of severe anemia and bleeding, where aggressive hospitalization and transfusions are needed, prognosis is more guarded (uncertain). These rodenticides can be lethal to dogs and cats.

SPECIAL INSTRUCTIONS:

Aplastic Anemia

Kristi S. Lively, DVM, DABVP

BASIC INFORMATION

Description

The bone marrow is responsible for producing platelets, red blood cells (RBCs), and white blood cells (WBCs). These cells are formed from precursor cells that reside in the bone marrow, and many become mature while in the bone marrow. Diseases of the marrow can affect one or all of these cell lines, resulting in inadequate circulating numbers of mature cells. These cells are important for blood clotting (platelets), immune functions (WBCs), and oxygen delivery to tissues (RBCs). Aplastic anemia occurs when bone marrow function is so severely impaired that numbers of all three cell types diminish (called pancytopenia).

Causes

The cause of aplastic anemia is not always identified but may be related to infection with feline leukemia virus (FeLV) in cats, parvovirus in dogs or cats, or ehrlichiosis in dogs. Adverse reactions to drugs, such as estrogen, methimazole, azathioprine, griseofulvin, albendazole, captopril, phenylbutazone, trimethoprim-sulfa, and chemotherapeutic medications, may also cause pancytopenia. Tumors that secrete feminizing hormones (Sertoli cell and interstitial cell tumors) may be a cause. Immune-mediated destruction of precursor cells in the bone marrow is also a possible cause in some animals.

Clinical Signs

Clinical signs vary depending on the severity of the aplastic anemia. Signs often include weakness, pale gums, lethargy, blood in the feces or urine, nose bleeds, and abnormal bruising. If the WBCs are markedly affected, secondary infections may occur, because the immune system is compromised.

Diagnostic Tests

Aplastic anemia is usually recognized when a complete blood count (CBC) reveals a low platelet count (thrombocytopenia), a low WBC count (leukopenia), and a nonregenerative, low RBC count (anemia). A thorough history is then taken to determine possible exposure to ticks, toxins, or drugs that are potentially harmful to the bone marrow. Laboratory tests may be recommended to rule out infectious diseases and to determine the effects on other organs. A Coombs’ test may be performed to identify an immune-mediated component to the disease.

Bone marrow aspiration or biopsy is an important diagnostic procedure because it provides further information on the status of the precursor cells in the bone marrow, as well as information on the production and maturation of the different cell lines. With aplastic anemia, the precursor cells of all three cell lines are decreased or absent. Occasionally, infectious organisms may be found in the marrow samples.

If a cancerous process is suspected, imaging (x-rays, ultrasounds) of the chest, abdomen, and reproductive tract, as well as biopsy of any abnormal masses, may be recommended.

TREATMENT AND FOLLOW-UP

Treatment Options

When a primary cause of the pancytopenia is identified, treatment is directed at that condition. Potentially toxic substances or drugs are withdrawn. Supportive care may be needed, including hospitalization, oxygen therapy, blood transfusions, intravenous fluids, and antibiotics for secondary infections. If an autoimmune disorder is suspected, immune-suppressive medications, such as prednisone, azathioprine, cyclosporine, cyclophosphamide, or intravenous immune globulin, may be tried. Medications that stimulate the bone marrow, such as erythropoietin or granulocyte colony-stimulating factor, have been tried in only a small number of patients, and it is uncertain whether they provide much benefit. Whereas people with aplastic anemia may undergo bone marrow transplantation, this procedure is not routinely available for animals.

Follow-up Care

The CBC is monitored approximately every 3 days at first, and then weekly to monthly if the patient improves. Other monitoring is based on the underlying cause.

Prognosis

Prognosis is guarded (uncertain) to poor, depending on the underlying cause. Some toxins and infections cause irreversible bone marrow damage, whereas the effects of others are reversible once treated or once exposure to the toxin is eliminated. Secondary infections may develop into life-threatening sepsis (widespread infection in multiple organs) because the immune system is compromised. Patients are also at risk for life-threatening bleeding from the low numbers of platelets. When recovery does occur, it requires weeks to months of therapy and monitoring, which can be expensive.

SPECIAL INSTRUCTIONS:

Babesia Infection in Dogs

Kristi S. Lively, DVM, DABVP

BASIC INFORMATION

Description

Babesia is a blood parasite that causes anemia (an abnormally low red blood cell count) in dogs all over the world. The anemia arises from destruction of red blood cells. Babesia rarely affects cats. It is spread by ticks and occurs most commonly in the southeastern United States and in the Great Lakes region. Babesial infections affect greyhounds and pit bulls more often than other breeds. Puppies younger than 8 months of age may be more susceptible.

Causes

Even though more than 100 species of Babesia species exist, currently Babesia canis and Babesia gibsoni are the only two species known to infect dogs. Babesia infection (babesiosis) occurs most commonly when a tick carrying the Babesia organism attaches to a dog (for at least 2 days) and releases the infection into the dog’s bloodstream. The organisms multiply and infect red blood cells. New ticks pick up the infection from an infected dog and spread it to other dogs. Pregnant dogs can spread the infection to their unborn puppies. Infection may also be transmitted from dog to dog through bite wounds and via blood transfusion.

The dog’s immune system recognizes the infected red blood cells and destroys them in an effort to kill the parasite. The resulting anemia may be mild to severe.

Severe inflammation may also arise in other body systems, including the liver, kidneys, eyes, neurologic system, and respiratory system.

Clinical Signs

The infection typically incubates 10-21 days before clinical signs develop. Most infected dogs clear the infection and never become ill, but they may become carriers. Signs may occur in carrier dogs when they are stressed. Babesiosis may be classified as uncomplicated or complicated.

In uncomplicated cases, dogs are acutely ill, with fever, loss of appetite, depression, pale gums, enlargement of the spleen, and dark urine. Signs may be mild to severe, depending on the extent of the anemia. Symptoms of the anemia include weakness, jaundice, fever, depression, sudden collapse, and red- or orange-colored urine.

Complicated babesiosis may manifest as acute kidney failure, neurologic or blood clotting disorders, liver or breathing problems, inflammation of the heart muscle, low blood pressure, inflammation of the pancreas or eyes, or swelling of the legs. Shock, severe weakness, vomiting, and death may also occur.

Diagnostic Tests

The best diagnostic test for babesiosis is demonstrating the parasite on a blood smear; however, the parasite may not always be present in the sample, so a negative blood smear does not rule out infection. Because the organisms are hard to find, alternative testing is often necessary and may require sending samples to a laboratory. Some tests to confirm the diagnosis do not differentiate well among the various Babesia species and may give false-negative results early in the infection. These false-negative results complicate the screening process for carriers of the disease.

Other laboratory tests may be needed to detect problems in other organs, to evaluate blood clotting, to rule out other causes of anemia, and to assess the immune system’s reaction to the disease.

TREATMENT AND FOLLOW-UP

Treatment Options

Treatments are aimed at reversing the anemia and suppressing or clearing the infection. To stabilize the anemia, many dogs require a blood transfusion. A steroid (such as prednisone) may be given to decrease destruction of the red blood cells. Other complicating factors must also be addressed with appropriate therapy.

No known treatment clears all Babesia infections. Imidocarb dipropionate is the only drug approved in the United States for treatment of babesiosis. A single injection of the drug often clears B. canis and probably B. gibsoni. Side effects include pain at the injection site, tremors, elevated heart rate, fever, drooling, facial swelling, vomiting, and breathing problems. For B. gibsoni and the other small Babesia species, multiple injections may be needed.

A vaccine is available in France that is 89% effective against certain strains of Babesia. The best prevention is strict tick control.

Follow-up Care

All blood donors should be screened for babesiosis before donating, especially greyhounds and dogs from areas of the country where Babesia species are known to exist. Dogs that clear the initial infection but become carriers may have relapses when subjected to stress, such as surgery, pregnancy, or other illness. Females that test positive should not be used for breeding.

Prognosis

Prognosis is best when the infection is caught before the anemia becomes severe. Severe and complicated cases require more supportive care, and prognosis depends on the severity of anemia, severity of other organ involvement, and response to treatment.

SPECIAL INSTRUCTIONS:

Chronic Lymphocytic Leukemia

Kristi S. Lively, DVM, DABVP

BASIC INFORMATION

Description

Chronic lymphocytic leukemia (CLL) is a cancer of lymphocytes, a type of white blood cell (WBC). Lymphocytes are formed in the bone marrow and other lymphoid organs. When malignant proliferation occurs, these cells are released into the bloodstream.

With CLL, so many cancerous lymphocytes are released into the blood that the WBC count becomes very elevated (leukocytosis). Leukocytosis can occur in response to infection, stress, or inflammation but with these conditions the WBCs appear normal. Leukemia differs from other forms of leukocytosis in that the WBCs being produced are abnormal and represent a malignancy.

Lymphocytic leukemia may be acute (sudden in onset) or chronic (developing slowly), depending on the stage of the lymphocyte precursor involved. Acute leukemia forms when immature blast cells proliferate, whereas chronic leukemia involves more developed lymphocytes. In general, acute leukemia is more aggressive than CLL. CLL is a slowly progressive disease, often of older dogs and cats.

Causes

The cause of CLL has not been identified in either dogs or cats. CLL in dogs tends to involve a particular type of lymphocyte, called the T cell. CLL is rare in cats.

Clinical Signs

About 50% of patients with CLL have no clinical signs, and the disease is discovered when a blood count is done for another reason. Lethargy is the most common sign. Other signs include weight loss, loss of appetite, and enlargement of the spleen, liver, or lymph nodes (glands). Vomiting or diarrhea may be present if the gastrointestinal tract is affected.

A condition called hyperviscosity syndrome is a potential complication of CLL and arises when the lymphocytes produce a protein that builds up in the blood. The malignant lymphocytes all tend to form the same type of protein, which is a monoclonal antibody. Excessive levels of these proteins cause the blood to thicken and may cause small blood vessels to bleed. Signs of hyperviscosity syndrome may include nose bleeds, seizures, blurred vision, or blindness.

Diagnostic Tests

The complete blood count (CBC) reveals a persistent, unexplained, elevated lymphocyte count. Sometimes the count is so elevated the diagnosis of leukemia is obvious. However, CLL can be confused with leukocytosis from other causes if the lymphocyte count is only moderately elevated. Low blood counts of red blood cells (anemia) and neutrophils (another type of WBC) may also occur. It may be necessary to submit a blood sample for further analysis if the diagnosis of leukemia is not definite. Special stains and tests may be performed to identify the cancer cells and their stage of development.

A protein electrophoresis test may be done to confirm that blood protein is elevated and to determine whether the protein is a monoclonal antibody. A bone marrow aspiration may be recommended to evaluate the various cells present in the marrow and to confirm the identity of the cancerous cells. A fine-needle aspiration or biopsy of enlarged lymph nodes may be needed to differentiate leukemia from lymphoma, another cancer of lymphocytes.

Other laboratory tests, x-rays, and possibly an ultrasound may be recommended to assess involvement of other organs, to rule out other causes of leukocytosis, and to differentiate CLL from acute lymphocytic leukemia, other forms of lymphoma, and other types of leukemia.

TREATMENT AND FOLLOW-UP

Treatment Options

Since the course of this disease is very slowly progressive, treatment may not be indicated at the time of diagnosis. If the lymphocyte count is less than 60,000-75,000 cells per microliter (µL) and the patient has no abnormalities in other blood cells, treatment may be delayed. Treatment is usually started right away if clinical signs develop, if hyperviscosity syndrome is detected, if the lymphocyte count rises above 75,000/µL, or if anemia, low platelet counts, or low neutrophil counts occur.

Chemotherapy is the treatment of choice, and protocols may include drugs such as chlorambucil, prednisone, and vincristine. Occasionally other supportive treatments are needed, depending on the animal’s clinical signs and the presence of other abnormal laboratory results.

Follow-up Care

If no treatment is started, the CBC is repeated periodically to monitor the lymphocyte count. During chemotherapy, CBCs are also rechecked to assess response to treatment and to monitor for side effects from the chemotherapeutic medications.

Prognosis

Prognosis for remission is good, with survival times of 2-3 years being common. Even without chemotherapy, patients may live 1-2 years beyond diagnosis. In some animals, chemotherapy may be stopped if remission lasts for longer than 1 year.

SPECIAL INSTRUCTIONS:

Coagulopathy Associated with Liver Disease

Kristi S. Lively, DVM, DABVP

BASIC INFORMATION

Description

The liver is responsible for producing many of the proteins involved in the normal blood clotting (coagulation) process, particularly factors VII, IX, X, and XI. When the liver is severely diseased, these proteins are not produced in normal amounts. If production of these proteins falls below 10% of normal, spontaneous bleeding may occur.

Causes

For liver function to be affected enough that the production of these proteins is diminished, the underlying liver disease must be widespread and serious. Diseases of the liver causing widespread damage include toxins, inflammation, vascular shunts, cancer, fatty infiltration, and terminal scarring (cirrhosis).

Clinical Signs

The underlying liver disease may cause decreased appetite, fever, weight loss, lethargy, vomiting, or diarrhea. Some patients with significant liver dysfunction become jaundiced, with yellow discoloration of the skin, the gums, and the white part of the eyes (sclera). If liver disease is significant enough to cause a bleeding tendency, the patient may have bruising of the skin, gums, and sclera. The urine may be a dark, yellow-orange color if jaundice is present, or it may be blood tinged.

Diagnostic Tests

In patients with liver disease, liver blood tests are usually elevated, and other laboratory tests, such as blood protein, glucose, and bilirubin, may also be abnormal. Your veterinarian may recommend additional liver function tests, such as measurement of blood ammonia levels or bile acids. If a bleeding disorder is suspected, a coagulation panel of several different clotting tests is often performed. X-rays and an ultrasound of the liver may be done to evaluate any structural changes. A liver biopsy may be performed to determine the underlying cause of the liver disease, but it may not be recommended until coagulation tests improve and the concern for secondary bleeding decreases. Other tests may be recommended to rule out other diseases that cause similar clinical signs, as well as other clotting disorders.

TREATMENT AND FOLLOW-UP

Treatment Options

Treatment is aimed at correcting the underlying cause of the liver disease whenever possible. Such treatment may include antibiotics, steroids, intravenous fluids, nutritional support, plasma transfusions, blood transfusions, or chemotherapy, depending on the cause. Supplements that improve liver health or replace deficiencies caused by the liver disease may also be administered. These include vitamin B, vitamin K, SAM-e (S-adenosylmethionine), milk thistle, taurine, and carnitine. Seriously ill animals may require an extended hospital stay.

Follow-up Care

Laboratory testing of liver function and blood clotting is repeated every few days initially, to assess response to therapy and progression of the disease. Periodic laboratory monitoring and repeated x-rays and/or ultrasounds may be needed long term.

Prognosis

Liver disease that is so advanced that it causes significant clotting factor deficiencies has a guarded (uncertain) to poor prognosis. In some cases, however, the disease may be reversed with aggressive and intensive therapy. The reversibility of the disease depends largely on whether the underlying cause is treatable and the extent of liver damage present at the time of diagnosis.

SPECIAL INSTRUCTIONS:

Disseminated Intravascular Coagulation

Kristi S. Lively, DVM, DABVP

BASIC INFORMATION

Description

Disseminated intravascular coagulation (DIC) is a life-threatening condition caused by widespread, excessive activation of clotting proteins and the formation of microscopic blood clots. Widespread, extensive microclotting results in consumption of these proteins. Once the level of circulating clotting proteins falls, a severe bleeding tendency develops. DIC is sometimes called consumptive coagulation or consumptive coagulopathy.

Causes

DIC is not a primary disorder; that is, it does not arise spontaneously by itself. Rather, it is a secondary disorder that develops in association with serious underlying diseases. Underlying causes include infections such as bacterial, viral, tick-borne, and parasitic diseases. Severe inflammation associated with heat stroke, burns, cancer, trauma, shock, snake bites, autoimmune diseases, and other diseases may also predispose a patient to DIC.

Clinical Signs

Clinical signs are initially related to the primary disease condition. In severe or fulminant DIC, evidence of abnormal hemorrhaging is present, such as bruising of the skin, gums, inner aspect of the ear flaps, and sclerae (white part of the eyes). Bleeding may develop at sites where blood samples were drawn or in the urinary or intestinal tracts. Sudden respiratory distress and neurologic signs may occur but are less common. Life-threatening clot formation or bleeding, heart failure, or multiple organ failure may cause sudden death.

Diagnostic Tests

Thorough diagnostic testing is usually needed to identify the underlying disease. The presence of DIC is confirmed by performing a coagulation panel that includes a platelet count, various blood clotting assays, measurement of a blood protein called fibrinogen, and/or measurement of D-dimer levels in the blood. D-dimers are fragments of material produced during degradation of a blood clot. Results of the coagulation panel often reveal prolonged bleeding time, a decreased platelet count, and increased levels of D-dimers or fibrinogen degradation products.

TREATMENT AND FOLLOW-UP

Treatment Options

Treatment is aimed at stabilizing or reversing the underlying disorder whenever possible. Extended hospitalization for intensive therapy and advanced supportive care may be required. Attempts may be made with medications, such as heparin, to minimize dangerous clot formation and maintain adequate circulation in tissues. Intravenous fluids may be administered to help support circulation, and plasma or blood transfusions are often indicated for significant blood loss.

Follow-up Care

Coagulation tests are repeated periodically to assess the effects of therapy and to monitor recovery from DIC. Other monitoring and testing are based on the underlying disease or condition.

Prognosis

Prognosis is guarded (very uncertain) to poor, depending on the severity of the underlying disease. If tiny blood clots (thrombi) form in single or multiple organs and organ failure ensues, the prognosis becomes grave. Treatment and ongoing monitoring can be intense and expensive.

SPECIAL INSTRUCTIONS:

Fever of Unknown Origin

Kristi S. Lively, DVM, DABVP

BASIC INFORMATION

Description

A fever is a body temperature higher than the normal range. In dogs and cats, normal body temperature is approximately 100-102.5° F (38-39.5° C). Fever of unknown origin (FUO) is diagnosed when the fever is chronic (lasting for 3 weeks or longer) or recurs frequently and physical examinations and routine laboratory tests have not identified the source of the fever.

Causes

The most common causes of fever are infection, immune disease, inflammation, and cancer. Infectious causes include, but are not limited to:

• Tick-related infections, such as Rocky Mountain spotted fever, ehrlichiosis, Lyme disease, and babesiosis in dogs

• Viruses such as feline immunodeficiency virus (FIV), feline leukemia virus (FeLV), and feline infectious peritonitis (FIP) virus in cats

• Bacterial or fungal infections from bite wounds, pneumonia, or infections of the heart valves, uterus, urinary tract, joints, or bones

• Infections with protozoal agents, such as toxoplasmosis (cats and dogs) and neosporosis (dogs), or blood parasites, such as hemobartonellosis (cats)

Inflammatory and immune-mediated causes include:

• Drug or vaccine reactions

• Immune-mediated anemia, thrombocytopenia, or joint disease

Any type of cancer can cause a fever from release of inflammatory chemicals or destruction of tissue by tumor cells.

Clinical Signs

Clinical signs depend largely on the underlying cause but are often vague and nonspecific. Many patients are lethargic and have a poor appetite; they may lose weight and may become dehydrated. These patients tend to be ill for several weeks as the fever persists and the underlying cause goes unidentified.

Diagnostic Tests

A very thorough history is needed to determine the cause of the fever, so be sure to relay to your veterinarian all the medications and supplements recently administered to your pet, its vaccine status and dates, travel history, and exposure to other animals. A detailed physical examination is done to look for potential sources of the fever. Numerous laboratory tests are usually needed to rule out the various causes of fever. Some of the most common tests are the following:

• Complete blood count, serum biochemistry panel, electrolytes

• Urinalysis, urine culture

• Viral testing for FIV, FeLV, FIP

• X-rays of the chest and abdomen, including the spine

• Specialized tests for the common tick-borne, fungal, and protozoal diseases in your geographic area

• Blood smear evaluation and specialized tests for blood parasites

If these screening tests come back negative or nondiagnostic, then additional, more advanced diagnostics may be recommended, such as the following:

• Abdominal ultrasound and echocardiogram (heart ultrasound)

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Sep 11, 2016 | Posted by admin in SMALL ANIMAL | Comments Off

Fastest Veterinary Medicine Insight Engine

9: Hemolymphatic System

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