ANAEMIC PATIENT. Specific erythrocyte disorder v's systemic disorder

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1 ANAEMIC PATIENT Specific erythrocyte disorder v's systemic disorder Anaemia indicates decreased RBC mass so decreased red blood cells, decreased haematocrit or haemoglobin. It is classified as regenerative or non-regenerative. Maturation of red blood cells takes 7 days. Evidence of reticulocyte presence indicates regeneration. SIGNALMENT: Some breeds are predisposed to IMHA, young to middle aged commonly, females more than males. Older animals are more likely to get primary disease causing anaemia. HISTORY: is usually non specific lethargy episodic weakness exercise intolerance collapse increased respiratory rate increased heart rate changed urine colour changed skin colour pale mucous membranes drug/vaccination history is relevant signs of underlying disease process eg: PUPD, diarrhoea, malaenia, weight loss. PHYSICAL EXAMINE: PCV that's low in a well patient suggests chronic disease low PCV in collapsed patient suggests acute disease HAEMATOLOGY: TP when decreased suggests acute blood loss Blood smear essential acanthocytes suggest haemangiosarcoma anisocytosis and polylchromasia suggest regerative anaemia spherocytes suggest haemolytic disease reticulocyte count important typical regenerative anaemia: macrocytosis (increased MCV sometimes) hypochromasia (decreased MCHC) regeneration with normal MCV suggests disease associated with microcytosis such as chronic blood loss or bleeding disorder haemolytic anaemias tend to regenerate better than haemorrhagic anaemias as the byproducts are re-usable. Nucleated RBC's doesn't always mean regeneration, it can occur with bone marrow pathology, splenic disease, lead poisoning and in miniature schnauzers. Microcytosis may be from iron deficiency anaemia due to chronic blood loss

2 gastrointestinal tract lung urinary tract disease portosystemic shunt BIOCHEM: may reflect underlying disease bilirubinuria/hyperbilirubinaemia may suggest haemolysis Other tests: Thoracic/abdo xrays and ultrasounds for underlying disease or haemorrhage coagulation tests B12 Bone marrow aspirates CAUSES: regenerative haemorrhage vs haemolysis HAEMORRHAGE: ACUTE: if severe will cause hypovolaemic shock (increased heart rate and splenic contraction) initially PCV/TP will not change (normocytic/normochromic) erythropoiten will increase causing regeneration in 2-3 days platelets may decrease acutely but will normalise quickly may see stress leucogram TP should fall (panhypoproteinaemia) GENERALISED haemorrhagic disorder more likely if bleeding into body cavity: - trauma - bleeding disorder - neoplasia TREATMENT: restore circulating volume, control haemorrhage crystalloids usually volume replaced is usually 2-4x volume lost shock rates initially 90ml/kg/hr (ensure low potassium fluids) acute blood loss may require transfusion NOTE: if blood loss is peracute, wont see drop in PCV. Make judgement on clinical signs expect PCV to take 1-2 weeks to return to normal CHRONIC: aetiology: GIT: ulceration, inflamation, neoplasia, malabsorption: may cause malaenia or pica chronic bleeding neoplasia

3 parasites: endoparasites or ectoparasites iatrogenic urinary disease iron deficiency is usually external loss, eg from gut or urinary tract, will see decreased haemoglobin and PCV BLOOD TESTS: microcytic, hypochromic anaemia increased central pallor cells stiffer so more fragment marked reticulocytosis may occur leucogram maybe normal if gut disease may see eosinophilia thrombocytosis common panyproteinaemia may be only change on biochemistry HAEMOLYTIC: Average lifespan RBC in dogs days, 70-80days in cats RBC destruction-> iron is recycled ->bilirubin binds to albumin Bilirubin is absorbed by hepartocytes, excreted thru bile caniliculi. Massive haemolysis overflows caniliculi, bilirubin then circulates in plasma, plasma will go yellow Intravascular haemolysis releases haemoglobin causing plasma to go pink. CAUSES (excluding IMHA) Dogs 1. onions most common cause in dogs 2. propylene glycol ingestion 3. inherited causes Pyruvate kinase deficiency: beagles, WHWT,Cairn terriers Phosphofructokinase deficiency: English springer or cocker spaniels (cockers: PFK deficiency is ph sensitivity, alkalaemia can cause haemolysis, so exercise/panting causes haemolysis) Cats 1. methylene blue, propylene glycol, paracetamol 2. vitamin K3, copper 3. lymphosarcoma, diabetes, hyerthyroidism CLINICAL SIGNS: typically mild anaemia jaundice lethargy anorexia fever dark urine

4 Mechanical trauma can cause microangiopathic anaemias: DIC haemangiosarcoma valvular heart disease hepatic disease caval syndroms glomerulonephritis red belly black envenomation Histiocytic disease: BREEDS:Golden or Flat coated retrievers,rottweilers, bernese mountain dogs, labradors regenerative anaemia thrombocytopaenia splenomegaly hypoalbuminaemia? Hypocholesterolaemia? Coombs test NEGATIVE

5 IMMUNE MEDIATED HAEMOLYTIC ANAEMIA type II hypersensitivity: intravascular v's extravascular primary v's secondary primary disease is truly autoimmune, target is the RBC membrane secondary disease causes indirect attachment to antigen on RBC membrane infections drugs or vaccinations inflammation neoplasia SLE Most IMHA cause extravascular haemolysis, macrophages remove part of RBC membrane causing spherocytes then splenic removal. PRIMARY IMHA: often younger to middle aged dogs, females more than males common breeds: cocker spaniels springer sdpaniels poodles collies OESD irish setters SECONDARY IMHA: not a typical signalment CLINICAL SIGNS IMHA: usually acute onset: pale mucous membranes icterus tachycardia, tachypnoea splenomegaly fever? Haemic murmur, systolic usually if sever enough aneamia historically: anaemia exercise intolerance weakness collapse DIAGNOSIS: low PCV TP -haemorrhage TP will be low, haemolysis TP should be normal regenerative anaemia: anisocytosis, polychromasia, spherocytes plasma colour extravascular yellow plasma - intravascular pink plasma autoagglutination is present is diagnositic for IMHA

6 To test for agglutination: 1 or 2 drops of blood onto slide then 2x the volume of saline. If agglutination occurs, the clumps of blood cannot be broken up by mixing. Can see clupms form on edta tube walls also. Alternatively 1 drop of blood into plain tube then 10 drops of saline, then examine a drop of this on a slide. HAEMATOLOGY: reticulocyte count should be increased MCV should be increased neutrophilic leucocytosis can be massive, possibly with left shift platelets should be normal except with decrease with thrombocytopaenia BIOCHEMISTRY: Increased ALT, ALP usually secondary to hypoxia possibly increased BUN, CRE either pre-renal due to dehydration or renal due to hypoxia or damage from hyperbiliruninaemia increased bilirubin URINALYSIS: bilirubinuria if extravascular haemolysis haemoglobinuria if intravascular haemolysis proteinuria if secondary renal disease bilirubin crystals possible SECONDARY IMHA: search for underlying disease and treat this TREATMENT: Immunosuppression 1. glucocorticoids most common, suppress erythrophagocytosis rather than decrease antibody production, IV or oral prednisalone 2-4mg/kg/d dogs 3-6ml/kg/d cats (may take up to 14 days to work) 2. blood transfusion: decision based on clinical signs not just PCV (tachycardia, tachypnoea, weak) 3. cant interpret cross match if autoagglutination present 4. azathioprine 1-2 mg/kg q24-28hrs (takes 14 days) side effects not common: myelosuppression hepatotoxicity nephrotoxicity pancreatitis monitor blood counts 5. cyclosporine: monitor bloods after few days and alter dose accordingly side effects: gingival hyperplasia GI upset hepatotoxicity nephrotoxicity increased risk of lymphosarcoma?? 6. Cyclophosphamide: oral or IV. Rapid onset. 200Mg/m2 weekly side effects: myelosuppresion GI upset sterile haemorrhagic cystitis (less severe if medicate in morning) 7. Leflunomide: inhimbis DNA synthesis so decreases antibody formation Monitor response to treatment and continue medication until normal PCV, slowly decreased prednisalone 20-25% every fortnight. Some patients need lifelong treatment.

7 ONLY 30% of IMHA sufferers survive long that 1 year Thromboembolic disease is potential complication of IMHA, especially if autoagglutination present. It is made worse by corticosteriods as they cause hypercoagulablity. Jaundice also increase the risk. Pulmonary thromboembolism most common: tachypnoea, dyspnoea exercise intolerance cyanosis Primary IMHA is less common in cats, it is usually secondary due to: infections, drugs or neoplasia cats dont have spherocytes do bloods, FIV, Felv, mycoplasma PCR, chest and abdo x-rays to find underlying disease Treat the underlying disease. Can also use prednisalone, cyclosporine, chloraembucil Can have non-regenerative IMHA due to bone marrow disease DO NOT USE PENICILLIN OR CEPHALEXIN IN DOGS WITH IMHA AS IT CAN ATTACH TO RBC USE DOXYCYCLINE