Regenerative anaemias Flashcards
(54 cards)
Causes of acute haemorrhage
Trauma
Bleeding tumours
Coagulopathies
Severe thrombocytopaenia
Signs of acute haemorrhage
Collapse
Tachycardia with weak pulses
Pallor
Hypovolaemic shock
What happens immediately after acute haemorrhage?
PCV and plasma protein will be unchanged (as equal volumes lost)
Splenic contration - releases more red cells, compensating for red cell loss
Fluid moves from interstitium into vessels, dilutes the remaining red cells and platelets
What happens after acute internal haemorrhage?
Most erythrocytes will be reabsorbed
Plasma proteins are rapidly reabsorbed
Acute phase response leading to production of globulins, thus plasma protein concentrations normalise quickly
Around 65% of red cells will be reabsorbed within 2-3 days and 80% will return to the circulation within 2 weeks.
What happens after acute external haemorrhage?
Marked regenerative response
Plasma protein will normalise more quickly then PCV
May also have a mild-moderate thrombocytopaenia
Chronic haemorrhage
Often associated with GI bleeding (may see melaena or haematochezia), sometimes urinary tract
Body is able to adapt to reduced oxygen carrying capacity
Signs usually mild
How to check for GI bleeding
Faecal occult blood test
may need to feed white meat for 3 days prior as myoglobin from red meat can be registered
What to do if you suspect chronic haemorrhage (low PCV, or low normal and low iron), but there is no obvious cause?
Urinalysis, dipstick and sediment
Feacal analysis (for ectoparasites and faecal occult blood)
Abdominal ultrasound examination/contrast radiography of the GI tract or urinary tract
Hypochromasia
red cells have a larger area of central pallor.
Usually this is secondary to iron deficiency.
Reticulocytes are also hypochromatic although they have grey-blue colouration.
Differences between haemolytic and haemorrhagic anaemias
Haemolytic: plasma protein normal or increased (usually decreased in haemorrhage)
Haemolytic tend to be more regenerative as not losing iron (unless damage to precursor cells in bone marrow)
Extravacsular haemolysis
Occurs when erythrocytes are phagocytosed by macrophages in the spleen and liver
Often associated with splenomegaly and spherocytes
Insidious onset
Mild to severe anaemia
Intravascular haemolysis
Erythrocytes are lysed within blood vessels
Usually due to red cell membrane damage -> ghost cells
often rapid onset, severe anaemias
Poor prognosis
Clinical signs of intravascular haemolytic anaemia
Haemoglobinaemia
Haemoglobinuria
May have
Hyperbilirubinaemia
Bilirubinuria
Signs of extravascular haemolytic anaemia
Hyperbilirubinaemia
Bilirubinuria
Splenomegaly
Haemoglobin is broken down to bilirubin by macrophages so dont see haemoglobinaemia/uria
Causes of haemolytic anaemias
Immune mediated
- Primary: idiopathic
- Secondary: drugs, vaccines, infectious agents, alloimmune, neoplasia
Bacteria, protozoal, viral infection
Oxidative damage
Disorders causing erythrocyte fragmentation
Inherited erythrocyte metabolic disorders
Severe hypophosphataemia
Evenomation
Haemophagocytic histiocytic sarcome
IMHA - general info
Dogs: common, usually primary (idiopathic), females overrepresented, Cocker spaniel, English Springer spaniel, poodles, Irish setter
Cats: less common, more often secondary
What can IMHA be secondary to?
Drugs (e.g. potentiated sulphonamides, cephalosporins, NSAIDs)
Vaccination? (controversial).
Infections; e.g.
o Dogs – Babesia, Anaplasma, Ehrlichia, leishmania.
o Cats – FeLV, Mycoplasma.
Neoplasia (especially lymphoproliferative diseases)
Following improperly cross matched transfusions
Neonatal isoerythrolysis
What is Evans syndrome?
IMHA and IMTP seen together
Pathophysiology of IMHA
Immune system produces antibodies directed against the surface of red cells most often IgG, but sometimes IgM.
Recognised by macrophages
Macrophages either destroy whole RBC or remove part of membrane to give spherocytes
What are spherocytes?
Small round densely staining red cells, which lack central pallor.
RBC membrane has been partially phagocytosed by macrophage, leaving less membrane to maintain the biconcave discoid shape, therefore the cells become spheroid in shape. They are difficult to see in species other than dogs due to the lack of central pallor in normal cells from other species (i.e. cat). Low numbers can also be seen in normal blood smears, especially at the tail of the smear (artefact).
Differentials for spherocytosis
IMHA (if >20 per hpf)
PFK deficiency
Zinc toxicity
Evenomation
Clinical signs of IMHA
Acute severe anaemia or more insidious, less severe anaemia
Lethargy, pallor, weakness, exercise intolerance, tachycardia
Pyrexia
Jaundice (hyperbilirubinaemia, bilirubinuria)
Haemoglobinaemia and consequent haemoglobinuria
Splenomegaly and hepatomegaly if extravascular
+/- lymphadenopathy (mild)
Tachypnoea
Diagnostic features suggestive of IMHA
Regenerative anaemia (moderate to severe)
Bilirubinuria/haemoglobinuria
Hyperbilirubinaemia/ haemoglobinaemia
Spherocytosis (in dogs)
Ghost cells
Marked anisocytosis and increase in RDW due to the presence of large reticulocytes and small spherocytes
Neutrophilia (may be marked)
Liver enzymes may be elevated due to hypoxic damage
Definitive diagnosis of IMHA
Autoagglutination
- grossly in tube or in saline agglutination test (SAT)
- can be non-specific, if unsure wash and retest
- only moderately sensitive
Coombs test
- serial dilurtions of Coombs reagent with washed RBCs from patient
- if IMHA present will cause autoagglutination
- diagnostic