From:
Hope RA, Longmore JM, Oxford Hanbook of Clinical Medicine, Third Edition.

The peripheral blood film
Many haematological (and other) diagnoses can be made by careful examination of the peripheral blood film. It is also necessary for interpretation of the FBC indices.
Acanthocytes: RBCs show many spicules (in abetalipoproteinaemia).
Anisocytosis: Variation in size, eg in megaloblastic anaemia, thalassaemia as well as iron-deficiency anaemia (IDA).
Basophilic stippling of RBCs is seen in lead poisoning, thalasssemia and other dyseritropoetic anaemias.
Blasts: nucleated precursor cells (eg in myelofibrosis or leuksemea). They are not normally seen in peripheral blood.
Burr cells: Irregularly shaped cells occurring in uraemia.
Dimorphic picture: A mixture of RBC sizes eg partially treated iron deficiency, mixed deficiency (Fe + B₁₂/folate), post-transfusion, sideroblastic anaemia.
Hovvell-Jolly bodies: Nuclear remnants seen in RBCs post-splenectomy, rarely leukaemia, megaloblastic anaemia, IDA. Hypochromia: Less dense staininjg of RBCs seen in IDA, thalasseemia and sideroblastic anaemia (iron stores unusable).
Left shift: Immature white cells seen in circulating blood in any marrow outpouring, eg infection.
Leptocytes: See target cells.
Leucoerythroblastic anaemia: Immature cells (myelocytes and normoblasts) seen in film. Due to marrov infiltration (eg by malignancy), hypoxia or severe anaemia.
Leukaemoid reaction: A marked reactive Ieucocytosis. Usually granulocytic eg in severe infection, burns, acute haemolysis, metastatic cancer.
Myelocytes, promyelocytes, metamyelocytes, normoblasts: Immature cells seen in the blood in Ieucoerythroblastic anaemia.
Normoblasts: Immature red cells, with a nucleus. Seen in leucoerythroblastic anaemia, marrow infiltration, haemolysis, hypoxia.
Pappenheimer bodies: Granules of siderocytes, eg lead poisoning, carcinomatosis, post-splenectomy.
Poikilocytes: Variably shaped cells, eg seen in IDA.
Polychromasia: RBCs of different ages stain unevenly (the young are bluer). This is a response to bleeding, haematinics (eg ferrous sulphate, B₁₂), haemolysis or dyserythropoiesis.
Reticulocytes: (NR: 0,8-2% of RBCs). Young, larger RBCs signifying active erithropoiesis. Increase in heamolysis, haemorrhage, and if B₁₂, iron or folate is given to marrow which lack these.
Right shift: Hypersegmented polymorphs (>5 lobes to nucleus) seen in megaloblastic anaemia, uraemia and liver disease.
Rouleaux formation:  Red cells stack on each other (the visual 'analogue' of a high ESR).
Schystocytes: Fragmented RBCs sliced by fibrin bands. Seen in intravascular haemolysis.
Spherocytes: Spherical cells; seen in haemolysis (or, rarely, in hereditary spherocytosis).
Target cells: (Also called Mexican hat cells) These are RBCs with central staining, a ring of pallor and an outer rim of staining seen in liver disease, thalassaemia or sickle-cell disease—and, in small numbers, in iron-deficiency anaemia.

The differential white cell count
The neutrophils 2-7.5 x 10⁹/l (40-75%) of white blood cells; but absolute values are more meaningful than percentages).
Increased in: Bacterial infections, trauma, surgery, burns, haemorrhage, inflammation, infarction, polymyalgia, PAN, myeloproliferative disorders and drugs (eg steroids). Marked increase in leuksemias, disseminated malignancy, severe childhood infection.
Decreased in: Viral infections; brucellosis; typhoid; kala-azar; TB. Also drugs, eg carbimazole; sulphonamides. They may be used up during septicaemia or destroyed by hypersplenism or neutrophil antibodies (seen in SLE and rheumatoid arrhritis). There is reduced manufacture in B₁₂ folate deficiency and in bone marrow failure.

The Iymphocytes 1.3-3.5 x 10⁹/l (20-45%).
Increased in: Viral infecrions—EBC, CMV, rubella; toxoplasmosis; whooping cough; brucellosis; chronic lymphatic leukaemia. Large numbers of abnormal ("atypical") Iymphocytes are characreristically seen with EBV infecrion: these are T-cells reacting against EBV-infected B-cells.
Decreased in: Steroid theropy; SLE; uraemia; legionnaire's disease; AIDS; marrow infiltration; post chemotherapy or radiotherapy.
T-lymphocyre subset reference values: CD4 count: 537-1571/mm³, (low in HIV infection). CD8 count: 235-753/mm³; CD4/CD8 ratio: 1.2-3.8.

The eosinophlis 0.04-0.44 x 10⁹/l (1-6%).
Increased in: Asthma and allergic disorders; parasitic infections (especially invasive helminths); PAN; skin disease especially pemphigus; urticaria; eczema; malignant disease (including eosinophilic leukaemia); irradiation; Loffler's syndrome; during rhe convalescent phase of any infection.
The hypereosinophilic syndrome is seen when there is development of end organ damage (restrictive cardiomyopathy, neuropathy, hepatosplenomegaly) in association with a raised eosinophil count (>1.5 x 10⁹/l) for more than 6 weeks. Steroids or cyroroxic drugs may give temporary relief.
The eosinophilia-myalgia syndrome consists in myalgia, arthralgia, fever, rashes, sweiling of the arms, and an intense eosinophilia. It is seen in the USA. and is thought to be due to contaminants in L-tryptophan-containing proprietary dietary supplements.

The monocytes 0.2-0.8 x 10⁹/l (2-10%).
Increased in. Acute and chronic infections (eg TB, brucellosis, protozoa); malignant disease (including M4 & M5 acute myeloid leukaemia and Hodgkin's disease); myelodysplasia.

The basophils 0.01 x 10⁹/l (0-1%).
lncreased in: Viral infections; urticaria; myxaedema; post-splenectomy; CML; UC; malignancy; systemic mastocytosis (urticaria pigmentosa); haemolysis; polycythaemia rubra vera.

Anaemia
Anaemia is a low haemoglobin due a decreased red cell mass. If the low Hb is due to dilution from an increased plasma volume (as occurs in pregnancy), the 'anaemia' is called physiological. A low Hb (at sea level) is <13.5 g/dl for men and <11.5 g/dl for women. It may be due to reduced production or increased loss of RBC and has many cause. These will often be distinguishable by history, examination, and inspection of the blood film.
Symptoms: These may be due to the underlying cause or to the anaemia itself and include fatigue, dyspnoea, palpitations, headache, tinnitus, anorexia and bowel disturbance.
Signs: Pallor, retinal haemorrhages. In severe anaemia (Hb < 8g/dl) there may be signs of a hyperdynamic circulation eg tachycardia, murmurs and cardiac enlargement. Later heart failure may occur and in this state rapid blood transfusion may be fatal.
Anaemia due to excessive red cell destruction is called haemolytic anaemia. Suspect haemolysis if there is a rericulocytosis, mild macrocyrosis, bilirubin and
urobilinogen.
The next step in determining the cause of anaemia is to look at the MCV (normal 76-96 femptolitres, 10¹⁵fl = litre).
Low MCV (microcytic) The common cause is iron deficiency anemia (IDA) with a microcytic, hypochromic blood film showing anisocytosis and poikilocytosis. It may be confimned by showing serum iron and ferririn (more representative of total body iron) with total iron binding capacity (TIBC). Other causes include thalasssemia (suspect if thc MCV is "too low" for the level of anaemia and the red cell count is raised), and congenital sideroblastic anaemia (very rare). These are iron loading conditions and will show serum iron; ferrirint; but TIBC.
Normal MCV (normocytic) The causes are anaemia of chronic disease (AoCD), bone marrow failure, haemolysis, hypothyroidism, renal failure and pregnancy. If there is a reduced white cell or platelet count suspect bone marrow failure and perform a bone marrow biopsy.
High MCV (macrocytic) Causes: B₁₂ and folate deficiency, alcohol ingestion, liver disease, reticulocytosis (eg, haemolysis), marrow infiltration, acquired sideroblastic anaemia and hypothyroidism.
Blood transfusion:  Avoid unless Hb dangerously low. The decision will depend on the severity and cause. If there is risk of haemorrhage (eg active peptic ulcer) transfuze up to 8g/dl. If there is severe anaemia and heart failure, transfusion is vital to restore Hb to safe level, eg 6-8g/1dl, but must be done with great care. Give packed cells slowly with 40mg frusemide IV/PO with alternate units (do not mix with blood). Check for rising JVP and basal crepitations and consider CVP line. If CCF gets worse, and immediate transfusion is essential, try a 2-3 unit exchange transfusion, removing blood at same rate as transfused.

Iron-deficiency anaemia (IDA)
This is common, occurring in up to 14% of pre-menopausal women. The major regulator of body iron (total 5g) is GI absorption which averages 1mg/day. Anaemia may the due to dietary deficiency, malabsorption or blood loss. By far the commonest cause is blood loss, usually menorrhagia (eg if >80ml/cycle) or GI bleeding. In women with menorrhagia it is justifiable to start treatment without further tests, although follow up is vital. In men and post-menopausal women the commones cause is GI bleeding (eg from peptic ulcer, gastric or colonic carcinoma, hiatus hernia or diverticulitis).
Dietary deficiency is rarely the major factor in the developed world but may occur in babies and those on unusual diets. Malabsorption may be cause of IDA, eg in coeliac disease. Signs of chronic iron deficiency (tissue Fe): koilonychia (spoon-shaped nails), atrophicglossitis and post cricoid webs.
Investigations. Faecal occult blood, sigmoidoscopy, barium enema and microscopy for ova as appropriate. Hookworm is the major cause of GI blood loss outside the Western world.
Treatment: This is of underlying cause, then iron replacement eg ferrous sulphate 200mg/8h PO. SE. constipation; black stools, Hb should rise by 1g/dl/week (accompanied by a rericulocyrosis). Continue until Hb is normal and for 3 months to replenish stores.

The anaemia of chronic disease
This is associated with a variety of diseases: eg infection collagen vascubr disease, malignancy and renal disease. There is Anile normoc~n,anaemia (eg Hb>8g/dl), sometimes confused with iron-defic~enc~ sa~.is but T'scl and "rum ferritin normal or I. Treatment is of the underlying disease. Erythropoietin lack is a cause of the anaemia of renal failure—genetically engineered erythropoietin is effective in raising the haernoglobin level (dose example: 7S-4SO units/kg/week; SE: flu-l~k~ symptoms, hypertension, mild rise in the platelet count).

Sideroblastic anaemia
Hypochromic RBCs are seen on the blood film with sideroblasts in the marrow (erythroid precursors with iron deposited in mitochondria in a ring around the nucleus). It may be congenital (rare, X-linked) or acquired and is usually idiopathic, but may follow alcohol or lead excess, myeloproliferative disease, malignancy, malabsorption, anti-TB drugs. Treatment is supporrive; pyridoxine may help (10-100mg/24h PO). Iron loading (haemosiderosis, ie endocrine, liver and cardiac demage) can be a problem as GI iron absorption is increased.

Refractory anaemia
The usual reason for IDA to fail to respond to iron replacement is failure of compliance, often because of Gl disturbance, and altering the dose of elemental iron may help. There may be continued blood loss, malabsorption or misdiagnosis (eg thalassemia). Occasionally, there is myelodysplasia with abnormal marrow maturation. This is refractory to most treatments and may be pre-leukemic.