Haematology
The ageing haematopoietic system
There are very few changes as the bone marrow ages. Be very reluctant to ascribe changes seen on testing to age alone—pathology is much more likely.
Haemoglobin
Epidemiological studies show that population haemoglobin (Hb) concentration gradually declines from age 60
There is debate as to whether the reference range should be adjusted since lower Hb levels are associated with increased morbidity and mortality compared with older patients who maintain normal levels
Thus anaemia is common in old age (between 10-20% will have Hb less than 12g/dL in females or 13g/dL in males), but this is due to disease(s) not ageing per se
The decision about whether to investigate anaemia should be made not on the absolute value but the clinical scenario. Consider symptoms, past medical history, severity of anaemia and rate of fall of Hb, the mean cell volume (MCV) and finally patient’s wish/tolerance of investigation
A fit elderly man with no significant past history merits investigation with an Hb of 11.5 g/dL (especially if his Hb g/dL was 13 last year or if the MCV is abnormal) while a patient with known rheumatoid arthritis, renal failure and heart failure who has a normocytic anaemia 10.5 g/dL for years usually does not
Erythrocyte sedimentation rate (ESR)
The height of the red cells in a standard bottle of blood, after being allowed to sediment for 60min
This is a simple, old fashioned and non-specific test however it is inexpensive and remains useful for screening and monitoring disease in older people. CRP is often used in conjunction
Red cells fall gradually because they are more dense, but the rate of fall increases where the cells clump together
ESR rises with age and is slightly higher in women so values up to 30mm/hr for men and 35mm/hr for women can be normal at age 70
Anaemia can cause a mild elevation in ESR
A high ESR occurs in disorders associated with elevated plasma proteins (fibrinogen and globulins). Numerous acute and chronic disorders can cause modest elevation
Very high levels (>90) are commonly found with paraproteinaemias, giant cell arteritis and chronic infections such as tuberculosis
Investigating anaemia in older people
A low haemoglobin is a frequently encountered abnormality in geriatric practice. It is worth remembering the following:
Other parameters, usually documented in the full blood count report (eg MCV) will greatly assist in characterising the anaemia, and should be scrutinized
Looking up old FBC results will often reveal a pattern eg a frail older person may run a chronically low Hb because of chronic disease or marrow failure. If there is a recent change, this should prompt more urgent investigation
Unwell older patients may have low Hb as a result of fluid overload or marrow suppression. Repeat FBC as they recover, and see if it persists
Multiple aetiology is common, so check a full range of blood tests in all anaemic older patients
It is very important to check that the laboratory have received the correct blood specimens for these tests before arranging blind replacement therapy or a transfusion—subsequent samples will be invalid for haematinics
Most anaemic patients will require:
Blood film
Ferritin, serum iron and total iron binding capacity (or transferrin)
B12, folate
Renal, liver and thyroid function testing
Blood and urine electrophoresis and look for Bence Jones proteins in urine if the ESR is raised
If the anaemia has been characterized (eg iron deficient, macrocytic etc.), then decisions can be made about the nature and extent of further testing. See ‘Iron deficiency anaemia: diagnosis’, p.454 for details.
If the picture is mixed, then there may be multiple contributing factors (eg chronic kidney disease, minor gastritis, early myelodysplasia)—list these and address each in turn.
Iron deficiency anaemia: diagnosis
This is the most common cause of microcytosis (but beware the occasional patient with lifelong microcytosis who has an inherited thalassaemia or sideroblastic anaemia).
Causes
Most common is occult blood loss in the gut especially in patients taking NSAIDs (even 75mg aspirin)
Malabsorption (eg coeliac disease, gastrectomy, achlorhydria due to atrophic gastritis or use of PPIs)
Malnutrition as a sole cause is very unusual
▶Multifactorial aetiology is common—eg mild chronic blood loss, borderline dietary intake and mild malabsorption syndromes
Diagnosis
History is vital (ask about weight loss and gut, kidney, urogenital, or ENT blood loss). Pallor (conjunctivae, nail beds) may be found. The emphasis of examination should be to find rectal or abdominal masses, hepatomegaly, and lymphadenopathy.
Investigations
Microcytosis usual but not in combined deficiency or acute blood loss
Low serum ferritin levels (<12micrograms/L) are diagnostic. Moderately low levels (12-45micrograms/L) may also point to the diagnosis as ferritin levels rise with age. Ferritin is an acute phase reactant so normal/high levels don’t rule out deficiency
Serum iron levels will be low with high iron binding capacity, ie the ratio of iron/iron binding will be low (<15%). This is a useful way of distinguishing the anaemia of chronic disorder where both iron and iron binding are low (and the ratio will be normal) (see also Table 16.1)
Low iron stores on a bone marrow trephine are diagnostic but this investigation is painful and rarely required
Faecal occult blood is of limited value in cases of established iron deficiency—it is usually positive and you may feel that further gastrointestinal tests are needed anyhow
Haematuria sufficient to cause anaemia is rare, and usually severe. Urinalysis may be indicated in patients with poor vision or cognition to look for renal tract blood loss
Iron deficiency without anaemia should still be investigated but the lower the Hb the higher the likelihood of finding attributable pathology
Table 16.1 Characteristic findings in iron deficiency and chronic disease | ||||||||||||||||||
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HOW TO … Investigate iron deficiency anaemia
The main dilemma is deciding how far to take investigations.
A fit patient, who would be a candidate for surgery, should have a minimum of OGD and colon imaging (see ‘HOW TO … Image the older colon’, p.373). These should proceed regardless of the degree of anaemia and whether there are symptoms. The finding of oesophagitis or an upper gastrointestinal ulcer should not stop a screening test for the colon to rule out a coexisting neoplasm. If these tests are negative, screen for coeliac disease (eg endomysial antibody) and haematuria. Small bowel barium studies or capsule endoscopy are sometimes helpful. If there is intermittent overt gastrointestinal blood loss mesenteric angiograms can demonstrate small angiodysplastic lesions if there is active haemorrhage.
At the other extreme a frail, bed-bound nursing home patient with dementia will probably merit empirical iron and PPI therapy without further investigations.
In between these extremes physicians often adopt a ‘half way house’. Some examples of this compromise include:
Not proceeding to lower gastrointestinal tests if upper gastrointestinal pathology is found
Where NSAIDs are the likely problem, stop the drug, give iron, and a PPI, and only investigate if the anaemia or evidence of bleeding continues after a suitable therapeutic trial
Not performing lower gastrointestinal tests if the patient is not fit for, or not consenting to surgical intervention
Performing a flexible sigmoidoscopy rather than a full colonoscopy (80% of tumours can be excluded this way without complete bowel preparation and with less risk and discomfort)
Using oral contrast-enhanced CT colography to image the colon (better tolerated) will miss small lesions but excludes large tumours
Assuming that very longstanding and stable iron deficiency (several years) presents low risk for a malignant sourceStay updated, free articles. Join our Telegram channel
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