For Patients

The commonly used scans include ultrasound (U/S), plain X ray, computerised tomography (CT), magnetic resonance imaging (MRI) and positron emission tomography (PET).  Contrast medium is frequently used to enhance the outline and blood flow to various organs. 

Ultrasound detects different tissues’ reflection of high frequency sound waves.  Plain X ray detects different tissues’ absorption of radioactive rays to compose a 2-dimensional image. CT uses a rotating set of emitters and detectors of X-rays to collect data about the density and location of the body tissues and the data is then assembled into a 3-dimensional image using advanced computer algorithms.  MRI detects body tissues’ response to a strong magnetic field and uses computer algorithm to form a 3-dimensional dynamic picture of the area studied.  PET detects body tissues’ uptake of a radioactive tracer in relation to changes in glucose metabolism and it is often combined with a low dose CT to provide further information. No radiation is involved with ultrasound or MRI.

The different scans provide a range of information on blood flow, anatomical changes and functional changes, hence are often complementary to one another.  Your doctor will recommend the scan(s) best suited to study the question in hand.

As far as the testing is concerned there should be no significant difference because all laboratories practise to the same standard as required by the Government. However, there may be slightly different instruments and methods used, resulting in minor variations in readings.  It is often more convenient to go to the nearest laboratory to have the testing done.  The results will still go back to your doctor.  However, if you have all your tests in the same pathology laboratory, your results may be easier to compare over time and will be all in one place.  This will make it easier for your doctor to access results from different time points.

For a small number of conditions, blood test results are not directly comparable between different laboratories. In those instances, your doctor will give specific advice regard the lab to go to. 

Anaemia describes a fall in haemoglobin levels in your blood. Haemoglobin is packaged in red blood cells in the circulation and carry oxygen around the body. A fall in haemoglobin causes tiredness, fatigue, shortness of breath, paleness, palpitations and other symptoms.   Low haemoglobin levels may be a result of decreased production or increased loss of red blood cells.

The bone marrow act as a factory to produce red cells. For successful production, four things are required: raw materials, a signal to guide production, the recipe for production, and the factory itself. A change in any of these factors will cause anaemia from lack of production.

The most common cause of anaemia in otherwise healthy individuals is lack of raw materials, in either iron, vitamin B12 or the vitamin folate. Whilst this may reflect an individual’s eating habits, potentially important medical disorders may interfere with absorption of these vital ingredients even with a normal diet. Low levels of these vitamins and minerals can be checked using a simple blood test and, if abnormal, may prompt further testing to look for underlying causes. (See below: “How do I become low in iron and how would that affect me?”)

Erythropoietin (Epo) act as a signal to guide the rate of production. It is produced by the kidneys and patients with poor renal function may need Epo supplementation to maintain red cell production.

All cells have a genomic code that resides in the DNA. In red cells, its DNA guides its maturation and production of haemoglobin. Mutations in the DNA causes production of defective red cells – defective in shape and altered haemoglobin content. In later life, it may be seen in a bone marrow disease called myelodysplasia. In the young, haemoglobinopathy and thalassemia are inherited mutations in the DNA of the haemoglobin genes.

Finally, the factory itself may be damaged. Common causes here include marrow invasion by infection, scarring, solid cancer, blood cancers, previous radiotherapy to the spine / pelvis, or interference by medications.

Increased losses may be due to internal or external blood loss (bleeding).  Destruction of red blood cells may also occur by immune mechanisms secondary to autoimmune conditions, drugs, infections or leukaemia/lymphoma.  Destruction of red blood cells by other mechanisms such as genetic abnormalities of cell membrane, enzymes and protein may also cause anaemia.  A number of systemic disorders such as kidney, liver, thyroid diseases, extensive blood vessel damage, abnormal splenic function and mechanical damage such as artificial heart valves also cause increased red cell destruction.  

A mild anaemia, defined as haemoglobin level of 100 or above (but less than the reference range), usually does not cause undue fatigue or loss of energy.  The actual effect of anaemia is dependent on heart and lung functions, concurrent illnesses, your level of physical activity, prior fitness, emotional and mental states and the period of time which the body has to adapt to it.  Depending on the extent an individual is affected and the cause of the anaemia, your doctor may consider a blood transfusion when the haemoglobin level has dropped to 70-80.  However, transfusion is not necessarily the best treatment and it is important to identify and treat the cause of the anaemia.

Symptoms of fatigue, loss of energy and concentration are usually evident when the haemoglobin level drops below 70-80.  People with heart and lung insufficiency are often more affected, and angina may be precipitated by moderate or severe anaemia.  Conversely people with chronic and stable anaemia often handle the anaemia better than those with rapidly dropping haemoglobin. 

Blood and blood components provided by Red Cross in Australia are, for the most part, donated by healthy Australian volunteer donors. There is a very minor quantity of speciality manufactured plasma derived products imported into Australia.

All blood donors are stringently screened via comprehensive questionaries as to their health before they are eligible to donate. After donation, each unit is tested for blood borne infections and only released when quality requirements are met. The risk of blood borne infection related to transfusion in current modern practice is very low.

However, there are other risks to blood transfusion. Each bag of red cells also adds to iron stores, in the recipient, which may not be efficiently disposed. Iron build up over the long term may cause further problems due to organ damage. A recipient may also be sensitised to develop antibodies that may react to incoming blood products as foreign objects. These allergic reactions cause rash, fever, shortness of breath and palpitations.

Finally, administration and clerical errors (for example, giving a patient the wrong blood group) also needs to be considered as a risk of transfusion. Thankfully, with modern blood banking practices and stringent attention to detail, this risk can be minimised.

The Australian Red Cross has more information on this. https://mytransfusion.com.au/about-blood/ensuring-blood-safety

Yes, too much haemoglobin can be a problem. This is commonly defined as a blood test result of >165 g/L haemoglobin in men, or >160 g/L in women (or if haematocrit, one of the other blood test result is used, >49 percent in men or >48 percent in women). This can be a normal, physiological response to training (e.g. in elite athletes) to enhance oxygen delivery to muscles, though more commonly in Australia, it is caused by disease.

In situations where oxygen levels in the blood are low, the body produces more red cells to compensate. This may happen in patients with lung disease (e.g. smoking, emphysema or obstructive sleep apnoea), certain congenital heart diseases or in patients with inherited disorders where haemoglobin produced is defective (e.g. thalassemia).

Red cell over production can also occur when there is excess Epo in the system (see above “What causes anaemia” for an explanation on Epo).

When the bone marrow produces an excess number of red cells inappropriately without another identified cause, the disease is called polycythaemia vera. This is usually caused by a mutation in a bone marrow stem cell. The switch that governs red cell production is stuck in the ‘On’ position as a result of this mutation, and inappropriate over production of red cell ensues.

Over the long term, high red cell numbers in the circulation can cause slowing of circulation and even clotting in arteries. This may lead to heart attacks, strokes and claudication.

For patients with high haemoglobin, it is important to be assessed as to the cause, and the correct treatment given. Sometimes, this may be just as simple as having venesections (where blood is taken away deliberately, like blood donations for healthy volunteers, except more frequently).

White cells, also known as leukocytes, fight infection. In a normal healthy individual, there are usually between 4 to 11 million of white cells per mL of blood. In disease, the number of white cells in the blood can be abnormal, or that the types of white cell present can be different to that seen in health. There are many different types of white cells, each doing different jobs.  The main type are as follows.

• Lymphocytes: These are vital for producing antibodies that help the body to defend against bacterial, viruses, and other threats.

• Neutrophils: These are powerful scavenger cells that destroy bacteria and fungi.

• Basophils: These alert the body to infections by secreting chemicals into the bloodstream, mostly to combat allergies.

• Eosinophils: These are responsible for destroying parasites and cancer cells, and they are part of an allergic response.

• Monocytes: These are responsible for attacking and breaking down germs or bacteria that enter the body.

In a normal healthy individual, there are usually between 4 to 11 million of white cells per mL of blood.

The most common cause of an increased white cell is infection, where it is part of a normal immune response. Other types of tissue injury that causes stress on the marrow, such as smoking, trauma or burns can also lead to an increased white cell count. Some medications can also raise the white cell count, as can auto-immune diseases.

Bone marrow disorders can also cause an increased white cell count. Most of these disease states are caused by mutations in the marrow stem cells that in many instances, disrupting the regulation of cell production. Again, the switch to cell production may be stuck in the ‘On’ position as a result of these mutations. Additionally, over production of one type of cell may be associated with an underproduction of other types of cells, which may lead to anaemia, infections, and bleeding. In some patients, the spleen and the lymph nodes may also be enlarged, being taken over by the excess of newly formed white cells.

Depending on which specific type or types of white cell being overproduced, the treatment and implications are different, and some of these disorders are classified as blood cancers, whilst others are medical emergencies. Acute leukemia, chronic leukemia and myeloproliferative neoplasms are some of the disorders that belong to this spectrum. Most of these conditions are treatable; comprehensive specialist assessment is usually necessary for a proper diagnosis and management plan.

Although it is possible for white cell numbers to fall from being used up, such as in severe infections, the more common cause of low white cells (leucopenia) is underproduction.

As with red cells, the bone marrow acts as a factory to produce white cells. A number of disorders will affect white cell production. Most common causes of low white cell counts are drugs (including over the counter medications) and infections (viral, bacterial and others). Patients having chemotherapy or radiotherapy treatments can be expected to have low cell counts during their treatments. Liver disease, excess alcohol consumption, and having an enlarged spleen are less common causes. Importantly, a number of bone marrow disorders are associated with low white cell counts, and some of them may have severe consequences if left untreated.

Low white cells may put you at risk of infections. In many circumstances severe deficiencies are regarded as medical emergencies. A number of tests may be necessary to find the cause of low white cell counts.

Blasts are immature cells that usually reside in the bone marrow during blood cell development. It is normal to have a small number of blasts. Over time, blasts grow and mature into normal blood cells in a process called differentiation.  

Blasts may become detectable in the blood in situations of severe stress such as life-threatening infection, severe burns or haemorrhage. This is a normal response in order to increase white cell production to cope with increased demand and should resolve when a patient gets better from their illness. Diseases that cause inappropriate production of blood cells, such as myeloproliferative neoplasms, can also increase blast numbers (see above: “What causes high white cell counts, how high is dangerous?”)

If mutations are present in marrow stem cells that interferes with blood cell maturation, then blast cells may increase in number to very high levels due to the block in maturation. Normal cell production is affected such that numbers of normal red cells, white cells and platelets may be deficient. This is the most common presentation of acute leukaemia. This disorder warrants urgent medical attention.

Platelets are small cells produced by the bone marrow that plug any holes in the wall of blood vessels and release chemicals to initiate clotting. They help clotting in response to injury. Adults who are otherwise healthy have between 150 – 450 million platelets per mL of blood. Increased platelet counts may occur as a response to bleeding, trauma, infection or anaemia as a natural response. These increases are usually mild.

If there is an overproduction of platelets without an obvious stimulus, then the suspicion falls to the bone marrow where a number of disorders can cause an inappropriate over-production of platelets. These disorders include chronic myeloid leukaemia, polycythaemia vera, essential thrombocythaemia, or early myelofibrosis, and are grouped under the broad term myeloproliferative disorders or myeloproliferative neoplasms.  Increased circulating platelet numbers over the long term may contribute to blocked blood vessels, causing heart attacks or strokes. Aspirin-like compounds can be used to reduce such risks when the platelet count is mildly elevated. To control the high platelet counts, chemotherapy and removal of platelets from the circulation by a special procedure called apheresis may be needed. Treatment for these conditions are usually worked out between the patient, their GP and a haematologist.

Low platelets can result from under-production or excess consumption. Having low platelets is also called thrombocytopenia.

As with anaemia, the causes of platelet underproduction include the lack of raw materials and bone marrow disorders. Low platelets may result from deficiencies in vitamin B12 and folate; deficiency from thrombopoietin (TPO) due to liver disorders; DNA mutations causing myelodysplasia or congenital thrombocytopenia; and marrow infiltration. A number of drugs and infections can also interfere with platelet production (the list of drugs with the potential to do this is quite long, though quinine, commonly used for cramps and an active ingredient in tonic water in the past, was notorious for doing this. To a haematologist, chemotherapy is the most common agent that causes low platelets).

Conversely, platelet counts may fall due to inappropriate consumption or destruction. For instance, the immune system may mistake platelets for foreign objects and mark them for destruction in a disorder called immune-mediated thrombocytopenia (ITP).  Inappropriate activation of platelets to clot off vessels where no injury exists causes disorders such as disseminated intravascular coagulation or thrombotic thrombocytopenic purpura (DIC and TTP). Patients who have liver disease may also have increase trapping of platelets in liver and spleen, where they are destroyed.

Patients with low platelet counts are at risk of spontaneous bleeding and bruising. Internal bleeding (into the brain or into the gut) are considered medical emergencies and urgent hospital treatment is required (including platelet transfusions). Luckily, this does not occur unless the platelet count is very low. Moderately decreased platelet counts may subject an individual to bleeding under certain conditions of stress, such as an operation or during dental surgeries.

Aspirin like compounds may reduce the chemical content of platelets and blood thinners (anticoagulants) reduce blood clot formation so both medications can be dangerous in people with low platelet counts.

In normal day to day life, a number of events can cause bleeding. These may be from noticeable trauma, or inconspicuous breaks in vessels too small to be noticed. Forming blood clots is a natural mechanism to stop bleeding and to repair blood vessels.  

Just like a wall is made of bricks and mortar, a normal blood clot also has these 2 components. The bricks in the clot are made of platelets – small blood cells. The mortar that glue the platelets together are called clotting proteins. Deficiency in either of these 2 components can cause abnormal bleeding. Under normal circumstances, clotting proteins only become sticky (activated) when there is bleeding.

There are many different types of clotting proteins in the blood. When bleeding occurs, platelet particles adhere together to form a platelet plug at the injury site and release specific chemical signals to activate other platelets and clotting proteins. A number of different clotting proteins can then activate, binding platelets together to form a stable clot.

In health, normal levels of anti-clotting proteins (also called anti-coagulants) prevent excessive or inappropriate activation of clotting proteins. A healthy individual always has the right balance of clotting and anti-clotting proteins in the blood.

Altering the balance between clotting and anti-clotting factors may lead to disease. Increased function of clotting factors, or mutations leading to their inappropriate activation will lead to clots being inappropriately formed. Clots in the long veins of the legs is called deep vein thrombosis (DVT). Clots thus formed may break off and travel to the lung, blocking off major arteries in the circulation in a disease called pulmonary embolism (PE). Conditions leading to a fall in anti-clotting factors will do the same. Some of these conditions of abnormal clotting may be inherited, whilst others are associated with medications, hormone use, liver disease and cancer.

Conversely, a fall in production of clotting factors, or production of defective clotting factors, leads to bleeding. Haemophilia is a good example of an inherited bleeding disorder caused by low production of either clotting factors VIII or IX.

To have a normal clotting response to bleeding, 2 components are necessary: platelets and clotting factors. (see above: “Why do blood clots form?”) Any defects in either number or quality of these 2 components will cause abnormal bleeding. 

Abnormally low production of clotting factors, or production of defective clotting factors, leads to bleeding. This may be due to drugs, such as warfarin, which is used deliberately in some patients to prevent excessive clotting. It be also be caused by liver failure, or inherited conditions, such as haemophilia.

Platelet problems can also cause bleeding. Abnormally low platelet numbers, called thrombocytopenia, is covered above: “How dangerous is a low platelet count?” A number of conditions can change platelet function and may predispose to bleeding even if platelet numbers are normal. For instance, aspirin is commonly used in patients with artery disease to prevent complete blockages, through inhibition of platelet function. Other medications, including over the counter types, can cause this. There are also inherited disorders that can predispose to bleeding through platelet dysfunction.

The body may become low in iron due to reduced oral intake or increased loss.  Dietary deficiency is uncommon in developed countries with the abundance of food.  However low intake of iron may occur with individual dietary habits, particularly those which are restricted and limited in animal products, or secondary to diseases such as malabsorption or after extensive bowel surgery.  In general, the commonest conditions are excessive or prolonged bleeding such as with heavy periods, multiple pregnancies, bleeding from peptic ulcers, hiatus hernia, haemorrhoids or more seriously, bowel cancers. It is therefore important to identify the cause of iron deficiency. 

Iron deficiency commonly presents as iron deficiency anaemia.  Those affected may look pale, lack energy or have poor concentration, a poor appetite and heavy periods (both which may also aggravate the iron deficiency). Students may suffer in their schoolwork and workers in their productivity.  People with heart disease may notice in increase in angina.

Iron can be replaced orally or intravenously. Your doctor will advise which is the best treatment for you.  It is important to note that many health food /natural preparations may claim to contain iron, but their concentration is much lower than needed to replenish the bodies iron stores. Furthermore, iron from some food sources / medicines are more easily absorbed compared to others, and the raw iron content should not be the only determinant of its value as an iron replacement therapy.

Iron is vital to many body functions but too much iron (iron overload) can cause tissue damage, particularly in the heart, liver and pancreas.

Normally, iron stores are tightly regulated through changing the rate of absorption. There is natural mechanism for the body to get rid of its excess iron, so when the bodies iron stores are full, absorption mechanisms are switched off, and no more is absorbed through the diet. 

In an inherited genetic disorder called haemochromatosis, patients cannot switch off iron absorption even when their iron stores are full. They continue to pile on iron stores to levels that poison body organs. In patients who need chronic transfusions, red cells given to them eventually break down and release iron contained within. This iron is left behind in the body and accumulates.

The excess iron is stored in tissues in a haphazard manner. Overtime, with high iron levels, this can cause widespread damage. Iron deposits in the heart lead to heart failure, in the liver lead to cirrhosis, in endocrine glands lead to abnormal hormone production and diabetes, in the joints lead to arthritis, and in the skin leading to increased pigmentation. Overtime, such patients literally turn bronze. Such multiorgan failure can be fatal.  

Iron stores can be tested using a simple blood test, where we look for the iron concentration in the blood, and the presence of an iron binding protein called ferritin. Ferritin that circulate in the blood is a good indication of iron being present. However, in some disease states, such as auto-immune disease, infection or liver disease, ferritin can be released without iron being high, and be artificially elevated. Oral or intravenous iron replacement may also lead to a transient increase in serum ferritin, as can an iron rich meal. Sometimes, repeat measurements of iron studies or extra tests may be necessary to determine a patient’s iron status.

Long distance travel and prolong periods of sitting / immobility whether in a car or on a plane may lead to deep vein thrombosis (DVT), where clots form in the long veins of the legs. This leads to pain and swelling. More importantly, these clots can travel through the venous system and lodge themselves in the lung, causing shortness of breath due to loss of functional lung tissue. In rare instances, cardiac arrest can occur where the clots lodged in the lungs are sizeable. Other risk factors for DVT include hormone treatments, pregnancy and cancer.  

In general, keeping active including in-chair exercises, plenty of fluids, avoiding sleeping tablets, use of pressure stockings are recommended to reduce the risk of deep vein thrombosis on long distance journeys.  Alcohol leads to dehydration by promoting urine production, and excess drinking is best avoided.

There has been suggestion that low dose aspirin, with its anti-platelet effect, may be used to reduce the risk of DVTs. Whilst aspirin may help in individuals with increased risk of DVTs, its benefits in otherwise healthy individuals is unclear, and it may be adequate to merely follow healthy travel guidelines. On the other hand, individuals at high risk of developing DVTs, being on low dose aspirin may not be adequate as protection. The decision on whether anticoagulant medications should be used to reduce the risk of DVTs should therefore be taken on an individual basis after a discussion with your doctor.

Blood glucose, lipids studies, serum beta crosslaps, B12 and folate levels and serum iron studies.