Disorders of Blood

Conditions affecting the

components of whole blood
Learning Outcomes

To be able to describe the major disorders of the blood

To build upon your physiological knowledge and develop a clinical

understanding of the signs and symptoms of common blood
disorders

To understand where osteopathic treatment may be contra-

indicated.
Plan

Introduction
Clinical aspects
Anaemia
Bleeding tendencies
Clotting tendencies
Bone marrow failure
Leukaemia
Lymphoma
Myeloma
Osteopathic implications.
Blood Disorders
Included here are disorders of the
formed elements of blood

As they may arise within bone marrow from

cells of myeloid and lymphoid origin they
can be classified as diseases of lymphoid
and haemopoietic tissue

The formed elements of blood are;

Erythrocytes (and haemoglobin)
Thrombocytes (and blood clotting)
Leucocytes
Formed Elements of Blood
Normal range Unit
Hb 13-18 g/dl
Mean red Cell Vol 80-96 fl
(MCV)

Haematocrit 0.42:0.53 (ratio)

(HCT;PCV)*

Total white cell count 4-11 X109/l

WBC
Neutrophils 2-7.5 X109/l
Eosinophils 0.04-0.4 X109/l
Lymphocytes 1.5-3.5 X109/l

Platelets (PLTS) 150-400 X109/l

* PCV packed cell volume
Blood Disorders

Disorders of Erythrocytes

Anaemia

Polycythaemia
Formation of Red Blood Cells
Formation of Red Blood Cells
Erythropoiesis is stimulated by hypoxia (lack of oxygen) which stimulates the
production of a hormone, erythropoietin.

Erythropoietin is a glycoprotein formed within the kidney. It is inactivated by the

liver and excreted in the urine

Various other factors can affect the rate of erythropoiesis by influencing

erythropoietin production.

Thyroid hormones, thyroid-stimulating hormone, adrenal cortical steroids,

adrenocorticotrophic hormone, and human growth hormone (HGH) all promote
erythropoietin formation and so enhance red blood cell formation (erythropoiesis

However, very high doses of steroid hormones seem to inhibit erythropoiesis.

 Anaemia
Anaemia is the commonest form of blood disorder.
It is defined as a lack of haemoglobin rather than a reduction in red blood cells
Signs & Symptoms
Symptoms Signs
Fatigue Low [Hb]
Dyspnoea Abnormal MCV
Palpitations Abnormal TIBC
Headache Pallor
Tinnitus Tachycardia
Anorexia Murmur
Dyspepsia Cardiac enlargement
Bowel disturbance (Heart failure)
Angina (if CHD)

MCV = mean cell volume; TIBC = total iron binding capacity

Anaemia
Classifications

Hypocytic

Normocytic

Hypercytic

Hypochromic Normochromic Hyperchromic

Anaemia
Classifications

The most common form of anaemia (about 30% of the world

population) is mycrocytic hypochromic anaemia.

Classic clinical signs are;

Koilonychia Atrophic Glossitis

Anaemia

Classifications

In the UK we often see normocytic anaemia where the erythrocytes

are averaged sized but low in numbers within the formed blood.

Typically this will be as a result of;

Chronic Disease
Kidney Disease
Pregnancy
Bone Marrow Failure
Anaemia
Classifications

The other commonly observed form of anaemia is macrocytic

which can present;

Where large immature dysfunctional erythrocytes are present

in bone marrow due to defective DNA synthesis
(Megaloblastic)

Less common is Non-megaloblastic anaemia which is usually

caused by alcohol abuse. DNA synthesis is not defective, and
there are no megaloblastic changes in the bone marrow
Anaemia
Anaemia

Causes

Blood loss e.g. Trauma

Decreased production e.g. Iron

deficiency

Increased destruction e.g. Sickle Cell

Sequestration e.g. Polycythaemia

Anaemia

Blood loss

Trauma such as accidents or injury

Iatrogenic intervention such as operations

Failure in body tissues such as the gut

Pregnancy or from very heavy

menstruation.
Anaemia
Decreased production Commonest cause through
malnutrition, gut disease or loss of
Iron gastric tissue

Required in DNA synthesis, leads

Nutritional Vitamin B12 to megaloblastic RBC. 3yr store in
Deficiency liver (Pernicious Anaemia)

Decreased
Production

Defective
Cells
Anaemia
Pernicious Anaemia

Commonly caused by loss of gastric parietal cells, and subsequent inability to

absorb vitamin B12. May also be linked to other reasons for malabsorbtion
e.g. Crohns disease or inflammatory conditions of the small intestine.

Can also be due to dietary insufficiency common in vegetarians and vegans

May be due to increased requirement, such as in pregnancy or where

cancers may be widespread in tissue

Less commonly due to parasitic competitive upteake e.g fish tapeworm

Anaemia
Decreased production Commonest cause through
malnutrition, gut disease or loss of
Iron gastric tissue

Required in DNA synthesis, leads

Nutritional Vitamin B12 to megaloblastic RBC. 3yr store in
Deficiency liver (Pernicious Anaemia)

Folate
As above, but body stores of only
Decreased a few weeks
Production
Chronic Second commonest form due to
Disease neoplasms, RA, SLE, AS, PMR,
Defective GIT disease and liver disease
Cells Sideroblastic RBC progenitor cells abnormal
and Iron accumulates in
mitochondria
Haemolytic Increased destruction in spleen or
liver
 Anaemia
Increased destruction
Sickle Cell Linked to malaria resistance.
Hb RBC osmotically fragile
Formation

Genetic

Increased
destruction

Non
Genetic
Anaemia
Sickle Cell Anaemia Signs & Symptoms

Episodes of pain during a sickle cell crisis are one of

the most common symptoms

A sickle cell crisis is triggered when the abnormal

blood cells block the small blood vessels that supply
the bodys tissue.

As a child grows older, pain can affect any area of the

body, although the most common areas are:
ribs
spine
pelvis
abdomen
sternum (breastbone)
long bones in the legs and arms
 Anaemia
Increased destruction
Linked to malaria resistance.
Sickle Cell
Hb RBC osmotically fragile
Formation
Thalassaemias Frame shift in DNA base of Hb

Enzyme Enzymes act as anti-oxidants,

Genetic Deficiency common in malaria zones

Cell Hereditary, RBC spherical and fragile

Membrane
Non Auto- Haemolytic disease of newborn
Increased
Immune Rh- mothers with Rh+ children
destruction
Immunity Auto-
Production of IgG which damages
Based Immune
RBC
Non
Genetic Mechanical Heart valve prosthesis, contact sports
Non
Immunity
Based Infection Malaria

Chemicals/Burns
Anaemia
Sequestration

Erythrocytes become entraped within organs or other tissue commonly in an

enlarged spleen (Feltys Syndrome)

Splenomegaly results from the chronic inflammatory state.

The increased miles of sinusoids in this massive spleen leads to;

Shortened RBC life span (extravascular haemolysis)

Thromobytopaenia (easy of bruising) and
Leukopaenia, which leads to chronic bacterial infections

Often aggrivated by a dilutional anaemia due to increased plasma volume.

Polycythaemia

A range of disorders which have an increased number of circulating erythrocytes

The normal Hematocrit (packed cell volume PCV) is 52% for males and 47% for
females.

Two forms;

Relative Polycythaemia where there is a decrease in plasma volume

Absolute Polycythaemia where there is an increase in erythrocyte numbers
Polycythaemia
Haemochromatosis

Not to be confused with Polycythaemia increase in RBC

A recessive genetic disorder causing the body to absorb an excessive amount of

iron from the diet

The iron is then deposited in various organs, mainly the liver, but also the
pancreas, heart, endocrine glands, and joints

Once believed to be rare, but now accepted as one of the most common genetic
disorders

Blood tests identify the condition which is treated by weekly removal of blood.

Significant for osteopaths as arthritic symptoms are part of the common and
earliest presentation
Haemochromatosis
Signs & Symptoms

Chronic fatigue, weakness, lethargy

Abdominal pain; sometimes in the stomach region or the upper right hand side,
sometimes diffuse
Arthritis; may affect any joint but particularly common in the knuckle and first joint
of the first two fingers (the bronze fist - illustrated on the right)
Diabetes (late onset type)
Liver disorders; abnormal liver function tests, enlarged liver, cirrhosis
Sexual disorders; loss of sex drive, impotence in men, absent or scanty menstrual
periods and early menopause in women, decrease in body hair
Cardiomyopathy; disease of the heart muscle (not to be confused with disease of
the arteries of the heart)
Neurological/psychiatric disorders; impaired memory, mood swings, irritability,
depression
Bronzing of the skin, or a permanent tan
Blood Disorders
Disorders of Leucocytes

Increase or decrease in the number of leucocytes in

the blood, leads to different diseases and disorders of
white blood cells. Neutropenia, HIV/AIDS and
lymphocytopenia are caused due to low white blood
cell count, while leukemia is caused due to high white
blood cell count.
 Leucocyte Disorders

Primary Primary Immunodeficiency - Genetic

Secondary Immunodeficiency
Qualitative Splenectomy, Steroid Therapy,
Secondary Diabetes, Renal Failure, Alcohol,
Leukaemia, Glandular Fever

Disorders

Quantitative
Leukaemia
Summary

Neoplasia of white blood cell precursors within lymphoid (lymphatic) or myeloid

(bone marrow) tissues

Classified as acute or chronic, where acute conditions tend to be curable if

treated early, whereas chronic conditions are much more difficult to treat

Acute Lymphocytic Leukaemia (ALL)

Acute
Relatively
Acute Myeloid Leukaemia (AML)
Leukaemia rare but fatal
if untreated
Chronic Lymphocytic Leukaemia

Chronic
Chronic Myeloid (Granulocytic) Leukaemia
Acute Leukaemia
Aetiology

ALL; Infants 2-4 years old most at risk, but can

occur in later life. 2/3 of children cured upto the age
of 5, decreasing success in later life.

AML; More common in later life though infants and

adolescents can develop it. Only 25% of sufferers
live for longer than 5 years.

Treated with chemotherapy and antibiotics, plus

blood replacements with the aim of eliminating the
abnormal tissue and allowing it to repopulate. Bone
marrow transplants commonly carried out.
Acute Leukaemia

Signs & Symptoms

Aches & pains (hence the visit to an osteopath)

Bone pain (especially in children hence the visit to the osteopath
Non-specific flu like symptoms
Fever, malaise
Anaemia
Bleeding gums, noses and purpura present
Infections of bacteria and fungi due to neutropenia
Headaches, fits, convulsions and comas (due to increased blood viscosity)
Enlargement of lymph nodes, liver and spleen
Chronic Leukaemia

Aetiology

CLL; Commonest type of leukaemia in the UK (30% of

presentations) affects mature lymphocytes only.

CML; Several cell types involved (myeloproliferative)

accounts for 15-20% of lymphomas.

Treated with cytotoxic chemotherapy, radiotherapy and

steroids to control autoimmune complications. Newer
treatments utilise monoclonal antibodies which attach to
the abnormal lymphocytes and destroy them.
Chronic Leukaemia

Signs & Symptoms

Lethargy & fatigue

Splenomegaly in severe cases the spleen fills the abdominal and pelvic
cavities
Moderate anaemia
Hepatomegaly
Friction rub and tender abdomen common (hence visit to osteopath)
Enlarged lymph nodes
Glandular Fever
Not a failure of leucocytes by often a cause for dynamic change in numbers

Aetiology

An infectious mononucleosis

Common in young adults often asymptomatic but

can also cause acute illness

Spread via saliva droplets

Incubation 4-5 weeks

Caused by Epstein-Barr Virius (EBV) which

invades the B Lymphocyte cells
Glandular Fever

Signs & Symptoms

May be asymptomatic
Sore throat and fever
Severe fatiguem loss of apetite and depression (may continue for months)
Muscle pains (may visit and osteopath)
Oedema around eyes in 20% of cases
Headache (may visit and osteopath)
Increased sweating
Swollen lymph glands
Hepatitis & jaundice
Anaemia
 Leucocytes
Primary Primary Immunodeficiency - Genetic

Secondary Immunodeficiency
Qualitative Splenectomy, Steroid Therapy,
Secondary Diabetes, Renal Failure, Alcohol,
Leukaemia, Glandular Fever

Myeloid hyperplasia of bone marrow

Increase (reactive leucocytosis)
In Numbers
(Leucocytosis) Chronic granulocytic leukaemia
Disorders

Autoimmune e.g rheumatoid

Increased Glandular Fever
Quantitative Destruction Anaphylactic Shock
Decrease
Hypersplenism
In Numbers
(Leucopaenia)
Decreased Bone Marrow Failure
Production Megaloblastic Anaemia
Myeloma
Aetiology

Often known as multiple myeloma

Neoplasm affecting plasma cells which arise in bone marrow and causing a breakdown in
the production of antibodies instead paraproteins are created which have no capacity to
fight disease
Commoner in males than females, incidence is increasing due to better detection
Common in elderly (over 75) with higher incidence in Afro-Caribbean origin
Causes bone marrow failure, as well as bone destruction which means sufferers are
contra-indicated for HVT
Signs & Symptoms

Bone pain or insidious fractures due to resorbtion (may visit an osteopath)

Red Blood Cells aggregation due to increased paraprotein in blood
Kidney damage due to an increase in calcium deposition and effects of the paraprotein.
Lymphoma
Aetiology

Neoplasm of lymphoid cells, principally affecting the lymph nodes (neoplastic

lymphadenopathy)

Two main categories;

Hodgkins Lymphomas (Hodgkins Disease)

Non-Hodgkins Lymphomas
Lymphoma

Hodgkins Lymphomas Aetiology

Syndrome rather than a single disease typified by characteristic malignant

cells (Reed-Sternberg Cells)

1% of malignant diseases, with male to female ratio of 1.5:1

Bimodal age distribution with peaks at 20-30 and over 65

Possible links with the Epstein-Barr Virus (EBV) and reported association
with HIV

Treated with chemotherapy & radiotherapy with hypothyroidism a common

complication. 75% survival rate after 5 years. Fatal if not treated
Lymphoma
Hodgkins Lymphomas Signs & Symptoms

Painless enlarged lymph nodes which are firm, rubbery and mobile.
Can be mediastinal and affect breathing
Weight loss & night sweats with flu-like symptoms
Pruritis common itchy skin in the area of enlarged tumor due to decreased
drainage
Lymphoma
Non-Hodgkins Lymphomas Aetiology

A more prevalent condition than Hodgkins Lymphomas accounting for 3%

of all malignancies.

Complex scheme of classification but the most common affects the older
age group and is known as Follicular Lymphoma

Similar signs & symptoms to Hodgkins Lymphomas but extranodal

involvement is more likely, with the lymphomas being more widespread
than the patient is aware.

Radiotherapy, chemotherapy and bone marrow suppression with stem cell

transplants may be used in treatment. Breakdown of tumours may lead to
cardiac arrest due to release of high levels of potassium
Blood Disorders

Disorders of Thrombocytes & Haemostasis

Disorders of coagulation and haemostasis can generally

be considered alongside disorders of thrombocytes
(platelets)

A haemorrhage may become apparent on soft tissue

treatment, as the patient develops bruising.

The potential causes need to be considered.

Haemorrhage

Blood Loss may be;

Acute a large volume is lost over a short time

Chronic small volumes are lost over long periods

Compensatory mechanisms occur with chronic haemorrhage, but

eventually iron stores are depleted and iron deficient anaemia
occurs.
Haemorrhage

Commonest sites of blood loss are;

Uterine menstrual loss especially in the case of menorrhagia

Gastric/Gut peptic ulcers, haemorrhoids, NSAIDS, neoplastic
disease.

Also;

In Urine, haematuria due to damaged glomeruli

Internally from damaged blood vessels (risk of septacaemia)
From capilliaries resulting in small petechial haemorrhages
Haemorrhage

Skin Haemorrhage Classification

Purpura are a collection of petechial haemorrhages in the skin and

mucus membranes e.g. Senile purpura

Ecchymosis (bruise) is a large, subcutaneous haemorrhage

Haematoma is a large haemorrhage a lump of clotted blood

 Bleeding Disorders Congenital thrombocytopenia Uncommon and
associated with other defects e.g. Eczema
Thrombocyte
Defects Congenital defects in function e.g. Membrane
defects, defective granlues or absent fibrinogen

Absence of a single clotting factor

Congenital e.g.Haemophilia
Coagulation
Defects

Disorders
Haemophilia
Two types, both are sex-linked recessive disorders

Haemophilia A (Classical)
Haemophilia B (Christmas Disease)

Specific clotting factors are absent

Males affected and females carriers, but with 50% deficiency in clotting
factor therefore a mild form may be present.

Severity varies between families

No purpura but frequent haemorrhaging into large joints (haemarthrosis)

resulting in synovial hypertrophy, erosion of articular cartilage and severe
osteoarthritis.

Bleeding into muscle and urinary tract may also occur

Haemophilia
Haemophilia

Replacement therapy (blood transfusion) is used, risk of hepatitus

C infection and HIV in past.

Patients may develop antibodies to administered clotting factor.

HAEMOPHILIA & OSTEOPATHY

Patients with haemophilia exhibit many symptoms of dysarthria

and are suitable for treatment with care.

Very few of our interventions are likely to instigate bleeding but

may exacerbate that already present.

Joint mobilisation will assist in reduced inflammation and

maintenance of mobility
 Bleeding Disorders Congenital thrombocytopenia Uncommon and
associated with other defects e.g. Eczema
Thrombocyte
Defects Congenital defects in function e.g. Membrane
defects, defective granlues or absent fibrinogen

Absence of a single clotting factor

Congenital e.g.Haemophilia
Coagulation
Defects Absence of a carrier protein e.g. Von
Willebrands disease
Defects of Ehlers-Danlos Syndrome
vessels & Osteogenesis imperfecta Blood vessels leak
supporting Marfans Syndrome
tissues

Disorders Thrombocyte
Defects

Acquired Coagulation
Defects

Defects of
vessels &
supporting
tissues
 Ehlers Danlos Syndrome
A spectrum of inherited
genetic conditions affecting
Type I or II collagen.
Various presentations ranging
from mild to lethal.
Marfans Syndrome
Autosomal dominant genetic
condition which affects the
fibrillin component of
connective tissue.
Varying degrees of expression
may occur even within
families
Osteogenesis Imperfecta
Typically seen as an
autosomal dominant genetic
condition affecting Type 1
collagen, substituting complex
amino acids into the structure
rather than glycogen.
Recessive forms have now
been identified.
 Bleeding Disorders
Decreased Usually associated with
production other marrow dysfunction
Congenital Increased Autoimmune, drug &
Quantitative destruction neonatal causes most
common
Sequestration Splenomegaly
Thrombocyte Increase in Thrombocythaemia
Defects numbers (myeloproliferative)
(Thrombocytosis) Reactive (chronic
Disorders inflammation e.g.
rheumatoid)
Coagulation
Defects
Drugs Asprin, NSAID, Penecillin, Alcohol
Acquired
Renal failure leads to decreased
Defects of Uraemia platelet size & aggregation
vessels & Qualitative
supporting Myeloplastic & Polycythaemia rubra
tissues Myeloproliferative vera for instance
 Bleeding Disorders
Congenital

Liver disorder; e.g. Cirrhosis, hepatitis or

Thrombocyte paracetamol overdose. Death may result
Defects due to lack of clotting

Autoantibodies to clotting factors e.g.

Disorders Rheumatoid arthritis, post partum and
May result in the elderly
Coagulation serious bleeding
Defects e.g. Into joints Vitamin K deficiency; required to
Acquired even after minor produce clotting factor in liver. Dietary
trauma due to; deficit or malabsorbtion. Can be due to
Defects of antibiotics effect on gut flora.
vessels &
supporting Anti-coagulant drugs e.g. warfarin
tissues
Drug effects e.g. steroids
 Bleeding Disorders
Ageing senile purpura
Congenital
Trauma cut vessel, chemical damage etc

Steroid use

Thrombocyte
Defects Cushings Disease, under production of glutocorticoids

Disorders
Vitamin C deficiency (alocholism)
Coagulation
Defects
Acquired Structural weakness e.g. syphilis

Defects of Hypoxia
vessels &
supporting
tissues Amyloidosis accumulation of protein in tissue
Osteopathic Considerations

We need to be aware of all of a

patients presenting conditions which
includes FBC results if available.
Family history is vital if we suspect
an inherited condition

Certain conditions directly contra-

indicate osteopathic treatment,
others need a careful approach,
whilst others have been shown to
have beneficial effects.
Osteopathic relevance

Blood is a vital organ, and has

significant osteopathic relevance...

Still considered that displaced joints

would obstruct the free flow of blood
and lead to disease. He came to the
conclusion that the role of the artery is
absolute it must be unobstructed or
disease will result
FURTHER READING

Rowett HGQ, Basic Anatomy and Physiology, 4th Edition, John Murray, 1999. Very
simple, very basic, therefore very admirable.
Guyton and Hall, Textbook of Medical Physiology, 10th Edition, Saunders, 2000.
Standard physiology text, cant go wrong.
Underwood JCE, General and Systematic Pathology, 3rd Edition, Churchill
Livingstone, 2000. All you need unless you want something more gruesome. (4th Ed
now available 2004.)
Kumar and Clarke, Clinical Medicine, 4th Edition, Saunders 1998. Covers this
material very well. New edition out.
Ward RC (American Osteopathic Association), Foundations for Osteopathic Medicine,
2nd Edition, Lippincott Williams and Wilkins, 2002. Good for the biceps.
Lederman E, Fundamentals of Manual Therapy, Churchill Livingstone, 1997. Has a
lot of interesting things to say about tissues.