11/14/24, 10\:40 AM Thrombocytopenia

Thrombocytopenia

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Thrombocytopenia\: abnormally low platelet count (\<150 x 10 /L), increasing the risk of bleeding.
Platelet life span\: around 5 days; brief disruptions to production or survival can lead to thrombocytopenia.
Causes\:
Reduction in platelet production\: viral infections (e.g., herpes, CMV, HIV), chemotherapy, aplastic anaemia, haematological
malignancies, B12/folate de
Decreased platelet survival\:
Immune-mediated\: idiopathic thrombocytopenic purpura, SLE, rheumatoid arthritis, sarcoidosis, antiphospholipid
syndrome.
Non-immune\: medications (e.g., heparin, carbamazepine), splenomegaly, haemolytic uraemic syndrome, HELLP syndrome,
thrombotic thrombocytopenic purpura.
Pseudothrombocytopenia\: false low reading due to platelet clumping.
Symptoms\: often asymptomatic until platelets fall below 10; symptoms include spontaneous bruising, bleeding gums,
epistaxis, gastrointestinal bleeding, genitourinary bleeding, menorrhagia.
History\:
Assess for recent infections, surgical history, dental procedures, obstetric history, medication history, family history of
bleeding disorders.
Screen for symptoms of malignancy\: bone pain, night sweats, weight loss, splenomegaly, excessive thirst, urination,
constipation (myeloma).
Examination\: look for petechiae, purpura, lymphadenopathy, hepatosplenomegaly.
Investigations\:
Blood tests\: FBC, blood
Bone marrow biopsy\: if concerned about malignancy or aplastic anaemia.
Genetic screening\: if a congenital cause is suspected.
Management\:
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Secondary care referral\: not usually required for modest isolated thrombocytopenia (100-150 x 10 /L); monitor FBC,
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urgent referral if severe thrombocytopenia (\<20 x 10 /L), severe bleeding, or red cell fragments on blood
Patient education\: avoid contact sports, NSAIDs, maintain dental hygiene, avoid deep intramuscular injections.
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Platelet transfusion\: for severe thrombocytopenia (\<10 x 10 /L) or active bleeding.
Tranexamic acid\: increases clot stability; can be used orally, intravenously, or as soaked gauze.
Steroids\: for immune-mediated thrombocytopenia (e.g., ITP).
TPO agonists\: Eltrombopag, Romiplostim for stimulating platelet production in ITP or aplastic anaemia.
Bone marrow transplantation\: for severe unresponsive thrombocytopenia (e.g., aplastic anaemia).
Complications\: major risk is excessive and uncontrolled bleeding (e.g., gastrointestinal haemorrhage, intracranial
haemorrhage).
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Introduction

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Thrombocytopenia is a condition characterised by an abnormally low platelet count (\<150 x 10 /L). Platelets (also known
as thrombocytes) are disc-shaped cell fragments whose function is to react to blood vessel injury by clumping to initiate
the formation of a blood clot. Thrombocytopenia increases the risk of bleeding, however, most cases of thrombocytopenia
are detected on a routine full blood count (FBC) in otherwise asymptomatic patients.

Aetiology and risk factors

There are many causes of thrombocytopenia, which can be broken down into three broad categories; reduction in platelet
production, a reduction in platelet survival and dilution of platelet numbers.
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The average platelet life span is around 5 days, meaning even brief disruption to platelet production or survival can
result in thrombocytopenia.

Reduction in platelet production

Reduced platelet production will quickly translate to reduced numbers of platelets in the circulation due to their relatively
short life span (5 days).
Some causes of reduced platelet production include\:
Viral infections such as herpes simplex virus, cytomegalovirus, varicella-zoster virus, Epstein-Barr virus, rubella,
enterovirus, mumps, hepatitis, and HIV.
Chemotherapy agents\: result in direct bone marrow toxicity, inhibiting the production of platelets.
Aplastic anaemia\: a form of bone marrow failure typically of idiopathic aetiology.
Haematological malignancy such as leukaemia\: due to crowding of the bone marrow by malignant cells.
Non-haematological metastatic malignancy\: again due to invasion and crowding of the bone marrow by malignant cells.
B12 and folate de
Excess alcohol intake\: results in direct bone marrow toxicity and liver cirrhosis.
Congenital conditions including Fanconi's anaemia, Wiskott-Aldrich syndrome (WAS) and many others.

Decreased platelet survival

If platelets survive for a shorter duration and the bone marrow is unable to adequately increase its production of platelets
to match those being lost, thrombocytopenia will develop.
Platelet survival can be reduced by immune and non-immune causes.
Immune-mediated decreased platelet survival
Immune-mediated destruction of platelets typically occurs as a result of antibodies being directed at various platelet
components.
Some immune causes of decreased platelet survival include\:
Idiopathic thrombocytopenic purpura (ITP)\: antibodies directed at the surface of platelets result in their destruction.
Systemic lupus erythematosus
Rheumatoid arthritis
Sarcoidosis
Antiphospholipid syndrome
Non-immune decreased platelet survival
Some non-immune causes of decreased platelet survival include\:
Medications (e.g. heparin, carbamazepine, ibuprofen, rifampin, trimethoprim, vancomycin)
Splenomegaly\: the spleen sequesters more platelets than normal, decreasing the total circulating number of platelets.
Haemolytic uraemic syndrome (HUS)\: toxins from E .c o l i cause increased thrombogenicity of the vascular endothelium
which results in the consumption of platelets due to thrombotic microangiopathy.
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HELLP syndrome\: platelets are consumed due to increased exposure to von Willebrand's factor resulting in widespread
thrombotic microangiopathy.
Thrombotic thrombocytopenic purpura (TTP)\: reduction in the function of the enzyme ADAMTS13 normally responsible
for the breakdown of von Willebrand's factor results in platelets being excessively consumed due to a similar
mechanism as that described in HELLP syndrome.

Pseudothrombocytopenia

Pseudothrombocytopenia occurs when platelets undergo a phenomenon called ‘clumping’
, in which they stick together
causing a false low reading when passed through an auto-analyser.

Clinical features

History

Patients with thrombocytopenia are often asymptomatic until platelets fall to very low levels (often below 10) and as a
result, most cases are detected incidentally on full blood counts performed for unrelated reasons.
However, if a patient injures themselves or undergoes a procedure whilst signi
surgery) they are at risk of developing major haemorrhage.
If you suspect a patient may have thrombocytopenia, it is important to take a thorough bleeding history.
Typical symptoms associated with thrombocytopenia include\:
Spontaneous bruising or excessive bruising as a result of a minor injury
Bleeding gums
Epistaxis which may be excessive, frequent and prolonged
Gastrointestinal bleeding\: haematemesis, haematochezia and melaena
Genitourinary bleeding\: haematuria, post-coital bleeding
Menorrhagia
Other important areas to cover\:
Recent infections
Surgical history\: ask about previous surgery and if there were any issues with bleeding or bruising.
Dental history\: ask about previous dental procedures and if there was signi
Obstetric history\: ask about delivery and associated complications (e.g. post-partum haemorrhage)
Medication history\: ask about current medications (including blood thinning medication) and any recently prescribed
medication or dose changes.
Family history\: ask about any history of bleeding problems in the family.
Symptoms of occult malignancy should also be screened for including\:
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Bone pain
Night sweats
Weight loss
Left upper quadrant discomfort (e.g. splenomegaly)
Excessive thirst, urination and constipation (myeloma)

Clinical examination

Typical clinical
Petechiae (\<2 mm)
Purpura (0.2-0.1 cm)
These can be found on the skin and the oral mucosa.
A lymphoreticular examination should be performed to look for evidence of underlying haematological malignancy (e.g.
lymphadenopathy and/or hepatosplenomegaly).
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Petechiae on the lower leg from thrombocytopenia 4

Investigations

Blood tests
Blood tests relevant to thrombocytopenia include\:
Full blood count (FBC)
Blood
U&Es
Prothrombin time (PT) and activated partial thromboplastin time (aPTT)
B12 and folate
Bone marrow biopsy
Bone marrow biopsy may be indicated if there are concerns about underlying malignant invasion of the bone marrow (e.g.
leukaemia) or aplastic anaemia.
Genetic screening
Patients may undergo genetic screening if a congenital cause of thrombocytopenia is suspected.
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Blood
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Management

There is a wide range of management options for thrombocytopenia which di
Below is a brief overview of a range of di
thrombocytopenia.
Secondary care referral
Hospital referral is not usually required if the patient has modest isolated thrombocytopenia (platelet count 100-150
9 1
x 10 /L), without atypical features such as lymphadenopathy or fever. FBC should, however, be monitored closely in
primary care to ensure that platelets and other blood counts are not continuing to deteriorate (e.g. aplastic anaemia).
Patients should be advised to seek review if they experience any bleeding or spontaneous bruising.
Indications for urgent referral to haematology include\:
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severe thrombocytopenia (20 x 10 /L)
severe bleeding
red cell fragments or blasts on the blood
a history of constitutional symptoms (e.g. fever, weight loss, night sweats), spontaneous bruising/bleeding or
abnormalities on examination of the blood
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Consider a discussion with a haematologist if the platelet count is less than 100 x 10 /L.

Patient education

Patients with severe thrombocytopenia are advised\:
to avoid contact sports and activities which increase their risk of signi
to avoid NSAIDs (which impair platelet function)
to maintain good dental hygiene (to minimise the risk of gingival bleeding and the need for dental procedures)
to avoid deep intramuscular injections if possible
If patients with thrombocytopenia require surgical or dental procedures, they may be provided with treatments to
temporarily increase their platelet count (e.g. platelet transfusion, steroids) or increase clot stability (e.g. tranexamic acid).
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Platelet transfusion

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Platelet transfusions are often required for patients with severe thrombocytopenia (e.g. \<10 x 10 /L) or for those who
need a temporary boost to their levels for a procedure (e.g. major surgery). Transfusions should be used sparingly as there
is a risk of alloimmunisation against HLA antigens and/or platelet glycoproteins.
Platelet transfusions are also used in the emergency setting if patients with thrombocytopenia are actively bleeding.

Tranexamic acid

Tranexamic acid reduces the conversion of plasminogen to plasmin, preventing
stability.
Gauze soaked in tranexamic acid may be used to manage super
Oral or intravenous preparations of tranexamic acid may also be used in the peri/post-operative period to increase clot
stability and reduce the risk of bleeding.

Steroids

Steroids (e.g. prednisolone) are commonly used in the management of immune-mediated thrombocytopenia (e.g. ITP) to
suppress immune-mediated destruction of platelets allowing for count recovery.

Thrombopoietin receptor (TPO) agonists

TPO agonists such as Eltrombopag (daily tablet) and Romiplostim (weekly subcutaneous injection) directly stimulate the
production of platelets by the bone marrow. They are typically used as a second-line treatment in ITP (if steroids fail) and
also in the management of aplastic anaemia.

Bone marrow transplantation

Allogenic bone marrow transplantation is only used in cases of severe thrombocytopenia unresponsive to other
therapies (e.g. aplastic anaemia). Treatment involves induction chemotherapy to wipe out the host's stem cells and then
infusion of donor stem cells in the hope of curing the underlying pathology. There is a wide range of serious acute and
chronic complications of allogeneic bone marrow transplantation which are beyond the scope of this article.

Complications

The major potential complication of thrombocytopenia is excessive and uncontrolled bleeding (e.g. gastrointestinal
haemorrhage, intracranial haemorrhage).
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References

Patient.info, T h r o m b o c y t o p e n i a a n d P l a t e l e t F u n c t i o n D i s o r d e r s , Published 14.01.2015. Available BMJ Best Practice, A s s e s s m e n t o f T h r o m b o c y t o p e n i a , Published 2018. Available from\: [LINK]
National Heart, Lung and Blood Institute, T h r o m b o c y t o p e n i a . Available from\: [LINK]
James Heilman, MD. Licence\: CC BY-SA. Available from\: [LINK]
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AfroBrazilian. Licence\: CC BY-SA. Available from\: [LINK]
Prof. Erhabor Osaro. Licence\: CC BY-SA. Available from\: [LINK]

Acute Myeloid Leukaemia
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Anaemia Overview
Chronic Myeloid Leukaemia
Disseminated Intravascular Coagulation (DIC)
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