Platelets (Sources: Revision notes) Flashcards

1
Q

When should you consider investigating a decrease in platelet count?

A

If < 100 or falls by >30%

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2
Q

What are the common and less common but important causes of thrombocytopenia in ICU pts?

A
Sepsis
DIC
Haemodilution
Haemofiltration and extracorporeal circuits
Drugs e.g. G2a/3b inhibitors, chemo
Excess alcohol 
Hypersplenism
Liver disease
Post-surgery e.g. bypass
Macrophage activation syndrome
Blood bourne viruses e.g. HIV, CMV
Folate deficiency
Myelodysplasia
Less frequent are TTP, HUS, HIT, ITP, HELLP, malaria
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3
Q

How should you investigate low platelets in ICU patients?

A
R/V history, exam and medications
Blood film - may be diagnostic, can exclude clumping
B12, folate
D-dimer
LFTs
coag screen
Renal function
LDH
bHCG
HIV
Bone marrow aspirate
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4
Q

Whos guidance should we follow with regards to platlet transfusion in the UK?

A

The joint United Kingdon Blood Transfusion and Tissue Transplantation Services Professional Advisory Committee (JPAC)

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5
Q

According to JPAC what are the triggers for platelet transfusion in the critically unwell?

A

Non-bleeding pts without sepsis or haemostatic abnormalities - not indicated
Prophylaxis in non-bleeding pts with severe sepsis or haemostatic abnormality - 20 x 10(9)/L
DIC with bleeding - >50
Plt dysfucntion with non-surgically correctable bleeding - may bleed despite plts count normal - give one pool and rpt according to clinical response
Major haemorrhage - >75 if multiple traum or trauma to the CNS

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6
Q

Describe heparin-induced throbocytopenia

A

Rare
Immune mediated
Occurs between 5 and 10 days post heparin exposure, but can occur within hours if the pt has had previous heparin exposure
Plt count is typically 50-80
It’s a prothombotic state and can manifest as necrotic skin leisons and arterial and venous thrombosis

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7
Q

How should you investigate whether a patient may have HIT?

A

Calculate a pre-test probability score - e,g, the Warkentin 4T score
A low score reliably excludes HIT
A moderate score should prompt further investigation
- a HIT screen involves an ELISA test for anti-heparin PF4 antibodies and a functional screen

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8
Q

How should you manage suspected HIT?

A

Heparin should be stopped
Switch to non-heparin anti-coagulation e.g. danaparoid, lepirudin, valirudin or argatroban
Platelet transfusion is contra-indicated in HIT

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9
Q

What is thrombotic thrombocytopenia purpura?

A

A rare disease
Significant mortality
It’s a thrombotic microangiopathy (TMA)
It has an autoimmune aetiology associated with low levels of ADAMTS-13
May be associated in some cases with HIV infection, pregnancy and some drugs e.g. quinine, clopidogrel, aciclovir

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10
Q

How does TTP manifest clinically?

A

Thrombocytopenia
Microangiopathic haemolytic anaemia (MAHA)
Microvascular thrombosis and its consequences e.g. cerebrovascular comp-lications, cardiac ischaemia, renal dysfunction; haematuria

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11
Q

How do you investigate for TTP?

A

Check ADAMTS-13 levels

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12
Q

How is TTP managed?

A
Management in a specialist centre
Plasma exchange
Immunosuppression
Organ support if required
Platelet transfusion is contraindicated
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13
Q

Describe the Warkentin 4T scoring system

A

Used for pretest probability scoring in HIT

  1. Thrombocytopenia - 2 if > 50% fall in plts, 1 if 30-50% fall
  2. Timing - 2 if onset within 5 days (or <1 day if heparin within last 30 days), 1 if > day 10 or timing unclear
  3. Thrombosis - 2 if proven new thrombosis, skin necrosis; 1 if progressive or recurrent thrombosis
  4. Other cause for platelets to fall - 2 non evident, 1 possible
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14
Q

What is haemolytic uraemic syndrome?

A

HUS is predominantly a renal TMA
Characterised by MAHA, AKI and throbocytopenia
Typical HUS is associated with diarrhoea (usually bloody) and infection with shiga toxin-producing pathogens e.g. E.Coli 0157

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15
Q

How is HUS managed?

A

Supportive

Plasma exchange and immunosuppression

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16
Q

Does RRT in renal failure improve platelet function

A

Yes

17
Q

Describe Von Willebrand’s disease

A

Deficiency of Von Willebrand’s factor leading to impaired platelet interaction with the vasculature and subsequent increased bleedig tendancy
Familial or aquired
Desmopression and antifibrinolytic agents are used in the treatment

18
Q

What aetiologies result in acquired Von Willebrand’s?

A

Autoimmune
Mechanical stress from extracorporeal circuits
Myeloproliferative disorders