How do we approach

thrombocytopenia in critically ill

patients?
Jecko Thachil
Theodore E. Warkentin

2016 John Wiley & Sons Ltd, British Journal of

Haematology
The incidence of critical illness
thrombocytopenia
type of care provided
(medical, surgical or mixed) Thrombocytopenia can
and the threshold used for develop prior to arrival or
defining thrombocytopenia during the ITU stay
(< 150.000)

develops after arrival in the

ITU is likely to be caused by
development of a
an intervention (e.g. surgery,
complication (e.g. sepsis or
resuscitation fluids causing
liver impairment) in the ITU
haemodilution or drugs like
vancomycin)
Mechanisms for
thrombocytopenia in
ITU
patients
Mechanisms for
thrombocytopenia in
ITU
patients Histones Induce Thrombocytopenia
Practice Pointer

• Rapidity of development of
thrombocytopenia
• Timing of onset of
thrombocytopenia
• Thrombocytopenia in
combination with thrombosis
• The value of an absolute
platelet count
• Thrombocytopenia in patients
confirmed to have sepsis
• Thrombocytopenia with
abnormal coagulation profile
• Thrombocytopenia in patients
with artificial devices
• Bone marrow disorders
Diagnosing Heparin Induce Thrombocytopenia
Thrombocytopenia as a marker of poor
prognosis
Count < 100.000 associated with increase intensive treatment and
hospital stay, also higher in mortality
• Mild thrombocytopenia (100.000-150.000) increase 12% of mortality
• Moderate thrombocytopenia (50.000 – 100.000) increase 47% of mortality
• Severe thrombocytopenia increase (20.000-50.000) 56% of mortality
• Very severe thrombocytopenia increase (<20.000) 67% of mortality

Severe thrombocytopenia suggestive of severe underlying disease

and can be usefull during the course of intensive treatment
Management of the critically ill
thrombocytopenic patient (Fig 4)
• Bleeding in the thrombocytopenic patient
• Platelet count thresholds for transfusions
• Thrombocytopenia as a risk for organ impairment
• Antiplatelet therapy for sepsis?
• Thrombosis in the thrombocytopenic patient
Bleeding in the thrombocytopenic patient

• Bleeding is the biggest fear in relation to thrombocytopenia although

It is unusual for patient to bleed unless platelet count in < 20.000
• Most common cause of thrombocytopenia in intensive treatment
patient cause by increase in platelet consumption  platelet
transfusion is not likely beneficial
• In severe thrombocytopenia, patients may not bleed since endothelial
activation that cause the release of large amount of Von Wilebrand
factor which compensate for low platelet count ( has been
demonstrated in patient with liver disease)
Platelet count thresholds for transfusions
Most commonly accepted platelet
Stanworth et al (2013) showed count threshold for transfusion
that up to 30% of critical patient are level of 10.000 for without
receive a transfusion  majority bleeding, 20.000-30.000 for those
for prophylaxis rather than with additional risk factors for
treatment of bleeding bleeding ( DIC or severe hepatic
or renal dysfunction)

In those patient who are not

bleeding, platelet transfusion may
be required for surgical or
radiological intervention
Thrombocytopenia as a risk for organ impairment

• Platelet aggregation and adhesion to endothelium, circulating platelet

leucocyte aggregates, DIC lead to microvascular ischaemia which
manifest as organ failure
• Multiple organs are affected with the features of excess thrombin
generation (abnormal PT and APTT)  need antithrombotic therapy if
the risk of bleeding is no high
• Choices : low molecular weight heparin  need close supervision to
detect any bleeding early in such cases
• Avoid giving anticoagulation if platelet count < 25.000 unless there is
evidence of macrovasculer thrombus (DVT) or concern microvascular
thrombosis (Symetrical peripheral gangrene)
Thrombocytopenia as a marker of organ
impairment in critically ill
• Acute Kidney Injury
• Ono et al (2006) incidence of ARF and increase serum creatinine levels in patient
with sepsis and thrombocytopenia
• Clause et al (2009) systemic inflammation in sepsis  platelet aggregation  kidney
impairment
• Acute Lung Injury
• During mechanical ventilation  platelets promote leucocyte and inflammatory 
ALI
• Thrombocytopenia in critically ill disrupt barrier integrity  lead into pulmonary
edema  Lung Injury
• Vascular leakage
• Platelet maintain stability of vascular endothelial. Thrombocytopenia leads to
vascular leakage  red cell leakage ( ptechiae/bruising) and extravascular fluid (
edema and effusions)
 Antiplatelet therapy for sepsis?
There are several observational studies which show the use of aspirin may
have a beneficial effect

• Patient with CAP who were receiving anti-platelet therapy were less likely to need intensive
treatment and shorter hospital stay ( Boyle et al, 2015)
• Intensive treatment patients who were on antiplatelet therapy have better survival and lesser
risk of developing ALI and multiorgan failure and lesser mortality ( Winning et al, 2010; Harr et
al, 2013; Valerio rojas et al, 2013; Boyle et al, 2015)
• But there is still lack of radomised controlled trial in this setting

Author would continue antiplatelet agent if the patient were already

receiving it and has not acquired bleeding risk in intensive treatment up to a
platelet count threshold 25.000
Thrombosis in the thrombocytopenic patient

• Managing acute venous thrombosis in patient with thrombocytopenia is

dilemma
• Rule out condition which can present with this combination ( HIT, APS, DIC)
• Anticoagulation if platelet count above 50.000
• 30.000-50.000 unfractionated heparin may be chosen as the anticoagulant
of choice because of its easy reversibility and renal safety
• If less than 30.000 anticoagulant is not administered or given at reduced
dose but mechanical thromboprophylaxis is ensured and any thrombotic
risk factors (removal central lines)
Summary
• Thrombocytopenia is a common haemotological abnormality
encountered in intensive treatment
• Several different etiologies need to be kept in mind when trying to
identify the cause
• Thrombocytopenia can predict organ impairment and prognosis
• Certain clinical variables including timing and severity are useful
• Platelet transfusion may needed as prophylaxis or treatment
• Treatment Thrombosis in thrombocytopenic patient still a difficult
dilemma