Thrombocytopaenia

OVERVIEW

  • definition of thrombocytopenia is a platelet count < 150 × 10E9/L
  • most common haemostatic abnormality in ICU patients
  • 15-60% incidence in ICU (higher in surgical/ trauma patients than medical)
  • about 50% is pre-existing, otherwise it tends to occur in the first 4 days in ICU

PROGNOSIS

  • increased mortality associated with severity of thrombocytopenia
  • severity of thrombocytopenia correlates with prognostic scores (e.g. SAPS, MODS, APACHE)
  • associated with increased hospital and ICU LOS

PATHOPHYSIOLOGY

  • thrombopoietin produced by the liver and kidneys stimulates thrombopoiesis
  • platelets are derived from megakaryocytes
  • average platelet lifespan is 9 days, and destruction occurs by phagocytosis in the spleen and liver
  • decreased production typically leads to a gradual fall in platelets over a week
  • immune destruction typically leads to an abrupt fall in platelets
  • aggregation is the main mechanism of thrombocytopenia in sepsis and MODS, sequestration also occurs in sepsis through binding to endothelium
  • the spleen normally sequesters 1/3 of the body’s platelets, this increases to 90% in massive splenomegaly
  • spleen contraction stimulated by the sympathetic nervous system can release additional platelets

CAUSES

Decreased production due to bone marrow failure (myelosuppression or infiltration)

  • drugs (temporal association with starting a drug, typically improves a few days)
  • alcohol
  • infection (e.g. viruses such as rubella, mumps, varicella, CMV, EBV; chronic: HCV, HIV; tropical: Dengue, chikungunya)
  • nutritional e.g. B12, folate, copper
  • infiltration
  • hematological disorders (e.g. leukemia)
  • liver cirrhosis (decreased thrombopoietin)

Increased destruction

  • sepsis
  • immune – ITP e.g. post-viral, post-transfusion purpura, HITTS
  • intravascular device (IABP, ECMO, PAC, bypass)
  • drug induced (antibiotics, thiazides, H2 antagonists)
  • antiphospholipid syndrome
  • TTP
  • HUS
  • DIC
  • HELLP
  • haemolysis
  • massive haemorrhage (consumption of platelets in clot formation)

Increased aggregation

  • early sign of MODS
  • sepsis (e.g. bacterial and fungal infections)
  • massive PE
  • thrombotic storm (widespread thrombosis in multiple organs)

Dilution

  • post resuscitation
  • massive transfusion (dilution in addition to consumption in haemorrhage)

Sequestration

  • splenomegaly e.g. cirrhosis, congestive heart failure, portal hypertension, infection and myeloproliferative disorders

Spurious

  • look for clumping on blood film

Often multifactorial in the critically ill (e.g. drug-induced thrombocytopenia amy not improve if sepsis then supervenes)

CLINICAL FEATURES

  • often asymptomatic when first detected (significant or spontaneous bleeding rarely occurs with a platelet count > 50 × 10E9/L; 5-fold increase in risk <50 x 10E9/L)
  • purpura, petechiae and bleeding
  • bleeding from venepuncture sites
  • Spontaneous intracerebral haemorrhage (<0.5% in ICU, higher risk if platelets <10 x 10E9/L)
  • generalised edema (platelets are required for vascular integrity, thrombocytopenia contributes to capillary leak in the critically ill)

INVESTIGATIONS

Assess clinically for:

  • drug history and timing of onset (e.g. abrupt drop in platelets within 2 weeks of transfusion or drugs)
  • exposure to heparin (including line flushes and RRT)
  • evidence of bleeding or microthrombosis
  • splenomegaly

Investigations are tailored to the presentation and may include:

  • blood film – clumping, schistocytes (microangiopathy), leukoerythroblastic profile (bone marrow disorder), RBC macrocytosis (B12, folate, EtOH, hypothyroidism)
  • malaria screen (splenomegaly)
  • Coagulation profile (DIC, sepsis, MODS)
  • LFTs
  • Haemolysis screen
  • HIT screen
  • vasculitis screen
  • B12 and folate levels
  • Septic screen
  • Viral screen (e.g. HIV,HCV, EBV, CMV)
  • investigation for source of bleeding if suspected

MANAGEMENT

  • control bleeding
  • treat underlying cause
  • platelets best avoided in TTP and HITS unless active, life-threatening bleeding present
  • As a rule of thumb, give 1 adult bag if:
    • platelets <10 x10E9/L
    • platelets <20 x10E9/L and patient has septic shock or is severely ill (expect ongoing consumption)
    • platelets <50 x10E9/L and an invasive interventional procedure is required
    • platelets <50 x10E9/L and patient requires anti-platelet drugs
    • platelets <100 x10E9 and severe traumatic brain injury / intracranial haemorrhage (Australian massive transfusion guidelines)
  • platelets are also given for critical bleeding according to massive transfusion protocols

References and Links

Journal articles

  • Crowther MA, Cook DJ, Meade MO, Griffith LE, Guyatt GH, Arnold DM, Rabbat CG, Geerts WH, Warkentin TE. Thrombocytopenia in medical-surgical critically ill patients: prevalence, incidence, and risk factors. J Crit Care. 2005 Dec;20(4):348-53. PMID: 16310606.
  • Greinacher A, Selleng K. Thrombocytopenia in the intensive care unit patient. Hematology Am Soc Hematol Educ Program. 2010;2010:135-43. PMID: 21239783.
  • Rice TW, Wheeler AP. Coagulopathy in critically ill patients: part 1: platelet disorders. Chest. 2009 Dec;136(6):1622-30. PMID: 19995764.
  • Wang HL, Aguilera C, Knopf KB, Chen TM, Maslove DM, Kuschner WG. Thrombocytopenia in the intensive care unit. J Intensive Care Med. 2013 Sep-Oct;28(5):268-80. PMID: 22232201.

CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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