• Thrombocytopenia is defined as a platelet count <150,000/µL; it can result from decreased production, increased destruction, dilution, and errors with measurement. The platelet count is not, by itself, a predictor of platelet function and perioperative bleeding.
• Occasionally thrombocytopenia is associated with hypercoagulability and an increased risk of thrombosis.

• Impaired production:
  • Congenital
  • Acute leukemia, myelodysplasia
  • Osteoporosis
  • Toxins: Chemotherapy, alcohol
  • Infections: HIV
  • Radiotherapy
• Increased intravascular destruction:
  • Autoimmune:
    • Primary causes: Idiopathic thrombocytopenia, systemic lupus erythematous
    • Secondary causes: Drug-induced (HIT), post-transfusion, neonatal autoimmune thrombocytopenia
  • Non-autoimmune:
    • Disseminated intravascular coagulopathy (DIC)
    • Thrombotic thrombocytopenic purpura (TTP)
    • Hemolytic uremic syndrome (HUS)
    • Infection
    • Preeclampsia/HELLP syndrome
• Increased extravascular destruction:
  • Hypersplenism
• Dilutional:
  • Massive transfusion
• Pseudothrombocytopenia

• Idiopathic thrombocytopenia: Attachment of antibodies or immune complexes to platelets resulting in their premature removal from the circulation by the reticuloendothelial system.
• Systemic lupus erythematous: Antiplatelet antibodies or circulating immune complexes bind to platelets.
• HIT
  • HIT type 1: A benign, non-autoimmune condition. Mild thrombocytopenia occurs within 1–2 days after heparin therapy and resolves spontaneously within a few days even with continued heparin therapy.
  • HIT type II: IgG antibodies bind to heparin bound to platelet factor 4. Together, this IgG–heparin–PF4 complex binds to platelet receptors and activates them. Venous thrombosis occurs more commonly than arterial thrombosis. Occurs 5–10 days after the initiation of therapy.
• Post-transfusion thrombocytopenia occurs about 10 days after a blood transfusion and is due to antibodies in the recipient against human platelet antigen 1a (HPA–1a) on transfused platelets.
• Neonatal alloimmune thrombocytopenia (NAIT) results from transfer of maternal IgG antiplatelet antibodies across the placenta to the fetus. The antibody attaches to the HPA-1a inherited from the father and is lacking in the mother. Severe thrombocytopenia during the early phase of the second trimester can occur and may cause intracranial hemorrhage (20% incidence).
• DIC results from an abnormal, systemic activation of the coagulation cascade. This leads to deposition of fibrin in the microcirculation and aggregation and "consumption" of platelets with consequent thrombosis causing ischemia and organ necrosis. The blood becomes "unclottable" and severe hemorrhage occurs.
• TTP is due to an inability to cleave large multimers of von Willebrand factor (vWF). These large multimers bind to platelets and cause thrombosis of the small vessels. TTP may result in renal failure and impaired neurological function.
• HUS is similar to TTP in that there is a failure of cleavage of large multimers of vWF. It is characterized by the acute onset of microangiopathic hemolytic anemia, renal injury, and a low platelet count. HUS can be triggered by infection (e.g., Escherichia coli and HIV), genetic predisposition, medication, and systemic diseases that cause microvascular injury (e.g., systemic lupus).
• HELLP syndrome results in microvascular injury with endothelial cell damage along with progressive platelet activation and consumptive thrombocytopenia.
• Infection. Viral (e.g., HIV, EBV, and CMV), rickettsial, and parasitic infections (e.g., malaria) can reduce platelet production causing thrombocytopenia. Also sepsis in the critically ill is associated with an increase in macrophage colony-stimulating factor; it is responsible for histiocyte engulfment of megakaryocytes.
• Splenomegaly. Up to 90% of platelets may be sequestered in the spleen but it is not usually associated with bleeding.
• Dilutional thrombocytopenia can occur in patients who have received multiple units of whole blood or packed RBCs (pRBCs). Blood stored at 4°C for 24 hours has few viable functioning platelets (after 6 hours storage at 4°C, platelets lose 50–70% of their activity.
• Pseudothrombocytopenia. Occurs due to in vitro agglutination of platelets by EDTA anticoagulant and can result in falsely low platelet counts being recorded with automated measurements.
• Pregnancy associated thrombocytopenia is mild, asymptomatic, and present in 5% of pregnant women at term.

• A thrombocytopenic patient should be evaluated for the underlying cause, the possibility of qualitative platelet dysfunction, other coagulation defects, and signs and symptoms of impaired hemostasis.
• Each unit of transfused platelets increases the platelet count by 10,000/µL assuming that there is no immediate sequestration and destruction by hypersplenism or dilution by IV fluids and pRBCs.
• Ensure that the blood bank has a recent type and cross-match with pRBCs and platelets available and ready for immediate transfusion, if needed. Of note, cross-matching the recipient's platelets with those of the donor is not necessary; however incompatibility can reduce post-transfusion counts.

Hematemesis, hemoptysis, hematochezia, melena

Dependent on the etiology and severity

• ITP: Steroids, IV immunoglobulin (IVIG), splenectomy
• TTP, HUS: IVIG, plasmapheresis
• HIT: Discontinue heparin, consider alternative anticoagulant if blood thinning is still needed
• Hypersplenism: Splenectomy

Depends on underlying cause and can include

• Renal failure
• Liver cirrhosis
• Bone marrow failure
• Anemia and hypovolemia
• Thrombocytopenic thrombotic disorders may result in deep venous thrombosis (DVT), pulmonary embolism (PE), myocardial infarction (MI), and cerebrovascular accident (CVA)

• for complex causes of thrombocytopenia, a hematology consult may be warranted to optimize the patient preoperatively and continue appropriate therapy intraoperatively and postoperatively.
• Spontaneous bleeding occurs with platelet counts <20,000/µL (1).
• Neurosurgery and ophthalmic surgery, where even minimal bleeding can have a deleterious effect, should be performed only with a platelet count 100,000/µL.
• Major invasive surgery including cardiac surgery can be safely performed with platelet counts of 50,000/µL only if platelet function is normal and no other coagulation abnormalities exist (2).
• Obstetrics patients with HELLP syndrome. Platelet transfusions should be considered when the count is <30,000/µL for vaginal delivery or <50,000/µL for Cesarean section (2).
• Lumbar puncture for intrathecal chemotherapy should not be performed with platelet counts <20,000/µL (4).

• Impaired production
• Increased destruction (intravascular or extravascular)
• Dilutional
• Pseudothrombocytopenia

Depends on the surgical procedure, comorbidities, and intraoperative events (e.g., massive transfusion and ongoing bleeding).

• Corticosteroids, when appropriate, should be continued in the postoperative period.
• Follow-up platelet counts
• Hematology consult may be required

• Thrombocytopenia related
  • Postoperative bleeding
  • Bleeding or hematoma at IV, central line, and arterial line sites
  • Postoperative thrombosis: DVT, PE, MI, CVA
• Platelet transfusion related
  • Alloimmunization can be minimized by using leukocyte-depleted platelet concentrates or HLA-matched platelets.
  • Graft-versus-host disease can be prevented by gamma-irradiation of platelet concentrates prior to transfusion in patients with immunodeficiencies (6).
  • Increased risk of disease transmission
• Perioperative thrombosis: DVT, PE, MI, CVA.

• Platelets
• Heparin-Induced Thrombocytopenia
• Preeclampsia
• Von Willebrand's Disease

• 287.30 Primary thrombocytopenia,unspecified
• 287.49 Other secondary thrombocytopenia
• 287.5
• 289.84 Heparin-induced thrombocytopenia (HIT)

• D69.49 Other primary thrombocytopenia
• D69.59 Other secondary thrombocytopenia
• D69.6 Thrombocytopenia, unspecified
• D75.82 Heparin induced thrombocytopenia (HIT)
• D69.3 Immune thrombocytopenic purpura

Mona G. Sarkiss , MD, PhD