What are Platelets?
Platelets (thrombocytes) are small, disc-shaped cell fragments derived from megakaryocytes in the bone marrow. They are essential for hemostasis (stopping bleeding) by forming platelet plugs at sites of vascular injury and providing a surface for blood clotting.
Platelet Function and Lifespan
- Lifespan: 7-10 days in circulation
- Production: Produced from megakaryocytes in bone marrow; regulated by thrombopoietin (TPO)
- Primary hemostasis: Platelets adhere to damaged vessel walls, activate, and aggregate to form platelet plug
- Secondary hemostasis: Provide phospholipid surface for coagulation cascade (fibrin clot formation)
- Destruction: Removed by spleen and liver after 7-10 days or after activation
How Platelets Work in Hemostasis
When blood vessels are injured, platelets respond through a series of steps:
- Adhesion: Platelets stick to exposed collagen via von Willebrand factor (vWF)
- Activation: Activated platelets change shape, release granule contents (ADP, serotonin, thromboxane A2)
- Aggregation: Released factors recruit more platelets, forming platelet plug
- Clot stabilization: Fibrin mesh reinforces platelet plug to form stable clot
Why is Platelet Count Important?
Platelet count provides critical information for clinical decision-making:
- Bleeding risk assessment: Low platelets increase bleeding risk, especially with procedures or trauma
- Transfusion guidance: Determines need for platelet transfusion before surgery or in bleeding patients
- Medication monitoring: Many medications cause thrombocytopenia (heparin, chemotherapy, antibiotics)
- Clotting disorder screening: Detects ITP, TTP, HUS, DIC, and hematologic malignancies
Platelet Count vs. Platelet Function: Normal platelet count doesn't guarantee normal hemostasis. Some patients with normal counts have defective platelet function (e.g., aspirin use, von Willebrand disease, uremia). Conversely, patients with mild thrombocytopenia (50,000-100,000/μL) rarely bleed spontaneously if platelets function normally.
Platelet counts are relatively consistent across age and sex, though pregnant women and newborns may have slightly different ranges.
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| Population | Normal Range (/μL) | SI Units (× 10⁹/L) |
|---|---|---|
| Adults (male and female) | 150,000-450,000 | 150-450 |
| Pregnant Women | 100,000-400,000 | 100-400 |
| Newborns (0-2 weeks) | 150,000-450,000 | 150-450 |
| Infants and Children | 150,000-450,000 | 150-450 |
Important Considerations:
- Critical values: Platelets <10,000 or >1,000,000 should be reported immediately
- Gestational thrombocytopenia: 5-10% of pregnant women develop mild thrombocytopenia (100,000-150,000) in third trimester; usually benign
- Pseudothrombocytopenia: Falsely low platelet count due to EDTA-induced platelet clumping (1-2% of samples)
- Platelet clumping: Always check peripheral smear if unexplained thrombocytopenia
- Ethnic variations: Some populations have slightly lower baseline counts without pathology
Thrombocytopenia (Low Platelet Count <150,000/μL)
Thrombocytopenia is classified by mechanism: decreased production, increased destruction, or sequestration.
Decreased Platelet Production
- Bone marrow failure: Aplastic anemia, myelodysplastic syndrome
- Marrow infiltration: Leukemia, lymphoma, metastatic cancer, myelofibrosis
- Nutritional deficiencies: Vitamin B12, folate deficiency (megaloblastic anemia affecting all cell lines)
- Medications: Chemotherapy agents, alcohol (direct marrow toxicity)
- Viral infections: HIV, hepatitis C, EBV (marrow suppression)
Increased Platelet Destruction
- Immune Thrombocytopenia (ITP): Autoantibodies destroy platelets; most common cause in otherwise healthy patients
- Drug-induced: Heparin (HIT), quinine, sulfonamides, vancomycin, valproic acid, linezolid
- Thrombotic Thrombocytopenic Purpura (TTP): Microangiopathic hemolytic anemia with schistocytes, fever, renal failure, neurologic changes
- Hemolytic Uremic Syndrome (HUS): Similar to TTP; often follows E. coli O157:H7 diarrhea in children
- Disseminated Intravascular Coagulation (DIC): Consumption of platelets and clotting factors; prolonged PT/PTT, low fibrinogen, elevated D-dimer
- Post-transfusion purpura: Rare; severe thrombocytopenia 5-10 days after transfusion
Platelet Sequestration
- Hypersplenism: Enlarged spleen sequesters up to 90% of platelets (cirrhosis, portal hypertension, lymphoma)
- Splenic sequestration crisis: Acute in sickle cell disease
Dilutional Thrombocytopenia
- Massive transfusion: Transfusion of >10 units packed RBCs without platelet replacement
- Massive fluid resuscitation: Dilutes circulating platelets
Pregnancy-Related
- Gestational thrombocytopenia: Benign; platelets 100,000-150,000 in third trimester
- HELLP syndrome: Hemolysis, Elevated Liver enzymes, Low Platelets; severe preeclampsia complication
- Preeclampsia/eclampsia: Platelet activation and consumption
Thrombocytosis (High Platelet Count >450,000/μL)
Elevated platelet count is classified as primary (clonal) or secondary (reactive).
Primary (Clonal) Thrombocytosis
- Essential thrombocythemia: Myeloproliferative neoplasm with JAK2, CALR, or MPL mutations; platelets often >600,000-1,000,000
- Polycythemia vera: Myeloproliferative disorder with elevated RBCs, WBCs, and platelets
- Chronic myeloid leukemia (CML): BCR-ABL positive; marked leukocytosis with thrombocytosis
- Myelodysplastic syndromes: Especially 5q deletion syndrome
Secondary (Reactive) Thrombocytosis
- Acute inflammation or infection: Pneumonia, UTI, inflammatory bowel disease
- Chronic inflammatory conditions: Rheumatoid arthritis, Crohn's disease, ulcerative colitis
- Tissue damage: Recent surgery, trauma, burns
- Iron deficiency: Thrombocytosis common even before anemia develops
- Malignancy: Lung, gastric, ovarian, breast cancer (paraneoplastic)
- Post-splenectomy: Loss of splenic sequestration; can reach 600,000-1,000,000
- Rebound thrombocytosis: After chemotherapy or severe infection recovery
- Medications: All-trans retinoic acid (ATRA), G-CSF
Distinguishing Primary vs. Secondary Thrombocytosis: Primary (clonal) thrombocytosis is persistent, often >600,000, associated with other cytopenias or cytoses, and carries thrombosis risk. Secondary (reactive) thrombocytosis is usually <600,000, transient, improves when underlying condition treated, and rarely causes thrombosis. If platelets >600,000 or persistent elevation, refer to hematology.
Bleeding Risk by Platelet Count
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| Platelet Count (/μL) | Bleeding Risk | Clinical Implications |
|---|---|---|
| >100,000 | Minimal | Safe for most procedures; no spontaneous bleeding |
| 50,000-100,000 | Mild | Increased surgical bleeding; generally safe for minor procedures |
| 20,000-50,000 | Moderate | Increased bleeding with trauma; bruising common; avoid major surgery |
| 10,000-20,000 | High | Spontaneous mucosal bleeding (epistaxis, gingival bleeding); consider transfusion |
| <10,000 | Severe | High risk spontaneous bleeding including intracranial hemorrhage; transfuse |
Platelet Transfusion Guidelines
Platelet Transfusion Thresholds:
- Active bleeding: Transfuse if platelets <50,000/μL (some say <30,000 for minor bleeding)
- Major surgery or invasive procedures: Target platelets >50,000/μL pre-procedure
- Neurosurgery or ophthalmic surgery: Target platelets >100,000/μL
- Prophylactic (no bleeding): Transfuse if <10,000/μL to prevent spontaneous bleeding
- Minor procedures (LP, central line): Target >20,000-50,000/μL
DON'T transfuse platelets in:
- TTP/HUS: Platelet transfusion can worsen microvascular thrombosis
- HIT (Heparin-Induced Thrombocytopenia): Risk of thrombosis, not bleeding
- ITP: Transfused platelets are rapidly destroyed; reserve for life-threatening bleeding
Expected Response to Platelet Transfusion
- One unit platelets (apheresis): Raises platelet count by ~30,000-50,000/μL in average adult
- One unit platelets (pooled): Raises count by ~5,000-10,000/μL per unit (typically 4-6 units pooled)
- Post-transfusion check: Measure platelet count 10-60 minutes and 24 hours post-transfusion
- Poor response: Suggests platelet refractoriness (alloimmunization, HLA antibodies, splenomegaly, DIC, sepsis)
Approach to Thrombocytopenia
Step 1: Confirm thrombocytopenia - rule out pseudothrombocytopenia by checking peripheral smear
Step 2: Assess bleeding risk and clinical urgency
Step 3: Review medication list for culprit drugs
Step 4: Categorize by mechanism:
- Isolated thrombocytopenia (normal WBC/Hgb): ITP, drug-induced, infection
- Pancytopenia (low WBC, RBC, platelets): Bone marrow failure, megaloblastic anemia, hypersplenism
- Microangiopathic hemolytic anemia (schistocytes on smear): TTP, HUS, DIC, HELLP
Step 5: Order targeted testing:
- PT/PTT, fibrinogen, D-dimer (if DIC suspected)
- Peripheral smear (schistocytes, platelet clumping)
- HIV, HCV (if risk factors present)
- Consider bone marrow biopsy if unexplained or concern for malignancy
Factors That Decrease Platelets
- Medications (most common cause): Heparin (HIT), chemotherapy, valproic acid, antibiotics (vancomycin, linezolid, sulfonamides), anticonvulsants, quinine
- Alcohol: Direct bone marrow toxicity and splenic sequestration
- Viral infections: HIV, hepatitis C, EBV, CMV, dengue
- Hypothermia: Platelet sequestration and dysfunction
Factors That Increase Platelets
- Iron deficiency: Even without anemia, iron deficiency commonly causes thrombocytosis
- Inflammation: Acute infection, trauma, surgery, inflammatory diseases
- Medications: All-trans retinoic acid (ATRA), G-CSF/GM-CSF, epinephrine
- Exercise: Strenuous exercise transiently increases platelet count
- Smoking: Chronic smokers have mildly elevated platelet counts
Pseudothrombocytopenia
- EDTA-induced clumping: Platelets clump in EDTA tubes, causing falsely low automated count (1-2% of samples)
- Diagnosis: Review peripheral smear showing platelet clumps; normal platelet count on smear estimation
- Solution: Redraw in citrate tube or heparin tube; perform manual platelet count
- Clinical significance: No clinical consequence; platelets function normally
Pre-analytical Errors
- Clotted sample: Platelets consumed in clot; falsely low count
- Delayed processing: Platelets degrade over time; process within 4 hours
- Giant platelets: May be counted as small RBCs or WBCs by automated analyzers
- Hemolysis: Can interfere with optical platelet counting
Clinical Pearl
"Spontaneous bleeding rare above 10,000-20,000/μL": Patients with platelet counts above this threshold rarely bleed spontaneously unless they have concurrent platelet dysfunction (uremia, aspirin, NSAIDs) or coagulopathy. Focus prophylactic transfusions on those <10,000/μL.
Always check peripheral smear for unexplained thrombocytopenia: Pseudothrombocytopenia (EDTA-induced clumping) occurs in 1-2% of samples. The smear will show platelet clumps and normal platelet numbers. Don't panic and transfuse based on automated count alone.
Clinical Pearl
HIT (Heparin-Induced Thrombocytopenia) causes thrombosis, not bleeding: Despite low platelet count (typically 50,000-150,000), HIT causes dangerous arterial and venous thrombosis. If platelets drop >50% after starting heparin (days 5-14), stop heparin immediately, check HIT antibody, and start alternative anticoagulant (argatroban, bivalirudin). Never transfuse platelets in HIT.
Don't transfuse platelets in TTP/HUS: Thrombotic microangiopathies (TTP, HUS) involve platelet-rich microvascular thrombi. Platelet transfusion worsens microvascular thrombosis and can precipitate stroke or MI. Treatment is plasmapheresis (TTP) or supportive care (HUS), not platelets. Reserve platelet transfusion for life-threatening bleeding only.
Clinical Pearl
ITP diagnosis is exclusion: Immune Thrombocytopenia (ITP) causes isolated thrombocytopenia with normal WBC, hemoglobin, and peripheral smear (except low platelets). Rule out drugs, HIV, HCV, and other causes first. Treatment: corticosteroids, IVIG, or anti-D for platelets <30,000 or bleeding.
Gestational thrombocytopenia is common and benign: 5-10% of pregnant women develop platelet counts 100,000-150,000 in third trimester. This is physiologic, not pathologic. Differentiate from HELLP, preeclampsia (hypertension, proteinuria, elevated LFTs), or ITP (platelets usually <100,000).
Clinical Pearl
Iron deficiency causes thrombocytosis: Even without anemia, iron deficiency commonly elevates platelets to 500,000-700,000. This is reactive thrombocytosis and rarely causes thrombosis. Treat the iron deficiency and platelets will normalize.
Essential thrombocythemia threshold is >450,000: But most patients have counts >600,000-1,000,000. If persistent platelets >600,000 without obvious reactive cause (infection, inflammation, iron deficiency), refer to hematology for JAK2/CALR/MPL mutation testing. ET carries thrombosis risk; may need aspirin or cytoreductive therapy (hydroxyurea).
Clinical Pearl
Post-splenectomy thrombocytosis peaks at 7-21 days: After splenectomy, platelet count rises (loss of splenic sequestration) and can reach 600,000-1,000,000. Usually benign and self-limited. Consider aspirin prophylaxis if >1,000,000 or thrombosis risk factors. Counts typically normalize over weeks to months.
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