Chronic Degloving Injury and Thrombocytosis
No, chronic tissue damage from a degloving injury many years ago would not be expected to cause persistent thrombocytosis. While tissue damage is a recognized cause of secondary thrombocytosis, this is an acute phenomenon that resolves once healing occurs, not a chronic condition persisting years after the initial injury.
Understanding Secondary Thrombocytosis from Tissue Damage
Tissue damage causes reactive thrombocytosis during the acute healing phase only. In a large cohort analysis of 732 patients with elevated platelet counts, tissue damage accounted for 42% of secondary thrombocytosis cases, but this represented acute injury and active healing processes 1. The mechanism involves inflammatory cytokines (particularly IL-6 and thrombopoietin) released during tissue repair that stimulate platelet production 1.
Key Temporal Considerations
- Acute phase response: Thrombocytosis from tissue damage occurs during active inflammation and healing, typically resolving within weeks to months as tissues heal 1
- Degloving injuries heal: Even severe degloving injuries undergo definitive reconstruction and healing, whether through replantation, free flaps, or skin grafting 2, 3
- No chronic stimulus: Once tissue healing is complete (which occurs within months, not years), there is no ongoing inflammatory stimulus to maintain elevated platelet production 1
What You Should Actually Investigate
If your patient has persistent thrombocytosis years after a degloving injury, you must search for an alternative cause. The elevated platelets are coincidental to the old injury, not caused by it.
Primary Thrombocytosis Evaluation
- Essential thrombocythemia is the most common primary cause, accounting for 45% of primary thrombocytosis cases 1
- Primary thrombocytosis presents with significantly higher platelet counts (often >600-800 × 10⁹/L) and carries increased risk of arterial and venous thromboembolism 1
- Laboratory features distinguishing primary from secondary causes include elevated hematocrit, elevated leukocyte count, elevated lactate dehydrogenase, and elevated serum potassium 1
Secondary Causes to Consider
- Active infection (24% of secondary thrombocytosis) 1
- Occult malignancy (13% of secondary thrombocytosis) 1
- Chronic inflammatory conditions such as inflammatory bowel disease or rheumatologic disease (10% of secondary thrombocytosis) 1
- Iron deficiency (common and often overlooked)
- Chronic infection or osteomyelitis (could theoretically relate to the old injury site if chronic infection persists, but this would be ongoing active pathology, not simply "old tissue damage")
Clinical Significance and Risk Assessment
The thromboembolic risk depends entirely on whether this is primary or secondary thrombocytosis.
- Primary thrombocytosis carries significant risk for both arterial and venous thromboembolism regardless of other risk factors 1
- Secondary thrombocytosis causes venous thromboembolism only when additional risk factors are present (immobility, malignancy, surgery) 1
- Unless additional risk factors exist, secondary thrombocytosis alone does not require antiplatelet or anticoagulation therapy 1
Common Pitfall to Avoid
Do not attribute current laboratory abnormalities to remote trauma without evidence of ongoing pathology. A degloving injury from "many years ago" is healed tissue. If thrombocytosis persists, conduct a thorough evaluation for primary myeloproliferative disorders, active infection, malignancy, chronic inflammation, or iron deficiency rather than assuming the old injury is responsible 1.