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Mohamed Magdy Badr: When Blood Disorders Break the Skin
Mohamed Magdy Badr, MD, WCSP/LinkedIn
Nov 9, 2025, 10:20

Mohamed Magdy Badr: When Blood Disorders Break the Skin

Mohamed Magdy Badr, Wound Care Consultant at Armed Force Rehabilitation Center, posted on LinkedIn:

”When Blood Disorders Break the Skin – Hematologic Causes of Leg Ulcers

1. Sickle Cell Disease (SCD)

Mechanism: Vaso-occlusion and chronic hemolytic anemia → tissue ischemia and poor oxygen delivery.

Features:

  • Common around the medial or lateral malleolus.
  • Painful, punched-out ulcers with hyperpigmented margins.
  • Delayed healing, often recurrent.

Other clues: Anemia, reticulocytosis, leg swelling, history of painful crises.

2. Thalassemia and Severe Anemias

Mechanism: Chronic hypoxia and iron overload → impaired collagen synthesis and tissue repair.

Ulcer characteristics:

  • Usually shallow with pale granulation tissue.
  • Often associated with hemosiderosis and fragile skin.

 

3. Polycythemia Vera

Mechanism: Hyperviscosity and microthrombi → tissue ischemia.

Typical lesions:

  • Painful, necrotic ulcers (often on lower legs).
  • May worsen with hydroxyurea therapy (drug-induced ulcers).

4. Leukemia and Myeloproliferative Disorders

Mechanism: Leukostasis, anemia, thrombocytopenia → poor perfusion + impaired immunity.

Findings:

  • Necrotic ulcers, gangrenous changes.
  • May present with leukemia cutis or neutrophilic dermatoses (Sweet’s syndrome, pyoderma gangrenosum-like lesions).

 

5. Thrombophilic States (Inherited or Acquired)

Examples:

  • Antiphospholipid syndrome (APS)
  • Factor V Leiden mutation
  • Protein C/S deficiency
  • Antithrombin III deficiency

Mechanism: Recurrent microvascular thrombosis → ischemic ulceration.

  • Clinical features: Livedo reticularis, painful ulcers, history of miscarriages or DVTs (especially in APS).

 

6. Cryoglobulinemia and Cold Agglutinin Disease

Mechanism: Immune complex deposition → small-vessel vasculitis → ulceration.

Features:

  • Painful purpura, ulcers on acral parts (toes, heels).
  • Triggered by cold exposure.

7. Paraproteinemias (e.g., Multiple Myeloma, Waldenström)

Mechanism: Hyperviscosity and immune complex deposition → vascular occlusion.

Findings: Livedo, ulcers, necrosis, poor wound healing.

 

8. Disseminated Intravascular Coagulation (DIC) / Thrombotic Microangiopathies

Mechanism: Microthrombosis → tissue ischemia and necrosis.

Seen in: Sepsis, malignancy, HELLP syndrome, TTP/HUS.

Lesions: Painful purpura → necrotic ulcers or gangrene.

 

Key Diagnostic Workup

  • CBC, peripheral smear
  • Reticulocyte count
  • Coagulation profile
  • ESR, CRP
  • Autoimmune and thrombophilia screening (ANA, APL antibodies, Protein C/S, AT III)
  • Serum electrophoresis for paraproteins
  • Skin biopsy (if vasculitis or malignancy suspected)

Management Principles

  • Treat the underlying hematologic disorder (transfusion, cytoreduction, anticoagulation, immunotherapy).
  • Optimize perfusion and oxygenation.
  • Meticulous local wound care and infection control.
  • Compression therapy where safe.
  • Adjuvant measures such as hyperbaric oxygen or pentoxifylline for resistant cases

Clinical Insight

When a “vascular” ulcer fails to heal despite proper blood flow, think hematologic.

“Healing the wound begins with healing the blood.” ”

Leg Ulcers

Keep up with Hemostasis Today.

Dermatology DIC Disseminated Intravascular Coagulation Health Hematology Hemostasis Hemostasis Today Leg Ulcers Leukemia Medicine Mohamed Magdy Badr Myeloproliferative Disorders Paraproteinemias polycythemia vera SCD Severe Anemias Sickle Cell Disease Thalassemia Thrombophilic States thrombosis Thrombotic Microangiopathies
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