Msk Dermatology · Year 2 · from Msk Dermatology

Case 3: Wound Healing Phases

Patient Presentation

Demographics: 45-year-old male with diabetes

Chief Complaint: Non-healing foot ulcer for 3 months

History of Present Illness: The patient has a chronic diabetic foot ulcer on the plantar surface of his right great toe. The wound has been present for 3 months despite wound care. He has peripheral neuropathy and does not feel pain in the affected area. He continues to walk on the foot without offloading.

Past Medical History:

  • Type 2 diabetes mellitus (HbA1c 9.2%)
  • Peripheral neuropathy
  • Peripheral arterial disease

Physical Examination:

  • Right foot:
  • 2 cm x 1.5 cm ulcer on plantar great toe
  • Wound bed: Pale, granular tissue with some slough
  • Minimal drainage
  • No surrounding erythema or warmth
  • Peripheral pulses: Diminished dorsalis pedis
  • Sensory: Absent protective sensation (10g monofilament negative)

Workup and Results

Ankle-Brachial Index:

  • Right ABI: 0.65 (moderate PAD)

Wound Culture:

  • Mixed flora, no signs of deep infection

X-ray Foot:

  • No osteomyelitis on plain films

Clinical Image

Photograph of chronic diabetic foot ulcer demonstrating impaired wound healing with poor granulation tissue, reflecting the failure of normal wound healing progression from proliferative to remodeling phase.

Diagnosis

Chronic Non-Healing Diabetic Foot Ulcer

Contributing factors:

  • Impaired wound healing (hyperglycemia)
  • Peripheral arterial disease (poor perfusion)
  • Continued pressure/trauma (neuropathy)
  • Failure to progress through normal wound healing phases

Discussion

This case illustrates wound healing phases and impairment:

  • Hemostasis and Inflammation: The lecture describes the initial phases involving platelet plug formation, fibrin clot, and inflammatory cell recruitment. Chronic wounds often get "stuck" in the inflammatory phase.
  • Proliferation Phase: The lecture explains that granulation tissue formation, angiogenesis (driven by VEGF), and re-epithelialization occur during proliferation. This patient shows poor granulation, indicating impaired proliferation.
  • Remodeling Phase: The lecture describes how type III collagen is gradually replaced by type I collagen during remodeling, increasing wound strength to approximately 80% of normal.
  • Factors Impairing Healing: Diabetes impairs multiple wound healing phases through hyperglycemia-induced cellular dysfunction, impaired angiogenesis, and increased infection risk. PAD reduces oxygen and nutrient delivery.

Treatment Plan

  1. Optimize Systemic Factors:
  • Improve glycemic control (target HbA1c <7%)
  • Vascular assessment/intervention if indicated
  • Nutritional optimization
  1. Offloading:
  • Total contact cast or removable walking boot
  • Essential to remove pressure from wound
  1. Wound Bed Preparation:
  • Debridement of non-viable tissue
  • Moisture balance with appropriate dressings
  • Consider advanced wound therapies
  1. Infection Control:
  • Monitor for signs of infection
  • Antibiotics if clinical infection develops
  1. Advanced Therapies (if no progress):
  • Growth factors (becaplermin/PDGF)
  • Negative pressure wound therapy
  • Cellular/tissue-based products

Teaching Points

  1. Wound healing occurs in four phases: hemostasis, inflammation, proliferation, remodeling
  2. VEGF drives angiogenesis during proliferation phase
  3. Type III collagen is replaced by type I collagen during remodeling
  4. Maximum wound strength is ~80% of normal skin
  5. Chronic wounds often stall in the inflammatory phase

Image Reference

For visual reference of skin structure concepts, see:


Learning Points

  1. Skin Layers: Epidermis (from ectoderm), dermis (from mesoderm), hypodermis
  1. Keratinocyte Turnover: ~28 days from stratum basale to stratum corneum
  1. Melanocyte Origin: Neural crest; reside in stratum basale
  1. DEJ Function: Connects epidermis to dermis; type VII collagen forms anchoring fibrils
  1. Wound Healing Phases: Hemostasis, inflammation, proliferation (VEGF/angiogenesis), remodeling (type III to type I collagen)

All cases for this lecture as Markdown