Not all wounds hurt the same, and not all pain is visible.

In wound care, clinicians are often struck by a puzzling disconnect: two patients with similar-looking wounds may report drastically different pain levels. One barely flinches at dressing changes, while the other is in tears from the moment the tape is peeled.

What explains this gap? Beyond size, depth, and infection status, a complex mix of molecular, neurological, and systemic factors may influence how pain manifests in chronic wounds. Understanding these drivers and what we can do about them is critical to improving quality of life and outcomes for patients living with chronic wounds.

Pain Is More Than a Symptom; It’s a Signal

Pain in chronic wounds isn’t just an uncomfortable side effect. It’s a clinical signal that something deeper is happening, often tied to underlying inflammation, tissue hypoxia, or neuropathic disruption.¹

While acute pain is typically protective, chronic wound pain can become a self-perpetuating burden. Studies have found that more than 80% of patients with chronic wounds report ongoing pain, with half rating it as moderate-to-severe. Clinically, this pain may be nociceptive (due to tissue damage), neuropathic (due to nerve injury or sensitization), or a blend of both.¹

The Inflammation-Pain Loop: A Vicious Cycle

One of the strongest predictors of wound pain is chronic inflammation. In normal healing, inflammation acts as a controlled response to injury. But when healing stalls, this phase becomes prolonged, possibly triggering ongoing pain through multiple pathways: inflammatory cytokines and proteases flood the wound bed; local nerves become hypersensitive to stimuli; tissue edema reduces oxygen delivery; and acidosis from anaerobic metabolism activates pH-sensitive pain receptors.² This creates a feedback loop where pain fuels inflammation and vice versa.

Why Do Some Patients Feel It More?

Two patients. Two wounds. Different experiences with pain. Why?

Peripheral neuropathy may blunt pain perception.³ Psychosocial stressors can amplify reported pain.⁴ Medication use, previous wound experiences, or even genetic variability can shape pain thresholds.⁵ This means chronic wound pain is multidimensional. The wound we see only tells part of the story.

Dressing Changes: The Hidden Flashpoint

In a multinational survey of wound care professionals, dressing removal was consistently rated as the most painful aspect of care.⁶

The noted causes include⁶:

• Adhesive trauma

• Exposed nerve endings

• Anticipatory anxiety

• Poor moisture management

Using atraumatic dressings whenever possible and involving patients in their care decisions can contribute to mitigating these concerns.

Breaking the Cycle: Clinical Strategies

While there’s no one-size-fits-all approach to chronic wound pain, several interventions have been shown to help when they are clinically appropriate:

• Foam and hydrogel dressings to protect and hydrate the wound¹

• Compression therapy to reduce edema and restore perfusion³

• Adjunctive therapies, such as physical activity, moisture management, impregnated dressings, social programs, and/or a combination of nonpharmalogical interventions⁵

• Pain-specific assessment tools that account for both physical and emotional drivers⁴

Treating pain means acknowledging its complexity and honoring the patient’s voice, even when visual cues don’t match their symptoms.

Conclusion

Wound pain is personal. When we recognize that pain isn’t just a symptom but a signal shaped by biology, experience, and inflammation, we move closer to truly personalized wound care. And in doing so, we create space not just for healing, but for dignity, trust, and relief.

About the Author

Matthew Davis is the Vice President of Administration and Corporate Development at Shared Health Services, a national wound care and hyperbaric consulting firm. He focuses on simplifying clinical data and translating complex strategies into tools that improve program performance and patient outcomes.

References

1.     Woo KY, et al. Chronic wound pain: a conceptual model. Adv Skin Wound Care. 2008;21(4):175-188.

2.     Dubin AE, Patapoutian A. Nociceptors: the sensors of the pain pathway. J Clin Invest. 2010;120(11):3760–3772.

3.     Dinh T, Veves A. Microcirculation of the diabetic foot. Curr Pharm Des. 2005;11:2301-2309.

4.     Blome C, Baade K, Debus ES, Price P, Augustin M. The "Wound-QoL": a short questionnaire measuring quality of life in patients with chronic wounds based on three established disease-specific instruments. Wound Repair Regen. 2014;22(4):504-514. doi:10.1111/wrr.12193

5.     Holloway S, Ahmajärvi K, Frescos N, Jenkins S, Oropallo A, Slezáková S, Pokorná A. Holistic management of wound-related pain. J Wound Management. 2024;25(1 Sup1).

6.     Moffatt CJ, Franks PJ, Hollinworth H. Understanding wound pain and trauma: an international perspective. EWMA Position Document: Pain at Wound Dressing Changes. EWMA Journal. 2002;2:2–7. Accessed June 23, 2025. https://amca-admin.rachel.puxdesign.cz/CSLR/media/amca/ewma/dokumenty/s…

7.     Gottrup F, Jørgensen B, Karlsmark T. Less pain with Biatain-Ibu: initial findings from a randomized, controlled clinical investigation. Int Wound J. 2007;4(Suppl 1):24–34.