Why Do Some Wounds Hurt While Others Don’t? Key Insights
- mdavis107
- Sep 15, 2020
- 10 min read
Updated: 2 days ago
Pain is a common symptom among patients with chronic wounds — often persistent, under-treated, and deeply disruptive to quality of life.⁹,⁶⁵,⁶⁶ More than 80% of patients with chronic wounds report persistent pain, and nearly half describe it as moderate to severe¹⁻⁴. Despite its prevalence, the nature of wound pain is highly subjective. As McCaffery classically stated, “pain is whatever the patient says it is — and exists whenever the patient says it does.”⁶⁷
But beneath that subjectivity lies a complex pathophysiology rooted in inflammation, oxygen deprivation, and metabolic disruption. Understanding why some wounds hurt more than others can help clinicians intervene earlier, ease suffering, and improve quality of life for medically complex patients.
The Connection Between Pain and Chronicity
In a large study of 758 patients, researchers found that the longer a wound persisted, the more severe the reported pain⁵. As chronicity increases, so does the likelihood of entering a downward spiral: one where prolonged inflammation leads to worsening tissue damage — and worsening pain. Without early and aggressive pain treatment, this cycle can become self-sustaining — worsening both the wound and the patient's quality of life.⁵,⁶⁴
Over the past two decades, awareness of chronic wound pain has grown — with international surveys highlighting its frequency and clinical impact.⁶,⁷,¹² Notably, in 2002, a multinational survey of more than 39,000 wound care practitioners across 11 countries, dressing removal was identified as the most painful moment in care.¹² Although research on chronic wound pain remains limited, much of it has focused specifically on dressing-related pain.⁶⁻¹¹ While this finding has informed product development and procedural best practices⁶⁻¹¹, it also underscores a larger trend: chronic wound pain is deeply tied to inflammatory processes⁶⁻⁷,¹¹.
The Inflammation–Pain Loop
This article outlines a clinical pathway for chronic wound pain — showing how prolonged inflammation contributes to pain, and how breaking that cycle can support healing.
Despite mounting evidence linking inflammation to chronic wound pain, an extensive literature search reveals no clearly defined clinical pathway to guide management. This gap underscores the importance of understanding how prolonged inflammation fuels pain — and how that cycle might be interrupted.
Their model remains one of the most accurate depictions of the chronic wound microenvironment to date — validated by decades of subsequent research.²⁴–³⁵
After tissue injury, the body initiates inflammation to begin repair. But when that inflammatory phase is prolonged, it initiates a “vicious cycle” — first described by Mast and Schultz in 1996¹³. As the inflammatory phase drags on and healing stalls, patients often experience heightened wound pain.⁵ This cycle, characterized by elevated cytokines and proteases, senescent cells, and reduced mitogenic activity, prevents wounds from progressing to healing¹³,²⁴⁻³⁵. While inflammatory profiles may vary between wound types, this dysfunctional environment — marked by poor cellular response to growth factors — is a shared trait across most chronic wounds.¹³,²⁴,²⁵
As inflammation persists, nociceptors (pain receptors) in the wound and surrounding tissue become hypersensitive, increasing both nociceptive and neuropathic pain. In effect, the wound environment itself becomes a pain amplifier¹³⁻¹⁵. When the microenvironment transitions from chronic inflammation to active repair, wound pain typically decreases — reinforcing the link between inflammation and pain.⁵⁻⁷,¹¹
How Edema and Hypoxia Fuel the Cycle
One of the body’s first inflammatory responses is edema — but chronic edema leads to pericapillary cuffing, impairing oxygen and nutrient delivery³⁹⁻⁴⁰. Infection further deepens this oxygen debt⁴¹. This hypoxic state reinforces the chronic inflammatory cycle described by Mast and Schultz — pushing the wound deeper into a self-sustaining loop.¹³ As edema worsens, tissue shifts from a hypoxic state toward ischemia, with fibrin cuffs forming around collapsed capillaries⁴²⁻⁴⁴. As pressure builds, sluggish blood flow and leukocyte adhesion further obstruct perfusion — a process known as capillary “plugging.”⁴²⁻⁴⁴
This sets the stage for ischemia-reperfusion injury, microvascular damage, and tissue acidosis⁴⁵⁻⁵⁶. Oxygen deprivation triggers anaerobic metabolism, reducing ATP and leading to metabolic acidosis — a cascade that lowers pH and elevates lactate. The resulting low pH and lactate buildup “excite” nociceptors and trigger pH-sensitive ion channels — intensifying pain¹⁴⁻²³.
Why Some Wounds Hurt Less
In contrast, wounds with sufficient oxygen availability can complete aerobic metabolism. The byproducts — carbon dioxide and water — are non-toxic and non-inflammatory¹⁵. This metabolic balance helps explain why acute wounds tend to hurt less than chronic ones, and why improved oxygenation often brings pain relief.
This principle may also explain the effectiveness of NSAID-based dressings like ibuprofen foam. Studies show that topical ibuprofen can downregulate proinflammatory cytokines and reduce wound pain⁵⁷⁻⁶³.
A Pathway Toward Relief
Despite the extensive literature on chronic wound pain, few resources outline a clear clinical pathway for addressing it. The evidence suggests one central truth: when we interrupt the cycle of chronic inflammation, we can reduce pain and improve healing outcomes.
Tools such as transcutaneous oxygen tension (TcPO₂) monitoring reinforce this theory. Studies show that edema reduces TcPO₂ levels — and that once edema is controlled, oxygenation improves and pain often declines.³⁶⁻³⁸
Final Thoughts
Wound pain is not just a symptom — it’s a signal. One that reflects the molecular state of the wound and the systemic burden on the patient. By recognizing the connection between pain and inflammation, healthcare teams can intervene earlier and more effectively.
SHS Spotlight
With more than 25 years of experience in wound care and hyperbaric program development, Shared Health Services equips hospitals and healthcare providers with the resources, tools, and peer-to-peer expertise needed to build successful, sustainable HBOT programs. We work directly with center staff—serving as trusted liaisons—to provide clinical guidance, compliance support, and training aligned with the highest standards of care. Our goal is to empower teams, elevate outcomes, and strengthen local wound care efforts through proven strategies and hands-on collaboration.
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