Longevity & AgingResearch PaperOpen Access

Skin Failure in Critical Illness Lacks a Verified Diagnosis, Experts Conclude

A multidisciplinary think tank found 'skin failure' remains poorly defined and unsupported as a standalone ICD-10 diagnosis for critically ill patients.

Sunday, July 12, 2026 1 view
Published in J Wound Ostomy Continence Nurs
Close-up of aged human skin under clinical lighting, showing subtle discoloration and texture changes near a bony prominence, hospital setting

Summary

In August 2024, the National Pressure Injury Advisory Panel convened a multidisciplinary think tank to evaluate whether 'skin failure' in critically ill adults warrants its own diagnostic code. After reviewing the literature and deliberating, experts concluded that non-pressure-related skin failure lacks a clearly established etiology, pathophysiology, or histopathology distinct from pressure injury. While hypoperfusion is hypothesized as a key mechanism, no published photographs or biopsy data confirm a unique clinical entity. The panel defined skin failure as injury occurring despite standard preventive care with no identifiable alternative cause, but emphasized that this definition is insufficient to support a specific ICD-10-CM code. Substantial further research is required before skin failure can be codified as a separate diagnosis.

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Detailed Summary

The concept of skin failure has circulated in wound care and critical care medicine for decades, yet it remains loosely defined and clinically contested. The National Pressure Injury Advisory Panel (NPIAP) convened a think tank in August 2024, prompted by a request from the American Hospital Association to evaluate whether an ICD-10-CM diagnostic code for skin failure was warranted. The multidisciplinary panel included specialists from dermatology, critical care, geriatrics, palliative care, wound/ostomy/continence nursing, and surgery.

The panel conducted a systematic literature review spanning MEDLINE, CINAHL, Embase, Scopus, and Cochrane databases, covering terms including acute skin failure, Kennedy Terminal Ulcer, Trombley-Brennan Terminal Tissue Injury, and Skin Changes at Life's End (SCALE). Members reviewed full-text reprints prior to a face-to-face deliberation session. The review traced the term's origins to Irvine (1991) and the subsequent framework proposed by Langemo and Brown (2006), who categorized skin failure as acute, chronic, or end-stage, all rooted in hypoperfusion during organ dysfunction.

A central challenge identified was distinguishing skin failure from pressure injury, particularly on pressure-bearing surfaces like the sacrum and heels. Research by Nowicki and colleagues found that critically ill patients with severe multi-organ dysfunction (mean SOFA score 11.9) who developed stage 3–4 hospital-acquired pressure injuries all required multiple vasoactive agents, with many needing renal replacement therapy or ECMO. Yet studies by Kalowes and Lee demonstrated that foam sacral dressings prevented ulceration even in patients on vasopressors, undermining the hypothesis that vasopressors alone cause non-pressure skin failure. This evidence suggests the etiology is multifactorial and not cleanly separable from pressure-related mechanisms.

The think tank reached five key conclusions: (1) non-pressure-related skin failure should be defined as skin injury occurring despite standard preventive interventions with no identified alternative etiology; (2) no distinct etiology separates it from pressure injury; (3) hypoperfusion is a proposed but unconfirmed contributor; (4) histopathology has not been described; and (5) no published photographs depict acute skin failure. The panel was unambiguous that the current evidence base does not support assigning a specific diagnostic or billing code to skin failure.

The clinical implications are significant: the term is widely used in hospitals, sometimes to reclassify what may be pressure injuries as unavoidable skin failure events, potentially obscuring quality metrics and liability. Until a reproducible morphological description, natural history, and histopathological profile are established through rigorous research, using skin failure as a formal diagnosis risks conflating distinct pathologies and undermining pressure injury prevention accountability.

Key Findings

  • Skin failure in critically ill adults currently lacks a distinct, evidence-based etiology separate from pressure injury.
  • Hypoperfusion is hypothesized as the primary mechanism, but no histopathological data or clinical photographs confirm this.
  • Foam sacral dressings prevented ulceration even in vasopressor-dependent patients, challenging a simple vasopressor-skin failure link.
  • The think tank defined skin failure as injury despite standard prevention with no identified cause, insufficient for a diagnostic code.
  • Critically ill patients with severe multi-organ failure (mean SOFA 11.9) show the highest risk for deep tissue pressure injuries, confounding skin failure diagnosis.

Methodology

A multidisciplinary think tank of 13 experts convened in August 2024, preceded by a structured literature search across five databases (MEDLINE, CINAHL, Embase, Scopus, Cochrane). The panel used concept analysis and expert deliberation rather than primary data collection or meta-analysis.

Study Limitations

The think tank relied on expert consensus and a narrative literature review rather than systematic review with formal evidence grading. No primary data were collected, and the absence of published histopathology or clinical photographs for acute skin failure represents a fundamental evidentiary gap. Representation from geriatrics was limited as no American Geriatric Society delegate was available.

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