An Unusual Presentation of Deep Tissue Injury, Do We Really Understand It? A Case Report and Literature Review

Deep tissue injury (DTI) is an injury to the soft tissue under the skin due to pressure and is usually over boney prominence. This injury is commonly seen in bedridden patients in hospitals and nursing homes. Although many efforts were made to elucidate the precise mechanism and clinical presentation, the pathogenesis and the final clinical outcome are yet to be determined. Although the current agreed upon presentation describes DTI as purple- or maroon-colored skin with ulceration, presented herein is an unusual case where DTI presented with only erythema and induration over the sacrum and right gluteal area.

Deep tissue injury (DTI) was described as early as 1873 when Sir James Paget defined purple areas of unbroken skin that sloughed and turned into cavities.¹ In 1942, Groth, a German scientist, applied an external pressure to create ulcers in an animal and described these ulcers that started in the muscles as malignant.² Taking Groth’s study further, Darrell Shea was the first to introduce classification to pressure ulcers and added closed pressure ulcers into the staging system in 1975.^3,4 

The idea of another cause for pressure ulcers was debated by the National Pressure Ulcer Advisory Panel (NPUAP) in 2001.² These pressure ulcers emerged as maroon-purple colored tissue, and many of them tended to become stage IV ulcers.² 

The term “deep tissue injury” was chosen because the most likely cause of these pressure ulcers was a great level of pressure at the bone-soft tissue crossing point. At first, DTI was defined as a pressure-related injury to subcutaneous tissues under intact skin that initially have the appearance of a deep bruise and may herald the development of a Stage III-IV pressure ulcer, even with optimal treatment.³ According to the NPUAP, DTI is unbroken skin with nonblanchable purple or maroon discoloration that may be preceded by pain. This area of skin could be different in texture (mushy, boggy, firm) as compared with neighboring skin area, and the . maroon or purple color is hard to recognize in dark skin.⁵ This type of ulcer is severe and hard to diagnose. Indeed, if such type of ulceration reaches an advanced level, it becomes hard to treat and the prognosis is unprivileged. Thus, focusing on skin cannot reflect the extent of the total damage induced by the pressure.⁶ Deep tissue injury is commonly seen in bedridden patients in nursing homes and hospitals. Although many attempts have been made to explain the exact mechanism and clinical presentation, the pathophysiology and the final clinical outcomes have yet to be determined.

The authors have seen many patients with DTI in their practice. The presentations and outcomes may vary from healing without tissue necrosis and sequelae to complete tissue necrosis evolving into stage IV pressure wounds needing surgical debridement. Although the currently agreed upon presentation describes DTI as purple- or maroon-colored skin with ulceration, herein the authors present a case where DTI presented with only erythema, induration, and pain over the sacrum and right gluteal areas. A DTI diagnosis was made on the clinical examination, which was later confirmed intraoperatively.

A 67-year-old man with an early stage of dementia and major peripheral neuropathy with difficulty walking presented to the outpatient wound clinic with a 1-week history of painful sacral and right gluteal indurated areas with erythema and heterogeneous pigmentation. A small area of macerated skin was also found on the lower sacrum and coccyx (Figure 1). The involved area was covered with a protective foam dressing, an air mattress was ordered for his home, and he was asked to remain on either side while in bed, where he spent most of his time at home. 

During the next follow-up visit 1 week later, the symptoms remained the same with increased pain. The patient was then taken to the operating room for wound exploration. A 5-cm angular incision was made over the lower part of the sacrum and extended to the right gluteal area, which was indurated and painful on palpation. Subcutaneous fat necrosis was discovered extending down to the right gluteal fascia and a thin layer of the muscle itself. The skin flap was intact, and the necrotic tissue was excised down to healthy bleeding tissue. After achieving hemostasis using electrocautery and vessel ligation with 3-0 Vicryl sutures (Ethicon, Somerville, NJ), the wound was irrigated with normal saline and packed with a wet dressing made of gauze and quarter strength Dakin’s solution. The dressing was changed daily for 7 days then negative pressure wound therapy (NPWT) was applied at continuous 125 mm Hg. The patient was seen at the wound center 1 week following surgery (Figure 2) with regular weekly visits thereafter until complete wound healing was achieved 2 months postoperatively. Figure 3 shows the wound 1 week prior to complete healing.

Pressure ulcers develop as a result of ischemic insult to the soft tissue when compressed between the bony tuberosity and the patient’s chair or bed. If permanent capillary occlusion occurs, then tissue necrosis will follow. Subcutaneous fatty tissue is avascular and the first to die upon excessive pressure. The skin is very resilient to ischemia due to support from the rich vasculature of the subdermal plexus and is the last to succumb to excessive pressure. This can explain how DTI may only present with erythema and induration, which represent the calcified necrotic fatty and muscular tissue surrounded by inflamed tissue, like the authors found in this case after exploring the injured area intraoperatively. The term DTI is used loosely by clinicians; thus, it may create staging confusion that may result in legal implications. This issue is due to the lack of strong evidence-based science to confirm early diagnosis and predict the clinical outcomes of DTI. In the authors’ experience, DTIs may heal without sequelae, or they may evolve into stage IV pressure ulcers.

They can develop from the bottom up, from the top down, or remain in the middle, as seen in this case.

This unusual clinical presentation of DTI with only pain, induration, and discoloration should serve as a reminder of the possibility of this diagnosis. This patient did not present with the typical features of DTI, including bruised purple discoloration described by the NPUAP.⁵

While the skin was mostly intact during surgical exploration, the subcutaneous tissue, fascia, and part of the muscle were necrotic. A surgical exploration was prompted by the increased pain exacerbated by pressure at the involved area. Furthermore, the lumpy, indurated area had raised the suspicion for subcutaneous fat and muscle necrosis, and it warranted exploration to confirm the diagnosis and to determine the extent of necrosis needing debridement to hasten the healing process. 

Early diagnosis of DTI is critical to prevent the development of pressure ulcers and to prevent their worsening. In fact, infrared thermography could serve as an efficient tool for early detection of DTI lesions.⁷ Further clinical investigations are needed to help clinicians understand the pathophysiology of DTI, better evaluate the extent of injury, and predict its clinical outcome. This will finally help establish a clear definition of DTI. 

This case represents an unusual presentation of DTI. The skin, with its rich blood supply, is more resilient to pressure in comparison to muscle and adipose tissue, which has limited blood supply. Furthermore, skin may be the last layer to be affected. This may mask the underlying process. Therefore, clinicians should be aware that DTI could present itself with only painful subcutaneous tissue induration and without purple and maroon skin discoloration. Ultimately, early detection of DTI and proper treatment will improve clinical outcomes.

From the Department of Pharmacology and Toxicology, Boonshoft School of Medicine, Wright State University, Dayton, OH; and Department of Dermatology, Boonshoft School of Medicine, Wright State University 

Address correspondence to:
Richard Simman, MD, FACS, FACCWS
Plastic and Reconstructive Surgery 
Professor
Boonshoft School of Medicine
Wright State University
4000 Miamisburg-Centerville Road, Suite 104
Miamisburg, OH 45354
richard.simman@wright.edu

Disclosure: The authors disclose no financial or other conflicts of interest.