Sacral Wound: An Integral Part of Wound Care

If you ask most wound care specialists, pressure injuries are among the most challenging skincare conditions to treat. They’re generally slower to heal, often costly to treat, and can impact a patient’s overall quality of life, mainly when they occur in certain locations. For instance, one pressure injury that can stump even the most experienced practitioners is the sacral wound. 

Because they’re common and more challenging to manage, we’ll take a deep dive into sacral wounds. Clinicians will be able to walk away knowing what they are, how they come about, treatment strategies, and more. This insight can aid in improving patient outcomes, lowering costs, and more. 

What Is a Sacral Wound? 

When people say “sacral wound”, they’re referring to a type of pressure injury located in the sacral region (i.e., the tailbone). In addition, they’re occasionally referred to by other names, such as sacral decubitus ulcer, sacral pressure ulcer, or sacrum wound or injury. 

According to current research, 70% of the time pressure injuries are located at the sacrum, ischial tuberosity (sit bones), and greater trochanter (part of the femur bone at the hip). Each of these locations are categorized by bones close to the surface of the skin. Overall, the most frequently affected site for pressure injuries is  the sacrum, representing almost 40% of cases in one study. 

Sacral Wound Stages

It’s important to understand that not all sacral injuries are created equal, as they have varying levels of severity requiring different types of treatment. To signify how they may differ, the National Pressure Injury Advisory Panel (NPIAP) has categorized them into the following stages.

• Stage 1: Skin is intact, but there’s an observable alteration to the area, and non-blanchable redness. Sometimes patients experience other sensations, such as warmth or firmness at the wound site, before noticing visual changes.
• Stage 2: There’s partial-thickness skin loss and exposure to the dermis. It may present as a shallow open ulcer with a moist pink or red wound bed without sloughing or bruising. There might also be an intact or ruptured serum-filled blister. 
• Stage 3: Full-thickness skin loss, where adipose tissue may be visible in the ulcer, and wound edges may be rolled. There may be eschar or slough, as well as tunneling or undermining. However, bone, muscle, and tendons are not exposed. 
• Stage 4: Characterized by full-thickness skin and tissue loss, with exposed muscle, tendon, or bone. Slough or eschar may be present, with rolled edges, tunneling, or undermining.  
• Unstageable: In this stage, there’s full-thickness skin and tissue loss, but the level of damage can’t be determined due to eschar or slough. 

The Pathogenesis of Sacral Injuries

To fully grasp sacral wounds, it helps to have a solid understanding of how pressure injuries occur in the first place. So to make sure we’re all on the same page there, let’s explore some of the biological processes associated with pressure wound development. 

When patients present with a bedsore, as pressure injuries are occasionally termed, it signals that they’ve experienced localized damage to their skin and underlying tissue. This occurs when there’s extended external pressure on the area, and when this pressure isn’t relieved, it can eventually result in three primary mechanisms of injury: 

• Ischemia-reperfusion injury
• Impaired lymphatic drainage
• Cellular deformation

Ischemia-Reperfusion Injury

Normal capillary pressure is between 12 and 32 mm Hg. When mechanical pressure exceeds that, it can cause s capillary blockage that restricts blood flow. This results in reduced oxygen levels, in this case, in the sacral region, and the development of local ischemic tissue. When paired with venous obstruction, it leads to swelling that begins in the deep tissue and extends to the superficial level.  

A host of processes  are triggered by ischemia, like impaired mitochondrial oxidative phosphorylation. When this happens, adenosine triphosphate (ATP) generation is decreased, which is necessary for protein synthesis and cellular processes. There’s a boost in leukocyte activation and heightened levels of inflammation, as well. The hypoxia can lead to  cell death and the accumulation of toxic metabolites in a sacral wound. 

The Effects of Removing Pressure

Once pressure is removed, you might assume that cellular processes  will return to normal once the pressure is removed, but that’s not quite what happens. Once pressure is alleviated, the restoration of blood flow elevates oxidative stress and reactive oxygen species (ROS). The reperfusion process diminishes the expression of nitric oxide, impedes vascular relaxation, and more. These actions, in turn, exacerbate pro-inflammatory signal production and ROS, making it difficult for debris and apoptotic cells to be cleared. 

Understand that a patient being bedridden for even two hours is enough to create the foundation of  a pressure injury. There’s also research showing that the onset of pressure sores can progress from muscle tissue to superficial skin within 48 hours and advance to gangrene within seven to 10 days. Numerous physiological changes can occur in tissue below the skin’s surface before clinicians observe visual changes, making these wounds particularly dangerous. 

Impaired Lymphatic Drainage 

The lymphatic system plays a crucial role in the body, including: 

• Absorbing interstitial fluid 
• Clearing debris and toxic metabolites 
• Moving the immune cells from soft tissues into the arteriovenous circulation 

However, when pressure is applied to the skin, lymphatic clearance is reduced, and it has the potential to cause lymphedema. Lymphedema is said to be a component of pressure ulcer pathophysiology, with its ability to induce sacral wound development. 

The dysfunction of lymphatic clearance has a trickle-down effect. It can cause an unregulated infiltration of excess leukocytes due to inadequate cytokine removal and ROS. It also reduces T-regulatory cells that are meant to help resolve inflammation. 

Cellular Deformation

External pressure can result in cellular deformation and hinder cell viability. This damage can happen when:

• Elevated amounts of pressure are applied for short periods, or
• Small amounts of pressure are exerted for prolonged periods of time 

Contorted cells, like those that occur with pressure injuries, can compromise plasma membrane permeability, an activity meant to help cells regulate and maintain their internal components . The increased permeability allows for the influx of harmful molecules into the soft tissues and muscle cells, aka myocytes. When not relieved, it’s common to see cytoskeletal damage and necrosis. 

How Are Sacral Wounds Caused? 

Now that we’ve clarified how they’re developed, it’s time to understand why these sacral injuries occur. As we’ve discussed, and what you’ve likely observed in practice, these wounds are intricate and have several interconnected parts. For instance, there are external factors besides pressure, like: 

• Friction. The skin scraping against something, like bedding, can break down the superficial dermis and epidermis. 
• Moisture. Incontinence, whether fecal or urinary, can irritate the skin and heighten the risk of infection. 

Also, although shearing forces don’t cause sacral wounds, they influence and can contribute to the damage they cause. 

Then there are several internal factors as well.

• Malnutrition: Research shows that one’s nutritional status is significantly connected to pressure injury development. 
• Impaired sensation: Some patients don’t feel discomfort due to preexisting nerve damage, and therefore don’t always feel prompted to change positions.  
• Poor circulation: Pressure injuries result from mechanical force reducing the blood supply. That, coupled with a condition like peripheral artery disease, further interrupts nutrient and oxygen delivery to the site. 
• Decreased mobility/immobility: Evidence reveals that limited mobility is the greatest risk factor for developing pressure injuries. In that study, patients with immobility also had the most severe bedsores, making up nearly 50% of those with hospital-acquired Stage 3, Stage 4, Unstageable, and deep tissue injuries. 

Together, external and internal factors work simultaneously to create sacral wounds. 

Which Patients Are Most at Risk for Sacral Wounds? 

Anyone can have  a sacral injury, but some individuals are more likely to be at risk than others. Understanding who’s most at-risk allows clinicians to be proactive and observant when supporting patients who align with those characteristics. The best protocol for sacral decubitus ulcers is to prevent them from occurring in the first place. 

Consider the following high-risk populations.

Individuals with Paraplegia

Those with spinal cord injuries, neurological diseases, or meningitis are at a high risk of forming sacral ulcers. Motor paralysis combined with sensory loss requires providers and staff to take a multidisciplinary approach. Sacral pressure injury prevention might include  using innovative support surfaces to redistribute the patient’s weight, using the 30-degree side-lying position, and avoiding prolonged use of prone positioning. 

Older Adults 

As people age, skin integrity changes, often becoming thinner, drier, and less elastic. These factors can make the skin more sensitive and increase the likelihood of bruising, but it’s also a risk factor for sacral wound development. 

Older adults are particularly vulnerable, because they’re more likely to have poor nutrition, limited mobility, incontinence, comorbidities , and/or take multiple medications that could result in  various side effects. 

Those in nursing homes and hospitals are at an even greater risk, as they often have to rely on healthcare professionals for mobility assistance. Many spend prolonged periods of time sitting or lying down, leading to  pressure on the sacrum. 

One study found that: 

• Pressure injury prevalence, incidence, and nursing home-acquired pressure injury rate are 11.6 %, 14.3 %, and 8.5 %, respectively.
• Nursing home residents are most likely to develop Stage 1 and Stage 2 injuries. 
• The most common bodily areas are the heel (34.1%), sacrum (27.2%), and foot (18.4%).

Children 

Children in hospitals are also at a higher risk of pressure injuries, but the severity of it is largely unknown, as most research is geared towards adults. 

Among hospitalized children, the body sites that pressure injuries are most likely to occur include the occiput (16.7%), sacrum and coccyx (15.6%), and ears (9.9%). Interestingly, researchers also found that  sacral ulcers most often occurred in the general ward, while those on the occiput and ears developed in intensive care units (ICU). 

How to Treat a Sacral Wound

When practitioners identify that a patient has a sacral wound, research suggests they begin aggressively managing modifiable factors. This may look like: 

• Positioning changes
• Dietary adjustments 
• Medical comorbidity assessment
• Pressure from medical devices evaluation and elimination
• Incontinence assessment (e.g., different absorbent products or product size, more frequent toileting assistance, temporary constipating agents, etc.)

Ultimately, though, which treatment practitioners decide to implement largely depends on the stage of the sacrum wound. Sacrum wound management options span from cutting-edge mattresses and negative pressure wound therapy to ultraviolet heat lamps and surgery. 

Stage 1 and Stage 2 Sacral Wound Treatment

Care of Stage 1 and 2 sacral wounds is often conservative and doesn’t require surgical intervention. Clinicians can initially focus on washing, cleaning, and maintaining the wound’s surface, then look at ways to optimize the patient’s health. 

This might involve increasing hydration and boosting their intake of certain proteins, vitamins, and minerals. Smoking cessation, better pain control, and ensuring proper blood volume can optimize a patient’s health enough to promote healing, as well. 

Stage 3 and 4 Sacral Wound Treatment 

A Stage 3 or 4 sacrum wound might require all of the above, plus surgical intervention. For instance, wounds with devitalized tissue are a breeding ground for bacteria and possible infection. Damaged tissue also acts as a physical barrier to new skin tissue development. 

Debridement, a process for removing infected, damaged, or dead tissue, helps prepare the wound bed for re-epithelialization. It’s important to note that there are different debridement approaches, and practitioners should aim to select the appropriate technique based on their treatment goals. Consider the two types of debridement listed  below, but keep in mind that there are others. 

• Autolytic Debridement: Deemed the most conservative and slowest approach, it uses the body’s enzymes and endogenous phagocytic cells to break down necrotic tissue. 
• Surgical Debridement with Sharp Instruments: This may be done if it’s decided that the sacral wound will need  reconstruction. It can be performed at the bedside or in an operating room, but it must be done by someone licensed to conduct surgical treatment.  

Reconstructive Treatment of Advanced Sacral Wounds

Sacral pressure injuries are associated with high morbidity, with some even resulting in death due to severe sepsis. To minimize the risks of sacral wounds, skin grafts or flap techniques may be implemented. Skin grafts, in particular, are more likely to cause hypertrophic scarring and are prone to recurrence. 

Research finds that the most common local flaps used for sacral pressure ulcer reconstruction are:

• ​​Unilateral or bilateral fasciocutaneous flaps (V-Y advancement or rotation). Best for smaller sacral wounds, as they restrict one’s range of movement
• Myocutaneous gluteus maximus flaps. Often more distressing, this approach may interfere with gluteus maximus function, depending on the amount of muscle removed.
• Perforator-based flaps. Requires complex planning and dissection, with a mean complication rate of 19.6%.  

The bilobed flap, a type of transposition flap, has gained much attention because it provides a robust blood supply, has an abundance of subcutaneous tissue, and is simpler to perform. The procedure doesn’t require dissection through the gluteal maximus, thus helping preserve muscle fibers. Research also shows that patients are less likely to experience complications with the bilobed flap, especially compared to the other flap interventions. 

Sacral Wounds: A Common and Potentially Costly Injury

Known for being complex, sacral injuries require diligent and timely intervention for the best results. However, admittedly, this isn’t always easy for clinicians. Despite good intentions, heavy workloads and challenging demands often hinder sacral wound prevention and treatment. This not only results in poorer patient outcomes but also financial penalties, as Medicare may not reimburse for Stage 3 and Stage 4 hospital-acquired sacral wounds.  Practitioners and healthcare system leaders should assess how technology can help them prevent and manage sacral pressure injuries to avoid financial pitfalls and patient complications.