Non-Surgical Management and Debridement

A long-standing pressure injury management procedure is to excise diseased tissue in and around the wound to reduce the risk of wound progression and infection (Conway & Griffith 1956). Although the most common method of debridement is surgical, non-surgical debridement methods are also beneficial to the healing of pressure sores in people with SCI. For people with SCI, three types of non-surgical debridement methods have been studied that are also useful in regular pressure injury management: pulsatile lavage, maggot therapy and silicone moulding. Autolytic debridement using occlusive dressings is discussed in section 3.8 (Effectiveness of Dressings for Treatment of Pressure injuries Post SCI) above since dressings are used predominantly for routine care of pressure injuries and contraindicated in the presence of infection where debridement is often required.


Hydrotherapy is considered a form of mechanical debridement that is gentle and almost free of pain (Krasner 1990). However, hydrotherapy via daily whirlpool (Burke et al. 1998) can be costly in terms of personnel and facility resources and potentially can be a source of cross-contamination, especially when wounds are draining heavily (Maragakis et al. 2004). Conversely, Ho et al. (2012) found that pressurized saline hydrotherapy directed on the wound at the bedside is an effective form of hydrotherapy that is less resource-intensive and reduces the potential for cross-contamination. This form of pulsatile lavage therapy has been successfully used in intra-operative joint cleansing during orthopaedic surgery. As such, pulsatile lavage therapy can also be used for non-debridement-related cleansing of wounds at the bedside. The findings by Bogie et al. (2013) on cleansing and debridement for grade III and IV align with those by Ho et al. (2012) in that it is beneficial. In both studies, the wound dimensions decreased significantly in the pulsatile lavage group with a significantly faster rate of healing.

In the retrospective chart review undertaken by Bogie et al. (2013), adverse events were reported as a result of pulsatile lavage therapy used to promote pressure injury healing. One adverse event was reported Bogie et al. (2013) but none by Ho et al. (2012). However, an outbreak of multidrug-resistant Acinetobacter baumannii associated with pulsatile lavage wound treatment was reported at Johns Hopkins Hospital as a result of extensive environmental contamination during pulsatile lavage (Maragakis et al. 2004). In addition to multidrug-resistant Acinetobacter baumannii transmission between patients, and caregiver splash injuries, the authors postulated additional potential adverse events such as pain, bleeding, and autonomic dysreflexia with subsequent hypertensive crisis, myocardial infarction and cerebrovascular accident. The one adverse event reported for one of 28 patients in Bogie et al. (2013) was described as minor wound bleeding leading to interruption of treatment. Although environmental contamination could not be evaluated in the 2013 retrospective chart review after examination of the circumstances of the Johns Hopkins outbreak, Bogie et al. (2013) suggested that standard infection control practices would eliminate the potential for clinical safety concerns. These standard infection control practices include low-pressure pulsatile lavage, avoidance of common wound care treatment areas (e.g., bedside lavage is preferred), and wound area draping.

The beneficial effects of fly larvae have been known for centuries but the intentional use of fly larvae (maggot therapy) for the treatment of wounds was used extensively the 1930s and 1940s. It then fell out of favour when antimicrobials and other forms of debridement (including surgical) were introduced. Maggot therapy, using sterilized larvae of Phaenicia sericata species, was reintroduced to treat intractable wounds in the 1990s (Mumcuoglu et al. 1999; Sherman 1995, 2002). Maggot therapy is believed to work through three processes: debridement of necrotic tissue, disinfection of the wound and promotion of tissue growth (as cited by Sherman 2002). In a non-RCT, Sherman et al. (1995) reported that 8 of 20 patients diagnosed with stage III and IV pressure injuries were treated with maggot therapy. All eight patients underwent three weeks of conventional treatment, followed by maggot therapy. All necrotic wounds were debrided within one week of maggot treatment and wound healing was faster among those who had received maggot therapy than those who had not. Another maggot study that included only 42% SCI patients (Wang et al. 2010, SCIN/N=18/43) was included in this discussion given the dearth of studies on this intervention. Wang et al. (2010) examined maggot bio-debridement and reported that all SCI-related pressure injuries healed more quickly as evidenced by bacterial negativity, granulation (p<0.05), and no recurrence after an average follow-up of 3.5 months.

Effective mechanical and sharp debridement requires clear visualization of the necrotic tissue in order to be thorough and also to not cause additional damage by perforating healthy and/or regenerating tissue. Methylene blue diluted with hydrogen peroxide instilled in the wound can leave a visual guide for tissue excision. However, the wound cavity shape itself can be a barrier to effective visualization even if the necrotic tissue deeper in the cavity has been stained. To overcome this barrier, Erba et al. (2010), with a convenience sample of 10 paraplegic patients presenting with grade IV ischial ulcers, injected silicone to fill the ulcer cavity. Within six minutes, the silicone vulcanized into a tumor-like mass that was an imprint of the ulcer cavity. Under palpatory control, the imprint was then expelled and examined for completeness of excised necrotic tissue. Wheelchair mobilization at six weeks after the procedure, discharge after ten weeks and four consecutive 6-month follow-up assessments (including clinical assessment for potential adverse events (e.g., hematoma, infection, seroma) and photographic documentation), revealed no observation of early or late postoperative consequences including recurrence.


There is level 1 evidence (from one RCT: Ho et al. 2012) that underpins the use of pulsatile lavage hydrotherapy debridement for Stage III and IV pressure injuries secondary to SCI.

There is level 5 evidence (from one observational study: Bogie et al. 2013) that pulsatile lavage therapy, used in conjunction with standard infection control standards, is likely a safe debridement method for Stage III and IV pressure injuries in people with SCI.

There is level 2 evidence (from one prospective controlled trial and one observational study: Wang et al. 2010; Sherman et al. 1995) that supports the use of maggot therapy as an adjunctive therapy for pressure injury debridement post-SCI.

There is level 4 evidence (from one post-test study: Erba et al. 2010) that supports the use of silicone moulding as a radical en bloc debridement method for pyramidal-shaped grade IV pressure injury cavities in people with SCI.

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