Pressure area prevention and management

Questions about pressure areas have usually presented the candidates with pictures of decomposed sacral ulcers. The questions then ask the candidate to talk about risk factors, prevention and management. Previous such questions have included the following:

Generally, the best published resource for this is probably the 2015 article by Krupp and Monfre, which is a review and update on the then-current state of the art. Unfortunately, only the first two pages are available to the homeless and destitute- the rest you have to pay for. The CEC has a gross brochure about the classification of pressure injuries, which would probably be enough to answer the 20% section on that subject in Question 20 from the first paper of 2022. Official guidelines can also be offered, if anybody has time to explore them, specifically these offerings from the Australian Wound Care Association 

The time-poor exam candidate is warned against actually using these documents for revision, as even the abridged versions extend to 64 pages. It is hoped that the brief summary below is enough to answer the past paper questions on this topic.

Risk factors for pressure ulcers in ICU

Modifiable risk factors

  • Prolonged immobility
  • Use of neuromuscular junction blockers
  • Use of steroids
  • Hemodynamic instability preventing pressure area care
  • Incontinence with soiling
  • Low albumin
  • Poor nutrition
  • Oedema
  • Hypotension

Non-modifiable risk factors and comorbidities

  • Low BMI (no padding!)
  • Altered mental state
  • Peripheral vascular disease
  • Diabetes
  • Age over 60
  • Severe illness (APACHE II score over 13)

Associated disease states:

  • malignancy
  • stroke
  • pneumonia
  • sepsis
  • heart failure

Prevention of pressure ulcers in ICU

  • Use of a "skin integrity care bundle", for example the InSpPiRE protocol (Coyer et al, 2015)
  • Risk assessment and monitoring
  • Mobility
  • Minimise sedation and restraints to allow for self-repositioning
  • Management of incontinence (rectal pouches, IDC)
  • 2 hourly repositioning
  • Air mattress or specialised foam (evidence is not strong)
  • Adequate skin care (clean and dry)
  • Adequate nutrition
  • Control of modifiable risk factors (eg. hypotension, oedema, low albumin, steroids)

Classification of pressure injuries

In case the CEC chart is not sufficient, the discerning reader can be directed to the Australian Wound Management Association website, where the Pan Pacific Clinical Practice Guideline for the Prevention and Management of Pressure Injury contains their preferred staging system, which is the NPUAP/EPUAP system (2009). An international 2019 edition is also available, but you have to pay for it. The classification is a plain language guide to the assessment of these lesions on the basis of their depth, and is used both for documentation and to guide management.

  • Stage I: non-blanchable erythema
  • Stage II: partial thickness skin loss
  • Stage III: full thickness skin loss
  • Stage IV: full thickness tissue loss
  • Unstageable pressure injury: depth unknown
  • Suspected deep tissue injury: depth unknown

Management of pressure ulcers in the ICU

  • Engagement of a multidisciplinary wound care team
  • Debridement
  • Antibacterial (silver sulfadiazine) dressings
  • Frequent dressing changes
  • Exudate-absorbing dressings
  • Promote wound healing:
    • Adequate nutritional supplementation, particularly of protein (2g/kg/day)
    • Control of diabetes
    • Avoidance of corticosteroids
    • Optimisation of tissue perfusion
    • Avoidance of oedema

Negative pressure wound therapy systems (VAC)

Question 20 from the first paper of 2022 specifically asked how this wound management systems "potentially contribute to wound healing", presumably because there is also the potential that they don't. Weird wording aside, the exact question was to "list the mechanisms". After a cursory review of the evidence, it appears that these mechanisms are common to the effect of VAC (Vacuum-Assisted Closure) on all forms of deep wounds, not just pressure injuries. It is possible to say this because pressure injury literature that discusses their mechanisms tends to reference non-pressure-injury-specific reviews and experiments, such as this article by Panayi et al (2017)

So then, those mechanisms are:

  • Stabilisation of the wound environment is usually mentioned as a mechanism, or "alteration" of the wound environment, which is basically a way of saying that the VAC acts as a dressing. It moisturises the wound edges, maintains its temperature, minimises microorganism colonisation, prevents contamination, and removes all kinds of electrolytes and proteins that might produce an oedema-generating osmotic and oncotic effect. 
  • Removal of extracellular fluid: Oedema fluid in the extracellular space of the wound edge tissues inhibits perfusion, increases the distance between capillaries and compresses the microvasculature. The suction applied by the vacuum pump removes the oedema fluid, which improves wound edge perfusion. This fluid removal is a parallel mechanism to normal lymphatic drainage (or a replacement where this drainage is deficient).
  • Contraction of the wound,  sometimes referred to as "macrodeformation": the negative pressure dressing constantly applies pressure to the wound edges, slowly bringing them together. The negative pressure on the foam in the wound causes the pores in the foam to collapse, decreasing the size of the foam-occupied space and shrinking the wound. This counteracts the inherent tension of the skin, which constantly tends to stretch the wound open.
  • Microdeformation at the foam-wound interface refers to the mechanical strain exerted by the foam on the wound surface at a microscopic scale. All the little bubbles push and pull on the inner surface of the deep wound, and these forces end up being transmitted below the wound surface. How could this possibly be beneficial, you might ask? Well: the deformation and shear of the cytoskeleton of the cells and the extracellular matrix apparently upregulates the signalling cytokines that bring more fibroblasts and help to establish granulation tissue. 
  • Neurogenesis is promoted due to the release of neuropeptides, which are directly linked to the microdeformation mechanism. 
  • Angiogenesis results from microscopic regions of hypoperfusion which occur due to microdeformation. The result of this is the release of VEGF, which promotes the development of arterioles and capillaries
  • Modulation of inflammation: the effects of removing cytokines and other immune mediator molecules along with the oedema fluid are almost always antiinflammatory (as the cytokine milieu in chronic wounds is almost always proinflammatory)
  •  Stimulus for cellular proliferation: at a basic level most tissues undergo proliferation and division when exposed to mechanical stresses, so VAC suction tends to stimulate the growth of tissues other than granulation tissue

Complications of negative pressure wound therapy systems were also asked for in the same SAQ. These ones listed below come from reviews by Li & Yu (2014) and Fagerdahl et al (2014):

  • Seal failure and pump blockage (i.e. where the VAC doesn't vac)
  • Bleeding, eg. where the dressing is applied over vessels, or where dressing change disturbs haemostatic thrombi
  • Protein loss  because the fluid being sucked out is relatively protein-rich; in this fashion these patients lose more protein per area VACed than do burns patients
  • Fluid loss which is often an accountable volume, perhaps measured in litres per day
  • Infection, eg. introduced during dressing changes or as the result of a failed seal
  • Pain, both constant and acutely severe during dressing changes (which often require sedation)

Additionally, where these systems are being used for things other than pressure injuries, it is important to note that site-specific complications can arise, and of these the most disturbing is probably the formation of an enterocutaneous fistula when the VAC dressing is used to close an abdominal wound.

References

Keller, Paul B., et al. "Pressure ulcers in intensive care patients: a review of risks and prevention." Intensive care medicine 28.10 (2002): 1379-1388.

Cullum, N., et al. "Beds, mattresses and cushions for pressure sore prevention and treatment." The Cochrane Library (2000).

REULER, JAMES B., and THOMAS G. COONEY. "The pressure sore: pathophysiology and principles of management." Annals of Internal Medicine94.5 (1981): 661-666.

Health Quality Ontario. "Pressure Ulcer Prevention: An Evidence-Based Analysis." Ontario health technology assessment series 9.2 (2009): 1.

Stratton, Rebecca J., et al. "Enteral nutritional support in prevention and treatment of pressure ulcers: a systematic review and meta-analysis." Ageing research reviews 4.3 (2005): 422-450.

Henzel, M. Kristi, et al. "Pressure ulcer management and research priorities for patients with spinal cord injury: consensus opinion from SCI QUERI Expert Panel on Pressure Ulcer Research Implementation." J Rehabil Res Dev 48.3 (2011): xi-xxxii.

Theaker, C., et al. "Risk factors for pressure sores in the critically ill."Anaesthesia 55.3 (2000): 221-224

Krupp, Anna E., and Jill Monfre. "Pressure Ulcers in the ICU Patient: an Update on Prevention and Treatment." Current infectious disease reports 17.3 (2015): 1-6.

Coyer, Fiona, et al. "Reducing Pressure Injuries in Critically Ill Patients by Using a Patient Skin Integrity Care Bundle (Inspire)." American Journal of Critical Care 24.3 (2015): 199-209.

Panayi, Adriana C., Tripp Leavitt, and Dennis P. Orgill. "Evidence based review of negative pressure wound therapy." World J Dermatology 6.1 (2017).

Li, Zonghuan, and Aixi Yu. "Complications of negative pressure wound therapy: a mini review." Wound Repair and Regeneration 22.4 (2014): 457-461.

Fagerdahl, Ann-Mari, et al. "Risk factors for unsuccessful treatment and complications with negative pressure wound therapy." Wounds 24.6 (2012): 168.