Incontinence causes pressure ulcers…but does it??

Seriously though…how can incontinence cause a pressure injury (PI) /ulcer??
If you ‘micro-think’ about this you will see that it makes no sense whatsoever!When a patient is incontinent of urine and / or faeces the wettest, soggiest area is the perineum, vulva, penis and testicles….isn’t it?…not the sacrum and certainly not the heels!
Sure the sacrum might get wet and pooey.. BUT … it is not where the greatest concentration of gloop is found in the incontinentpatient; the sacrum might get damp…but so might the symphysis pubis…both are equidistant from the perineum but I have never seen a Stage 4 PI over the symphsis pubis or abdomen.
Yet people still say that incontinence can cause a PI. If incontinence was a risk factor we’d see stacks of Stage 4 perineal PI – more so than on the sacrum…….makes sense?? But in > 20 years of looking at pressure ulcers I have never, ever, seen a perineal pressure ulcer!!!   Patients get excoriated…sure… in the same way that babies get nappy rash…but neither babies nor toddlers have huge Stage 4 PI inside their nappies… do they now?!
Many PI risk assessment tools still include incontinence when assessing patients for risk of PI??
I need to hear a good reason why!! Does anyone have any idea why?
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9 Responses to “Incontinence causes pressure ulcers…but does it??”
  1. Jo Otero says:

    Good morning Kate

    An excellent point & one perhaps not really considered by those who have actually developed the assessment tools nor clinicians who are lead to believe because of this that they are related.

    Neglect in pressure prevention strategies & flagging the at risk patient has always been the the findings of investigations I have conducted in this area.

    Absolutely it places the patient at further risk from a contamination point of view but again generally failure to adequately manage the incontinent patient may lead to this.

    I did have a patient who had developed a stage 4 pressure ulcer sacrally extending to the anal wall who developed faecal incontinence because of the trauma to area but again this was post Surgery neglect (for a fractured neck of femur).

    Whilst the two were not directly related managing the two issues was a priority & pleased to say that with appropriate wound management, pressure prevention & continence re-established, this patient progressed well eventually.



  2. Jonathan Hastings says:

    I just graduated so I’m not pretending my opinion matches your 20 years in wound care, but the fact that incontinence does not initiate pressure sores seems irrelevant to me. Pressure sores (and by this i mean Stage I … erythema with skin intact) happen (occasionally) even with good care and these areas are a breach in the skin’s defense. Combine this breach with a skin irritant like urine and the moisture and bacteria in feces and you’re welcoming infection and consequent progression of the wound. So whether a soiled diaper causes pressure sores or not, I think incontinence remains a “risk factor”–NOT OF CAUSING a PI but of exacerbating it. And I can’t think that small distinction warrants removal of incontinence from existing protocols.

    That said, I think the baby example is a great comparison and it illustrates your point well. Babies/Toddlers as you said don’t get stage IV ulcers despite incontinence because: 1) their skeletons weigh less (less pressure); 2) they are more mobile than the majority of bedridden adults (less stasis); and 3) they have a thicker fat layer (further distributing the already lessened pressure) and 4) they probably have better circulation than most elderly and/or diabetic patients, despite underdeveloped immunity systems. Still even though dirty diapers don’t cause PI’s would you really maintain that they play no part in their progression? And if they play even the smallest part in any wounds progression why remove it from the list of risk factors?

  3. Jo Otero says:

    Hi Jonathan
    It is great that you have expressed your views on this matter so well.
    I am a firm believer that it’s not about the years of experience that matters to your practice but rather what you do with the knowledge you have gained.
    I commend you for questioning this whilst your learning is still fresh & for taking the time to reflect on this.

    Whilst I do support Kate on this specific clinical point I can also see where you are coming from.
    It is a risk factor to be considered in assessing & implementing nursing care plans even though it is not the direct cause pressure related ulcers.

    It’s a worthy flag/alert for nurses to consider how potential contamination may jeopardize further already compromised skin integrity.
    Managing incontinence faecal or urine is critical for patients already at risk of developing sacral decubitus ulcers.
    So with this in mind I think it is important that continence is considered in the overall patient assessment but whether it belongs on the pressure risk assessment or other general admission/assessment form is open to debate.

  4. Martyn Butcher says:

    Hi guys,

    This is interesting and Kate’s comments support the view I have had for a number of years. If incontinence in itself was a determining feature in pressure ulcer development we’d see a much greater incidence of damage than is currently recorded, and in a wider patient population (including neonates). The whole moisture debate doesn’t stack-up on its own either; if this were the case cross-channel swimmers and the likes of David Walliams (a UK comedian who recently undertook a charity swim 140 miles down the Thames to London) would be in a sorry state when they left the water!

    I think we need to dig deeper.

    Moisture undoubtedly has an effect on the mechanisms of friction and shear transmission in epithelial and underlying tissues; we see this in healthy individuals as well as compromised patients. Maternity-based pressure damage to the pelvic region appears to be precipitated by the interplay of moisture (amniotic fluid) insensibility (particularly from epidural anaesthetic) and high levels of shear (through poor positioning).

    It makes sense that once compromised, the epidermal tissues exposed to faecal material are open to enzymatic attack. However I have doubts that the majority of stools have sufficient enzymatic load to cause significant damage (once again, if this was the case we’d see a much higher incidence of the problem). From my experience, the group most frequently plagued with this problem are those patients with explosive diarrhoea (eg Norovirus) and patients exposed to poor care practices (frequent use of soap, abrasive cleansing cloths, poor manual handling techniques and poor patient positioning).

    The issue therefore doesn’t seem to be incontinence, but what is done to manage it and how the presence of moisture (and the resultant changes to the epidermal structure) affects the bodies natural defence to external stress.

    Why we keep incontinence in pressure ulcer risk assessment is in my mind simply because it is easier to use “labels” rather than thinking things through to their logical conclusion. For many clinicians, a simple “tick-box” yes/no is deemed as more beneficial in assessing risk, and therefore more likely to be undertaken and documented than grey areas of practice and research. for instance, it is interesting that shear is recognised as a significant factor in pressure ulcer development (the US even had a working party looking at it for several years) and yet very few pressure ulcer risk assessment tools adequately take this mechanism into account, possibly because shear is so difficult to measure and quantify.


  5. Jo Otero says:

    Excellent Points Martyn
    As I suggested also it is about how you manage any bodily fluids that pose a contamination risk.
    I agree nurses do have a tendency to like the tick style of documentation as a quick form of perhaps demonstrating that they have a least gone through the motions of what is legally required.
    My concern however with these designs is that it may not always encourage more action oriented, reflective & lateral thinking as demonstrated in many adverse outcomes such as the development of decubitus ulcers.

    The tendency to not review & visually reassess patients once the boxes are ticked is generally why patients suffer the most. (Add to this often placed because of bed pressures in wards not familiar with their conditions or set up with resources ready to use)

    Given that there are the multifactorial contributors to these adverse outcomes we must encourage nurses to not only use the tools to assess but to work collaboratively in evaluating regularly the risks.
    Compromised Weight, Nutritional status, Skin Integrity/conditions oedema, Age related, mobility status, medications, Neurological deficits, surgery/sedation, smoking, vascular disorders, dehydration, endocrine disorders, continence disorders etc must be considered in the equation.

    I suggest that the lack of recognition and acceptance by clinicians that a cascade of events & the omission in the steps required (failure to act on multifactorial conditions) is the fundamental cause of any adverse outcome.

    Shear is difficult to measure but perhaps mobility & the ability to reposition self or not holds the clue. (This was certainly a consistent factor with vascular patients unilateral & bilateral amputees).

  6. Martyn Butcher says:

    I agree Jo. But isn’t it sad that many clinicians are more concerned with ensuring they meet the legal requirements of “tick-box form filling” than the clinical and humanitarian issues of assessing and delivering good (and fundamental) care?

    Just to go back and expand on some of my earlier comments….

    Although relatively rare, pressure ulceration in the perineal region can occur.

    By far the commonest are those caused by devices such as urinary catheters. These tend to occur in female patients where the patient effectively sits on the device causing localised high areas of pressure. These may be seen as ulceration in the perineum and/or the labial structures. Although this can occur in male patients, the differing anatomy means such damage may be seen on the penis/scrotum/glans penis and is less likely to be seen in the actual perineum. These can result in small, discreet, but deep (grade 3) damage. This is obviously avoided by the correct positioning of such devices.

    Another group seen are among patients who are forced to sit for prolonged periods due to medical conditions such as paraplegia. Whether these are truly perineal damage or extensions of deep ischial damage is open to interpretation. I certainly have seen individuals without obvious ischial damage (ie no sign of palpable induration in the overlying ischial area) who present with deep (grade 3-4) damage, though this is a rare occurrence and one is left to ponder on whether such damage is influenced by poor body posture or the use (or mis-use) of positioning aids, particularly cushions and seating aids with anterior pommels. In my experience these form of pressure injuries are more likely to be seen in patients cared for by informal carers in home environments where the carer may not be aware of the risks of incorrectly using rolled-up incontinence products, bedding or foam wedges etc.

    Finally, some male patients present with grade 2-3 damage to the scrotum. These tend to be more common in individuals who may be considered to be somewhat “well endowed” particularly with a large, flaccid scrotum. From my experience these may be easily overlooked (particularly by female nurses – no offence intended) and simply referred to as “severe diaper rash”. However if you look into how these arise, although moisture from sweat and/or urinary incontinence is an undoubted feature, friction shear and pressure has a part to play in their development. Once again, many of these gents effectively sit on the area affected. This is more likely to occur if upright positioning when sitting is difficult to maintain. The patient with poor core stability often slouches and the pelvis is forced forward by the effects of gravity. The scotum in such individuals is therefore dragged under the buttocks. Abrasions quickly develop on the moist epidermal tissue which can lead to ulceration unless quickly identified and corrective action is initiated. Thankfully, the vascular nature of the scrotum means that healing of these ulcers is usually aproblematic provided repeated damage and secondary infection is avoided. This is just as well as trying to apply dressing to this area is pretty tricky!

    I think the big issue is whether moisture causes pressure damage or whether it is a factor in pressure ulcer formation. My view is that pressure damage is caused by pressure, shear and friction. These mechanisms result in changes within the macro and micro vascularisation of the skin and other underlying soft tissues. Moisture simply acts as a mechanism which alters the body’s natural defence mechanism; it provides an environment in which shear forces and friction co-efficients are increased. It also changes the ability of the stratum corneum to withstand these forces by rehydrating skin squames.

    Catheter-related pressure damage is not significantly associated with incontinence as the urinary flow is already diverted away from the area. The issue here is how the relatively hard surface of the catheter induces capillary occlusion when the patient sits on it.

    Urine and faeces (due to their water content) have similar effects, but can also increase bacterial bioburden, increase the presence of enzymatic agents (therefore increasing the risk of protein degradation) and change the natural pH balance (and therefore its endogenous protective ability) of the skin.

    As such, is incontinence any more of a risk than say washing the skin regularly with aggressive soaps? I think the difference is that:
    • incontinence is a common phenomenon
    • many incontinent individuals have other co-morbidities which increase PU risk
    • incontinence will precipitate the use of other interventions (such as cleansing) which may also have negative effects on skin health
    • the effects of urine and faeces on the skin may have prolonged and exponential effects on factors such as skin pH

    Personally, I think it’s very easy to get drawn into the “what makes risk-factors a risk” debate. For instance, does patient sex really make a difference? Sure, there are some hormonal variance that might impact on tissue repair etc, but many of our elderly ladies have a similar androgen profile to our old guys? If it’s about fat distribution and muscle mass then what about the influence of obesity and our more sedentary modern lifestyle – are young, fat, computer geeks at more risk than slim, fit, mobile, female 60-somethings?? In these days when everyone is spouting the Gospel of “research-based care” there appears to be very little research behind the relative values placed on individual risk factors within risk assessment tools. I have read some good work coming from our Japanese colleagues, however even here most of this relates to extrapolations of lab-based findings.

    One thing that has been raised is why don’t we see complete destruction (grade 4 damage) of the perineum (ie scotum, testes, vulva) when patients develop perineal pressure damage?

    I think the issue of lack of total destruction of structures within the perineum is one which relates to the intervention that is undertaken and the specific vascularisation of this anatomical area. The blood supply of the testes is derived from the testicular artery, pampiniform plexus and to a lesser degree the fascia. This is highly efficient, (unlike the blood supply to most of the skin) and is independent to the dermal plexus. Unless the testes are themselves subjected to ischaemic insult they are unlikely to necrose (unless there is secondary bacterial infection). Therefore these remain intact despite the damage made to other, less vascularised structures (ie the scrotal skin). The limitation in depth and therefore severity of pressure-related vulval damage is slightly more difficult to explain, however once again we have structures that are naturally endowed with a great blood supply therefore it is unlikely that complete arterial occlusion is easy to achieve.

    As stated above, we have to remember that pressure ulcers are predominantly the sequelae of an ischaemic event – even in more commonly occurring pressure damage (such as sacral or heel damage) the ulcer is caused by degradation of ischaemic tissue. True pressure ulcer “extension” should therefore only relate to further ischaemic insult in surrounding tissue, ie further shear and pressure (however, it could be argued that the proliferation of bacterial bioburden within the wound will cause ischaemia from competition for available oxygen and the release of toxins which interfere with microvascularisation).

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  9. john says:

    It is important to clarify that incontinence does not cause pressure ulcers, and it is important to point out that managing incontinence through proper attention to the patient is better for helping a patient to heal these ulcers than a foley or a rectal tube. The reason I say this is because patients are needlessly subjected to these tubes to help prevent wounds and help them heal. These interventions are not without a price tag of increased morbidity for our patients.

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