Dr. Jenny Alderden and colleagues at the University of Utah and at Duke have just published the results of a study evaluating the risk factors for superficial (Stage 2) pressure injuries vs. severe (Stage 4 and Deep Tissue Injury – DTI) in critical care patients. Despite the intense focus on pressure injury prevention, the endless clinician blaming, and the “get to zero” campaigns, severe pressure injuries continue to occur at a predictable rate, particularly among critical care patients. There’s a reason. We aren’t targeting the right factors for prevention, if indeed it is always possible.
For many years, ICU nurses and critical care physicians have observed the relationship between hypotension and DTI. We postulated that if severe pressure injuries were related to hypotension, we’d be more likely to see hypotension among the ICU patients who got severe pressure injuries than among those who had superficial lesions. Additionally, if the angiosome concept is valid, we would expect to see more DTIs that are NOT over bony areas (e.g. the buttocks), because these tissues are “downstream” from the vascular infarction that causes them. This small study suggests our hypothesis was correct.
Data was evaluated on 206 critical care patients (n=146 stage 2; n=60 DTI), and the results indicate that Stage 2 ulcers are more likely to be over a bony prominence and the patients who got them were less likely to have been hypotensive (P<.001). Patients with DTIs were more likely to have had a diastolic blood pressure <50 mmHg (P<.001) or receive an epinephrine infusion (P=.008). DTIs were also more likely to occur on the fleshy parts of the body (e.g. buttocks) – an anatomical reality that has always called into question the “direct compression of capillaries” theory for their development.
This matters for a lot of reasons. The biggest one is that I do not know of any “pressure injury prevention protocols” that attempt to mitigate risk factors like hypotension. It matters because if there are hemodynamic factors that control whether a patient gets a DTI, and we can’t control those factors, then the DTI is medically unpreventable. We ought to be able to define medical unpreventability of DTIs in objective terms (e.g. minimum diastolic pressure). We might be able to improve mitigation strategies and help prevent a few of them; and when we can’t, we could avoid hospitals paying millions of dollars in lawsuits over unpreventable problems.
It’s time for a new paradigm of severe pressure injuries. There’s an epidemic of them in ICUs right now due to Covid. If the Angiosomal infarction/diastolic hypotension theory holds water, they are more likely to occur in ventilated patients on high PEEP (positive end expiratory pressure).
- Here’s Dr. Alderden’s online article:
Alderden J, Amoafo L, Zhang Y, Fife C, Yap D, Yap T
Comparing Risk Profiles in Critical Care Patients With Stage 2 and Deep Tissue Pressure Injuries: Exploratory Retrospective Cohort Study
JMIR Dermatol 2021;4(2):e29757 - Here’s a link to a case we published that further discusses this mechanism:
Yap TL, Alderden J, Lewis M, Taylor K, Fife CE.
Angiosomal Vascular Occlusions, Deep-Tissue Pressure Injuries, and Competing Theories: A Case Report
Adv Skin Wound Care. 34(3):157-164, 2021.
