Hypoperfusion Major Contributor to Deep Tissue Injury in ICUs
Holly Kirkland-Kyhn PhD, FNP, GNP, CWCNOleg Teleten, MS, RN, CWCNUC Davis Medical Center
Synopsis: In this population, DTI risk was significantly associated with DBP < 49 mmHg, hemodialysis, or prolonged surgery. The Braden Score was not associated with DTI occurrence rate.
Background: Deep tissue injuries (DTI) often develop in critically ill patients in the intensive care units (ICU), presenting as a “purple or maroon localized area of discolored intact skin or blood-filled blisters, due to damage of underlying soft tissue from pressure and/or shear.”1 These skin changes that occur with DTI most often evolve into stage 3, 4 and unstageable pressure injuries 2,3 known as- hospital acquired pressure injuries (HAPI) which can develop in all health care settings (acute hospitals, long term care, skilled nursing facilities, and home) despite best practices for prevention.1 The incidence of HAPI in ICUs in the United States has been reported as ranging from 14 percent to 42 percent.4
Both DTI and pressure injuries are localized areas of tissue necrosis that develop most frequently over a bony prominence, when soft tissue is compressed by an external surface over a period of time.1 The consequences of pressure induced injury to skin ranges from non-blanchable erythema of the skin (stage 1) to full thickness deep injuries involving muscle and bone (osteomyelitis) in stage 4 pressure injuries.1 The National Pressure Ulcer Advisory Panel suggests that applied pressure, shear, friction, and moisture contribute to the development of a pressure injury.1 However, other patient related factors may provide a greater contribution to the development of DTI that evolve into stage 3,4, or unstageable pressure injuries, especially in those patients who have interventions implemented that were designed to prevent the modifiable risk factors of pressure, shear, friction, and moisture. The National Pressure Ulcer Advisory Panel published a white paper in 2009, suggesting that occurrences of HAPIs, despite all prevention interventions in critically ill patients, may not be preventable.1
Previous identified and modifiable risk factors included in the Braden Risk Assessment Scale include a) interface pressure, b) shearing forces, c) friction, moisture, d) and nutrition.1 Although other scales and tools have been developed for risk assessment, the Braden scale has been most commonly used worldwide.5 The Braden scale has six constructs in the areas of sensory perception, mobility, activity, moisture, friction/shear, and nutrition. These constructs are assigned a score on a scale of 1- 4 with higher scores showing a lower risk of the development of HAPI. Nurses hold the responsibility to perform the HAPI risk assessment at regular pre-defined intervals according to the institutional policy. However, the Braden scale was developed for use in long term care facilities and has been adopted by the acute care setting without further validation for acute care patient risk assessment.6
Methods: We collected possible risk data on patients who developed DTI that evolved into stage 3, 4, and HAPI over 5 years. The specific aim was to perform a comparative risk analysis of ICU patients that develop DTIs, to ICU patients that didn’t develop DTIs. We analyzed the patient related risk data to quantify the most significant factors that contribute to the development of DTIs.
Ten variables were identified as risk factors for the development of DTIs. The variable data was collected for patients with sacral DTIs (n=47) that evolved into stage 3, 4, or unstagable HAPI. The general ICU patient data was collected for comparison (n=72).
The summary and averages for variables are found in table 1.
General ICU pts
General ICU pts
LOS=length of stay, SBP=systolic blood pressure, DBP=diastolic blood pressure, Hct=hematocrit, BMI=body mass index.
The analysis of the data was compared to determine specific parameters of patient related risk factors in patients who developed DTIs. A backwards regression was then preformed to find the most significant risk factors and to quantify those risk factors (pending publication in peer review journal).
Results: We found a decrease in perfusion (hypotension) as the most significant contributor to DTI. Patients with diastolic blood pressure below 49mmHg had 10 times greater chance of developing a DTI. Patients on dialysis had 4 times greater chance of developing a DTI. Surgical patients were at higher risk of DTI; for every 1 hour in surgery the likelihood of a DTI increased by 20 percent. We did not find any significant difference in the Braden Score between those patients that developed DTI and those patients who did not develop DTI. In addition, all Braden risk related interventions were implemented on all patients at the time of admission.
Conclusion: This study advances the knowledge of the patient related risk factors that contribute to the development of sacral DTIs that evolve into stage 3, 4, and unstageable HAPIs. The findings from this study suggest that the Braden risk score does not predict risk of HAPI development in ICU patients. Perhaps the National Pressure Ulcer Advisory Panel should consider changing the terminology of DTIs in order to represent deep tissue ischemia that evolves into stage 3, 4, or unstable pressure injuries.
NPUAP, ed National Pressure Ulcer Advisory Panel, Europian Pressure Ulcer Advisory Panel and Pan Pacific Pressure Injury Alliance. Perth, Australia: Cambridge Media; 2014. Haesler E, ed. Prevention and Treatment of Pressure Ulcers: Clinical Practice Guideline.
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This 67 year old male was admitted for an emergent Aortic aneurysm repair. He had two cardiac arrests during the 15 hour surgery. Picture 1 depicts a sacral DTI; the photo was taken while the patient was standing in the ICU, 6 hours after returning from the OR.
Picture 2 is the same sacral wound 18 days later and was then an unstageable HAPI. It is now 6 months after this HAPI occurred and this wound has not closed completely despite expert treatment.