Early Skin Temperature Characteristics of the Kennedy Lesion (Kennedy Terminal Ulcer)

Recommendation 2.4 in the 2019 EPUAP/NPIAP/PPPIA International Guideline on the Prevention and Treatment of Pressure Ulcers/Injuries is to “Assess temperature of skin and soft tissue.”¹ The majority of studies using objective measures of temperature in skin injuries have been primarily limited to diabetic ulcers^2,3 and pressure ulcers.^4-11 The updated term Pressure Injuries (PIs) (vs. pressure ulcers) will be used in this paper. Studies examining PIs consistently report that within areas of intact discolored skin, temperature changes over areas of inflammation or hyperemia are warmer than surrounding skin and temperature changes over areas of ischemia are cooler than surrounding skin.^4-11 Studies describing skin temperature characteristics of other skin injuries such as the Kennedy Lesion (KL) are needed.

The Kennedy Lesion (also termed Kennedy Terminal Ulcer/KTU) was described by Karen Kennedy in 1989 in a population of intermediate care facility residents.¹² Over the last decades other authors have likewise described the observable characteristics of KLs as intact skin discoloration that occur suddenly, primarily in the sacrococcygeal area, that can be red, yellow, purple, pink, and black in color, are generally in the shape of a butterfly, pear, or horseshoe with irregular borders,   and are generally associated with death within weeks or months.^13-18 In 2017 the Center for Medicare Services published these observable characteristics to help surveyors in long term care facilities distinguish between pressure ulcers and the KTU or end-of-life ulcers.¹⁹ While historically known as the KTU,¹³ the term Kennedy Lesion (KL) will be used in this paper to acknowledge that with the increased use of advanced technologies to sustain lives, the terms “terminal” or “end-of-life” may not always apply.¹⁴ Characterizing early skin temperature of the KL is a valuable next step toward further defining the KL.

Concerning selecting an objective method for measuring the temperature of skin injury, it is of note that an implementation consideration under the 2019 EPUAP/NPIAP/PPPIA International Guideline recommendation is to “Consider using an infrared thermographic imaging device or infrared thermometer as an adjunct to clinical examination of the skin.”¹ Long-Wave Infrared Thermography (LWIT) is based on the physiologic principle that body heat is produced by cellular metabolism and is distributed by blood to the rest of the body, and particularly to the overlying skin, for loss by radiation and convection.  A thermographic sensor captures the skin’s long-wave, infrared thermal radiation and converts it into an electrical signal corresponding to a given temperature.²⁰ Contemporary LWIT systems include digital and infrared cameras that provide visual and thermal images, respectively, as well as sophisticated software for analysis of skin injury size and temperature. Several studies conducted over the last decade confirm that LWIT is an objective, reliable, valid and easy-to-use method to assess skin temperature when healthcare professionals are trained in its use.^20-24 

The purpose of this study was to describe early skin temperature changes in KLs using LWIT. The major finding from this study was that there were no early (ie, within 24 hours of first observed discoloration) skin temperature differences between KLs and surrounding skin. Larger studies are needed to confirm and expand the scope of this small study; however, these findings may indicate the KL has a unique early skin temperature signature. The findings of this study also support the recommendation of the 2019 EPUAP/NPIAP/PPPIA International Guideline to routinely incorporate thermography in assessment of skin injury. 

In a retrospective case study design, KLs were identified from chart review in 10 patients from 3 acute care hospitals of similar size in the midwest and northeast United States. In the study hospitals, visible and thermographic skin assessments were performed on admission. In addition, if new areas of skin discoloration became visible, wound care nurses were consulted and thermographic data was obtained within 24 hours of the new discoloration. Thus, for this study, “early” skin temperature change was defined as occurring within 24 hours of a newly identified area of discoloration. Inclusion criteria were adult patients admitted without skin discoloration and normal skin temperatures who developed new skin discoloration during hospitalization. Patients were excluded if a KL was present at the time of admission. The diagnosis of KL was confirmed by a certified wound care clinician according to standard hospital criteria. All patients were in the intensive care unit at the time of data collection. IRB approval was obtained from each of the hospitals. All patient information was de-identified. Patient permission and approval to image the skin was obtained from each facility’s general consent to treat.
 
Demographic data was collected including age, admitting diagnosis, location prior to admission, general skin color, comorbidities, weight, Body Mass Index (BMI), first discoloration in relation to the start of a vasopressor, and the Braden risk score.  Laboratory data including White Blood Cell Count (WBC), Red Blood Cell Count (RBC), Hemoglobin (Hgb), Hematocrit (Hct), Glucose, Blood Urea Nitrogen (BUN), Creatinine, Calcium, Albumin, Platelets, Prothrombin Time (PT), and Partial Thromboplastin Time (PTT) were collected when available.  

As noted earlier, routine skin protocols in the study hospitals were in place prior to this study.  As part of the protocols, skin temperature assessments using LWIT were done within 24 hours of newly identified areas of skin discoloration. Thermal skin assessments were performed using a commercially available, FDA-approved, long-wave infrared thermography (LWIT) imaging system (Scout; WoundVision LLC).  Wound care teams in each hospital were trained by the manufacturer. Standard methods were used to obtain images (Figure 1). Briefly, after the skin was exposed to acclimate the tissue to the ambient temperature, the hand-held device was positioned at a 90-degree angle to the skin surface and a standardized 18 inches from the area of interest (standardized distance is achieved when two red dots from the range-finding laser merge). The image was then captured by engaging a trigger on the device.  Each LWIT image yields an image pair consisting of a digital (visual) image and a mirror thermal image. 

The thermography imaging software produces wound size and temperature measurements from the captured images (Figure 1). An outline of the entire perimeter of the discolored area was made, and the length (cm) x width (cm), area (cm²), perimeter (cm), and perimeter area (cm²) were calculated. The outline of the discolored area from the digital image was overlaid onto the thermal image.  The wound (entire discolored area) mean temperature, minimum temperature, maximum temperature, and the gradient between the minimum and maximum temperatures (°C) were then determined. The Scout software calculates a Relative Temperature Differential (RTD) between the discolored area and a selected control point. The control point was defined as an area of unaffected intact tissue proximal to the area of discoloration which was affected by similar environment and intrinsic host factors as the discolored area. 

The image software provides both a color and number scale to assist operators easily identify thermal patterns. For example, a red thermal color observed on the thermal image corresponds to the red square and a +5 RTD on the color and number scales, respectively. Based on previous research, for this study abnormal skin temperature is defined as a RTD of > +1.2°C or < -1.2°C (Cai 2021, Farid K 2012, Cox J 2016, Sae-Sia W 2005). 

Additional wound data was collected describing the number of days from admission to the first indication of skin discoloration and the number of days from the first indication of skin discoloration to death. Furthermore, data was also collected on the location and observable characteristics of the KL, specifically, if the skin was intact or open, if open to what depth, and the color, shape, and edge characteristics. Descriptive data was analyzed and expressed as mean +/- standard deviation or frequencies, as appropriate.

Patient demographics. 
Demographic information was not available for all patients.  In this and the following sections, the number of patients for which data was obtained is noted. Table 1 describes patient demographics and wound characteristics not measured by imaging. The average age of patients was 61.5 +/- 18.6 years (N=6); the majority of these patients (5 of 6) were over 60 years of age. Only 2 of 5 were overweight; none were obese (mean BMI 22.58 +/- 3.9 kg/m²). All patients (6 of 6) were at home prior to hospitalization and there was no discernable pattern in admitting diagnosis or comorbidities among patients. The majority of patients (4 of 6) were receiving vasopressors at the time of the first visible sign of skin discoloration. The average Braden Score was 13 (6 scores across 4 patients). 

The majority of patients had normal WBC values (4 of 6) and 2 of 6 had significantly elevated WBC values. Only one patient had a significantly high glucose value. Hemoglobin, hematocrit, and albumin values were abnormally low (5 of 5). Platelet values were low in half (3 of 6) of the patients. Partial thromboplastin time was abnormally high in 2 of 4 patients.

Observable characteristics of Kennedy Lesions. 
Observable KL characteristics are presented in Table 2. With respect to the timing of the appearance of early skin discoloration, 6 of 9 (67%) patients developed the first skin discoloration less than 10 days after admission, 1 (11%) within approximately 2 weeks, and 2 (22%) developed skin discoloration at approximately a month after admission. The majority of patients (5 of 7, 71%) expired within two weeks after the first sign of skin discoloration. One patient lived for approximately a month and another for a year after developing skin discoloration. One hundred percent of KLs were in the sacrococcygeal area; the buttock was involved in one patient. The majority (90%) of KLs had a bilateral distribution and 80% had intact skin at onset. The color of KLs was variegated in all patients; the predominant colors were purple, pink, red and black. Eighty percent of KLs presented as butterfly shaped, and all had irregular edges.  

Temperature characteristics of Kennedy Lesions. 
A summary of KL size and temperature characteristics is presented in Table 3. Average wound area based on conventional length and width measurements was larger (141.8 +/- 86.1 cm²) than the wound area based on the perimeter measurement (93.4 +/- 45.9 cm²). The range of Relative Temperature Differentials (RTD) of KLs was -1.0 °C to + 0.5 °C. The mean of all 10 RTDs was 0.4 °C +/- 0.5°C, values within the same range as control skin temperatures.

Figures 2 and 3 are visual and thermal images of normal skin and a pending PI, respectively, presented for comparison to the KL.  In Figure 2, normal skin temperature appears as light blue, green and yellow (sprinkles) on the thermal color scale. 

Figure 3 is an example of the thermal temperature change of a pending PI. The skin was blanchable and presented as a butterfly shape and red in color. The RTD of the discolored area was +2.5 °C (abnormally warm/inflamed) and appeared as an orange color on the thermal color scale.

Figures 4-6 are visual and thermal images of KLs obtained within 24 hours of the first sign of discoloration. All images were of the sacrococcygeal area. In all 10 patients, RTDs were within the normal range; that is, the temperature of the KLs were not different than the temperature of the reference skin points. This translated to green, yellow and light blue on the thermal color scale.

In the current study we used LWIT to objectively measure early skin temperature characteristics of KLs; early temperature characteristics were defined as those occurring within 24 hours of newly identified discoloration. The novel finding from this small sample of ICU patients demonstrated that early skin temperatures of visibly discolored KLs do not differ from surrounding, unaffected tissue. While other studies examining skin temperatures of KLs have not been reported, our findings confirm the findings from recent NPIAP poster and podium presentations which described the lack of skin temperature change in several patients with KLs.^23,25,26 

In addition to the early temperature findings of the KL, the current study confirms previous observations that KLs present as large, intact skin with purple/purple-red lesion and are butterfly or pear shaped. In many cases, death occurred within days or weeks after the discoloration was first observed. While all KLs in this study occurred in the sacrococcygeal area, KLs can occur in other areas such as the heel and lower legs.^12,19,27,28 

The observable characteristics of KLs are similar to the Trombley Brennan Terminal Tissue Injury (TB-TTI) with respect to color and sudden onset. Characteristics of the TB-TTI not always seen in the KL are a shorter time to death after first discoloration and skin that remains intact. Of note is that all patients in the TB-TTI studies were receiving palliative care.  Also, in contrast to the KL, more linear discoloration patterns in the extremities are observed in TB-TTI (vs. large discoloration patterns in the sacrococcygeal area in KLs).^29,30 At the time of this writing, skin temperature characteristics of the TB-TTI have not been reported. 

The lack of abnormal early skin temperature findings in the KL contrast with the majority of studies examining skin temperature changes of PIs, which show either a significant decrease or increase in skin temperatures compared to control skin temperature.^4-11 Direct comparisons of skin temperature findings in PIs to findings from this study are difficult, as the methods used to measure temperature often differ and the timing of temperature measurements relative to the first sign of skin discoloration are often unknown. Nonetheless, previous studies examining skin temperature in PIs can be used as examples for studying skin temperatures in other forms of skin injuries; selected studies are described below.  

Sprigle et al (2001) measured skin temperatures using adhesive temperature strips on 80 ulcers of outpatient and inpatients presenting with pressure-induced erythema (Stage I PU). They found that 63% of pressure ulcers were significantly warmer (inflamed), 23% were cooler (ischemic), and 15% were the same as control skin temperature (no explanation of this finding was provided). Using a handheld infrared thermographic device, Farid et al (2012) measured temperatures of pressure related intact discolored areas of skin (PRIDAS) in 85 hospitalized patients to predict PRIDAS progression to necrosis. Mean PRIDAS temperatures were either significantly warmer (greater than 1.2°C) or cooler (less than 1.2°C) than control skin temperature. Temperature measurement relative to the onset of skin discoloration was not indicated in either of these studies. Cai et al (2021) used mobile phone-based infrared thermography in 82 hospitalized patients before sacral skin discoloration was observed and found that skin was significantly cooler than control skin in all cases. Using a taped thermocouple skin probe, Sae-Sai et al (2005) found that before skin discoloration was observed, sacral skin temperatures of nine neurologically impaired hospitalized patients were significantly warmer than control skin temperatures. Finally, a recent study by Simman and Angel (2022) used LWIT to assess skin temperature in sacral and heel areas in 70 hospitalized patients on admission and at 3, 7, 14 and 25 days. In 4 PUs that developed they found an increase (N =3) or decrease in relative skin temperature (N = 1) before the PU was visibly discernable. Findings from these studies indicate that there may indeed be differences between skin temperature of PIs and early skin temperature of KLs. Larger studies are needed to confirm these differences. As a result of these studies, there is consensus that in pressure injuries, compared to unaffected skin, a decrease in skin temperature reflects tissue ischemia resulting from decreased or absence of blood flow and an increase in skin temperature reflects tissue inflammation as a result of ischemia-reperfusion or progression to necrosis.¹ 

In a recent concept review, Levine describes the KTU (KL) as an injury within the “spectrum of skin failure.”¹⁴ As such, risk factors contributing to the development of KLs would parallel those of skin failure. Commonly cited risk factors for skin failure include multiple organ dysfunction, hypotension, use of vasopressors, use of mechanical ventilation, co-morbid conditions (eg, cardiovascular disease, smoking, diabetes, pneumonia, sepsis), abnormal white cell counts, malnutrition/low albumin levels, and immobility.^{14,15,18,31,32} In addition, aging is associated with altered immune responses and changes in vascular structure and can be a risk factor for skin failure.^14,33 

To advance our understanding of the pathophysiology of the KL, it is important to understand the connection between the risk factors contributing to their development and the mechanisms that might account for the lack of early skin temperature change. One possibility is that the injury in the early stage of KL may be restricted to the superficial cutaneous microcirculation and does not yet involve surrounding tissue, therefore no abnormal skin temperature is observed. Several lines of evidence support this idea. First, it is well known that both acute and the risk factors associated with chronic illness, including end of life events, damage the systemic vascular endothelium.^33-35 Second, it is known that the function of the cutaneous microcirculation reflects systemic vascular dysfunction.^37,38 

Like the microcirculation in other organs, the superficial cutaneous microcirculation is comprised of terminal arterioles, capillaries, and postcapillary venules. Both the blood-supply side (arterioles and capillaries) and the blood-outflow side (postcapillary venules) of the microcirculation can be affected by acute and chronic conditions. Conditions at the end of life and/or as a result of serious illness (described above) may result in solitary or multiple bouts of low blood flow within arterioles and capillaries, leading to transient local ischemia followed by reperfusion.^34,39-41 Thus, when examining the pathophysiology of KLs, not only are supply side (artery/arteriole) events leading to transient lack of blood flow/ischemic episodes critical to identify, but events in the post capillary venule are also important to consider as this is the segment of the microcirculation that bears the brunt of ischemia-reperfusion associated inflammatory processes.^39,40 

Acute and chronic conditions can result in the release of cytokines from multiple cell types and activation of plasma complement, kinin, and coagulation systems, all which contribute to microvascular endothelial damage. These conditions are also associated with activation of circulating immune cells, specifically neutrophils and monocytes. When activated, these immune cells express surface molecules that promote their adhesion to ischemia-activated, damaged microvascular endothelium of the postcapillary venule. Once adhered, these immune cells release more damaging inflammatory cytokines such as interleukins (eg, IL-1, IL-6), TNFα and IFNγ, as well as enzymes that degrade the proteins of the blood vessel.  As a result of these inflammatory processes, postcapillary venules become structurally unsound and highly permeable.^{34-36,39,40,42} 

It may be that the inflammatory processes associated with transient episodes of ischemia-reperfusion play a more significant role in the development of KLs than previously considered. During the first 24 hours of observable KL skin discoloration, damage to the postcapillary venule might reach a point at which structural breakdown of the micro vessel occurs, leading to significantly increased permeability and subsequent outward leakage of multiple blood components. It is at this critical point when the sudden, observable superficial skin discoloration of the KL may occur. However, because the deeper tissue of the discolored area is not ischemic or inflamed in this early period, no skin temperature abnormalities are observed. These ideas remain hypothetical and certainly require further study.

The retrospective case study design, small sample size, and lack of a control group limit the generalizability of the study findings.  In this study, only KLs in the sacrococcygeal area were available for analysis.  Terminal skin injuries can occur in other locations and should be included, when available, in future studies.  Skin temperature measurements were noted at only one early time point in the trajectory of the injury, specifically, within 24 hours of a newly identified discoloration. It is possible that over time, observable characteristics and skin temperature of the KL will change. Tracking skin temperatures over time would provide a more comprehensive understanding of the KL.

The novel finding from this small study is that early skin temperatures of KLs were normal. While more study is needed to clarify the pathophysiologic mechanisms that explain the KL, it may be that the injury of the KL is mostly due to damage of the superficial skin microcirculation and not due to damage of the deeper tissue associated with the discolored area. In alignment with the 2019 EPUAP/NPIAP/PPPIA International Guideline recommendation, the findings of this study, combined with studies by others examining temperature in other forms of skin injury, support a practice shift toward routine, standardized use of objective skin temperature measurements as part of skin injury assessment.

1 Wound Consultant, KL Kennedy LLC
2 Director Clinical Solutions Specialist, WoundVision, Indianapolis, Indiana
3 Professor Emerita, College of Nursing, University of Arizona, Tucson, Arizona
4 Wound Care Coordinator, Mount Carmel Health System, Columbus, Ohio
5 Inpatient Wound Service, Saint Francis Hospital and Medical Center, Hartford, Connecticut

none disclosed

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