Abstract
Pressure ulcers (PUs), i.e. bed sores, are chronic injuries largely affecting over 2.5 million patients annually.[1] Although considered preventable, present standards to detect PUs have low specificity and sensitivity or are difficult to implement due to time or cost constraints. PUs are caused by prolonged pressure, resulting in ischemia and tissue necrosis. Since pressure-induced ischemia alters blood reperfusion and oxygen concentration levels, measuring O2 changes prior to and after reperfusion is a promising indicator for PU formation. We have a created a low-cost, handheld device that induces reperfusion (via an automated loading mechanism) and measures the changes in O2 (via reflectance pulse oximetry), thus quantitatively assessing PU formation based on the change in O2 in clinical settings.
Background
Over 2.5 million Americans annually suffer from pressure ulcers (PUs), with 60,000 dying due to related complications. PUs cost the United States $11 billion and are the second most common cause for medical malpractice litigation.[1] The current standard involves repositioning patients every 2-4 hours to prevent the formation of PUs;[2] this technique is combined with the Braden Scale, whereby caretakers visually inspect patients’ risk areas for impending PUs. Current prevention methods lack in sensitivity, specificity, and are difficult to implement widely due to cost or time constraints. Additionally, there is a lack of quantitative, evidenced-based methods to prevent PUs. The quality of life for millions of patients can be greatly increased with the development of a solution that detects Pre-stage I PUs, therefore assisting the prevention of PU formation. Our team has developed a novel solution to sense the early formation of PUs.
Statement of Problem
Although easily preventable, PUs still are a common and costly problem, largely due to a lack of an effective, low-cost, adaptable, easy-to-implement detection method. We aim to develop a device to detect formation of PUs in patients in clinical settings. It will be low-cost such that hospitals and nursing homes can afford it, portable and easy-to-use so that it can be adopted into current care regimens, and be able to accurately, precisely, and non-invasively detects the presence of pre-stage I ulcers. Furthermore, it will be effective with a variety of patients.
Design
Overview
PUs are caused by the application of prolonged pressure, resulting in ischemia and subsequent tissue necrosis. Since pressure-induced ischemia alters blood reperfusion and oxygen concentration levels, measuring O2 changes prior to and after reperfusion is a promising indicator for PU formation.[3,4] Our device (Figure 1) thus uses a transient loading method to measure the changes in oxygen concentration during blood reperfusion within the areas of skin with potential PUs. A reflectance pulse oximetry sensor is used to measure the oxygen saturation of the tissue before, during, and after pressure loading, while a linear actuator applies a controlled amount of pressure to allow for accurate sensor readings and slight blood occlusion. The loading is controlled via feedback between the actuator and an embedded load cell, preventing excessive forces from being applied to the patient.
Figure 1. a) Side view of the device, with LCD screen and LED highlighted in green, and automated loading mechanism highlighted in red.
b) Angled view of the device, with reflective pulse oximetry sensor highlighted in blue and microSD card reader highlighted in yellow.
Device Usage
The caretaker will use this device to quantitatively check for the formation of PUs within patient risk areas, such as the sacrum, heel, or hip, as shown in Figure 2. The user will turn the device on, select the patient and location of measurement, and hold it flush against the suspected area. The device will apply a minimal amount of pressure (50mmHg) to allow for the sensor to obtain an accurate oxygen concentration reading. It will then apply 170mmHg for 10 seconds, causing temporary blood occlusion. Afterwards, it will return to the initial, minimal pressure, triggering blood reperfusion. After 8 seconds, the device will then calculate the change in O2 from the initial and reperfusion stages and indicate to the user, via the LCD user interface, whether the area is a PU. A simplistic representation of our device is shown below in Figure 3.
Figure 2. Illustration of device usage on the heel of the patient Figure 3. a) Initial stage, where the device measures the O2, b) Occlusion stage, where pressure is applied via extension of the linear actuator shaft, c) Reperfusion stage, where the shaft retracts and the device measures the O2
Reflectance Pulse Oximetry
Pulse oximetry noninvasively measures the PPG and oxygen concentration levels within the blood, factors that have been shown to change during pressure ulcer formation in literature. We chose to use reflectance pulse oximetry due to its adaptability with different bodily locations. Unlike the traditional transmission pulse oximetry system, the photodiode measures the amount of light reflected back from the tissue, using the changing absorbances from the red and infrared lights to calculate the oxygen concentration. As a result, the measurement of oxygen concentration is no longer limited to thin parts of the patients body, allowing areas commonly susceptible to PU development, such as the heel, sacrum, or hips, to be monitored. Our system uses a Nonin 8000R sensor and OEM III module, which measures the amount of light reflected back from the blood and determines the resulting O2 concentration. The sensor contains the red and IR LEDs and the photodiode. The OEM III alternates the illumination of the LEDs, collects the voltage readings, applies digital signal processing techniques, and converts the resulting signal into oxygen saturation. The ratio of absorbance between the red and IR LEDs is then calculated using the AC and DC voltages, which can then be used to determine the O2 concentration, using existing calibration curves. Figure 4 details the components of the reflectance pulse oximetry system.
Figure 4. The basic circuitry of the reflectance pulse oximetry system
Automatic Loading Mechanism
To create temporary blood occlusion our device uses an automatic loading mechanism. The system uses a linear actuator and uses a load cell to monitor and control the applied pressure via a feedback loop. A TI SN754410 Quadruple Half-H Driver is used to drive the motor within the linear actuator, allowing for the automatic application and release of loading; an ATmega32U4 microcontroller collects the varying voltage readings from the load cell, converts it into the applied pressure, and controls the motor and shaft movement of the linear actuator based on the measured, inputted values, allowing for motional user feedback. An additional LED indicator light provides visual feedback, allowing the user to determine if the applied pressure is within the appropriate range. Figure 5 details the feedback control system.
Figure 5. Closed-loop control system measures and adjusts applied pressure on the patient.
User Interface
Our device has an LCD screen to allow the user to view the O2 values and results for the test. In addition, the device has data storage and transfer capabilities, with a microSD card reader allowing users to store their data, allowing nurses or caretakers to easily monitor and record various patients’ health over time.
Evaluation
To validate our measure of detecting pressure ulcers (i.e. measuring the change of O2 before and after reperfusion), we compared changes in O2 for patients with no PU and patients with simulated PUs. Due time and resource restrictions, we were unable to gain access to patients with PUs for initial testing. As result, we simulated the development of ulcers by loading 120 mmHg onto the sacrum of the test subject, as done in prior literature. After 20 minutes of loading, the pressure was removed, and the device was used on that area of skin. The average change in O2 before and after the device occlusion was 0.00% +/- 0.00%. In contrast, a patient without PUs (i.e. one who did not under the prior loading) had an average change of 3.07 +/- 1.74%. The statistically significant difference between the changes in O2 (p<0.05) therefore implies that measuring changes in O2 before and after reperfusion could be an accurate method of detecting pressure ulcers. In addition to validating our approach for PU detection, our device was able to meet our set design criteria. Its calculated unit manufacturing cost (as calculated by a labor, burden and manufacturing cost analysis) fell below our target cost of $2000, at $678 per device, an affordable price point for hospitals and nursing homes. It met our portability standards, as measured through weighing the final device and calculating the estimated volume of the outer casing, and was easy-to-use, having data storage and transfer capabilities and a device use time of under 5 minutes. In addition, it was adaptable, working with a variety of different skin tones and in different bodily locations (i.e. the sacrum and heel).
Discussion/Conclusion
Our device was shown to be low-cost, easy-to-use, portable, and adaptable on a variety of patients and body locations, making it an attractive and feasible option for many hospitals and nursing homes, areas with high rates of PU development. Our method of quantitatively detecting ulcer formation was validated by the statistically significant difference in O2 change between the healthy patient and patient with a simulated PU, and by monitoring blood reperfusion, our device will be a lower cost alternative to many products currently in development, such as the SEM scanner or portable ultrasound technologies. Thus, our device can act as a low cost, quantitative method for detecting PUs, a necessity that currently doesn’t exist for healthcare settings.
Acknowledgements
We would like to thank Dr. Eric Richardson, Dr. Gary Woods, Dr. Catherine Ambrose, and Professor Lex Frieden for their help and support. The project was sponsored by Carolyn and Harrell L. Huff. The design work for this project was supported by the resources of the Oshman Engineering Design Kitchen.
References
[1] Berlowitz, Dan, Carol VanDeusen Lukas, and Victoria Parker. “Preventing Pressure Ulcers in Hospitals.” (n.d.): n. pag. Agency for Healthcare Research and Quality. Web. 22 Sept. 2014.
[2] de, L.E.H., et al., Epidemiology, risk and prevention of pressure ulcers in critically ill patients: a literature review. J Wound Care., 2006. 15(6): p. 269-75.
[3] Liu, Mon Hsia, David R. Grimm, Victoria Teodorescu, Steven J. Kronowitz, and William A. Bauman.”Transcutaneous Oxygen Tension in Subjects with Paraplegia with and without Pressure Ulcers: A Preliminary Report.” Journal of Rehabilitation Research & Development 36.3 (1999): n. pag. Web.
[4] Herrman, Eric C., Charles F. Knapp, James C. Donofrio, and Richard Salcido. “Skin Perfusion Responses to Surface Pressure-induced Ischemia: Implication for the Developing Pressure Ulcer.” Journal of Rehabilitation Research & Development 36.2 (1999): n. pag. Web.