A Prospective, Descriptive Study to Determine the Rate and Characteristics of and Risk Factors for the Development of Medical Device-related Pressure Ulcers in Intensive Care Units

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Ostomy Wound Management 2016;62(2):12–22
Seval Hanonu, RN, MSN; and Ayise Karadag, RN, ET/WOCN, MsN, PhD, Prof. Dr.

Abstract

Pressure ulcers do not develop only in areas with bony prominences; they can develop in any tissue under pressure, including pressure exerted by medical devices. A prospective, descriptive study was conducted from December 15, 2013 to March 25, 2014 to determine the prevalence, risk factors, and characteristics of medical device-related hospital-acquired pressure ulcers (MDR HAPUs) among all patients  (N = 175) in 5 adult intensive care units (ICUs) in a university hospital in Turkey.

The previously established point prevalence of hospital-acquired pressure ulcers (HAPUs) in these ICUs was 15%. Patients were evaluated in the first 24 hours after admission and observed 6 times thereafter in intervals of 48 hours. Demographic (eg, age, gender, body mass index) and medical device-related pressure ulcer data (eg, location, device type, stage), and Braden Scale scores were collected and analyzed; frequencies and percentages were calculated and Mann-Whitney U Test, t-test, and odds ratios were applied. Twenty-seven (27) patients (15.4%) developed nonMDR HAPUs and 70 (40.0%) developed MDR HAPUs. MDR HAPUs occurred most frequently (45.0%) in patients with an endotracheal tube. The most frequent type (42.6%) was Stage II. The highest rates of MDR HAPUs were observed among internal medicine ICU patients (OR 7.041), patients who also had a nonMDR HAPU (OR 6.6), patients in the high Braden risk score group (OR 1.8), or patients who received enteral feeding (OR 2.12). Because of the high rate of MDR HAPUs noted, policies and procedures aimed at preventing medical device-related pressure ulcers are needed. 

 

Despite advancements in medical treatment, care, and technology, pressure ulcers (PUs) remain an important health problem worldwide.1,2 PUs commonly occur at bony prominences such as the sacrum or heels,3 but recent research shows PUs also occur in mucous membranes and skin lying over soft tissue. Because of external pressure on the tissue on which they are positioned, medical devices such as nasal cannulas, endotracheal tubes (ETs), and continuous positive airway pressure (CPAP) masks cause tissue damage, resulting in medical device-related pressure ulcers (MDR PUs).3,4 Despite numerous studies on PUs,1,5-8 studies on MDR hospital-acquired pressure ulcers (HAPUs) are limited in number.3,4,9 The proportion of MDR HAPUs to general PUs reported in these studies is high: a cross-sectional point prevalence study3 conducted on 2,178 patients in the United States to determine PU incidence and prevalence reported the overall prevalence of MDR HAPUs was 34.5%, one third of all PUs reported in this study.

A variety of medical devices can cause MDR HAPUs. In a prospective, clinical evaluation study (N = 166) by Davis et al10 among patients wearing a cervical collar <5 days, 33% developed MDR PUs; among patients whose wear time exceeded 5 days, 44% developed MDR PUs. A nonexperimental, descriptive study11 conducted on 148 trauma patients reported wearing a cervical collar for >2 days is the second most important cause of skin damage (23.7%) and the tracheostomy-related PU rate is 10.5%.

In a prospective, descriptive study by Wille et al12 involving 125 surgical intensive care unit (ICU) patients attached to pulse oximeter probes, 6 (5%) developed a device-related ulcer. In Jaul’s13 cohort study of patients treated at a psychogeriatric inpatient health care facility (N = 174), 166 atypical PUs were observed, of which 23 (35%) were related to medical devices.

Due to their immobility, sensory perception loss, and insufficient circulation, patients receiving care in an ICU are at high risk of developing PUs.3 ICU patients generally receive treatment involving multiple medical devices more than nonICU patients.2,14,15 ICU patient characteristics increase their vulnerability to the numerous medical devices used during treatment. The different degrees of pressure exerted by the medical device and the tolerance level of the patient’s skin also affect PUs occurrence.3 PUs reduce patient quality of life and increase treatment costs; upon discharge from ICU, recovery from PUs may take several months.6,16,17

Many medical devices such as nasal cannulas, oxygen masks, ETs, CPAP masks, nasogastric (NG) tubes, Foley catheters, peripheral oxygen saturation of hemoglobin (SpO2) probes, blood pressure (BP) cuffs, cervical collars, and splints are used for the treatment and monitoring of patients in ICUs.3,4 These devices exert pressure on the tissue on which they are positioned and cause changes  in  tissue humidity and temperature. The increase in temperature and moisture between the medical device and skin causes microchanges in the skin.3,4 Moreover, the moisture that occurs causes the skin to become more susceptible to compromise3; furthermore, a medical device attached to the skin may hinder assessment of the skin beneath it.3 The materials used to fasten the devices compress the tissue, can disturb the blood and lymph circulation, and cause edema. All of these factors are thought to increase the risk for MDR HAPUs.3,4,9

For effective treatment, a health problem needs to be diagnosed at an early stage and available preventive measures must be implemented.5 Nurses need to be vigilant in preventing MDR HAPUs in ICU patients. As with nonMDR HAPUs, nurses play an important role in MDR HAPU prevention. When MDR HAPUs are prevented, the prevalence and incidence rates of HAPUs will be reduced as well.3

As far as the authors could determine, no publication is available on the rate of MDR PUs in Turkey. The purpose of this prospective, descriptive study was to address the following research questions:

1.         What is the prevalence of MDR HAPUs in ICUs?

2.         What are the characteristics of MDR HAPUs?

3.         What are the risk factors for MDR HAPUs?

 

Methods

Ethical considerations. This study was conducted according to the ethical guidelines and principles of the International Declaration of Helsinki. Before the study, the approval of Gazi University Faculty of Medicine Ethics Board for Non-invasive Clinical Research was obtained. Written consent was obtained from the chairpersons of the departments of the relevant ICUs included in the study via the Gazi University Health Research and Application Center Directory. During the study, conscious patients were informed about the aim of the study and their oral consent to participate was obtained. Unconscious patients were consented via their guardians.

Study setting and sample. The research sample consisted of anesthesia reanimation, cardiovascular surgery, internal medicine, neurosurgery, and thoracic disease patients treated in the 5 ICUs. The literature reports patients treated in ICUs are at high risk of developing PUs2,3,14,15 and that ICUs are among the units with the highest PU rates.4,9,16,17 Moreover, more medical devices are used in the treatment and monitoring of patients in ICUs  than nonICUs,3,4 guiding the choice of patient sample.

To determine which ICUs should be included in the study sample, the hospital’s 2012 PU point prevalence records were examined; these records showed PU prevalence rates were 100% in the anesthesia-reanimation, 71.4% in the thoracic diseases and surgery, 43.9% in internal medicine, 42.9% in the neurosurgery, and 16.7% in the cardiovascular surgery ICUs.18 Following expert opinion, the other units, including neurology, general surgery, and coronary ICUs, with PU prevalence rates below 15% were excluded from the study.

The number of participants was determined using the following formula19:

owm_0216_hanonu_formula

 

where n = number of individuals to be sampled, p = frequency of incidence occurrence (probability), q = frequency of nonobservance of the phenomenon (1-p), t = theoretical value t from the table at a certain standard error and degree of freedom, and d = the standard deviation from incidence frequency. When numerical values were inserted, P = 0.11.

A review of the literature3,10-13  revealed MDR HAPU prevalence rates range between 5% and 44%. Based on these data, a statistician suggested setting the frequency of incidence occurrence at 11%: q = 0.78,  t = 1.96, d =0.05 (± 5% deviation was desired), (1.96)² x 0.11 x 0.89/(0.05)², n = 150. According to this formula, the sample size was calculated to be 150.

Data collection. Data were collected using the systematic observation method. To obtain the data, a Patient Characteristics Form, an MDR PU Form, the Braden Scale for Predicting Pressure Ulcer Risk, and the Pressure Ulcer Staging Form were used. Forms were completed by the researcher, a certified stoma and wound nurse.

Patient characteristics. The patient characteristics form was developed by the researchers based on the literature.1,3,20,21 The form consisted of 25 items regarding demographic information (eg, gender, age, body mass index [BMI]) and information on health conditions (eg, diagnosis, accompanying diseases, nutrition).

PU characteristics. The MDR PU form was developed based on the literature3,4,9,13,21,22 and included 5 questions regarding PU characteristics (eg, occurrence of nonMDR HAPU and MDR PU), as well as the observations and related information such as type of medical device, PU location on the body, and PU stage obtained at each observation. To facilitate the data recording, the form included codes to refer to medical device, body site, and ulcer stage. Both the patient characteristics and PU forms were developed specifically for and used for the first time in this study.

PU risk. The Braden Scale for Predicting Pressure Ulcer Risk was used to assess the risk of PUs. The total possible score on the scale ranges from 6 to 23. Accordingly, a score of 12 points or lower indicates very high risk, 13–14 points high risk, and 15–16 points low risk. For patients 75 years and older, 15–18 points is considered low risk for PU.23

PU staging. PU staging was based on the National Pressure Ulcer Advisory Panel/European Pressure Ulcer Advisory Panel24 (NPUAP-EPUAP) staging system standards of 2009. The stages include Stage I, Stage II, Stage III, Stage IV, unstageable, and suspected deep tissue injury.

Procedure. After obtaining the necessary approval and consent of the Hospital Directorate (IRB-equivalent), a pilot study was conducted with 15 patients from the cardiovascular surgery, internal medicine, neurosurgery, and thoracic surgery ICUs to determine the applicability and comprehensibility of the data collection forms. No changes were made to the forms after pilot study. In a prospective, cross-sectional study conducted in ICUs in the US and Australia, Coyer et al4 found MDR PUs developed within 3 to 13 days following admission to the unit; therefore, data for the study were collected from patients newly admitted (<24 hours) to the ICUs included in the study. Patients then were observed for PUs at 48-hour intervals. Data collection took place between November 15, 2013 and March 25, 2014.

Each study participant was examined at least once to a maximum of 6 times (2 weeks). Once a person was examined 6 times, data collection stopped, even if he/she was not discharged from the ICU. Assessment of MDR PUs was limited to only those body sites to which a medical device was attached at the first examination. Any information regarding any medical device attached to the patient after the initial examination was disregarded.

Examination. The patient’s skin was evaluated completely from head to toe, paying special attention to bony prominences, and the tissue under and around all attached medical devices was examined and palpated. Removing devices that can be unattached for a short period of time, such as oxygen masks, nasal cannulas, and SpO2 probes, allowed for examination of the tissue underneath. Using the Braden Scale, the patient’s PU risk was assessed; staging information was recorded for patients who had developed PUs. BMI data were grouped according to the World Health Organization25 (WHO) classification criteria. Accordingly, low BMI was considered <18.50, normal BMI 18.50–24.99, heavy BMI 25.00–29.99, and obese 30.00.

Data analysis. The data obtained from each patient were coded and entered into Statistical Packages for Social Sciences (SPSS) by the researcher. Data were stored according to research and publishing ethics and analyzed using SPSS for Windows, Version 20.0 (SPSS Inc, Chicago, IL, USA).The frequency and percentage distributions of the items pertaining to patient characteristics information were calculated. Group differences were evaluated using the normality test, and the Mann Whitney U test was used for paired group variables exhibiting nonnormal distribution. To evaluate the relationship among variables, the chi-square (2) and Fisher exact tests were used. The statistical significance level was determined to be 0.05, and significant differences among groups were observed when P <0.05. Data for risk factors were presented as crude or adjusted odds ratios (ORs) with 95% confidence intervals (95% CI).

 

Results

Patient demographics. From the 5 participating ICUs, 175 persons were assessed. Participant mean age was 62.50  ± 16.67 years, average BMI was 26.49 ± 5.26, and 57.1% of the patients were men. ICU breakout included internal medicine (26.2%), cardiovascular surgical (24.5%), and neurosurgical (23.4%). The most common primary patient diagnoses were cardiovascular (28.0%) and neurological (28.0%) system diseases. Prescribed medications included antibiotics (79.4%), steroids (56.0%), and anticoagulant medication (53.7%); 39.4% received oral feeding and 36.0% were attached to mechanical ventilation (see Table 1). owm_0216_hanonu_table1

Ulcer data. Of the 175 patients included in the study, 27 (15.4%) developed nonMDR HAPUs, 70 (40.0%) developed MDR HAPUs, 16 (9.1%) developed pre-ICU nonMDR PUs, and 14 (8.0%) developed pre-ICU MDR PUs (see Table 2). owm_0216_hanonu_table2

Of the 175 participants, 70 (40%) developed a total of 211 device-caused MDR HAPUs, which were caused by ETs (95, 45.0%), CPAP masks (22, 10.4 %), SpO2 probes (17, 8.0%), oxygen masks (15, 7.1 %), and nasal cannulas (14, 6.6%). No MDR HAPUs were observed in patients with orogastric tubes, cervical collars, splints, and percutaneous endoscopic gastrostomy tubes (see Table 3). owm_0216_hanonu_table3

The MDR HAPU stages encountered were assessed initially as Stage II (42.6%), Stage I (37.9%), unstageable (17.5%), and suspected deep tissue injury (1.9%) (see Figure 1). In terms of MDR HAPU rate, the difference in the observations between 11.8% and 60.2% was found to be statistically significant (P <0.05). The rate of MDR PUs at Stage I (1.2%), Stage II (3.3%), and unstageable (2.7%), determined at the first screening, increased to 60.0%, 67.7%, and 64.8%, respectively, at the sixth observation. owm_0216_hanonu_figure1

MDR PUs occurred on the lips (44.0%), nose (15.6%), fingers (7.5%), ears (6.1%), and other sites (17.6%) (see Figure 2). owm_0216_hanonu_figure2

Risk factors. Generally, patients that developed nonMDR HAPUs were 6.60 times more likely to develop MDR HAPUs; specifically, patients in the internal medicine, neurosurgery, and thoracic disease ICUs were, respectively, 7.04, 6.22, and 6.01 times more likely to increase MDR HAPUs risk, a statistically significant difference (P <0.05). Moreover, for enterally fed patients, PU risk increased 2.12 times and as the Braden risk score moved from low to high risk, MDR HAPU risk increased 1.81 times (P <0.5).

Although not statistically significant, MDR HAPUs occurred 1.23 times more often in male patients, 2.07 times more in patients attached to a mechanical ventilator, 2.07 times more in patients on anticoagulants, and 2.56 times more in patients receiving sedation. Although not statistically significant, MDR HAPU development was 1.02 higher as age increased and 1.17 higher as hemoglobin levels dropped (>0.05) (see Table 4). owm_0216_hanonu_table4

Length of stay. In this study, 340 (60.2%) of MDR HAPUs developed with a total of 211 devices. More MDR HAPUs developed as the number of days in hospital increased: 11.8% occurred during the first 24 hours (7/59 sites); on the fourth day, the number of occurrences rose to 48.0% (37/77 sites) and on the eleventh day to 82.3% (215/261 sites) (P <0.05)  (see Table 5). owm_0216_hanonu_table5

 

Discussion

Prevalence. The prevalence rate for MDR HAPUs in this study was 40.0% — approximately 1 in 2 patients admitted to an ICU developed a MDR HAPU. This rate was higher than nonMDR HAPUs prevalence (15.4%), which corresponds to the findings in the relevant literature. In a cross-sectional point prevalence study by Black et al3 conducted on 2,079 patients, nonMDR HAPU prevalence was 5.4% and MDR HAPU prevalence was 34.5%. In a cross-sectional study by Coyer et al4 conducted on 483 ICU patients in Australia and the US, the MDR PU rate was 12.8% (17/132) for Australian patients and 8.8% (3/351) for American patients. In a descriptive study by Apold and Rydrych22 among 255 cases of severe PUs, 74 (29%) were caused by medical devices. In a study by Jaul13 conducted among 174 patients in a geriatric ICU, 35 developed atypical PUs, of which 10 (28.5%) were medical device-related. In a cross-sectional study by van Gilder et al26 conducted in ICUs and other wards, 149 out of 1,631 PUs (9.1%) were caused by medical devices.

Location. MDR HAPU location varies depending on where a medical device is attached to a patient. In the present study, MDR HAPUs developed most commonly on the lips (44.0%), followed by nose (15.6%), fingers (7.5%), and ears (6.11%), whereas nonMDR HAPUs occurred in the sacrum, ischium-sacrum, and sacrum-ischium-trochanter regions. This is underscored in the literature; MDR PUs develop at sites of medical device use. In Black et al’s study,3 the locations of most MDR HAPUs were the ears (35%), lower leg (11%), and heels (8%). In the study by VanGilder et al,26 the most observed MDR PUs locations were the ears (20%), sacrum (17%), heels (12%), and buttocks (10%). In the studies by Watts et al11 and Apold and Rydrych,22  the most common location of PUs was the cervical collar region. These studies support that nonMDR HAPUs and MDR HAPUs occur in different locations from one another.

Stages. PU stages vary in the literature as well. In the current study, the most frequently observed PU stages of MDR HAPUs were Stage II, Stage I, and unstageable, respectively. In the study by Apold and Rydrych,22 the most observed MDR PUs stages were unstageable (52.7%), Stage II and Stage III (20.3%), and Stage I (5.4%). The MDR PU stages reported in Black et alare Stage I (35%), Stage II (32%), and unstageable (24%). The different frequencies in MDR HAPU stages reported is thought to be due to the differences in medical device use, differences and indefiniteness with respect to tissue examination scope and frequency, and the inability to determine the presence of MDR HAPUs until they have reached an advanced stage.22 Methodological differences in research also may account for these differences.3,4,22 In Apold and Rydrych,22 one fourth of MDR PUs (74%) was not identified until they reached Stage III, Stage IV, and unstageable, versus 54% for nonMDR HAPUs. The Stage I MDR PU identification rate is 5.0% and 20.0% for Stage I nonMDR HAPUs. In addition, the fact MDR PUs develop in relatively lean body sites with little fat tissue under the skin (eg, nostrils, behind the ears, neck, back of the head, nose bone) also allows the ulcers to reach Stage III, Stage IV, and unstageable faster than nonMDR HAPUs.22 Furthermore, in some cases, early-stage MDR PUs are mistakenly identified as dried exudate (oral, nasal, gastric) instead of PUs. These misidentifications tend to delay the timely and appropriate staging of PUs and thus their treatment.22 As with nonMDR HAPUs, the prevention and early diagnosis of MDR HAPUs greatly depends on nurses’ accurate staging and recording of ulcers forming on the skin on which medical devices are positioned.3,4,22

The MDR HAPU literature focuses mainly on skin ulcers.3,11,22,25 Coyer et al4 state to accurately determine the rate of MDR PUs, evaluations of mucous membrane ulcers as well as skin ulcers need be conducted in order to avoid classifying mucous ulcers as coagulum.

Devices. With advancements in medical technology, the number of available medical devices that may cause MDR PUs has increased. In the current study, more than 20 medical devices were used, among which ETs, CPAP masks, SpO2 probes, and oxygen masks caused the most MDR PUs. The device causing the most MDR PUs, the intubation tube is also a device widely used in ICUs, findings that correspond to those of Coyer et al.4

Risk factors. Although the literature includes studies on MDR HAPUs, no study to determine the impact of the relevant risk factors has been found. Therefore, the results of the present study provide important data for the literature. Advanced age, obesity, low hemoglobin, low albumin, lower Braden risk scores, chronic diseases, medications used, length of hospital stay, and the type of clinic are factors reported to influence the occurrence of nonMDR HAPUs.3,22,26 According to the literature, nonMDR HAPUs and MDR HAPUs share common risk factors, the most important of which is the use of a medical device. Studies3,4,22,26 report MDR PUs develop in high-risk patients whose risk evaluation score on the Braden Scale is low. The findings of the current study are supported by the literature: patients in internal medicine ICUs developed 7 times more MDR HAPUs, and those in neurosurgical and chest disease ICUs 6 times more than other ICUs. Moreover, in enterally fed patients, and as the Braden risk scores move from low risk to high risk, MDR HAPU rates doubled. Patients developed MDR HAPUs 7 times more than nonMDR HAPUs (P <0.05) (see Table 4). In addition, advanced age (67.4 ± 16.1 years); attachment to a mechanical ventilator; low hemoglobin and albumin values; and the use of steroid, anticoagulant, and sedative medications were found to be risk factors influencing MDR PU development (see Table 4).

NonMDR HAPU development risk is high in ICUs, where high-risk patients are treated.4,26 In this study, the highest MDR HAPU development rate was observed in patients admitted to the internal medicine ICU, followed by chest disease ICU and neurosurgical ICU. In the study by VanGilder et al,26 general ICU ranked first, followed by coronary ICU and surgical ICU. However, in these studies, ICU data are reported in terms of ulcers rather than patients, which limits the possibility of comparing studies with respect to MDR PU developing patient numbers. Yet in a study by Black et al,3 no difference was found between ICU and nonICU patients in terms of MDR PU development. Moreover, nonMDR HAPU development risk is higher in patients with medical devices.

Among the patients in the current study, fewer than half (63/175) were attached to a mechanical ventilator or received enteral feeding (43/175) (see Table 1). Although the number of mechanical ventilator-attached patients was smaller, a higher rate of MDR HAPU development was observed in these patients (see Table 4). The literature4 supports that ventilation devices cause more MDR PUs than other devices. Similarly, despite the small number of enteral feeding patients (see Table 1), MDR PUs were observed at high rates in these patients (see Table 4). In the study by Jaul,13 the incidence rate of MDR PUs was higher in enteral feeding  patients. This may be attributed to the fact that patients who receive enteral feeding and are attached to ventilation devices are usually also those at higher risk with respect to life functions, and thus more often exposed to treatments with more medical devices.

In the current study, patients at advanced ages (67.4 ± 16.1 years) developed MDR HAPUs at a high rate. This is supported by Coyer et al,4 where the average age of patients developing a MDR PU was 60.5 ± 20.6 years.

Low hemoglobin (9.7 ± 1.7) and albumin (2.8 ± 0.7) values, use of medication (eg, sedatives, steroids), and high PU risk scale score increase MDR PU risk.3,4,22,27  Low hemoglobin negatively affects circulation and thus leads to insufficient blood flow to tissues.6,28 Low albumin leads to interstitial leakage and thus to edema, which in turn results in increased pressure and deterioration in the nutrient exchange in tissues. This situation may facilitate the formation of MDR HAPUs in edematous tissue.28 The use of steroids prevents the formation of collagen fibers, and the use of sedatives impairs the patients’ sensory perception of pain. Therefore, patients on these medications do not feel the pain resulting from medical device-related tissue damage and thus do not adequately voice their discomfort. Because patients are usually prescribed anticoagulants to address circulation problems, MDR PUs may be more likely to develop in these patients.3,29

Patients in the high Braden Scale score risk group have low activity levels, nourishment problems, and weak stimulus perception and are mostly bedbound and attached to 1 or more medical devices. All these risk factors associated with nonMDR HAPUs occurrence are considered to be relevant for MDR HAPU occurrence as well.

Timing. In this study, MDR HAPUs occurred as early as 24 hours after admission to the ICU and continued to occur through to day 11. Within the first 24 hours, MDR HAPUs developed most commonly on persons using nasal cannulas and ETs. In Coyer et al,4 MDR PUs were found to develop between 3 and 13 days after admission.

Location as a factor of time. In the patients participating in the study, the rate of body sites where MDR HAPUs developed in the first 24 hours of hospitalization (11.8%) increased 7 times by the eleventh day. As the patients’ length of stay in the ICU increased, their days attached to medical devices increased as well, along with the risk of medical device pressure on the body site. As the pressure time increases, blood and lymph circulation in the compressed tissue decreases, resulting in inadequate tissue nourishment and thus increased PU risk.30-32 The same hypothesis appears to be valid for MDR PUs. As the time a medical device stays attached to the tissue increases, circulation under the tissue decreases. Moreover, factors related to the medical device such as the friction/shear and local temperature increase, the edema caused by tight attachment straps, skin softening, and maceration caused by excessive moisture accumulation are all considered to decrease skin tolerance and to contribute to MDR PU development.3,9,13,33

 

Limitations 

In this study, patients newly admitted to the ICU and examined within 24 hours were included. The evaluation of skin beneath medical devices was limited to the first examination — the skin beneath whichever medical device was present in the first examination was evaluated for MDR HAPU development in subsequent examinations. The skin sites of other medical devices attached to the patients after the first examination or later in their treatment and MDR HAPU due to these devices were excluded from the study. Due to the differences in the death, discharge from hospital, and transfer of patients to other departments, the observation periods of these patients were different. The observation period was limited to a maximum of 2 weeks. In addition, after completing the observation period  (a total of 6 examinations), patients were not evaluated again, even if their stay in the same ICU continued. Because this study was limited to patients in the internal medicine, cardiovascular surgery, neurosurgical, and anesthesia-resuscitation ICUs in an academic hospital with a MDR HAPU prevalence rate of 15%, the results cannot be generalized to other ICUs. Moreover, preventive measures taken by nurses to prevent MDR HAPUs were not evaluated.

 

Conclusion

The findings of this study, conducted to determine the prevalence of MDR HAPUs and to identify risk factors for and characteristics of MDR HAPUs development rate through systematic observation, showed MDR HAPUs occurred 3 times more often than nonMDR HAPUs. MDR HAPUs occurred most frequently due to ET, CPAP masks, and SpO2 probes and mostly on the lips, nose, and fingers. The stages of the MDR HAPUs observed were Stage II, Stage I, and unstageable, respectively.

In this study, the MDR HAPU development rate in patients treated in internal medicine, neurosurgical, and chest disease ICUs, who exhibited high Braden risk values, who were enterally fed, who developed nonMDR HAPUs, and who stayed in hospital for a greater number of days, were found to have a higher MDR PU development rate (P <0.05). Based on the findings, additional studies are needed to help develop evidence-based policies and procedures aimed at preventing MDR HAPUs. 

 

References

1.         Karadağ A. Basınç ülserleri: değerlendirme, önleme ve tedavi. C.Ü.Hemşirelik Yüksek Okulu Dergisi. 2003;7(2):41–46.

2.         Elliott R, McKinley S, Fox V. Quality improvement program to reduce the prevalence of pressure ulcers in an intensive care unit. Am J Crit Care. 2008;17(4):328–335.

3.         Black JM, Cuddigan JE, Walko MA, Didier LA, Lander MJ, Kelpe MR. Medical device related pressure ulcers in hospitalised patients. Int Wound J. 2010;7(5):358–365.

4.         Coyer FM, Stotts NA, Blackman VS. A prospective window into medical device related pressure ulcers in intensive care. Int Wound J. 2013;11(6):656–664.

5.         Lindgren M, Unosson M, Krantz MA. A risk assessment scale for the prediction of pressure sores development: reliability and validity. J Adv Nurs. 2002;38(2):190–199.

6.         Lindgren M, Unosson M, Fredrikson M, Ek AC. Immobility—a major risk factor for development of pressure ulcers among adult hospitalized patients: a prospective study. Scand J Caring Sci. 2004;18(1):57–64.

7.         Lahmann NA, Halfens RJG, Dassen T. Prevalence of pressure ulcer in Germany. J Clin Nurs. 2005;14(2):165–172.

8.         Schoonhoven L, Bousema MT, Buskens E. The prevalence and ıncidence of  pressure ulcers in hospitalised patients in the Netherlands: a prospective inception cohort study. Int J Nurs Stud. 2007;44(6):927–935.

9.         Black J, Alves P, Brindle CT, Dealey C, Santamaria N, Call E, Clark M. Use of wound dressings to enhance prevention of pressure ulcers caused by medical devices. Int Wound J. 2015;12(3):322–327.

10.       Davis JW, Parks SN. Detlefs CL, Williams GG, Williams JL, Smith RW. Clearing the cervical spine in obtunded patients: the use of dynamic fluoroscopy. J Trauma Nurs. 1995;39(3):435–438.

11.       Watts D, Abrahams E, MacMillan C, Sanat J, Silver R, Van Gorder S, et al. Insult after injury: pressure ulcers in trauma patients. Orthop Nurs J. 1998;17(4):84–91.

12.       Wille J, Braams R, van Harren W, van der Werken C. Pulse oximeter-induced digital injury: frequency rate and possible causative factors. Crit Care Med. 2000;28(10):3555–3557.

13.       Jaul E. Cohort study of atypical pressure ulcers development. Int Wound J. 2014;11(6):696–700.

14.       Strand T, Lindgren M. Knowledge, attitudes and barriers towards prevention of pressure ulcers in intensive care units: a descriptive cross-sectional study. Intensive Crit Care Nurs. 2010;26(6):335–342.

15.       Mattox E. Medical devices and patient safety. Crit Care Nurs. 2012;32(4):60–68.

16.       Tel H, Özden D. Güneş ÇP. Yatağa bağımlı hastalarda basınç yarası gelişme riski ve hemşirelerin bu hastalara uyguladıkları önleyici bakım. Hemşirelikte Araştırma Geliştirme Dergisi. 2006;1(2):35–45.

17.       Schoonhoven L, Defloor T, Grypdonck MH. Incidence of pressure ulcers due to surgery. J Clin Nurs. 2002;11(4):479-487.

18.       Karadağ A, Baykara ZG, Özaltan G. Bir üniversite hastanesinde nokta prevalans çalışması. In: 15 Ulusal İç Hastalıkları Kongresi 2013. Antalya, Turkey: MİKİ Matbaacılık; 2013:429.

19.       Karataş N. Araştırmada Örnekleme. In: Erefe İ (ed). Hemşirelikte Araştırma İlke, Süreç ve. Yöntemleri, Ankara, Turkey: Hemar Ge Yayınevi;2012:124–125

20.       Black J, Baharestani MM, Cuddigan J, Dorner  B, Edsberg L, Langemo D. National Pressure Ulcer Advisory Panel’s updated pressure ulcer staging system. Adv Skin Wound Care. 2007;20(5):269–274.

21.       Karadağ M, Gümüşkaya N. The incidence of pressure ulcers in surgical patients: a sample hospital in Turkey. J Clin Nurs. 2006;15(4):413–421.

22.       Apold J, Rydrych D. Preventing device-related pressure ulcers: using data to guide statewide change. J Nurs Care Qual. 2012;27(1):28–34.

23.       Pınar R, Oğuz S. Norton ve Braden Bası Yarası Değerlendirme Ölçeklerinin yatağa bağımlı aynı hasta grubunda güvenirlilik ve geçerliliklerinin sınanması. In: Uluslararsı katılımlı VI. Ulusal Hemşirelik Kongresi 1998. Kongre kitabı. Ankara, Turkey: Damla Matbaacılık;1998:172–175.

24.       National Pressure Ulcer Advisory Panel and European Pressure Ulcer Advisory Panel. Prevention and treatment of pressure ulcers: clinical practice guideline. Washington: National Pressure Ulcer Advisory Panel, 2009.  Available at: www.npuap.org/resources. Accessed October 10, 2014.

25.       World Health Organization. Global Data Base on Body Mass Index. Available at: http://apps.who.int/bmi/index.jsp?introPage=intro_3.html. Accessed October 7, 2014.

26.       VanGilder C, Amlung S, Harrison P, Meyer S. Results of the 2008–2009 International Pressure Ulcer Prevalence Survey and a 3-year, acute care, unit-specific  analysis. Ostomy Wound Manage. 2009;55(11):39–45.

27.       Karadağ A, Karabağ Aydın, A. Basınç Ülserlerinde Etiyoloji ve Fizyopataloji. In: Baktıroğlu S, Aktaş Ş (ed). Kronik yarada güncel yaklaşımlar. İstanbul, Turkey: İstanbul Üniversitesi Kronik Yara Konseyi;2013:120–125.

28.       Kozier B, Erb GL. Fundamentals of Nursing. Pearson International Edition, 2009. Sidney, Australia: Mosby Elsevier;2009:904–910.

29.       Wolverton CL, Hobbs LA, Beeson T, Benjamin M, Campbell K, Forbes C, et al. Nosocomial pressure ulcer rates in critical care. J Nurs Care Qual. 2004;20(1):56–62.

30.       Bryant RA, Shannon ML, Pieper B, Braden BJ and Morris DJ. Pressure ulcers. In: Bryant RA. Acute and Chronic Wounds – Nursing Management. St Louis, MO: Mosby;1992:105–163.

31.       Morison JM. The Prevention and Treatment of Pressure Ulcers. Toronto, Canada: Mosby;2001:20–32.

32.       Myers BA. Wound Management Principles and Practice. Upper Saddle River, NJ: Pearson Prentice Hall;2004:260–296.

33.       Jaul E. A prospective pilot study of a typical pressure ulcer presentation in skilled geriatric nursing unit. Ostomy Wound Manage. 2011;57(2):49–57.

 

Potential Conflicts of Interest: none disclosed

 

Ms. Hanonu is a research assistant, Gazi University Faculty of Health Sciences, Department of Nursing, Ankara, Turkey. Dr. Karadag is a Professor, Koç University School of Nursing, Istanbul, Turkey. Please address correspondence to: Seval Hanonu, RN, MSN, Emniyet Mah, Muammer Yasar Bostancı Sokak No:1606560 Besevler/Akara, Turkey; email:sevalhanonu@yahoo.com.

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