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International Wound Journal logoLink to International Wound Journal
. 2020 Apr 1;17(4):944–956. doi: 10.1111/iwj.13363

Pressure injury development in critically ill patients with a cervical collar in situ: A retrospective longitudinal study

Harn‐Rong N Wang 1, Jill Campbell 1,2, Anna Doubrovsky 1, Veeranjit Singh 3, Johnathon Collins 4, Fiona Coyer 5,6,
PMCID: PMC7948998  PMID: 32239663

Abstract

Trauma patients with a serious injury to the head or neck can remain immobilised with a cervical collar (C‐collar) device in situ and are subsequently exposed to device‐related skin integrity threats. This study aimed to determine the incidence and risk factors associated with the development of C‐collar‐related pressure injures (CRPIs) in an intensive care unit. This retrospective longitudinal cohort study was conducted in an Australian metropolitan intensive care unit. Following ethical approval, data from patients over 18 years, who received a C‐collar were retrieved over a 9‐year period. Chi square and t‐tests were used to identify variables associated with CRPI development. A logistic regression model was employed to analyse the risk factors. Data from 906 patients were analysed. Nine‐year pressure injury incidence was 16.9% (n = 154/906). Pressure injury development directly associated with a C‐collar increased by 33% with each repositioning episode (odds ratio 1.328, 95% confidence interval 1.024‐1.723, P = .033). Time in the C‐collar (10.4 to 2.5 days, P = .002) and length of stay in intensive care unit (ICU) (20.1 to 16.1 days, P < .001) were associated with pressure injury development. Patients with C‐collar devices are a vulnerable group at risk for pressure injury development because of their immobility and length of ICU stay.

Keywords: cervical collar, critically ill patients, incidence, intensive care, pressure injury

1. INTRODUCTION

Cervical collar (C‐collar) is a life‐saving medical device, used to immobilise the cervical spine (C‐spine) and reduce the risk of secondary spinal cord injury by keeping the head in a comfortable gravity aligned position and maintaining normal cervical lordosis (normal inward curvature).1, 2, 3 C‐collars are manufactured as either soft collars or firm to rigid collars.4, 5 Soft collars are made from thick and soft foam rubber covered with a cotton stockinette, whereas rigid C‐collars are made from moulded plastic. Although both soft and rigid collars limited head and neck motions, 5 soft collars mitigate the complications associated with the use of rigid collars, including patient discomfort, aspiration risk, increased intracranial pressure, and soft tissue injury formation.3, 6 While the application of a C‐collar is an essential and live‐saving intervention for potential/and spinal cord injury patients, the application of this device places patients at risk of skin integrity threats. 7

The length of time in C‐collar is determined by the time taken to rule out or diagnose a C‐spine injury. 8 Clinically, C‐spine injuries are excluded if both computed tomographic (CT) radiographs and clinical examination of the C‐spine are negative. 9 For unconscious patients, if the CT radiograph is not definitive, and a magnetic resonance image (MRI) is recommended.8, 9, 10 In some patients, immobilisation in a C‐collar is often continued for prolonged periods because clinical examination is only effective in patients who are awake and an MRI investigation may be delayed because of its significant costs and sufficiently potential risks. 9 Consequently, C‐collars can remain in situ for an extended period, with the patient repositioned using the log roll strategy during this time. 9 It is postulated that in such cases, the development of pressure injuries (PI) related to the C‐collar device may increase.

Literature directly purporting to PI development in patients with C‐collars in situ (C‐collar related [CR] PIs) are limited.8, 10, 11, 12, 13, 14, 15, 16, 17 The incidence of CRPI has been identified in international context with vide variation. Studies conducted in the United States of America report CRPI incidence ranging from 1.1% to 44%,12, 13, 16, 17 while in European studies incidence ranged from 23.9% to 55%10, 15 and incidence reported in one Australian study was 9.7%. 11 Previous studies have reported PIs located in a wide variety of locations such as the chin, shoulders, chest, back, clavicle, and occiput, as attributed to the presence of a C‐collar.11, 12, 14 However, these studies did not specifically distinguish PIs that developed as a result of direct skin contact with the C‐collar and PIs that may have developed in association with the presence of a C‐collar. This is because the aforementioned studies were all conducted prior to the release of a national consensus definition of what constitutes a medical device‐related pressure injury (MDRPI). Currently, the American National Pressure Injury Advisory Panel defines MDRPI as a “PI that results from the use of devices designed and applied for diagnostic or therapeutic purposes. The resultant PI generally conforms to the pattern or shape of the devices”. 18

The severity of PIs has been reported as an aggregate result in studies conducted by Watts et al 17 and Ham et al, 8 with PI stages reported for all PIs rather than differentiating between the stages attributed directly and indirectly to the C‐collar. Only two studies have focused solely on the severity of PIs related to the C‐collars. Molano et al 15 reported Stage II (42.1%, 16/38) as the most commonly identified severity of CRPI, and Davis et al 13 also found Stage II CRPIs to be the most prevalent (52%, 23/44). Furthermore, the time in the C‐collar11, 12, 14, 16, 17 and the length of stay in the intensive care unit (ICU)14, 15 have been described as possible risk factors for CRPI development in trauma patients.

Given the lack of information pertaining to CRPI and in light of the consensus definition of MDRPI, 18 this study aimed to identify the longitudinal incidence, severity, and anatomical locations of CRPIs, the risk factors associated with PI development, and the time to develop a CRPI in patients in the ICU.

2. MATERIALS AND METHODS

2.1. Study design and setting

A retrospective longitudinal cohort study of adult critically ill patients with a C‐collar in situ was conducted in the 26‐bed ICU of an Australian quaternary metropolitan hospital. At this centre, patients admitted to the ICU are high acuity and medical admission diagnoses include acute neurological disorders, respiratory diseases, renal dysfunction, burns, sepsis, and major multi‐trauma injuries. Approximately 2500 patients per year are admitted to ICU with an Acute Physiology and Chronic Health Evaluation II (APACHE II) mean score of 18 and a mean length of ICU stay of 3.1 days. 19

2.2. Participants

The study population comprised all patients admitted to the ICU for a 9‐year period, between 1st July 2010 and 30th June 2019. All patients 18 years and over who/ admitted to the ICU with a C‐collar in situ during this time period were included. Patients admitted with burns to the head and neck and community acquired pressure injuries (CAPIs) defined as PIs that were presented upon admission to the hospital or documented in the first 8 hours of hospitalisation 20 were excluded from the study.

2.3. Variables

Patients' demographic and clinical characteristics included age, gender, ICU admission diagnosis, APACHE II score (a score of patient acuity on admission to the ICU with the score ranging from 0 to 71, where higher scores correspond to more severe disease states and higher mortality risks for intensive care patients,21, 22 Glasgow Coma Scale score ([GCS]; the level of the patient's consciousness based on elements of eye opening, verbal response, and motor response, 23 which can be scored individually and then added together to give a sum score, ranging from 3 to 15,24, 25 length of time with C‐collar in situ, frequency of patient repositioning per day and the position the patient was placed in, e.g. supine, left or right lateral, or logrolled, use of mechanical ventilation, vasopressor use, and length of stay in the ICU.

If patients developed a PI, the clinical characteristics captured comprised the date and time of initial documentation, anatomical location, and stage according to the international guideline classification system at the time of original data entry.18, 26, 27 Documented PIs were then classified by the researchers into three groups;

  1. Direct C‐collar‐related pressure injury (direct CRPI) was defined as PIs that developed where the C‐collar directly comes in contact with the skin (chin, all sides around the neck, and clavicle). 18

  2. Indirect C‐collar‐related pressure injury (indirect CRPI) was defined as PIs that occurred on the posterior body surface (back, occiput, shoulder, elbow, heel, buttocks, and sacrum). This term ‘indirect CRPI’ was unique to this study, based on the fact that a patient with a C‐collar in situ may be supine for prolonged periods and repositioned using a logroll technique. Subsequently, PIs in these locations were indirectly attributable to the presence of the C‐collar and the associated reduced mobility.

  3. Other PIs were defined as any other PIs that developed in patients with a C‐collar in situ on other anatomical locations (ears, nose, cheek, lip, tongue, trunk, leg, and arm), that is, those not associated with the supine position. In addition, any PI, no matter the location that is detected 24 hours after C‐collar removal is classified as ‘other PI’.

2.4. Procedure

As this was a retrospective study, following ethical approval (local site approval number; HREC/16/QRBW/16), and site governance approval, the Medical Director of Intensive Care Services was approached to provide authorisation to access patient data captured on the Intellivue Clinical Information Portfolio (Philips Healthcare, Andover MA) (2010‐2014) and MetaVision (iMDsoft, Australia) (2014‐2019) clinical databases. All patient information was retrieved from the clinical databases in a de‐identified format by the department information systems administrator. A de‐identified report was provided to the researchers in a Microsoft Excel (2007) spreadsheet. The investigator exported the data from Microsoft Excel (2007) into the Statistical Package for the Social Sciences (SPSS) (2018, Version 25.0, Chicago, Illinois). Nine random cases were entered into the SPSS data and crosschecked with the Microsoft Excel (2007) spreadsheet before any statistical analysis was undertaken to ensure the reliability and accuracy of data preparation and cleaning.

2.5. Statistical methods

Descriptive statistics were analysed using frequencies and percentages for categorical variables, means, and SD or median and interquartile ranges for continuous variables. A frequency distribution statistical analysis was used to check whether there were any invalid, missing, or duplicate values. 28 Incidence of hospital acquired pressure injury ([HAPI] defined as any PI not presented at admission but acquired during hospitalisation) was measured using the proportion of participants who developed a HAPI divided by the total number of participants with a C‐collar at risk of PI development. 29 The nine‐financial year incidence of HAPI development was compared between three groups, direct CRPIs, indirect CRPIs, or other PIs.

Length of time in ICU was calculated from admission date to discharge date; the time patients had the C‐collar in situ was computed from admission date to the time the C‐collar removal was documented; repositioning frequency (mean daily turn totals) was calculated from the number of daily turns during the time the C‐collar was on and was compared with the time the C‐collar was removed; GCS score was recorded as the lowest score on every day of the patient's admission up to 28 days and was analysed by examining the proportion of days patients had a GCS score less than 8, less than 11, and 15; time to direct CRPI, indirect CRPI, and other PI development were defined as the number of days between ICU admission date and the first documented time of a PI.

Pearson Chi square test, Fisher's exact test, and t‐tests were used as appropriate to identify variables associated with PI development across patient groups, and those with a significance value of P ≤ .2 formed the basis for multivariate logistic regression. Logistic regression modelling was employed to analyse the risk factors of CRPI development. The patient admission date and the first direct and indirect CRPI development time were included to measure the fraction of patients with a C‐collar for a certain amount of time and those who developed a CRPI. Odds ratios (ORs) with 95% confidence intervals (CIs) and a P value less than .05 was considered statistically significant.

3. RESULTS

3.1. Patient demographics/characteristics

During the nine financial year (2010‐2019) study period, 925 patients were admitted to the ICU with a C‐collar in situ. Of these, 19 were excluded because they had CAPIs upon admission leaving 906 patients included for analysis (Table 1). Patient mean age was 46.1 years (SD 19.4, range 29‐62) and most were male (69%, n = 625). The average APACHE II score was 17 (SD 8). The patients' admission diagnosis was mainly trauma, inclusive of non‐operative trauma (52%, n = 468) and operative trauma (19.4%, n = 175). The majority of patients were admitted to the ICU from the emergency department (51.2%, n = 464). Over half of patients had vasopressor medications administered (n = 461, 50.9%) and were mechanically ventilated (n = 762, 84.1%) during their ICU admission. The mean length of stay in the ICU was 8.19 days (SD 14.19). The mean repositioning frequency for patients with a C‐collar in situ was 6.4 position changes (SD 2.61) per day, and this increased to 7 (SD 2.7) position changes when the C‐collar was removed. Of the remaining 906 patients, 154 (17%) developed a HAPI (including CRPI or any other PI).

TABLE 1.

Patients' demographic and clinical characteristics (n = 906)

Variable/year 2010‐2011 (n = 89) 2011‐2012 (n = 81) 2012‐2013 (n = 81) 2013‐2014 (n = 66) 2014‐2015 (n = 72) 2015‐2016 (n = 91) 2016‐2017 (n = 143) 2017‐2018 (n = 141) 2018‐2019 (n = 142) Total patients (n = 906)
Age (y)
Mean ± SD 42.1 ± 20.1 42.6 ± 19.2 42.8 ± 17.9 44.3 ± 20.7 47.7 ± 19.5 44 ± 17.5 50 ± 19.6 47.8 ± 19.1 48.2 ± 19.5 46.1 ± 19.4
Median, interquartile range 38 (24‐57) 41 (24‐55) 41.5 (27‐59) 39.8 (23‐65) 46.5 (30‐63) 45 (28‐57) 52 (32‐66) 48 (32‐63) 49.5 (30‐65) 46 (29‐62.1)
Gender (number, %)
Male 64 (71.9) 62 (76.5) 57 (70.4) 46 (69.7) 55 (76.4) 61 (67) 97 (67.8) 89 (63.1) 94 (66.2) 625 (69)
Female 25 (28.1) 19 (23.5) 24 (29.6) 20 (30.3) 17 (23.6) 30 (33) 46 (32.2) 52 (36.9) 48 (33.8) 281 (31)
Admission diagnosis (number, %)
Non‐operative trauma 54 (60.7) 50 (61.7) 42 (51.9) 41 (62.1) 40 (55.6) 56 (61.5) 63 (49.3) 60 (42.9) 56 (40) 468 (52)
Operative trauma 19 (21.3) 17 (21) 23 (28.4) 15 (22.7) 16 (22.2) 16 (17.6) 17 (12.1) 27 (19.3) 25 (17.9) 175 (19.4)
Neurological 6 (6.7) 4 (4.9) 7 (8.6) 4 (6.1) 6 (8.3) 5 (5.5) 15 (10.7) 13 (9.3) 27 (19.3) 87 (9.7)
Respiratory 2 (2.2) 1 (1.2) 4 (4.9) 3 (4.5) 1 (1.4) 3 (3.3) 9 (6.4) 9 (6.4) 7 (5) 39 (4.3)
Cardiovascular 3 (3.4) 1 (1.2) 1 (1.2) 1 (1.5) 4 (5.6) 4 (4.4) 5 (3.6) 9 (6.4) 11 (7.9) 39 (4.3)
Metabolic 2 (2.2) 5 (6.2) 1 (1.2) 1 (1.5) 2 (2.8) 2 (2.2) 4 (2.9) 6 (4.3) 4 (2.9) 27 (3)
Sepsis 1 (1.1) 0 0 1 (1.5) 1 (1.4) 4 (4.4) 10 (7.1) 5 (3.6) 3 (2.1) 25 (2.8)
Gastrointestinal 0 0 2 (2.5) 0 1 (1.4) 0 6 (4.3) 6 (4.3) 6 (4.3) 21 (2.3)
Others 1 (1.1) 1 (1.2) 0 0 1 (1.4) 0 2 (1.4) 2 (1.4) 0 7 (0.8)
Musculoskeletal 1 (1.1) 0 1 (1.2) 0 0 1 (1.1) 0 2 (1.4) 0 5 (0.6)
Haematological 0 1 (1.2) 0 0 0 0 2 (1.4) 0 0 3 (0.3)
Gynaecological 0 0 0 0 0 0 0 1 (0.7) 1 (0.7) 2 (0.2)
Renal 0 0 1 (1.2) 0 0 0 1 (0.7) 0 0 2 (0.2)
APACHE II score
Mean ± SD 15 ± 8 14 ± 7 15 ± 6 16 ± 8 17 ± 8 17 ± 8 18 ± 8 19 ± 8 17 ± 7 17 ± 8
Median, interquartile range 14 (9‐19) 14 (9‐18) 14 (10‐18) 16 (9‐20) 17 (12‐22) 15 (11‐21) 16 (12‐24) 17 (12‐24) 16 (12‐22) 16 (11‐21)
ICU admission source (number, %)
Emergency department 51 (57.3) 51 (63) 34 (42) 27 (40.9) 36 (50) 51 (56) 65 (45.5) 75 (53.2) 74 (52.1) 464 (51.2)
Operating room 25 (28.1) 19 (23.5) 32 (39.5) 17 (25.8) 19 (26.4) 20 (22) 26 (18.2) 37 (26.2) 42 (29.6) 237 (26.2)
Other hospital 8 (9) 8 (9.9) 9 (11.1) 11 (16.7) 10 (13.9) 11 (12.1) 25 (17.5) 6 (4.3) 9 (6.3) 97 (10.7)
Ward transfer 4 (4.5) 2 (2.5) 2 (2.5) 6 (9.1) 2 (2.8) 5 (5.5) 19 (13.3) 18 (12.8) 12 (8.5) 70 (7.7)
Other hospital ICU 1 (1.1) 1 (1.2) 4 (4.9) 5 (7.6) 5 (6.9) 4 (4.4) 8 (5.6) 5 (3.5) 5 (3.5) 38 (4.2)
GCS proportion (mean ± SD) a
<8 0.37 ± 0.43 0.23 ± 0.38 0.2 ± 0.36 0.22 ± 0.34 0.65 ± 0.4 0.78 ± 0.35 0.63 ± 0.39 0.58 ± 0.4 0.66 ± 0.39 0.51 ± 0.43
<11 0.63 ± 0.4 0.61 ± 0.42 0.45 ± 0.43 0.48 ± 0.42 0.76 ± 0.35 0.85 ± 0.32 0.74 ± 0.38 0.69 ± 0.38 0.74 ± 0.37 0.67 ± 0.4
15 0.1 ± 0.24 0.12 ± 0.25 0.13 ± 0.28 0.12 ± 0.25 0.03 ± 0.14 0.04 ± 0.16 0.08 ± 0.21 0.08 ± 0.18 0.1 ± 0.25 0.08 ± 0.22
C‐collar time (d)
Mean ± SD 4.27 ± 12.78 2.08 ± 4.22 3.57 ± 5.45 4.59 ± 7.33 2.84 ± 5.27 2.57 ± 4.36 5.09 ± 19.37 3.52 ± 6.23 3.61 ± 7.47 3.66 ± 10.11
Median, interquartile range 1.2 (0.5‐2.9) 0.6 (0.3‐1.6) 0.87 (0.4‐4) 1.66 (0.5‐4.6) 0.6 (0.2‐1.5) 0.59 (0.17‐3) 1.13 (0.5‐4.5) 1.34 (0.5‐3.7) 0.81 (0.4‐3.8) 0.8 (0.3‐3.5)
Mechanical ventilation (number, %)
Yes 73 (82) 67 (82.7) 69 (85.2) 55 (83.3) 64 (88.9) 71 (78) 121 (84.6) 117 (83) 125 (88) 762 (84.1)
Vasopressor (number, %)
Yes 36 (40.4) 24 (29.6) 28 (34.6) 29 (43.9) 32 (44.4) 52 (57.1) 89 (62.2) 81 (57.4) 90 (63.4) 461 (50.9)
ICU length of stay (d)
Mean ± SD 7.88 ± 14.9 5.74 ± 5.55 7.93 ± 13.67 7.41 ± 8.4 7.69 ± 7.67 8.35 ± 7.21 11.3 ± 27 7.7 ± 9.31 7.81 ± 10.18 8.19 ± 14.19
Median, interquartile range 3.6 (1.7‐10.4) 3.6 (1.7‐8.5) 3.96 (1.7‐9.8) 3.7 (2.1‐10.7) 4.47 (2‐10) 5.9 (2.8‐12) 5.65 (2.7‐12) 4.67 (2.6‐9.8) 4.55 (2.4‐9.3) 4.5 (2.1‐10.6)
ICU outcome (number, %)
Survived 81 (92) 79 (97.5) 78 (96.3) 59 (89.4) 65 (90.3) 79 (86.8) 130 (90.9) 123 (87.2) 129 (90.8) 823 (90.9)
Died 7 (8) 2 (2.5) 3 (3.7) 7 (10.6) 7 (9.7) 12 (13.2) 13 (9.1) 18 (12.8) 13 (9.2) 82 (9.1)
Repositioning frequency
C‐collar in situ
Mean ± SD 5.4 ± 2.37 5.71 ± 2.43 5.79 ± 2.44 6.69 ± 2.61 6.39 ± 2.93 6.52 ± 3.29 6.88 ± 2.48 6.61 ± 2.65 6.57 ± 2.39 6.4 ± 2.61
Median, interquartile range 5.5 (3.5‐7) 5.5 (4.5‐7) 5.71 (4‐7.56) 6.66 (5‐8) 6 (4‐8) 6 (4‐8.86) 7 (5.5‐8.17) 6.67 (5‐8.25) 6.45 (5‐8) 6.15 (4.5‐8)
C‐collar removed
Mean ± SD 7.08 ± 3 7.66 ± 2.9 6.97 ± 2.97 6.15 ± 3.64 6.68 ± 3.21 7.58 ± 2.62 6.84 ± 2.23 7.18 ± 2.24 6.65 ± 2.55 7 ± 2.7
Median, interquartile range 7.8 (5.5‐9.2) 8.2 (6.25‐9.6) 7.4 (5‐8.69) 7 (3.5‐9) 7 (5‐8.81) 8 (6.5‐9) 7.29 (5.38‐8) 7.5 (6‐8.33) 7 (5‐8) 7.25 (5.5‐8.5)
Mean repositioning type
C‐collar in situ (mean ± SD)
Supine 1.65 ± 1.58 1.85 ± 1.49 1.6 ± 1.46 1.78 ± 1.48 2.97 ± 1.76 3.16 ± 1.78 3.32 ± 1.25 3.27 ± 1.43 3.29 ± 1.49 2.7 ± 1.67
Logrolled 2.49 ± 1.67 2.52 ± 1.59 3.09 ± 1.63 3.25 ± 1.90 2.3 ± 1.53 2.1 ± 1.75 1.49 ± 1.65 1.65 ± 1.7 1.34 ± 1.45 2.08 ± 1.75
Lateral 0.83 ± 1.18 0.77 ± 0.83 0.7 ± 1.03 0.88 ± 1.32 0.79 ± 1.16 1.03 ± 1.34 1.77 ± 1.61 1.45 ± 1.5 1.63 ± 1.49 1.2 ± 1.4
Lateral left 0.48 ± 0.7 0.49 ± 0.52 0.34 ± 0.53 0.47 ± 0.77 0.38 ± 0.61 0.54 ± 0.76 0.94 ± 0.91 0.81 ± 0.89 0.89 ± 0.89 0.65 ± 0.81
Lateral right 0.36 ± 0.59 0.28 ± 0.48 0.36 ± 0.62 0.41 ± 0.6 0.41 ± 0.66 0.49 ± 0.71 0.82 ± 0.85 0.64 ± 0.78 0.74 ± 0.84 0.55 ± 0.74
Other 0.25 ± 0.67 0.36 ± 0.78 0.19 ± 0.45 0.48 ± 1 0.25 ± 0.51 0.1 ± 0.26 0.14 ± 0.4 0.1 ± 0.35 0.12 ± 0.33 0.19 ± 0.54
Sitting out of bed 0.05 ± 0.18 0.09 ± 0.23 0.05 ± 0.14 0.23 ± 0.57 0.04 ± 0.16 0.05 ± 0.21 0.08 ± 0.2 0.05 ± 0.16 0.1 ± 0.32 0.08 ± 0.26
Reverse Trendelenburg 0.09 ± 0.39 0.13 ± 0.56 0.15 ± 0.76 0.05 ± 0.23 0.03 ± 0.17 0.05 ± 0.32 0.08 ± 0.39 0.08 ± 0.36 0.08 ± 0.38 0.08 ± 0.42
Trendelenburg 0.04 ± 0.18 0 0.01 ± 0.11 0.01 ± 0.07 0.01 ± 0.12 0.03 ± 0.22 0 0 ± 0.01 0.01 ± 0.06 0.01 ± 0.11
C‐collar removal (mean ± SD)
Supine 2.73 ± 1.56 2.73 ± 1.42 1.8 ± 1.11 1.42 ± 1.49 3.03 ± 1.77 3.69 ± 1.54 3.38 ± 1.37 3.32 ± 1.5 3.32 ± 1.16 3.05 ± 1.61
Lateral 2.38 ± 2 2.13 ± 1.47 1.76 ± 1.58 1.78 ± 2.23 2.23 ± 1.77 2.55 ± 1.75 2.57 ± 1.55 2.83 ± 1.54 2.43 ± 1.37 2.39 ± 1.65
Lateral left 1.3 ± 1.16 1.19 ± 0.88 0.94 ± 0.97 0.82 ± 0.93 1.18 ± 0.98 1.37 ± 1.03 1.37 ± 0.99 1.53 ± 0.89 1.3 ± 0.91 1.29 ± 0.98
Lateral right 1.08 ± 0.97 0.93 ± 0.85 0.76 ± 0.89 0.76 ± 0.91 1.05 ± 1.01 1.18 ± 0.94 1.2 ± 0.82 1.3 ± 0.89 1.13 ± 0.86 1.11 ± 0.9
Logrolled 0.92 ± 0.87 1.63 ± 1.25 1.85 ± 1.46 1.57 ± 1.55 0.82 ± 1.72 0.73 ± 1.57 0.32 ± 0.85 0.42 ± 1.2 0.27 ± 1.04 0.74 ± 1.34
Other 0.63 ± 1.24 0.83 ± 1.13 1.29 ± 2.28 1.31 ± 2.54 0.43 ± 1.03 0.4 ± 0.8 0.29 ± 0.87 0.37 ± 1.08 0.42 ± 1.22 0.54 ± 1.32
Sitting out of bed 0.38 ± 0.48 0.34 ± 0.67 0.32 ± 0.56 0.27 ± 0.57 0.12 ± 0.29 0.14 ± 0.24 0.27 ± 0.49 0.21 ± 0.33 0.19 ± 0.34 0.24 ± 0.44
Reverse Trendelenburg 0.05 ± 0.28 0 0.01 ± 0.04 0 0.04 ± 0.24 0.04 ± 0.23 0.01 ± 0.05 0.03 ± 0.23 0.01 ± 0.05 0.02 ± 0.16
Trendelenburg 0 ± 0.02 0.01 ± 0.04 0 ± 0.01 0 0 0.03 ± 0.22 0 ± 0.02 0 ± 0.01 0 ± 0.01 0 ± 0.08
Patient with PI (number, %) b 2 (2.2) 11 (13.6) 16 (19.8) 13 (19.7) 20 (27.8) 19 (18.7) 31 (21.7) 26 (18.4) 16 (11.3) 154 (17)
Numbers of PIs per patient (number, %)
One 2 (2.2) 8 (9.9) 10 (12.3) 6 (9.1) 12 (16.7) 10 (11) 20 (14) 18 (12.8) 11 (7.7) 97 (10.7)
Two 0 3 (3.7) 3 (3.7) 4 (6.1) 3 (4.2) 5 (5.5) 6 (4.2) 6 (4.3) 3 (2.1) 33 (3.6)
Three 0 0 2 (2.5) 2 (3) 2 (2.8) 0 4 (2.8) 2 (1.4) 2 (1.4) 14 (1.5)
Four 0 0 1 (1.2) 1 (1.5) 3 (4.2) 1 (1.1) 1 (0.7) 0 0 7 (0.8)
Six 0 0 0 0 0 1 (1.1) 0 0 0 1 (0.1)

Abbreviations: APACHEII, Acute Physiology and Chronic Health Evaluation II; GCS, Glasgow Coma Scale; ICU, intensive care unit; PI, pressure injury.

a

Population mean of the proportion of days each patient's GCS score was less than 8; less than 11 or 15.

b

PI of any kind.

3.2. Incidence rate of CRPI

Over the 9‐year period, the incidence of direct CRPI was 0.7% (6/906), the incidence of indirect CRPIs was 5.4% (49/906), and other PI was 10.9% (99/906). The overall HAPI incidence was 16.9% (154/906). Incidence year by year is reported in Table 2.

TABLE 2.

Incidence rates of HAPIs

Financial year Patients with direct CRPI (number, %) Patients with indirect CRPI (number, %) Patients with other PI (number, %) Total patients with any HAPI (number, %)
2010‐2011 (n = 89) 1 (1.1) 0 1 (1.1) 2 (2.2)
2011‐2012 (n = 81) 0 3 (3.7) 8 (9.9) 11 (13.6)
2012‐2013 (n = 81) 0 7 (8.6) 9 (11.1) 16 (19.8)
2013‐2014 (n = 66) 0 7 (10.6) 6 (9.1) 13 (19.7)
2014‐2015 (n = 72) 1 (1.4) 5 (6.9) 14 (19.4) 20 (27.8)
2015‐2016 (n = 91) 2 (2.2) 7 (7.7) 8 (8.8) 19 (18.7)
2016‐2017 (n = 143) 1 (0.7) 9 (6.3) 21 (14.7) 31 (21.7)
2017‐2018 (n = 141) 1 (0.7) 8 (5.7) 17 (12.1) 26 (18.4)
2018‐2019 (n = 142) 0 3 (2.1) 13 (9.2) 16 (11.3)
Total patients (n = 906) 6 (0.7) 49 (5.4) 99 (10.9) 154 (16.9)

Abbreviations: CRPI, C‐collar‐related pressure injury; HAPI, hospital acquired pressure injury; PI, pressure injury.

3.3. The severity and anatomical locations of CRPI (direct and indirect) and other PI

Total 239 HAPIs were recorded in 154 patients. Direct CRPIs were detected in three regions where C‐collars were directly contacted with the skin. These were the neck (3.3%, 8/239; one Stage I, four Stage II, two Stage III, and one deep tissue PI), chin (0.4%, 1/239; one deep tissue PI), and clavicle (0.4%, 1/239; one Stage I). Indirect CRPIs were mainly located on the sacrum (17.2%, 41/239). The most frequent location for other PIs was the mouth (17.2%, 41/239) where 24 mucosal PI, two Stage I, 12 Stage II, two Stage III, and one unstageable PI were found. Of the total 239 HAPIs identified (including nine missing data for the PI severity), the most frequently recorded classification was Stage II (99/239, 41.4%) (Table 3).

TABLE 3.

HAPI anatomical location and stage 2010‐2019 (n = 239)

Location/severity Mucosal Stage I Stage II Stage III Stage IV Unstageable Suspected deep tissue injury Total number of PIs
Direct CRPI (number, %)
Neck 0 1 (0.4) 4 (1.7) 2 (0.8) 0 0 1 (0.4) 8 (3.3)
Chin 0 0 0 0 0 0 1 (0.4) 1 (0.4)
Clavicle 0 1 (0.4) 0 0 0 0 0 1 (0.4)
Total 0 2 4 2 0 0 2 10
Indirect CRPI (number, %)
Sacrum 0 11 (4.6) 22 (9.2) 3 (1.3) 0 1 (0.4) 4 (1.7) 41 (17.2)
Heels 0 12 (5) 5 (2.1) 2 (0.8) 0 1 (0.4) 6 (2.5) 26 (10.9)
Occiput 0 1 (0.4) 9 (3.8) 2 (0.8) 1 (0.4) 4 (1.7) 3 (1.3) 20 (8.4)
Buttocks 0 3 (1.3) 11 (4.6) 0 0 1 (0.4) 4 (1.7) 19 (7.9)
Back 0 2 (0.8) 3 (1.3) 0 0 0 0 5 (2.1)
Elbow 0 2 (0.8) 0 0 0 0 0 2 (0.8)
Shoulder 0 0 0 0 0 0 0 0
Total 0 31 50 7 1 7 17 113
Other PI (number, %)
Mouth 24 (10) 2 (0.8) 12 (5) 2 (0.8) 0 1 (0.4) 0 41 (17.2)
Nose 6 (2.5) 5 (2.1) 18 (7.5) 1 (0.4) 0 1 (0.4) 1 (0.4) 32 (13.4)
Facial 0 0 7 (2.9) 0 0 1 (0.4) 2 (0.8) 10 (4.2)
Leg 0 5 (2.1) 2 (0.8) 1 (0.4) 0 0 1 (0.4) 9 (3.8)
Chest 0 2 (0.8) 3 (1.3) 1 (0.4) 0 0 0 6 (2.5)
Genitalia 1 (0.4) 1 (0.4) 1 (0.4) 1 (0.4) 0 0 0 4 (1.7)
Arm 0 2 (0.8) 2 (0.8) 0 0 0 0 4 (1.7)
Trachea 0 0 0 1 (0.4) 0 0 0 1 (0.4)
Total 31 17 45 7 0 3 4 107
Missing data 9 (3.8)
Total numbers of PIs 31 (13) 50 (20) 99 (41.4) 16 (6.7) 1 (0.4) 10 (4.2) 23 (9.6) 239 (100)

Abbreviations: CRPI, C‐collar‐related pressure injury; HAPI, hospital acquired pressure injury; PI, pressure injury.

3.4. Risk factors associated with CRPI development

The predictor variables used for this analysis were age, gender, APACHE II score, GCS score, length of time with C‐collar in situ, repositioning frequency, use of medical ventilation, vasopressor use, and the length of stay in the ICU. The mean of total position changes per day was found to be a significant predictor for patients to develop a direct CRPI (n = 6) compared with patients with no PI development (n = 760), where the odds of developing a direct CRPI increased 33% with each daily repositioning episode (OR: 1.328, 95% CI: 1.024‐1.723, P = .033). No other variables evaluated in this study had a significant impact on the incidence of direct CRPI.

Time in the C‐collar was significantly higher in patients who developed an indirect CRPI (n = 49, 15.5 days, SD 31.8) as compared with patients who did not develop an indirect CRPI (n = 794, 2.53 days, SD 6.12) (OR: 1.101, 95% CI: 1.061‐1.143, P < .001). APACHE II score was a significant predictor of indirect CRPI development (OR: 1.084, 95% CI: 1.045‐1.124, P < .001), as well as admission to the ICU from the emergency department (OR: 0.391, 95% CI: 0.197‐0.778, P = .007).

The mean (SD) time of stay in ICU was 17.2 days (15.4) for the patients who developed any other PI (n = 99), compared with 6.03 days (7.87) for patients who did not develop the complication (n = 853) (P < .001). There was an increase in odds of other PI development related to the length of time C‐collar was in situ (P < .001). There was an increase in the odds of other PI development when APACHE II score (P = .001) was added as an additional predictor variable in this equation (Tables 4 and 5).

TABLE 4.

Bivariate analysis of variables comparing between patients with no PIs and those with direct CRPIs, indirect CRPIs, and other PIs

Variable Patients without PIs (N = 754) Patients with direct CPRI (N = 6) Patients with indirect CRPI (N = 49) Patients with other PI (N = 99)
Value Value Test P value Value Test P value Value Test P value
Age (mean ± SD) 45.35 ± 19.14 56.2 ± 29.7 1.372 .170 50.7 ± 19.2 1.898 a .058 48.8 ± 20.2 1.681 a .093
GCS < 8 0.50 ± 0.44 0.5 ± 0.4 −0.159 .874 0.5 ± 0.4 −0.145 a .885 0.6 ± 0.4 3.111 a <.001 d
GCS < 11 0.66 ± 0.41 0.6 ± 0.2 −0.323 .747 0.7 ± 0.3 0.425 a .671 0.8 ± 0.3 2.961 a <.001 d
GCS = 15 0.09 ± 0.23 0.02 ± 0.06 −0.746 .456 0.06 ± 0.14 −1.135 a .257 0.04 ± 0.12 −2.495 a .013 d
Mean of total turns 6.20 ± 2.69 8.6 ± 2.6 2.176 .030 d 7.4 ± 2.2 3.004 a .003 d 7.0 ± 2.3 2.888 a .004 d
ICU LOS 6.03 ± 7.87 20.1 ± 20.3 4.289 <.001 d 22 ± 43 8.334 a <.001 d 17.2 ± 15.4 11.523 a <.001 d
APACHE II score 16.08 ± 7.54 20.2 ± 9.6 1.320 .187 22 ± 9 5.245 a <.001 d 19.8 ± 7 4.698 a <.001 d
C‐collar time (day) 2.53 ± 6.12 10.4 ± 6.7 3.126 .002 d 15.5 ± 31.8 8.976 a <.001 d 6.1 ± 8.5 5.212 a <.001 d
Gender (number, %) c .384 0.047 b .828 0.341 b .559
Male 519 (69) 3 (50) 33 (67.3) 71 (71.7)
Female 235 (31) 3 (50) 16 (32.7) 28 (28.3)
Ventilation use (yes) 614 (81) 6 (100) c .599 49 (100) 10.864 b .001 d 93 (93.9) 9.40 b .002 d
ICU outcome (survived) 685 (91) 6 (100) c 1 43 (87.8) c .451 91 (91.9) 0.097 b .755
Vasopressor use (yes) 346 (46) 3 (50) c 1 39 (79.6) 20.941 b <.001 d 75 (75.8) 31.23 b <.001 d
ICU admission source 5.025 b .285 48.033 b <.001 d 8.964 b .062
Emergency 405 (54) 2 (33.3) 13 (26.5) 44 (44.4)
Operating room 202 (27) 1 (16.7) 10 (20.4) 24 (24.2)
Other hospital 73 (10) 1 (16.7) 7 (14.3) 17 (17.2)
Other ICU 25 (3) 1 (16.7) 10 (20.4) 3 (3)
Ward transfer 49 (6) 1 (16.7) 9 (18.4) 11(11.1)

Abbreviations: APACHE II, Acute Physiology and Chronic Health Evaluation II; CRPI, C‐collar‐related pressure injury; GCS, Glasgow Comma Scale; ICU, intensive care unit; LOS, length of stay; PI, pressure injury.

a

t‐test.

b

Pearson Chi Square test.

c

Fisher's exact test.

d

Significance at P < .05.

TABLE 5.

Risk factors of PI using binary logistic regression

Independent variables B SE Wald df Sig. Exp(B) 95% CI for EXP(B)
Lower Upper
A) For direct CRPIs (n = 6) compared with patients with no PI (n = 760)
Total turns (mean) 0.284 0.133 4.564 1 0.033 1.328 1.024 1.723
Constant −7.096 1.237 32.893 1 0.000 0.001
B) For indirect CRPIs (n = 49) compared with patients with no PI (n = 794)
C‐collar time (days) 0.096 0.019 25.845 1 0.000 1.101 1.061 1.143
APACHE II score 0.080 0.019 18.676 1 0.000 1.084 1.045 1.124
ICU admission source (emergency department) −0.938 0.351 7.156 1 0.007 0.391 0.197 0.778
Constant −3.684 0.650 93.118 1 0.000 0.012
C) For other PIs (n = 99) compared with patients with no PI (n = 853)
ICU LOS (days) 0.140 0.018 61.367 1 0.000 1.150 1.110 1.191
C‐collar time (days) −0.092 0.025 13.505 1 0.000 0.913 0.869 0.958
APACHE II score 0.050 0.015 10.586 1 0.001 1.051 1.020 1.083
Constant −2.830 0.357 134.788 1 0.000 0.020

Note: Panel A: Negelkerke R 2 = .063; Panel B: Negelkerke R 2 = .233; Panel C: Negelkerke R 2 = 0.241.

Abbreviations: APACHE II, Acute Physiology and Chronic Health Evaluation II; CRPI, C‐collar‐related pressure injury; ICU, intensive care unit; LOS, length of stay; PI, pressure injury.

3.5. The time for patients to develop CRPI

The median time from ICU admission to documentation of a direct CRPI was 5.7 days (range 1.2‐10.1), 2.9 days to develop an indirect CRPI (range 1.1‐6.8), and 5.5 days to develop any other PI (range 2.9‐9.4). Of the patients who had developed a direct CRPI (n = 6), most patients (66.7%, 4/6) developed a direct CRPI when the C‐collar was in situ for more than 6 days after ICU admission. A similar tendency was observed in those patients who developed indirect CRPIs (n = 49) where more than half of the patients (63.3%, 31/49) developed indirect CRPIs with the C‐collar in situ for longer than 6 days (Table 6).

TABLE 6.

Time to PI and C‐collar time between direct, indirect CRPI, other PI, and HAPI

Variables Patients with No PI (N = 754) Patients with direct CRPI (N = 6) Patients with indirect CRPI (N = 49) Patients with other PI (N = 99) Patients with HAPI (N = 154)
No Yes Yes Yes Yes
Time to event
Mean ± SD 5.7 ± 4.3 6 ± 10.7 7.2 ± 5.4 6.7 ± 7.5
Median, range 5.7 (1.2‐10) 2.9 (1.1‐6.9) 5.5 (2.9‐9.4) 3.7 (1.9‐8.0)
C‐collar in situ
Mean ± SD 2.5 ± 6.1 10.4 ± 6.7 15.5 ± 31.8 6.1 ± 8.5 9.3 ± 19.7
Median, range 0.7 (0.3‐2.4) 10.92 (5.6‐12) 10.6 (2.8‐17.3) 2.4 (0.6‐8.2) 5 (0.7‐13.1)
C‐collar in situ (number, %)
<3 days 1 (16.7) 13 (26.5) 51 (51.5) 65 (42.8)
3‐6 days 1 (16.7) 5 (10.2) 14 (14.1) 20 (13.2)
6‐10 days 0 5 (10.2) 13 (13.1) 18 (11.8)
>10 days 4 (66.7) 26 (53.1) 21 (21.1) 51 (32.2)

Abbreviations: CRPI, C‐collar‐related pressure injury; HAPI, hospital acquired pressure injury; PI, pressure injury.

4. DISCUSSION

This is the first study to report a 9‐year overview of PIs in patients with a C‐collar in situ in the ICU. The incidence rate of direct CRPI (0.7%) in this study was lower than the findings of previous international studies of 1.1%, 10 6.8%, 16 6.8% to 38%, 14 9.7%, 11 23.9%, 15 38%, 12 and 44%. 13 This may be explained in part by the different categorisation of CRPIs in each earlier study as well as differing care practices, types of collar used, and patient characteristics. The differences in categorisation/staging of CRPIs between studies make comparison difficult. That is, when other studies were conducted, the definition of MDR PI did not exist. Our study is the first study to apply this definition to C‐collar device‐related injuries and as a result, it is impossible to contrast our findings with previous literature.

Undeniably, the application of C‐collar generated high risk for PI development in our sample of patients in the ICU. Although the incidence of direct (0.7%) and indirect (5.4%) CRPIs was low, the overall HAPI incidence (16.9%) was high. Our results may indicate that patients with C‐collars are more likely to develop any kind of PI. This is most likely attributable to several key issues. Firstly, patients with a C‐collar in situ are predominantly trauma patients with a longer ICU admission. The mean ICU length of stay was 8.2 days in our study, which is substantially higher than the length of stay of other ICU patient groups (surgical and medical patients in the same study hospital), who had a mean length of stay of 3.6 days, the latter being consistent with the average duration of stay in Queensland public hospital ICUs.19, 30 Secondly, patients with a C‐collar in situ are largely immobile, are repositioned less frequently with pressure points not off loaded for long periods, and require logroll repositioning to keep the cervical spine in alignment.8, 9, 10, 31

The overall HAPI incidence rate in our study decreased from 21.7% in 2016‐2017 to 11.3% in 2018‐2019. This reduction may be because of the completion of a number of research studies translating best‐available PI prevention strategies into the local ICU research site.32, 33, 34 Additionally, we acknowledge that clinical practices changed during the 9‐year data collection period of this study. The most significant practice change noted was by the Queensland Ambulance Service (QAS) and the research site where rigid C‐collars were replaced with soft C‐collars. 3 Although the exact date of the transition to soft collars by QAS was not able to be determined, the use of soft collars would have been a clinically important factor in the downward trend of direct CRPIs in this study.

Our study found that direct CRPIs were mainly located all around the neck and most were documented as Stage II. The sacrum was found to be the most frequent location for indirect CRPIs development. It is difficult to directly compare the results with other studies again because of the variations in reporting of CRPIs. For example, Watts et al 17 and Ham et al 8 described PI stages as an aggregate result, with PI stages reported for all PIs rather than differentiating between the stages attributed directly and indirectly to the C‐collar, whereas Davis et al 13 and Molano et al 15 reported stages only related to the C‐collar.

Interestingly, we found that the development of direct CRPI increased by 33% with each repositioning episode (OR: 1.328, 95% CI: 1.024‐1.723, P = .033). One possible explanation for this result may be that the movement associated with more frequent repositioning may have caused increased friction and shear forces (known to contribute to PI development) at the interface between the skin and the collar, contributing to the development of a direct CRPI.18, 35, 36

Time in a C‐collar should be kept as short as clinically possible. In our study, the time in the C‐collar was identified as an important risk factor for both indirect CRPIs and other types of PI development, which is consistent with previous work.11, 12, 13, 14, 16, 17 Davis et al 13 found that patients with C‐collar for 5 days or longer were more likely to develop a CRPI (P = .029). Ackland et al 11 reported that the risk of CRPI development increased by 66% for each 1 day increase in C‐collar time. In our study, the risk for indirect CRPIs increased by 8.1% for every day in the C‐collar.

In addition, APACHE II score was reported as an important risk factor for both the indirect CRPI and other PI development. Ham et al 14 and NPUAP, EPUAP, and PPPIA 27 all report that trauma patients with a high severity of illness have an increased risk of any PI development. The APACHE II score is calculated on admission, consequently the higher the APACHE II score, the higher severity of illness, resulting in a potentially longer length of stay in ICU and an increase in the probability of PI development. 37 Further to this, our study found length of stay in the ICU had a statistically significant association with the development of other PIs. Again, it is difficult to compare these findings with other studies because of the differences in reporting of the categories of PIs. We found no other studies focusing on CRPI have reported an ‘other PI’ category. However, Molano et al 15 reported that patients who developed CRPI had a longer length of stay in the ICU (24.6 days) compared with patients without a CRPI (10 days). The finding by Molano et al 15 and our study point to an association between length of stay and PI development, although further research is warranted.

The average time for patients to develop a direct CRPI from ICU admission was 5.7 days, with two‐thirds of patients more likely to develop a direct CRPI with a C‐collar in situ for more than 10 days. A possible explanation for the association between the duration of C‐collar placement and indirect CRPI development may be that patients with C‐collars are cared for with cervical spine precautions, such as logrolling, limited reposition turns, and maintaining cervical spine alignment. 3 Thus, if patients are largely supine and logroll repositioned, the risk of a PI developing on the posterior body surface (back, occiput, shoulder, elbow, heel, buttocks, and sacrum) will increase.

This study introduced the terms ‘direct CRPI’ and ‘indirect CRPI’ that distinguish PIs that develop as a result of direct contact with the C‐collar and PIs that develop in association with the presence of a C‐collar. This proposed classification of CRPIs advances clarity in the reporting of these injuries and makes an important contribution to the understanding of CRPIs in critically ill intensive care patients. Future studies should standardise different terms for CRPIs and the way they are categorised and reported in order to facilitate benchmarking and comparison of research results. Further prospective studies are required to investigate the risk of PIs for patients with C‐collars in the ICU.

The duration of C‐collar placement and APACHE II score were significantly associated with the development of indirect CRPIs and other PIs. Therefore, healthcare providers should be aware of the increased risk of CRPI and other PI development in these patient categories. Furthermore, the longer length of days spent in a C‐collar, the more likely the patient is to develop indirect CRPIs and other PIs. It is therefore important to focus on education programs about the importance of C‐spine clearance procedure and interdisciplinary collaboration to facilitate rapid clearance of C‐spine in order to remove the C‐collar as soon as possible. Further, it is recommended that ICUs develop evidence‐based practice guidelines to standardise nursing practice and improve care of patients in C‐collars. Ongoing monitoring of CRPI incidence is recommended. The development and delivery of education programs regarding the importance of a C‐spine clearance protocol will assist healthcare providers and health professionals to understand the increased PI risk prolonged C‐collar time poses for patients and promote interdisciplinary collaboration in reducing the time patients are exposed to C‐collars.

A limitation of this study was the retrospective design of the data collection and the use of a single site, both of which could decrease the generalisability of the study findings. Another limitation was it was not possible to compare the sample population with a similar cohort of patients over time who did not have a C‐collar in situ. A final limitation was that the type of C‐collar used was also unable to be determined. It is plausible that the type of C‐collar may have influenced the incidence, locations, and severity of CRPI development.

5. CONCLUSION

The incidence of direct CRPI (0.7%) development in this study was lower than other studies; however, a high risk of overall HAPI (16.9%) development remained. This study found that patients with C‐collars are more likely to develop any kind of HAPI. Future studies could emphasise the understanding of the association between increased HAPI incidence and patients with C‐collars in situ to identify the reason for patients with a C‐collar who are at risk and to apply effective preventive interventions for HAPI development.

Wang H‐RN, Campbell J, Doubrovsky A, Singh V, Collins J, Coyer F. Pressure injury development in critically ill patients with a cervical collar in situ: A retrospective longitudinal study. Int Wound J. 2020;17:944–956. 10.1111/iwj.13363

Institution where work was performed: Intensive Care Services, Royal Brisbane and Women's Hospital.

REFERENCES

  • 1. Corsar K. Semirigid cervical spine collar and risk of missing significant soft tissue injuries. BMJ Case Rep. 2019;12(4):e228761. 10.1136/bcr-2018-228761. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2. Oteir A, Smith K, Stoelwinder J, Middleton J, Jennings P. Should suspected cervical spinal cord injury be immobilised: a systematic review. Injury. 2015;46(4):528‐535. 10.1016/j.injury.2014.12.032. [DOI] [PubMed] [Google Scholar]
  • 3.Queensland Ambulance Service. Clinical practice procedures: trauma/cervical collar. Clinical Quality and Patient Safety Unit, Queensland Government; 2016. https://www.ambulance.qld.gov.au/%5Cdocs%5Cclinical%5Ccpp%5CCPP_Cervical%20collar.pdf
  • 4.Agency for Clinical Innovation. Use of foam collars for cervical spine immobilisation: Initial management principles; 2018. https://www.aci.health.nsw.gov.au/__data/assets/pdf_file/0009/450882/ACI18080_Foam-Collars_Report_D4-final.pdf
  • 5. Barati K, Arazpour M, Vameghi R, Abdoli A, Farmani F. The effect of soft and rigid cervical collars on head and neck immobilisation in healthy subjects. Asian Spine J. 2017;11(3):390‐395. 10.4184/asj.2017.11.3.390. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 6. Quinn J, Enraght‐Moony E. Spinal immobilisation: evidence review. Queensland Ambulance Service. 2016. https://prehospitalandretrievalmedicine.files.wordpress.com/2015/05/spinal-immobilisation_evidence-review_170314_v3_eem.pdf
  • 7. Montgomery N, Goode D. Managing patients with cervical spine injury. Emerg Nurs. 2014;22(2):18‐22. 10.7748/en2014.04.22.2.18.e1216. [DOI] [PubMed] [Google Scholar]
  • 8. Ham W, Schoonhoven L, Schuurmans M, Leenen L. Pressure ulcers in trauma patients with suspected spine injury: a prospective cohort study with emphasis on device‐related pressure ulcers. Int Wound J. 2017;14(1):104‐111. 10.1111/iwj.12568. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9. Worsley PR, Stanger ND, Horrell AK, Bader DL. Investigating the effects of cervical collar design and fit on the biomechanical and biomarker reaction at the skin. Med Devices (Auckl). 2018;11:87‐94. 10.2147/MDER.S149419. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10. Ham W, Schoonhoven L, Galer A, Shortridge‐Baggett L. Cervical collar‐related pressure ulcers in trauma patients in intensive care unit. J Trauma Nurs. 2014;21(3):94‐102. 10.1097/JTN.0000000000000046. [DOI] [PubMed] [Google Scholar]
  • 11. Ackland H, Cooper J, Malham G, Kossmann T. Factors predicting cervical collar‐related decubitus ulceration in major trauma patients. Spine. 2007;32(4):423‐428. 10.1097/01.brs.0000255096.52871.4e. [DOI] [PubMed] [Google Scholar]
  • 12. Chendrasekhar A, Moorman DW, Timberlake GA. An evaluation of the effects of semi‐rigid cervical collars in patients with severe closed head injury. Am Surg. 1998;64(7):604‐606. https://gateway.library.qut.edu.au/login?url=https://search-\proquest-com.ezp01.library.qut.edu.au/docview/212804751?accountid=13380. [PubMed] [Google Scholar]
  • 13. Davis J, Parks S, Detlefs C, Williams G, Williams J, Smith R. Clearing the cervical spine in obtunded patients: the use of dynamic fluoroscopy. J Trauma. 1995;39(3):435‐438. [DOI] [PubMed] [Google Scholar]
  • 14. Ham W, Schoonhoven L, Schuurmans MJ, Leenen LP. Pressure ulcers from spinal immobilization in trauma patients: a systematic review. J Trauma Acute Care Surg. 2014;76:1131‐1141. 10.1097/TA.0000000000000153. [DOI] [PubMed] [Google Scholar]
  • 15. Molano AE, Murillo P, Salobral V, Domingue C, Cuenca S, Garcia F. Pressure sores secondary to immobilization with cervical collar: A complication of acute cervical injury. Enferm Intensiva. 2004;15:112‐122. [DOI] [PubMed] [Google Scholar]
  • 16. Powers J, Daniels D, McGuire C, Hilbish C. The incidence of skin breakdown associated with use of cervical collars. J Trauma Nurs. 2006;13(4):198‐200. 10.1097/00043860-200610000-00016. [DOI] [PubMed] [Google Scholar]
  • 17. Watts D, Abrahams E, MacMillan C, et al. Insult after injury: pressure ulcers in trauma patients. Orthop Nurs. 1998;17(4):84‐91. 10.1097/00006416-199807000-00012. [DOI] [PubMed] [Google Scholar]
  • 18.National Pressure Ulcer Advisory Panel. Pressure injury and stages. Washington: National Pressure Ulcer Advisory Panel; 2016. https://www.npuap.org/wp-content/uploads/2012/03/NPUAP-Staging-Poster.pdf
  • 19. Royal Brisbane and Women's Hospital . Intensive Care Services Annual Report. Brisbane: Royal Brisbane and Women's Hospital; 2018. [Google Scholar]
  • 20.The National Database of Nursing Quality Indicators (NDNQI). Pressure ulcer training; 2009. https://www.nursingquality.org/ndnqipressureulcertraining/default.aspx
  • 21. Knaus A, Draper A, Wagner P, Zimmerman E. APACHE II: a severity of disease classification system. Crit Care Med. 1985;13(10):818‐829. [PubMed] [Google Scholar]
  • 22. Naved SA, Siddiqui S, Khan FH. APACHE‐II score correlation with mortality and length of stay in an intensive care unit. J Coll Physicians Surg Pak. 2011;21:4‐8. [PubMed] [Google Scholar]
  • 23. Mclernon S. The Glasgow Coma Scale 40 years on: a review of its practical use. BJNN. 2014;10(4):179‐184. 10.12968/bjnn.2014.10.4.179. [DOI] [Google Scholar]
  • 24. Reith F, Brande R, Synnot A, Gruen R, Maas A. The reliability of the Glasgow Coma Scale: a systematic review. Intens Care Med. 2016;42(1):3‐15. 10.1007/s00134-015-4124-3. [DOI] [PubMed] [Google Scholar]
  • 25. Teasdale G, Allan D, Brennan P, McElhinney E, Mackinnon L. Forty years on: updating the Glasgow Coma Scale. Nurs Times. 2014;110(42):12‐16. http://search.proquest.com/docview/1620411352/. [Google Scholar]
  • 26.National Pressure Ulcer Advisory Panel, European Pressure Ulcer Advisory Panel. Prevention and treatment of pressure ulcers: clinical practice guideline. Washington: National Pressure Ulcer Advisory Panel; 2009.
  • 27.National Pressure Ulcer Advisory Panel, European Pressure Ulcer Advisory Panel, Pan Pacific Pressure Injury Alliance. Prevention and treatment of pressure ulcers: clinical practice guideline. 2nd ed. Perth, Australia: Cambridge Media; 2014.
  • 28. Pallant J. SPSS survival manual: a step by step guide to data analysis using IBM SPSS. 6th ed. Crows Nest, NSW: Allen & Unwin; 2016. [Google Scholar]
  • 29. Baharestani M, Black J, Carville K, et al. Dilemmas in measuring and using pressure ulcer prevalence and incidence: an international consensus. Int Wound J. 2009;6(2):97‐104. 10.1111/j.1742-481X.2009.00593.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 30.Australian Institute of Health and Welfare. Admitted patient care 2015‐16: Australian hospital statistics, Health services series no.75, Canberra: AIHW; 2017. https://www.aihw.gov.au/getmedia/3e1d7d7e-26d9-44fb-8549-aa30ccff100a/20742.pdf.aspx?inline=true
  • 31. Conrad B, Rossi G, Horodyski M, Prasarn M, Alemi Y, Rechtine G. Eliminating log rolling as a spine trauma order. Surg Neurol Int. 2012;3:188‐197. 10.4103/2152-7806.98584. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 32. Coyer F, Gardner A, Doubrovsky A, et al. Reducing pressure injuries in critically ill patients by using a patient skin integrity care bundle (inspire). Am J Crit Care. 2015;24(3):199‐209. 10.4037/ajcc2015930. [DOI] [PubMed] [Google Scholar]
  • 33. Coyer F, Miles S, Gosley S, et al. Pressure injury prevalence in intensive care versus non‐intensive care patients: a state‐wide comparison. Aust Crit Care. 2017;30(5):244‐250. [DOI] [PubMed] [Google Scholar]
  • 34. Coyer F, Cook J, Doubrovsky A, Campbell J, Vann A, McNamara G. Understanding contextual barriers and enablers to pressure injury prevention practice in an Australian intensive care unit: An exploratory study. Aust Crit Care. 2019;32(2):122‐130. 10.1016/j.aucc.2018.02.008. [DOI] [PubMed] [Google Scholar]
  • 35. Coleman S, Nixon J, Keen J, et al. A new pressure ulcer conceptual framework. J Adv Nurs. 2014;70(10):2222‐2234. 10.1111/jan.12405. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 36. Reger SI, Ranganathan VK, Orsted HL, Ohura T, Gefen A. Shear and friction in context. In International review. Pressure ulcer prevention: pressure, shear, friction and microclimate in context. A consensus document. Lond Wounds Int. 2010;11‐18. [Google Scholar]
  • 37. Gulin F, Menegueti M, Auxiliadora‐Martins M, et al. APACHE II Death risk and length of stay in the ICU are associated with pressure injury in critically ill patients. J Clin Med Res. 2018;10(12):898‐903. 10.14740/jocmr3636. [DOI] [PMC free article] [PubMed] [Google Scholar]

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