Study on the relationship between sublingual microcirculation disorder and pressure injury in patients with acute infection

1. FOREWORD

A pressure injury is defined as a localized injury to the skin and/or underlying soft tissue at the bony prominence area or at the point of contact with medical devices due to severe and/or prolonged pressure or pressure combined with shear, usually with deep tissue damage but intact skin or open ulcers with pain.

In recent years, the incidence and prevalence of pressure injuries have remained at high levels, bringing a heavy burden to patients, families, society and medical and healthcare facilities, and there is still a lack of effective clinical prevention and control methods, and the absence of more accurate and effective assessment methods are one of the key reasons. ¹ , ² , ³ More and more evidence shows that there is a close relationship between microcirculation function and organ damage and prognosis of critically ill patients. ⁴ As the direct place where the body participates in tissue nutrient exchange and waste metabolism, the continuous disturbance of microcirculation function can lead to the imbalance of tissue oxygen supply and metabolism. ⁵ The ability of cells to utilize oxygen is still hindered with tissue and cellular edema, even if the tissue blood perfusion is sufficient. ⁶ At present, it is known that the perfusion state and functional state of local tissues are the key factors leading to the occurrence of pressure injury, ¹ and the relationship between microcirculation disorder and pressure injury is still unknown. Therefore, a clinical experiment is designed to study the connection between the two.

2. OBJECT AND METHOD

This study is a single‐centre prospective observational study. Patients with acute infectious diseases admitted to the Emergency Medicine Clinical Research Center of Beijing Chaoyang Hospital affiliated to the Capital Medical University were selected and included in different groups according to the inclusion and exclusion criteria, and divided into pressure injury group (PI) and non‐pressure injury group (NPI) depending on whether the patient had developed a skin pressure injury.

2.1. Inclusion criteria

①Patients with acute infectious disease as primary disease; ② Age >18 years; ③ No pressure injury when the patient came to the hospital.

2.2. Exclusion criteria

① Patients with primary disease requiring surgical intervention; ② Patients with tumours and connective tissue diseases; ③ Patients with long‐term use of oral or intravenous hormones; ④ Patients who died within 48 h after admission; ⑤ Patients who used anticoagulants and patients with acute poisoning; ⑥ Patients with clear pressure injury when admitted; ⑦ Patients on whom the sublingual microcirculation test cannot be performed because of invasive or noninvasive mechanical ventilation.

2.3. Shedding/rejection criteria

① Those who have not completed 48 h of relevant monitoring due to various reasons; ② Those who cannot be followed up for pressure injury within 5 days of symptom onset; ③ Those who cannot tolerate the collection of sublingual microcirculation; ④ Those who cannot complete relevant laboratory tests according to the requirements of the observation items.

2.4. Observation indicators

Gender, age, underlying health condition, site of acute infection, white blood cell count, platelet count, haemoglobin, D‐dimer level, blood lactate, base excess, procalcitonin (PCT), C‐reactive protein (CRP), SOFA score, APACHII score, sublingual microcirculation parameters (MFI, De Backer score, TVD, PPV, FHI, PVD), mechanical ventilation or not, 28‐day death, etc. For sublingual microcirculation parameters, the 24‐h change rate and the 48‐h change rate were further calculated.

$$48\mathrm{h}\text{rate of change}=\begin{array}{l}\left(48\mathrm{h}\text{value}-24\mathrm{h}\text{value}\right)/24\mathrm{h}\text{value}\\ \times 100\%\end{array}$$

$$72\mathrm{h}\text{rate of change}=\begin{array}{l}\left(72\mathrm{h}\text{value}-24\mathrm{h}\text{value}\right)/24\mathrm{h}\text{value}\\ \times 100\%\end{array}$$

2.5. Specimen collection

After the patients were admitted to the hospital, the collection of basic information was improved. Arterial blood and venous blood samples were collected within 24, 48 and 72 h respectively, to improve the detection of relevant observation indicators, and complete the clinical score. At 24, 48 and 72 h of admission, the MicroSee sublingual microcirculation monitor with side‐stream dark field (SDF) technology was used to detect the sublingual microcirculation status of the patients, and the images were collected and analysed according to the European Society of Intensive Care Medicine's Consensus on the assessment of sublingual microcirculation in critically ill patients in 2018, ⁷ requirements includes:

Give patients with a lot of oral secretions sufficient suction or gauze to clean the oral secretions; give patients with dry sublingual mucosa necessary saline to moisten, and clean up the viscous secretions under the tongue; use the location with capillaries, venules and even arterioles as sublingual microcirculation measurement points; avoid choosing location with much venous rings or venules; choose at least three sublingual areas as observation points; adjust the focus to a level where individual red blood cells in capillaries could be clearly seen and avoid artefacts caused by saliva or air bubbles; monitor at least 4 s and optimal duration is 20 s; eliminate the artefact caused by probe pressure; blood perfusion of small veins with a diameter greater than 20 μm can be used as an indicator tot image quality.

Sublingual microcirculation images were analysed by a well‐trained professional who was not involved in the acquisition of images and other clinical data.

2.6. Medical ethics review

This clinical study has been reviewed and approved by the Medical Ethics Committee of Beijing Chaoyang Hospital (approval batch number: 2021‐ke‐474). All experimental processes were conducted in strict accordance with ethical review standards, and all the patients included in the study signed the Informed Consent Form to confirm their consent, and for the patients without the ability to act independently, their legal immediate family members signed the Informed Consent Form to confirm the consent.

2.7. Statistical methods

SPSS 23.0 was used for processing. Mean ± SD (x ± s) was used to express normal distribution measurement data. Median (P25, P75) was used to describe the skewed distribution measurement data. The independent samples t‐test was used for comparison between groups. One‐way ANOVA was used to compare the same group before and after admission. Two‐way repeated measures ANOVA was used to determine the variance between groups. The χ ² test was used for comparison between groups. The difference was statistically significant when p < 0.05.

3. RESULTS

3.1. General situation

A total of 70 patients participated in this study, of which 15 patients failed to complete 72 h of relevant monitoring, and three patients were not followed up for pressure injury and dropped out of the study. A total of 52 patients completed this study, of which 21 patients (40.4%) developed pressure injury during treatment, 31 patients (59.6%) did not have pressure injury (as shown in Figure 1), and the time of occurrence of pressure injury was 89.90 ± 19.74 (68 [58, 126]) hours after admission. Among them, 11 cases (52.4%) were mainly due to stage 1 pressure injury, and one case (4.8%) was associated with pressure injury with wound infection complication (Table 1). Of all the patients who completed the study, a total of 24 patients (46.2%) were finally diagnosed with sepsis, which met the diagnostic criteria of Sepsis‐3.0, ¹ of which 17 patients (32.7%) had pressure injuries, and seven cases (13.5%) did not, and there was a significant difference between the two groups (p = 0.000). A total of 10 patients (19.2%) died within 28 days after the onset of the disease, among them, four patients (7.7%) had pressure injury and six patients (11.5%) did not. There were no significant differences between the two groups in terms of age, gender, evaluation of nutritional status on admission, underlying diseases, infection lesions and laboratory indicators (Table 2).

FIGURE 1.

Experimental flow chart.

TABLE 1.

Description of pressure injuries.

Occurrence time (h)	Staging of pressure injuries (n = 21)					Wound infection
(Mean ± SD)	1(%)	2(%)	3(%)	5(%)	Others(%)	n (%)
89.90 ± 17.74	11 (52.4%)	5 (23.8%)	2 (9.5%)	1 (4.8%)	2 (9.5%)	1 (4.8%)

TABLE 2.

General condition of patients on admission.

General	Total (n = 52)	PI (n = 21)	NPI (n = 31)	p
Age (mean ± SD)	74.35 ± 12.14	74.67 ± 11.40	74.13 ± 12.80	0.196
Gender male (%)	39 (75.0%)	15 (28.8%)	24 (46.2%)	0.624
Gender female (%)	13 (25.0%)	6 (11.5%)	7 (13.5%)	0.351
Time to appear pressure injury (h)	89.90 ± 19.74 [68 (58, 126)]
Diagnosed sepsis (%)	24 (46.2%)	17 (32.7%)	7 (13.5%)	0.000*
28 days of death, n (%)	10 (19.2%)	4 (7.8%)	6 (11.5%)	0.978
Nutritional status assessment
BMI	23.30 ± 4.08	23.26 ± 4.28	23.17 ± 4.02	0.664
Triceps skinfold thickness (mean ± SD)	15.08 ± 6.04	14.81 ± 6.39	15.27 ± 5.89	0.765
NRS2002 (mean ± SD)	3.31 ± 1.85	3.62 ± 1.99	3.10 ± 1.76	0.497
NUTRIC (mean ± SD)	2.19 ± 1.40	2.10 ± 1.22	2.26 ± 1.53	0.271
GCS (mean ± SD)	13.52 ± 2.85	13.52 ± 2.89	13.52 ± 2.87	0.964
Underlying disease
Hypertension	27 (51.9%)	10 (19.2%)	17 (32.7%)	0.778
Coronary heart disease	16 (30.8%)	5 (9.6%)	11 (21.2%)	0.542
Diabetes	16 (30.7%)	6 (11.5%)	10 (19.2%)	0.777
History of cerebrovascular disease	11 (21.3%)	7 (13.5%)	4 (7.8%)	0.095
History of chronic lung disease	14 (26.9%)	3 (5.7%)	11 (21.2%)	0.118
Chronic cardiac insufficiency	7 (13.5%)	3 (5.7%)	4 (7.8%)	1.000
Chronic kidney insufficiency	4 (7.7%)	3 (5.7%)	1 (2.0%)	0.291
Bedridden for various reasons	8 (15.4%)	5 (9.7%)	3 (5.7%)	0.244
Site of infection
Respiratory infection	45 (86.5%)	18 (34.6%)	27 (51.9%)	0.408
Urinary tract infection	2 (3.8%)	1 (1.9%)	1 (1.9%)	‐
Biliary infection	2 (3.8%)	1 (1.9%)	1 (1.9%)	‐
Intra‐abdominal infection	3 (5.7%%)	1 (1.9%)	2 (3.8%)	‐
Laboratory metrics
Albumin (g/L) (mean ± SD)	36.24 ± 5.68	35.31 ± 5.84	36.87 ± 5.58	0.749
Prealbumin (g/L) (mean ± SD)	0.11 ± 0.07	0.12 ± 0.09	0.11 ± 0.06	0.081
Haemoglobin (g/L) (mean ± SD)	120.60 ± 24.40	118.10 ± 26.83	122.29 ± 22.91	0.392
White blood cells (*109) (mean ± SD)	12.09c5.45	11.34 ± 5.32	12.59 ± 5.57	0.377
Platelets (*109) (mean ± SD)	219.60 ± 91.42	226.19 ± 105.22	215.13 ± 82.31	0.479

^*Comparison of the data between the pressure injury group and the non‐pressure injury group, p < 0.05.

The heart rate and mean arterial pressure of all patients included in the study were recorded at 24, 48 and 72 h of admission, and the serum D‐dimer, blood lactate and base excess were detected at the same time, and APACHEII score and SOFA score were calculated combined with relevant results. The patients were divided into two groups according to whether there was pressure injury or not. The indexes at different time points in the two groups were compared, and the indexes at the same time point between the two groups were compared. The results showed that the SOFA score of patients in the pressure injury group at 48 and 72 h was significantly higher than that at 24 h (3.29 ± 1.96 vs. 2.35 ± 1.12, p < 0.05) (3.65 ± 1.84 vs. 2.35 ± 1.12, p < 0.05), heart rate was significantly lower than that at 24 hours after admission (104.71 ± 18.35 vs. 92.18 ± 18.17, p < 0.05) (104.71 ± 18.35 vs. 85.06 ± 17.08, p < 0.05); the SOFA score of patients in the pressure injury group at 72 h after admission was significantly higher than the patients in the peer group (3.65 ± 1.84 vs. 2.97 ± 2.81, p < 0.05); at 24, 48 and 72 h of admission, the blood lactate level in the pressure injury group was significantly higher than that in the non‐pressure injury group (2.15 ± 2.32 vs. 1.56 ± 1.02, p < 0.05) (1.82 ± 1.44 vs. 1.30 ± 0.48, p < 0.05) (1.46 ± 0.71 vs. 1.32 ± 0.41, p < 0.05), while the base excess was lower than that of the non‐pressure injury group (−1.62 ± 9.36 vs. 1.78 ± 7.76, p < 0.05) (−1.32 ± 6.71 vs. 2.03 ± 7.02, p < 0.05) (0.85 ± 6.58 vs. 3.13 ± 7.03 p < 0.05). There were no significant differences in other indicators within or between groups (Figure 2) (Table 3).

FIGURE 2.

Schematic diagram of 24, 48 and 72 h index monitoring in the pressure injury group and the no pressure injury group. *: Comparison of data at the same time point between the group with pressure injury and the group without pressure injury, p < 0.05. #: 48 h data was compared with 72 and 24 h respectively within the same group, p < 0.05.

TABLE 3.

24, 48, 72 h index monitoring in pressure injury and non‐pressure injury.

Item	24 h after admission	48 h after admission	72 h after admission
APACHEII(mean ± SD)
PI (n = 21)	12.12 ± 4.82	11.12 ± 5.05	10.71 ± 4.99
NPI (n = 31)	11.90 ± 4.92	10.83 ± 5.01	10.90 ± 5.75
SOFA(mean ± SD)
PI (n = 21)	2.35 ± 1.12	3.29 ± 1.96 #	3.65 ± 1.84 #
NPI (n = 31)	2.28 ± 1.41	3.10 ± 2.38 #	2.97 ± 2.81*
Mean arterial pressure, mmHg, (mean ± SD)
PI (n = 21)	87.08 ± 11.87	90.00 ± 6.03	89.31 ± 7.86
NPI (n = 31)	90.48 ± 8.68 *	89.03 ± 7.58	87.21 ± 9.39
Heart rate, bmp, (mean ± SD)
PI (n = 21)	104.71 ± 18.35	92.18 ± 18.17 #	85.06 ± 17.08 #
NPI (n = 31)	96.48 ± 17.70	90.07 ± 15.73	86.83 ± 16.33 #
D‐dimer, (mg/L), (mean ± SD)
PI (n = 21)	4.73 ± 4.55	5.31 ± 5.02	5.31 ± 4.91
NPI (n = 31)	3.75 ± 8.10	5.14 ± 9.09 #	5.50 ± 7.74 #
Blood lactate, (mmol/L), (mean ± SD)
PI (n = 21)	2.15 ± 2.32	1.82 ± 1.44	1.46 ± 0.71
NPI (n = 31)	1.56 ± 1.02*	1.30 ± 0.48*	1.32 ± 0.41*
Base excess, (mmol/L), (mean ± SD)
PI (n = 21)	−1.62 ± 9.36	−1.32 ± 6.71	0.85 ± 6.58
NPI (n = 31)	1.78 ± 7.76*	2.03 ± 7.02*	3.13 ± 7.03*

^*Comparison of data at the same time point between the group with pressure injury and the group without pressure injury, p < 0.05.

^# 24 h data was compared with 48 and 72 h respectively within the same group, p < 0.05.

The related data of sublingual microcirculation, including De Backer score, small blood vessel density (TVD), Microvascular Flow Index (MFI), Homogeneity Index (FHI), Perfusion Vessel Proportion (PPV) and Perfusion Vessel Density (PVD), was recorded for all patients included in the study at 24, 48 and 72 h of admission, the results showed that within the same group, there was no significant difference in sublingual microcirculation indexes at different times; MFI at 24, 48 and 72 h in the no injury group (2.68 ± 0.23 vs. 2.40 ± 0.51, p < 0.05) (2.60 ± 0.27 vs. 2.42 ± 0.39, p < 0.05) (2.65 ± 0.20 vs. 2.45 ± 0.36, p < 0.05), PPV (92.78 ± 5.70 vs. 88.34 ± 12.36, p < 0.05) (93.74 ± 4.10 vs. 91.22 ± 7.93, p < 0.05) and PVD (13.47 ± 2.90 vs. 11.82 ± 3.18, p < 0.05) (13.14 ± 3.00 vs. 11.66 ± 3.46, p < 0.05) (13.30 ± 2.11 vs. 12.41 ± 2.56, p < 0.05) were significantly higher than those in the pressure injury group, while FHI (0.24 ± 0.12 vs. 0.34 ± 0.26, p < 0.05) (0.27 ± 0.17 vs. 0.38 ± 0.18, p < 0.05) (0.24 ± 0.15 vs. 0.36 ± 0.21, p < 0.05) was significantly lower than that in the pressure injury group (Figure 3) (Table 4).

FIGURE 3.

Schematic diagram of sublingual microcirculation at 24, 48 and 72 h in PI and NPI. *: Comparison of data at the same time point between the group with pressure injury and the group without pressure injury, p < 0.05. #: 48 h data was compared with 72 and 24 h respectively within the same group, p < 0.05.

TABLE 4.

Sublingual microcirculation parameters in patients with and without pressure injury.

Item	24 h after admission	48 h after admission	72 h after admission
De Backer(mean ± SD)
PI (n = 21)	8.71 ± 1.97	9.16 ± 2.43	9.36 ± 1.69
NPI (n = 31)	9.91 ± 1.89	9.56 ± 1.97	9.74 ± 1.70
TVD, mm/mm2(mean ± SD)
PI (n = 21)	13.01 ± 2.87	13.16 ± 3.42	13.56 ± 2.37
NPI (n = 31)	14.45 ± 2.79	14.09 ± 2.83	14.25 ± 2.13
MFI(mean ± SD)
PI (n = 21)	2.40 ± 0.51	2.42 ± 0.39	2.45 ± 0.36
NPI (n = 31)	2.68 ± 0.23*	2.60 ± 0.27*	2.65 ± 0.20*
FHI (mean ± SD)
PI (n = 21)	0.34 ± 0.26	0.38 ± 0.18	0.36 ± 0.21
NPI (n = 31)	0.24 ± 0.12*	0.27 ± 0.17*	0.24 ± 0.15*
PPV (mean ± SD)
PI (n = 21)	90.01 ± 12.36	88.34 ± 12.36	91.22 ± 7.93
NPI (n = 31)	92.91 ± 5.29	92.78 ± 5.70*	93.74 ± 4.10*
PVD, mm/mm2 (mean ± SD)
PI (n = 21)	11.82 ± 3.18	11.66 ± 3.46	12.41 ± 2.56
NPI (n = 31)	13.47 ± 2.90*	13.14 ± 3.00*	13.30 ± 2.11*

^*Comparison of data at the same time point between the group with pressure injury and the group without pressure injury, p < 0.05.

Among the 21 patients with pressure injury, the 48 h and 72 h change rate of sublingual microcirculation parameters of MFI (−3.81 ± 11.26 vs. −5.67 ± 12.51, p = 0.195), PPV (−2.67 ± 11.48 vs. −1.76 ± 9.09, p = 0.548), PVD (4.62 ± 17.99 vs. 7.62 ± 21.00, p = 0.412) and FHI (72.43 ± 111.37 vs. 93.76 ± 167.77, p = 0.470) had no significant difference (Table 5).

TABLE 5.

Comparison of the change rate of sublingual microcirculation in patients with pressure injury.

Item	48 h	72 h	p
MFI % (mean ± SD)	−3.81 ± 11.26	−5.67 ± 12.51	0.195
FHI % (mean ± SD)	72.43 ± 111.37	93.76 ± 167.77	0.470
PPV % (mean ± SD)	−2.67 ± 11.48	−1.76 ± 9.09	0.548
PVD % (mean ± SD)	4.62 ± 17.99	7.62 ± 21.00	0.412

At 24, 48 and 72 h after admission, the sublingual microcirculation state of the patients in the pressure injury group was worse than that of the patients in the group without pressure injury at the same time. The sublingual microvascular branch was cut off, the vascular shape was not clear, red blood cells and platelets were stagnated inside and the fluidity of red blood cells in the microvascular was poor by dynamic observation. The results are shown in Figure 4, and the differences are indicated by coloured arrows (PI group blue arrows, NPI group orange arrows).

FIGURE 4.

Diagram of sublingual microcirculation at 24, 48, and 72 h in patients with pressure injury and non‐pressure injury. PI: The blue arrows indicate that the sublingual microvascular branches are cut off, the vascular shape is not clear, red blood cells and platelets stagnation can be seen, and the red blood cell fluidity is poor. NPI: The orange arrows indicate that the filling, vascular shape and red blood cell fluidity of the sublingual microvessels were better than those in the pressure injury group.

4. DISCUSSION

Pressure injury is a difficult problem for clinical medical staff, which not only increases the pain and economic burden of patients, prolongs hospitalization time, but also causes infection and even death in severe cases. Although many effective nursing measures have been applied in clinical practice, the incidence of pressure injury still has no obvious declining trend. In 2016, the Canadian Registered Nurses' Association of Ontario (RNAO) issued the third edition of the ‘Assessment and management of pressure injuries for the interprofessional team’, which provided optimal assessment and management advice for interprofessional team services for people aged 18 and over with pressure injuries. ⁸ In 2019, the National Pressure Injury Advisory Panel (NPIAP), the European Pressure Ulcer Advisory Panel (EPUAP) and the Pan Pacific Pressure Injury Association (PPPIA) updated the ‘Pressure Injury Prevention and Treatment: Clinical Practice Guidelines’ (Prevention and treatment of pressure ulcers/injuries: clinical practice guideline), which provided recommendations for health professionals worldwide to develop effective preventive and therapeutic measures for people at risk of developing or with existing pressure injuries. ⁹ In practice, however, identifying individuals with the probability of pressure injury from a clinical population remains a challenge for medical professionals.

In our study of acutely infected patients admitted to the emergency department, we found that 40.4% of the patients had pressure injuries of varying degrees, which was higher than that in the ward but lower than that in the ICU. ¹⁰ Pressure injury occurred at 89.90 ± 17.74 h after admission. Compared with non‐occurring patients, the basic status of age, gender, underlying diseases, vital signs on admission, nutritional status and lesion location were not significantly different. However, in patients with a final diagnosis of sepsis, pressure injuries occurred at a significantly higher rate than those who did not. This result suggests that the progression of the primary disease is associated with the occurrence of pressure injury. We further compared the indicators of the two groups of patients at 24, 48 and 72 h after admission, and found that the SOFA score of the patients with pressure injury at 48 and 72 h was not only significantly higher than that of the patients at 24 h, but also significantly higher than that of the patients without pressure injury. It is known that the SOFA score has a very good predictive value for organ function damage and prognosis in patients with sepsis. ⁴ Therefore, we have reason to believe that the progression of the primary disease is closely related to the occurrence of pressure injury, and the monitoring of pathophysiological processes will help us identify individuals with a high probability of developing pressure injury.

The occurrence of pressure injury is related to a variety of factors, ¹¹ and in clinical work we have been looking for effective means to prevent and treat it. Since the 1960s, the pressure ulcer scale has been widely used to assess and predict the risk of pressure injury in patients, and has achieved certain results. ¹² However, up to now, there is still a lack of clinical indicators that can reflect the individual characteristics of pressure injuries, as well as more accurate or effective means to assess pressure injuries. ⁹ In our study, we found that there were no significant differences in heart rate, mean arterial pressure, APACHII score and D‐dimer at 24, 48 and 72 h after admission in patients with pressure injury, and there was no significant difference between patients without pressure injury and those with pressure injury. This suggests that the macrocirculation state cannot be used as a characteristic indicator to reflect the occurrence of pressure injury. Although some studies have shown that the local perfusion state, compression and skin moisture are related to the occurrence of pressure injury, it is clear that this conclusion does not help effectively identify individuals at high risk of developing pressure injury. ¹³ In our study, we found that under the same treatment and nursing conditions, the occurrence of pressure injury in patients with acute infection was between 72 and 110 h after admission, and there was no significant difference in the nutritional status, vital signs, primary disease and underlying diseases at admission, and at 72 h after admission. This result suggests that the mechanism and risk factors of pressure injury in acute and critically ill patients are different from those in patients with chronic diseases. It will be the focus of our clinical work to define indicators that help to assess the risk of such patients, and to conduct effective monitoring.

In our study, we found that the blood lactate and base excess at 48 and 72 h after admission in patients with pressure injury were significantly different from those at 24 h, and also significantly different from those in patients without pressure injury at the same time. Studies have confirmed that the blood lactate and base excess reflect the microcirculation status of patients with sepsis, and microcirculation disorders are closely related to the prognosis of patients. ¹⁴ The blood lactate level in patients with pressure injury was higher than that in the patients without pressure injury, while the base excess level lower than the latter, this suggests that there is a link between abnormal microcirculation function and the occurrence of pressure injury. In this study, we performed sublingual microcirculation monitoring in patients at 24, 48 and 72 h and the results showed that the sublingual microcirculation index of patients with pressure injury was significantly worse than that of patients without pressure injury. Among the 21 patients with pressure injury, there was no significant difference in the sublingual microcirculation status at each time point. Taking the 24 h admission result as the benchmark, there was no significant difference in the 48 and 72 h change rates of corresponding microcirculation indicators, which suggests that the difference in the sublingual microcirculation state between the two groups of patients is persistent and stable, and further suggests that the microcirculation state is related to the occurrence of pressure injury.

More and more studies have confirmed that microcirculation disorders cause tissue hypoperfusion and hypoxia, thereby impairing the function of organs, ¹⁵ especially in the microcirculation ischemic period, while sympathetic nerves are excited, vasoconstriction contracting factors are released and the systemic microcirculation blood vessels continue to spasm, in particular the precapillary contraction is more obvious with increasing resistance, and a large number of true capillary networks are closed, resulting in a marked reduction in tissue perfusion, ¹⁶ while in the microcirculatory failure period, aggregation, activation of platelets and formation of microthrombi, blood flow cessation, severe disturbance of tissue oxygen supply and metabolism, continue to aggravate the damage of organ function. ¹⁷ Therefore, for acute and critically ill patients, microcirculation dysfunction often occurs earlier than systemic circulation dysfunction, and its severity and duration are significantly related to prognosis. ¹⁸ In our study, we used Sidestream Dark Field (SDF) technology to monitor sublingual microcirculation, and analysed the SOFA, mean arterial pressure and heart rate of patients, and the results suggest that the microcirculatory perfusion state can better indicate the risk of pressure injury than the macrocirculation, and monitoring the sublingual microcirculation can help in the early identification of those patients with potential pressure injury and provide a more accurate and easy‐to‐implement monitoring tool. In addition, we also found in our study, among the 10 deceased patients, that there was no significant difference in the proportion of patients with and without pressure injury. This result suggests that the occurrence of pressure injury may be one of the manifestations of systemic organ function damage caused by the primary disease, and its impact on the prognosis of patients is affected by a variety of clinical factors. Therefore, a comprehensive prevention and treatment strategy should be adopted for pressure injury.

5. CONCLUSION

The occurrence of pressure injury is one of the manifestations of systemic organ function damage caused by primary diseases. At present, there is no effective method for early prediction and identification of patients at high risk of pressure injury in clinical practice. The microcirculation status of patients with pressure injury is significantly different from that of patients without pressure injury, and this difference shows earlier than the occurrence of other abnormal clinical indicators, and the difference in microcirculation status remains relatively stable throughout the disease process, which could facilitate clinical medical staff to identify patients with high risk of pressure injury early and provide a new idea for the prevention and treatment of pressure injury.

CONFLICT OF INTEREST STATEMENT

The authors declare no conflicts of interest.

Zuo D, Li P, Guo S, Wei B, Yang J. Study on the relationship between sublingual microcirculation disorder and pressure injury in patients with acute infection. Int Wound J. 2024;21(3):e14749. doi: 10.1111/iwj.14749

DATA AVAILABILITY STATEMENT

All data generated or analysed during this study are included in this published article.