Prognostic utility of on-admission pulse pressure in hospitalized patients with traumatic brain injury

Abstract

BACKGROUND

Traumatic brain injury (TBI) remains a significant cause of morbidity and mortality worldwide. Given the pivotal role of proper triage and timely management in patients with TBI, physicians are seeking a readily informative, straightforward tool for evaluating patients in the emergency department.

AIM

To evaluate the association between on-admission pulse pressure (PP) and clinical outcomes, including severity of injury, complications, and mortality, among patients hospitalized with TBI.

METHODS

A retrospective observational study was conducted using data from adult patients with TBI admitted to the Hamad Trauma Center from 2011 to 2021. Patients were categorized into five PP groups at presentation in the emergency department: ≤ 30 mmHg, 31-40 mmHg, 41-50 mmHg, 51-60 mmHg, and > 60 mmHg.

RESULTS

A total of 5029 patients with TBI (mean age 33.1 ± 12.6 years; 87% male) were included. Low PP (PP ≤ 30) was significantly associated with younger age; higher injury severity; worse physiological parameters; and increased rates of transfusion, intubation, and acute respiratory distress syndrome (P < 0.001). Mortality was higher in the low-PP group (24%) compared with mid- and high-PP groups (5%-7%, P < 0.001). Bivariate analysis revealed that PP was positively correlated with age (r = 0.21), mean arterial pressure (r = 0.35), and Glasgow Coma Scale score (r = 0.098), and negatively correlated with shock index (r = -0.47), Injury Severity Score (r = -0.115), and blood units transfused (r = -0.18). Multivariable regression identified age, head Abbreviated Injury Scale score, PP, transfused blood units, and acute respiratory distress syndrome as independent predictors of mortality (P < 0.001).

CONCLUSION

Admission PP reflects both hemodynamic stability and injury severity in patients with TBI. Low PP (≤ 30 mmHg) independently predicts higher mortality, whereas moderate PP (41-60 mmHg) is associated with optimal outcomes, suggesting this range represents a potential hemodynamic target. PP is a simple, rapid bedside adjunct marker that may aid early risk stratification and guide timely intervention in the management of TBI.

Key Words: Traumatic brain injury; Pulse pressure; Hemodynamics; Mortality; Prognostic marker

Core Tip: Traumatic brain injury is a major contributor to long-term disability. Hemodynamic parameters, including mean arterial pressure and pulse pressure (PP), play a critical role in maintaining cerebral perfusion, regulating intracranial pressure, and mitigating secondary brain injury. Admission PP reflects both hemodynamic stability and injury severity in patients with brain injury. Low PP (≤ 30 mmHg) independently predicts higher mortality, whereas moderate PP is associated with optimal outcomes, suggesting that this range represents a potential hemodynamic target. PP is a simple bedside adjunct marker that aids early risk stratification and guides timely intervention in patients with traumatic brain injury.

INTRODUCTION

Traumatic brain injury (TBI) is a major contributor to long-term disability and neurological impairment among trauma patients[1], with an estimated global incidence of approximately 55.5 million cases annually[2]. A systematic review from the Middle East and North Africa region reported a TBI mortality rate of 13%[3]. Numerous studies have consistently demonstrated that advanced age, preexisting comorbidities, and greater initial severity of injury are strongly associated with worse clinical prognoses in TBI[4-6]. Hemodynamic parameters, including systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and pulse pressure (PP), play a critical role in maintaining cerebral perfusion, regulating intracranial pressure (ICP), and mitigating secondary brain injury. Guidelines for severe TBI emphasize the importance of maintaining adequate blood pressure to improve outcomes[7].

The prognostic value of PP, defined as the difference between SBP and DBP, remains inadequately characterized in the context of TBI. In the context of isolated systolic hypertension, increases in PP are significantly amplified, reaching levels that can disrupt cerebral blood flow autoregulation and increase the risk of stroke and mortality[8,9]. Excessively high PP may compromise the integrity of cerebral microvasculature by exceeding the upper limit of autoregulatory capacity, potentially leading to ischemic injury. In non-demented individuals, the presence of cerebral microhemorrhages (capillary microbleeds) has been associated with older age, hypertension, and cognitive decline[10].

An elevated PP has been identified as a key predictor of increased stroke risk and recurrence and is independently associated with adverse cerebrovascular outcomes. However, its relationship with incident stroke is partly mediated by SBP[11-13]. A narrow PP has been independently associated with the need for massive transfusion and urgent surgical intervention in hemodynamically stable trauma patients[14]. At the same time, deviations in PP may reflect impaired cerebral perfusion, ongoing hemorrhage, or disrupted autoregulatory functions. Narrow PP has also been associated with major surgical interventions in normotensive trauma patients[15]. Notably, PP tends to increase with age and may serve as a useful hemodynamic indicator in older individuals[16-18]. Although numerous studies[14,15,19] have explored PP in the context of spontaneous intracerebral hemorrhage[11,12,16,19], its clinical significance in TBI remains unclear. Moreover, the prognostic value of PP as a marker for outcome prediction or risk stratification in TBI has not been well addressed in clinical trials. Therefore, we aimed to evaluate the association between on-admission PP and clinical outcomes, including injury severity, complications, and mortality, among patients hospitalized with TBI.

MATERIALS AND METHODS

A retrospective analysis was conducted using data from the Qatar National Trauma Registry to identify patients admitted to the Hamad Trauma Center with a diagnosis of TBI. TBI cases were defined according to the International Classification of Diseases, Ninth Revision, and the Abbreviated Injury Scale (AIS). The Hamad Trauma Center is the only level 1 trauma care facility in Qatar, providing comprehensive care for patients with moderate to severe injuries. The study included all adult patients aged 14 years or older who were admitted with TBI from January 2011 to April 2021. Pediatric population (< 14 years), those declared dead on arrival, those who died within 24 hours of admission, inter-facility transfers, and patients with incomplete or missing relevant data were excluded.

Collected variables included demographic and clinical characteristics such as age; sex; mechanism of injury; vital signs at the scene and upon hospital admission (SBP, DBP, PP, MAP); shock index in the emergency department (ED); ethanol levels; associated injuries (chest, abdomen, pelvis, lower and upper extremities, acute kidney injury); AIS for the head, chest, abdomen, and pelvis; Injury Severity Score (ISS); Glasgow Coma Scale (GCS) score at the scene and in the ED; intubation; exploratory laparotomy; craniotomy/craniectomy; need for blood transfusion; massive transfusion protocol activation; hospital and intensive care unit length of stay; ventilator days; acute respiratory distress syndrome (ARDS); and in-hospital mortality. The shock index was defined as the initial heart rate divided by the initial SBP. Patients were stratified into five groups based on their initial PP at presentation: Group 1 (PP ≤ 30 mmHg), group 2 (PP: 31-40 mmHg), group 3 (PP: 41-50 mmHg), group 4 (PP: 51-60 mmHg), and group 5 (PP > 60 mmHg), consistent with previously published classifications[20]. The Institutional Review Board (MRC-01-21-990) of Hamad Medical Corporation approved this retrospective observational study and granted a waiver of informed consent.

Statistical analysis

Data were expressed as proportions, means ± standard deviation (SD), 95% confidence intervals (CI), or medians with ranges, as appropriate. Normality of PP was assessed using the Kolmogorov-Smirnov test (Figure 1). Comparisons among groups were performed using the χ² test for categorical variables and the one-way analysis of variance for continuous variables, as appropriate. Yates’ corrected χ² was used for categorical variables if the expected cell frequencies were less than 5. Pearson’s correlation analysis was used to assess the relationship between PP and selected continuous variables, including age, shock index in the ED, MAP in the ED, ISS, GCS score in the ED, and the number of blood units transfused. Multivariable logistic regression analysis was performed to identify independent predictors of mortality in patients with TBI, adjusting for age, sex, head AIS, PP, blood units transfused, and the presence of ARDS. Results were expressed as adjusted odds ratios (aORs) with corresponding 95%CIs. A two-tailed P value less than 0.05 was considered statistically significant. Data were analyzed using the Statistical Package for the Social Sciences version 26 (IBM, Armonk, NY, United States).

Figure 1 Normality test for pulse pressure using a histogram and normal Q-Q plot.

RESULTS

A total of 5029 patients were included in the analysis and stratified into five groups based on their initial PP. Table 1 summarizes and compares the demographic characteristics and injury profiles of patients with TBI across these five PP categories. Age demonstrated a progressive increase with rising PP, from a mean age of approximately 29 years in patients with PP ≤ 30 mmHg to 36.5 years in those with PP > 60 mmHg (P = 0.001). Although male predominance was consistent across all groups, it did not reach statistical significance (P = 0.05). Traffic-related injuries were most frequent in both the lowest and highest PP groups. In contrast, falls were more common with mid-range PP values (P = 0.001), suggesting that lower PP may be associated with higher-energy trauma mechanisms.

Table 1 Clinical characteristics, management, and outcome in traumatic brain injury based on pulse pressure (n = 5029), n (%)/mean ± SD.

	PP ≤ 30 mmHg	PP: 31-40 mmHg	PP: 41-50 mmHg	PP: 51-60 mmHg	PP > 60 mmHg	P value
Number (n = 4963)	578 (11.5)	1010 (20.1)	1409 (28.0)	1102 (21.9)	930 (18.5)
Age (yr)	28.7 ± 16.2	28.4 ± 14.7	29.1 ± 15.0	31.2 ± 15.3	36.5 ± 19.6	0.001
Males	517 (89.4)	910 (90.1)	1276 (90.6)	1023 (92.8)	857 (92.2)	0.05 for all
Females	61 (10.6)	100 (9.9)	133 (9.4)	79 (7.2)	73 (7.8)
Mechanism of injury
Traffic-related	238 (41.2)	359 (35.5)	499 (35.4)	387 (35.1)	376 (40.4)	0.001 for all
Pedestrians	114 (19.7)	155 (15.3)	195 (13.8)	144 (13.1)	121 (13.0)
Fall from height	166 (28.7)	348 (34.5)	523 (37.1)	419 (38.0)	317 (34.1)
Fall of a heavy object	14 (2.4)	52 (5.1)	71 (5.0)	66 (6.0)	46 (4.9)
Others	46 (8.0)	96 (9.5)	121 (8.6)	86 (7.8)	70 (7.5)
Vitals at scene
Pulse (n = 3718)	101.2 ± 27.0	94.9 ± 24.2	93.4 ± 23.4	89.1 ± 20.8	90.4 ± 21.8	0.001
SBP (n = 3618)	126.0 ± 27.6	129.9 ± 23.3	130.3 ± 21.9	135.4 ± 20.9	143.9 ± 27.7	0.001
DBP (n = 3606)	82.2 ± 22.2	81.1 ± 20.6	81.8 ± 16.8	83.6 ± 17.6	86.2 ± 18.6	0.001
GCS (mean, 95%CI) (n = 3794)	10.0 (9.6-10.5)	11.4 (11.1-11.7)	12.4 (12.1-12.6)	12.7 (12.4-12.9)	12.3 (11.9-12.6)	0.001
Vital signs at hospital admission (ED)
Pulse	107.1 ± 26.8	97.5 ± 24.5	93.5 ± 22.3	90.2 ± 20.6	91.2 ± 22.1	0.001
SBP	100.7 ± 22.6	113.7 ± 15.8	123.2 ± 14.7	133.1 ± 14.2	151.2 ± 22.3	0.001
DBP	76.2 ± 22.2	76.3 ± 15.8	76.5 ± 14.3	77.0 ± 13.6	77.0 ± 16.9	0.733
GCS (mean, 95%CI) (n = 4931)	8.4 (7.8-8.9)	10.3 (9.9-10.7)	11.3 (11.0-11.6)	11.9 (11.5-12.2)	11.3 (10.9-11.7)	0.001
Shock index in the ED	1.15 ± 0.49	0.88 ± 0.29	0.77 ± 0.22	0.69 ± 0.18	0.62 ± 0.18	0.001
Ethanol levels	41.4 ± 21.9	41.5 ± 22.2	43.2 ± 19.7	40.0 ± 24.9	39.0 ± 23.7	0.79
Ethanol positive	55 (9.5)	110 (10.9)	124 (8.8)	77 (7.0)	51 (5.5)	0.001
MAP in the ED	84.4 ± 22.2	88.8 ± 15.8	92.1 ± 14.3	95.7 ± 13.7	101.7 ± 17.9	0.001
Associated injuries
Chest	282 (48.8)	343 (34.0)	389 (27.6)	264 (24.0)	265 (28.5)	0.001
Abdomen	167 (28.9)	193 (19.1)	166 (11.8)	102 (9.3)	55 (5.9)	0.001
Pelvis	110 (19.0)	122 (12.1)	113 (8.0)	74 (6.7)	57 (6.1)	0.001
Lower extremity	121 (20.9)	158 (15.6)	170 (12.1)	125 (11.3)	93 (10.0)	0.001
Upper extremity	182 (31.5)	221 (21.9)	298 (21.1)	200 (18.1)	207 (22.3)	0.001
Acute kidney injury	25 (4.3)	21 (2.1)	15 (1.1)	9 (0.8)	15 (1.6)	0.001
Head AIS score	3.6 ± 1.0	3.4 ± 0.9	3.3 ± 0.9	3.3 ± 0.9	3.4 ± 0.9	0.001
Chest AIS score	2.8 ± 0.7	2.7 ± 0.7	2.7 ± 0.6	2.6 ± 0.7	2.5 ± 0.7	0.001
Abdomen AIS score	2.7 ± 0.9	2.5 ± 0.9	2.4 ± 0.8	2.3 ± 0.8	2.3 ± 0.9	0.001
Pelvis AIS score	2.3 ± 0.8	2.2 ± 0.6	2.1 ± 0.4	2.1 ± 0.3	2.1 ± 0.3	0.004
MAP = SBP + 2 (DBP)/3, PP = SBP-DBP; SI = HR/SBP

PP: Pulse pressure; SBP: Systolic blood pressure; DBP: Diastolic blood pressure; GCS: Glasgow Coma Scale; CI: Confidence intervals; ED: Emergency department; MAP: Mean arterial pressure; AIS: Abbreviated Injury Scale; SI: Shock index; HR: Heart rate.

Vital signs at the scene and upon hospital admission showed distinct patterns. Patients with PP ≤ 30 mmHg had significantly worse physiological and neurological parameters both prehospital and at admission (P = 0.001 for all), except for DBP in the ED. Additionally, the PP ≤ 30 mmHg group had significantly elevated shock index in the ED (P = 0.001) and the lowest MAP at ED presentation (P = 0.001). Furthermore, patients in the PP ≤ 30 mmHg group showed a significantly higher rate of associated injuries to the chest, abdomen, pelvis, and extremities (P = 0.001 for all). The AIS analysis revealed that head AIS was highest in the lowest PP group (mean 3.6), consistent with more severe neurological injury. Similarly, AIS scores for other regions were also highest in the PP ≤ 30 mmHg group, further indicating greater overall injury severity among patients with lower PP. Figure 2 shows no significant difference between sexes across PP categories.

Figure 2 Distribution of pulse pressure categories stratified by sex. PP: Pulse pressure.

Outcomes

Table 2 presents the management, complications, and outcomes of patients with TBI stratified by PP groups. The mean ISS was highest among patients in the PP ≤ 30 mmHg group (P = 0.001). The need for intubation (P = 0.001), exploratory laparotomy (P = 0.001), blood transfusion (P = 0.001), and massive transfusion protocol activation was also significantly more frequent in this group. Moreover, the incidence of ARDS was also highest among patients with PP ≤ 30 mmHg compared with other groups (P = 0.001). Also, patients in the lowest PP group experienced prolonged intensive care unit and hospital stays. The rate of in-hospital mortality (Figure 2) was significantly higher in the PP ≤ 30 mmHg group (24%) compared with other PP groups (P = 0.001). Figure 3 illustrates in-hospital mortality across the five PP groups, highlighting that mortality was highest in the lowest PP group (≤ 30 mmHg) and lowest in the 41-60 mmHg range.

Figure 3 In-hospital mortality across the five pulse pressure (PP) groups. Mortality was highest in the lowest PP group (≤ 30 mmHg) and lowest in the moderate PP range (41-60 mmHg). PP: Pulse pressure.

Table 2 Management, complications, and outcome of traumatic brain injury patients across pulse pressure groups, n (%)/mean, 95% confidence intervals.

	PP ≤ 30 mmHg	PP: 31-40 mmHg	PP: 41-50 mmHg	PP: 51-60 mmHg	PP > 60 mmHg	P value
Number	578 (11.5)	1010 (20.1)	1409 (28.0)	1102 (21.9)	930 (18.5)
Injury Severity Score (n = 5016), mean ± SD	24.7 ± 12.0	19.7 ± 10.9	18.1 ± 10.0	17.5 ± 9.0	18.3 ± 9.2	0.001
Intubation	358 (61.9)	414 (41.0)	461 (32.7)	337 (30.6)	355 (38.2)	0.001
Exploratory laparotomy	60 (10.4)	54 (5.3)	35 (2.5)	20 (1.8)	7 (0.8)	0.001
Craniotomy/craniectomy	63 (10.9)	92 (9.1)	153 (10.9)	110 (10.0)	116 (12.5)	0.17
Blood transfusion	303 (52.4)	287 (28.4)	292 (20.7)	173 (15.7)	175 (18.8)	0.001
Blood units transfused	6 (1-79)	4 (1-49)	3 (1-62)	3 (1-20)	4 (1-51)	0.001
Massive transfusion protocol activation	117 (20.2)	73 (7.2)	43 (3.1)	17 (1.5)	17 (1.8)	0.001
ARDS	21 (3.6)	11 (1.1)	13 (0.9)	11 (1.0)	11 (1.2)	0.001
Intensive care unit length of stay	7 (1-115)	5 (1-155)	5 (1-161)	5 (1-70)	5 (1-126)	0.001
Ventilator days	6 (1-115)	6 (1-180)	5 (1-55)	5 (1-84)	6 (1-100)	0.15
Hospital length of stay (days; n = 5010)	10 (1-304)	7 (1-360)	6 (1-217)	6 (1-218)	8 (1-186)	0.001
In-hospital mortality	139 (24.0)	96 (9.5)	77 (5.5)	65 (5.9)	67 (7.2)	0.001

PP: Pulse pressure; ARDS: Acute respiratory distress syndrome.

Correlation coefficient

Table 3 illustrates the bivariate correlations between PP and other clinical variables. Significant positive correlations were identified between PP and age (r = 0.21), MAP (r = 0.35), and GCS score in the ED (r = 0.098). In contrast, PP showed significant negative correlations with shock index in the ED (r = -0.47), ISS (r = -0.115), and the number of transfused blood units (r = -0.18).

Table 3 Bivariate correlation between pulse pressure and other relevant factors.

Variables	Pearson correlation	P value
Age	0.210	0.001
Shock index in the ED	-0.474	0.001
MAP in the ED	0.346	0.001
Injury Severity Score	-0.115	0.001
Glasgow Coma Scale score	0.098	0.001
Blood transfusion units	-0.184	0.001

ED: Emergency department; MAP: Mean arterial pressure.

Predictors of mortality

Table 4 summarizes the results of the multivariable logistic regression analysis for predictors of mortality. After adjusting for potential confounders, significant independent predictors included age (aOR: 1.022; 95%CI: 1.012-1.032, P = 0.001), head AIS score (aOR: 2.757; 95%CI 2.307-3.295; P = 0.001), PP in the ED (aOR: 0.986; 95%CI: 0.978-0.994; P = 0.001), blood units transfused (aOR: 1.061; 95%CI: 1.037-1.084; P = 0.001) and ARDS (aOR: 2.781; 95%CI: 1.533-5.044; P = 0.001).

Table 4 Multivariable logistic regression analysis of predictors of mortality.

Variable	Adjusted odd ratio	95% confidence interval	P value
Age	1.022	1.012-1.032	0.001
Sex (male)	1.364	0.796-2.337	0.259
Head AIS1	2.757	2.307-3.295	0.001
Pulse pressure at TRU1	0.986	0.978-0.994	0.001
Blood transfusion units	1.061	1.037-1.084	0.001
ARDS	2.781	1.533-5.044	0.001

¹Continuous variable.

AIS: Abbreviated Injury Scale; TRU: Triage and reception unit; ARDS: Acute respiratory distress syndrome.

DISCUSSION

This retrospective study of 5029 patients with TBI demonstrated that lower admission PP (≤ 30 mmHg) was significantly associated with younger age, higher injury severity, greater hemodynamic instability, and increased mortality compared with patients with moderate or higher PP values. Conversely, patients with moderate PP (41-60 mmHg) exhibited the most favorable physiological parameters, neurological status, and survival outcomes, suggesting that this range represents an optimal hemodynamic window for patients with TBI. In contrast, high PP (> 60 mmHg) was observed predominantly among older individuals and was associated with a slightly increased mortality rate. Multivariable analysis further identified PP as an independent predictor of mortality alongside age, head injury severity, bleeding, and ARDS. These findings suggest the role of PP as an integrative hemodynamic marker reflecting both cardiovascular function and trauma severity. Prior studies have demonstrated that significant fluctuations in SBP are strongly associated with worse outcomes in traumatic intraparenchymal hemorrhage[21].

Hemodynamic indices are fundamental to maintaining cerebral perfusion, regulating ICP, and preventing secondary brain injury[7]. The prognostic relevance of PP remains insufficiently characterized by TBI. Markedly elevated PP, particularly in isolated systolic hypertension, can impair cerebral blood flow autoregulation and increase the risk of stroke and mortality[8,9], potentially causing microvascular injury when autoregulatory limits are exceeded. High PP is an established predictor of stroke risk and recurrence, with associations partly mediated by SBP[11-13]. Conversely, low PP has been independently linked to massive transfusion and urgent surgical intervention in trauma patients, even in the absence of hypotension[14,15]. Deviations in PP may therefore indicate impaired perfusion, active hemorrhage, or disrupted autoregulation. Although PP generally increases with age and may serve as a useful hemodynamic marker in older adults[16-18], its clinical significance in TBI remains inadequately defined despite investigations in trauma and spontaneous intracerebral hemorrhage cohorts[11,12,14-16,19,22].

Prognostic relevance of PP

Fluctuations in blood pressure may impair cerebral autoregulation, which may lead to cerebral edema and hematoma expansion. Similarly, ICP waveform parameters, including mean amplitude and pulse shape index, correlate with mortality, even in patients with relatively normal ICP values[22]. These observations suggest that both absolute PP and its variability reflect the degree of cerebrovascular stress and may predict adverse outcomes following TBI. The physiological mechanisms underlying this relationship are multifactorial. The Cushing reflex, characterized by widened PP, hypertension, bradycardia, and irregular respiration, is a classic sign of elevated ICP and reduced cerebral perfusion pressure[23]. Moreover, paroxysmal sympathetic hyperactivity following TBI can produce transient surges in PP (> 80 mmHg) that are associated with poor neurological outcomes[24]. Conversely, low PP may signal hypovolemia, impaired cardiac output, or loss of vascular tone, leading to inadequate cerebral perfusion and secondary ischemic injury[25]. Despite these observations, a notable gap remains in the literature regarding the role of PP variability in TBI.

In our study, patients with higher PP tended to be relatively older, which may reflect underlying vascular stiffness or age-related comorbidities. Specifically, the mean age in the PP > 60 mmHg group was significantly higher compared to that in the PP ≤ 30 mmHg group. This trend aligns with established physiology, as PP generally increases with advancing age and may serve as an indicator of arterial compliance and vascular health in older individuals[26]. These findings suggest that elevated PP in older patients is likely to reflect chronic vascular remodeling rather than acute hemodynamic disturbance.

In our study, traffic-related injuries predominated in both the lowest and highest PP groups. In contrast, falls were more frequent among patients with mid-range PP values, indicating that lower PP may be linked to high-energy trauma mechanisms and greater injury severity. One possible explanation is that high-impact mechanisms, such as motor vehicle collisions, often lead to significant blood loss, hypovolemia, and impaired cardiac output, resulting in reduced PP due to decreased stroke volume and vascular tone[27]. Conversely, elevated PP observed in some traffic-related cases may reflect a stress-induced catecholamine surge and transient sympathetic overactivation following severe trauma[28]. In contrast, low-energy mechanisms such as falls typically produce moderate physiological responses with relatively preserved hemodynamic stability, corresponding to mid-range PP values[29]. These findings underscore the complex interaction between trauma mechanism, physiological compensation, and vascular response following TBI[30].

In our study, patients with PP ≤ 30 mmHg exhibited markedly greater hemodynamic instability and neurological status, reflected by lower GCS scores and higher shock index values. This observation likely reflects hypovolemia, reduced cardiac output, and impaired cerebral perfusion secondary to severe hemorrhage or systemic shock[31]. In TBI, such hemodynamic compromise can exacerbate secondary brain injury by impairing cerebral blood flow and oxygen delivery, leading to ischemia and worsening neurological outcomes[32]. Prior studies have shown that shock and hypotension at presentation are strong predictors of mortality and poor neurological recovery in patients with TBI[33,34]. These findings suggest that a low PP with concurrent elevated shock index and reduced GCS score represents a state of compromised perfusion and severe physiological stress.

Moreover, in our study, PP showed positive correlations of varying strengths with age, MAP, and GCS score, and negative correlations with shock index, ISS, and transfusion requirements, further supporting PP as a marker of hemodynamic stability. These relationships are consistent with prior studies linking low PP with hemorrhagic shock and high transfusion needs in trauma populations[35,36].

In our study, analysis of associated injuries revealed that chest and abdominal injuries were most prevalent among patients with low PP, with the incidence of these injuries progressively decreasing as PP increased. This pattern supports the notion that patients presenting with low PP are more likely to sustain severe multisystem trauma, reflecting greater overall injury burden, physiological compromise, and the need for emergent interventions[15,37].

In our cohort, the requirement for blood transfusion was highest among patients with low PP and progressively declined with increasing PP. This trend suggests that low PP is associated with higher transfusion demand, likely reflecting underlying hypovolemia and hemodynamic instability. Although most studies on TBI have focused on SBP thresholds (e.g., hypotension < 90 mmHg) as critical determinants of outcome, PP is increasingly recognized as an independent hemodynamic marker with prognostic significance. In a study of spontaneous subarachnoid hemorrhage, a U-shaped relationship between baseline PP and mortality was reported, with the lowest mortality observed at PP values between 57 and 68 mmHg, and higher mortality associated with both low (< 56 mmHg) and high (> 69 mmHg) PP levels[38]. Consistent with these observations, our study demonstrated a significantly higher in-hospital mortality rate among patients with PP ≤ 30 mmHg, and multivariable analysis confirmed PP as an independent predictor of mortality. This finding aligns with recent evidence indicating that PP is an independent predictor of in-hospital mortality[13,39]. Similar trends were observed in the INTERACT2 trial, where higher SBP variability during the early stages of hospitalization was significantly associated with a higher risk of death or severe disability in patients with acute intracerebral hemorrhage[40].

The precise mechanisms through which SBP and PP variability influence outcomes in TBI remain unclear. Excessive fluctuations in SBP or PP may disrupt this autoregulatory balance. In hemorrhagic stroke, such variability has been linked to increased cerebral edema and hematoma expansion[19]. A similar pathophysiological mechanism is believed to operate in TBI, wherein blood pressure fluctuations may impair baroreflex sensitivity and exacerbate secondary brain injury[21].

Taken together, these findings suggest that on-admission PP provides valuable prognostic information in TBI, capturing both vascular and systemic components of the injury response. While its predictive strength is modest compared with established indicators such as head AIS and ARDS, PP offers a simple, rapid, and noninvasive tool that can complement existing triage and monitoring strategies in patients with TBI.

Limitations

This study has several limitations that should be acknowledged. First, its retrospective observational design limits causal inference between PP and clinical outcomes. Second, all data were derived from a single national trauma center, which, despite being the only level I facility in the country, may limit the generalizability of findings to other populations or healthcare settings. Third, PP measurements were obtained only upon admission, without accounting for subsequent fluctuations or trends that may have occurred during hospitalization. Finally, preexisting comorbidities, medication use (e.g., antihypertensives or beta-blockers), and fluid resuscitation before arrival were not fully captured, which could have affected the accuracy of baseline PP measurements. Additionally, correlations between PP and other variables, although statistically significant, were modest and should be interpreted with caution.

CONCLUSION

Admission PP reflects both hemodynamic and injury severity in patients with TBI. Low PP was associated with younger age, greater injury burden, hemodynamic instability, higher transfusion requirements, and the highest mortality. Moderate PP was associated with favorable physiological stability, neurological status, and the lowest complication and mortality rates, suggesting that it may represent an optimal PP range for improved outcomes. Moreover, high PP was more frequent among older patients and was associated with mildly increased mortality, likely reflecting age-related vascular changes rather than acute hemodynamic derangement. Multivariable analysis demonstrated that PP was an independent predictor of mortality, alongside established risk factors. These findings underscore the potential value of PP as a simple, noninvasive bedside adjunct marker for early risk stratification and triage in TBI. Future prospective multicenter studies incorporating serial hemodynamic monitoring and comprehensive assessment of cardiovascular and neurological parameters are warranted to validate and expand upon these findings.