Traumatic brain injury and variants of shock index

Abstract

Traumatic Brain Injury is a major cause of death and long-term disability. The early identification of patients at high risk of mortality is important for both management and prognosis. Although many modified scoring systems have been developed for improving the prediction accuracy in patients with trauma, few studies have focused on prediction accuracy and application in patients with traumatic brain injury. The shock index (SI) which was first introduced in the 1960s has shown to strongly correlate degree of circulatory shock with increasing SI. In this editorial we comment on a publication by Carteri et al wherein they perform a retrospective analysis studying the predictive potential of SI and its variants in populations with severe traumatic brain injury.

Key Words: Predictive tools; Traumatic brain injury; Shock index; Neurocardiogenic stress; Myocardial ischemia

Core Tip: Traumatic brain injury is associated with an unacceptable morbidity and mortality. Brain injury has been shown to increase acute cardiovascular disease risk in the form of neurocardiogenic shock. Shock index (SI) is recognized to be a reliable early indicator of hemodynamic instability compared to traditional vital signs. Early identification is crucial as it helps with risk stratification of patients and predict prognosis. There are numerous variants of SI proposed over the years with the more well studied one being age adjusted SI.

INTRODUCTION

Shock index (SI), defined as the ratio of heart rate (HR) to systolic blood pressure (SBP) was first introduced by Allgöwer and Burri[1] in 1967. Although the individual HR and SBP alone are not reliable in determining the presence of circulatory shock, their ratio as reflected by the SI, has shown to adequately measure hemodynamic instability and to risk stratify patients for intravenous fluid, vasopressors, transfusion requirements and outcomes. It was also proven to be a useful clinical indicator for acute hypovolemia in patients with both HR and SPB within normal range. The normal SI ranges from 0.5 to 0.7, and a higher value is associated with a higher mortality. In a retrospective study performed by Mutschler et al[2], 21853 patient’s vital signs in emergency department were analyzed. It showed that increasing SI values correlated with the degree of circulatory shock along with the need for intravenous fluids, vasopressors, and blood products.

There are multiple variations of SIs proposed over the years. Some of the well-known ones are the Modified SI which is the ratio of HR and mean arterial pressure (MAP), and the Age SI which is the ratio of HR and SBP multiplied with age. SI has been studied most extensively in patients with traumatic injury. Numerous studies have decoded potential benefits of using SI in predicting mortality and admission duration in trauma patients, predicting mortality in pneumonia, predicting ruptured ectopic pregnancy, categorization of pulmonary emboli patients, and predicting prognosis in acute myocardial infarction. In this editorial we comment on a publication by Carteri et al[3]. wherein they perform a retrospective analysis studying the predictive potential of SI and its variants in populations with severe traumatic brain injury.

PROGNOSTIC VALUE OF SHOCK INDEXS AND THEIR VARIANTS

Traumatic brain injury (TBI) refers to any injury to the brain caused by an external force, such as a blow to the head. It can result from various incidents, including falls, car accidents, sports injuries, or violence. TBIs range from mild concussions to severe brain damage and can have long-lasting effects on both physical and cognitive functions. It is a major cause of long-term disability and premature death. A widely used bedside clinical assessment using Glasgow Coma Score categories TBI as mild (14-15) moderate (9-13), and severe (3-8). TBI has been shown to increase acute cardiovascular disease risk, but associations between TBI, chronic cardiovascular disease, and risk factors for cardiovascular disease have received little attention in comparison with neurological or psychiatric conditions after injury. The relationship between the brain and the heart is complex and fundamental in the preservation of normal hemodynamics.

Cardiac dysfunction is a well-recognized sequala of any sort of intracranial damage including ischemic strokes, intracranial hemorrhage, and trauma. This entity is referred to as neurocardiogenic stunning or neurogenic stress cardiomyopathy[4]. There are three proposed mechanisms for this type of cardiomyopathy: (1) Ischemic myocardial stunning due to epicardial coronary spasm; (2) ischemic myocardial stunning due to coronary microvascular dysfunction; and (3) catecholamine-mediated myocardial injury[4]. Patients with brain injury are shown to have inflated peripheral sympathetic and catecholamine activity with increased plasma catecholamine levels, which may contribute to cardiac toxicity. Management of stress cardiomyopathy is largely supportive and is usually reversible in the absence of underlying obstructive coronary artery disease.

Independent predictors evidencing cardiac dysfunction such as serum biomarkers (troponin, CK-MB, brain natriuretic peptide) are disproportionate to the extent of wall motion abnormality. Recognizing a pattern for neurocardiogenic stunning is important because an early diagnosis has implications for management and prognosis. There have been a great number of publications that studied and researched models to predict prognosis for patients with trauma, including the Revised Trauma Score[5], Trauma and Injury Severity Score[6], Injury Severity Score[7] and New Injury Severity Score[8]. All these scoring systems proved to be effective in predicting survival probability, however they are restricted in use because it needs data of all the injured organs to calculate scores. This makes their utilization in prehospital settings and emergency departments limited. A brisk and effortless tool that provides both prognostic value and risk stratification would be valuable in managing patients with traumatic injury. The use of SIs and their variants would provide immense prognostic value in patients with traumatic injury.

SHOCK INDEXES IN EARLY RECOGNITION OF IMPAIRED CEREBRAL PERFUSION PRESSURE

In this issue of Journal, Carteri et al[3] contributed to existing literature by implementing a retrospective analysis to study the predictive potential of SI and their variants in predicting mortality following severe traumatic brain injury. In their cohort they compared SIs amongst surviving and non-surviving patients. They found no significant difference in using the SIs, reverse SI (rSI), or rSI multiplied by Glasgow Coma Score (rSIG) in predicting outcomes of severe traumatic brain injury. However, the use of age multiplied SI (ageSI) showed promise in predicting outcomes of severe TBI at 48 hours. This study adds to the work by Zarzaur et al[9] where they retrospectively analyzed 189574 trauma patients showing Age multiplied by SI has a better prediction effect of mortality at 48 hours compared to heart rate, SBP, and SI.

Interestingly, Odom et al[10] used a multivariate logistic regression model to show a bimodal relationship between SI and mortality in patients with TBI even after correcting for various confounding variables. In their study (n = 10420), they exhibited that SIs with both high and low values are correlated with mortality. However, it did show that only those with a high SI predicted death in patients without traumatic brain injury. It also exhibited that SI is a better predictor of hemodynamic instability than either isolated pulse rate or blood pressure values in both groups of patients with and without traumatic brain injury.

One of the most controversial areas of TBI is the management of cerebral perfusion pressure (CPP). CPP is defined as the difference between the systemic MAP and intracranial pressure (ICP). When hemodynamic autoregulation is impaired after TBI, the cerebral blood flow is affected because of its dependence on CPP which in turn is dependent on MAP and inversely correlated with ICP. A normal ICP is usually well-regulated at 5 mmHg or less in healthy individuals without intracranial pathology, and the changes observed in CPP are a reflection of alterations in the systemic blood pressures or MAP. CPP has a narrow range of normal values, and a change in the ICP or MAP will be disadvantageous and have consequences with the effective CPP. CPP and cerebral vascular resistance provide a tight homeostasis to maintain cerebral blood flow, and this homeostasis is disrupted in situations involving brain injury, hypercapnia, hypoxemia, intravenous fluids, and anesthetics. The traditional approach of focusing on the systolic and diastolic blood pressures in predicting impairment of CPP would lead to a delay in identifying occult hypotension. The use of ageSI could therefore aid in early recognition of impaired CPP before a decrease in MAP is recognized.

CONCLUSION

Trauma, in particular traumatic brain injury, is one of the most important global causes of morbidity and mortality, presenting a significant challenge to healthcare systems worldwide. Rapid assessment and appropriate intervention are crucial in managing trauma patients effectively, especially in the context of traumatic brain injury, where early recognition and intervention are paramount for improved outcomes. Among the various tools available for assessing shock severity, the SI has emerged as a simple yet valuable parameter in guiding clinical decision-making.