Traumatic brain injury (TBI) remains a major cause of death and disability worldwide. For all ages and TBI severities, crude incidence rates ranged from 47.3 to 694 per 100,000 population per year (country-level studies) and from 83.3 to 849 per 100,000 population per year (regional-level studies). Mortality rates ranged from 9 to 28.10 per 100,000 population per year (country-level studies) and from 3.3 to 24.4 per 100,000 population per year (regional-level studies). The most common mechanisms of injury were traffic accidents and falls [1]. Patients with TBI are most commonly categorised into mild, moderate, and severe based on Glasgow Coma Scale (GCS) [2], as well as findings from computed tomography (CT) for the head [3]. Magnetic resonance imaging (MRI) is routinely performed at a growing number of centres and is particularly helpful in the quantification of diffuse axonal TBI. The more recently developed diffusion tension DT-MRI can detect in even greater detail alterations in the microstructure of the white matter, and it shows considerable promise in the assessment of neuronal damage [4]. However, these neuroimaging techniques reveal little or no information regarding secondary injury processes such as excitotoxicity, neuroinflammation, blood–brain barrier breakdown, ischemic damage, and cell death. New biomarkers are a promising tool for clinicians for obtaining additional, patient-specific information.

A substantial subgroup of patients with TBI admitted to hospitals includes patients with traumatic intracerebral haemorrhage (TICH). In these cases, damage to the neuronal structure is apparent on admission CTs. The earliest consequences of TICH are increased vascular permeability, leading to brain oedema and complex inflammatory response [5,6,7,8]. Alterations in blood–brain barrier permeability may contribute to secondary brain injury through an abnormal passage of blood-borne substances into the extravascular space, increasing neuronal vulnerability [9,10]. Increased vascular permeability is associated with multiple post-traumatic inflammatory events [9,11]. Trauma-induced mechanical damage to vascular cell membranes results in endothelial cell necrosis and red blood cell extravasation [12,13]. Endothelial and leukocyte adhesion molecules are upregulated as a result of primary traumatic events, leading to the recruitment and extravasation of circulating leukocytes into the brain parenchyma [14]. Blood-borne circulating monocytes gain access to the brain parenchyma and may contribute to macrophage-induced secondary injury mechanisms. Moreover, a brain injury is often accompanied by multi-organ trauma, which is often severe and difficult to diagnose and treat and may influence prognosis [15].

The prognosis of patients with TICH is still unclear, and multiple studies have tried to identify predictors of outcome in these patients [9]. An assessment of the level of consciousness with the Glasgow Coma Scale at admission remains the most reliable prognostic factor, which unfortunately can be subject to human error. It may also be underestimated due to drug or alcohol intoxication [16]. Thus, the need for more objective prognostic factors should be addressed. The immunological studies demonstrate diagnostic potential and provide information regarding both the acute as well as long-term cerebrovascular consequences of brain injury leading to mortality, disability, and cognitive impairment [17]. In the past few years, many studies reported that the combinations of the haematological components of the systemic inflammatory responses, such as the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), the lymphocyte-to-monocyte ratio (LMR), and systemic immune inflammation index (SII) were effective prognostic indicators in patients with a severe traumatic brain injury [10,17,18], neoplasms [19,20,21,22,23], obesity [24,25], coronary artery disease [26,27], diabetes [28], and acute ischaemic stroke [29]. The components of these easily calculated parameters are readily available, inexpensive, and routinely measured in daily practice as part of the complete blood count [30]. The calculation of these haematological components of the systemic inflammatory response may provide clinicians with a further valuable and objective tool that would support the clinical assessment of the head trauma patients in their management and prognosis.

2. Discussion