Role of Monocyte-to-lymphocyte Ratio, Mean Platelet Volume-to-Platelet Count Ratio, C-Reactive Protein and Erythrocyte Sedimentation Rate as Predictor of Severity in Secondary Traumatic Brain Injury: A Literature Review

Abstract

BACKGROUND: Secondary traumatic brain injury (TBI) is injury to the brain following primary TBI because of neuroinflammation as consequences of neuronal and glial cell injury which cause release of various inflammation cytokine and chemokine. Biomarker examination to predict the severity of secondary TBI is important to provide appropriate treatment to the patient. This article reviews possibility several common laboratory parameter such as monocyte-to-lymphocyte ratio (MLR), mean platelet volume-to-platelet count (PC) ratio (MPV-PCR), c-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) to predict severity of secondary TBI. LITERATURE REVIEW: TBI activates microglia which increase infiltration and proliferation of monocyte. Neuroinflammation also increases thrombopoiesis which leads to increase megakaryocytes production. In the other hand, due to disruption of brain blood vessels because of trauma, coagulation cascade is also activated and leads to consumptive coagulopathy. These are reflected as high monocyte count, low PC, and high MPV. Lymphocyte count is reported low in TBI especially in poor outcome patients. CRP is an acute phase reactant that increased in inflammation condition. In TBI, increased production of Interleukin-6 leads to increase CRP production. In head injured patients, ESR level does not increase significantly in the acute phase of inflammation but last longer when compared to CRP. CONCLUSION: MLR, MPV-PCR, CRP, and ESR could be predictor of severity in secondary TBI.

Correlation of MLR with CRP and MPVPCR with LED in Traumatic Brain Injury

“…This elevation may be seen in the acute phase of TBI (first 72 h). As opposed to MLR, ESR count is not related to any acute neuroinflammatory process [11], [32].…”

“…In this study, we found that MLR and CRP have a positive correlation in patients with TBI and are statistically significant (r = 0.215, p = 0.045). Upregulation of monocyte may be due to microglia activation after TBI and acute inflammatory response in a patient with TBI [31], [32], [33]. Escalation of monocyte leads to upregulation of proinflammatory cytokine, then activates hepatocyte to synthesize CRP [29].…”

“…Platelets may be classified as an immune factor due to their ability to recognize pathogens and attract other immune cells, such as neutrophils, macrophages, and lymphocytes, to the inflamed area [36], [37]. Conversely, CRP is specific to expressing acute inflammatory process [32]. In the early phase of the neuroinflammatory process, there is an increase in platelet count as a reaction to increasing in thrombopoietin in the blood that will lead to thrombocytosis.…”