Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2022 Oct 8;17(3):435-441.
doi: 10.1055/s-0042-1757217. eCollection 2022 Sep.

Prognostic Role of Catecholamine in Moderate-to-Severe Traumatic Brain Injury: A Prospective Observational Cohort Study

Affiliations

Prognostic Role of Catecholamine in Moderate-to-Severe Traumatic Brain Injury: A Prospective Observational Cohort Study

Anamika Singh et al. Asian J Neurosurg. .

Abstract

Objective Traumatic brain injury leads to the activation of sympathetic nervous system and elevation in serum catecholamine levels. The aim of this study was to determine whether catecholamine level obtained within 24 hours of traumatic brain injury provides a reliable prognostic marker for outcome. Materials and Methods This study was a prospective observational cohort study on 36 moderate-to-severe traumatic brain injury. Plasma epinephrine (E), norepinephrine (NE), and dopamine (DA) levels were measured by using computed tomography enzyme-linked immunosorbent assay test and compared with Glasgow coma scale (GCS) that was obtained concurrently. Neurological outcome was determined by GCS at day 7 of treatment and by Glasgow outcome scale at mean follow-up of 9.73 ± 2.26 months. Results Patients with GCS 3 to 4 had markedly increase in baseline mean E (771.5 ± 126.0), NE (2,225.0 ± 215.4), and DA (590.2 ± 38.8) levels as compared with control, while patients with better GCS (11-12) had mildly elevated levels. Patients with GCS 5 to 10 had intermediate values. Cases with markedly elevated baseline E, NE, and DA level were either died or remained in poor GCS (3 or 4) at day 7 of treatment and remained in persistent vegetative state at mean follow-up of 9.73 ± 2.26 months. Cases with only mildly elevated E, NE, and DA level were improved to better GCS on treatment and had good recovery on follow-up. Conclusion These data indicate that a markedly elevated catecholamine level was an excellent endogenous and readily quantifiable marker that appears to reflect the extent of brain injury and predict the likelihood of recovery.

Keywords: Glasgow coma scale; catecholamine; moderate-to-severe; outcomes; traumatic brain injury.

PubMed Disclaimer

Conflict of interest statement

Conflict of Interest None declared.

Figures

Fig. 1
Fig. 1
Polynomial line diagram showing changes in baseline mean catecholamine levels during the hospitalization with respect to Glasgow coma scale (GCS) at admission.
Fig. 2
Fig. 2
Correlation of baseline catecholamine level with outcome at day 7 of treatment. GCS, Glasgow coma scale.
Fig. 3
Fig. 3
Correlation of baseline catecholamine level with Glasgow outcome scale at mean follow-up of 9.73 ± 2.26 months. GR, good recovery; MD, moderate disability; PV, persistent vegetative state; SD, severe disability.

References

    1. Hyder A A, Wunderlich C A, Puvanachandra P, Gururaj G, Kobusingye O C. The impact of traumatic brain injuries: a global perspective. NeuroRehabilitation. 2007;22(05):341–353. - PubMed
    1. Lingsma H F, Roozenbeek B, Steyerberg E W, Murray G D, Mass A I. Early prognosis in traumatic brain injury: from propheciesto predictions. Lancet Neurol. 2010;9(05):543–554. doi: 10.1016/s1474-4422(10)70065-X. - DOI - PubMed
    1. Woolf P D, Hamill R W, Lee L A, Cox C, McDonald J V. The predictive value of catecholamines in assessing outcome in traumatic brain injury. J Neurosurg. 1987;66(06):875–882. - PubMed
    1. Chesnut R M, Marshall L F, Klauber M R. The role of secondary brain injury in determining outcome from severe head injury. J Trauma. 1993;34(02):216–222. - PubMed
    1. Kinoshita K. Traumatic brain injury: pathophysiology for neurocritical care. J Intensive Care. 2016;4:29. - PMC - PubMed