Volume 1, Issue 4, November 2017, Page: 96-103
Role of Propranolol and Clonidine in Sympathetic Hyperactivity After Severe Traumatic Brain Injury
Mohamed Mostafa Megahed, Critical Care Medicine, Critical Care Department, Faculty of Medicine, Alexandria University, Alexandria, Egypt
Tamer Nabil Habib, Critical Care Medicine, Critical Care Department, Faculty of Medicine, Alexandria University, Alexandria, Egypt
Zeyad Moqbel, Radiodiagnosis Department, Faculty of Medicine, Alexandria University, Alexandria, Egypt
Riyad Abdullah Almogahed, Critical Care Medicine, Critical Care Department, Faculty of Medicine, Alexandria University, Alexandria, Egypt
Islam El Sayed Mohamed Ahmed, Clinical Pharmacy Specialist, Faculty of Pharmacy, Alexandria University, Alexandria, Egypt
Received: Jun. 5, 2017;       Accepted: Jun. 22, 2017;       Published: Oct. 24, 2017
DOI: 10.11648/j.cnn.20170104.14      View  2070      Downloads  88
Abstract
Sympathetic hyperactivity following severe traumatic brain injury (TBI) has compounding negative consequences on many body organs. Adrenergic blockade using beta blockers and alpha 2 agonists demonstrated positive effects in decreasing sympathetic hyperactivity and increasing survival. This study was conducted on 50 adult patients with severe TBI randomly assigned into two groups. Intervention group received propranolol 40 mg BID and clonidine 150 µg BID for 7 days. Control group didn’t receive any beta blockers or alpha 2 agonists. The primary outcome was plasma norepinephrine level on day 8. Intervention group showed 20% reduction in plasma norepinephrine, while control group showed 10% reduction only. Glasgow coma score (GCS) and full outline of unresponsiveness (FOUR) score didn’t show any significant differences (p = 0.554). Heart rate was significantly decreased in intervention group (p = 0.002), mean arterial pressure also decreased (p = 0.007), as well as respiratory rate (p = 0.001). Ventilator free days, coma free days, ICU length of stay, and mortality didn’t differ significantly between the two groups. Propranolol and clonidine at the specified doses may decrease the sympathetic hyperactivity in patients suffering from severe traumatic brain injury.
Keywords
Critical, Neurology, Trauma, β-Blocker, α-Agonist
To cite this article
Mohamed Mostafa Megahed, Tamer Nabil Habib, Zeyad Moqbel, Riyad Abdullah Almogahed, Islam El Sayed Mohamed Ahmed, Role of Propranolol and Clonidine in Sympathetic Hyperactivity After Severe Traumatic Brain Injury, Clinical Neurology and Neuroscience. Vol. 1, No. 4, 2017, pp. 96-103. doi: 10.11648/j.cnn.20170104.14
Copyright
Copyright © 2017 Authors retain the copyright of this article.
This article is an open access article distributed under the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Reference
[1]
Traumatic Brain Injury (TBI) - Definition and Pathophysiology [Internet].: Overview, Epidemiology, Primary Injury. [cited 2017 March 18]. available at: http://emedicine.medscape.com/article/326510-overview
[2]
Teasdale G, Jennett B. Assessment of Coma and Impaired Consciousness. The Lancet 1974; 304(7872): 81–4.
[3]
Faul M, Xu L, Wald MM, Coronado V, Dellinger AM. Traumatic brain injury in the United States: national estimates of prevalence and incidence, 2002-2006. Injury Prevention 2010; 16 (Supplement 1).
[4]
Zygun DA, Laupland KB, Hader WJ et al.: Severe traumatic brain injury in a large Canadian health region. Can J Neurological Sci 2005, 32(1): 87-92.
[5]
Campbell CG, Kuehn SM, Richards PM et al.: Medical and cognitive outcome in children with traumatic brain injury. Can J Neurological Sci 2004, 31(2): 213- 19.
[6]
Rose JM: Continuum of care model for managing mild traumatic brain injury in workers. Compensation context: a description of the model and its development. Brain Injury 2005, 19(1): 29-39.
[7]
Woolf PD. The Catecholamine Response to Multisystem Trauma. Arch Surg Archives of Surgery 1992; 127(8): 899.
[8]
Woolf PD, Hamill RW, Lee LA, Cox C, Mcdonald JV. The predictive value of catecholamines in assessing outcome in traumatic brain injury. Journal of Neurosurgery 1987; 66(6): 875–82.
[9]
Perkes I, Baguley IJ, Nott MT, Menon DK. A review of paroxysmal sympathetic hyperactivity after acquired brain injury. Annals of Neurology Ann Neurol 2010; 68(2): 126–35.
[10]
Rabinstein AA, Benarroch EE. Treatment of paroxysmal sympathetic hyperactivity. Curr Treat Options Neurol Current Treatment Options in Neurology 2008; 10(2): 151–7.
[11]
Kim E, Lauterbach EC, Reeve A, Arciniegas DB, Coburn KL, Mendez MF, et al. Neuropsychiatric Complications of Traumatic Brain Injury: A Critical Review of the Literature (A Report by the ANPA Committee on Research). Journal of Neuropsychiatry 2007; 19(2): 106–27.
[12]
Nott MT, Chapparo C, Heard R, Baguley IJ. Patterns of agitated behaviour during acute brain injury rehabilitation. Brain Injury 2010; 24(10): 1214–21.
[13]
Baguley IJ, Nicholls JL, Felmingham KL, Crooks J, Gurka JA, Wade LD. Dysautonomia after traumatic brain injury: a forgotten syndrome? Journal of Neurology, Neurosurgery and Psychiatry 1999; 67(1): 39–43.
[14]
Tong C, König MW, Roberts PR, Tatter SB, Li X-H. Autonomic Dysfunction Secondary to Intracerebral Hemorrhage. Anesthesia & Analgesia 2000; 91(6): 1450–1.
[15]
Srinivasan S, Lim CT, Thirugnanam U. Paroxysmal autonomic instability with dystonia. Clinical Autonomic Research Clin Auton Res 2007; 17(6): 378–81.
[16]
Cuny E, Richer E, Castel JP. Dysautonomia syndrome in the acute recovery phase after traumatic brain injury: relief with intrathecal Baclofen therapy. Brain Injury 2001; 15(10): 917–25.
[17]
Baguley IJ, Heriseanu RE, Cameron ID, Nott MT, Slewa-Younan S. A Critical Review of the Pathophysiology of Dysautonomia Following Traumatic Brain Injury. Neurocritical Care Neurocrit Care 2007; 8(2): 293–300.
[18]
Baguley IJ. The excitatory: inhibitory ratio model (EIR model): An integrative explanation of acute autonomic overactivity syndromes. Medical Hypotheses 2008; 70(1): 26–35.
[19]
Neuroanatomical basis of paroxysmal sympathetic hyperactivity: A diffusion tensor imaging analysis Holly E. Hinson1 Brain Inj. 2015; 29(4): 455–461.
[20]
Tran TY, Dunne IE, German JW. Beta blockers exposure and traumatic brain injury: a literature review. Neurosurgical FOCUS 2008; 25(4).
[21]
Payen D, Quintin L, Plaisance P, Chiron B, Lhoste F. Head injury. Critical Care Medicine 1990; 18(4): 392–5.
[22]
Nordström C-H. Physiological and Biochemical Principles Underlying Volume-Targeted Therapy The "Lund Concept". Neurocritical Care NCC 2005; 2(1): 083–96.
[23]
Choi Y, Novak JC, Hillier A, Votolato NA, Beversdorf DQ. The Effect of alpha-2 Adrenergic Agonists on Memory and Cognitive Flexibility. Cognitive and Behavioral Neurology 2006; 19(4): 204–7.
[24]
Schneider J, Tinker J, Decamp E. Clonidine improves attentional and memory components of delayed response performance in a model of early Parkinsonism. Behavioural Brain Research 2010; 211(2): 236–9.
[25]
Asgeirsson B, Grände P-O, Nordström C-H, Berntman L, Messeter K, Ryding E. Effects of hypotensive treatment with α2-agonist and β1-antagonist on cerebral haemodynamics in severely head injured patients. Acta Anaesthesiologica Scandinavica 1995; 39(3): 347–51.
[26]
Ara Ko et al. Early Propranolol after Traumatic Brain Injury is Associated with lowerMortality Journal of Trauma and Acute Care Surgery 2016
[27]
Didier Payen et al. Head injury: Clonidine decreases plasma catecholamines, Critical Care Medicine May 1990
[28]
Patel et al. Decreasing adrenergic or sympathetic hyperactivity after severe traumatic brain injury using propranolol and clonidine (DASH After TBI Study): study protocol for a randomized controlled trial Trials 2012, 13: 177.
Browse journals by subject