Distant Organs Complications Post Traumatic Brain Injury (TBI)

Abstract

Background: Central Nervous System (CNS) plays integral role in controlling body organs, there is a constant interplay of neurotransmitters between CNS and extracranial organs. Hence, an isolated traumatic brain injury may be associated with various physiological responses of other body organs. Extra cranial injuries such as polytrauma and infection may also be associated with changes of neuropathology in patients with TBI. The aim of this paper is to highlight the systematic organs complications post TBI.

Methods: A literature review of extracranial organs complications post TBI was conducted. Literature review findings were presented in a lecture format, using head to toe systematic assessment format. Starting with changes in pituitary gland, followed by heart and lungs changes, then gastro-intestinal and renal changes as well as a brief on immune system changes. The main mechanism of these physiological changes was discussed such as inflammation, catecholamine surge, and increased sympathetic tone affecting systematic organs.

Result: Literature identified pituitary changes in up to 47% of traumatic subarachnoid hemorrhage. Hormonal insufficiency and antidiuretic hormone secretion abnormalities are the most common forms of pituitary dysfunction in patients with TBI. Diabetes Insipidus is reported in up to 51% of TBI cases, and it is associated with 57% to 69% mortality rate among patients with TBI. Cardiac dysfunctions are reported in up to 74% of TBI cases in which ECG abnormalities are the most common form of cardiac changes. Cardiovascular failure was reported on 18% of TBI cases. Catecholamines surge leads to structural change in cardiomyocytes due to direct effect of norepinephrine on cardiac muscles. Severe dysregulation of catecholamine homeostasis affects pulmonary vessels leading to increased blood pressure and generates massive blood shifts to the pulmonary vasculature causing Neurogenic Pulmonary Edema (NEP). In contrast, NPE can further the harm of the brain due to hypoxia and inadequate oxygen supply to brain cells. Brain injury insults the renal system indirectly in the form of electrolytes disturbances such as hypo and hyper natremia. Hyponatremia is reported in 51% of TBI cases. Stress ulcer is the most common form of gastrointestinal system changes among patients with TBI. In addition, CNS injury stimulates the immune system leaving patients with TBI highly susceptible to infection due to release of pro-inflammatory cytokines such as IL-1, IL-6 and TNF-α. Systematic inflammatory response state impacts organs hemostasias resulting on tissue hypoperfusion.

Conclusion: Cerebral injury is not only a brain disease, but it also affects the body as whole leading to systematic changes that require holistic therapeutic approach to manage. Autonomic imbalance caused by CNS dysfunction may lead to various systematic complications. Understanding the mechanism of extra-cranial organs injuries are key to prevent and manage complications.  Elevation of inflammatory biomarkers such may predict mortality and morbidity in patient post TBI.