scholarly journals Disorders of sodium balance in patients with hypothalamic-pituitary lesions in traumatic brain injury

2021 ◽  
Vol 17 (8) ◽  
pp. 61-65
Author(s):  
O.Ya. Ilchyschyn ◽  
Ya.M. Pidhirnyі
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Endocrine System ◽  
Electrolyte Imbalance ◽  
Sodium Balance ◽  
Cerebral Contusion ◽  
Hypothalamic Region ◽  
Severity Of Injury ◽  
Working Age ◽  
Pituitary Lesion

Background. Traumatic brain injury (TBI) still remains the leading cause of death in people of working age. In Ukraine, the frequency of TBI varies from 2.3 to 6 cases (average of 4–4.2) per 1,000 population annually depending on the regions. Patients with primary damage to the brain and hypothalamic-pituitary system are at risk of developing cerebral edema due to the water-electrolyte imbalance and, accordingly, osmolar imbalance between cellular and extracellular spaces. Water-electrolyte imbalance as a result of damage to the hypothalamic-pituitary system in traumatic brain injury is not described enough in the literature. The functioning of the central and peripheral links of the endocrine system depending on the location, nature and severity of injury is examined not enough. The question of diagnostic and prognostic values of various indicators of volume status in patients with trauma is also underinvestigated. The purpose of this study was to examine the types of disorders of sodium balance in patients with isolated TBI and hypothalamic-pituitary lesions; to clarify the influence of sodium imbalance type on mortality in patients with TBI and hypothalamic-pituitary lesions. Material and methods. We examined 74 patients (men/women = 60/14) with focal cerebral contusion and lesions of the hypothalamic region. Forty-seven of them were diagnosed with hypovolemia combined with hyponatremia. Hypernatremia with hypervolemia was found in 15 patients. Intracranial pressure monitoring was performed using a multifunction monitor (BSM-3562, Japan, 2018, Nihon Kohden Corporation) with a line for invasive pressure measurement. Continuous non-invasive measurement of organ tissue oxygenation (rSO2) was carried out using Somanetics Invos Oximeter Cerebral/Somatic monitor (Covidien, Mansfield, MA, USA, 2020). Plasma electrolytes were evaluated in all patients. Conclusions. Patients with TBI and hypothalamic-pituitary lesion have different types of water-sodium imbalance, which demand the differentiated approach to their treatment. Given the small number of observations, we do not dare to link the type of sodium imbalance with lethality in patients with brain trauma and hypothalamic-pituitary lesions. We consider this requires further researches.

White Matter Integrity Following Traumatic Brain Injury: The Association with Severity of Injury and Cognitive Functioning

2013 ◽  
Vol 26 (4) ◽  
pp. 648-660 ◽  
Author(s):  
Gershon Spitz ◽  
Jerome J. Maller ◽  
Richard O’Sullivan ◽  
Jennie L. Ponsford
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
Cognitive Functioning ◽  
White Matter Integrity ◽  
Severity Of Injury

scholarly journals The Roles of Neurotrophins in Traumatic Brain Injury

Life ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 26
Author(s):  
Ping-Hung Lin ◽  
Lu-Ting Kuo ◽  
Hui-Tzung Luh
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neural Development ◽  
Tissue Destruction ◽  
Compensatory Mechanisms ◽  
Injured Brain ◽  
Severity Of Injury ◽  
Brain Barrier Permeability ◽  
Post Traumatic ◽  
Related Proteins

Neurotrophins are a collection of structurally and functionally related proteins. They play important roles in many aspects of neural development, survival, and plasticity. Traumatic brain injury (TBI) leads to different levels of central nervous tissue destruction and cellular repair through various compensatory mechanisms promoted by the injured brain. Many studies have shown that neurotrophins are key modulators of neuroinflammation, apoptosis, blood–brain barrier permeability, memory capacity, and neurite regeneration. The expression of neurotrophins following TBI is affected by the severity of injury, genetic polymorphism, and different post-traumatic time points. Emerging research is focused on the potential therapeutic applications of neurotrophins in managing TBI. We conducted a comprehensive review by organizing the studies that demonstrate the role of neurotrophins in the management of TBI.

Abstract 3942: Mild Controlled Hypothermia Induction is Safe and Feasible for the Treatment of Intracranial Hypertension in Patients with Aneurysmal Subarachnoid Hemorrhage.

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Mohammad Ibrahim ◽  
Mohammad Moussavi ◽  
Elzbieta Wirkowski ◽  
Adel Hanna ◽  
Cecilia Carlowicz ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Electrolyte Imbalance ◽  
Surface Cooling ◽  
Conventional Methods ◽  
Rebound Increase

Introduction Hypothermia has been increasingly used for cerebral resuscitation in comatose survivors of cardiac arrest. A large number of studies have been undertaken in patients with traumatic brain injury to asses the efficacy of hypothermia for reduction of intracranial hypertension. Hypothermia has also been shown to reduce mortality and increase functional outcome if used for longer duration in patients with severe traumatic brain injury. Due to the risk of rebound cerebral edema during re-warming, medical complications and other factors, hypothermia has not been widely utilized for other neurologic catastrophes. To determine the safety and feasibility of hypothermia to treat intracranial hypertension in patients with aneurysmal subarachnoid hemorrhage (SAH), we performed this study. Methods Retrospective analysis was performed on 11 consecutive patients with poor grade (Hunt and Hess IV and V) SAH who had high intracranial pressure that was either non responsive or poorly responsive to conventional methods (head of bed at 30 degrees, sedation, CSF drainage and osmotherapy). All patients had intracranial pressure (ICP) monitoring via an external ventriculostomy drain (EVD) catheter. Hypothermia was induced non-invasively via surface cooling pads (Artic Sun Temperature Management System). Intravenous sedation and paralysis was used via intravenous infusion to control shivering. Hypothermia (target temperature of 32 to 34 degree C) was maintained until ICP normalized. Results Duration of hypothermia ranged from 79 hours to 190 hours. One patient required re-induction due to rebound increase in ICP during re-warming. Modified rankin scale was recorded at 3 month after the ictus. Eight patients (72%) survived with good recovery, one patient (9%) survived with severe disability and two patients (18%) died. The most common side effect was electrolyte imbalance seen in seven patients (63%), thrombocytopenia in three patients (27%), and pneumonia in four patients(36%). All complications were successfully treated and major consequences of complications (bleeding diathesis, septic shock syndrome and death) were not observed in any of these patients. Two patients had decompressive hemicraniectomy prior to hypothermia induction. Out of nine patients who did not undergo hemi-craniectomy, two died and seven did not require surgical intervention after induction of hypothermia. Conclusions Mild hypothermia induction for 72 hours or more for the treatment of intracranial hypertension refractory to other conventional methods in patients with SAH appears safe and feasible. Hypothermia may potentially be an earlier treatment option than currently recommended. This study serves as a template for future efficacy trials.

scholarly journals Serum electrolyte imbalance and prognostic factors of postoperative death in adult traumatic brain injury patients

Medicine ◽  
2018 ◽  
Vol 97 (45) ◽  
pp. e13081 ◽  
Author(s):  
Pathomporn Pin-on ◽  
Ananchanok Saringkarinkul ◽  
Yodying Punjasawadwong ◽  
Srisuluck Kacha ◽  
Drusakorn Wilairat
Keyword(s):  
Traumatic Brain Injury ◽  
Prognostic Factors ◽  
Brain Injury ◽  
Electrolyte Imbalance ◽  
Serum Electrolyte ◽  
Postoperative Death

Associations between disability and employment 1 year after traumatic brain injury in a working age population

Brain Injury ◽  
2012 ◽  
Vol 26 (3) ◽  
pp. 261-269 ◽  
Author(s):  
Nada Andelic ◽  
Lillian Flores Stevens ◽  
Solrun Sigurdardottir ◽  
Juan Carlos Arango-Lasprilla ◽  
Cecilie Roe
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Working Age ◽  
Working Age Population

scholarly journals Attenuation of Brain Nitrostative and Oxidative Damage by Brain Cooling during Experimental Traumatic Brain Injury

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Jinn-Rung Kuo ◽  
Chong-Jeh Lo ◽  
Ching-Ping Chang ◽  
Mao- Tsun Lin ◽  
Chung-Ching Chio
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Oxidative Damage ◽  
Jugular Vein ◽  
External Jugular Vein ◽  
Motor Deficits ◽  
Sham Operation ◽  
Brain Cooling ◽  
Cerebral Contusion ◽  
Oxide Synthase

The aim of the present study was to ascertain whether brain cooling causes attenuation of traumatic brain injury by reducing brain nitrostative and oxidative damage. Brain cooling was accomplished by infusion of 5 mL of 4°C saline over 5 minutes via the external jugular vein. Immediately after the onset of traumatic brain injury, rats were randomized into two groups and given 37°C or 4°C normal saline. Another group of rats were used as sham operated controls. Behavioral and biochemical assessments were conducted on 72 hours after brain injury or sham operation. As compared to those of the sham-operated controls, the 37°C saline-treated brain injured animals displayed motor deficits, higher cerebral contusion volume and incidence, higher oxidative damage (e.g., lower values of cerebral superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, but higher values of cerebral malondialdehyde), and higher nitrostative damage (e.g., higher values of neuronal nitric oxide synthase and 3-nitrotyrosine). All the motor deficits and brain nitrostative and oxidative damage were significantly reduced by retrograde perfusion of 4°C saline via the jugular vein. Our data suggest that brain cooling may improve the outcomes of traumatic brain injury in rats by reducing brain nitrostative and oxidative damage.

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