Management of traumatic brain injury

Author(s):  
Alistair A. Gibson ◽  
Peter J. D. Andrews

Traumatic brain injury (TBI) is a leading cause of death and disability worldwide and although young male adults are at particular risk, it affects all ages. TBI often occurs in the presence of significant extracranial injuries and immediate management focuses on the ABCs—airway with cervical spine control, breathing, and circulation. Best outcomes are achieved by management in centres that can offer comprehensive neurological critical care and appropriate management for extracranial injuries. If patients require transfer from an admitting hospital to a specialist centre, the transfer must be carried out by an appropriately skilled and equipped transport team. The focus of specific TBI management is on the avoidance of secondary injury to the brain. The principles of management are to avoid hypotension and hypoxia, control intracranial pressure and maintain cerebral perfusion pressure above 60 mmHg. Management of increased intracranial pressure is generally by a stepwise approach starting with sedation and analgesia, lung protective mechanical ventilation to normocarbia in a 30° head-up position, maintenance of oxygenation, and blood pressure. Additional measures include paralysis with a neuromuscular blocking agent, CSF drainage via an external ventricular drain, osmolar therapy with mannitol or hypertonic saline, and moderate hypothermia. Refractory intracranial hypertension may be treated surgically with decompressive craniectomy or medically with high dose barbiturate sedation. General supportive measures include provision of adequate nutrition preferably by the enteral route, thromboembolism prophylaxis, skin and bowel care, and management of all extracranial injuries.

2021 ◽  
Author(s):  
Brandon Lucke-Wold ◽  
Kevin Pierre ◽  
Sina Aghili-Mehrizi ◽  
Gregory Murad

Abstract Background:Over half of patients with facial fractures have associated traumatic brain injury. Based on previous force dynamic cadaveric studies, Lefort type 2 and 3 fractures are more associated with severe injury. Whether this correlates to neurosurgical intervention have not been well characterized. The purpose of this retrospective data analysis is to characterize fracture pattern types in patients requiring neurosurgical intervention and to see if this is different from those not requiring intervention. Methods:Retrospective data was collected from the trauma registry from 2010-2019. Inclusion criteria: adults over 18, confirmed facial fracture with available neuroimaging, reported traumatic brain injury, and admission to ICU or floor bed. Exclusion criteria: patients less than 18 years old, patients with no neuroimaging, and patients that were deceased prior to initiation of neurosurgical intervention. Data included: basic demographic data, presenting Glasgow Coma Scale (GCS) score, mechanism of injury, type of traumatic brain injury, neurosurgical intervention, and facial fracture type. Retrospective Contingency Analysis with Fraction of Total Comparison was used with Chi-Square analysis for demographic and injury characteristic data.Results:1172 patients met inclusion criteria. 1001 required no neurosurgical intervention and 171 required intervention. No significant difference was seen between the non-intervention group and intervention group in terms of demographic data or baseline injury characteristics except for presenting GCS. A significant difference was seen between groups for presenting Glasgow Coma Scale (c2=67.71, p<0.001). The intervention group had greater number of patients with GCS<8 compared to the non-intervention group. Fracture patterns were overall similar between the non-intervention group compared to intervention group (c2=4.518, p=0.92), however subset analysis did reveal a 2 fold increase in Lefort type 2 fractures and notable increase in Lefort type 3 and panfacial fractures in the intervention group. The intervention group was further divided into those requiring external ventricular drain or intracranial pressure monitor only vs. patients requiring craniectomy, craniotomy, or burr holes with or with external ventricular drain or intracranial pressure monitor. A significant difference was seen between groups (c2=20.02, p=0.03). The craniectomy, craniotomy, or burr hole group was much more likely to have Lefort type 2 or 3 fractures compared to the external ventricular drain or intracranial pressure monitor group only. Conclusions:Lefort type 2 and type 3 fractures are significantly associated with requiring neurosurgical intervention. An improved algorithm for managing these patients has been proposed in the discussion. Ongoing work will focus on validating and refining the algorithm in order to improve patient care for trauma patients with facial fracture and traumatic brain injury.


2020 ◽  
pp. 1-6 ◽  
Author(s):  
Jon Pérez-Bárcena ◽  
Catalina Crespí ◽  
Guillem Frontera ◽  
Juan Antonio Llompart-Pou ◽  
Osman Salazar ◽  
...  

OBJECTIVEThe objectives of this study were to evaluate levels of inflammasome-signaling proteins in serum and CSF of patients with traumatic brain injury (TBI), and to correlate these protein levels with intracranial pressure (ICP) and clinical outcomes at 6 months after injury.METHODSThis is a prospective and observational study in patients with moderate and severe TBI who required an external ventricular drain as part of their treatment. Serum and CSF samples were collected 3 times a day for the first 5 days after TBI. The authors have determined the protein concentration of caspase-1 in the CSF and serum of patients with TBI by using commercially available enzyme-linked immunosorbent assays. The ICP value was recorded hourly. The 6-month outcome was assessed using the Glasgow Outcome Scale–Extended.RESULTSA total of 21 patients were included in this study, and a total of 234 paired serum-CSF samples were analyzed. The area under the curve (AUC) value of caspase-1 in CSF during the 5-day period was 2452.9 pg/mL·hr in the group of patients with high ICP vs 617.6 pg/mL·hr in the patients with low ICP. The differences were mainly on day 2 (19.7 pg/mL vs 1.8 pg/mL; p = 0.06) and day 3 (13.9 pg/mL vs 1 pg/mL; p = 0.05). The AUC value of caspase in CSF during the 5-day period was 1918.9 pg/mL·hr in the group of patients with poor outcome versus 924.5 pg/mL·hr in the patients with good outcome. The protein levels of caspase-1 in CSF were higher in patients with unfavorable outcomes during the first 96 hours after TBI.CONCLUSIONSIn this cohort of patients with TBI who were admitted to the neurosurgical ICU, the inflammasome protein caspase-1 is increased in the CSF of patients with high ICP, especially on days 2 and 3 after TBI. Also the protein levels of caspase-1 in CSF were higher in patients with poor outcome during the first 96 hours after TBI. Moreover, not only the absolute value of caspase-1 in CSF but also its trend is associated with poor outcomes.


2012 ◽  
Vol 23 (2) ◽  
pp. 186-203
Author(s):  
Patricia A. Blissitt

Despite progress in the management of adults with severe traumatic brain injury, several controversies persist. Among the unresolved issues of greatest concern to neurocritical care clinicians and scientists are the following: (1) the best use of technological advances and the data obtained from multimodality monitoring; (2) the use of mannitol and hypertonic saline in the management of increased intracranial pressure; (3) the use of decompressive craniectomy and barbiturate coma in refractory increased intracranial pressure; (4) therapeutic hypothermia as a neuroprotectant; (5) anemia and the role of blood transfusion; and (6) venous thromboembolism prophylaxis in severe traumatic brain injury. Each of these strategies for managing severe traumatic brain injury, including the postulated mechanism(s) of action and beneficial effects of each intervention, adverse effects, the state of the science, and critical care nursing implications, is discussed.


2009 ◽  
Vol 30 (3) ◽  
pp. 628-637 ◽  
Author(s):  
Guoyi Gao ◽  
Yasutaka Oda ◽  
Enoch P Wei ◽  
John T Povlishock

This study examined the effect of posttraumatic hypoxia on cerebral vascular responsivity and axonal damage, while also exploring hypothermia's potential to attenuate these responses. Rats were subjected to impact acceleration injury (IAI) and equipped with cranial windows to assess vascular reactivity to topical acetylcholine, with postmortem analyses using antibodies to amyloid precursor protein to assess axonal damage. Animals were subjected to hypoxia alone, IAI and hypoxia, IAI and hypoxia before induction of moderate hypothermia (33°C), IAI and hypoxia induced during hypothermic intervention, and IAI and hypoxia initiated after hypothermia. Hypoxia alone had no impact on vascular reactivity or axonal damage. Acceleration injury and posttraumatic hypoxia resulted in dramatic axonal damage and altered vascular reactivity. When IAI and hypoxia were followed by hypothermic intervention, no axonal or vascular protection ensued. However, when IAI was followed by hypoxia induced during hypothermia, axonal and vascular protection followed. When this same hypoxic insult followed the use of hypothermia, no benefit ensued. These studies show that early hypoxia and delayed hypoxia exert damaging axonal and vascular consequences. Although this damage is attenuated by hypothermia, this follows only when hypoxia occurs during hypothermia, with no benefit found if the hypoxic insult proceeds or follows hypothermia.


Critical Care ◽  
2021 ◽  
Vol 25 (1) ◽  
Author(s):  
Daniel Agustin Godoy ◽  
Rafael Badenes ◽  
Paolo Pelosi ◽  
Chiara Robba

AbstractMaintaining an adequate level of sedation and analgesia plays a key role in the management of traumatic brain injury (TBI). To date, it is unclear which drug or combination of drugs is most effective in achieving these goals. Ketamine is an agent with attractive pharmacological and pharmacokinetics characteristics. Current evidence shows that ketamine does not increase and may instead decrease intracranial pressure, and its safety profile makes it a reliable tool in the prehospital environment. In this point of view, we discuss different aspects of the use of ketamine in the acute phase of TBI, with its potential benefits and pitfalls.


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