Pediatric traumatic brain injury and elevated intracranial pressure

2008 ◽  
Vol 2 (4) ◽  
pp. 237-238
Author(s):  
Lawrence F. Marshall
2018 ◽  
Author(s):  
Ryan Martin ◽  
Lara Zimmermann ◽  
Marike Zwienenberg ◽  
Kee D Kim ◽  
Kiarash Shahlaie

The management of traumatic brain injury focuses on the prevention of second insults, which most often occur because of a supply/demand mismatch of the cerebral metabolism. The healthy brain has mechanisms of autoregulation to match the cerebral blood flow to the cerebral metabolic demand. After trauma, these mechanisms are disrupted, leaving the patient susceptible to episodes of hypotension, hypoxemia, and elevated intracranial pressure. Understanding the normal and pathologic states of the cerebral blood flow is critical for understanding the treatment choices for a patient with traumatic brain injury. In this chapter, we discuss the underlying physiologic principles that govern our approach to the treatment of traumatic brain injury. This review contains 3 figures, 1 table and 12 references Key Words: cerebral autoregulation, cerebral blood flow, cerebral metabolic rate, intracranial pressure, ischemia, reactivity, vasoconstriction, vasodilation, viscosity


Author(s):  
Ruchir Gupta

In this chapter the essential aspects of anesthesia for traumatic brain injury are discussed. Subtopics include manifestations and treatment of elevated intracranial pressure (ICP), Glasgow Coma Scale (GCS), drugs used to lower ICP, and patient monitoring. The case presented is an emergent craniotomy. The chapter is divided into preoperative, intraoperative, and postoperative sections with important subtopics related to the main topic in each section. Preoperative topics discussed are evaluation of trauma, use of the GCS in this case, assessing intracranial hypertension, history of substance abuse, and clearing the cervical spine. Issues related to intraoperative management in this case include induction and use of blood products. Postoperative concerns addressed include polyuria and acute respiratory distress syndrome.


2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Stuart H. Friess ◽  
Todd J. Kilbaugh ◽  
Jimmy W. Huh

While the cornerstone of monitoring following severe pediatric traumatic brain injury is serial neurologic examinations, vital signs, and intracranial pressure monitoring, additional techniques may provide useful insight into early detection of evolving brain injury. This paper provides an overview of recent advances in neuromonitoring, neuroimaging, and biomarker analysis of pediatric patients following traumatic brain injury.


2007 ◽  
Vol 73 (10) ◽  
pp. 1023-1026 ◽  
Author(s):  
Kenji Inaba ◽  
Pedro G.R. Teixeira ◽  
Jean-Stephane David ◽  
Carlos Brown ◽  
Ali Salim ◽  
...  

There are no independent computed tomography (CT) findings predictive of elevated intracranial pressure (ICP). The purpose of this study was to evaluate brain density measurement on CT as a predictor of elevated ICP or decreased cerebral perfusion pressure (CPP). A prospectively collected database of patients with acute traumatic brain injury was used to identify patients who had a brain CT followed within 2 hours by ICP measurement. Blinded reviewers measured mean density in Hounsfield Units (HU) within a 100-mm2 elliptical region at four standardized positions. Brain density measurement was compared for patients with an ICP of 20 or greater versus less than 20 mm Hg and CPP of 70 or greater versus less than 70 mm Hg. During a 2-year period, 47 patients had ICP monitoring after brain CT. Average age was 40 ± 18 years old; 93.6 per cent were male; mean Injury Severity Score was 25 ± 10; and Glasgow Coma Scale was 6 ± 4. There was no difference in brain density measurement for observer 1, ICP less than 20 (26.3 HU) versus ICP 20 or greater (27.4 HU, P = 0.545) or for CPP less than 70 (27.1 HU) versus CPP 70 or greater (26.2, P = 0.624). Similarly, there was no difference for observer 2, ICP less than 20 (26.8 HU) versus ICP 20 or greater (27.4, P = 0.753) and CPP less than 70 (27.6 HU) versus CPP 70 or greater (26.2, P = 0.436). CT-measured brain density does not correlate with elevated ICP or depressed CPP and cannot predict patients with traumatic brain injury who would benefit from invasive ICP monitoring.


2008 ◽  
Vol 2 (4) ◽  
pp. 240-249 ◽  
Author(s):  
Jay Jagannathan ◽  
David O. Okonkwo ◽  
Hian Kwang Yeoh ◽  
Aaron S. Dumont ◽  
Dwight Saulle ◽  
...  

Object The management strategies and outcomes in pediatric patients with elevated intracranial pressure (ICP) following severe traumatic brain injury (TBI) are examined in this study. Methods This study was a retrospective review of a prospectively acquired pediatric trauma database. More than 750 pediatric patients with brain injury were seen over a 10-year period. Records were retrospectively reviewed to determine interventions for correcting ICP, and surviving patients were contacted prospectively to determine functional status and quality of life. Only patients with 2 years of follow-up were included in the study. Results Ninety-six pediatric patients (age range 3–18 years) were identified with a Glasgow Coma Scale score < 8 and elevated ICP > 20 mm Hg on presentation. The mean injury severity score was 65 (range 30–100). All patients were treated using a standardized head injury protocol. The mean time course until peak ICP was 69 hours postinjury (range 2–196 hours). Intracranial pressure control was achieved in 82 patients (85%). Methods employed to achieve ICP control included maximal medical therapy (sedation, hyperosmolar therapy, and paralysis) in 34 patients (35%), ventriculostomy in 23 patients (24%), and surgery in 39 patients (41%). Fourteen patients (15%) had refractory ICP despite all interventions, and all of these patients died. Seventy-two patients (75%) were discharged from the hospital, whereas 24 (25%) died during hospitalization. Univariate and multivariate analysis revealed that the presence of vascular injury, refractory ICP, and cisternal effacement at presentation had the highest correlation with subsequent death (p < 0.05). Mean follow-up was 53 months (range 11–126 months). Three patients died during the follow-up period (2 due to infections and 1 committed suicide). The mean 2-year Glasgow Outcome Scale score was 4 (median 4, range 1–5). The mean patient competency rating at follow-up was 4.13 out of 5 (median 4.5, range 1–4.8). Univariate analysis revealed that the extent of intracranial and systemic injuries had the highest correlation with long-term quality of life (p < 0.05). Conclusions Controlling elevated ICP is an important factor in patient survival following severe pediatric TBI. The modality used for ICP control appears to be less important. Long-term follow-up is essential to determine neurocognitive sequelae associated with TBI.


2018 ◽  
Author(s):  
Ryan Martin ◽  
Lara Zimmermann ◽  
Marike Zwienenberg ◽  
Kee D Kim ◽  
Kiarash Shahlaie

The management of traumatic brain injury focuses on the prevention of second insults, which most often occur because of a supply/demand mismatch of the cerebral metabolism. The healthy brain has mechanisms of autoregulation to match the cerebral blood flow to the cerebral metabolic demand. After trauma, these mechanisms are disrupted, leaving the patient susceptible to episodes of hypotension, hypoxemia, and elevated intracranial pressure. Understanding the normal and pathologic states of the cerebral blood flow is critical for understanding the treatment choices for a patient with traumatic brain injury. In this chapter, we discuss the underlying physiologic principles that govern our approach to the treatment of traumatic brain injury. This review contains 3 figures, 1 table and 12 references Key Words: cerebral autoregulation, cerebral blood flow, cerebral metabolic rate, intracranial pressure, ischemia, reactivity, vasoconstriction, vasodilation, viscosity


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