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Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents. Chapter 9. Use of sedation and neuromuscular blockade in the treatment of severe pediatric traumatic brain injury
... Infection rates are also higher with intraventricular catheters (up to 5%), compared with about 2% with intraparenchymal devices [33]. In circumstances of intractable elevated ICP with a working ventriculostomy in place, open basal cisterns, and no major mass lesions or shift, the use of a lumbar drain is considered a treatment option [34], but this technique is not widely used. ...
... Hypertonic saline does not cause diuresis , so the intracellular and interstitial volumes within the vascular compartment are maintained. Standard dosage The published guidelines suggest a dosing range from 0.1 to 1.0 mL/kg per hour of 3% saline [19]. Peterson et al. [24] reported that a similar dosage of 11 to 27 mL/kg per day was well tolerated, and that the mortality rate was signifi cantly lower than predicted from the Trauma and Injury Severity Score (TRISS). ...
... Pontine myelinolysis or renal failure is a theoretical risk, but these are not limiting problems in practice. Special point Serum osmolarity levels of up to 360 mOsm are well tolerated [19]. ...
The primary goal in treating any pediatric patient with severe traumatic brain injury (TBI) is the prevention of secondary insults such as hypotension, hypoxia, and cerebral edema. Despite the publication of guidelines, significant variations in the treatment of severe TBI continue to exist, especially in regards to intracranial pressure (ICP)-guided therapy. This variability in treatment results mainly from a paucity of data from which to create standards and from the heterogeneity inherent in pediatric TBI. The approach to management of severe TBI based on the published guidelines should be focused on ICP control, which should ultimately improve cerebral perfusion pressure. After identifying and surgically evacuating expanding hematomas, the first-tier treatment approach requires placing an ICP monitor. This is accompanied by medical management of elevated ICP, initially with simple maneuvers such as elevating the head of the bed to improve venous drainage, instituting sedation and analgesia to decrease metabolic demands of the brain, and draining cerebrospinal fluid. If these measures fail, then further first-tier interventions include hyperosmolar therapy to decrease cerebral edema and controlled ventilation to decrease cerebral blood volume. For elevations of ICP resistant to first-tier therapies, treatment escalates to second-tier therapy, which includes more aggressive measures such as placing jugular catheters to measure cerebral oxygenation with moderate hyperventilation, placing lumbar drains to remove more cerebrospinal fluid, administering high-dose barbiturates to suppress cerebral electrical activity, inducing hypothermia as a protective measure, and performing decompressive craniectomy to open the cranial vault. To properly execute these interventions, appropriate neuromonitoring is essential, starting from standard physiological parameters such as ICP, mean arterial blood pressure, and temperature. Additional modalities of neurologic monitoring are becoming more readily available and can provide additional clinically useful information about the pediatric patient with TBI; these include cerebral oxygenation, continuous electroencephalography, noninvasive blood flow monitoring, and advanced neuroimaging.
... The most recent guidelines for management of severe TBI in pediatric patients do not make specific recommendations on the use of sedatives and analgesics, yet these medications are commonly used as first line therapy -91% of practitioners report using sedatives as first tier ICH-directed therapy [4,7,8]. Specifically, fentanyl and midazolam are commonly used in the management of critically ill children, primarily for the sedative-analgesic effect that facilitates mechanical ventilation and lowers oxygen consumption in respiratory failure and shock states [9]. ...
... The mechanism for this response is not fully understood, although opioidmediated vasodilation has been proposed (leading to increased brain blood volume in the presence of abnormal brain compliance) [34]. In recognition of these data, and the lack of evidence supporting use in children, the 2003 consensus guidelines recommended that use of fentanyl in pediatric TBI be left to physician discretion [7]. The most recent guidelines do not specifically address the use of fentanyl due to the continued lack of clinical studies in children [4]. ...
Objective:
To evaluate the clinical effectiveness of bolus-dose fentanyl and midazolam to treat episodic intracranial hypertension in children with severe traumatic brain injury.
Design:
Retrospective cohort.
Setting:
PICU in a university-affiliated children's hospital level I trauma center.
Patients:
Thirty-one children aged 0-18 years with severe traumatic brain injury (Glasgow Coma Scale score of ≤ 8) who received bolus doses of fentanyl and/or midazolam for treatment of episodic intracranial hypertension.
Interventions:
None.
Measurements and main results:
The area under the curve from high-resolution intracranial pressure-time plots was calculated to represent cumulative intracranial hypertension exposure: area under the curve for intracranial pressure above 20 mm Hg (area under the curve-intracranial hypertension) was calculated in 15-minute epochs before and after administration of fentanyl and/or midazolam for the treatment of episodic intracranial hypertension. Our primary outcome measure, the difference between predrug and postdrug administration epochs (Δarea under the curve-intracranial hypertension), was calculated for all occurrences. We examined potential covariates including age, injury severity, mechanism, and time after injury; time after injury correlated with Δarea under the curve-intracranial hypertension. In a mixed-effects model, with patient as a random effect, drug/dose combination as a fixed effect, and time after injury as a covariate, intracranial hypertension increased after administration of fentanyl and/or midazolam (overall aggregate mean Δarea under the curve-intracranial hypertension = +17 mm Hg × min, 95% CI, 0-34 mm Hg × min; p = 0.04). The mean Δarea under the curve-intracranial hypertension increased significantly after administration of high-dose fentanyl (p = 0.02), low-dose midazolam (p = 0.006), and high-dose fentanyl plus low-dose midazolam (0.007). Secondary analysis using age-dependent thresholds showed no significant impact on cerebral perfusion pressure deficit (mean Δarea under the curve-cerebral perfusion pressure).
Conclusions:
Bolus dosing of fentanyl and midazolam fails to reduce the intracranial hypertension burden when administered for episodic intracranial hypertension. Paradoxically, we observed an overall increase in intracranial hypertension burden following drug administration, even after accounting for within-subject effects and time after injury. Future work is needed to confirm these findings in a prospective study design.
... While there have been cases of propofol providing adequate sedation and successfully treating intracranial hypertension [47,48], several pediatric traumatic brain injury case reports have reported metabolic acidosis and death in patients on prolonged (24 hrs) continuous infusion of propofol [49][50][51][52][53]. In the 2003 published guidelines for the care of severe pediatric traumatic brain-injured patients, "continuous infusion of propofol is not recommended" [54]. ...
Sedation and analgesia performed by the pediatrician and pediatric subspecialists are becoming increasingly common for diagnostic and therapeutic purposes in children with developmental disabilities and neurologic disorders (autism, epilepsy, stroke, obstructive hydrocephalus, traumatic brain injury, intracranial hemorrhage, and hypoxic-ischemic encephalopathy). The overall objectives of this paper are (1) to provide an overview on recent studies that highlight the increased risk for respiratory complications following sedation and analgesia in children with developmental disabilities and neurologic disorders, (2) to provide a better understanding of sedatives and analgesic medications which are commonly used in children with developmental disabilities and neurologic disorders on the central nervous system.
... The most encouraging clinical data come from the pediatric patients who have sustained TBI. Most institutions that have adopted HTS as a first-line therapy for intracranial hypertension use a continuous infusion of 3% normal saline [74]. Potential adverse events that have been associated with HTS include renal failure, central pontine myelinoysis, and rebound ICP elevation [45]. ...
Traumatic brain injury (TBI) refers to the potential for significant injury to the brain parenchyma following head trauma. This article covers pertinent principles, management approaches, and current controversies in severe, moderate, and minor TBI. Controversies covered include hypertonic saline (HTS) for increased intracranial pressure (ICP), prehospital intubation of patients who have experienced TBI, and the use of recombinant factor VIIa (rFVIIa). Traumatic head injury has plagued humankind since the beginning of civilization. The writings of Hippocrates refer to trephination [1], and early writings on the practice of neurosurgery describe the management of head trauma. Although the most common mechanism for TBI has changed since antiquity from assaults to motor vehicle-associated injuries, TBI remains the single largest cause of trauma morbidity and accounts for nearly one third of all trauma deaths (Fig. 1) [2-4]. An estimated 1.1 million patients are evaluated each year in emergency departments for acute TBI [3]. TBI occurs most. often in young people, with a peak incidence at 15 to 24 years of age [4]. Smaller peaks occur in children younger than 5 years of age and in individuals older than 85 years [4]. Child abuse is common in children younger than 4 years of age who present with severe to moderate TBI (Fig. 2) [5]. TBI is commonly categorized by means of the Glasgow Coma Scale (GCS) [6] as severe (GCS <= 8), moderate (GCS 9-13), and minor (GCS 14-15). Severe TBI accounts for approximately 10% of all cases, whereas moderate TBI accounts for another 10%; the remaining 80% are classified as minor [4].
Trauma patients present a unique challenge to anesthesiologists, since they require resource-intensive care, often complicated by pre-existing medical conditions. This fully revised new edition focuses on a broad spectrum of traumatic injuries and the procedures anesthesiologists perform to care for trauma patients perioperatively, surgically, and post-operatively. Special emphasis is given to assessment and treatment of co-existing disease, including surgical management of trauma patients with head, spine, orthopedic, cardiac, and burn injuries. Topics such as training for trauma (including use of simulation) and hypothermia in trauma are also covered. Six brand new chapters address pre-hospital and ED trauma management, imaging in trauma, surgical issues in head trauma and in abdominal trauma, anesthesia for oral and maxillofacial trauma, and prevention of injuries. The text is enhanced with numerous tables and 300 illustrations showcasing techniques of airway management, shock resuscitation, echocardiography and use of ultrasound for the performance of regional anesthesia in trauma.
The perioperative management of a child posted for a neurosurgical intervention is based on a robust understanding of the pediatric neurophysiology, the pathophysiologic effects of myriad neurosurgical entities, and the interplay between anesthetic drugs and cerebral pathophysiology in this subset of patients. From the preoperative period, until the child is discharged to the wards, the anesthesiologist’s role is paramount in achieving the harmonious amalgamation of safe neuroanesthesia principles with high-end pediatric neurocritical care. There have been giant strides in modern-day neurosurgical practice, and it is imperative to develop high-level sub-specialty pediatric neuroanesthesia and neurocritical care to improve outcome measures. The ensuing treatise attempts to present practical aspects for the hands-on management of children presenting for neurosurgical procedures.
Sugammadex is a novel pharmacologic agent, which reverses neuromuscular blockade with a mechanism that differs from acetylcholinesterase inhibitors such as neostigmine. There is a growing body of literature demonstrating its efficacy in pediatric patients of all ages. Prospective trials have demonstrated a more rapid and more complete reversal of rocuronium-induced neuromuscular blockade than the acetylcholinesterase inhibitor, neostigmine. Unlike the acetylcholinesterase inhibitors, sugammadex effectively reverses intense or complete neuromuscular blockade. It may also be effective in situations where reversal of neuromuscular blockade is problematic including patients with neuromyopathic conditions or when acetylcholinesterase inhibitors are contraindicated. This paper reviews the physiology of neuromuscular transmission as well as the published literature regarding the use of sugammadex in pediatric population including the pediatric intensive care unit population. Clinical applications are reviewed, adverse effects are discussed, and dosing algorithms are presented.
Objectives:
The devastating effect of traumatic brain injury is exacerbated by an acute secondary neuroinflammatory response, clinically manifest as elevated intracranial pressure due to cerebral edema. The treatment effect of cell-based therapies in the acute post-traumatic brain injury period has not been clinically studied although preclinical data demonstrate that bone marrow-derived mononuclear cell infusion down-regulates the inflammatory response. Our study evaluates whether pediatric traumatic brain injury patients receiving IV autologous bone marrow-derived mononuclear cells within 48 hours of injury experienced a reduction in therapeutic intensity directed toward managing elevated intracranial pressure relative to matched controls.
Design:
The study was a retrospective cohort design comparing pediatric patients in a phase I clinical trial treated with IV autologous bone marrow-derived mononuclear cells (n = 10) to a control group of age- and severity-matched children (n = 19).
Setting:
The study setting was at Children's Memorial Hermann Hospital, an American College of Surgeons Level 1 Pediatric Trauma Center and teaching hospital for the University of Texas Health Science Center at Houston from 2000 to 2008.
Patients:
Study patients were 5-14 years with postresuscitation Glasgow Coma Scale scores of 5-8.
Interventions:
The treatment group received 6 million autologous bone marrow-derived mononuclear cells/kg body weight IV within 48 hours of injury. The control group was treated in an identical fashion, per standard of care, guided by our traumatic brain injury management protocol, derived from American Association of Neurological Surgeons guidelines.
Measurements and main results:
The primary measure was the Pediatric Intensity Level of Therapy scale used to quantify treatment of elevated intracranial pressure. Secondary measures included the Pediatric Logistic Organ Dysfunction score and days of intracranial pressure monitoring as a surrogate for length of neurointensive care. A repeated-measure mixed model with marginal linear predictions identified a significant reduction in the Pediatric Intensity Level of Therapy score beginning at 24 hours posttreatment through week 1 (p < 0.05). This divergence was also reflected in the Pediatric Logistic Organ Dysfunction score following the first week. The duration of intracranial pressure monitoring was 8.2 ± 1.3 days in the treated group and 15.6 ± 3.5 days (p = 0.03) in the time-matched control group.
Conclusions:
IV autologous bone marrow-derived mononuclear cell therapy is associated with lower treatment intensity required to manage intracranial pressure, associated severity of organ injury, and duration of neurointensive care following severe traumatic brain injury. This may corroborate preclinical data that autologous bone marrow-derived mononuclear cell therapy attenuates the effects of inflammation in the early post-traumatic brain injury period.
Purpose of Review
This article reviews the pathophysiology, evaluation, and management of pediatric TBI, as well as highlights recent updates in the literature. Traumatic brain injury (TBI) is a leading cause of death and permanent disability worldwide, and its prevalence presents a significant public health concern. Since the second edition of the Guidelines for the Acute Medical Management of Severe Traumatic Brain Injury in Infants, Children, and Adolescents was released, several recent studies have broadened our understanding of pediatric TBI.
Recent Findings
While there remains a paucity of high-level evidence on which to base precise consensus guidelines for care in pediatric patients, recent studies have addressed therapeutic hypothermia, pharmacologic treatment of elevated intracranial pressure, and abusive head trauma.
Summary
Understanding the pathophysiology and treatment strategies for pediatric TBI, while preventing secondary insults, remains a cornerstone for improving patient outcomes.
Analgosedation is a fundamental part of traumatic brain injury (TBI) treatment guidelines, encompassing both first and second tier supportive strategies. Worldwide analgosedation practices continue to be heterogeneous due to the low level of evidence in treatment guidelines (level III) and the choice of analgosedative drugs is made by the treating clinician. Current practice is thus empirical and may result in unfavourable (often hemodynamic) side effects. This article presents an overview of current analgosedation practices in the paediatric intensive care unit (PICU) and addresses pitfalls both in the short and long term. We discuss innovative (pre-)clinical research that can provide the framework for initiatives to improve our pharmacological understanding of analgesic and sedative drugs used in paediatric severe TBI and ultimately facilitate steps towards evidence-based and precision pharmacotherapy in this vulnerable patient group.
Abhängig vom Schädigungsmechanismus kann das Schädel-Hirn-Trauma (SHT) in fokale und diffuse, geschlossene und offene sowie primäre und sekundäre Hirnschädigungen unterteilt werden. Diese Unterscheidungen gehen mit verschiedenen pathophysiologischen Vorgängen, klinischen Erscheinungsbildern, Verläufen, Behandlungsnotwendigkeiten und Prognosen einher. Die klinische Differenzierung des Schweregrades in leichte, mittelschwere, schwere SHT anhand der Glasgow Coma Scale (Tab. 217.1) ist für das klinische Management des verletzten Patienten relevanter als die nur rückblickend mögliche Unterscheidung in Commotio mit kurz dauernder neurologischer Funktionsstörung ohne Herdsymptomatik, Amnesie, Kopfschmerzen, Erbrechen und Contusio mit länger dauernder Depression der zerebralen Funktionen mit oder ohne Herdsymptomatik.
Verschiedene epidemiologische Studien lassen den Schluss zu, dass jährlich ca. 270.000 Menschen Kopfverletzungen bei Unfällen erleiden. Mehr als die Hälfte dieser schädelhirnverletzten Menschen ist jünger als 25 Jahre, in 15 % der Fälle handelt es sich um Kinder bis zum 5. Lebensjahr. Während ca. 90 % aller SHT als leicht eingestuft werden und häufig ohne wesentliche Folgen ausheilen, ist das schwere SHT mit einer Mortalität von 9–15 % für die Hälfte aller Todesfälle im Kindesalter verantwortlich und damit die häufigste Todesursache jenseits des 1. Lebensjahres. In Industrienationen sterben 5-mal mehr Kinder an einem SHT als an Leukämie. Darüber hinaus haben Verletzungen des Gehirns wegen der zum Teil schweren Langzeitbehinderungen eine enorme ökonomische Bedeutung.
Background:
Diagnosis and treatment of children with mild traumatic brain injury (mTBI) remain a challenge since initial signs and symptoms do not always indicate the severity of the trauma. Therefore, guidelines regarding the decision upon imaging methods and ambulatory or hospitalized treatment are needed. The goal of our study was to investigate if the standard that was allied from the PECARN rules and is applied in this study can ensure that patients with clinically important brain injury are recognized and leads to outcomes with a low complication rate, a high patient satisfaction and minimal post-concussion syndrome incidence.
Methods:
We enrolled 478 children with mTBI and contacted their families with a questionnaire. Out of these, 267 valid questionnaires were received. Patient records and questionnaires were analyzed yielding a number of 140 ambulatory and 127 hospitalized patients.
Results:
Patients with mild TBI were admitted according to the above-mentioned guidelines or sent home for observation through their parents after thorough patient examination and information. Among ambulatory patients only 13 children (9%) underwent any imaging procedure; however, none of those showed any pathological findings. Next, in 41 of 127 hospitalized patients (32.2%) an imaging study was performed and of these only 3 according to 2.4% of hospitalized patients showed pathological findings, namely a skull fracture, two of them in combination with an intracranial hemorrhage. The duration of inpatient observation was 48 h in most cases (55.3%). Moreover, a majority of all patients (72.4%) did not seek any follow-up visit and did not need any further treatment. Of all patients in the study, only 10 patients according to 3.7% developed a post-concussion syndrome. Patient satisfaction was very high in both, the ambulatory and hospitalized patient group.
Conclusion:
This study confirms that PECARN rules as administered in this study can ensure safe decision-making regarding ambulatory or inpatient treatment.
Definition. Abhängig vom Schädigungsmechanismus kann das Schädel-Hirn-Trauma (SHT) in fokale und diffuse, geschlossene und offene sowie primäre und sekundäre Hirnschädigungen unterteilt werden. Diese Unterscheidungen müssen beachtet werden, da sie mit verschiedenen pathophysiologischen Vorgängen, klinischen Erscheinungsbildern, Verläufen, Behandlungsnotwendigkeiten und Prognosen einhergehen. Die klinische Unterscheidung des Schweregrades in leichte, mittelschwere, schwere SHT anhand der Glasgow Coma Scale (Tab. 207.1) ist für das klinische Management des verletzten Patienten relevanter als die nur rückblickend mögliche Unterscheidung in Commotio mit kurzdauernder neurologischer Funktionsstörung ohne Herdsymptomatik, möglicher Amnesie, Kopfschmerzen, Erbrechen und Contusio mit längerdauernder Depression der zerebralen Funktionen mit oder ohne Herdsymptomatik.
Abhängig vom Schädigungsmechanismus kann das Schädel-Hirn-Trauma (SHT) in fokale und diffuse, geschlossene und offene sowie primäre und sekundäre Hirnschädigungen unterteilt werden. Diese Unterscheidungen gehen mit verschiedenen pathophysiologischen Vorgängen, klinischen Erscheinungsbildern, Verläufen, Behandlungsnotwendigkeiten und Prognosen einher. Die klinische Differenzierung des Schweregrades in leichte, mittelschwere, schwere SHT anhand der Glasgow Coma Scale ist für das klinische Management des verletzten Patienten relevanter als die nur rückblickend mögliche Unterscheidung in Commotio mit kurz dauernder neurologischer Funktionsstörung ohne Herdsymptomatik, Amnesie, Kopfschmerzen, Erbrechen und Contusio mit länger dauernder Depression der zerebralen Funktionen mit oder ohne Herdsymptomatik.
Objective:
The purpose of this study is to determine whether the use of neuromuscular blockade agents (NMBAs) in pediatric patients following tracheostomy is associated with increased rates of complications or a prolonged length of stay.
Methods:
This was a single-center retrospective chart review of pediatric patients undergoing tracheostomy placement between 2010 and 2013 who were admitted to the pediatric or neonatal intensive care units and did or did not receive NMBA within 7 days post-procedure.
Results:
Out of 114 included patients, 26 (23%) received NMBAs during the postoperative period. Patients receiving NMBAs were more likely to have cardiac disease and preoperative respiratory failure but less likely to have neurologic disease. Patients receiving NMBAs had a longer median postoperative length of stay (33 vs. 23 days, p=0.043) and were more likely to have postoperative ileus (12% vs. 3%, p=0.037).
Conclusion:
In patients undergoing tracheostomy placement, use of NMBAs is associated with prolonged postoperative hospital courses. NMBAs are not associated with a higher likelihood of postoperative complications.
Introduction In developed countries, head injury is the leading cause of death in children over 1 year of age. The goal of therapy in managing head injury is to prevent secondary injury and mitigate the cascade of events resulting in the delayed primary insult. The systemic secondary insults that have the most impact on outcome are hypotension and hypoxia, and their identification and prevention is the priority in the management of head injury. Case history A 5-year-old, previously healthy boy fell through the screen of a second-floor window on to concrete below. There was no initial loss of consciousness. On arrival in the Emergency Room, he was drowsy but responsive to voice and moving all limbs purposefully and to command. Cervical spine immobilization was undertaken with an appropriately sized semi-rigid collar. His initial vital signs were respiratory rate of 24 min-1, oxygen saturations of 96% in air, a heart rate of 76 min-1, a blood pressure of 114/60 mmHg, and a GCS score of 14 (E3/V5/M6). Oxygen was administered, IV access obtained and blood sent for routine trauma panel (FBC, blood group and screen, urea and electrolytes, creatinine, glucose, liver function tests, and also serum amylase). The initial chest x-ray and cervical spine plain films were normal. The secondary survey failed to identify other significant injuries. Approximately 60 minutes after his arrival to the hospital, the child became unresponsive with dilating sluggish pupils bilaterally.
Anesthesia for neurosurgery presents an interesting challenge to the pediatric anesthesiologist. One has little control over the patient's primary lesion, but the selection of anesthetic technique and the recognition of perioperative events and changes may profoundly reduce or prevent significant morbidity. Current neuroanesthetic practice is based on the understanding of cerebral physiology and how it can be manipulated in the presence of intracranial pathology. The pediatric neuroanesthesiologist also must contend with the physiological differences in developing children. In addition to the common problems of administering anesthesia to the general pediatric population, special consideration must be given to the effects of anesthesia on the central nervous system of children with neurological diseases. This chapter reviews the fundamentals of the clinical management in neurosurgical patients. Discussion of specific neurosurgical conditions and their respective anesthetic management is designed to highlight the common and sometimes unique problems encountered by the pediatric neuroanesthesiologist.
We describe the protocolised use of 23.4% hypertonic saline solution (HTS) for intracranial hypertension in the context of traumatic brain injury in the paediatric population. This study represents the largest published data on the use of 23.4% HTS in the paediatric population. In this retrospective cohort, we focus on the efficacy, biochemical and metabolic consequences of 23.4% HTS administration in a Level 1 paediatric trauma centre. Mortality in the first seven days was 6% (2/32) with a mean intensive care unit length-of-stay of ten days (range 2 to 25, standard deviation [SD] 6). All-cause hospital mortality was 6%, with no deaths after the seven-day study period. Mean intracranial pressure (ICP) response to HTS was 10 mmHg (range 1 to 30, SD 8). For biochemistry data, the mean highest daily serum sodium was 148 mmol/l (139 to 161, SD 6), mean highest serum chloride was 115 mmol/l (range 101 to 132, SD 8) with matched mean serum base excess of -1.5 mmol/l (range 2 to -8, SD 3) and mean peak serum creatinine was 73 mmol/l (range 32 to 104, SD 32). Glasgow outcome scores of >3 (independent function) were achieved in 74% of patients. We describe the use of 23.4% HTS, demonstrating it to be a practical and efficacious method of delivering osmoles and may be advantageous in minimising total fluid volume. Thus, the bolus versus infusion debate may best be served via combining both approaches.
To evaluate the association between neuromuscular blocking agents and outcome, intracranial pressure, and medical complications in children with severe traumatic brain injury.
A secondary analysis of a randomized, controlled trial of therapeutic hypothermia.
Seventeen hospitals in the United States, Australia, and New Zealand.
Children (< 18 yr) with severe traumatic brain injury.
None for this secondary analysis.
Children received neuromuscular blocking agent on the majority of days of the study (69.6%), and the modified Pediatric Intensity Level of Therapy scores (modified by removing neuromuscular blocking agent administration from the score) were increased on days when neuromuscular blocking agents were used (9.67 ± 0.21 vs 5.48 ± 0.26; p < 0.001). Children were stratified into groups based on exposure to neuromuscular blocking agents (group 1 received neuromuscular blocking agents each study day; group 2 did not). Group 1 had increased number of daily intracranial pressure readings more than 20 mm Hg (4.4 ± 1.1 vs 2.4 ± 0.5;p = 0.015) and longer ICU and hospital length of stay (p = 0.003 and 0.07, respectively, Kaplan-Meier). The Glasgow Outcome Score-Extended for Pediatrics at hospital discharge and 3, 6, and 12 months after traumatic brain injury and medical complications observed during the acute hospitalization were similar between groups.
Administration of neuromuscular blocking agents was ubiquitous and daily administration of neuromuscular blocking agents was associated with intracranial hypertension but not outcomes-likely indicating that increased injury severity prompted their use. Despite this, neuromuscular blocking agent use was not associated with complications. A different study design-perhaps using randomization or methodologies-of a larger cohort will be required to determine if neuromuscular blocking agent use is helpful after severe traumatic brain injury in children.
Traumatic brain injury (TBI) remains the leading cause of death of children in the developing world. In 2012, several international efforts were completed to aid clinicians and researchers in advancing the field of pediatric TBI. The second edition of the Guidelines for the Medical Management of Traumatic Brain Injury in Infants, Children and Adolescents updated those published in 2003. This article highlights the processes involved in developing the Guidelines, contrasts the new guidelines with the previous edition, and delineates new research efforts needed to advance knowledge. The impact of common data elements within these potential new research fields is reviewed.
Traumatisch hersenletsel is een frequente oorzaak van morbiditeit en mortaliteit door ongevallen of mishandeling op de kinderleeftijd. Ernstig neurotrauma wordt gedefinieerd als een neurotrauma met een glasgow-comascore kleiner dan 9 op de plaats van het ongeval. Gebaseerd op de geldende richtlijnen voor de behandeling van ernstig neurotrauma bij kinderen en volwassenen en aanvullende recente literatuur wordt een overzicht gegeven van de beste huidige behandeling van deze patiënten gericht op de Nederlandse situatie. Hypotensie, shock en hypoxie zijn geassocieerd met een slechte uitkomst en moeten actief bestreden worden. Transport dient primair naar een gespecialiseerd traumacentrum te geschieden. Zo spoedig mogelijk dient een CT-scan verricht te worden, en een herhaling van dit onderzoek moet overwogen worden bij iedere neurologische verslechtering. Een operabele intracraniële bloeding met massa-effect is een indicatie voor chirurgische evacuatie. De basisbehandeling bestaat uit adequate ventilatie, normothermie, sedatie en het intact houden of optimaliseren van het interne milieu. De intracraniële druk dient door middel van frequent neurologisch onderzoek met gebruik van de (pediatrische) glasgow-comaschaal en/of via een ICP-meter te geschieden. Als behandeling van intracraniële drukverhoging zijn osmotische therapie, diepere sedatie, liquordrainage, opgelegde hypothermie, kortdurende hyperventilatie en decompressie craniëctomie effectief, hoewel de effecten op de uitkomst niet geheel duidelijk zijn. Voor het profylactisch gebruik van anti-epileptica, voor het barbituratencoma en voor spierverslappers is in het algemeen geen indicatie. Corticosteroïden zijn gecontra-indiceerd.
This article reviews aspects of management of traumatic brain and spinal cord injury. A discussion of management of intracranial pressure after traumatic brain injury is followed by a discourse on cerebrovascular trauma and pediatric injuries. Specific management methods are discussed, including medical and surgical management in intracranial hypertension. A special attempt is made to include the current recommendations for management of brain and spinal cord injuries. Spinal cord injuries are discussed in the final section. With an increasing number of patients surviving after devastating spinal cord injuries, the special issues in their management are evaluated.
To investigate whether ventilatory management using a temperature-corrected (pH-stat) or uncorrected (alpha-stat) blood gas analysis strategy improves brain tissue oxygen tension (PbrO(2)) in children prophylactically treated with moderate hypothermia for traumatic brain injury.
Double crossover study conducted in the intensive care unit of a tertiary children's hospital. Nine children aged 3-14 years with severe traumatic brain injury were randomly allocated twice to a 6-hour period of either alpha- or pH-stat management while being kept hypothermic at 32.5°C.
PbrO(2), intracranial pressure (ICP) and PbrO(2)/PaO(2).
PbrO(2) was significantly higher during pH-stat management (alpha-stat, 23.2mmHg [95% CI, 22.4- 24.0mmHg] v pH-stat, 28.7mmHg [95% CI, 27.9- 29.5mmHg]; P < 0.001). PbrO(2)/PaO(2) was significantly higher during pH-stat (alpha-stat, 0.190 [95% CI, 0.187- 0.193] v pH-stat, 0.251 [95% CI, 0.246-0.259]; P < 0.05). ICP was non-significantly higher during pH-stat (alpha-stat, 8.8mmHg [95% CI, 8.1-9.5mmHg] v ph-stat,10.2mmHg [95% CI, 9.6-10.8]).
PbrO(2) may be improved using a pH-stat blood gas management strategy in prophylactic hypothermia for paediatric patients with traumatic brain injury without any clinically relevant increase in ICP.
A 9-year-old previously healthy girl presented with 3 weeks of intermittent emesis and headache to a community emergency department, where she had rapid decompensation due to increased intracranial pressure. Head computed tomography revealed a calcified suprasellar mass consistent with a craniopharyngioma. Despite medical and surgical intervention, the patient had progression of herniation with global cerebral infarction, and care was withdrawn. Although craniopharyngiomas are typically thought to be benign, slow-growing intracranial tumors, this case emphasizes the need for an expeditious diagnostic evaluation when symptoms that may be referable to intracranial hypertension are evident. Craniopharyngiomas and emergency management of intracranial hypertension are reviewed.
Severe traumatic brain injury (TBI) in children is associated with substantial long-term morbidity and mortality. Currently, there are no successful neuroprotective/neuroreparative treatments for TBI. Numerous preclinical studies suggest that bone marrow-derived mononuclear cells (BMMNCs), their derivative cells (marrow stromal cells), or similar cells (umbilical cord blood cells) offer neuroprotection.
To determine whether autologous BMMNCs are a safe treatment for severe TBI in children.
Ten children aged 5 to 14 years with a postresuscitation Glasgow Coma Scale of 5 to 8 were treated with 6×10 autologous BMMNCs/kg body weight delivered intravenously within 48 hours after TBI. To determine the safety of the procedure, systemic and cerebral hemodynamics were monitored during bone marrow harvest; infusion-related toxicity was determined by pediatric logistic organ dysfunction (PELOD) scores, hepatic enzymes, Murray lung injury scores, and renal function. Conventional magnetic resonance imaging (cMRI) data were obtained at 1 and 6 months postinjury, as were neuropsychological and functional outcome measures.
All patients survived. There were no episodes of harvest-related depression of systemic or cerebral hemodynamics. There was no detectable infusion-related toxicity as determined by PELOD score, hepatic enzymes, Murray lung injury scores, or renal function. cMRI imaging comparing gray matter, white matter, and CSF volumes showed no reduction from 1 to 6 months postinjury. Dichotomized Glasgow Outcome Score at 6 months showed 70% with good outcomes and 30% with moderate to severe disability.
Bone marrow harvest and intravenous mononuclear cell infusion as treatment for severe TBI in children is logistically feasible and safe.
Severe traumatic brain injury (TBI) is the most common cause of death and disability in pediatric trauma. This review looks at the strategies to treat TBI in a temporal fashion. We examine the targets for resuscitation from field triage to definitive care in the pediatric ICU.
Guidelines for the management of pediatric TBI exist. The themes of contemporary clinical research have been compliance with these guidelines and refinement of treatment recommendations developing a more sophisticated understanding of the pathophysiology of the injured brain. In the field, the aim has been to achieve routine compliance with the resuscitation goals. In the hospital, efforts have been directed at improving our ability to monitor the injured brain, developing techniques that limit brain swelling, and customizing brain perfusion.
As our understanding of pediatric TBI evolves, the ambition is that age-specific and perhaps individual brain injury strategies based upon feedback from continuous monitors will be defined. In addition, vogue methods such as hypothermia, hypertonic saline, and aggressive surgical decompression may prove to impact brain swelling and outcomes.
Despite being the leading cause of death and disability in the paediatric population, traumatic brain injury (TBI) in this group is largely understudied. Clinical practice within the paediatric intensive care unit (PICU) has been based upon adult guidelines however children are significantly different in terms of mechanism, pathophysiology and consequence of injury.
To review TBI management in the PICU and gain insight into potential management strategies.
To conduct this review, a literature search was conducted using MEDLINE, PUBMED and The Cochrane Library using the following key words; traumatic brain injury; paediatric; hypothermia. There were no date restrictions applied to ensure that past studies, whose principles remain current were not excluded.
Three areas were identified from the literature search and will be discussed against current acknowledged treatment strategies: Prophylactic hypothermia, brain tissue oxygen tension monitoring and decompressive craniectomy.
Previous literature has failed to fully address paediatric specific management protocols and we therefore have little evidence-based guidance. This review has shown that there is an emerging and ongoing trend towards paediatric specific TBI research in particular the area of moderate prophylactic hypothermia (MPH).
Deepening sedation is often needed in patients with intracranial hypertension. All widely used sedative and anesthetic agents (opioids, benzodiazepines, propofol, and barbiturates) decrease blood pressure and may therefore decrease cerebral perfusion pressure (CPP). Ketamine is a potent, safe, rapid-onset anesthetic agent that does not decrease blood pressure. However, ketamine's use in patients with traumatic brain injury and intracranial hypertension is precluded because it is widely stated that it increases intracranial pressure (ICP). Based on anecdotal clinical experience, the authors hypothesized that ketamine does not increase-but may rather decrease-ICP.
The authors conducted a prospective, controlled, clinical trial of data obtained in a pediatric intensive care unit of a regional trauma center. All patients were sedated and mechanically ventilated prior to inclusion in the study. Children with sustained, elevated ICP (> 18 mm Hg) resistant to first-tier therapies received a single ketamine dose (1-1.5 mg/kg) either to prevent further ICP increase during a potentially distressing intervention (Group 1) or as an additional measure to lower ICP (Group 2). Hemodynamic, ICP, and CPP values were recorded before ketamine administration, and repeated-measures analysis of variance was used to compare these values with those recorded every minute for 10 minutes following ketamine administration.
The results of 82 ketamine administrations in 30 patients were analyzed. Overall, following ketamine administration, ICP decreased by 30% (from 25.8 +/- 8.4 to 18.0 +/- 8.5 mm Hg) (p < 0.001) and CPP increased from 54.4 +/- 11.7 to 58.3 +/- 13.4 mm Hg (p < 0.005). In Group 1, ICP decreased significantly following ketamine administration and increased by > 2 mm Hg during the distressing intervention in only 1 of 17 events. In Group 2, when ketamine was administered to lower persistent intracranial hypertension, ICP decreased by 33% (from 26.0 +/- 9.1 to 17.5 +/- 9.1 mm Hg) (p < 0.0001) following ketamine administration.
In ventilation-treated patients with intracranial hypertension, ketamine effectively decreased ICP and prevented untoward ICP elevations during potentially distressing interventions, without lowering blood pressure and CPP. These results refute the notion that ketamine increases ICP. Ketamine is a safe and effective drug for patients with traumatic brain injury and intracranial hypertension, and it can possibly be used safely in trauma emergency situations.
Raised intracranial pressure (ICP) is a life threatening condition that is common to many neurological and non-neurological illnesses. Unless recognized and treated early it may cause secondary brain injury due to reduced cerebral perfusion pressure (CPP), and progress to brain herniation and death. Management of raised ICP includes care of airway, ventilation and oxygenation, adequate sedation and analgesia, neutral neck position, head end elevation by 20 degrees-30 degrees, and short-term hyperventilation (to achieve PCO(2) 32-35 mm Hg) and hyperosmolar therapy (mannitol or hypertonic saline) in critically raised ICP. Barbiturate coma, moderate hypothermia and surgical decompression may be helpful in refractory cases. Therapies aimed directly at keeping ICP <20 mmHg have resulted in improved survival and neurological outcome. Emerging evidence suggests that cerebral perfusion pressure targeted therapy may offer better outcome than ICP targeted therapies.
To evaluate potential side effects of continuous hypertonic 3% saline (CHS) as maintenance fluid in patients with brain injury.
Retrospective chart analysis of prospectively collected data.
Patients admitted to the neurosurgical intensive care unit for >4 days with traumatic brain injury, stroke, or subarachnoid hemorrhage with a Glasgow Coma Scale <9 and elevated intracranial pressure (ICP) or at risk of developing elevated ICP were included. Based on physician preference, one group was treated with 3% CHS at a rate of 1.5 mL/kg/bw as maintenance fluid. The other group received 0.9% normal saline (NS). Two percent saline was used in the CHS group to wean patients off 3% CHS or when sodium was above 155. Data on serum sodium, blood urea nitrogen, creatinine, ICP, infection rate, length of stay, rates of deep vein thrombosis, and pulmonary emboli and dural thrombosis were collected prospectively.
One hundred seven patients in the CHS group and 80 in the NS group met the inclusion criteria. The incidence of moderate hypernatremia (Na >155 mmol/L) and severe hypernatremia (Na >160 mmol/L) was significantly higher in the CHS therapy group than in the NS group. No significant relationship between CHS infusion and renal dysfunction was found. Moderate and severe hypernatremia was associated with a higher risk of elevated blood urea nitrogen and creatinine levels. Acute renal failure was not seen in these patients. A total of 53.3% in the CHS group and in 16.3% in the NS group (p < 0.0001) had raised ICP (>25 mm Hg), consistent with the physicians decision to use CHS in patients with elevated ICP.
CHS therapy was not associated with an increased rate of infection, deep vein thrombosis, or renal failure. However, there was a significant risk of developing hypernatremia. We conclude that CHS administration in patients with severe injuries is safe as long as sodium levels are carefully monitored.
Seizures are common in pediatric emergency care units, either as the main medical issue or in association with an additional neurological problem. Rapid treatment prolonged and repetitive seizures or status epilepticus is important. Multiple anti-convulsant medications are useful in this setting, and each has various indications and potential adverse effects that must be considered in regard to individual patients. This review discusses new data regarding anticonvulsants that are useful in these settings, including fosphenytoin, valproic acid, levetiracetam, and topiramate. A status epilepticus treatment algorithm is suggested, incorporating changes from traditional algorithms based on these new data. Treatment issues specific to complex medical patients, including patients with brain tumors, renal dysfunction, hepatic dysfunction, transplant, congenital heart disease, and anticoagulation, are also discussed.
Traumatic brain injury (TBI) is the leading cause of death in childhood; however only very few studies focusing on the specific pathophysiology and treatment have been published to date. Head trauma is more likely in young children than in adults given the same deceleration of the body due to their large and heavy heads and weak cervical ligaments and muscles. Resulting brain injury is more severe due to their thin, pliable skulls and the yet unfused sutures. Accordingly, children below the age of 4 years have lower chances of a full recovery after severe TBI, although in general, neurologic recovery after severe brain injury in children is better than in adults.
The past decade has witnessed a resurgence of interest in the use of hypertonic saline for low-volume resuscitation after trauma. Preliminary studies suggested that benefits are limited to a subgroup of trauma patients with brain injury, but a recent study of prehospital administration of hypertonic saline to patients with traumatic brain injury failed to confirm a benefit. Animal and human studies have demonstrated that hypertonic saline has clinically desirable physiological effects on cerebral blood flow, intracranial pressure, and inflammatory responses in models of neurotrauma. There are few clinical studies in traumatic brain injury with patient survival as an end point. In this review, we examined the experimental and clinical knowledge of hypertonic saline as an osmotherapeutic agent in neurotrauma.
Dexmedetomidine is a centrally acting alpha(2)-adrenergic agonist which is currently FDA-approved for the short-term (less than 24 h) sedation of adults during mechanical ventilation.
Given its beneficial physiologic properties, there has been increasing use of this agent in the pediatric population. As with any agent used for sedation in the Pediatric ICU setting, dose escalations may be necessary. Unlike benzodiazepines and opioids, there are limited data regarding the administration of dexmedetomidine above the current package insert dosing recommendations of 0.7 microg/kg/h.
We report a 2-year-old child with traumatic brain injury who developed hypertension following the administration of a dexmedetomidine infusion at 4 microg/kg/h for several hours. Investigation into the etiology of the hypertension was negative and the blood pressure returned to baseline with a decrease in the infusion rate.
Subsequent to this, no further issues with hypertension were noted.
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