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Anesthetic considerations and care management of children with traumatic brain injury
Sangeetha R Palaniswamy1, Rajeeb Mishra1, Dwarakanath Srinivas2
1 Department of Neuroanaesthesia and Neurocritical Care, Bengaluru, India
2 Department of Neurosurgery, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India
| Date of Submission | 15-Apr-2021 |
| Date of Decision | 05-Dec-2021 |
| Date of Acceptance | 07-May-2022 |
| Date of Web Publication | 30-Jan-2023 |
Correspondence Address:
Dwarakanath Srinivas,
Department of Neurosurgery, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India.
India
 Source of Support: None, Conflict of Interest: None DOI: 10.4103/jpn.JPN_87_21
 Abstract | | |
Traumatic brain injury (TBI) in the pediatric population persists to be a global health burden contributing to significant morbidity and mortality. The in-hospital management of pediatric TBI differs from adult TBI due to the various inherent age-specific anatomical, physiological, and pathological differences. Their peri-operative care encompasses initial stabilization in the emergency room, sedation for diagnostic imaging, medical management in the intensive care unit, anesthesia for emergent decompressive craniotomies in the operating room, support of recovery from anesthesia in the postoperative suite, and postoperative management in the emergency trauma care unit until hospital discharge. Disturbed cerebral autoregulation and compromised intracranial compliance predispose to cerebral ischemia and edema. Refractory intracranial hypertension is observed to be the most important predictor of poor outcome and mortality in these patients. Multimodal neuromonitoring paves the way for a better contemplation of the underlying intracranial pressure, cerebral hemodynamics, cerebral oxygenation, and neuronal electrical activity. The peri-operative goals revolve around the maintenance of cerebral and systemic homeostasis, the key components of which are discussed here. This review also discusses the key recommendations and practice guidelines proposed by the Brain Trauma Foundation for the critical care management of pediatric patients with severe TBI. A thorough knowledge about pediatric neuroanatomy and neuropathophysiology of TBI in concordance with the multidisciplinary application of best management practices fosters the best possible neurocognitive outcome among pediatric TBI survivors.
Keywords: Pediatric neurotrauma, pediatric traumatic brain injury, perioperative management of traumatic brain injury
| Introduction | |  |
The pediatric population is a nation’s asset and core determinant of our society’s future. Periodic statistical data shed light on the unfortunate reality that this cohort continues to be an innocent victim of trauma-related consequences frequently culminating in lethality. Trauma is a prime health concern accounting for a significant proportion of hospital admissions and nearly 49% of mortality in the age group under 16.[1] Pediatric trauma under the age of 15 years has an incidence of 45 per 100,000 in the United States of America, contributing to significant morbidity and mortality. The most typical occurrence follows a bimodal pattern wherein, very young (0–3 years) and older (15–18 years) children are frequent sufferers. A bewildering fact is that unintentional falls and road traffic accidents are predominant causative etiologies.[2] Due to deficient registry, pediatric injuries’ epidemiology is difficult to estimate in low- and middle-income countries. Various centers have tried to outline the clinical-epidemiological patterns of demography, etiology, presentation, and outcomes in these children. A high-volume tertiary care hospital from South India reported that 1587 out of 8464 admissions to the emergency department with trauma history over one year during 2017 were pediatric victims of unintentional trauma under the age of 15 years.[3] Of these 28.2% had a history of fall on level ground, 26.5% sustained road traffic accidents (RTA), 21.5% due to falling from a height, 3.5% from domestic injuries, 0.7% were sports-related injuries, 0.6% due to cracker blast, 0.3% due to assault and 0.6% from other causes. This retrospective analysis revealed a 0.4% in-hospital mortality. Of these, 21% were neurotrauma only second to orthopedic injuries (56.5%). A three-year data from a North Indian tertiary care center reported a 19.86% incidence of head injury among trauma admissions, with an in-hospital mortality rate of 5.57% and residual disability in 6.5% of survivors.[4]
The requisites of pediatric in-hospital management do differ from that of an adult traumatic brain injury (TBI) due to the various anatomical, physiological, and pathological differences. The threshold for decompensation following a severe TBI is alarmingly low in children. Therefore, there is a need to modify anesthetic and surgical practice to achieve a good outcome. Coordinated multidisciplinary approach involving the neurosurgeon, neuroanesthetists, neuroradiologist, neurointensivist, and the nursing team is crucial for the early diagnosis, triaging, and successful management of these patients. We aim to review the existing literature on the perioperative management of pediatric TBI. The uniqueness of pediatric head, neck, and brain[5],[6],[7],[8],[9],[10],[11] is as described in [Table 1]. | Table 1: Differences in pediatric anatomy and physiology with clinical implications
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| Need for Comprehensive Care | | |
The role of an anesthesiologist in the care of these patients extends from the time of hospital admission during initial stabilization in the emergency room (ER), sedation for diagnostic imaging, medical management in the intensive care unit (ICU), anesthesia services for emergent decompressive craniotomies in the operating room (OR), support of recovery in the postoperative suite to the postoperative management in the emergency trauma care unit until hospital discharge.
A thorough, updated knowledge of pediatric trauma care practices is prudent for the effective management of these patients.
| Initial Stabilization in the Emergency Department | | |
A trauma victim’s primary survey begins with a short brief, relevant history from a reliable source. A rapid clinical assessment of the nervous system with simultaneous quick systemic examination should rule out other systemic injuries. Assessment and stabilization of airway, breathing, circulation in conjunction with evaluation and treatment of disability, and hypothermia avoidance are initial factors to be addressed.
The clinician must perform a comprehensive head-to-toe examination to detect systemic injuries with ongoing post-resuscitation monitoring and care in addition to a detailed focal neurological assessment for level of consciousness, pupillary responsiveness, and brainstem reflexes. Pain should be managed without undue drug-induced respiratory depression. In any neurological deterioration during the secondary survey, one should repeat the primary survey and address the problem before proceeding with definitive patient care.
Most children with TBI are managed conservatively. Only few children, especially those with severe TBI require surgery. Fine-tuning pediatric anesthetic techniques’ inherent intricacies optimize perioperative care and recovery to foster favorable outcomes.
| Cerebral Injury Classification | | |
- 1.Diffuse cerebral injury is the most common presentation of severe TBI caused by acceleration and deceleration forces in the pediatric age group, in contrast to focal contusions being common in adult TBI. A diffuse axonal injury is an extreme form of diffuse brain injury. Diffuse cerebral swelling following severe TBI is more common among infants and children than adults.[12] Post-traumatic vasospasm is an uncommon finding among children.[13]
- 2.Focal brain injury leading to contusions, bleeding into the epidural/subdural/subarachnoid space may also require immediate surgical evacuation depending on the presentation. Pediatric subdural hematomas are associated with more severe parenchymal damage and injuries to the venous sinuses and the cortical veins.[14] Linear skull fractures hint to underlying significant parenchymal injury. Growing skull fractures are a unique feature of a pediatric skull injury.[15] Occipital and sub-occipital fractures are particularly concerning due to the risk of a posterior fossa hematoma, which can rapidly compress the brainstem and cause hydrocephalus by fourth ventricular or aqueduct obstruction.[16]
- 3.TBI and injury above the clavicle level should raise a suspicion of associated cervical spine injury (CSI). Approximately 1%–2% of children with TBI can have co-existent CSI, which should be ruled out based on imaging.[17] Mortality can be as high as 33% in children with upper cervical spine injury as against 8.3% in lower cervical spine injuries.[18]
| Perioperative Anesthetic Management of Pediatric TBI | | |
Preoperative evaluation
Patient factors
The following points need to be considered while evaluating a child. Age, comorbid illness, association with congenital anomalies, systemic injuries (primary and secondary), neurological status, ease of intravenous access, allergy history, recent upper respiratory tract infection, nil per oral status, hydration status owing to hyperosmotic agent administration.
Surgical factors
Critical factors of consideration are the primary diagnosis, surgical options, surgical positioning, anticipated blood loss, availability of adequate cross-matched blood and blood products for perioperative transfusion.
| Anesthetic Management of Pediatric TBI | | |
Anesthetic concerns
- a)Pediatric airway: An inherently challenging pediatric airway can be rendered more difficult in the setting of craniofacial fractures, oral bleed, unstable cervical spine, and an unfasted status. The large protuberant occiput, relative macroglossia, anteriorly placed funnel-shaped short larynx (5 cm in infants and 7 cm at 18 months) that bifurcates at a higher level and floppy epiglottis make the pediatric airways different from that of an adult.[19] In association with traumatic gastroparesis, aerophagia predisposes them to pulmonary aspiration even with a fasting status. Cricoid pressure, as a part of rapid sequence induction (RSI), prevents gastroesophageal reflux. It should be applied only after careful exclusion of unstable cervical spine injuries and the absence of active vomiting and suspected cricoid and tracheal injury.
- b)Respiratory system: Compliant chest wall explains a pulmonary contusion’s greater incidence in the absence of rib fractures.[20] Neurogenic pulmonary edema/ associated rib fractures induced hemothorax or pneumothorax must be carefully ruled out pre-induction. Always avoid hypoxia and hypercarbia to avoid further increases in ICP.
- c)Hemodynamic challenges: Associated sympathetic overactivity can manifest with electrocardiographic changes and hemodynamic instability, which can be worse as bradycardia with associated hypertension. Episodes of direct laryngoscopy-induced vagal stimulation can accentuate pre-existing intracranial hypertension-induced bradycardia, especially when combined with the use of succinylcholine as a part of a rapid sequence intubation regimen. These can synergistically create a favorable scenario for sinus arrest or asystole. The anticipation of complications and adequate preparedness with preloaded emergency drugs are saviors during critical emergent scenarios.
Anesthetic management
The key anesthetic goals that should be aimed and planned for, are highlighted in [Figure 1]. Anesthetic induction should be carefully planned and executed to avoid hypoxia, hypercapnia, and a hemodynamic stress-induced surge in the ICP. The perioperative management strategies are as outlined in [Table 2]. | Figure 1: Intraoperative goals for the anesthetic management of patients with pediatric TBI undergoing surgery
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,  | Table 2: Key phases and principles in the anesthetic management of patients with pediatric TBI undergoing surgery
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Anesthetic induction
Intravenous induction using Propofol or Thiopentone with neuromuscular blockade to facilitate tracheal intubation is preferred over inhalational induction except in the absence of intravenous access or difficulty securing it. Post-induction hypotension should be avoided to preserve cerebral perfusion pressure. Attempts to attenuate hemodynamic stress response should be followed to avoid intracranial hypertension precipitation.
Endotracheal intubation with/without rapid sequence induction
The routine practice of rapid sequence induction (RSI) and intubation requires careful consideration for the pediatric airway. Continuous aspiration is done if an NG tube is in place. A 20° head-up position is essential during preoxygenation and induction. Adequate preoxygenation using four full vital capacity breaths with 100% oxygen may be hindered by the lack of co-operation especially in younger children, further complicated by alteration in sensorium secondary to the primary pathology.
In the absence of adequate patent IV access, inhalational induction using sevoflurane may be contemplated. In children with a secured IV access, RSI is done using IV Inj. Thiopentone at 3–5 mg/kg or IV Inj. Propofol 2 mg/kg, with the dosage titrated to clinical effect. Anticipation and preparedness for post-induction hemodynamic instability are essential.
Following anesthetic induction, cricoid pressure is routinely indicated in anticipation and prevention of gastroesophageal reflux and pulmonary aspiration, in the case of adults. However, the routine use of cricoid pressure is questionable in the pediatric population. The cricoid cartilage is small and placed more cephalad, making its identification difficult. The pediatric larynx is fragile and requires careful manipulation to avoid fractures or injuries. When the cricoid cartilage is depressed, the lower esophageal sphincter tone reduces, predisposing to aspiration. Further, its contraindication in suspected cervical spine injury can be extrapolated to the pediatric counterparts as well. If applied, lower cricoid compression pressures of 7.7 Newton (N), as against 30N in adults should be considered. One may consider routine atropine premedication to avoid succinylcholine and laryngoscopy-induced bradycardia as children are known to have a robust parasympathetic tone. Rapid sequence intubation is done following administration of IV Inj. Succinylcholine at 1–2 mg/kg (2 mg/kg for neonates and 1 mg/kg for older children) or Rocuronium as in modified RSI at a dose of 1.2 mg/kg IV. The controlled RSI concept permits gentle bag-mask ventilation with insufflation pressures not exceeding 12 cm H2O in desaturating patients. Once the trachea is intubated its correct position is confirmed, the cricoid pressure is released. If an NG tube is not in situ, it should be placed to facilitate gastric decompression.[21]
Intraoperative management
Adequate large-bore iv access in a dehydrated child loaded with mannitol in the ER can be another challenge. Time to secure central venous access and arterial cannulation for beat-to-beat cardiac monitoring and frequent blood gas analysis should not add to delay in the start of surgery. Quick bladder catheterization should follow for continuous urine output monitoring. Optimal positioning of the patient avoids impedance to normal cerebral venous drainage. An immature thermoregulation status and a disproportionately greater body surface area to body mass ratio add to the fluid and heat loss from exposed surgical sites. Hypothermia to be avoided to prevent worsening of coagulopathy and hemodynamic instability.[22],[23]
Anesthetic maintenance
This can be done by a balanced technique using low-end-tidal inhalational anesthetics or total intravenous infusion supplemented with short-acting opioids. Propofol infusion can be considered for intracerebral hematoma evacuations until durotomy. Regional anesthesia using bilateral scalp block has an opioid-sparing effect. Mechanical ventilation should be titrated to ensure normoxia and normocapnia.[24],[25]
Intraoperative complications
Management of a tight-brain scenario is not different from that of an adult. Optimization of head position, reassessment of the depth of anesthesia, re-evaluation of ventilation parameters to rule out raised intrathoracic pressure and mild hyperventilation should precede hyperosmolar therapy and surgical intervention.[26],[27] Systemic hypotension should be anticipated post-decompression. The injury severity and preoperative sympathetic and parasympathetic balance are the identified risk factors in adults.[28] Sympathetic hyperactivity-related hemodynamic changes usually subside, at times, to the point of hemodynamic compromise. One must hence be watchful to attend to such changes promptly.
Intracranial bleeding, including EDH, can cause significant exsanguination considering the relatively small total body volume. Adequate cross-matched blood should be made available inside the OT before starting the case. Simultaneous arrangements for the same should be made in parallel to surgical preparation. Avoidance of extremes of temperature is vital for cerebral and systemic homeostasis.[26] A small volume intracranial bleed in a child may cause a substantial circulating volume deficit. Perioperative mannitol infusion with/without diuretic therapy can aggravate the resulting hypovolemia and hypotension. Hypotension should be promptly recognized and treated, even if it occurs for a brief period. Systolic pressure (5th percentile) = 70 mm Hg + 2 X (age in years).[29] The heart rate is a more accurate correlate of the hemodynamic status in the pediatric cohort.
The hemodynamic goal is to maintain stability with normovolemia. Mild hyperosmolarity explains the preferential use of normal saline as intraoperative maintenance fluid. Dextrose-containing fluid infusion contributes to hyperglycemia and the worsening of cerebral ischemia. However, young children and neonates are more prone to undesirable hypoglycemia. Close monitoring of blood glucose levels targeting normoglycemia can be supplemented with intravenous glucose infusion at 5–6 mg/kg/min.[23]
Rapid restoration of circulating blood volume in patients unresponsive to crystalloid infusions can prove lifesaving in most patients. Type-specific or unmatched O negative packed cell transfusion at a dose of 10-20ml/kg is recommended for transfusion. Trauma or blood transfusion-induced coagulopathy requires co-transfusion of fresh frozen plasma at a 10ml/kg dose. Although the fixed formula of 1:1:1 ratio of PC, FFP, and platelet transfusion is not a universal recommendation, various studies advocating similar rationing of blood products have observed favorable outcomes. Significant and ongoing blood loss requiring massive blood transfusion (MBT) aims to minimize coagulopathy associated with bleeding despite its innate overload-related complications.[30] Early prediction of the need for perioperative MBT is critical to optimize the judicious use of resources. MBT replaces the entire total blood volume within 24 h and half of it in 3 h.[31] Evidence supporting the use of MBT to improve outcomes in children is limited. An observational study conducted in 55 children with significant hemorrhage reported no difference in mortality between the recipients and non-recipients of MTP. The 22 patients in the MTP group had a significantly higher severity of injury requiring transfusion of either 80 mL/kg within 24 h or 40 mL/kg in 12 h. They were recipients of per-protocol transfusion at a ratio of 1:1:1 of PRBCs, FFP, and platelets. The incidence of thromboembolic events was lower in the MTP group than the 33 children of the non-MTP group.[32]
Postoperative recovery phase
Disturbed cerebral autoregulation and compromised intracranial compliance are common after surgery leading to postoperative cerebral ischemia and edema. The intra-operative goals of cerebral and systemic homeostasis should continue in the postoperative period. Recovery must be smooth and non-combative.
Tracheal extubation policies
A planned delay in extubation with further management in the ICU is desirable for those patients in whom, cardio-respiratory and neurological recovery is expected to occur over a prolonged period, especially following intraoperative major fluid shifts, and where significant risk of cerebral ischemia is possible. Planned delayed recovery provides a window for optimization of oxygenation and ventilation, achieving cardiovascular, metabolic and thermal stability and attenuation of edema associated with neural tissue handling.[33]
| Intensive Care in the Neurocritical Care Unit | | |
Post-operative care following TBI surgery and brain injuries not amenable to surgical intervention necessitate focused care to facilitate recovery from the primary pathology and avoid and promptly manage secondary insults. Hypotension, hypoxia, hypoglycemia, hyperglycemia, and hyperthermia are prime influencers of pediatric TBI patients’ outcomes.[34]
The third edition of the Guidelines for the Management of Pediatric Severe Traumatic Brain Injury, proposed by the Brain Trauma Foundation (BTF) has outlined the practice guidelines for the conservative and critical care management of pediatric patients with severe TBI.[35] However, there are currently only four level 2 recommendations for therapeutic interventions in these patients. We describe their critical care management based on the evidence available to date.
Mechanical ventilation titrated to adequate arterial partial oxygen and carbon-dioxide pressures support recovery.[36] Adequate pain relief should be instituted with sedation to avoid ventilator desynchrony and rise in ICP. Strict adherence to infection control practices minimizes complications and facilitates early discharge from the ICU. The prophylactic anti-epileptic treatment alleviates early (within 7 days) post-traumatic seizures. The pediatric TBI guidelines recommend against routine corticosteroid use to reduce ICP or improve outcomes. However, if instituted for chronic steroid replacement, steroid therapy, in those with adrenal suppression, and hypothalamic-pituitary steroid axis injury, regular scrutiny with rapid tapering and discontinuation should be done (as the primary diagnosis permits) to avert complications.[37]
| Multimodal Advanced Neuromonitoring | | |
Multimodal neuromonitoring paves the way for a better contemplation of the underlying ICP, cerebral hemodynamics, oxygenation, and electrical activity.[38] The pediatric TBI guidelines recommend few thresholds for advanced neuromonitoring in children with TBI. When brain parenchymal tissue oxygenation (PbrO2) monitoring is employed, maintaining more than 10 mm Hg level is suggested.[39],[40]
One must target a cerebral perfusion pressure between 40- and 50-mm Hg.[41] Age-specific thresholds may be followed with infants at the lower and adolescents at/above the upper end of this range.
Intracranial hypertension
The quality of evidence to support ICP monitoring and appropriate treatment thresholds in pediatric TBI is currently low. Acceptable levels of ICP probably vary with age, neurological disease, and the state of cerebral autoregulation.[42] The treatment threshold for intracranial hypertension is currently at 20 mm Hg lasting for 5 minutes.[43]
The decision for choice of hyperosmolar therapy between and mannitol and hypertonic saline (HTS) remains to be resolved as in the adult population. Intravenous Mannitol when administered, is at a dose of 0.5–1 g/kg. The pediatric BTF guidelines recommend hyperosmolar therapy with a bolus of 2–5 mL/kg of 3% HTS over 10–20 minutes for acute use and a continuous infusion of 3% HTS at doses of 0.1 -1.0mL/kg of body weight per hour.[44],[45],[46],[47] The dose selected is the minimum needed to maintain ICP less than 20 mm Hg. For refractory ICP, consider administering a bolus of 23.4% HTS at 0.5 mL/kg with a maximum of 30 mL. It is crucial to avoid sustained (>72 h) serum sodium greater than 160 mEq/L.[48]
The pediatric TBI guidelines by the BTF do not recommend prophylactic moderate (32–33°C) hypothermia over normothermia to improve the overall outcomes. However, if hypothermia is used and rewarming initiated, it should not exceed 0.5–1.0°C per 12–24 h to avoid complications.[49],[50]
There is no recommendation for prophylactic hyperventilation to Pco2 of less than 30 mm Hg in the initial 48 h after injury. However, if used in the management of refractory intracranial hypertension, evaluation of cerebral ischemia using advanced neuromonitoring is suggested.[43]
In hemodynamically stable children with refractory intracranial hypertension, high-dose barbiturate therapy plays an important role. In such cases, continuous arterial blood pressure monitoring and cardiovascular support adequate CPP maintenance.[51]
Early (within 72 h from injury) initiation of enteral nutritional support is suggested to reduce mortality and improve outcomes.[52]
Further neurologic deterioration, herniation, or intracranial hypertension refractory to medical management may be considered to benefit from decompressive craniectomy.
The incidence of coagulopathy in isolated pediatric severe TBI has an incidence of is exceedingly high at 40% and reflects the head injury severity with a mortality rate as high as 17.5% in coagulopathic patients in contrast to 0.5% in versus non-coagulopathic patients. Poor GCS, increasing age, injury severity score ≥16, and intraparenchymal lesions are independent predictors of TBI coagulopathy.[53] Pediatric data on management of trauma-induced coagulopathy are limited and practices are essentially extrapolated from the adult trauma experience. The main age-dependent differences include decreased plasma concentrations of tissue plasminogen activator, plasminogen, and α-antiplasmin with increased plasma concentrations of plasminogen activator inhibitor-1, along with a decrease in both plasmin generation and overall fibrinolytic activity.[54]
An evidence statement in November 2012 issued by The Royal College of Paediatrics and Child Health in the United Kingdom, entitled “Major trauma and the use of TXA in children” proposes the pediatric dosing consensus for children 12 years of age and older as a 1 g loading dose over 10 minutes within the first 3 h post-injury, followed by a 1 g infusion over 8 h. For children under 12 years of age, the loading dose was 15 mg/kg (maximum dose 1 g) followed by an infusion of 2 mg/kg/h for at least 8 h or until the cessation of bleeding. This dosage is significantly lower than the doses for pediatric spinal, cardiac and craniofacial surgery. Post-administration seizures have not been reported at this dose.[55]
| Outcomes | | |
A retrospective review of more than 750 pediatric TBI patients revealed that the extent and severity of primary cerebral and systemic injuries strongly correlated with the long-term quality of life. Refractory intracranial hypertension was the most important predictor of poor outcome and mortality in these patients.[56]
| Future of Pediatric TBI Research | | |
Challenges exist in the conduct of further research to bridge the existing gaps in the care of pediatric TBI due to ethical concerns. The Approaches and Decisions in Acute Pediatric TBI Trial (ADAPT) is one of the recent multicenter prospective observational studies that has attempted in exploring the impact of interventions namely, ventilation, hyperosmolar therapy, nutrition, advanced neuromonitoring, and CSF diversion on the 6-month outcome of pediatric TBI survivors, to redefine the existing practices for the care of pediatric TBI.[57],[58]
| Conclusion | | |
An ingrained knowledge about pediatric neuroanatomy and neuropathophysiology of TBI in concordance with the multidisciplinary application of best management practices fosters the best possible neurocognitive outcome among pediatric TBI survivors.
Financial support and sponsorship
Not applicable.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1]
[Table 1], [Table 2]
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