Annual Meeting Reviews

Session II: Trauma and Traumatic Brain Injury

Submitted by Zulfiqar Ahmed, MD, FAAP
Director of Pediatric Anesthesia and CME Anesthesia Associates of Ann Arbor
Ann Arbor MI

The second session of the day was themed “Trauma and Traumatic Brain Injuries.” The moderator of the session was Kenneth Brady, MD (Texas Children’s Hospital) and the speakers included David Shellington, MD, Jennifer K. Lee-Summers MD and Nina K. Hardcastle, MD

The title of Dr. David Shellington’s (University of California San Diego) speech was “Pediatric Trauma-Damage Control and Resuscitation.” Dr. Shellington currently serves as an assistant professor of Pediatric Respiratory Medicine and Critical Care and shared his experience during his time spent in Kandahar Afghanistan, during Operation Enduring Freedom.

Dr. Shellington’s presentation primarily revolved around:

• Reviewing the types of injuries encountered in Operation Iraqi Freedom and Operation Enduring Freedom
• Discussing damage control resuscitation principles for these injuries
• Describing how these advances in care may influence current civilian practice

He started his talk with an introduction of the basics of blast injury in pediatric patients. When Dr. Shellington arrived in Afghanistan he played a key role in transforming a local community hospital into a highly functional trauma unit capable of offering pediatric care. Dr. Shellington showed a number of graphic pictures and videos detailing devastating results of blast injuries such as amputations, shrapnel injuries, IED blasts and diffuse brain injuries. Evolution and improvement in the quality of tourniquets available to soldiers was one major achievement. Dr. Shellington also reiterated the three important principles of damage control surgery:

• Prevent hypothermia;
• Prevent acidosis;
• Delay definitive repair till stabilization of the patient.

Major unanswered challenges in traumatic pediatric brain injury include:

• When to perform decompressive craniectomy to manage ICP; and
• Degree of hypotension tolerated in patients with increased intracranial pressure.

Dr. Lee-Summers (Johns Hopkins University) addressed the topic “Trauma and Traumatic Brain Injury: When Trauma is No Accident.” Her presentation objectives were:

• Describe the epidemiology of non-accidental trauma in children;
• Differentiate patterns of injury following accidental trauma versus those observed in non-accidental trauma;
• Review the medical, surgical, and anesthetic management strategies in children who have suffered non-accidental trauma.

In the journal Pediatrics in 1974, Caffey et al defined “Shaken Baby Syndrome” as “long bone fractures and subdural hematomas in children that were “shaken”. Dr. Lee-Summers presented grim data that abusive head trauma is the most common cause of death from child abuse and the most common cause of severe traumatic brain injury (TBI) in infants. Outcomes after abusive head trauma are worse than after non-inflicted TBI of similar severity. Shien et al have shown that children with moderate abusive head trauma (GCS 9 –11) have a mortality rate similar to that of children with severe accidental TBI (GCS < 9).

An important question Dr. Lee-Summers raised was whether treatment needs to be altered for abusive head trauma given the complex injury mechanisms. Dr. Lee-Summers emphasized the need to adhere to the Severe Pediatric TBI guidelines published by Society of Critical Care Medicine in 2012. Evidence has shown that adherence to these guidelines improves patient survival (Vavilala M.S. CritCare Med 2014). Intracranial hypertension can and does occur in infants with open fontanelles and ICP monitoring should be considered in some of these patients if the GCS is <9. Finally, she recommended following general TBI guidelines to maintain CPP above 40 to 50 mmHg and maintain ICP < 20 mmHg.

The third speaker of the day was Dr. Nina Hardcastle (Alberta Children’s Hospital). The topic of her talk was “Rescuing the Injured Brain” and the objectives of her talk were to review:

1. Pediatric TBI Guidelines
2. Mechanisms of injury and why they matter
3. TBI Interventions – physiology and targets
4. TBI Interventions – tiered strategies

Pediatric TBI guidelines were first published in 2003 (many level III evidence). In 2012 the guidelines were revised to include higher quality data from randomized control trials (mostly level II evidence). Primary injury is defined as the primary damage occurring to the brain and secondary injuries are defined as those resulting from consequential cerebral ischemia/hypoxia/elevated ICP, hypotension, hypercapnia, acidosis and hypothermia.  First tier strategies of TBI management include 30 degree elevation of the head of the bed, maintaining neutral head position, maintaining normocarbia (PaCO2 35-40 mmHg), preventing hypoxia (PaO2>60 mmHg), maintaining normothermia (35.6-37.5o C). These strategies should be implemented in all patients with TBI. 

Second tier strategies include hyperosmolar therapy (3% saline), mannitol and mechanical decompression in cases of elevated ICP refractory to management. Surgical interventions include CSF drains and craniectomy. Hyperventilation is not recommended (level III) for prolonged or prophylactic use. Skippen et al (Critical Care Medicine 1997) have shown the effects of hyperventilation on regional ischemia. According to their data, 28.9% of the brain was ischemic in normocapneac patients, 59.4% was ischemic with PaCO2 of 25-35 mmHg and 73.1% was ischemic with PaCO2 of <25mmHg. Furthermore, prolonged hyperventilation has been shown to exacerbate secondary injury and may worsen outcome (Curry et al; Critical Care Medicine 2008).

There is level II evidence for hyperosmolar therapy in the TBI guidelines. Hypertonic saline should be considered for treatment of severe pediatric TBI associated with intracranial hypertension. Doses for acute use range between 6.5 and 10 mL/kg. The 2012 Guidelines recommend Level II evidence for hypertonic saline bolus therapy and level III evidence for hypertonic saline infusion therapy. Although Mannitol has been used widely, at present there is no data available with respect to efficacy plus concerns exist that it may accumulate in the brain.  On the other hand although there is less clinical experience with hypertonic saline, its use has shown reasonably good clinical performance in clinical trials.  Decompressive craniectomy should be considered in patients with severe TBI and:

• Early signs of neurologic deterioration or herniation;
• Intracranial hypertension (ICH) refractory to medical therapies.

Unanswered questions include whether craniectomy should be performed early vs. late, as a solo treatment or as rescue only.

Therapeutic hypothermia has limited evidence for efficacy. Moderate hypothermia (32-33oC) may be considered in the treatment of refractory intracranial hypertension but should be limited to less then 24 hours with a rewarming rate of (0.5-1oC/hr). Barbiturate coma also has limited evidence but may be used in refractory coma. Drugs such as pentobarbital or phenobarbitone may be used with close cardiopulmonary monitoring and support and in conjunction with continuous EEG monitoring to achieve burst suppression. The use of this technique is complicated by a long half life and zero order kinetics. Etomidate bolus has shown to be successful as an intervention for elevated ICP, but may cause adrenal suppression (Bramwell et al, 2006) Propofol should be avoided per FDA recommendations.

The conclusion of Dr.Hardcastle’s talk included the following,

• Optimal CPP is >40mmHg, and up to 60mmHg approaching adult age.
• Hyperventilation presents significant risk for cerebral ischemia.
• Increased usage of 3%NaCl (bolus and infusion) for ICP management is warranted.
• Decompressive craniectomy and CSF drainage help with ICP control.
• Barbiturates offer good ICP control, albeit with side effects.
• Hypothermia should be limited to 24 hours duration followed by slow rewarming.