Chapter 11: Trauma and Traumatic Brain Injury

INTRODUCTION

Metabolic alterations following injury in children significantly affect survival. Though the response occurs in a predictable manner, much controversy exists in the medical literature on the mode, timing, and amount of feeding. With better understanding of the various approaches to providing nutrition support, additional opportunities for decreasing mortality after trauma can be identified.

Improving nutrition support of the pediatric trauma patient can not only affect survival, but also shorten the time needed for rehabilitation. Caloric support can ameliorate the protein catabolism that occurs following trauma. Wound healing and immune response are also reliant on adequate protein stores. Muscle breakdown can be ameliorated using nutrition support with parenteral and enteral approaches.

Enteral nutrition (EN) should be an early priority soon after achieving hemodynamic stability using adequate resuscitation. Parenteral nutrition (PN) can be an adequate substitute until injuries have been addressed and enteral access has been obtained. Both underfeeding and overfeeding can lead to unintended consequences.

Specific injuries after trauma require additional nutrition support and careful monitoring of nutritional needs. Burns, traumatic head injury, multiorgan system injury, and concomitant abdominal compartment syndrome all have unique characteristics that need to be addressed. In this chapter, we will focus on the metabolic response after injury, followed by parenteral and enteral approaches to providing nutrition, and finally, specific traumatic injuries that require distinct practices.

METABOLIC RESPONSE TO TRAUMA

As originally outlined by Cuthbertson in 1932, injury leads to a series of metabolic events that in turn lead to a loss of nitrogen in the urine from protein breakdown.¹ The response follows an “ebb and flow” pattern where there is an initial decrease in blood pressure, cardiac output, and temperature, with a subsequent increase in temperature, heart rate, and release of catabolic enzymes. Though the normal state of health prior to injury differs among individuals, the response involves release of catabolic enzymes promoting glycolysis, lipolysis, gluconeogenesis,² and an increase in the basal metabolic rate, which correlates with the severity of the injury.³ Details of the metabolic stress response can be found in chapter 1.

In children, the metabolic response can be more challenging to predict than in adults. Children have a higher per weight baseline energy expenditure, which does not increase with injury. Instead, calories are shunted away from growth, as exhibited by the high rates of protein turnover.⁴ Children are also more vulnerable to protein loss and more readily demonstrate complications secondary to this loss. Misinterpreting the metabolic response can lead to either underfeeding or overfeeding, and each may produce unintended consequences.

Adverse effects of the response also include insulin resistance and hyperglycemia; sarcopenia, osteopenia, and growth restriction; and deficient immune response and sepsis. Long-term metabolic effects of injury from a prolonged response or severe injury have been reported, including cardiovascular events, type 2 diabetes mellitus, and early-onset ...