Moderate-to-Severe Traumatic Brain Injury in Children

Complications and Rehabilitation Strategies

Myra L. Popernack, MSN, RN, CPNP; Nicola Gray, BSN, RN; Karin Reuter-Rice, PhD, CPNP-AC, FCCM, FAAN


J Pediatr Health Care. 2015;29(3):e1-e7. 

In This Article

Physiologic Mechanisms

When a TBI is sustained, the damage to the brain can be separated into primary injury and secondary injury. Primary injury is the instantaneous damage to the intracranial contents resulting from mechanical forces. Secondary injury is the subsequent damage that occurs over hours to days as a result of altered cerebral blood flow and inflammatory processes. The initial stabilization of the injured child in the prehospital and emergency department setting is focused on minimizing sequelae of the primary injury. Prevention of secondary injury and maximizing positive outcomes is ongoing throughout the intensive care and rehabilitation settings.

Primary injury occurs at the time of impact and is a direct effect of kinetic energy transferred from the mechanical force to the parenchyma. Some common mechanisms of injury include direct impact from an object, rapid acceleration/deceleration as seen in motor vehicle accidents, penetrating injury, and blast waves, which can be the result of an explosion. The acute injury of the parenchyma can be manifested as contusions, hematomas, shearing of white matter tracts, and cerebral edema.

Secondary injury occurs over time as a result of repercussions of the acute injury. Cerebral blood flow is often altered as a result of vasospasm, focal microvascular occlusion, and vascular injury. This secondary ischemia can lead to hypoxia, altered electrolytes and cell metabolism, and neuronal cell death. Cerebral edema of either cytotoxic or vasogenic origin is also a major contributor to secondary injury and often results in increased intracranial pressure and further compromise to cerebral blood flow (Greve & Zink, 2009).