Neurologic Emergencies and Stabilization

Neurocritical Care Principles

The brain has high metabolic demands, which are further increased during growth and development. Preservation of nutrient supply to the brain is the mainstay of care for children with evolving brain injuries. Intracranial dynamics describes the physics of the interactions of the contents—brain parenchyma, blood (arterial, venous, capillary), and cerebrospinal fluid (CSF)—within the cranium. Normally, brain parenchyma accounts for up to 85% of the contents of the cranial vault, and the remaining portion is divided between CSF and blood. The brain resides in a relatively rigid cranial vault, and cranial compliance decreases with age as the skull ossification centers gradually replace cartilage with bone. The intracranial pressure (ICP) is derived from the volume of its components and the bony compliance. The perfusion pressure of the brain (cerebral perfusion pressure, CPP) is equal to the pressure of blood entering the cranium (mean arterial pressure, MAP) minus the ICP, in most cases.

Increases in intracranial volume can result from swelling, masses, or increases in blood and CSF volumes. As these volumes increase, compensatory mechanisms decrease ICP by (1) decreasing CSF volume (CSF is displaced into the spinal canal or absorbed by arachnoid villi), (2) decreasing cerebral blood volume (venous blood return to the thorax is augmented), and/or (3) increasing cranial volume (sutures pathologically expand or bone is remodeled). Once compensatory mechanisms are exhausted (the increase in cranial volume is too large), small increases in volume lead to large increases in ICP, or intracranial hypertension ( Fig. 85.1 ). As ICP continues to increase, brain ischemia can occur as CPP falls. Further increases in ICP can ultimately displace the brain downward into the foramen magnum—a process called cerebral herniation, which can become irreversible in minutes and may lead to severe disability or death; Fig. 85.2 notes other sites of brain herniation.

Oxygen and glucose are required by brain cells for normal functioning, and these nutrients must be constantly supplied by cerebral blood flow (CBF). Normally, CBF is constant over a wide range of blood pressures (i.e., blood pressure autoregulation of CBF) via actions mainly within the cerebral arterioles. Cerebral arterioles are maximally dilated at lower blood pressures and maximally constricted at higher pressures so that CBF does not vary during normal fluctuations ( Fig. 85.3 ). Above the upper limit of autoregulation, breakthrough dilation occurs, which if severe can produce hypertensive encephalopathy. Acid-base balance of the CSF, often reflected by acute changes in arterial partial pressure of carbon dioxide (Pa co ₂ ), body/brain temperature, glucose utilization, blood viscosity, and other vasoactive mediators (i.e., adenosine, nitric oxide), can also affect the cerebral vasculature.

Knowledge of these concepts is instrumental to preventing secondary brain injury. Increases in CSF pH that occur because of inadvertent hyperventilation (which decreases Pa co ₂ ) can produce cerebral ischemia. Hyperthermia-mediated increases in cerebral metabolic demands may damage vulnerable brain regions after injury. Hypoglycemia can produce neuronal death when CBF fails to compensate. Prolonged seizures can lead to permanent injuries if hypoxemia occurs from loss of airway control.

Attention to detail and constant reassessment are paramount in managing children with critical neurologic insults. Among the most valuable tools for serial, objective assessment of neurologic condition is the Glasgow Coma Scale (GCS) (see Chapter 81 , Table 81.3 ). Originally developed for use in comatose adults, the GCS is also valuable in pediatrics. Modifications to the GCS have been made for nonverbal children and are available for infants and toddlers. Serial assessments of the GCS score along with a focused neurologic examination are invaluable to detection of injuries before permanent damage occurs in the vulnerable brain. The full outline of unresponsiveness (FOUR) score is a modification of the GCS, with eye and motor response, but eliminates the verbal response and adds 2 functional assessments of the brainstem (pupil, corneal, and cough reflexes) and respiratory patterns ( Table 85.1 ).

The most studied monitoring device in clinical practice is the ICP monitor . Monitoring is accomplished by inserting a catheter-transducer either into the cerebral ventricle or into brain parenchyma (i.e., externalized ventricular drain and parenchymal transducer, respectively). ICP-directed therapies are standard of care in traumatic brain injury (TBI) and are used in other conditions, such as intracranial hemorrhage, some cases of encephalopathy, meningitis, and encephalitis. Other devices being used include catheters that measure brain tissue oxygen concentration, external probes that noninvasively assess brain oxygenation by absorbance of near-infrared light (i.e., near-infrared spectroscopy), monitors of brain electrical activity (continuous electroencephalography [EEG] or somatosensory, visual, or auditory evoked potentials), and CBF monitors (transcranial Doppler, xenon CT, perfusion MRI, or tissue probes). In the severe TBI guidelines, brain tissue oxygen concentration monitoring received level III support and thus may be considered.

Traumatic Brain Injury

Etiology and Epidemiology

Mechanisms of TBI include motor vehicle crashes, falls, assaults, and abusive head trauma. Most TBIs in children are from closed-head injuries ( Fig. 85.4 ). TBI is an important pediatric public health problem, with approximately 37,000 cases resulting in the death of >7,000 children annually in the United States.