Neurologic Emergencies and Stabilization

Published on 25/03/2015 by admin

Filed under Pediatrics

Last modified 25/03/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1280 times

Chapter 63 Neurologic Emergencies and Stabilization

The care of critically ill children has advanced greatly over the past decades, and mortality rates have fallen. A remaining challenge is optimizing recovery after critical neurologic insults.

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. 63-1). 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.

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 (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. 63-2). Acid-base balance of the CSF (often reflected by acute changes in PaCO2), body/brain temperature, glucose utilization, 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 (decreased PaCO2) 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 assessments of neurologic condition is the Glasgow Coma Scale (GCS) (see Table 62-3). Originally developed to assess level of consciousness after traumatic brain injury (TBI) in 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 (see Table 62-3). 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 best-studied monitoring device in clinical practice is the ICP monitor. Monitoring is accomplished by a catheter inserted either into the cerebral ventricle (externalized ventricular drain) or into brain parenchyma (parenchymal transducer). ICP-directed therapies are standard of care in TBI and are used in other conditions such as intracranial hemorrhage, Reye syndrome, and some cases of encephalopathy, meningitis, and encephalitis. Other devices being studied include catheters that measure brain tissue oxygen concentration (PbtO2), external probes that noninvasively assess brain oxygenation by absorbance of near-infrared light (near-infrared spectroscopy [NIRS]), 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).

Traumatic Brain Injury

Clinical Manifestations

The hallmark of severe TBI is coma (GCS score 3-8). Often, coma is seen immediately after the injury and is sustained. In some cases, such as with an epidural hematoma, a child may be alert presentation but may deteriorate after a period of hours. A similar picture can be seen in children with diffuse swelling, in whom a talk and die scenario has been described. Clinicians should also not be lulled into underappreciating the potential for deterioration of a child with moderate TBI (GCS score 9-12) with a significant contusion, because progressive swelling can potentially lead to devastating complications. In the comatose child with severe TBI, the second key clinical manifestation is the development of intracranial hypertension. The development of increased ICP with impending herniation may be heralded by new-onset or worsening headache, depressed level of consciousness, vital sign changes (hypertension, bradycardia, irregular respirations), and signs of 6th (lateral rectus palsy) or 3rd (anisocoria [dilated pupil], ptosis, down-and-out position of globe due to rectus muscle palsies) cranial nerve compression. Increased ICP can be appropriately managed only with continuous ICP monitoring. The development of brain swelling is progressive. Significantly raised ICP (>20 mm Hg) can occur early after severe TBI, but peak ICP generally is seen at 48-72 hr. Need for ICP-directed therapy may persist for longer than a week. A few children have coma without increased ICP, resulting from axonal injury or brainstem injury.

Laboratory Findings

Cranial CT should be obtained immediately after stabilization (Figs. 63-3 to 63-11). Generally, other laboratory findings are normal in isolated TBI, although occasionally coagulopathy or the development of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) or, rarely, cerebral salt wasting is seen. In the setting of TBI with polytrauma, other injuries can result in laboratory abnormalities, and a full trauma survey is important in all patients with severe TBI (Chapter 66).


Infants and children with severe or moderate TBI (GCS score 3-8 or 9-12, respectively) receive intensive care unit (ICU) monitoring. Evidence-based guidelines for management of severe TBI have been published (Fig. 63-12). This approach to ICP-directed therapy is also reasonable for other conditions in which ICP is monitored. Care involves a multidisciplinary team comprising pediatric caregivers from neurologic surgery, critical care medicine, surgery, and rehabilitation, and is directed at preventing secondary insults and managing raised ICP. Initial stabilization of infants and children with severe TBI includes rapid sequence tracheal intubation with spine precautions along with maintenance of normal extracerebral hemodynamics, including blood gas values (PaO2, PaCO2), MAP, and temperature. Intravenous fluid boluses may be required to treat hypotension. Euvolemia is the target, and hypotonic fluids should be rigorously avoided; normal saline is the fluid of choice. Pressors may be needed as guided by monitoring of central venous pressure (CVP), with avoidance of both fluid overload and exacerbation of brain edema. A trauma survey should be performed. Once stabilized, the patient should be taken for CT scanning to rule out the need for emergency neurosurgical intervention. If surgery is not required, an ICP monitor should be inserted to guide the treatment of intracranial hypertension.

During stabilization or at any time during the treatment course, patients can present with signs and symptoms of cerebral herniation (pupillary dilatation, systemic hypertension, bradycardia, extensor posturing). Because herniation and its devastating consequences can sometimes be reversed if promptly addressed, it should be treated as a medical emergency, with use of hyperventilation with an FIO2 of 1.0, and intubating doses of either thiopental or pentobarbital and either mannitol (0.25-1.0 g/kg, IV) or hypertonic saline (3% solution, 5-10 mL/kg IV).

ICP should be maintained <20 mm Hg; age-dependent CPP targets are ≈50 mm Hg for children 2-6 yr; 55 mm Hg for those 7-10 yr; and 65 mm Hg for those 11-16 yr. First-tier therapy includes elevation of the head of the bed, ensuring midline positioning of the head, controlled mechanical ventilation, and sedation and analgesia (i.e., benzodiazepines and narcotics). If neuromuscular blockade is needed, it may be desirable to monitor EEG continuously because status epilepticus can occur; this complication will not be recognized in a paralyzed patient and is associated with raised ICP and unfavorable outcome. If a ventricular rather than parenchymal catheter is used to monitor ICP, therapeutic CSF drainage is available and can be provided either continuously (often targeting an ICP > 5 mm Hg) or intermittently in response to ICP spikes, generally 20 mm Hg. Other first-tier therapies include the osmolar agents mannitol (0.25-1.0 g/kg IV over 20 min), given in response to ICP spikes >20 mm Hg or with a fixed (q4-6h) dosing interval, and hypertonic saline (often given as a continuous infusion of 3% saline at 0.1-1.0 mL/kg/hr). Choice of osmolar agent depends on the preference of the treating center. These two agents can be used concurrently. It is recommended to avoid serum osmolality >320 mOsm/L. A Foley urinary catheter should be placed to monitor urine output.

If ICP remains refractory to treatment, careful reassessment of the patient is needed to rule out unrecognized hypercarbia, hypoxemia, fever, hypotension, hypoglycemia, pain, and seizures. Repeat imaging should be considered to rule out a surgical lesion. Guidelines-based second-tier therapies for refractory raised ICP are available, but evidence favoring a given second-tier therapy is limited. In some centers, decompressive craniectomy is used. Others use a pentobarbital infusion, with a loading dose of 5-10 mg/kg over 30 min followed by 5 mg/kg every hour for 3 doses and then maintenance with an infusion of 1 mg/kg/hr. Careful blood pressure monitoring is required because of the possibility of drug-induced hypotension and the frequent need for support with fluids and/or pressors. Mild hypothermia (32-34°C) to control refractory ICP can be induced and maintained by means of surface cooling. Sedation and neuromuscular blockade are used to prevent shivering, and rewarming should be slow, no faster than 1°C every 4-6 hr. Hypotension should be prevented during rewarming. Refractory raised ICP can also be treated with hyperventilation (PaCO2 = 25-30 mm Hg). Other second-tier therapies (e.g., lumbar CSF drainage) are options.