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.
Figure 63-1 The Munro-Kellie doctrine describes intracranial dynamics in the setting of an expanding mass lesion (i.e., hemorrhage, tumor) or brain edema. In the normal state, the brain parenchyma, arterial blood, cerebrospinal fluid (CSF), and venous blood occupy the cranial vault at a low pressure, generally <10 mm Hg. With an expanding mass lesion or brain edema, initially there is a compensated state as a result of reduced CSF and venous blood volumes, and intracranial pressure (ICP) remains low. Further expansion of the lesion, however, leads to an uncompensated state when compensatory mechanisms are exhausted and intracranial hypertension results. See text for details.
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.
Figure 63-2 Schematic of the relationship between cerebral blood flow (CBF) and cerebral perfusion pressure (CPP). The diameter of a representative cerebral arteriole is also shown across the center of the y axis to facilitate understanding of the vascular response across CPP that underlies blood pressure autoregulation of CBF. CPP is generally defined as the mean arterial pressure (MAP) minus the intracranial pressure (ICP). At normal values for ICP, this generally represents MAP. Thus, normally, CBF is kept constant between the lower limit and upper limit of autoregulation; in normal adults, these values are ≈50 mm Hg and 150 mm Hg, respectively. In children, the upper limit of autoregulation is likely proportionally lower than the adult value relative to normal MAP for age. However, according to the work of Vavilala et al (2003), lower limit values are surprisingly similar in infants and older children. Thus, infants and young children may have less reserve for adequate CPP. See text for details.
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.
Traumatic Brain Injury
Etiology
Mechanisms of TBI include motor vehicle crashes, falls, assaults, and abusive head trauma. Most TBIs in children are from closed-head injury.
Epidemiology
TBI is one of the most important pediatric public health problems, resulting in the death of about 7,000 children annually in the USA.
Pathology
Epidural, subdural, and parenchymal intracranial hemorrhages can result. Injury to gray or white matter is also commonly seen and includes focal cerebral contusions, diffuse cerebral swelling, axonal injury, and injury to the cerebellum or brainstem. Patients with severe TBI often have multiple findings; diffuse and potentially delayed cerebral swelling is common.
Pathogenesis
TBI results in primary and secondary injury. Primary injury from the impact produces irreversible tissue disruption. In contrast, 2 types of secondary injury are targets of neurointensive care. First, some of the ultimate damage seen in the injured brain evolves over hours or days, and the underlying mechanisms involved (edema, apoptosis, and secondary axotomy) are therapeutic targets. Second, the injured brain is vulnerable to additional insults because injury disrupts normal autoregulatory defense mechanisms; disruption of autoregulation of CBF can lead to ischemia from hypotension that would otherwise be tolerated by the uninjured brain.
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).
Figure 63-3 Abusive head trauma in an infant. Note the subdural fluid collections, dilated ventricles, and blood.
Figure 63-5 Abusive head trauma with massive cerebral edema, with loss of gray matter–white matter differentiation, loss of the ventricular system, and probable herniation of the brainstem.
Figure 63-6 Abusive head trauma with significant intraventricular, intracerebral, and subdural hematomas, with loss of gray matter–white matter differentiation, suggestive of massive cerebral edema.
Figure 63-7 A depressed skull fracture due to traumatic delivery with forceps. Brain swelling can be seen.
Figure 63-8 Malignant brain edema. A common pattern in severe head injury that is associated with significant secondary brain injury and a very high mortality rate. Cisterns are absent on the CT scan. This type of injury is associated with hypoxia and hypoxemia and hypotension.
Figure 63-9 Significant closed-head injury with subgaleal hematoma, intracerebral hemorrhage, and loss of gray matter–white matter differentiation.
Figure 63-10 Severe traumatic brain injury with multiple depressed skull fractures and intraparenchymal hemorrhage.
Diagnosis and Differential Diagnosis
In severe TBI, the diagnosis is generally obvious from the history and clinical presentation. Occasionally, TBI severity can be overestimated because of concurrent alcohol or drug intoxication. The diagnosis of TBI can be problematic in cases of inflicted TBI or following an anoxic event such as near drowning or smoke inhalation.
Treatment
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.
Figure 63-12 Schematic outlining the approach to management of a child with severe traumatic brain injury (TBI). It is based on the 2003 guidelines for the management of severe TBI, along with minor modifications from later literature. The intracranial pressure (ICP) and cerebral perfusion pressure (CPP) targets are discussed in the text. This schematic is specifically presented for severe TBI, for which the experience with ICP-directed therapy is greatest. Nevertheless, the general approach provided here is relevant to the management of intracranial hypertension in other conditions for which evidence-based data on ICP monitoring and ICP-directed therapy are lacking. Please see text for details.
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.
Supportive Care
Euvolemia should be maintained, and isotonic fluids are recommended until resolution of intracranial hypertension. SIADH and salt wasting can develop and are important to differentiate, because management of the former is fluid restriction and that of the latter is sodium replacement. Severe hyperglycemia (blood glucose level >200 mg/dL) should be avoided and treated. The blood glucose level should be monitored frequently. Early nutrition with enteral feedings is advocated. Corticosteroids should generally not be used unless adrenal insufficiency is documented. Tracheal suctioning can exacerbate raised ICP. Timing of the use of sedation around suctioning events and/or use of tracheal or IV lidocaine can be helpful. Anticonvulsant prophylaxis with phenytoin or carbamazepine is a common treatment option.
Prognosis
Mortality rates for children with severe TBI who reach the PICU range between 10% and 30%. Ability to control ICP is related to patient survival, and the extent of cranial and systemic injuries correlates with quality of life. Motor and cognitive sequelae resulting from severe TBI generally benefit from rehabilitation to minimize long-term disabilities. Recovery from TBI may take months to achieve. Physical therapy, and in some centers methylphenidate, helps with motor and behavioral recovery.
Mild Traumatic Brain Injury
The majority (>90%) of children with blunt, closed-head trauma do not experience severe life- or brain-threatening complications. Children with mild TBI are defined as having a GCS score between 13 and 15 upon arrival at the hospital with or without the following acute symptoms: a history of loss of consciousness and antegrade or retrograde amnesia, as well as headache, vomiting, nausea, dizziness, or disorientation.
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