Etiology

CNS injury is the leading cause of death in children. In children younger than 2 years, serious head injuries (traumatic brain injuries [TBIs]) are commonly intentional (also called inflicted or non-accidental trauma). Children older than 3 years of age sustain head injuries secondary to falls or to motor vehicle, all terrain vehicle, bicycle, and pedestrian collisions. In high school-aged adolescents, football is the team sport most commonly linked with head injury.

Each year 1.5 million head injuries occur in the United States. Of this number approximately 300,000 children are hospitalized with head trauma. Nearly 90% of injury-related deaths are associated with head trauma. Males are twice as likely as females to sustain head trauma. Severe TBI or associated cardiorespiratory arrest can cause death within a few hours of injury.²⁰

Pathophysiology

The rigid cranium and the CSF cushion can protect the child's brain from injury during minor trauma. However, if distortion of the skull, shear injury, actual tissue damage, intracranial hemorrhage, or cerebral edema develop, the injury is likely to be complicated by increased ICP. Therefore, the child with head trauma requires assessment and treatment of the primary (or direct) injury, as well as careful assessment and treatment of secondary complications.

The types of cerebral injuries occurring with head trauma include concussions, contusions, skull fractures, vascular injuries, diffuse axonal injuries, penetrating injuries, and cerebral edema. Each lesion is summarized below.

Clinical Signs and Symptoms

The child with head injury requires frequent neurologic examinations and monitoring of neurologic function and responsiveness. Recently, evaluation of cerebral biomarkers has been shown to be helpful in the identification of head injury.

This section describes the use of serum biomarkers and the clinical signs and symptoms of each of the major forms of head injury. A review of the initial assessment of children with head trauma is included in the following section, Management.

Management

All children with moderate or severe head injury require critical care. Children with mild head injury usually are admitted to the critical or intermediate care unit for skilled continuous nursing observation. Because a small number of patients with apparently minor head injuries may deteriorate acutely as the result of rapid brain swelling and increased ICP, a CT scan is indicated when the child has a history or mechanism of injury consistent with a serious head trauma (e.g., a fall from a significant height, unrestrained occupant in a severe motor vehicle crash). This scan should be performed even if the child initially appears alert and oriented.⁵⁰

All children with serious head trauma are presumed to have a spinal cord injury until it has been ruled out. The cervical spine should be immobilized, and the child should be log rolled whenever turning is necessary. Until definitive radiographic studies and clinical examination can be performed, the nurse must frequently and carefully evaluate the patient's movement and sensation in all four extremities. The development of a progressive neurologic deficit in the patient with a spinal cord injury is a neurosurgical emergency that will require urgent intervention (see Spinal Cord Injury). When assessing movement and sensation, it is important to verify that movement is voluntary and intentional; the reflex withdrawal of an extremity may occur in response to stimulation of a spinal reflex arc despite complete spinal cord transection.

Etiology

Any trauma victim can sustain spinal cord injury (SCI). Traumatic SCI can be primary or can result from a secondary insult. The mechanisms most commonly associated with pediatric SCI include falls and pedestrian-related motor vehicle crashes. In adolescents, motor vehicle crashes, sports and diving injuries and gunshot wounds are common causes of SCI. Intentional injury may also cause SCI.

Pathophysiology

The young child's head is large and heavy in proportion to the rest of the body. The child ejected from or struck by a car often is propelled head-first into the ground or another object, and resulting hyperextension or flexion of the neck is likely to produce cervical spine injury. Flexion-rotation or hyperflexion injuries can cause dislocation or locking of the facets (articulation surfaces) of two contiguous vertebrae with resulting spinal cord compression.

The cervical spine is relatively unstable and is still developing in young children. As a result, SCI patterns in children differ from those in adults. The ligaments along the child's cervical vertebrae are relatively lax, and the paraspinous muscles are incompletely developed. The child's vertebral bodies are wedge-shaped and not completely ossified. In addition, the facet joints of the cervical vertebrae are relatively flat. For these reasons, the vertebrae can shift several centimeters during injury or the application of force to the spine, resulting in spinal cord injury without evidence of injury to the vertebrae. Although the pediatric spine is relatively more elastic than the adult spine, it will be injured if significant cervical subluxation occurs (Fig. 11-19).

Fig. 11-19 Spinal cord injury. Many injuries resulting in spinal cord damage produce visible radiographic changes, although a significant number (20%-60%) are not associated with any skeletal fracture or dislocation. A, Lateral cervical spine radiographs demonstrating skeletal abnormalities associated with cervical spine injury. The first radiograph is from a 4 year old who was restrained in a car seat that was not anchored in the car. The separation between the fifth and sixth cervical vertebrae is subtle but detectable (arrow), especially when compared with the line drawing of normal anatomy (far right). Radiopaque orogastric and nasogastric tubes are visible; they are slightly displaced anteriorly, indicating a small amount of edema surrounding the spinal cord injury. The location of the injury is unusual for this age. The second radiograph shows a 5-year-old pedestrian struck by an automobile and demonstrates significant separation between the first and second cervical vertebrae. This is a more common site of cervical spine injury in young children. Note the anterior displacement of the nasogastric tube (arrow) produced by edema surrounding the injury. An endotracheal tube is present but not visible. The line drawing depicts normal cervical spinal anatomy in a 3- to 4-year-old child. B, This scan film performed before a computed tomography scan demonstrates lumbar vertebral and spinal cord trauma associated with a lap belt injury. Separation of the lumbar vertebrae can be seen (arrow) and resulted in paraplegia. This injury resulted from flexion of the lumbar spine (see drawing). C, Flexion injury of the lower thoracic vertebrae and spine is visible on this anteroposterior chest radiograph. This radiograph shows an unrestrained 16-year-old driver who was thrown from the car. The lateral flexion resulted in compression of the spinal cord and fracture of the thoracic vertebrae (see arrow and corresponding illustration). The rod placed during surgery is visible. D, This magnetic resonance imagery scan shows in detail the skeletal and spinal damage resulting from a flexion-rotation injury. This 16-year-old motorcycle driver sustained displacement of two vertebrae (white arrows) and fracture of two vertebrae and one disc. Resulting compression of the cervical spine produced a complete spinal cord injury. A contusion is visible in the spinal cord (black arrow). The line drawing depicts the injury.

(A, courtesy Carol Gilbert and John Feldenzer, Roanoke, Va. Drawing reproduced from Riviello JJ, et al: Delayed cervical central cord syndrome after trivial trauma, Pediatr Emerg Care 6:116, 1990. B, courtesy Bennett Blumenkopf, Vanderbilt University Medical Center, Nashville, Tenn. Line drawing reproduced from Rudy EB: Advanced neurological and neurosurgical nursing, St Louis, 1984, Mosby. C, courtesy Noel Tulipan, Vanderbilt University Medical Center, Nashville, Tenn. Illustration reproduced from Rudy EB: Advanced neurological and neurosurgical nursing, St Louis, 1984, Mosby. D, courtesy Bennett Blumenkopf, Vanderbilt University, Nashville, Tenn. Line drawing reproduced from Rudy EB: Advanced neurological and neurosurgical nursing, St Louis, 1984, Mosby.)

The most common areas of SCI in children younger than 9 years include the atlas, axis, and upper cervical spine. Generally, ligamentous injuries are more common than bone injuries. In patients older than 9 years, injury patterns resemble those of the adult, with less cervical involvement.¹²³

Pediatric spinal cord injuries occur when vertebral bodies are fractured, or when vertebral subluxation (partial dislocation) occurs. Subluxation results in anteroposterior misalignment of contiguous vertebrae, with narrowing of the spinal canal and spinal cord compression. Young children are likely to sustain subluxation injuries without associated fractures. The severity of the neurologic deficit is related to the location and severity of the subluxation.¹²³

The neurologic dysfunction associated with SCI can result from the injury itself or from secondary compromise of spinal cord perfusion (ischemia or infarction), edema and necrosis. In laboratory experiments, SCI produces altered permeability of neuron membranes, electrolyte flux across the membranes, and the release of catecholamines and endorphins. Vasospasm and thrombosis in spinal cord vessels can contribute to ischemia, infarction, and dysfunction.⁹¹

Severe traumatic cervical spine injury (especially to the upper cervical spine) usually produces respiratory arrest at the scene of the injury, and the patient dies unless immediate resuscitation is provided. Occasionally, children with a cervical spinal injury sustain injury to the cervical vertebrae, rendering them unstable. These children can move all four extremities and breathe at the scene of the accident; however, if the cervical spine is not immobilized (particularly during intubation), spinal cord injury, respiratory arrest, and tetraplegia can result.

If a spinal cord injury is mild or moderate, complete recovery of neurologic function is possible despite the presence of complete neurologic deficit on admission.¹²³ However, if the initial insult is severe (particularly if severe subluxation occurred) or is associated with the development of edema, permanent loss of function and sensation below the level of injury can occur.

Traumatic atlantooccipital dislocation is the disruption of the supporting ligaments between the skull and the vertebral column, occurring in a transverse or vertical direction and resulting in complete transection of the spinal cord. Although this type of SCI is rare in children and adolescents, traumatic atlantooccipital dislocation is seen in infants and toddlers. Most children do not survive this initial insult, but as prehospital care has improved over recent years there are reports of survival when immediate CPR is provided at the scene or emergency responders arrive within a few minutes of the injury.¹²³

Clinical Signs and Symptoms

Management

Management of the child with SCI is designed to minimize the potential for further injury while supporting maximal recovery of spinal cord function. In general, the spinal cord is immobilized until the child's condition is stable, and then definitive therapy is provided.^47,50 The neck and spine are maintained in a neutral position, using the jaw-thrust maneuver when opening the airway and ensuring that manual stabilization is performed during intubation.

Steroid administration is advocated within the first 8   hours after injury to prevent secondary spinal cord edema and inflammation. A Cochrane meta-analysis of three studies documented that large dose methylprednisolone administration (a bolus dose of 30   mg/kg, followed by continuous infusion of 5.4   mg/kg per hour for 23   hours) significantly increased functional recovery of adult patients with SCI.²⁸ Although this steroid administration has now become standard,⁵⁰ controlled trials of this therapy have not been performed in children. There are no class I data to support the use of steroids in children younger than 18 years with SCI, and it should be avoided in children with brain injury.^13,123

Children with SCI require close observation for signs of neurogenic shock. These children experience a loss of vasomotor tone leading to venous pooling, decreased venous return, and ultimately decreased cardiac output. Bradycardia results from loss of sympathetic tone with resulting parasympathetic dominance. Management includes volume resuscitation and vasopressor support. SCI will also produce hypothermia, because the vasodilation leads to heat loss through the skin.

Urgent surgical intervention is rarely needed during the acute management of SCI, particularly when complete SCI is present. Urgent surgical intervention is indicated for incomplete SCI with compromise or for incomplete SCI with progressive neurologic dysfunction, because such progression often indicates the presence of an emerging but reversible problem, such as an epidural hematoma, or an unstable spinal injury.⁵⁰

If a cervical spine injury is unstable or subluxation is present, immobilization and alignment of the spine will be necessary through the use of Gardner-Wells tongs or halo traction. If the vertebral bodies are not reduced (i.e., they are misaligned), weight is added to the traction device, and clinical and radiographic examinations are repeated until the vertebrae are realigned or reduced. The alert patient will require analgesia during this procedure, but should not be sedated because the child must be responsive during clinical examination.^50,123

Once the vertebrae are aligned, the patient is maintained in halo traction for several weeks. In children, the use of a halo vest will facilitate ambulation.⁵⁰ If the area of injury continues to be unstable, spinal fusion occasionally is required, possibly several weeks later. Surgical stabilization is most likely to be required for children with SCI who are younger than 3 years.

Rehabilitation services should begin as soon as the pediatric patient with a SCI is stable. A physical medicine and rehabilitation consult should be obtained to provide guidance about the child's long term care needs. Physical and occupational therapy will be beneficial in maintaining range of motion, mobilization and integration into activities of daily living. Speech therapists will evaluate tolerance of oral intake and, if needed, can assist in providing alternative methods of communication. A bowel and bladder regimen should be initiated early and re-evaluated on a routine basis.

Etiology

Primary brain tumors are one of the most common forms of cancer in children, and medulloblastoma is the most common malignant brain tumor. Survival from brain tumors has now risen from approximately 60% in the 1980s to 80% to 85% in recent years.⁹⁸ This improved survival can be attributed to earlier and more complete tumor resection (particularly for medulloblastomas) as well as more aggressive and targeted chemotherapy and radiation therapy. The involvement of the disease at presentation, the amount of tumor resection possible, and tumor grades are part of the prognostic factors involved in the outcomes of most brain tumors (e.g., ependymoma).²¹

Tumors are abnormal masses that can arise from any tissue in the body. Their cause is unknown, although the role of hereditary factors and environmental carcinogens continues to be explored. Although few tumors are present from birth, many tumors of childhood arise from the inappropriate development of primitive neuroepithelial cells. Astrocytomas are the most common primary intraaxial brain tumor, and pilocytic astrocytomas typically manifest in the second decade of life.⁵⁰

Pathophysiology

Intracranial tumors in children produce an increase in intracranial volume; unless the skull can expand commensurately, the child will develop increased ICP. In addition, the tumor causes compression of the surrounding brain tissue, compromising important cerebral functions.

Tumors are classified according to their location, degree of malignancy, and histologic features. Classification by location is used here because it enables more straightforward prediction of the clinical consequences of tumor expansion and the possibility and risks of surgical tumor excision (Box 11-11).

Supratentorial tumors involve the cerebral hemispheres and all structures located above the tentorium cerebelli. Infratentorial tumors are those that involve the brain stem and cerebral structures located below the tentorium cerebelli.

Classification of tumors by cell type allows some predictions about the speed of tumor growth and spread and about recurrence risks. It is important to note that intracranial tumors in children may be malignant by position as well as by cell type. This means that the tissue itself is not malignant, but tumor growth can compress or erode vital brain tissue, resulting in serious neurologic compromise or death.

In the following section, the most common intracranial tumors in children are described. This description includes the clinical consequences of tumor growth.

Clinical Signs and Symptoms

Intracranial tumors in children can grow to a large size without producing significant symptoms until they invade vital brain tissue or cause increased ICP. In children up to 12 years of age, the skull can expand to accommodate a gradual increase in intracranial volume. Tumors may not be diagnosed in the young child with nonspecific signs of neurologic compromise, because testing of cognitive functions, fine motor skills, and sensation is very difficult in very young patients.

Signs and symptoms of any neoplasm in the child include a change in the child's appearance or growth patterns, swelling, lumps, masses, vague pains, or persistent irritability. The child may also change feeding patterns or bowel or bladder function or may develop unexplained clumsiness or stumbling or unexplained or persistent bleeding. General signs of an intracranial tumor during childhood include signs of increased ICP, headache, emesis, anorexia, ataxia, cranial nerve palsies, nystagmus, paresis, seizure activity, and hydrocephalus.

Specific signs of increased ICP caused by an intracranial tumor include papilledema, altered level of consciousness, visual disturbances (diplopia and blurring of vision), headache, and emesis. The headache is characteristically intermittent but progressive. It tends to be present after awakening, and it often is associated with vomiting. The child usually does not feel nauseated before vomiting. If vomiting or headaches are persistent, anorexia may develop.

As the tumor grows, an infant will develop a bulging fontanelle, and torticollis may result from the asymmetric compression of neck muscles by the tumor. Nuchal rigidity may be noted.³⁵

If the tumor compresses the sixth cranial nerve or if uncal (temporal-lateral) herniation develops from increased ICP, the child may develop strabismus, diplopia, or blurring of vision. Ataxia or nystagmus will develop if the tumor compresses or erodes the cerebellum.⁵⁰ Paresis will develop if the tumor compresses the brainstem or pyramidal tract. Seizures are rarely an early sign of an intracranial tumor, although they can develop late in the clinical course. If hydrocephalus is present, the tumor is obstructing CSF pathways.

The best means of diagnosing an intracranial tumor is with a thorough neurologic examination and a CT scan with and without contrast. MRI is also an essential tool in the diagnosis of brain tumors and is the preferred method of scanning for some brain stem tumors. (See Common Diagnostic Tests later in this chapter.) A plain skull radiograph may demonstrate characteristic changes associated with some tumors (e.g., calcification near the sella turcica that occurs with craniopharyngioma), but often the radiographs are not helpful. Arteriography can be performed to better locate and define the tumor.

Management

Care of the child with an intracranial tumor requires treatment of intracranial hypertension (see Increased Intracranial Pressure in the Common Clinical Conditions section of this chapter), surgical resection if possible, and initiation of chemotherapy or radiation therapy. Laser, stealth, and gamma knife surgeries are surgical techniques that have improved the efficacy of surgical intervention for intracranial tumors. Stealth or stereotactic guidance is especially useful in transsphenoidal tumor resection. Over the past decade, the development of frameless stereotaxy in combination with fluoroscopy assists the neurosurgeon in staying midline. It is considered safe and accurate and adds little cost and time to conventional surgical approaches.⁴⁴

Radiation therapy is typically prescribed for intracranial tumors, and chemotherapy recently has been found to be helpful in the treatment of some intracranial tumors in children.⁵⁰ Steroid therapy such as dexamethasone may be used for treatment of localized edema surrounding the tumor. Although the mechanism of action is unclear, the working theory is that the drug decreases the blood-tumor barrier permeability or it may increase parenchymal resistance to fluid transport.⁵⁰

The child with a brain tumor is typically admitted to the critical care unit following neurosurgery. The child may also require critical care for management of sepsis or infections secondary to chemotherapy-induced immunosuppression (see Chapters 6 and 16).

The child and family will require long-term physical and emotional support. If the tumor initially produced vague clinical signs and symptoms, and the parents ignored the child's initial complaints, they may feel guilty and frustrated. Unless deterioration is rapid, the child will require surgery, radiation, and possible chemotherapy with frequent hospitalizations. The child may, in fact, have a chronic neurologic disease and require prolonged treatment. The child and family will require long-term follow-up and ongoing support.

Etiology

Meningitis is an acute inflammation of the meninges and CSF. It occurs far more commonly in children than in adults, and it is seen most frequently in children between 1 month and 5 years of age. Meningitis most commonly is produced by bacteria (called purulent meningitis) or viruses (usually called aseptic meningitis), although it can also result from fungi, parasites, or mycobacteria.

Over the past decade there have been advances in testing technology. The addition of pneumococcal and meningococcal vaccines into the routine immunization schedule and the adjunctive use of steroids have changed the management of meningitis. However, meningitis remains a leading cause of infection in children, with significant morbidity and mortality.

The three major organisms responsible for meningitis worldwide are Haemophilus influenzae, Neisseria meningitidis, and Streptococcus pneumoniae, but the causative organisms vary depending on the geographic location and age of the child. In the United States, meningococcus and pneumococcus account for approximately 95% of acute bacterial meningitis in children. Group B streptococcus remains a leading cause of meningitis in the neonatal population. These forms of meningitis usually result from the extension of a localized infection, with transient bacteremia and CNS spread of the organism. Staphylococcal meningitis occurs most commonly after neurosurgery or after a skull fracture with a dural tear.^81,114

Pathophysiology

Most pathogens responsible for bacterial meningitis are introduced via the respiratory system. Colonization of the organism in the mucous membranes of the nasal passages causes injury to the epithelial cells, allowing access into bloodstream. After this hematogenous spread of bacteria (i.e., it is spread by blood), the bacteria then penetrate the blood-brain barrier, infecting the meninges. Once the CNS has been breached, the bacteria will multiply freely and rapidly spread throughout the entire surface of the spinal cord and brain. Inflammatory mediators and cytokines are then released causing an inflammatory response. Cerebral edema, inflammation, and ensuing increased ICP are frequently seen after bacterial invasion of the brain parenchyma. Cerebral vasculitis, thrombosis, and infarction are the consequence of endothelial damage at the vascular level. Edema or scarring of the outlet of the third ventricle produces stenosis of the Sylvian aqueduct and results in obstruction to CSF flow and hydrocephalus.⁵⁰

Clinical Signs and Symptoms

Clinical presentation depends on the age of the child, the time lapse between initial symptoms and medical treatment, the immunity of the child, and the infecting organism. Onset can be acute or slow. In the neonate or infant of younger than 6 months, the signs of meningitis are often nonspecific. The infant may be extremely irritable or lethargic with a history of poor feeding, vomiting, and fever. Seizures may develop. A high-pitched cry may be observed in infants with increased ICP.

Extremely malnourished or very small infants with meningitis may be afebrile.¹¹⁴ If the ICP is high, the anterior fontanelle will be full and may be tense. Although the presence of nuchal rigidity (stiff neck) provides an index of suspicion, it is often not present in the young infant. The diagnosis is only confirmed by the results of the spinal tap.

Older children with meningitis usually complain of headache and exhibit nausea, vomiting, anorexia, photophobia, acute onset of fever, decreased level of consciousness or seizures.¹¹⁴ Nuchal rigidity, neck pain, and sensitivity to touch are also present. Kernig's sign (pain with extension of the legs) and Brudzinski's sign (flexion of the neck stimulates flexion at the knees and hips) also may be present. Often there is a history of an antecedent upper respiratory or gastrointestinal infection.¹¹⁴

When meningitis is suspected, blood samples are obtained for a complete blood cell count with white blood cell differential, glucose, electrolytes, and blood cultures. The results will help detect evidence of a localized infection or sepsis. Additional urine, serum, or wound cultures are obtained as indicated.

A lumbar puncture is the definitive diagnostic test for meningitis. During the lumbar puncture, CSF samples are taken. From these samples, a culture, Gram staining, and cell count will be performed, and protein and sugar levels will be measured. The general appearance of the fluid and the opening and closing CSF pressures should be noted in the nursing record.

When bacterial meningitis is present, the glucose concentration of the CSF is low, but the protein content is high. In addition, there will be a large number of cells present in the fluid, predominantly neutrophils (Table 11-11). The culture and Gram stain will be positive.¹¹⁴

Table 11-11 Cerebrospinal Fluid Analysis in Bacterial and Viral Meningitis

When aseptic (viral or fungal) meningitis is present, the CSF glucose concentration is usually normal, and the protein content is only slightly elevated. In aseptic meningitis, there may be a moderate or large number of cells, predominantly polymorphonuclear leukocytes early in the course, and lymphocytes later in the course. The Gram stain is usually negative, and, with viral meningitis, the serologic culture is usually positive for virus.¹¹⁴

Untreated meningitis can cause rapid deterioration. The child may demonstrate mild irritability and fever and quickly progress to high fever, seizures, a decreased level of consciousness, and coma. Thus, the effectiveness of treatment can be related directly to the speed of diagnosis and the early initiation of appropriate treatment.

Management

Bacterial Meningitis

If the child is critically ill, support of airway, ventilation, and perfusion will be needed. However, the treatment of bacterial meningitis requires the prompt initiation (in less than 1   hour of first medical contact) and uninterrupted administration of appropriate IV antimicrobial agents. Vascular access must be established immediately and carefully maintained throughout therapy. Broad spectrum antibiotics are administered even before the results of the CSF cultures and sensitivities have been obtained. The infant or child is given nothing by mouth until systemic perfusion and neurologic function are acceptable.

Accurate recording of fluid intake and output and serum electrolyte concentrations is important, because many children will develop SIADH during or after the meningitis (see Chapter 12). The infant or child is typically given nothing by mouth, and IV maintenance fluids are administered. Fluid boluses may be required because these children usually are somewhat dehydrated related to fever and poor oral intake.

The infant's head circumference should be measured on admission and at least every 8   hours, because subdural effusions and obstructive hydrocephalus can develop after meningitis and can be detected by an increase in head circumference. The infant or child with H. influenzae or N. meningitidis meningitis is placed in respiratory isolation until antibiotic therapy has been administered for 24   hours.¹⁰¹

Treatment of bacterial meningitis should begin as soon as there is suspicion of infection. It is ideal to collect all cultures before beginning antibiotic therapy, but antibiotic administration should not be delayed if samples are difficult to obtain. Antibiotics should be given immediately, and the cultures can be obtained at a later time. Initially, broad spectrum antibiotics should be administered that will cover likely causative organisms for age (Table 11-12). The Gram stain is a guide for initial therapy, but coverage should not be narrowed based on this single test result. The CSF culture remains the gold standard for diagnosis of bacterial meningitis. The antimicrobial therapy can be modified once culture results (including organism and sensitivities) have been completed.

Table 11-12 Recommendations for Antimicrobial Therapy in Bacterial Meningitis Based on Predisposing Conditions or on Isolated Pathogen and Susceptibility Testing

Predisposing Factor	Common Bacterial Pathogens	Antimicrobial Therapy
Age
<1 month	Streptococcus agalactiae, Escherichia coli, Listeria monocytogenes, Klebsiella species	Ampicillin plus cefotaxime or ampicillin plus an aminoglycoside
1-23 months	Streptococcus pneumoniae, Neisseria meningitidis, S. agalactiae, Haemophilus influenzae, E. coli	Vancomycin plus a third-generation cephalosporin*,†
2-50 years	N. meningitidis, S. pneumoniae	Vancomycin plus a third-generation cephalosporin*,†
>50 years	S. pneumoniae, N. meningitidis, L. monocytogenes, aerobic gram-negative bacilli	Vancomycin plus ampicillin plus a third-generation cephalosporin*,†
Head trauma
Basilar skull fracture	S. pneumoniae, H. influenzae, group A β-hemolytic streptococci	Vancomycin plus a third-generation cephalosporin*
Penetrating trauma	Staphylococcus aureus, coagulase-negative staphylococci (especially Staphylococcus epidermidis), aerobic gram-negative bacilli (including Pseudomonas aeruginosa)	Vancomycin plus cefepime, vancomycin plus ceftazidime, or vancomycin plus meropenem
Postneurosurgery	Aerobic gram-negative bacilli (including P. aeruginosa), S. aureus, coagulase-negative staphylococci (especially S. epidermidis)	Vancomycin plus cefepime, vancomycin plus ceftazidime, or vancomycin plus meropenem
CSF shunt	Coagulase-negative staphylococci (especially S. epidermidis), S. aureus, aerobic gram-negative bacilli (including P. aeruginosa), Propionibacterium acnes	Vancomycin plus cefepime,‡ vancomycin plus ceftazidime,‡ or vancomycin plus meropenem‡

Microorganism, Susceptibility	Standard Therapy	Alternative Therapies
Streptococcus pneumoniae
Penicillin MIC
<0.1   mcg/mL	Penicillin G or ampicillin	Third-generation cephalosporin,* chloramphenicol
0.1-1.0   mcg/mL§	Third-generation cephalosporin*	Cefepime (B-II), meropenem (B-II)
≥2.0   mcg/mL	Vancomycin plus a third-generation cephalosporin*,	Fluoroquinolone¶ (B-II)
Cefotaxime or ceftriaxone MIC ≥1.0   mcg/mL	Vancomycin plus a third-generation cephalosporin*,	Fluoroquinolone¶ (B-II)
Neisseria meningitidis
Penicillin MIC
<0.1   mcg/mL	Penicillin G or ampicillin	Third-generation cephalosporin,* chloramphenicol
0.1-1.0   mcg/mL	Third-generation cephalosporin*	Chloramphenicol, fluoroquinolone, meropenem
Listeria monocytogenes	Ampicillin or penicillin G#	Trimethoprim-sulfamethoxazole, meropenem (B-III)
Streptococcus agalactiae	Ampicillin or penicillin G#	Third-generation cephalosporin* (B-III)
Escherichia coli and other Enterobacteriaceae ††	Third-generation cephalosporin (A-II)	Aztreonam, fluoroquinolone, meropenem, trimethoprim-sulfamethoxazole, ampicillin
Pseudomonas aeruginosa††	Cefepime# or ceftazidime# (A-II)	Aztreonam,# ciprofloxacin,# meropenem#
Haemophilus influenzae
β-Lactamase negative	Ampicillin	Third-generation cephalosporin,* cefepime, chloramphenicol, fluoroquinolone
β-Lactamase positive	Third-generation cephalosporin (A-I)	Cefepime (A-I), chloramphenicol, fluoroquinolone
Staphylococcus aureus
Methicillin susceptible	Nafcillin or oxacillin	Vancomycin, meropenem (B-III)
Methicillin resistant	Vancomycin**	Trimethoprim-sulfamethoxazole, linezolid (B-III)
Staphylococcus epidermidis	Vancomycin**	Linezolid (B-III)
Enterococcus species
Ampicillin susceptible	Ampicillin plus gentamicin
Ampicillin resistant	Vancomycin plus gentamicin
Ampicillin and vancomycin resistant	Linezolid (B-III)

Note: All recommendations are A-III, unless otherwise indicated.

* Ceftriaxone or cefotaxime.

† Some experts would add rifampin if dexamethasone is also given.

‡ In infants and children, vancomycin alone is reasonable unless Gram stains reveal the presence of gram-negative bacilli.

§ Ceftriaxone/cefotaxime-susceptible isolates.

Consider addition of rifampin if the MIC of ceftriaxone is 12   mg/mL.

¶ Gatifloxacin or moxifloxacin.

# Addition of an aminoglycoside should be considered.

** Consider addition of rifampin.

†† Choice of a specific antimicrobial agent must be guided by in vitro susceptibility test results.

Adapted from Tunkel, AR, Hartman BJ, Kaplan SJ, et al: Practice guidelines for the management of bacterial meningitis. Clin Infect Dis39:1267-1284, 2004.

The duration of antibiotic therapy is determined by the specific pathogen, but typically CNS infections are treated for 10 to 14 days. Infants infected with herpesvirus are generally treated for 28 days. In the neonate younger than 6 weeks, acyclovir is added because herpesvirus is a concern for CNS infection in the population. Vancomycin is added if the Gram stain is suggestive of pneumococcus. In the infant older than 2 months, vancomycin is added for empiric coverage because pneumococcal resistance to third-generation cephalosporins has emerged.^81,114

Additional days of therapy are indicated if the patient fails to demonstrate clinical improvement or if additional CSF findings indicate partially treated meningitis. Throughout therapy the nurse must monitor for side effects of the antibiotics.

The use of steroids (dexamethasone is 0.6   mg/kg per day divided into four doses for 4 days) in bacterial meningitis has been shown to reduce the incidence of hearing loss and decrease CNS inflammation. However, the first dose must be administered before or in conjunction with the first dose of antibiotics. The targeted bacteria include H. influenzae and pneumococcus. The use of steroids in the neonatal population is yet to be established. Although recommended by the American Academy of Pediatrics, widespread use has not been adopted. Often the infant has already received the first dose of antibiotics before the diagnosis of meningitis is made, so this may partially account for the lack of steroid use in this population. Steroids are not recommended in cases of viral meningitis.

Gastrointestinal prophylaxis with ranitidine or a proton pump inhibitor should be administered when steroids are used.^81,114 The nurse should be alert for signs of gastrointestinal hemorrhage or secondary infection that could complicate steroid administration.

A repeat lumbar puncture is not typically recommended at the end of therapy if the child's condition has improved and the child is afebrile. However, if the child is receiving appropriate therapy and does not show clinical improvement within 3 to 4 days of treatment, is experiencing new symptoms, culture results are positive for an unusual or resistant pathogen, or there is no improvement (i.e., in neurologic signs) or child remains febrile on specific therapy after 24 to 48 hours, then the lumbar tap should be repeated. In the neonate, Gram-negative meningitis is an indication for repeat lumbar puncture.^81,114

Prophylactic antibiotic administration is recommended for household, daycare, and nursery-school contacts of the patient with Neisseria spp. meningitis. These contacts should begin taking antibiotics within 24   hours of the patient's diagnosis. Prophylaxis also is recommended for anyone having intimate contact with the patient, including babysitters who may have kissed the child. Ceftriaxone, ciprofloxacin, and rifampin are used for prophylaxis in adults, and rifampin is the drug of choice for prophylaxis in most children.¹⁰¹

Etiology

A brain abscess is an isolated intracranial collection of purulent fluid, typically located in the cerebral hemispheres or the cerebellum. The abscess usually develops after bacteremia, but it also can result from chronic sinusitis or following a head injury with a skull fracture. Children with cyanotic congenital heart disease (especially if untreated and older than 2 years) or those with bacterial endocarditis are at increased risk for developing brain abscesses.

Pathophysiology

The pathogen enters the cerebral circulation at the site of intracranial surgery or compound skull fracture or as the result of a systemic or blood-borne infection. Abscesses also can spread into adjacent cerebral tissue from middle ear or mastoid infections.

The infected tissue initially is localized and is invaded quickly by white blood cells. Over a period of several weeks, necrotic tissue within the abscess liquefies, and the abscess becomes encapsulated by fibroblasts.⁶² As the abscess grows, it can produce signs of increased ICP. If it ruptures, it can produce diffuse meningoencephalitis.

Clinical Signs and Symptoms

The child with a brain abscess may be asymptomatic during the initial period or may demonstrate nonspecific signs and symptoms including headache, fever, malaise, vomiting, confusion, seizures, motor deficits, sensory deficits, speech deficits, and leukocytosis. As the brain abscess enlarges, it produces signs of increased ICP, including a progressive headache, decreased level of consciousness, pupil dilation with sluggish or absent response to light (especially if uncal herniation develops), papilledema, cranial nerve deficits, and seizures. With enlargement of the abscess, progressive signs of increased ICP develop (see Increased Intracranial Pressure section in this chapter).

A brain abscess also can produce localizing symptoms. The child with a frontal lobe abscess may have contralateral hemiparesis, frontal headache, aphasia, or seizures. Temporal lobe abscesses can produce a temporal lobe headache and contralateral facial weakness. A cerebellar abscess often produces a postoccipital headache, nystagmus, ipsilateral ataxia, and limb weakness.^62,114

A lumbar puncture will reveal an extremely high CSF pressure, a normal or increased cell count (with polymorphonuclear lymphocytes), an increased protein concentration, and a normal glucose concentration (see Table 11-4). The brain abscess can be localized with a CT scan or MRI.

Management

Prompt initiation and continued administration of IV antibiotics is the key treatment for a brain abscess. Treatment of increased ICP also may be required (see Management in the Increased Intracranial Pressure section of this chapter).¹¹⁴

The most common pathogens causing brain abscesses include anaerobic bacteria, Gram-negative organisms, streptococci, and staphylococci. The underlying cause of the abscess usually determines the causative organism. In children with heart disease, α-hemolytic streptococcus is the most common organism, whereas streptococcus and Staphylococcus aureus are common organisms associated with subacute bacterial endocarditis. S. aureus is commonly seen in abscesses associated with trauma, whereas streptococci, pseudomonas, or H. influenzae are the typical pathogens isolated in patients with otitis or sinusitis (see the Table 11-12 for specific antibiotic choices).

If the abscess appears to be well encapsulated, surgical excision may be attempted. If complete excision is not possible, serial aspiration and irrigation of the abscess may be required.

Throughout the child's care, it is important for the nurse to monitor for signs of neurologic deterioration, because increased ICP can develop and progress rapidly. Even with aggressive medical and surgical treatment of brain abscess, mortality is significant, and survivors may have neurologic deficits and seizures.^62,114

Etiology

Encephalitis is defined as an inflammation of the brain parenchyma. It can be associated with other CNS infections such as meningitis, or it can be related to viral illness such as rabies or herpes simplex. In the neonatal population, enterovirus and adenovirus are responsible pathogens. In children, arboviruses and enteroviruses are common causes of encephalitis. Adenovirus, Epstein-Barr virus, West Nile virus, measles, mumps and varicella are responsible for a small portion of pediatric encephalitis cases.

Encephalitis may appear during the course of an acute viral illness, or it may follow an infection. The term encephalitis is used to indicate an infective or inflammatory cerebral disorder. The term encephalopathy is used to refer to any neurologic disorder of unknown or noninfectious cause associated with a change in level of consciousness, irritability, seizures, and motor or sensory deficit.¹¹⁴

Pathophysiology

Encephalitis probably results from a toxic or infectious agent that enters the brain. The inflammatory mediators released or triggered by the agent produce an inflammatory response that results in cerebral edema, cellular damage, neuronal destruction, and transient neurologic dysfunction.

In the temporal region an acute inflammatory demyelination may be seen in association with viral infections or post immunization. In this circumstance if there is no direct viral involvement of the CNS it is called postinfectious encephalitis. In cases where the spinal cord is involved, it is referred to as acute disseminated encephalomyelitis (ADEM).¹¹⁴

Clinical Signs and Symptoms

Children with encephalitis demonstrate symptoms during or immediately after an acute viral illness or following exposure to a toxic or inflammatory agent. Affected children usually complain of a headache and may demonstrate irritability, lethargy, a change in level of consciousness, nuchal rigidity, visual, auditory and speech disturbances, seizures, or loss of consciousness. High fever is usually not present.

Herpes simplex virus encephalitis generally presents in children 6 months to 18 years of age and is equally distributed between males and females. Herpes simplex virus usually produces an acute, hemorrhagic, necrotizing encephalitis with associated cerebral edema.^50,62

A lumbar puncture usually is performed to rule out a bacterial cause of the neurologic symptoms. It reveals normal CSF pressure, normal or increased cell count (lymphocytes may be elevated), normal or slightly increased protein concentration, and normal glucose concentration. The CSF culture and Gram stain will yield no bacterial growth, but serologic tests can aid in the diagnosis of a viral agent (see Table 11-4).

An EEG will reveal diffuse cortical inflammation with high-voltage discharges, usually from the temporal lobes. CT scans typically fail to demonstrate localized areas of infection, but they will show defined areas of edema, predominantly in the temporal lobes. Hemorrhagic lesions are seen on approximately 12% of scans.^50,62 MRIs are more sensitive than CT scans, revealing edema as high signals on T2 weighted images, primarily in the temporal lobes.⁵⁰

Management

Treatment of encephalitis is largely supportive, but acute encephalitis is considered an emergency. The child should be admitted to the pediatric critical care unit for close neurologic monitoring. These children can develop rapid neurologic deterioration, including coma. As always, support of airway, oxygenation, ventilation, and perfusion are priorities. Antibiotic administration is not indicated if the disease is viral or toxic in origin. If the toxic agent can be identified (e.g., a drug) and an antidote is available, it should be administered. Antiviral agents such as amantadine and rimantadine can be used in cases influenza infection.

Steroid use has not been shown to change outcomes in cases of acute viral encephalitis; however, they may be used in an effort to decrease cerebral and neuronal inflammation.¹¹⁴ In cases of acute disseminated encephalomyelitis, steroid administration is the initial treatment of choice.⁶⁷

If seizures are present, they may be refractory to typical anticonvulsant therapy. Refractory status epilepticus in the child with encephalitis may require a induction of a barbiturate coma using either pentobarbital or thiopental (see Barbiturate Coma in the Management section under Status Epilepticus).

Plasmapheresis to remove circulating cytokines and other inflammatory mediators is an accepted mode of therapy in children with acute disseminated encephalomyelitis who are refractory to steroid therapy.^67,89,105 Before initiating this mode of therapy, a large-bore double-lumen central venous catheter (e.g., a hemodialysis catheter) is placed. Intravenous immune globulin (IVIG) may also be used in children with encephalitis who are unable to produce an effective immune response.^32,114

Children with encephalitis should be monitored closely for signs of neurologic deterioration that may indicate greater inflammation or the development of increased ICP. Analgesics that do not produce respiratory depression (e.g., codeine) can be prescribed to relieve a persistent or severe headache. If the child complains of sensitivity to light or noise, a private room or isolated bed space is usually necessary to enable reduction of room light and noise and to minimize stimulation.

Children with encephalitis may demonstrate mild symptoms and a rapid recovery or may develop progressive and fatal neurologic deterioration. The prognosis is determined by the causative agent and the general health of the patient.

Etiology

Metabolic encephalopathies can be divided into three subgroups: endogenous intoxication related to accumulation of neurotoxic metabolites, energy failure related to a lack of metabolites needed for brain function, and acute water-electrolyte-endocrine disturbances.

Pathophysiology

In several disease processes, including liver failure and inborn errors of metabolism, the products of amino acid catabolism are not cleared or detoxified by either the liver or kidneys. These waste products (e.g., ammonia and urea) accumulate and affect organ function, often causing neurologic problems such as cerebral edema. Examples of these disorders include maple syrup urine disease, methylmalonic aciduria, and propionic aciduria.

Energy failure encephalopathies include hypoglycemia, thiamine deficiency, and mitochondrial energy metabolism defects. Water and electrolyte encephalopathies include diabetic ketoacidosis, nonketotic hyperosmolar coma, hyponatremia, and hypernatremia (see Chapter 12). Cerebral edema again is the cause.^66,117

Clinical Signs and Symptoms

Children with metabolic encephalopathy can exhibit progressive confusion, motor and sensory deficits, hallucinations, and seizures. Respiratory failure develops as the level of consciousness deteriorates. Signs and symptoms of cerebral edema and increased ICP may also be present. (See Increased Intracranial Pressure in the Common Clinical Conditions section of this chapter.)

Management

Treatment is determined by the etiology of the encephalopathy. Patients usually are admitted to the critical or intermediate care unit for skilled continuous nursing observation. Initial priorities of care include establishing and maintaining an adequate airway, ventilation, oxygenation, and systemic perfusion. Careful monitoring for signs of increased ICP is imperative. Hypoventilation and hypercapnia will further exacerbate the already increased ICP. If the child is unable to maintain a patent airway or breathe spontaneously, elective intubation and mechanical ventilation are indicated before the development of airway obstruction, hypoxia, and hypercarbia (see Chapter 9).

Etiology

Stroke is an acute loss of blood flow to a region of the brain that results in a loss of neurologic function. More than 3200 new strokes are diagnosed annually in children younger than 18 years.^38,107 Approximately 30 neonates per 100,000 births are affected; in the pediatric population stroke incidence is approximately 2 to 13 per 100,000 children per year.³⁸ The remainder of this section addresses stroke in infants beyond the neonatal period and in children.

Ischemic strokes usually occur within the first year of life, and subarachnoid hemorrhages are more common in the teenage population.³⁹ Those at high risk are males and African-Americans.^38,39 Prognosis in children is much better than in adults.

Cerebral vascular accidents and strokes are rare occurrences in children, but carry significant morbidity and mortality. Stroke is among the top 10 causes of childhood deaths, and more than 50% of survivors have cognitive and motor dysfunction. Increasing prevalence is likely related to improved imaging and recognition in addition to advances that allow children with predisposing conditions such as cancer, sickle cell disease, heart disease and neurologic disease to survive longer.^38,39,65,99

Pathophysiology

Many factors and disease processes predispose children to strokes. A preexisting condition that increases the child's risk of stroke is identified in only about half of pediatric stroke victims. Common preexisting conditions include congenital heart disease and sickle cell anemia. Other known causes are leukemia, brain tumors, Down syndrome, trauma, recent infection, vasculitis, and bleeding disorders. Strokes can be classified as either ischemic or hemorrhagic.

Ischemic strokes are the result of either a thrombus or embolism and are responsible for approximately 85% of all strokes. Emboli generally originate in the heart, but extracranial arteries are another source. Thrombi are occlusive, and the most common sites are in the cerebral artery branches. Turbulent blood flow can also increase the risk for thrombus formation. Other causes include sickle cell disease, protein C disorders, polycythemia, hypoperfusion, anemia, and prolonged vasoconstriction.

Hemorrhagic strokes are intracerebral hemorrhages affecting the brain parenchyma. These hemorrhages can occur in small arteries damaged from hypertension, or they result from rupture of aneurysms, arteriovenous malformations, bleeding disorders, or cocaine abuse.⁹⁹

Clinical Signs and Symptoms

Acute stroke in children can produce signs and symptoms such as nausea, emesis, headache, altered mental status, abrupt onset of hemiparesis, visual disturbances, ataxia, and aphasia. Symptoms may be single or occur in combination. It is imperative to establish the precise time of the onset of symptoms, because it can affect the potential use of thrombolytics for ischemic stroke.

Management

All children suspected of having an acute stroke require blood sampling on admission for initial serum chemistries (electrolytes, glucose, calcium, and BUN), complete blood count, and coagulation studies, including activated partial thromboplastin time (aPTT). A comprehensive urine toxicology screen is performed to rule out any toxins or drugs that can produce signs similar to a stroke. Additional testing may include lupus anticoagulant; antiphospholipid antibody; dilute Russell viper venom time; anticardiolipin immunoglobulin (Ig) G, IgM, IgA; antiphosphotidyl serine IgG, IgM, IgA; anti-β2 glycoprotein IgG, IgM, IgA; fasting lipid profile; cholesterol; lipoprotein A; plasma homocysteine; varicella titers; organic and amino acids; factor V Leiden; antinuclear antibody, erythrocyte sedimentation rate; and C-reactive protein. The child is evaluated for mitochondrial myopathy, encephalomyopathy, lactic acidosis, and stroke—a family of inherited mitochondrial cyopathies.

Noncontrast CT, CT angiography, and MRI are the mainstays of imaging for stroke diagnosis. The noncontrast CT is completed and read soon after the child's arrival to quickly differentiate ischemic from hemorrhagic insults. In adult acute stroke guidelines, the recommended goal for completion of the CT image is 25   minutes or less from the time of hospital arrival, with CT image interpretation within 45   minutes of hospital arrival.⁴ Although the sensitivity and specificity of CT has not been shown in children, expert consensus supports its use.¹⁰⁷ However, it is often necessary to stabilize the child's condition before the CT scan.

CT angiography can identify filling defects and localize specific portions of the vessel that may be the cause of the stroke. MRI is sensitive in detecting both acute ischemic and hemorrhagic strokes. A cardiac echocardiogram should be obtained to rule out cardiac embolism as a cause of the stroke. Children with suspected strokes are admitted to the critical care unit for skilled continuous nursing observation. Obviously, establishing and maintaining an adequate airway, ventilation, and systemic perfusion are priorities.

Etiology

The term drowning is used to describe a submersion event producing primary respiratory impairment.⁸⁷ The victim typically requires some form of resuscitation (stimulation, rescue breathing, or compressions and ventilations). After a drowning event, the child may survive with or without significant neurologic impairment.

There are three categories of children at risk for drowning injuries: infants, children 1 to 4 years of age (toddlers and preschoolers), and adolescents. Infants usually drown in bathtubs and children 1 to 4 years of age are typically found submerged in shallow wading pools, home swimming pools, or spas.^22,33 Adolescents often drown in natural bodies of water, and alcohol or diving injuries are often involved.

Pathophysiology

The pulmonary complications of submersion are summarized in Chapter 9. The following paragraphs address only the potential neurologic complications of submersion. Within 3   minutes of submersion, most patients will develop sufficient hypoxia and cerebral ischemia to produce loss of consciousness. If submersion continues, CNS dysfunction develops; further ischemia and hypoxia can produce brain death.

The hypoxic-ischemic insult during the submersion may not be immediately fatal. Cardiopulmonary resuscitation can produce the return of spontaneous circulation. However, profound cerebral cellular damage, cerebral edema, and reperfusion injury may develop. This edema may produce signs of increased ICP as late as 48 to 72 hours or longer after the submersion episode.

The severity of neurologic sequelae following submersion is related to the severity of the primary hypoxic insult and any secondary insults that occur. The severity of the primary insult is affected by the duration of immersion, the temperature of the submersion water, and the time that elapsed before effective cardiopulmonary resuscitation was provided. Secondary neurologic insults (e.g., hypotension, further hypoxic episodes, hyperthermia, decreased CBF) may occur after initial return of spontaneous circulation.⁸⁷ The time of submersion as reported by bystanders is notoriously unreliable, so it is often impossible to determine the duration of cardiopulmonary arrest.

Submersion can stimulate the diving reflex. This reflex results in initial apnea, loss of consciousness, bradycardia, hypertension, and shunting of blood to vital organs and away from the skin and splanchnic vascular beds. When very small children are submerged in very cold water (<5° C), the diving reflex can slow metabolic rate and redistribute blood flow sufficiently to prevent profound neurologic injury. However, such protection cannot be assured, and intact survival following prolonged submersion is rare.²²

Clinical Signs and Symptoms

Unless the submersion is extremely brief, most children are apneic and flaccid when pulled from the water. If high-quality cardiopulmonary resuscitation is immediately initiated, many of these children will demonstrate a perfusing cardiac rhythm and spontaneous respirations on arrival in the emergency department; these children are likely to recover completely from the episode. The presence of any spontaneous movement or posturing on arrival in the emergency department and even within the first 24   hours after submersion is consistent with neurologic recovery.⁸⁷

No predictive factors evaluated during resuscitation can determine the outcome of drowning victims, so aggressive resuscitation and post-resuscitation care are generally indicated for the first hours following the submersion.⁸⁷

If skilled resuscitation was performed at the scene and during transport, and the normothermic child is asystolic on arrival in the emergency department, reported outcome is poor.²² Additional poor prognostic indicators include absence of purposeful movement at 24   hours after admission.⁸⁷

Serial neurologic examinations are required for children who remain comatose or severely impaired after return of spontaneous circulation and admission to the critical care unit.⁸⁷ If these children receive aggressive hemodynamic support, it may be possible to restore effective systemic perfusion, but the child with severe hypoxic brain injury may never recover significant neurologic function. Therefore, the indication for aggressive or prolonged resuscitation beyond the first 24   hours should be considered carefully, and the parents should be included in these discussions.

Management

If the drowning victim is responsive after resuscitation, further neurologic support is typically not required. The child should be monitored closely, and aggressive respiratory support may be needed to treat pulmonary complications (see Chapter 9).

If the child with severe neurologic injury is supported vigorously during the first hours after the drowning episode, the child may demonstrate some gasps within 12 to 24 hours. However agonal gasps indicate brain stem function and do not indicate neurologic recovery.

Signs of increased ICP can develop 48 to 72 hours after submersion. There is currently no evidence that aggressive therapy to treat increased ICP and limit secondary neurologic injury is beneficial for drowning victims with increased ICP. ^22,87 At this time, immediate resuscitation and therapeutic hypothermia are the only therapies that have been shown to improve neurologic outcome following hypoxic-ischemic brain injury, and evidence comes largely from the neonatal population. More data are needed regarding effectiveness of therapeutic hypothermia in children following resuscitation.

The parents of the drowning victim will need a great deal of compassionate support. They should be included in discussions and decisions to limit care or to pursue aggressive resuscitation and postresuscitation support (see Withholding and Withdrawing Care in Chapter 24).

If the child develops brain death, the parents should be offered the option of organ donation (see the Brain Death and Organ Donation section of this chapter). Support of the parents is reviewed in Chapter 3.

Definition and Purpose

A lumbar puncture, or spinal tap, is performed by introducing a needle into the subarachnoid space of the lumbar spinal canal. The needle is inserted with a stylette into the interspace between the third and fourth lumbar vertebrae; puncture at this level avoids damage to the spinal cord.^36,118

The lumbar puncture can be performed to examine the CSF, to measure CSF pressure, or to introduce medication, air, or radiopaque contrast material into the subarachnoid space. The lumbar puncture will aid in the diagnosis of intracranial or intraventricular hemorrhage if blood is present in the CSF.

The CSF can be sent for culture, Gram staining, cell count, and glucose and protein content to aid in the diagnosis of CNS infection or inflammation. In addition, anesthesia or antibiotics can be introduced into the subarachnoid space to reduce pain or treat infection, respectively. Finally, injected air or radiopaque contrast material can be used to outline subarachnoid structures or identify CSF obstructions or leaks. In the pediatric critical care unit, the lumbar puncture is used most often to confirm the diagnosis of CNS infection.¹¹⁸

Procedure

The lumbar puncture is safe when it is performed correctly by an experienced provider. Before the procedure, the child should be examined carefully for signs of increased ICP. If these signs are present in the infant, the lumbar puncture may proceed with caution if a CSF sample is absolutely necessary to identify and treat CNS disease. If, however, signs or suspicion of increased ICP are present in an older child with fused cranial sutures, the lumbar puncture should be postponed because the sudden release of CSF and pressure by the lumbar puncture can result in herniation of the medulla through the foramen magnum.

The procedure should be explained to the child carefully and in an age-appropriate manner. The child is placed in the knee-chest position, either sitting or lying on the side with the neck flexed toward the knees; this position maximizes separation of the vertebral bodies. The position must be modified if the child is intubated or has major trauma and fractures. The child should be held firmly to prevent excessive movement during the lumbar puncture.^36,118

Once the child is positioned, the back is draped and the puncture area is identified and scrubbed with a surgical preparation, such as chlorhexidine. The remainder of the procedure is then performed using strict sterile technique. Local anesthesia may be obtained by infiltrating lidocaine intradermally around the puncture site. If time is not a factor in obtaining samples, alternative anesthesia can be provided by using topical analgesic ointments (see Chapter 5). Such agents typically provide local numbness in 15 to 30 minutes.

The needle and stylette are inserted firmly into the subarachnoid space. Frequently a sharp sound is heard when the dura is pierced. The stylette should always remain in place when advancing the needle into the skin and past the subcutaneous tissue. This technique avoids introducing epidermal cells into the spinal canal that can lead to an iatrogenic epidermoid tumor. Once the needed is inserted into the subarachnoid space, the stylette is withdrawn.⁵⁰

As soon as the subarachnoid space is entered, the opening CSF pressure is obtained with a manometer. A few drops of CSF are then allowed to drain from the needle. Additional CSF is collected in three or more sterile sampling tubes as follows:

Additional tubes are used as needed for viral cultures or other special studies.

The nurse and provider performing the lumbar puncture will observe and later record the appearance of the CSF in the sampling tubes. If red blood cells result from a traumatic tap, the fluid should be clear by the time the final tube is filled. If intracranial hemorrhage is present, the final CSF sampling tube will still contain red blood cells. CSF cloudiness is usually abnormal and often indicates the presence of infection. Xanthochromia (yellow discoloration of the CSF) may be caused by hyperbilirubinemia or the presence of hemolyzed red blood cells. Changes in the CSF content with common CNS diseases are listed in Table 11-4.⁶²

After samples are obtained, the CSF closing pressure is measured, the needle is withdrawn, and a small dressing is placed over the area of the puncture site. If iodine was used as a preparation, it is removed before placing a dressing or adhesive bandage.

Nursing Responsibilities and Complications

It is the nurse's responsibility to prepare the child (as age appropriate) and family for the procedure. The nurse is also responsible for positioning, monitoring, and comforting the child throughout the procedure. The nurse will administer analgesics as ordered and monitor the child closely for effects and side effects of these drugs (see Chapter 5). In addition, the nurse is responsible for verifying the accurate labeling of all CSF samples and ensuring that samples are sent for analysis.

An uncommon but devastating potential complication of a lumbar puncture is brain stem herniation. Therefore, during and after the lumbar puncture, the nurse must monitor for signs of deterioration of neurologic status that could indicate brain stem herniation. These signs include decreased responsiveness, tachycardia or bradycardia, unilateral or bilateral pupil dilation with sluggish constrictive response to light, hypertension with widening pulse pressure, irregular breathing (including apnea), and abnormal posturing. These signs should be reported immediately to an on-call provider, and efforts should be made to reduce ICP.

Additional complications of the lumbar puncture include severe headache and bleeding from the puncture site.^50,62 The child should lie flat (unless signs of increased ICP are present) for 4 to 6 hours after the procedure to reduce the possibility and severity of headaches. Analgesics and intravenous fluids (unless contraindicated) will be given as needed to treat the headache, per provider order.

Definition and Purpose

The EEG is a recording of the electrical potentials that arise from the brain. These potentials can be quantified, localized, and compared with established, normal EEGs for the patient's age to aid in the diagnosis of seizure activity or CNS injury or dysfunction.⁶² An isoelectric (flat) EEG in the nonhypothermic, nonsedated patient is one of the criteria used to confirm cerebral death in patients with no clinical evidence of brain function.

Procedure

The EEG is recorded by placing approximately 17 to 21 electrodes on the surface of the frontal, parietal, occipital, and temporal areas of the scalp and over the ear. A unique electrode placement is required if the EEG is performed to confirm brain death (see Confirmatory Tests in the Criteria for Pronouncement of Brain Death section of this chapter). The EEG electrodes are fixed with an acetone-soluble paste to prevent electrode movement during the study. The EEG is performed when the patient is reclining and still. When this study is required in critically ill patients, it is usually performed in the critical care unit.

The EEG is typically recorded continuously for 20   minutes; longer recordings will be necessary if additional studies, such as the measurement of brain-stem evoked auditory potentials or the confirmation of brain death, are requested. Because the cerebral electrical activity must be magnified to provide a visible recorded signal, patient movement and electrical (equipment) artifact must be reduced to a minimum. Because extraneous or sudden noise or lights can stimulate cranial nerve electrical activity, they should also be minimized during the recording. If the child is alert and mobile, sedation may be required (see Chapter 5).

The EEG usually is recorded during sleep (or coma), and the recording often is continued during hyperventilation and with photic (rhythmic light flash) stimulation. The sleep EEG allows analysis of baseline activity, and hyperventilation is used to accentuate abnormal EEG findings. A 2-minute, rhythmic light flash (photic stimulation) may be used to attempt to induce seizure activity during the recording.

Brain stem-evoked responses can be tested to evaluate cranial nerve responses and to detect early evidence of cranial nerve damage. This testing is particularly useful in the newborn or comatose patient when response to painful stimuli is difficult or impossible to detect.

The brain stem-evoked auditory response is obtained by recording electrical activity over the auditory pathway after provision of a standard auditory stimulus. If the acoustic nerve itself is damaged, early conduction of the impulse through the nerve will be prolonged or diminished; this can occur, for example, as a complication of drug therapy and resultant ototoxicity. If brainstem disease or dysfunction is present, conduction of the auditory impulse through the nerve will be normal, but the time required for the impulse to travel between the auditory nerve and the brainstem will be prolonged.

Nursing Responsibilities and Complications

Before the EEG is obtained, the nurse will describe the procedure to the child (as age appropriate) and the parents. Important points to emphasize include the fact that the procedure is painless, and (if applicable) that the child will be given medication to make him or her drowsy during the procedure. In addition, the child should be told that some special soap (acetone) is used to clean the hair after the procedure, because the acetone has a distinctive and noxious odor. If the child is awake and alert, the nurse may administer a sedative if ordered. Care should also be taken to fully remove all traces of the electrode gel from the child's head after the EEG, because the paste can cause superficial burns if it remains in place during an MRI.

During the EEG, it is important that the nurse avoid touching or stimulating the patient more than is absolutely necessary. Lights should be dimmed and noises should be reduced to a minimum. The nurse should remain near the child's bedside throughout the EEG to monitor the child, answer questions, and provide hyperventilation or additional sedation as ordered and indicated. There are no complications resulting from a standard EEG.

Definition and Purpose

The CT scans the head in successive layers, using x-ray beams passing throughout the head in multiple directions. For a traditional CT, the information obtained is then constructed into images in a cross-sectional format. Each picture is referred to as a slice or cut. Multi-view imaging is now used to create 3-dimensional CT volume rendering images to evaluate structures of the head and brain (Fig. 11-20) and to create images in many views.

Fig. 11-20 Multi-view imaging of 10 month-old girl with head injury from a motor vehicle collision. A, Three-dimensional (3D) computed tomography (CT) volume rendering image shows a fracture of the frontal bone (see arrow). B, This traditional axial CT image provides a view looking up to the patient’s head (so the patient’s left side appears on the right of this image and the patient’s right side appears on the left side of this image; the front of the patient is at the top of the image and the back of the patient’s head is at the bottom of the image). Severe compression of the right lateral ventricle (CSF appears as a black density) is apparent, and a midline shift (toward the patient’s left side) is present. A large subdural hemorrhage is visible as a white density along the outer edge of the patient’s right cerebral hemisphere. C, Coronal CT image is interpreted as if the viewer is facing the patient. It shows the large subdural hemorrhage on the patient’s right side (the white density), the compression of the patient’s right lateral ventricle, and the midline shift toward the patient’s left. D, Sagittal CT image (from the side), shows the large subdural hemorrhage (it appears as white against the grey-white matter of the brain). In B, C, and D, there is diffuse loss of normal grey-white differentiation due to cerebral infarction.

(Images courtesy of Dr. Chetan Shah, Department of Pediatric Radiology, Arkansas Children’s Hospital.)

The CT scan is a reliable, painless, safe, and noninvasive method of visualizing a variety of neurologic disorders, including space occupying lesions, hematomas, hemorrhage, hydrocephalus, brain abscess, and cortical atrophy. The images produced by the scan allow differentiation of intracranial spaces and normal gray and white matter.^62,86 This scan has eliminated or reduced the need for many other more invasive diagnostic neurologic tests; it is the most useful test available in the evaluation of children with head trauma (see Fig. 11-12).⁸⁰

Procedure

This procedure must be performed in the neuroradiology department. The child is positioned supine on a mobile platform that is slid toward and into the scanner so the child's head is positioned within the scanner. A portion of the scanner will move around the child's head to direct the x-ray beam at many different angles; hundreds of radiographs are obtained and reconstructed during the scan.

The CT scan takes approximately 15   minutes. Occasionally, contrast agents are administered intravenously immediately before the scan to enable better visualization of intracranial structures.⁸⁰

Nursing Responsibilities and Complications

The nurse will prepare the child and family for the procedure, including a discussion of the noises that the child will hear during the scan. The nurse accompanies the child to the scanner, ensures that all tubes and catheters are secure during any movement into and out of the scanner and during the scan itself, and monitors the child during the procedure itself. Because the child must remain absolutely still throughout the procedure, sedatives and/or analgesics are administered before the procedure is performed on a conscious and alert child (see Chapter 5).

During the procedure, healthcare personnel and radiology technicians are positioned behind a lead screen to minimize stray radiation exposure. The nurse must be able to see the child throughout the procedure and ensure proper functioning of the child's IV equipment and mechanical ventilation support. Children in unstable condition must be monitored closely throughout the procedure.

The risk of complications associated with CT scans is relatively low. The typical dose of radiation emitted during a scan is essentially equivalent to natural sources of radiation.^62,86

If a contrast agent is injected before the scan, the nurse must monitor for signs of a reaction to the contrast material and for evidence of complications similar to those occurring after cerebral angiography. Before contrast agents are administered, it is important to identify any previous reaction to contrast agents. In addition the healthcare team must be aware of the patient's baseline renal function, including BUN and creatinine concentrations, because these may rise after the use of contrast media. After the procedure, the nurse must monitor the child's urine output and serum BUN and creatinine and notify an on-call provider if urine output is inadequate or if the BUN or serum creatinine rise significantly.

Definition and Purpose

MRI is the application of a strong external magnetic field around the patient to generate images of the body. This magnetic field causes rotation of the cell nuclei in a predictable direction at a predictable speed. The result of this rotation of nuclei is a resonant image that is extremely well defined, enabling visualization of soft tissues better than any other noninvasive device. Visualization of tumors, shunts, and organ or tissue thickness is excellent using MRI. The MRI scan enables detailed visualization of areas of spinal cord compression after trauma. Because this device does not use any radiation, there are no complications related to radiation exposure (Fig. 11-21).

Fig. 11-21 Magnetic resonance imaging. Normal midline sagittal magnetic resonance imaging scan of the entire spine. A, Cervical spine. B, Thoracic spine. Note in detail the cord (closed arrows), the conus medullaris (open arrow), and the bones and intervertebral discs.

(From Mercier LR: Practical orthopedics, ed 6, St Louis, 2008, Mosby, fig. 16-84, A-C.)

Procedure

The MRI scanner typically is located well away from critical care units. At present, scanning can be performed only on patients in relatively stable condition, because no metal-constructed mechanical devices can be placed in proximity to the magnetic field. Although all-plastic mechanical ventilators are available for use in the MRI scanner, monitoring systems cannot be used. Thus, MRI is most likely to be used in pediatric patients recovering from critical illness or injury.

Nursing Responsibilities

There are no known complications of MRI scanning. The nurse must be able to monitor the patient closely during the procedure, and this may be difficult with some units. MRI scanning is time consuming and requires the nurse and patient to be away from the unit for long periods of time. Prior to placing the patient in the MRI scanner, the nurse should insure that all metal objects have been removed from the patient and that appropriate MRI monitoring equipment is available.

Depending in the size of the child and the study ordered, a scan of the brain and entire spine with and without contrast can take up to hours to complete. The nurse should anticipate the need for additional doses of sedation and analgesia and possibly neuromuscular blockers if the patient is not receiving continuous infusions of these drugs (see Chapter 5).

When contrast media are used, it is important for the nurse to identify any history of previous reactions to contrast agents, and the child's current renal function, including BUN and serum creatinine. After the procedure, the nurse must monitor the child's urine output and serum BUN and creatinine and then notify an on-call provider if urine output is inadequate or the BUN or serum creatinine rise significantly. If a patient has a programmable ventriculoperitoneal shunt, the shunt programming is checked by a member of the neurosurgery team after the procedure to verify correct settings and function.

Definition and Purpose

Skull roentgenography (or a skull radiographs or films) enable evaluation of cranial bone relationships and densities and the size and shape of the skull. Skull radiographs are helpful in the diagnosis of skull deformities or fractures, head injuries, and bone erosion or calcification secondary to space occupying lesions. Skull radiographs, however, are often not helpful in the identification of intracranial abnormalities, such as brain tumors or head injury unless they also affect the bony structures.

A complete radiographic study of the skull includes anteroposterior and lateral views of the skull and an oblique anteroposterior view or other special angles as indicated by the child's presumed diagnosis.^62,78

Procedure

Preferably, skull radiographs are obtained in the radiology department so that the patient's head can be immobilized and good quality radiographs can be obtained. If this is impossible, portable radiographs are obtained in the critical care unit. The radiology technician will assist in positioning the child appropriately for each film.

Nursing Responsibilities and Complications

The child (as appropriate for age and clinical condition) and family require explanations about the need for radiographs and about any special positioning required. The nurse must monitor the child closely throughout the procedure. If an ICP monitoring system is in place, it is especially important to monitor the effects of changes in head position on the ICP and request modifications in these positions as needed to maintain the ICP under appropriate thresholds. The procedure is painless.

Definition and Purpose

In cerebral angiography, a radiopaque contrast agent is injected into the cerebral arterial system to enable radiographic visualization of the cerebral circulation. The progress of the contrast material through the cerebral circulation is recorded with radiographs for further study. Angiography is helpful in the diagnosis of intracranial tumor, hematoma, arterial aneurysm, and arteriovenous fistula and is the definitive diagnostic procedure for arteriovenous malformation (AVM).⁶²

Procedure

Contrast material, usually an iodine-containing material is injected into a selected cerebral vessel—typically the internal carotid artery. Sequential radiographs of the head are then made. This procedure usually is performed in the radiology department.

Nursing Responsibilities and Complications

The child (as appropriate for age and clinical condition) and parents require a brief explanation of the procedure. It is usually best to limit the explanation to the child to only those things that will be seen, heard, or felt; the alert child may be frightened or intrigued by the x-ray equipment.

Because the child will be transported to the radiology department for the angiography, the nurse is responsible for monitoring the child's condition during transport to and from the radiology department and throughout the procedure itself. If the child is intubated or in unstable condition, a provider able to re-intubate and prescribe drugs will accompany the bedside nurse and the child.

If contrast media are used, it is important for the nurse to be aware of the child's baseline renal function and current BUN and creatinine levels. A reaction to the contrast agent can occur after angiography. Mild symptoms may include urticaria, rhinorrhea, nausea, retching and/or vomiting, diaphoresis, coughing, and dizziness. Moderate symptoms may include vomiting, diffuse urticaria, headache, facial edema, laryngeal edema, mild bronchospasm, or dyspnea, tachycardia, bradycardia, hypertension, and abdominal cramps. Severe symptoms include life-threatening arrhythmias, hypotension, bronchospasm, pulmonary edema, seizures, syncope, and even death.^82,113 Treatment of anaphylactic shock requires volume administration and administration of vasopressors and antihistamines (see Chapter 6).

After the procedure, the nurse must monitor the child's urine output and serum BUN and creatinine levels. An on-call provider should be notified if urine output is inadequate or the BUN or serum creatinine levels rise significantly