46: The child with cerebral dysfunction

History

A family history can sometimes offer clues regarding possible genetic disorders with neurologic manifestations. A review of family members often identifies conditions that might otherwise be overlooked, especially increased number of miscarriages or siblings or relatives who died at an early age. The nurse asks questions regarding specific neurologic problems, such as intellectual and developmental disabilities, deafness, epilepsy, blindness, unusual movements, weakness, ataxia, stroke, and progressive mental deterioration. History of consanguinity is also important.

A health history provides valuable clues regarding the cause of neurologic dysfunction. A history is assessed for injury with loss of consciousness, febrile illness, an encounter with an animal or insect, ingestion of neurotoxic substances, inhalation of chemicals, past illness, and known diabetes mellitus or sickle cell disease. Sudden or progressive alterations in movement or mental abilities may provide clues for investigation. It is also important to ascertain the chronologic course of the illness.

Physical examination

Physical examination includes observation of the size and shape of the head (particularly in the infant and young child), spontaneous activity and postural reflex activity, and sensory responses. Note whether the patient is lethargic, drowsy, stuporous, alert, active, or irritable. The nurse also observes the overall tone, noting whether there is a normal flexed posture or one of extreme extension, opisthotonos, or hypotonia. Symmetry of movement is also assessed.

Facial features may suggest a specific syndrome. A high-pitched, piercing cry in an infant is often associated with CNS disorders. An abnormal respiratory cycle, such as prolonged apnea, ataxic breathing, paradoxic chest movement, and hyperventilation, may be the result of a neurologic problem.

Older children can be evaluated by the usual methods used in a neurologic examination. In addition, an estimation of the level of development provides essential information about neurologic function. This assessment is discussed throughout the book in relation to evaluation for specific disorders such as intellectual and developmental disabilities, failure to thrive, attention-deficit/hyperactivity disorder, cerebral palsy, cerebral tumors, and other physical or behavioral problems. Developmental screening tests can assess developmental progress in the young child.

Muscular activity and coordination, including ocular movements and gait, are valuable sources of information. Ocular movements, pupillary response, facial movements, and mouth functions provide clues regarding CNS involvement or impingement. (See Chapter 29 for CNS and reflex testing.) Testing reflexes, strength, and coordination and for the presence and location of tremors, twitching, tics, or other unusual movements is also an aspect of the neurologic assessment.

Etiology

An altered state of consciousness may be the outcome of several processes that affect the CNS. Impaired neurologic function can result from a direct or indirect cause. Some altered states, such as the diffuse changes observed in encephalitis, are directly related to cerebral insult. Others are the result of dysfunction in other organs or processes. For example, biochemical changes can impair neurologic function without morphologic findings, as in hypoglycemia.

Level of consciousness

Assessment of LOC remains the earliest indicator of improvement or deterioration in neurologic status. LOC is determined by observations of the child’s responses to the environment. Other diagnostic tests, such as motor activity, reflexes, and vital signs, are more variable and do not necessarily directly parallel the depth of the comatose state. The most consistently used terms are described in Box 46.2.

Coma assessment

Diminished alertness as a result of pathologic conditions occurs on a continuum and is designated as the comatose state, which extends from somnolence at one end to deep coma at the other. To produce coma, one of the following must occur: (1) extensive, diffuse, bilateral cerebral hemispheric destruction (the brainstem may be intact); (2) a lesion in the diencephalon; or (3) destruction of the brainstem down to the level of the lower pons.

Several scales have been devised in an attempt to standardize the description and interpretation of the degree of depressed consciousness. The most popular of these is the Glasgow Coma Scale (GCS), which consists of a three-part assessment: eye opening, verbal response, and motor response. The GCS was created to meet a clinical need to identify criteria for the consciousness level. For clinical purposes, the primary role of observation of the LOC is to detect a life-threatening complication such as cerebral edema. The GCS requires observational skills and is readily reproducible between observers.

A pediatric version of the GCS recognizes that expected verbal and motor responses must be related to the child’s age (Fig. 46.2). The pediatric coma scale does not assess verbal responses as such but records smiling, crying, and interaction. It uses a six-point motor scale that is inappropriate for children younger than 6 months of age. In children younger than 5 years of age, speech is understood to be any sound at all, even crying. Young children demonstrate orientation by identifying their parents correctly or giving their own names. When assessing LOC in young children, the nurse may find it helpful to have a parent present to help elicit a desired response. An infant or child may not respond in an unfamiliar environment or to unfamiliar voices.

Numeric values are assigned to the levels of response in each category. The sum of these numeric values provides an objective measurement of the patient’s LOC. The lower the score, the deeper the coma. A person with an unaltered LOC would score the highest, 15; a score of 8 or below is generally accepted as a definition of coma; the lowest score, 3, indicates deep coma or death.

The GCS in itself is not sufficient to determine depressed consciousness in all children. For example, because a child with quadriplegia cannot respond to commands physically, the child’s GCS can be very low but the child may be cognitively intact. Nevertheless, the GCS provides a more objective method for evaluating the state of consciousness in most cases. Severely injured children (GCS ≤ 8) may have a consistent grading of motor response, verbal response, and eye opening.

The GCS score performed during preadmission (i.e., assessment in the field), in the emergency department, and throughout the inpatient admission is universally accepted as one criterion to determine the patient’s prognosis (Braine & Cook, 2017). GCS scores of 5 or less are associated with poor outcome (Murphy, Thomas, Gertz, et al., 2017).

Vital signs

Pulse, respiration, and blood pressure provide information on the adequacy of circulation and the possible underlying cause of altered consciousness. Autonomic activity is most intensively disturbed in deep coma and in brainstem lesions. Body temperature is often elevated; sometimes the elevation is extreme. High temperature is most often a sign of an acute infectious process or heatstroke, but it may be caused by ingestion of some drugs (especially salicylates, alcohol, and barbiturates) or by intracranial bleeding, especially subarachnoid hemorrhage. Hypothalamic involvement may cause elevated or decreased temperature. Serious infection may produce hypothermia.

The pulse is variable and may be rapid, slow and bounding, or feeble. Blood pressure may be normal, elevated, or very low. The Cushing reflex, or pressor response that causes a slowing of the pulse and an increase in blood pressure, is uncommon in children; when it does occur, it is a very late sign of increased ICP. Medications can also affect vital signs. For assessment purposes, actual changes in pulse and blood pressure are more important than the direction of the change.

Respirations are more often slow, deep, and irregular. Slow and deep breathing often occurs in the heavy sleep caused by sedatives, after seizures, or in cerebral infections. Slow, shallow breathing may result from sedatives or opioids. Hyperventilation (deep and rapid respirations) is usually the result of metabolic acidosis or abnormal stimulation of the respiratory center in the medulla caused by salicylate poisoning, hepatic coma, or Reye syndrome (RS). A pattern of alternating hyperventilation and breath holding during wakefulness is common in Rett syndrome.

Breathing patterns have been described with a number of terms (e.g., apneustic, cluster, ataxic, Cheyne-Stokes). However, it is better to describe what is being observed rather than placing a label on it, because the terms are often used and interpreted incorrectly. Periodic or irregular breathing is a sign of brainstem (especially medullary) dysfunction. This is an ominous sign that often precedes complete apnea. The odor of the breath may provide additional clues (e.g., the fruity and acetone odor of ketosis, the foul odor of uremia, the fetid odor of hepatic failure, or the odor of alcohol).

Skin

The skin may offer clues to the cause of unconsciousness. The body surface should be examined for injury, needle marks, petechiae, bites, and ticks. Evidence of toxic substances may be found on the hands, face, mouth, and clothing—especially in small children.

Eyes

Assess pupil size and reactivity (Fig. 46.3). Pupils either do or do not react to light. Pinpoint pupils are commonly observed in poisoning (e.g., opiate or barbiturate poisoning) or in brainstem dysfunction. Widely dilated and reactive pupils are often seen after seizures and may involve only one side. Widely dilated and fixed pupils suggest paralysis of cranial nerve (CN) III (oculomotor nerve) secondary to pressure from herniation of the brain through the tentorium. A unilateral fixed pupil usually suggests a lesion on the same side. Bilateral fixed pupils, if present for more than 5 minutes, usually imply brainstem damage. Dilated and nonreactive pupils also occur in hypothermia, anoxia, ischemia, poisoning with atropine-like substances, or prior instillation of mydriatic drugs. Some of the therapies used (e.g., barbiturates) can alter pupil size and reaction.

The description of eye movements should indicate whether one or both eyes are involved and how the reaction was elicited. Ask the parents if the child has strabismus, which may cause the eyes to appear misaligned.

Blinking observed at rest or in response to a sudden loud noise or bright light implies that the pontine reticular formation is intact. The corneal reflex, blinking of the eyelids when the cornea is touched with a wisp of cotton, can test the integrity of the ophthalmic division of cranial nerve (CN) V (trigeminal nerve). Posttraumatic strabismus indicates CN VI (abducens nerve) damage.

Eye movements are assessed by the doll’s head maneuver, in which the child’s head is rotated quickly to one side and then to the other. When the brainstem centers for eye movement are intact, there is conjugate (paired or working together) movement of the eyes in the direction opposite the head rotation. Absence of this response suggests dysfunction of the brainstem or CN III. Downward or lateral deviation is often observed in association with pupillary dilation in dysfunction of CN III.

The caloric test, or oculovestibular response, is elicited by irrigating the external auditory canal with 10 mL of ice water over a period of approximately 20 seconds (with the head of bed elevated at a 30-degree angle). This test normally causes movement of the eyes toward the side of stimulation. This response is lost when the pontine centers are impaired and thus provides important information in assessment of the comatose patient.

Funduscopic examination reveals additional clues. Because it takes 24 to 48 hours to develop, papilledema (e.g., optic disc swelling, indistinct margins, hemorrhages, tortuosity of vessels, absence of venous pulsations), if it develops at all, will not be evident early in the course of unconsciousness. The presence of retinal hemorrhages in children is usually the result of accidental or inflicted trauma with intracranial bleeding (usually subarachnoid or subdural hemorrhage) but is sometimes caused by infection (Minns, Jones, Tandon, et al., 2017).

Motor function

Observation of spontaneous activity, posture, and response to painful stimuli provides clues to the location and extent of cerebral dysfunction. Asymmetric movements of the limbs or the absence of movement suggests paralysis. In hemiplegia the affected limb lies in external rotation and falls uncontrollably when lifted and allowed to drop. Observations should be described rather than labeled.

In the deeper comatose states, the child has little or no spontaneous movement, and the musculature tends to be flaccid. There is considerable variability in motor behavior in lesser degrees of coma. For example, the child may be relatively immobile or restless and hyperkinetic; muscle tone may be increased or decreased. Tremors, twitching, and spasms of muscles are common observations. The patient may display purposeless plucking or tossing movements. Combative or negativistic behavior is not uncommon. Hyperactivity is more common in acute febrile and toxic states than in cases of increased ICP. Seizures are common in children and may be present in coma as a result of any cause. Any repetitive movements and movements during seizures are described.

Posturing

Primitive postural reflexes emerge as cortical control over motor function is lost in brain dysfunction. These reflexes are evident in posturing and motor movements directly related to the area of the brain involved. Posturing reflects a balance between the lower exciting and the higher inhibiting influences. Strong muscles overcome weaker ones. Flexion posturing (Fig. 46.4A) occurs with severe dysfunction of the cerebral cortex or with lesions to corticospinal tracts above the brainstem. Typical flexion posturing includes rigid flexion, with arms held tightly to the body; flexed elbows, wrists, and fingers; plantar flexed feet; legs extended and internally rotated; and possibly fine tremors or intense stiffness. Extension posturing (see Fig. 46.4B) is a sign of dysfunction at the level of the midbrain or lesions to the brainstem. It is characterized by rigid extension and pronation of the arms and legs, flexed wrists and fingers, clenched jaw, extended neck, and possibly an arched back. Unilateral extension posturing is often caused by tentorial herniation.

Posturing may not be evident when the child is quiet but can usually be elicited by applying painful stimuli such as a blunt object pressed on the base of the nail. Nurses should avoid applying thumb pressure to the supraorbital region of the frontal bone (risk of orbital damage). Noxious stimuli (e.g., suctioning), turning, or touching will elicit a response. When the nurse is describing posturing, the stimulus needed to provoke the response is as important as the reaction.

Reflexes

Testing of certain reflexes, such as those present in an intact spinal cord, may be of limited value (see Chapter 46). In general, the corneal, pupillary, muscle-stretch, superficial, and plantar reflexes tend to be absent in deep coma. The state of reflexes is variable in lighter grades of unconsciousness and depends on the underlying pathologic process and the location of the lesion. The doll’s eye reflex maneuver, described previously, reflects paralysis of CN III. The absence of corneal reflexes (CN V) and the presence of a tonic neck reflex are associated with severe brain damage. The Babinski reflex, in which the lateral portion of the bottom of the foot is stroked and causes the big toe to go up, may be of value if it is found to be present consistently in children older than 1 year. A positive Babinski reflex is significant in the assessment of pyramidal tract lesions when it is unilateral and associated with other pyramidal signs. A fluctuating Babinski reflex is often observed after seizures.

Respiratory management

Respiratory effectiveness is the primary concern in the care of the unconscious child, and establishment of an adequate airway is always the first priority. Carbon dioxide has a potent vasodilating effect and will increase cerebral blood flow (CBF) and ICP. Cerebral hypoxia at normal body temperature that lasts longer than 4 minutes often causes irreversible brain damage.

Children in lighter stages of coma may be able to cough and swallow, but those in deeper states of coma are unable to manage secretions, which tend to pool in the throat and pharynx. Dysfunction of CNs IX and X (glossopharyngeal and vagus nerves) places the child at risk of aspiration and cardiac arrest. Therefore position the child with the head and body to the side to prevent aspiration of secretions and empty the stomach to reduce the likelihood of vomiting. In infants, the blockage of air passages from secretions can happen in seconds. In addition, upper airway obstruction from laryngospasm is a common complication in comatose children.

An oral airway can be used for the child who is suffering a temporary loss of consciousness, such as after a contusion, seizure, or anesthesia. For children who remain unconscious for a longer time, a nasotracheal or orotracheal tube is inserted to maintain the open airway and facilitate removal of secretions. A tracheostomy is performed in cases where laryngoscopy for introduction of an endotracheal tube would be difficult or dangerous or for a child who needs long-term ventilatory support. Suctioning is used only as needed to clear the airway, exerting care to prevent increasing ICP. Respiratory status is observed and evaluated regularly. Signs of respiratory distress may indicate a need for ventilator assistance.

Mechanical ventilation is usually indicated when the respiratory center is involved. Blood gas analysis is performed regularly, and oxygen is administered when indicated. Moderately severe hypoxia and respiratory acidosis are often present, but they are not always evident from clinical manifestations. Hypoventilation often accompanies unconsciousness and may lead to respiratory alkalosis, or it may represent the body’s attempt to compensate for metabolic acidosis. Blood gas and pH determinations are essential guides for electrolyte therapy. Chest physiotherapy is carried out on a regular basis, and the child’s position is changed at least every 2 hours to prevent pulmonary complications. Regular oral hygiene is recommended to reduce the risk of ventilator-associated pneumonia (VAP) (Hua, Xie, Worthington, et al., 2016).

Intracranial pressure monitoring

The role of ICP monitoring after traumatic brain injury (TBI) is controversial. Placement of the ICP monitor often occurs in the emergency department and where older in age (Kannan, Quistberg, Wang, et al., 2017). Early placement of ICP monitors may guide assessment management of patients with intracranial hypertension or those at higher risk for developing intracranial hypertension. ICP monitoring also may assist with decision making regarding transfer to the operating room or pediatric intensive care unit (PICU). However, in a large study using two national databases of 3084 children with severe TBI, no evidence was found of a benefit from ICP monitoring on functional survival of children with severe TBI (Bennett, DeWitt, Greene, et al., 2017). Development of noninvasive ICP sensors has the potential of decreasing the need for invasive interventions in pediatric patients in the future (Harary, Dolmans, & Gormley, 2018).

Direct ventricular pressure measurement remains the gold standard of ICP monitoring. The catheter method involves introduction of a catheter into the lateral ventricle on the nondominant side, if known, or placement in the subdural space. The catheter has the advantage of providing a means of extraventricular (or continuous) drainage of CSF to reduce pressure. A drainage bag attached to the system is kept at the level of the ventricles and can be lowered to decrease ICP. This device requires full penetration of the brain, requires skill and experience with placement, and carries the risk of infection. Infection risks can be lowered by always using aseptic technique when handling the external ventricular drainage (EVD) system, manipulating the EVD as little as possible, and sterile dressing changes only weekly or when the dressing is compromised, whichever occurs first (Hepburn-Smith, Dynkevich, Spektor, et al., 2016).

With the bolt method, the end of the bolt is placed into the subarachnoid space. The bolt cannot be adequately secured in a small child’s pliant skull, although special modifications have been developed for children younger than 6 years of age. The placement of the bolt is not adjusted by anyone except the neurosurgeon who placed the device. The neurosurgeon is notified if a satisfactory waveform is not observed.

An epidural sensor can be placed between the dura and the skull through a burr hole and connected to a stopcock assembly and a transducer, which provides a readout of the pressure. Although less invasive, the epidural sensor may have inconsistent correlation of pressure readings. In infants, a fontanel transducer can be used to detect impulses from a pressure sensor and convert them to electrical energy. The electrical energy is then converted to visible waves or numeric readings on an oscilloscope. ICP measurement from the anterior fontanel is noninvasive but may prove to be inaccurate if the equipment is poorly placed or inconsistently recalibrated. Intraparenchymal pressure-monitoring devices (e.g., Camino) use fiberoptic technology and perform reliably.

ICP can be increased by direct instillation of solutions; antibiotics are administered systemically if a positive CSF culture is obtained. However, ICP monitoring rarely causes infection. CSF is a body fluid; implement Standard Precautions according to hospital policy. (See Chapter 39, Infection Control.)

Nurses caring for patients with intracranial monitoring devices must be acquainted with the system, assist with insertion, interpret the monitor readings, and be able to distinguish between danger signals and mechanical dysfunction. Because systemic blood pressure, ICP, and therefore cerebral perfusion pressure (CPP) are normally lower in children, the child’s age must be taken into account when deciding what constitutes abnormally high ICP or abnormally low CPP.

Several medical measures are available to treat increased ICP resulting from cerebral edema. These include sedation, CSF drainage, and osmotic diuretics. Osmotic diuretics may provide rapid relief of ICP in emergency situations. Although their effect is transient, lasting only approximately 6 hours, they can be lifesaving in emergencies. These substances are rapidly excreted by the kidneys and carry with them large quantities of sodium and water. Mannitol (or sometimes urea) administered intravenously is the drug most commonly used for rapid reduction of ICP. The infusion is generally given slowly but may be pushed rapidly if there is herniation or impending herniation. Because of the profound diuretic effect of the drug, an indwelling catheter is inserted to ensure bladder emptying. Arterial carbon dioxide (PaCO₂) should be maintained at approximately 30 mm Hg to produce vasoconstriction, which reduces CBF, thereby decreasing ICP. Recording and analyzing the child’s volume state, plasma sodium concentration, and serum osmolarity can avert potential fluid and electrolyte problems. Administration of adrenocorticosteroids is not recommended for cerebral edema secondary to head trauma.

Nutrition and hydration

In the unconscious child, fluids and calories are supplied initially by the IV route. The type of fluid administered depends on the patient’s general condition. Children on the ketogenic diet and with certain metabolic disorders, such as pyruvate dehydrogenase deficiency, should receive normal saline rather than fluids containing dextrose, which can cause seizures and worsen their condition. Fluid therapy requires careful monitoring and adjustment based on neurologic signs and electrolyte determinations. Often unconscious children cannot tolerate the same amounts of fluid as when they are healthy. Overhydration must be avoided to prevent fatal cerebral edema. When cerebral edema is a threat, fluids may be restricted to reduce the chance of fluid overload. Examine skin and mucous membranes for signs of dehydration. Adjustments to fluid administration are based on urinary output, serum electrolytes and osmolarity, blood pressure, and arterial filling pressure. Observation for signs of altered fluid balance related to abnormal pituitary secretions is a part of nursing care.

Provide long-term nutrition in a balanced formula given by nasogastric or gastrostomy tube. The nasogastric tube is usually taped in place, with care taken to prevent pressure on the nares. Most children have continuous feedings. When bolus feedings are used, the tube is rinsed with water after each feeding. Tubes are replaced according to institutional policy. Irritation of the nasal mucosa is prevented by alternating nares each time the nasogastric tube is replaced.

Avoid overfeeding to prevent vomiting and the associated risk of aspiration. Stomach contents are aspirated with a syringe and measured before feeding to ascertain the amount remaining in the stomach. The removed contents may be refed. If the residual volume is excessive (depending on the child’s size), consult the dietitian and physician regarding the composition and amount to determine whether changes are required to provide calories and nutrients in a smaller volume.

Medications

The cause of unconsciousness determines specific drug therapies. Children with infectious processes are given antibiotics appropriate to the disease and the infecting organism. Corticosteroids are prescribed for inflammatory conditions and edema. Cerebral edema is an indication for osmotic diuretics. Antiepileptic medications are prescribed for seizure activity. Sedation in the combative child provides amnesic and anxiolytic properties in conjunction with a paralytic agent. This combination decreases ICP and allows treatment of cerebral edema. Usual drugs include morphine and midazolam. Midazolam is attractive because of its short half-life.

Deep coma induced by the administration of barbiturates is controversial in the management of ICP. Barbiturates are currently reserved for the reduction of increased ICP when all else has failed. Barbiturates decrease the cerebral metabolic rate for oxygen and protect the brain during times of reduced CPP. Barbiturate coma requires extensive monitoring. EEG monitoring can assess depth of coma, record EEG background abnormalities that can help to predict outcome, and evaluate any seizure activity. Cardiovascular and respiratory support and ICP monitoring are needed to assess response to therapy. Paralyzing agents such as vecuronium may be needed to aid in performing diagnostic tests, improving effectiveness of therapy, and reducing the risks of secondary complications. Elevation of ICP or heart rate in patients who are being given paralyzing agents or are under sedation may indicate the need for another dose of either or both medications or the need for pain medication.

Thermoregulation

Hyperthermia often accompanies cerebral dysfunction; if it is present, the nurse implements measures to reduce the temperature to prevent brain damage from hyperthermia and to reduce metabolic demands generated by the increased body temperature. Antipyretics are the method of choice for fever reduction; cooling devices are used for hyperthermia. (See Chapter 39, Controlling Elevated Temperatures.) Laboratory tests and other methods help to determine the cause, if any, of the hyperthermia. Treatment with hypothermia and barbiturates increases the risk of iatrogenic complications.

Elimination

A urinary catheter is usually inserted in the acute phase, but diapers may be used and weighed to record urinary output. The child who previously had bowel and bladder control is generally incontinent. If the child remains comatose for a long period, the indwelling catheter may be removed and periodic bladder emptying accomplished by intermittent catheterization. Stool softeners are usually sufficient to maintain bowel function, but suppositories or enemas may be needed occasionally for adequate elimination and to prevent fecal impaction. The passage of liquid stool after a period of no bowel activity is usually a sign of impaction. To avoid this preventable problem, daily recording of bowel activity is essential.

Hygienic care

Routine measures for cleansing and maintaining skin integrity are an integral part of nursing care of the unconscious child. Skinfolds require special attention to prevent excoriation. The child who is unable to move is prone to develop tissue breakdown and necrosis; the child is placed on a resilient appliance (e.g., alternating-pressure or water-filled mattress) to prevent pressure on prominent areas of the body. The goal is prevention by regular change of position and inspection of vulnerable areas (e.g., the ankle, heels, trochanter, sacrum, and shoulder). Unconscious children undergo numerous invasive procedures, and the skin sites used for these procedures require special assessment and intervention to promote healing and prevent infection. Keep bed linens and any clothing dry and free of wrinkles. Rubbing the back and extremities with lotion stimulates circulation and helps prevent drying of the skin. However, to prevent further tissue damage, do not massage reddened and nonblanching skin. (See Chapter 39, Maintaining Healthy Skin.) If the child requires surgery or radiography, the nurse checks all dressings, bony sites, catheters, and IV access lines before and after the procedure.

Oral care is performed at least twice daily because the mouth tends to become dry or coated with mucus. The teeth are carefully brushed with a soft toothbrush or cleaned with gauze saturated with saline. Commercially prepared cleansing devices, such as Toothettes, are convenient for cleansing the mouth and teeth. Lips are coated with ointment to protect them from drying, cracking, or blistering.

The unconscious child is also prone to eye irritation. The corneal reflexes are absent; therefore the eyes are easily irritated or damaged by linens, dust, or other substances that may come in contact with them. Excessive dryness results from incomplete closure of the lids and/or decreased secretions, especially if the child is undergoing osmotherapy to reduce or prevent brain edema.

Keep the child’s hair combed, and secure to prevent tangling. Keep the scalp clean with dry or wet shampoos as needed. The child’s head may need to be shaved for tests or surgical procedures. The family may want the hair to be saved.

Positioning and exercise

The unconscious child is positioned to minimize ICP and to prevent aspiration of saliva, nasogastric secretions, and vomitus. The head of the bed is elevated, and the child is placed in a side-lying or semiprone position. A small, firm pillow is placed under the head, and the uppermost limbs are flexed and supported with pillows. The weight of the body should not rest on the dependent arm. In the semiprone position the child lies with the dependent arm at the side behind the body; the opposite side is supported on pillows, and the uppermost arm and leg are flexed and resting on the pillows. This position prevents undue pressure on the dependent extremities. The dependent position of the face encourages drainage of secretions and prevents the flaccid tongue from obstructing the airway.

Normal range-of-motion exercises help maintain function and prevent contractures of joints. Perform exercises gently to minimize increasing ICP and with full range of motion. Place a small, rolled pad in the palms to help maintain proper positioning of fingers. Splinting may be needed to prevent severe contractures of the wrists, knees, or ankles.

Stimulation

Sensory stimulation is as important in the care of the unconscious child as it is in the care of the alert child. For the temporarily unconscious or semiconscious child, sensory stimulation helps arouse the child to the conscious state and orient the child in terms of time and place. Auditory and tactile stimulation are especially valuable. Tactile stimulation is not appropriate for a child in whom it may elicit an undesirable response. However, for other children tactile contact often has a relaxing and calming effect. When the child’s condition permits, holding or rocking the child is soothing and provides the body contact needed by young children.

Hearing is often intact in a state of coma. Hearing is the last sense to be lost and the first one to be regained; speak to the child as any other child. Conversation around the child should not include thoughtless or derogatory remarks. Soft music is often used to provide auditory stimulation. Singing the child’s favorite songs or reading a favorite story is a strategy used to maintain the child’s contact with a familiar world. Playing songs or favorite stories recorded in the parents’ voices can provide a continuous source of familiar stimulation.

Family support

Helping the parents of an unconscious child cope with the situation is especially difficult. They may demonstrate all of the guilt, fear, hostility, and anxiety of any parent of a seriously ill child (see Chapter 36). In addition, these parents face the uncertain outcome of the cerebral dysfunction. The fear of death, cognitive impairment, or permanent physical disability is present. Nursing intervention with parents depends on the nature of the pathologic condition, the parents’ coping skills, and the parent-child relationship before injury or illness.

Awakening from a coma is a gradual process; however, some children regain consciousness within a short time. If there is little or no residual effect, the child is discharged home fairly soon. The parents need the most intensive nursing intervention during the period of crisis and uncertainty. During the recovery phase the nurse gives them information, clarifies it as needed, and encourages them to become involved in the child’s care. Often the child’s hospitalization is brief; however, some children require extended hospitalization for intensive therapy and rehabilitation. The parents of children who die require support and guidance to cope with the reality of the death and to resolve their grief (see Chapter 36).

Probably the most difficult situations are those that involve children who never regain consciousness. Unlike losing a child through death, these children lack finality, which often leaves the parents in a state of suspended grief. Like parents of dying children, parents of comatose children search for any signs of hope. Well-meaning friends and relatives relate instances of miraculous recoveries. The parents seek confirmation and support for such possibilities and assign erroneous meanings to any sign in the child that might be interpreted as evidence of recovery (e.g., reflexive muscle contractions).

At these times nurses need to respond with compassion and honesty. They can acknowledge that miraculous recoveries do occur but are rare. The important message is to maintain open communication with the family.

Like parents who lose a child through death, the parents of a child who is unconscious attempt to construct a representation of the child. They bring items that belong to the child, such as favorite toys or music. This may be interpreted as an attempt to provide stimulation for the child in the hope of eliciting a response, to let the hospital staff know the child as the unique individual he or she was, and to reconstitute an image of the child “lost” to them and for whom they mourn. The nurses’ recognition and understanding of these behaviors and coping mechanisms are important to support the parents in their grief process.

In addition to the process of grieving for the “lost” child, the parents may face difficult decisions. When the child’s brain is so severely damaged that vital functions must be maintained by artificial means, the parents must make the final decision whether to remove the life support systems and allow a natural death. After parents are provided with information about what allowing a natural death and removal from life support mean, the parents may turn to both the provider and the nurses with their questions and concerns. Nurses play a critical role in assisting families in participating in their child’s care to the greatest extent possible and in planning the child’s death when that is the inevitable outcome of the neurologic disorder (Bloomer, Endacott, Copnell, et al., 2016).

Etiology

The most common causes of head injury in children are falls, being struck by or striking an object with one’s head, and motor vehicle accidents, in that order (Centers for Disease Control and Prevention, 2017a). Assaults are the leading cause of death from TBI in children 4 years of age or younger (Taylor et al., 2017). Neurologic injury accounts for the highest mortality rate, with boys usually affected twice as often as girls. There are a number of head trauma strategies, including safety gates on stairs, restricting sleeping in the top bunk to children older than 6 years of age, seat belts and car seat use, and helmets during recreational activities such as biking and skiing. Furthermore, preventing child abuse is necessary and possible.

Pathophysiology

The pathology of brain injury is directly related to the force of impact. Intracranial contents (brain, blood, CSF) are damaged because the force is too great to be absorbed by the skull and musculoligamentous support of the head. Although nervous tissue is delicate, it usually requires a severe blow to cause significant damage.

A child’s response to head injury is different from that of adults. The larger head size in proportion to body size and insufficient musculoskeletal support render the very young child particularly vulnerable to acceleration-deceleration injuries.

Primary head injuries are those that occur at the time of trauma and include skull fractures, contusions, intracranial hematomas, and diffuse injuries. Subsequent complications include hypoxic brain injury, increased ICP, and cerebral edema. The predominant feature of a child’s brain injury is the diffuse amount of swelling that occurs. Hypoxia and hypercapnia threaten the energy requirements of the brain and increase CBF. The added volume across the blood-brain barrier and the loss of autoregulation exacerbate cerebral edema. Pressure inside the skull that is greater than arterial pressure results in inadequate perfusion. Because the cranium of very young children has the ability to expand and the thin skull is more compliant, they may tolerate increases in ICP better than older children and adults.

Physical forces act on the head through acceleration, deceleration, or deformation. Acceleration or deceleration is more descriptive of the circumstances responsible for most head injuries. When the stationary head receives a blow, the sudden acceleration causes deformation of the skull and mass movement of the brain. Continued movement of the intracranial contents allows the brain to strike parts of the skull (e.g., the sharp edges of the sphenoid or the irregular surface of the anterior fossa) or the edges of the tentorium.

Although the brain volume remains unchanged, significant distortion and cavitation occur as the brain changes shape in response to the force transmitted from the impact to the skull. This deformation can cause bruising at the point of impact (coup) or at a distance as the brain collides with the unyielding surfaces opposite or far removed from the point of impact (contrecoup) (Fig. 46.5). Thus a blow to the occipital region can cause severe injury to the frontal and temporal areas of the brain.

When a moving head strikes a stationary surface, such as during a fall, sudden deceleration occurs and causes the greatest cerebral injury at the point of impact. Deceleration is responsible for most severe brainstem injuries.

Children with an acceleration-deceleration injury demonstrate diffuse generalized cerebral swelling produced by increased blood volume or by a redistribution of cerebral blood volume (cerebral hyperemia) rather than by the increased water content (edema).

Another effect of brain movement is shearing forces, which are caused by unequal movement or different rates of acceleration at various levels of the brain. A shearing force may tear small arteries that travel from the cerebral surfaces through the meninges to the dural sinuses and cause subdural hemorrhages. Shearing or stretching effects can also be transmitted to nerve fibers. Maximum stress from the shearing force occurs at the interface between structures of different density so that the gray matter (cell body) rapidly accelerates, whereas the white matter (axons) tends to lag behind. Although maximum shearing forces are at the cerebral surface and extend toward the center of rotation within the brain, the most serious effects are often in the area of the brainstem. Severe compression of the skull can cause the brain to be forced through the tentorial opening and produce irreparable damage to the brainstem.

A GCS value of 8 or less in pediatric patients indicates severe injury and requires aggressive therapeutic management (Hartman & Cheifetz, 2020). Three out of four children with a score of 3 or 4 will be severely disabled, be in a persistent vegetative state, or die within a year of their injury (Fulkerson, White, Rees, et al., 2015). A number of studies indicate that the Simplified Motor Scale (SMS) is equivalent to the GCS in predictive power but that the GCS is better for prognosticating death (Singh, Murad, Prokop, et al., 2013).

Complications

The major complications of trauma to the head are hemorrhage, infection, edema, and herniation through the brainstem. Infection is always a hazard in open injuries. Edema is related to tissue trauma. Vascular rupture may occur even in minor head injuries, causing hemorrhage between the skull and cerebral surfaces. Compression of the underlying brain produces effects that can be rapidly fatal or insidiously progressive.

Epidural hematoma

Epidural (extradural) hematoma is a hemorrhage into the space between the dura and the skull. As the hematoma enlarges, the dura is stripped from the skull; this accumulation of blood results in a mass effect on the brain, forcing the underlying brain contents downward as it expands (Fig. 46.6A). Because bleeding is generally arterial, brain compression occurs rapidly. The lower incidence of epidural hematoma in childhood is attributed to the fact that the middle meningeal artery is not embedded in the skull’s bone surface until approximately 2 years old. Therefore a temporal bone fracture is less likely to lacerate the artery. Neuroimaging studies in 210 infants and young children with isolated mild TBI showed skull fractures with extra-axial hemorrhage/no midline shift (30%), nondisplaced skull fractures (28%), and intracranial hemorrhage without fractures/midline shift (19%) (Noje, Jackson, Nasr, et al., 2019).

Child abuse accounts for a significant number of cases of epidural hematomas in infants and children, whereas motor vehicle accidents account for most epidural hematomas in adolescents.

Because bleeding is generally arterial, brain compression occurs rapidly. Most often the expanding hematoma is located in the parietal and temporal regions (Teichert, Rosales, Lopes, et al., 2012), which forces the medial portion of the temporal lobe under the edge of the tentorium, where it places pressure on nerves and blood vessels. Pressure on the arterial supply and venous return to the reticular formation causes loss of consciousness; pressure on CN III produces dilation and (later) fixation of the ipsilateral pupil. Pressure on the fibers of the pyramidal tract is evidenced by contralateral weakness or paralysis and increased deep tendon reflexes. Extreme pressure may cause brain herniation and death. Expanding epidural hemorrhages may be better tolerated in young children with open sutures that allow for expansion of the skull. In addition, young children have larger subarachnoid and extracellular spaces, which provide space for the expanding hematoma without compression on the brain parenchyma.

The classic clinical picture of an epidural hemorrhage is a lucid interval of minutes to hours followed by rapidly altered mental status, then loss of consciousness or coma due to blood accumulation in the epidural space and compression of the brain. The child may be seen with varying degrees of impaired consciousness, depending on the severity of the traumatic injury. Common symptoms in a child with no neurologic deficit are irritability, headache, and vomiting. In infants younger than 24 months of age, common symptoms are scalp swelling, irritability, and lethargy. They may also have seizures, reduced oral intake, and increasing head circumference (Sellin, Moreno, Ryan, et al., 2017).

An epidural hematoma can be detected by an initial CT scan. If the severity of the child’s symptoms is not recognized, herniation and death will result. Cushing triad (systemic hypertension, bradycardia, and respiratory depression) is a late sign of impending brainstem herniation.

NURSING ALERT

Children with a subdural hematoma and retinal hemorrhages should be evaluated for the possibility of child abuse, especially shaken baby syndrome.

Diagnostic evaluation

A detailed health history, both past and present, is essential in evaluating the child with head trauma. Certain disorders such as drug allergies, hemophilia, diabetes mellitus, or epilepsy may produce similar symptoms. Even a minor traumatic injury can aggravate a preexisting disease process, thereby producing neurologic signs out of proportion to the injury.

After a minor injury, initial unconsciousness (if present) is brief. The child ordinarily exhibits a transient period of confusion, somnolence, and listlessness; this period is most often accompanied by irritability, pallor, and one episode of vomiting. A severe head injury requires immediate evaluation and treatment. Because head injuries are often accompanied by injuries in other areas (e.g., spine, viscera, extremities), the examination is performed with care to avoid further damage. Box 46.3 lists manifestations of head injury.

Therapeutic management

Most children with mild TBI who have not lost consciousness can be cared for and observed at home after careful examination reveals no serious intracranial injury. The nurse should give parents both verbal and written instructions of signs and symptoms that warrant concern and the need for reevaluation. These include persistent or worsening headaches, vomiting, change in mental status or behavior, unsteady gait, or seizure. The child should have a physical examination 1 or 2 days after the injury. The manifestations of epidural hematoma in children do not generally appear until 24 hours or more after injury.

Maintaining contact with parents for continued observation and reevaluation of the child, when indicated, facilitates early diagnosis and treatment of possible complications from head injury, such as hematoma, cerebral edema, and posttraumatic seizures. Children are generally hospitalized for 24 to 48 hours of observation if their family lives far from medical facilities or lacks transportation or a telephone, which would provide access to immediate help. Other circumstances, such as language or other communication barriers or even emotional trauma, may hinder learning and make it difficult for families to feel confident caring for their child at home.

Children with severe injuries, those who have lost consciousness for more than a few minutes, and those with prolonged and continued seizures or other focal or diffuse neurologic signs must be hospitalized until their condition is stable and their neurologic signs have diminished. The child is maintained on nothing-by-mouth (NPO) status or restricted to clear liquids (if able to take fluids by mouth) until it is determined that vomiting will not occur. IV fluids are indicated in the child who is comatose, displays dulled sensorium, or is persistently vomiting.

The volume of IV fluid is carefully monitored to minimize the possibility of overhydration in case of SIADH and cerebral edema. However, damage to the hypothalamus or pituitary gland may produce DI, with its accompanying hypertonicity and dehydration. Fluid balance is closely monitored by daily weight, strict intake and output measurement, and serum osmolality (to detect early signs of water retention).

Sedating drugs are usually withheld in the acute phase. Headache is usually controlled with acetaminophen, although opioids may be needed. Antiepileptics are used for seizure control. Antibiotics are administered if there are lacerations or penetrating injuries. Prophylactic tetanus toxoid is given as appropriate. Cerebral edema is managed as described for the unconscious child. Hyperthermia is controlled with tepid sponges or a hypothermia blanket.

Nursing care management

The hospitalized child requires careful neurologic assessment and evaluation repeated as frequently as every 15 minutes to establish a correct diagnosis, identify signs and symptoms of increased ICP, determine clinical management, and prevent many complications. The goals of nursing management of the child with a head injury are to maintain adequate ventilation, oxygenation, and circulation; to monitor and treat increased ICP; to minimize cerebral oxygen requirements; and to support the child and family during recovery. (See Quality Patient Outcomes box.)

The child is placed on bed rest, usually with the head of the bed elevated slightly and the head in midline position. Appropriate safety measures, such as side rails kept up and seizure precautions, are implemented. If the child is extremely restless, hard surfaces may be padded and restraints used to prevent further injury. Individualize care according to the child’s specific needs.

A key nursing role is to provide sedation and analgesia for the child. The conflict between the need to promote the child’s comfort and relieve anxiety versus the need to assess for neurologic changes presents a dilemma. Both goals can be achieved with close observation of the child’s LOC and response to analgesics (using a pain assessment record) and effective communication with the provider. Decreasing restlessness after administration of an analgesic most likely reflects pain control rather than a decreasing LOC. (See Chapter 5, Pain Assessment and Pain Management.)

Children may be restless and irritable, but more often their reaction is to fall asleep when left undisturbed. A quiet environment can help reduce restlessness and irritability. Bright lights are irritating. This often makes checking the ocular responses more difficult and aggravating to the child.

Frequent examinations of vital signs, neurologic signs, and LOC are extremely important nursing observations. When possible, they should be performed by a single observer to better detect subtle changes that may indicate worsening of neurologic status. Pupils are checked for size, symmetry, reaction to light, and accommodation. Unless there is brainstem involvement, vital signs generally return to normal after the initial changes seen after injury.

The most important nursing observation is assessment of the child’s LOC. In the progression of an injury, alterations in consciousness appear earlier than alterations in vital signs or focal neurologic signs (see evaluation of responsiveness later in the chapter). Frequent examinations of alertness are fatiguing to the child; the child often desires to fall asleep, which may be confused with depressed consciousness. It is not uncommon to observe ocular divergence through the partially closed eyelids.

Observations of position and movement provide additional information. Note any abnormal posturing and whether it occurs continuously or intermittently. Questions nurses might ask include the following:

The child may report a headache or other discomfort. The child who is too young to describe a headache may be fussy and resist being handled. The child who suffers from vertigo often vigorously resists being moved from a position of comfort. Forcible movement causes the child to vomit and display spontaneous nystagmus. Seizures are relatively common in children at the time of head injury and may be of any type. Carefully observe any seizure activity and describe it in detail. Children in postictal states are more lethargic, with sluggish pupils.

Document drainage from any orifice. Bleeding from the ear suggests the possibility of a basal skull fracture. Clear nasal drainage is suggestive of an anterior basal skull fracture. Observe the amount and characteristics of the drainage.

Head trauma is often accompanied by other undetected injuries; therefore any bruises, lacerations, or evidence of internal injuries or fractures of the extremities are noted and reported. Associated injuries are evaluated and treated appropriately.

The child with a normal LOC is usually allowed clear liquids unless fluid is restricted. If the child has an IV infusion, it is maintained as prescribed. The diet is advanced to that appropriate for the child’s age as soon as the condition permits. Intake and output are measured and recorded with attention to the development of constipation. Any incontinence of bowel or bladder is noted for the child who has been toilet trained.

Assessment for unusual behavior can be made only in relation to the child’s typical behavior. For example, urinary incontinence during sleep would be of no consequence in a child who routinely wets the bed but would be highly significant for one who is always dry. Parents are invaluable resources in evaluating objective behaviors of their children. Information obtained from parents at or shortly after admission is essential in evaluating the child’s behavior (e.g., the ease with which the child is roused normally, the usual sleeping position, how much the child sleeps during the day, the child’s motor activities [rolling over, sitting up, climbing], hearing and visual acuity, appetite, and manner of eating [spoon, bottle, cup]). Documentation of the child’s baseline developmental and behavioral level is crucial. There is less concern about a child who falls asleep several times during the day if this is consistent with the child’s usual behavior.

When the child is discharged, advise the parents of probable posttraumatic symptoms they may observe, such as behavioral changes, sleep disturbances, phobias, and seizures. Parents should be taught seizure first aid. They should understand observations they need to make and when and how to contact the provider or health facility in case the child develops any unusual signs or symptoms. Emphasize the importance of follow-up evaluation.

Pathophysiology

Physiologically, most organ systems are affected, especially the pulmonary, cardiovascular, and neurologic systems. The major pulmonary changes that occur in submersion injury are directly related to the length of submersion (regardless of the type and amount of fluid aspirated), the victim’s physiologic response, and the development and degree of immersion hypothermia. Cerebral hypoxia is a major component of morbidity and mortality in these individuals. Therefore early and aggressive resuscitation is imperative.

Physiologic factors in submersion injuries are hypothermia, aspiration, and hypoxia. The temperature of the liquid plays an important role. Cold water decreases metabolic demands and activates the diving reflex, which causes blood to be shunted away from the periphery to vital organs (i.e., the brain and heart). Hypothermia occurs rapidly in infants and children, partly because of their large surface area relative to size and partly as a result of the cold water itself. Profound hypothermia is usually evidence of lengthy submersion. Prolonged submersion in cold liquids can impair cognition, coordination, and muscle strength that ultimately result in loss of consciousness, decreased cardiac output, and cardiac arrest (Thomas & Caglar, 2020). Submersion in cold water had previously been thought to be somewhat neuroprotective, but it is not (Quan, Mack, & Schiff, 2014).

Submerged children struggle initially to stay above water, and often breath-holding leads to air hunger. Reflex inspiration eventually occurs, which leads to aspiration (Thomas & Caglar, 2020). Fluid is quickly absorbed in the pulmonary circulation, resulting in pulmonary edema, atelectasis, and airway spasm. Hypoxia is the primary problem because it results in global cell damage, with different cells tolerating variable lengths of anoxia. Neurons, especially cerebral cells, sustain irreversible damage after 4 to 6 minutes of submersion. The heart and lungs can survive up to 30 minutes. Regardless of the amount of water aspirated, the victim suffers arterial hypoxemia (resulting from atelectasis and shunting of blood through the nonventilated alveoli), combined respiratory acidosis (resulting from retained carbon dioxide), and metabolic acidosis (caused by buildup of acid metabolites because of anaerobic metabolism). Although electrolyte imbalances are contributing factors, they are not the major causes of morbidity and mortality. The pathologic events are directly related to the duration of submersion. Approximately 10% of submersion injury victims die without aspirating fluid but succumb from acute asphyxia as a result of prolonged reflex laryngospasm.

Aspiration of fluid occurs in most submersion injuries. The aspirated fluid results in pulmonary edema, atelectasis, airway spasm, and pneumonitis, which aggravates hypoxia. Submersion in salt water is associated with better outcomes than submersion in fresh water, although duration of the submersion is the main factor that predicts outcome (Quan, Bierens, Lis, et al., 2016).

Clinical manifestations

Clinical manifestations are directly related to the duration of loss of consciousness and neurologic status after rescue and resuscitation.

Therapeutic management

With rapid treatment, some children can be saved. Resuscitative measures should begin at the scene, and the victim should be transported to the hospital with maximum ventilatory and circulatory support. In the hospital, intensive pulmonary care is implemented and continued according to the patient’s needs.

In general, management of the victim with a submersion injury is based on the degree of cerebral insult. The first priority is to restore oxygen delivery to the cells and prevent further hypoxic damage. A spontaneously breathing child does well in an oxygen-enriched atmosphere; the more severely affected child requires endotracheal intubation and mechanical ventilation. Blood gases and pH are monitored at frequent intervals as a guide to oxygen, fluid, and electrolyte therapies. Rewarming the hypothermic patient is initiated. Seizures may occur due to hypoxia and cerebral edema. Seizures result in increased cerebral oxygen consumption. Therefore it is imperative to aggressively control seizure activity. In addition, blood glucose should be monitored; both hypoglycemia and hyperglycemia are harmful to the brain.

All children who have a submersion injury should be hospitalized for observation. Although some children do not appear to have sustained adverse effects from the event, respiratory compromise or cerebral edema may occur within 24 hours after the incident. In the acute recovery period, fever should be prevented, although prophylactic antibiotics are not recommended. Aspiration pneumonia is a common complication that occurs approximately 48 to 72 hours after the episode. Bronchospasm, alveolar-capillary membrane damage, atelectasis, abscess formation, and acute respiratory distress syndrome are other complications that occur after aspiration of fluid.

Nursing care management

Nursing care depends on the child’s condition. A child who survives may need intensive respiratory nursing care with attention to vital signs, mechanical ventilation or tracheostomy, blood gas determination, chest physiotherapy, and IV infusion. Often the child has sustained a hypoxic insult and requires the same care as an unconscious child.

A difficult aspect in the care of the child who sustained a submersion injury is helping the parents cope with the grief, guilt, and anger reactions. Given the magnitude of the event, parents need repeated assurance that everything possible is being done to treat their child.

Nurses often have difficulty relating to the parents if obvious neglect has precipitated the accident and subsequent problems; it is important for those who care for these children and their families to assess their own feelings about the situation, in addition to assessing the family’s coping abilities and resources. Caring for victims of a submersion injury and their families requires the nurse to be sensitive to the needs of the child and the family and to recognize his or her own reactions and emotions.

Etiology

A variety of bacterial agents can cause bacterial meningitis. Since the introduction of vaccinations against most common causes of community-acquired pathogens, the incidence of bacterial meningitis has declined precipitously. The leading causes of neonatal meningitis are group B streptococcus (GBS) and Escherichia coli (Ku, Boggess, & Cohen-Wolkowiez, 2015).

Meningococcal meningitis is the only type readily transmitted by droplet infection from nasopharyngeal secretions and so has the potential to occur in outbreaks (Vetter, Baxter, Denizer, et al., 2016). Before the development of a vaccine, it occurred predominantly in school-age children and adolescents; currently it is most common in children younger than 12 months old, with a secondary peak in incidence in 16 to 23 year olds (Centers for Disease Control and Prevention, 2017b). Meningitis caused by pneumococcal and meningococcal infections can occur at any time but is more common in late winter and early spring.

Maternal factors, such as premature rupture of fetal membranes and maternal infection during the last week of pregnancy, are major causes of neonatal meningitis. It is a devastating disease with significant morbidity and mortality. Vaccination of pregnant women is being explored as a way to protect infants from meningitis (Jones, Munoz, Spiegel, et al., 2016). Children who survive neonatal meningitis are 10 times more likely to have moderate to severe disabilities than those who have not had meningitis (Ku et al., 2015). The incidence of early-onset GBS meningitis has been reduced by more than 70% with the adoption of antenatal screening and administration of intrapartum prophylactic antibiotics (Ku et al., 2015).

Risk factors for children developing meningitis include lack of immunization to the specific pathogen; recent exposure to someone with invasive Neisseria meningitidis or Hib disease; penetrating head trauma; cochlear implant devices; and anatomic defects such as midline facial defects, inner ear fistulas, or recent placement of a ventricular shunt (Swanson, 2015).

Pathophysiology

The most common route of infection is vascular dissemination from a focus of infection elsewhere. For example, organisms from the nasopharynx invade the underlying blood vessels, cross the blood-brain barrier, and multiply in the CSF. Invasion by direct extension from infections in the paranasal and mastoid sinuses is less common. Organisms also gain entry by direct implantation after penetrating wounds, skull fractures that provide an opening into the skin or sinuses, lumbar puncture or surgical procedures, anatomic abnormalities such as spina bifida, or foreign bodies such as an internal ventricular shunt or an external ventricular device. Once implanted, the organisms spread into the CSF, by which the infection spreads throughout the subarachnoid space.

The infective process is like that seen in any bacterial infection: inflammation, exudation, white blood cell accumulation, and varying degrees of tissue damage. The brain becomes hyperemic and edematous, and the entire surface of the brain is covered by a layer of purulent exudate that varies with the type of organism. For example, meningococcal exudate is most marked over the parietal, occipital, and cerebellar regions; the thick, fibrinous exudate of pneumococcal infection is confined chiefly to the surface of the brain, particularly the anterior lobes; and the exudate of streptococcal infections is similar to that of pneumococcal infections but thinner. As infection extends to the ventricles, thick pus, fibrin, or adhesions may occlude the narrow passages and obstruct the flow of CSF.

Clinical manifestations

The clinical manifestations of acute bacterial meningitis depend to a large extent on the child’s age. The type of organism, the effectiveness of therapy for antecedent illness, and whether it occurs as an isolated entity or as a complication of another illness or injury also influence the clinical manifestation (Box 46.4).

Diagnostic evaluation

A lumbar puncture is the definitive diagnostic test. The fluid pressure is measured, and samples are obtained for culture, Gram stain, blood cell count, and determination of glucose and protein levels. The findings are usually diagnostic. Culture and sensitivity are needed to identify the causative organism. Spinal fluid pressure is usually elevated, but interpretation is often difficult when the child is crying. Sedation with fentanyl and midazolam can alleviate the child’s pain and fear associated with this procedure (see Atraumatic Care box). If there is evidence or suspicion of increased ICP, a CT scan of the head may be warranted before the procedure (Weinberg & Thompson-Stone, 2018).

The patient generally has an elevated white blood cell count, often predominantly polymorphonuclear leukocytes. The glucose level is reduced, generally in proportion to the duration and severity of the infection. The relationship between the CSF glucose and serum glucose levels is important in evaluating the glucose content of CSF; therefore a serum glucose sample is drawn approximately a half-hour before the lumbar puncture. Protein concentration is usually increased.

Blood culture is advisable for all children suspected of having meningitis if antibiotics are started before obtaining CSF. Blood culture will occasionally be positive when CSF culture is negative. Nose and throat cultures may provide helpful information in some cases.

Therapeutic management

Acute bacterial meningitis is a medical emergency that requires early recognition and immediate therapy to prevent death and avoid residual disabilities. The initial therapeutic management includes the following:

The child is usually moved to an intensive care unit for close observation. An IV infusion is started to facilitate administration of antimicrobial agents, fluids, antiepileptic drugs, and blood, if needed. The child is placed in respiratory isolation.

Nursing care management

Nurses should take the necessary precautions to protect themselves and others from possible infection. Teach parents proper hand washing technique, and remind them as needed.

Keep the room as quiet as possible and environmental stimuli at a minimum because most children with meningitis are sensitive to noise, bright lights, and other external stimuli. Help the family limit the number and frequency of visitors until the child feels better. Most children are more comfortable without a pillow under their head but with the head of the bed slightly elevated. Use pillows alongside a child in a side-lying position and between the child’s knees for comfort in cases of nuchal rigidity. Avoid actions that cause pain or increase discomfort, such as lifting the child’s head. Evaluating the child for pain and implementing appropriate relief measures are important ongoing interventions. Measures are used to ensure safety because the child is often restless, disoriented, and subject to seizures. Prevention of falls is essential.

The nursing care of the child with meningitis is determined by the child’s symptoms and treatment (see Box 46.4). Observation of vital signs, neurologic signs, LOC, urinary output, and other pertinent data is carried out at frequent intervals. The child who is unconscious is managed as described previously, and all children are observed carefully for signs of the complications just described, especially increased ICP, shock, and respiratory distress. Frequent assessment of the open fontanels is needed in the infant because subdural effusions and obstructive hydrocephalus can develop as a complication of meningitis.

Administration of fluids and nourishment is determined by the child’s status. The child who is not alert and oriented is given nothing by mouth. Other children are allowed clear liquids initially and, if tolerated, progress to a diet suitable for their age. Careful monitoring and recording of intake and output are needed to determine deviations that might indicate impending shock or increasing fluid accumulation, such as cerebral edema or subdural effusion.

One of the most challenging issues in the nursing care of children with meningitis is maintaining IV infusion for the length of time needed to provide adequate antimicrobial therapy (usually 10 days). Because continuous IV fluids are usually not necessary, an intermittent infusion device is used. In some cases children who are recovering uneventfully are sent home with the device, and the parents are taught IV drug administration. (See Quality Patient Outcomes box.)