The Child with Cerebral Dysfunction

Brain Coverings

Within the skull, three membranes (the meninges) cover and protect the brain: the dura mater, arachnoid membrane, and pia mater (Fig. 37-1). The tough outer membrane, the dura mater, is a double layer that serves as the outer meningeal layer and the inner periosteum of the cranial bones. These two layers are separated by the epidural space. The dura is closely attached to the skull in infancy, causing slower spread of blood in epidural hemorrhage. Because of this adherence, epidural hemorrhages are uncommon in the first 2 years of life.

PATHOPHYSIOLOGY REVIEW

Between these layers of dura inside the skull lie large venous sinuses. Sheets of the dura mater also extend downward and inward to form partitions within the cranium. Projecting downward into the longitudinal fissure is a sheet of dura called the falx cerebri, which separates the cerebral hemispheres, and the falx cerebelli, which separates the cerebellar hemispheres. Another segment is a tentlike structure, the tentorium, which separates the cerebellum from the occipital lobe of the cerebrum. The large gap through which the brainstem passes is the tentorial hiatus, the site of herniation in untreated intracranial pressure (ICP).

The middle meningeal layer, the arachnoid membrane, is a delicate, avascular, weblike structure that loosely surrounds the brain. Between the arachnoid and the dura mater lies the subdural area, a potential space that normally contains only enough fluid to prevent adhesion between the two membranes. During cerebral trauma the fine blood vessels that bridge the subdural space are stretched and ruptured, causing venous blood to escape and spread freely, forming a subdural hemorrhage. The subdural space is small in children; therefore small amounts of blood can increase intracranial hemorrhage significantly.

The innermost covering layer, the pia mater, is a delicate, transparent membrane that, unlike the other coverings, adheres closely to the outer surface of the brain, conforming to the folds (gyri) and furrows (sulci). Within the pial layer lie the arteries and veins of the brain. Between the pia mater and the arachnoid membrane is the subarachnoid space. Cerebrospinal fluid (CSF) fills the entire subarachnoid space surrounding the brain and spinal cord and acts as a protective cushion for the brain tissue. Fibrous filaments known as arachnoid trabeculae provide further protection and help anchor the brain. When the head receives a blow, these attachments allow the arachnoid to slide on the dura, preventing excessive movement.

The Brain

Each section of the brain plays a vital role in regulation and control of body function. Each hemisphere is artificially divided into lobes. Pressure on or damage to these lobes produces observable signs or symptoms directly related to the area of pathology. These signs provide clues to the location of the damage.

Animation—Brain Lobes

The two large cerebral hemispheres that occupy the anterior and medial fossae of the skull are separated in the upper part by the longitudinal fissure. This separation is complete anteriorly and posteriorly, but centrally the hemispheres are joined by the block of fibers known as the corpus callosum, the largest fiber bundle in the brain. These fibers interconnect cortical areas of the right and left hemispheres. Destruction of the corpus callosum causes hemispheric independence, or “split brain.”

Situated deeply within each hemisphere and on each side of the midline are the basal ganglia (or cerebral nuclei), which serve as vital sorting areas for messages passing to and from the hemispheres. Connected to the hemispheres by thick bunches of nerve fibers is the brainstem, through which all nerve fibers traverse as they pass from the hemispheres to the cerebellum and spinal cord. The brainstem extends from the base of the hemispheres through the foramen magnum, where it is continuous with the spinal cord. Within the cranium and behind the brainstem is the cerebellum. Any pressure exerted on the intracranial structures can cause compression of the brainstem and prolapse of the cerebellum through the foramen magnum.

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. Is there a history of injury with loss of consciousness, febrile illness, an encounter with an animal or insect, ingestion of neurotoxic substances, inhalation of chemicals, past illness, or 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. (See Appendix A.)

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 6 for CNS and reflex testing, p. 176.) 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 (Box 37-2). Box 37-3 describes abnormalities of gait that indicate cerebral dysfunction.

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 level of consciousness (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 37-4.

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. 37-2). The pediatric coma scale does not assess verbal responses as such but records smiling, crying, and interaction. It uses a 6-point motor scale that is inappropriate for children below the age of 6 months. In children under 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 the responses of all children. For example, because a child with quadriplegia cannot respond to commands physically, the child can score very low but be cerebrally 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 at admission is predictive of abnormal neurologic findings at discharge only when profoundly depressed (≤6); otherwise the GCS is not useful as a prognostic tool when used alone (White, Farukhi, Bull, et al, 2001). GCS scores of less than 8 in combination with other abnormal findings (e.g., hypoxia on admission and abnormal computed tomography [CT] results) were associated with poor outcome (Ong, Selladurai, Dhillon, et al, 1996).

Vital Signs

Pulse, respiration, and blood pressure provide information regarding 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 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. 37-3). Pupils either react 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 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 usually imply brainstem damage if present for more than 5 minutes. 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 will cause the eyes to appear normal under compromise.

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 or a camel hair pencil, can test the integrity of the ophthalmic division of 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 (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 preretinal hemorrhages in children is usually the result of acute trauma with intracranial bleeding (usually subarachnoid or subdural hemorrhage).

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 or seizure movements 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, and strong muscles overcome weaker ones. Flexion posturing (Fig. 37-4, A) 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 (Fig. 37-4, B) 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) will elicit a response, as may turning or touching. 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 6.) 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 foot is stroked, 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. (See Fig. 8-10, B, p. 250.)

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 CBF and ICP. Cerebral hypoxia at normal body temperature that lasts longer than 4 minutes nearly always 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 CN 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 in which 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 ventilatory assistance.

Mechanical ventilation is usually indicated when the respiratory center is involved. (See Chapter 31.) Blood gas analysis is performed regularly, and oxygen is administered when indicated. Moderately severe hypoxia and respiratory acidosis are often present, but are not always evident from clinical manifestations. Hyperventilation often accompanies unconsciousness and may lead to respiratory alkalosis, or it may represent the body’s attempt to compensate for metabolic acidosis. Therefore 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.

Intracranial Pressure Monitoring

The selection of the type of ICP monitor should be guided by the clinical presentation and the therapeutic strategy chosen for each child. Indications for inserting an ICP monitor are (1) GCS evaluation of less than 7, (2) GCS evaluation of less than 8 with respiratory assistance, (3) deterioration of condition, and (4) subjective judgment regarding clinical appearance and response.

Four major types of ICP monitors are (1) intraventricular catheter with or without fibroscopic sensors attached to a monitoring system, (2) subarachnoid bolt (Richmond screw), (3) epidural sensor, and (4) anterior fontanel pressure monitor. Transducers for both ventricular and subarachnoid monitoring should be set up without the use of a flush device. 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.

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 under 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 wave form 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. Use of the intraparenchymal pressure monitoring device (e.g., Camino) uses fiberoptic technology and performs reliably.

ICP can be increased by direct instillation of solutions; therefore antibiotics are administered systemically if a positive CSF culture is obtained. However, ICP monitoring rarely causes infection. CSF is a body fluid; therefore implement Standard Precautions according to hospital policy. (See Infection Control, Chapter 27.)

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 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 about 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. Paco₂ should be maintained at 25 to 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. (See Chapter 28.) An IV infusion is started early, and the type of fluid administered depends on the patient’s general 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, but if 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 are refed. If the residual volume is excessive (depending on the child’s size), consult the dietitian and physician regarding the composition and amount of formula and whether changes are required to provide the needed 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, midazolam, and pancuronium (Pavulon). 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, including EEG monitoring to assess for seizure activity, cardiovascular and respiratory support, and ICP monitoring to assess response to therapy. Paralyzing agents such as pancuronium also 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.

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 Controlling Elevated Temperatures, Chapter 27.) Laboratory tests and other methods help 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; therefore 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 linen 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 Maintaining Healthy Skin, Chapter 27.) If the child requires surgery or radiography, the nurse checks all dressings, bony sites, catheters, and IV access lines before and after the procedure.

Mouth care is performed at least twice daily, since 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 linen, 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. If so, the hair should be saved, if possible, and given to the family.

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. Footboards or high-top shoes (e.g., running or tennis shoes) can help prevent footdrop, and in some cases splinting is needed to prevent severe contractures of the wrist, knee, or ankle in children.

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.

The auditory sense is often intact in a state of coma. Hearing is the last sense to be lost and the first one to be regained; therefore 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 the guilt, fear, hostility, and anxiety of any parent of a seriously ill child. (See Chapter 23.) 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’ personality, and the parent-child relationship before injury or illness (see Family-Centered Care box).

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 23.)

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 them 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 is 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. Since this decision is so difficult for parents, the practitioner is frequently placed in a position of making the decision indirectly. After providing the parents with information about what removal from life-support means, the practitioner may suggest that the child be removed from life support to “see if the child can make it without help.” This approach relieves the parents of the decision and can be effective, but it is based on an evaluation of the parents’ intellectual level and emotional state. Sometimes parents may choose to refuse treatment if they believe doing so is best for the child and the family (informed dissent). At other times parents request that “everything possible” be done for the child.

When the child has survived the cerebral insult but is physically and/or mentally limited, either minimally or severely, families must cope with and make decisions about the rehabilitation process and uncertain outcome. The family may need to make decisions whether to place their child in a chronic care facility or to care for their child at home. The drain on financial, emotional, and social resources can be enormous.

For parents who choose to care for their child at home, planning begins early in the recovery process. Family members should become involved with the child’s care as soon as they indicate an interest and ability to do so. They need education and support in learning to care for the child, regular follow-up observation and assessment of the home management, and planning for respite care. Parents need to understand that it is important to plan for periodic relief from the continuous care of the child. (See Discharge Planning and Home Care, Chapter 26, and Family-Centered Home Care, Chapter 25.)

Etiology

The three major causes of brain damage in childhood, in order of importance, are falls, motor vehicle injuries, and bicycle injuries (Fig. 37-6). Neurologic injury accounts for the highest mortality rate, with boys usually affected twice as often as girls. Falls are the major source of all head injuries in children between the ages 0 to 4 years (Langlois, Rutland-Brown, and Thomas, 2005; Marsh and Whitehead, 2005). In motor vehicle accidents children younger than 2 years of age are almost exclusively injured as passengers, whereas older children may also be injured as pedestrians or cyclists. The majority of deaths from brain trauma caused by bicycle injuries occur between the ages of 5 and 19 years. Bicycle helmet laws have effectively reduced the risk of head injury by 85% and brain injury by 88% (Rivara and Grossman, 2009).

Many of the physical characteristics of children predispose them to craniocerebral trauma. For example, infants are often left unattended on beds, in high chairs, and in other places from which they can fall. Because the head of an infant or toddler is proportionately large and heavy in relation to other body parts, it is the most likely to be injured. Incomplete motor development contributes to falls at young ages, and the natural curiosity and exuberance of children increase their risk for injury.

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 BBB along with the loss of autoregulation exacerbates 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. 37-7). 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 while the white matter (axons) tends to lag behind. Although shearing forces are maximum 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.

Another source of damage occurs when severe compression of the skull causes the brain to be forced through the tentorial opening. This can produce irreparable damage to the brainstem (Fig. 37-8).

Patients with mild head injuries have a GCS evaluation of 13 to 15, and those with moderate head injuries have a GCS of 9 to 12; a GCS value of 8 or less indicates severe injury (Marcin and Pollack, 2002).

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, and 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.

Diagnostic Evaluation

A detailed health history, both past and present, is essential in evaluating the child with craniocerebral 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, and the child ordinarily exhibits a transient period of confusion, somnolence, and listlessness; this period is most often accompanied by irritability, pallor, and one or more episodes of vomiting. A severe head injury requires immediate evaluation and treatment. Because head injuries are often accompanied by injuries in other areas (spine, viscera, extremities), the examination is performed with care to avoid further damage. Box 37-5 lists manifestations of head injury.

Therapeutic Management

The majority of children with mild traumatic brain injury 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. Parents should bring the child in for examination in 1 or 2 days. The manifestations of epidural hematoma in children do not generally appear until 24 hours or more after injury (see Family-Centered Care box and Emergency Treatment box, p. 1530).

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 NPO status (nothing by mouth) 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 (see p. 1519). Antiepileptics are used for seizure control. Antibiotics are administered if there are lacerations or penetrating injuries. Prophylactic tetanus toxoid is given as appropriate. (See Chapter 12.) Cerebral edema is managed as described for the unconscious child. Hyperthermia is controlled with a hypothermia blanket.

Nursing Care Management

The hospitalized child requires careful neurologic assessment and evaluation (see p. 1511) 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 the recovery phases.

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.

Skill—Implementing Seizure Precautions

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 practitioner. Decreasing restlessness after administration of an analgesic most likely reflects pain control rather than a decreasing LOC. (See Pain Assessment and Pain Management, Chapter 7.)

Children may be restless and irritable, but more often their reaction is to fall asleep when left undisturbed. A quiet environment helps reduce the restlessness and irritability. Bright lights are irritating. This often makes checking the ocular responses more difficult and more 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, equality, reaction to light, and accommodation. After the initial elevations usually seen after injury, the vital signs generally return to normal unless there is brainstem involvement.

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 of vital signs or focal neurologic signs (see p. 1512 for evaluation of responsiveness). Frequent examinations of alertness are fatiguing to the child; therefore the child often desires to fall asleep, which may be confused with depressed consciousness. When left alone, the child goes to sleep. 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 child may complain of 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, and any incontinence of bowel or bladder is noted for the child who has been toilet trained.

Observe the child for any unusual behavior, but interpretation of behavior is made in relation to the child’s normal 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]). There would be 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 that may be expected, such as behavioral changes, sleep disturbances, phobias, and seizures. They should understand observations they need to make and how to contact the practitioner 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 are imperative.

Physiologic factors that influence the extent of damage from immersion include resistance to asphyxia and anoxia, which shows some individual variation. The temperature of the water plays an important role in developing hypoxemia. Cold water decreases metabolic demands, thereby decreasing the effects of hypoxemia. Cold water also activates the diving reflex. This is a primitive neurologic response, often seen in children, of bradycardia and breath-holding. This neurologic response is triggered by immersion of the face in cold water. Blood is shunted away from the periphery to vital organs (i.e., the brain and heart). Submerged children struggle initially to stay above water, and often breath-hold leads to air hunger. Reflex inspiration eventually occurs, which leads to aspiration or reflex laryngospasm due to water contacting the lower respiratory tract (Salomez and Vincent, 2004). Cardiopulmonary arrest is secondary to hypoxemia and hypothermia.

Pathophysiologic features in submersion injuries are hypoxia, aspiration, and hypothermia. 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. The major difficulty is acute ventilatory insufficiency. Approximately 10% of submersion injury victims die without aspirating fluid but succumb from acute asphyxia as a result of prolonged reflex laryngospasm (see Research Focus box).

Aspiration of fluid occurs in the majority of submersion injuries. The aspirated fluid results in pulmonary edema, atelectasis, airway spasm, and pneumonitis, which aggravates hypoxia. It was previously thought that the physiologic response differed between submersion in salt water and fresh water. However, there is no clinically significant difference in human survivors, and the type of water does not alter the therapy or outcome. The duration of submersion and severity of the hypoxia are the main factors that determine outcome (American Heart Association, 2005).

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.

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. Many victims need care for some time after aspiration of fluid. 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 12 to 48 hours 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. 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 severe guilt reactions. Given the magnitude of the event, parents need repeated assurance that everything possible is being done to treat their child.

If the child dies, the sudden, unexpected nature of the death and the particular circumstances of the accident, especially in terms of guilt for not preventing it, compound the grief. (See Chapter 23.) The parents of the child who is saved from death face the anxiety of not knowing the final outcome—to what extent will their child recover? This situation generates such intense feelings of loneliness and guilt, it is important for families to know they are not alone. They should be reminded frequently that there are people to assist them through this crisis. Additional sources of support that can be recommended include psychiatric and social work consultants, community services, and religious support. Self-help groups are excellent if available in the community.

Nurses often have difficulty relating to the parents if obvious neglect has precipitated the accident and subsequent problems; therefore 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 new vaccinations (Hib and PCV7), the pathogens responsible for meningitis have changed. Currently S. pneumoniae and Neisseria meningitidis are the leading causes of bacterial meningitis in children between 3 months and 19 years. S. pneumoniae is the leading cause in children between 3 months and 10 years, and N. meningitidis is the leading cause in children between 10 and 19 years. The distribution of causative pathogens differs in children between 1 and 3 months. The leading causes of neonatal meningitis are group B streptococci (39%) and gram-negative bacilli (32%) (Nigrovic, Kuppermann, and Malley, 2008).

Meningococcal meningitis occurs in epidemic form and is the only type readily transmitted by droplet infection from nasopharyngeal secretions. Although this condition may develop at any age, the risk of meningococcal infection increases with the number of contacts; therefore it occurs predominantly in school-age children and adolescents. There appear to be some seasonal variations. Meningitis caused by pneumococcal and meningococcal infections can occur at any time, but is more common in later winter or 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. Risk factors for children developing meningitis include recent exposure to someone with meningococcal meningitis; recent ear or sinus infection; travel to areas where bacterial meningitis is common such as sub-Saharan Africa; penetrating head trauma; cochlear implant devices; and anatomic defects such as a dermal sinus, urinary tract anomaly, or recent placement of a ventricular shunt (Chavez-Bureno and McCracken, 2005).

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 BBB, 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 37-6).