Acute Head Trauma in Infancy and Childhood: Clinical and Radiologic Aspects

Symposium on Pediatric Emergencies

Acute Head Trauma in Infancy and Childhood

Clinical and Radiologic Aspects

N. Paul Rosman, M.D.,'~ Joel Herskowitz, M.D.,t Anthony P. Carter, M.B., B.S.,! and John F. O'Connor, M.D.§

Head trauma is one of the commonest causes for admission to hospital in the United States, accounting for nearly one quarter million children hospitalized annually. Indications for hospitalization generally include loss or other significant alteration of consciousness, memory deficit, focal neurologic signs, post-traumatic seizure, persisting posttraumatic vomiting, fever, severe headache, skull fracture, and/or suspicion of child abuse. Admission may also be justified if the specific circumstances of the head injury cannot be ascertained. The goals of such hospitalization include careful observation for signs of acute complications of head injury, with frequent monitoring of state of consciousness and vital signs, and specific treatment for problems such as compound skull fracture, post-traumatic seizures, and intracranial hemorrhage. The development of computerized tomographic (CT) scanning has revolutionized the role of radiology in the management of head trauma. The procedure is safe and can be repeated to reassess a changing neurologic picture, thereby correlating clinical and pathologic changes. Progressive improvement of CT scanners has enabled rapid examination of the brain (3 to 10 seconds per slice), virtually eliminating the need for 'Professor of Pediatrics and Neurology, Director of Pediatric Neurology, and Associate Director of Pediatrics, Boston University School of Medicine and Boston City Hospital, Boston, Massachusetts t Assistant Professor of Pediatrics and Neurology, Boston University School of Medicine; Assistant Visiting Physician for Pediatrics, Boston City Hospital, Boston, Massachusetts !Associate Professor of Radiology, Boston University School of Medicine; Chief of Neuroradiology, Boston City Hospital and University Hospital, Boston, Massachusetts §Professor of Radiology and Pediatrics, Boston University School of Medicine; Director of Pediatric Radiology, Boston City Hospital and Kennedy Memorial Hospital

Pediatric Clinics of North America-VoL 26, No.4, November 1979

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sedation. Resolution has improved greatly, and relatively thin slices (2 to 5 mm) are now achievable. It is established that CT scanning provides detailed information concerning gross structure of tissue and is anticipated that further development of CT scanners and contrast media will allow dynamic functional studies, such as ones involving cerebral blood flow and cerebrospinal fluid circulation. This discussion of clinical aspects of head injuries in childhood, with special focus on the radiologic role in management, takes place at a time of shared concern by patients, physicians, the public, and regulatory agencies that radiation dosage be minimized. Clearly, the indication for any radiologic procedure should be carefully assessed. When the clinical criteria for radiologic studies are met, however, the advantages to the patient far exceed the risk of radiation. Most children with head injury, including those hospitalized, will recover uneventfully. Others, however, will suffer seizures, motor handicaps, learning difficulties, and emotional impairment. A minority will succumb to the direct effects of head injury, to complications of head trauma, or to associated injury. In this article we summarize our approach to acute head trauma in infancy and childhood.

FUNCTIONAL ANATOMY The scalp, skull, and brain all may suffer injury as a result of head trauma. Figure 1 depicts a portion of brain, its surrounding structures. and pathologic entities that occur secondary to head trauma. The scalp,

ricranium

1. 2. 3. 4. 5. 6. 7. 8. Figure 1.

Caput succedaneum Subgaleal hematoma Cephalohematoma Porencephalic cyst or Leptomeningeal cyst Epidural hematoma Subdural hematoma Cerebral contusion Cerebral laceration

Subarachnoid space (CSF)

Brain, skull, surrounding structures, and pathologic entities relatedto trauma.

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lying outermost, is bounded on its inner surface by the galea aponeurotica, a tendinous sheath connecting the frontalis and occipitalis muscles. Beneath the galea is the subgaleal compartment, a potential space containing loose connective tissue. Immediately below lies the skull, the outermost portion of which is the pericranium, or periosteum. The outer and inner tables of the skull are separated by the diploic space, traversed by small veins. The dura, lying just below the inner table of the skull, adheres more closely to the cranium in the infant than in the older child and adolescent. It contains few blood vessels in contrast to the leptomeninges, which are closely applied to the brain. Small caliber veins from the leptomeninges traverse the subdural space to drain into dural sinuses. Other components of the intracranial vascular system include large vessels such as the internal carotid arteries and venous sinuses, intermediate sized vessels such as the middle cerebral arteries and veins, arterioles, venules and, ultimately, capillary networks. The brain itself, with cortex outermost and white matter lying more deeply, is bathed by cerebrospinal fluid within the subarachnoid space, which forms cisterns, ventricular cavities, interconnecting channels, and foramina.

MANAGEMENT OF THE CHILD WITH HEAD INJURY This section is devoted to the approach to the head-injured child: history, examination, investigation with special attention to plain radiography and CT scanning, and treatment. History

It is essential that the specific circumstances of head trauma be determined and that predisposing factors be identified. Such information should be sought directly from the child whenever possible and additionally from observers, who may include playmates, teachers, parents, or ambulance attendants. Under emergency circumstances such as post-traumatic status epileptic us or acute intracranial hemorrhage, it may be necessary for the history to be obtained by someone other than the person dealing specifically with the injured child. Details of the accident should be supplemented by observations as to memory loss, perseverative questioning, disorientation, and visual disturbance, as well as symptoms of increased intracranial pressure such as impaired consciousness, vomiting, severe headache, and altered vital signs. The infant or younger child may sustain head trauma from a fall from mother's arms, down stairs, or out of windows. This age group is also vulnerable to inflicted injury as part of a child abuse syndrome. 2 ,5.48 The older child or adolescent may sustain injuries in bicycle, skateboard, motorcycle, or automobile accidents. If the child was wearing a seat belt or other restraining device, inquiry should be directed to abdominal or lumbar spine trauma in addition to the more obvious head injury. Diving and tree-climbing accidents may involve cervical as well as head trauma. Athletic injuries and penetrating wounds occurring in suicidal or homicidal attempts are most commonly seen among adolescents. 29

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Factors predisposing to head trauma include alcohol or other drug abuse, seizure disorder, hyperactivity, gait disturbance, and disturbed parent-child interaction. Child abuse or neglect should be suspected in the child who has sustained repeated head trauma, which may have been associated with limb fractures or other injuries. General Physical Examination

Vital signs demand immediate diagnostic attention and, at times, emergency therapeutic intervention. Characteristic changes in pulse, blood pressure, and respiration may implicate shock (increased pulse, decreased blood pressure) or increased intracranial pressure (slowed and/or irregular respiration, decreased pulse, increased blood pressure). These and other signs of intracranial hypertension, as seen in infants and older children, are summarized in Table 1. A decrease in blood pressure in the child with head injury usually results from injury outside of the central nervous system, such as abdominal trauma resulting in a ruptured spleen or liver. Occasionally, however, sufficient extravasation of blood may occur extracranially as with subgaleal hematoma or intracranially as with epidural hematoma to produce shock. The entire body should be checked for signs of trauma. Examination should include a search for injl,lry to the neck, chest, abdomen, and long bones as well as a careful inspection of the skin. The neck should be examined with care because' of possible unsuspected injury. Initial assessment may be limited by sandbags or a cervical collar. Cervical abrasions or upper spine tenderness suggest neck injury. Meningismus may result from cervical trauma, subarachnoid bleeding, or cerebellar tonsillar herniation. The head must be examined carefully. The scalp should be inspected and the skull palpated for tenderness or depression. Tension of the anterior fontanelle should be assessed in the infant. Transillumination of the skull in infants and young children may detect abnormal accumulaTable 1. Signs of Acute~y Increased Intracranial Pressure Infants and children Altered mental state Vomiting Strabismus (palsies of cranial nerves VI and III) Altered vital signs (slowed respiration, decreased pulse, increased blood pressure) (Signs of herniation) Infants Full fontanelle Separated sutures (Macrocrania) (Papilledema) Children Headache Papilledema

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tions of fluid outside or inside the skull. Periorbital hemorrhage ("raccoon eyes"), ecchymosis behind the ear (Battle's sign), or bleeding from the nose or ears should be noted. These, along with cerebrospinal fluid otorrhea or rhinorrhea, are indications of a basal skull fracture. Neurologic Examination

Neurologic examination should include assessment of the child's state of alertness, orientation, memory functions, and neuroophthalmologic signs, in addition to motor, sensory, reflex, and coordinative functions. Level of consciousness may range from normal to clouding of consciousness (reduced wakefulness or awareness), stupor (relative unresponsiveness with arousal only by vigorous and repeated stimulation), or coma. Testing of orientation and memory functions, when possible, should include an account by the child of the incident of head trauma. The presence and extent of retrograde and anterograde (posttraumatic) amnesia should be determined. Additional assessment of memory should include testing of digit span and recall of three items after five minutes. A child's repeated asking of the same question, despite its having been answered several times previously, suggests a posttraumatic memory disturbance. Neuro-ophthalmologic assessment should include measurement of pupillary size under ambient illumination and upon exposure to bright light. Magnification may be required to detect subtle reactions. The fundi should be examined with care, and evidence of retinal hemorrhage and papilledema specifically sought. Abnormalities of ocular gaze and position may include roving eye movements, limitations in lateral and vertical gaze, and skew deviation. If there is no significant neck injury, the oculocephalic (doll's head) maneuver can be employed to assess extraocular movements. Lateral gaze may also be tested in the comatose patient through the oculovestibular reflex by means of caloric stimulation of the vestibular apparatus. Patency of the external auditory canal and intactness of the tympanic membrane should first be established. A combination of the oculocephalic maneuver and caloric irrigation provides a stronger stimulus than either technique alone. In the alert child, testing of visual fields and acuity should also be carried out. The extent of examination of the motor system will depend upon the state of alertness and orientation of the child. In the comatose patient, decorticate, decerebrate, or other abnormal posturing should be noted. Noxious stimulation such as sternal pressure may be required to produce such posturing. Flaccidity or spasticity may be seen in a hemiparetic or para paretic distribution. In the more alert child, motor impairment may be detected by individual muscle testing, examination of gait, or extension of supinated arms. Testing of deep tendon reflexes and plantar responses complete this portion of the examination. Radiologic Investigations

The radiologic evaluation of head injury includes plain radiography of the skull and cervical spine, CT scanning, cerebral arteriography, and isotope studies. Of these, plain skull radiographs and CT scans are the

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most frequently employed and most useful studies. Arteriography in the evaluation of head injury has declined dramatically whenever CT scanning is available. Isotope studies are not indicated in acute head injury, as the associated soft tissue changes negate the value of the brain scan. In subacute and chronic head injury, however, isotope studies still may be indicated occasionally, though much less often since the introduction of CT scanning. The use of skull radiography in head injury has been the subject of much discussion and controversy in the last decade. There has been an increasing tendency to eliminate radiographic investigation in patients with minor head injuries because of the infrequency of positive findings. 12,27 The following criteria have been found to give a high yield of radiologic findings following head trauma::l R Historical Unconsciousness more than five minutes Retrograde amnesia more than five minutes Vomiting Gunshot wound or accident at work Nonvisual focal symptoms General Physical Examination Palpable bony malalignment Discharge from ear Discharge from nose Ear drum discoloration Bilateral black eyes Neurologic Examination Stupor, semiconsciousness, or coma Irregular breathing or apnea Babinski reflex Other reflex abnormality Focal weakness Sensory abnormality Anisocoria Other cranial nerve abnormality

Utilizing these criteria, Phillips and others have demonstrated that the number of skull radiographs done for head trauma can be diminished by some 40 per cent. We have been using similar criteria for the past 10 years to determine the need for hospitalization of children with head injuries and feel that while these criteria may result in "missing" the occasional skull fracture, they identify essentially all children with head injuries requiring neurologic or neurosurgical intervention. Through adherence to these criteria, needless radiation of the eye and thyroid of infants and children has been minimized. It should be stressed, however, that radiographs of the skull need not be obtained in every child in whom high yield criteria are present; rather, their presence enhances the value of radiographic examination in the management of the patient's clinical course. We have added to the high yield criteria above a high velocity injury caused by a sharp or conical structure, such as a pencil or child's bow and arrow, which may cause a small depressed fracture, compound or otherwise, with or without symptoms.

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In relatively minor head injuries without high yield criteria, radiographs of the skull are probably unnecessary unless a significant scalp swelling or palpable skull defect is present. In other instances of head injury, plain radiographic studies may provide confirmatory or specifically diagnostic information. 13 Skull x-ray views should generally include anteroposterior, right and left lateral, and inclined anteroposterior (Towne) views, with at least one lateral view taken with a horizontal beam (cross-table). Fracture across the temporal bone may support a clinical impression of acute supratentorial epidural hemorrhage, whereas an occipital fracture might suggest a posterior fossa bleed. The crosstable lateral view is useful in demonstrating gas-fluid levels in the cranial cavity, parana sal sinuses, or ventricular system, a sign of compound fracture or basal skull fracture or both. With extensive head or facial trauma, a single Waters projection of the facial bones as well as films of the orbit may also prove to be useful. If a depressed skull fracture is suspected, a tangential view of the area should be obtained in addition to routine views. In the presence of severe head injury or when injury to the neck is evident or otherwise suspected, initial radiographic examination should include anteroposterior and lateral views of the cervical spine. In the child with major head trauma, cervical spine injury should be excluded as soon as possible, since manipulation of the neck, as may be required in the management of problems such as cardiorespiratory arrest, may result in cord transection and quadriplegia. Of course, the emergency nature of the clinical situation may not permit even portable skull or spine radiographs to be obtained if intracranial pressure is acutely elevated and cerebral herniation evident or impending. Following more severe head trauma with localizing or changing neurologic signs, other imaging modalities such as CT scanning and arteriography must be employed.1,9.30 In our opinion, all children with persistent or progressing neurologic signs should have a CT scan as soon as it can be performed, their clinical state permitting. Unilateral intracranial hemorrhage will usually be readily evident on CT scan as a relatively dense mass during the immediate post-traumatic period, when the scan may be done without infusion of contrast medium. After several days, extravasated blood incompletely broken down may be of the same density as contiguous brain tissue; therefore, it is important to do scans with and without contrast medium at that time. Vital signs and neurologic status should be carefully monitored throughout all radiologic procedures. It is well to recall that the potential for reactions to contrast medium is the same whether it is used for intravenous pyelography, angiography, or CT scanning. Provision should be made for management of these reactions at the time of the injection of contrast medium and for several hours thereafter. When contrast is not used and intracranial hemorrhage is not apparent, it may nonetheless be suspected through deformation of ventricular structures or by midline shift. It is important to remember that in bilateral lesions, such as acute subdural hematomas of infancy, a shift of midline structures may not occur.

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Bilateral intracranial hemorrhages may produce ventricular enlargement through blockage of the cerebral subarachnoid spaces, or may cause reduction in ventricular size owing to compression of brain tissue. Late subdural hematomas are often best defined by radionuclide scanning. One of the great values of CT scanning is that it can be safely repeated. Thus, a pathologic process such as cerebral contusion or subdural hematoma can be monitored. Initial studies performed within a few hours of the injury may be negative or show only minor changes. Repeat studies, however, may show progression of the lesion, as in cerebral contusion and intracranial hematoma, and may show changes of brain herniation. Follow-up studies will often demonstrate chronic structural complications associated with head injury such as hydrocephalus. Some radiologic centers have recommended that routine skull radiography be abandoned in favor of immediate CT scanning. While it is frequently true that clinical decisions can be made on the grounds of the CT scan alone, successive CT scan cuts may fail to demonstrate focal skull depressions, and associated facial or basal skull trauma may also be overlooked. We feel, therefore, that plain skull radiographs should be obtained before CT scanning is performed except in children with severe head injuries in whom the need for prompt treatment seems likely. Other Investigations

Lumbar puncture should not be performed in the child with head injury unless complicating central nervous system infection is suspected. It is usually contraindicated in the presence of significantly elevated intracranial pressure, and is absolutely contraindicated if there is evidence for a mass lesion. Lumbar puncture may provide evidence not only for infection, as with meningitis complicating basal skull fracture, but also of recent subarachnoid bleeding as with cerebral contusion, more remote subarachnoid bleeding as evidenced by xanthochromic cerebrospinal fluid following chronic subdural hematoma, and elevated intracranial pressure, which may complicate a variety of head injuries. Subdural taps may be indicated as a diagnostic measure, as a therapeutic measure, or for both reasons. Treatment

Treatment of the child with head injury must not be restricted necessarily to the head. The spine, long bones, chest, abdomen, and scalp may also require treatment. Respiratory support must be provided. as needed. Patency ofthe airway must be ensured with use of an oral airway or endotracheal intubation and assisted ventilation as required. The child should be placed in a lateral decubitus position, secretions removed by suction, the stomach emptied by nasogastric intubation, and an intravenous line established. Limb fractures should be splinted. If neck trauma is suspected, a cervical collar or sandbags should be applied. Circulatory failure must be treated promptly. External hemorrhage must be brought under control and blood volume maintained. Seizures should be treated with anticonvulsants. The child with an acute head injury may require emergency treatment if death or serious morbidity is to be averted. Slowed and/or

z

o

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Table 2. Medical Management of Acute Intracranial Hypertension in Head Trauma AGENT

DOSE

ADMINISTRATION

ONSET OF ACTION

PEAK ACTION

Passive hyperventilation

Reduce pCO, from 40 to 25 torr

Continuous

Minutes

2 to 30 min

Mannitol

0.25 to 2.0 gm per kg

Every 4 to 6 hr IV

20 to 30 min

20 to 360 min

Glycerol

0.5 to l.5 gm per kg

Every 6 hr IV or orally

15 to 30 min

Pentobarbital

3 mg per kg (loading dose: 5 mg per kg)

Every hr IV

Minutes

30 min (IV), 60 to 80 min (orally) Minutes

Hypothermia

29 to 31°C

Continuous

Approx. 1 hr

2 to 3 hr

No rebound

Dexamethasone

8 mg ("megadose")

Every 2 hr IV

12 to 18 hr

12 to 24 hr

No rebound

ADVANTAGES

Very prompt action; does not potentiate intracranial bleeding Prompt action

Prompt action by oral or IV route Prompt action; no rebound

SIDE EFFECTS OR LIMITATIONS

Effect may not be sustained; cerebral ischemia

Rebound; dehydration; renal failure; intracranial bleeding Rebound may occur; dehydration; intracranial bleeding Hypotension; renal failure; need for careful monitoring Cardiac arrhythmias; need for careful monitoring Slow onset of action; uncertain efficacy in head injury; GI hemorrhage

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irregular respirations, bradycardia, and elevated blood pressure suggest acutely raised intracranial pressure (see Table 1). Treatment of intracranial hypertension includes supportive therapy, particularly maintenance of airway and circulatory support, and one or more of the following modes of therapy: passive hyperventilation; intravenous mannitol, glycerol, pentobarbital, hypothermia, or corticosteroids; aspiration of epidural or subdural spaces; and ventricular drainage. The medical management of acute intracranial hypertension following head injury is outlined in Table 2, which details the administration, advantages, and limitations of the various therapies. 6.8.14.21.31,32.41,44.45.47,49,50

CLINICAL SYNDROMES IN CHILDREN WITH HEAD INJURIES This section presents specific clinical symptoms, signs, and syndromes associated with head trauma, including a discussion of scalp injuries, skull fractures, cerebral concussion, contusion, and laceration, post-traumatic epilepsy, transient post-traumatic blindness, and acute epidural and subdural hematomas. Scalp Injuries

Contusion and laceration are frequent manifestations of scalp injury. Most scalp swellings following head trauma in the older child are the result of a subgaleal hematoma. In the newborn or older infant, scalp swelling may be caused by subgaleal hemorrhage, caput succedaneum, cephalohematoma, or porencephalic or leptomeningeal cyst. These entities can be differentiated by noting whether the distribution of swelling is diffuse or focal and whether transillumination is increased or decreased (Fig. 2). Diffuse scalp swelling with decreased transillumination suggests subgaleal hematoma, whereas diffuse scalp swelling with increased transillumination indicates caput succedaneum. If the scalp swelling is focal (particularly in the parietal region) and transillumination is diminished, cephalohematoma is the likeliest cause (Fig. 3). Skull fracture, usually linear, has been associated with cephalohematoma in 0.2 to 25 per cent of cases.;;5 Focal swelling and increased transillumination sug-

Scalp Swelling

I

Diffuse

Increased

Caput succedaneum

Decreased

Subgaleal hematoma

I

I

Focal

Porencephalic or Leptomeningial cyst

{ Transillumination

Cephalohematoma

Figure 2. Clinical diagnosis of post-traumatic scalp swellings.

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Figure 3. Bilateral parietal cephalohematomas.

gest a porencephalic or leptomeningeal cyst, either of which may be associated with so-called "growing" fractures of the skull!8 Scalp laceration frequently will require suturing, preceded by thorough irrigation of the wound with sterile solution and hemostasis of the highly vascular injured tissue. Prevention of tetanus is essential. Specific tetanus prophylaxis will depend upon the nature of the penetrating object, the extent of the wound, the length of time the wound has been unattended, and the child's previous immunization status including allergic reaction to tetanus toxoid. A fully immunized child with a minor scalp laceration who has had a tetanus booster within the past 10 years need not be given tetanus toxoid or antitoxin. By contrast, the child with an open scalp wound who has not received medical attention for more than 24 hours should receive both passive and active immunization regardless of previous immunization status. 7 Scalp sweliing resulting from caput succedaneum does not require treatment, nor does that caused by cephalohematoma or subgaleal hematoma. Aspiration of such hematomas is of no benefit and may introduce infection. In rare instances, sufficient blood may be lost into the scalp in subgaleal hemorrhage that anemia or even shock may result. Such bleeding may be evident upon palpation of the skull and measurement of occipitofrontal circumference. In cases involving excessive scalp hemorrhage, it may be important to exclude a bleeding or clotting disorder. Skull Fractures

Linear, depressed, compound, basal, diastatic, and "growing" fractures may result from head trauma. Linear fractures make up about 75 per cent of skull fractures in childhood. The presence of such an injury does not itself necessitate

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Fig. 4

Fig. 5

Fig. 6

Figure 4. A lateral skull film in a three year old child shows a typical linear skull fracture in the frontal bone extending posteriorly across the coronal suture. When such fractures cross the grooves of the middle meningeal artery in the parietal or temporal bone, the patient is at greater risk for developing an epidural hematoma. Figure 5. An eight month old female has multiple linear skull fractures throughout both sides of the vault caused by child abuse. Associated soft tissue swelling, not apparent in this photographic reproduction, is best visualized by brightly lighting the edges of the radiograph. Fracture lines can be differentiated from suture lines by their location and lack of interdigitation: fracture line, closed arrows; suture line, open arrows. Figure 6. Films demonstrate a linear parietal skull fracture (closed arrows) in a 10 year old boy six months after the fracture was incurred. Most linear fractures either remain the same or gradually disappear over six to 12 months. Occasionally, the fracture line will expand, with a palpable mass projecting from the "growing" fracture.

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Fig. 7

Fig. 8

Fig. Fig . 99

Figure 7. Anteroposterior and both lateral films of a 16 year old boy struck on the head with·a lead pipe. Lateral films show the differing appearance of depressed skull fragments when the fracture site is seen in tangent (left film) as contrasted with the typical double density when the fracture fragment is seen superimposed on the contralateral vault (right film). Occasionally, the double density of bone fragments viewed on edge may be the only evidence of depressed skull fracture. Arrows point to the depressed fragment in all three views. Figure 8. A more typical, but less obvious, depressed skull fracture shows no evidence of a radiolucent fracture line in anteroposterior or lateral projections. Trauma was incurred in a motor vehicle accident, when the child's head presumably contacted a projection in the vehicle. Double densities are seen in both views (arrows). Figure 9. Lateral and anteroposterior films of a stellate depressed skull fracture resulting from a playground injury with a baseball bat. Note the radial fragments on the lateral view (open arrows). On the anteroposterior view, the double density of depressed fragments on edge (open arrows) is seen on the right side of the skull.

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specific treatment but indicates that a significant head injury has occurred, generally meriting hospitalization. Linear fracture across the petrous temporal bone may be associated with tear of the underlying middle meningeal artery and result in an epidural hemorrhage. A late complication of linear fracture, occurring within six months of head trauma, is a "growing" skull fracture. Linear fracture of the skull in the infant or younger child should raise the possibility of child abuse or neglect (Figs. 4 to 6). Depressedfractures involve disruption of the integrity of the skull or simply indentation, as in the "ping-pong ball" or "pond" fracture. The latter is seen in the normal infant only in the newborn period, when the cranium is less well mineralized and more easily distorted than in later life. Depressed skull fractures may be palpable or diagnosed only with tangential skull radiographs, which may demonstrate a characteristic double density (Figs. 7 to 10).4 Brain tissue underlying the depression can suffer contusion or laceration that may later serve as an epileptogenic focus. Elevation of depressed skull fractures has been advocated if the depression exceeds 5 mm or if the depressed fragment extends below the inner table of the skull, but such elevation appears not to diminish the risk of post-traumatic epilepsy,4 presumably because of brain injury sustained at impact. Compound fractures involve laceration of skin down to the site of bony fracture, which may be linear, depressed, or comminuted. Prompt surgical debridement should be carried out, unless contraindicated by the child's clinical state, with elevation and/or removal of depressed or fragmented bone. 35 Both antibiotic and antitetanus prophylaxis are indicated. Basalfractures involve a break in basal portions of frontal, ethmoid, sphenoid, temporal, or occipital bones. These fractures may be over-

Figure 10. Tangential views of a "ping-pong" fracture in a newborn inj'ant. These fractures are sometimes produced by obstetric forceps or other focal pressure on the cranial vault. A fracture line is usually not demonstrated.

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Figure 11. Periorbital hematomas resulting from a basal skull fracture of the floor of the anterior cranial fossa ("raccoon eyes" sign).

looked radiographically owing to the complicated radiologic features of the base of the skull and overlapping shadows. Hence, the diagnosis is usually established through characteristic clinical features. These include hemorrhage into the nose, nasopharynx, or middle ear (producing a hemotympanum if bleeding occurs behind the tympanic membranes), over the mastoid bone (Battle's sign), or about the eyes ("raccoon eyes" sign) (Fig. 11). Traumatic cranial nerve palsies may occur as well, and most frequently involve cranial nerves I, VIII, and VII, in order of decreasing likelihood. Cerebrospinal fl~id rhinorrhea and otorrhea reflect fracture of the cribriform plate or petrous temporal bone, respectively, with tearing of overlying meninges and subsequent leakage of cerebrospinal fluid from the subarachnoid space through the fracture site. A potential avenue for meningeal infection is thus established. The usual pathogens are S. pneumoniae and H. influenzae, type b. Cerebrospinal fluid rhinorrhea is more common than otorrhea and is more likely to persist. If either does persist, surgical repair may be required to prevent complications, particularly recurrent meningitis. ;)5.51 Occipital fractures extending to the foramen magnum may be readily discernible clinically. Characteristic signs are tachycardia, hypotension, and irregular respirations caused by brains tern compression associated with posterior fossa hemorrhage. Radiologic features of basal skull fracture include pneumocephaly and opacification of maxillary sinuses, typically seen best in lateral views taken with a horizontal beam (cross-

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table). Pneumocephaly is caused by introduction of air intracranially by a fracture through a paranasal or mastoid sinus. Air may be seen in the subdural space, subarachnoid space, intracerebrally, or intraventriculady. Sinus opacification results from hemorrhage into one or both maxillary sinuses. The risk of developing meningitis following basal skull fracture in children, particularly those in whom the only manifestation is hemotympanum, appears to be very small. 11 Although the efficacy of antibiotic prophylaxis has not been proved, a preventive regimen of intravenous ampicillin has been recommended: 300 mg per kg per day over four days, given in four hourly doses. 46 Diastatic fractures are traumatic separations of cranial bones at one or more suture sites. They most frequently affect the lambdoid suture and usually occur within the first four years oflife (Fig. 12). Specific therapy is not required unless a "growing" fracture occurs as a late complication. "Growing" fractures reflect the development of a cyst at the site of either a linear or a diastatic skull fracture which prevents fusion of fracture margins. Growth of such fractures has traditionally been attributed to a protrusion of leptomeninges ("leptomeningeal cyst") through a dural tear between the fracture margins (see Fig. 6). Recent data indicate, however, that such cysts more frequently are of porencephalic

Figure 12. 12. Anteroposterior, Anteroposterior, Figure lateral,and andtangential tangentialviews viewsof ofthe the lateral, cranial vault vault are are shown shown after after ococcranial cipital head head trauma. trauma. AA diastatic diastatic cipital separation of of the the right right lambdoid lambdoid separation sutureisisvisible visibleininall allthree threeviews. views. suture Compare the the separated separated portion portionof of Compare the suture suture ( closed (closed arrows) arrows) with with the the non nonseparated separated portion portion ( open (open the arrows ). arrows).

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type, usually in communication with the lateral ventricle on the same side. 28 Growing fractures are usually seen in children under three years of age, occur most frequently in the parietal bone, and develop within the first two to six months after head injury. Treatment consists of excision of the cyst, repair of the underlying dural tear, and cranioplasty.35 Cerebral Concussion

Concussion is characterized by transient impairment of consciousness (loss of awareness and responsiveness) following immediately upon head trauma. The period of unresponsiveness may last from several seconds to several hours. In the absence of reliably observed unconsciousness, the diagnosis of concussion is suggested strongly by characteristic memory deficits: temporary retrograde, permanent retrograde, and temporary post-traumatic (anterograde) amnesias. The temporary retrograde amnesia, in which memory of events that occurred for several years prior to head injury is lost, lessens considerably within a few hours of impact, and eventually disappears. The permanent retrograde amnesia, encompassing the few seconds to few minutes immediately before the injury, remains. This period is never directly recalled. The temporary post-traumatic amnesia is an especially valuable sign of concussion. It takes the form of a Korsakoff-like inability to lay down new memories, a failure to acquire or retain new information over the several minutes to hours after impact. Typically manifested by perseverative questioning, this memory disturbance usually clears spontaneously within 24 hours. In addition to these acute sequelae, a post-concussion syndrome can sometimes be seen following an otherwise uncomplicated concussion. Acceleration, particularly of rotational type, and deceleration have been demonstrated experimentally in animals to play major roles in causing cerebral ,concussion. 1O,:J6 Loss of consciousness has been attributed by these authors to shearing strains acting at the mesencephalic level. That no consistent pathologic entity in the brain has yet been identified in cerebral concussion underscores the probable subcellular basis of this disorder. Cerebral Contusion

Cerebral contusion is a bruising or crushing injury to brain. It generally results from blunt trauma to the head and, in contrast to laceration, is unaccompanied by interruption in continuity of adjacent structures. Several mechanisms have been identified in producing cerebral contusion. As a result of rotational and other accelerative influences, the orbital surfaces of the frontal lobes, the anterior temporal lobes, and the frontal-temporal junctions may sustain contusion as these portions of brain impact forcefully against the fixed, irregular surfaces of the orbital roofs, the lesser wings of the sphenoid, and the free edges of the tentorium respectively (Fig. 13). Depressed skull fracture, including the "ping-pong ball" variety, may cause contusion, or it may occur in head trauma without skull fracture. The contusion underlies the site of impact in the so-called "coup" injury in contrast to damage opposite the site of impact seen in the "contre coup" lesion.

't

724

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J.

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A. P.

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Figure 13. Parasagittal section of the brain shows contusions of the inferior frontal and anterior temporallobes.

The clinical diagnosis of contusion is based on the demonstration of focal neurologic signs, including focal seizures, known or presumed to be absent prior to the injury. The CT scan frequently will provide important radiologic confirmation (Figs. 14 to 16). The diagnosis of contusion based on prolonged unconsciousness alone is not uniformly accepted. Cerebral Laceration

Injury causing discontinuity of brain tissue is defined as laceration. As with contusion, dural septa or bony projections or both may produce cerebral laceration. More commonly, however, such a lesion is caused by penetrating wounds resulting from depressed skull fragments or missile injuries. Gunshot wounds of the head may be associated with direct injury to brain as well as laceration of intracranial vessels, producing major intracranial hemorrhage. Bone fragments and associated debris within the cranial cavity may provide a nidus for cerebral abscess and meningitis. CT scanning has been found to be valuable in the assessment of gunshot injuries to the head to detect operable intracranial hemorrhage. Early treatment with careful debridement and meticulous closure of the dura to prevent herniation of swollen brain and leakage of cerebrospinal fluid is indicated in such cases. 20 Post-Traumatic Epilepsy

Approximately 5 per cent of children hospitalized following head trauma will suffer a seizure within the first week after injury. Such early post-traumatic seizures are followed by epilepsy beyond the first week in 20 to 25 per cent of patients followed for a minimum of four years. 24 Skull fracture (linear or depressed), acute intracranial hemorrhage, focal signs (reflecting cerebral contusion), and post-traumatic amnesia of greater than 24 hours are all associated with increased risk of early posttraumatic epilepsy. If the first seizure occurs after the first week, so-called late posttraumatic epilepsy, the risk of a subsequent seizure in the next four years is nearly 75 per cent.24 The incidence of late post-traumatic epilepsy

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Fig. 14

Fig. 15

Fig. Fig. 16 16

Figure 14. Anteroposterior and lateral skull films of a two year old child with biparietal linear skull fractures (arrows) following trauma in a motor vehicle accident. Note that the fracture line on the side of the vault closer to the film (closed arrows) is sharper and narrower than the fracture line in the vault separated from the film by the width of the skull (open arrows). This is the result of geometric enlargement of the fracture line away from the film surface. Figure 15. On a CT scan taken four hours after the injury noted in Figure 14, a subgaleal hematoma is seen in both parietal regions (closed arrows). The ventricular system is symmetric and in the midline (open arrows). Figure 16. Because of progressing neurologic signs, a repeat CT scan was done six hours after the initial scan. A small left parietal subdural hematoma is seen along with contusion of the brain. The hematoma and contusion are outlined by closed arrows. Note that the ventricular system is compressed and has shifted away from the site of maximum swelling (open arrows).

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among unselected hospitalized patients, as with early post-traumatic epilepsy, is about 5 per cent. 25 The risk is significantly increased with depressed skull fracture, post-traumatic amnesia of greater than 24 hours, dural penetration, acute intracranial hemorrhage, and early posttraumatic epilepsy.26.52 Nearly 40 per cent oflate post-traumatic seizures are focal. Approximately one-half of these are of temporal lobe origin,25 reflecting the vulnerability to contusion of this portion of brain. The pathophysiology of post-traumatic epilepsy remains. obscure. It has been suggested that discrete pathogenetic mechanisms underlie immediate, early, and later post-traumatic seizures. 53 Experimental studies in animals indicate that traumatic depolarization o(neurons is the basis for seizures occurring immediately upon impact. Early posttraumatic seizures have been linked with focal injury to brain (contusion or laceration), associated with local ischemia and metabolic changes such as lactic acidosis. These changes are thought to alter cation transport and lead to states of recurrent depolarization. Late post-traumatic epilepsy has been attributed to scarring associated with distpftion, local vascular compromise, and mechanical irritation of brain. Other factors thought perhaps to contribute to post-traumatic epilepsy include diminution in neuronal dendritic branches, interference with glial uptake of potassium, impairment of inhibitory neurotransmitter function, and genetic influences. 40 •5:1 The therapy in post-traumatic convulsions in children is essentially the same as that employed in the management of non traumatic seizures, except that the child with head injury may also have suffered cranial, thoracic, abdominal, or other injuries that call for prompt surgical attention. Adequate ventilation must be ensured, vital signs maintained, and seizures controlled with intravenous medication. Phenytoin is the· drug of choice because of its rapid entry into brain and lack of prominent sedative effect. It should be given in slow intravenous infusion at 10 to 17 mg per kg (rate: 25 to 50 mg per min) while the pulse is being monitored continuously. If seizures have not fully subsided one-half hour after phenytoin has been given, paraldehyde in a dosage of 1.0 to 1.5 ml per year of age (maximum of 7 ml), mixed with an equal volume of mineral oil, can be given by rectum. Phenobarbital is another drug that may be used for the treatment of seizures complicating acute head injuries. It should be given intravenously in a dose of 5 to 10 mg per kg over 10 to 15 minutes. If seizure activity continues, diazepam can be employed as an alternative or adjunct to paraldehyde in a dosage of 0.3 mg per kg (maximum rate: 1 mg per min) with a total dosage not greater than 2 to 4 mg in the infant or 5 to 10 mg in the older child. This dosage of diazepam can be repeated every 30 minutes, if necessary. Phenobarbital and diazepam given together may act synergistically to cause respiratory depression or hypotension or both. Maintenance anticonvulsant therapy is clearly indicated in cases of late post-traumatic epilepsy and probably should be given to children with early post-traumatic epilepsy as well. Phenobarbital and phenytoin are the most useful drugs for long-term management of seizures. In either instance, the dosage is 5 to 8 mg per kg per day.

i

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The value of prophylactic anticonvulsant therapy following blunt head trauma in children has not been established. 42 Transient Post-Traumatic Blindness

A dramatic, though self-limited occurrence after blunt head trauma is total blindness. 15 This visual disturbance begins immediately after relatively minor head trauma or may follow it by 15 to 20 minutes. The blindness lasts for minutes to hours. The basic pathophysiology of this presumed cortical disturbance is unknown. Intracerebral Hemorrhages

Intracerebral hemorrhages are extensive intraparenchymal contusions. Accordingly, they are found most frequently in the subfrontal and anterior temporal regions. Shearing forces acting upon small blood vessels may also produce such lesions in the deep hemispheric white matter. The clinical features are discussed in the section on cerebral contusion. Epidural and Subdural Hematomas

These forms of intracranial hemorrhage are especially important considerations in the child with head injury. Either may occur following relatively mild head trauma, without associated skull fracture or loss of consciousness. Several features aid in defining and distinguishing intracranial extracerebral hematomas clinically and pathologically (Table 3).46 Both types of hematoma occur much more frequently above the tentorium

Clinical Features of Acute Epidural and Acute Subdural Hemorrhages

Table 3.

Supratentorial Frequency Skull fracture Source of hemorrhage Age Laterality Seizures (Pre-) retinal hemorrhages Increased intracranial pressure CT configuration Mortality Morbidity Infratentorial Frequency Skull fracture Source of hemorrhage

ACUTE EPIDURAL HEMATOMA

ACUTE SUBDURAL HEMATOMA

Less 75 per cent Usually arterial Usually older than 2 years U suall y unilateral Less than 25 per cent Less than 25 per cent

Greater 30 per cent Venous Usually younger than 1 year Usually bilateral 75 per cent 75 per cent

Present

Present

Usually lenticular 25 per cent Low

Usually crescentic Less than 25 per cent High

Greater Almost always Venous

Less Usually Venous

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than below. Supratentorially, the frequency of acute subdural hematoma is five to 10 times greater than that of acute epidural hemorrhage. The latter is associated with a fracture of the squamous portion of the temporal bone in about 75 per cent of cases and is usually caused by laceration of the underlying middle meningeal artery.22.33 At least one quarter of epidural hematomas in children are of venous origin, however, with hemorrhage derived from dural sinuses and diploic veins. Acute subdural hematomas characteristically are of venous origin, resulting from tearing of bridging meningeal veins. Underlying contusion is frequently associated. Shaking injury without direct trauma to the head may also produce subdural hemorrhage. 5 •16,48 Such hematomas when located above the tentorium have an associated skull fracture in only 30 per cent of cases. 17 Splitting of the cranial sutures may be seen when the subdural hematoma is sufficiently large to elevate intracranial pressure (Fig. 17). Acute subdural hemorrhages are usually seen in infancy, with a peak frequency at six months, whereas acute epidural hematomas tend to occur in children beyond infancy. The difference in age of presentation presumably reflects the close adherence of the dura to the inner table of the skull in infancy, rendering epidural blood collection less likely. Acute epidural hematomas are usually unilateral (Fig. 18), whereas at least 75 per cent of acute subdural hematomas are bilateral (Fig. 19). Seizures occur in less than 25 per cent of patients with acute epidural hemorrhages but in 75 per cent of those with acute subdural hemorrhages. Retinal and preretinal hemorrhages are frequently found with acute subdural hematomas (Fig. 20), but are relatively rare with epidural hemorrhage. The "biphasic course" described as characteristic of acute epidural hematoma (impairment of consciousness followed by a transient period of normalcy then lethargy or coma) is seldom seen in children. The relatively large volumes of extravasated blood in both types of hematoma characteristically produce symptoms and signs of acutely

Figure 17. In anteroposterior and lateral films of the skull of a patient with a subdurn'i hematoma following head trauma, note the wide separation of the coronal, lambdoid, and sagittal sutures.

729

ACUTE HEAD TRAUMA IN INFANCY AND CHILDHOOD

Fig. 18

Fig. Fig. 19 19 Figure 18. Figure 19. Figure 20.

Fig. 20

Acute left epidural hematoma. Acute bilateral subdural hematomas. Retinal and preretinal (subhyaloid) hemorrhages in acute subdural hematoma.

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elevated intracranial pressure (see Table 1). Certain of these signs, particularly appearance of an oculomotor (third cranial nerve) palsy and Cushing's triad of slowed and/or ataxic respirations, bradycardia, and elevation of blood pressure are ominous signs of acutely raised intracranial pressure and point to the need for emergency therapy to prevent irreversible brain herniation, with resulting compromise and death. Since the unfused sutures and open fontanelle(s) of the young infant's skull provide outlets for increases in intracranial pressure, herniation is less likely to occur in an infant with an acute subdural hematoma than with an acute epidural hematoma in an older child. With sufficient elevation of pressure in the supratentorial compartment as with an acute epidural hematoma, the temporal lobe on the affected side may be displaced into the only available supratentorial exit, the tentorial notch, to result in unilateral transtentorial herniation (Fig. 21). Such herniation may be more marked anteriorly (uncal herniation) or posteriorly (hippocampal herniation), and is usually accompanied by displacement of the ipsilateral cingulate gyrus under the falx (cingulate herniation). Clinical signs include third nerve palsy usually ipsilateral to the herniation, alteration of consciousness, respiratory irregularities, limb weakness usually contralateral to the herniation, deepening coma, decorticate or decerebrate posturing, and eventually cardiorespiratory failure."·30.39 A less well-recognized type of herniation but one that is actually more frequent than unilateral transtentorial herniation is bilateral or central trans tentorial herniation. This can occur, for example, with diffuse bilateral cerebral edema following head injury. In central herniation, there is symmetric downward displacement of both cerebral hemispheres, resulting in pupillary constriction, diminished consciousness, altered respirations, impaired upgaze, hypertonicity, and decorticate posturing. Altered body temperature, sometimes with diabetes insipidus, pupillary dilation, decerebrate posturing, and cardiorespiratory collapse may then ensue." The CT scan is particularly valuable in differentiating between acute subdural and epidural hematomas.1.9 The former tends to assume a crescentic configuration (Fig. 22) in contrast to the lens-like shape of the latter (Fig. 23). Exceptions to this rule are sufficiently frequent, however, to make such distinctions far from absolute. ls As many as 25 per cent of children with acute epidural hematoma die, but the survivors tend to be relatively free of neurologic sequelae. By contrast, the mortality in acute subdural hematoma is less than in acute epidural hematoma, but the morbidity is greater, doubtless because of the frequent coexistence of injury to underlying brain. Potential sequelae of subdural hematoma include motor deficits, seizures, hydrocephalus, and mental retardation. In contrast to their relative frequencies above the tentorium, acute epidural hematomas are two to three times more frequent in the posterior fossa than are acute subdural hematomas. 19,23,34,54 Occipital skull fracture almost invariably accompanies the posterior fossa epidural hematoma; it occurs less frequently with the infra tentorial acute subdural hemorrhage. In both types of hematoma, bleeding is of venous origin. Clinical

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ACUTE HEAD TRAUMA IN INFANCY AND CHILDHOOD

Figure 21. Temporal Temporal lobe lobe herniation arrow)) causing causing herniation ((curved curved arrow midbrain and secsecmidbrain compression and ondary arondary hemorrhages ((straight straight arrow). row ) .

Fig. 22 22 Fig.

Fig. 23 23 Fig.

Figure 22. CT scan shows crescentic density of an acute right subdural hematoma. Note compression of the right lateral ventricle. Figure 23. CT scan shows lenticular density of an acute right epidural hematoma.

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Figure 24. Cerebellar herniation with downward displacement of the cerebellar tonsils.

signs typically include loss or other impairment of consciousness, vomiting, altered respirations, meningismus, ataxia, and acute hydrocephalus. These findings may be complicated by those of upward displacement through the tentorial notch (upward cerebellar herniation) or more commonly by downward displacement, squeezing one or both cerebellar tonsils through the foramen magnum (cerebellar tonsillar herniation) (Fig. 24). With upward cerebellar herniation, paralysis of upgaze, pupillary dilation, and respiratory abnormalities may result. Cerebellar tonsillar herniation may be manifested by neck stiffness, head tilt, lower cranial nerve palsies, respiratory irregularities, or sudden cardiorespiratory arrest. 3 ,35,39 If epidural hemorrhage is suspected clinically, the diagnosis should generally be confirmed by CT scan or arteriography. Acute epidural hematoma may progress so rapidly, however, with hemiparesis and/or acutely elevated intracranial pressure that radiologic studies cannot be undertaken without delay that might jeopardize the patient. Urgent neurosurgical treatment is required: craniotomy, removal of blood clot, and identification of bleeding source. If subdural hemorrhage is suspected clinically, the diagnosis can generally be confirmed by CT scan. Arteriography or radioisotope brain scan may also provide diagnostic assistance. In acutely elevated intracranial pressure in infants, aspiration of the subdural space may need to be carried out as a combined diagnostic-therapeutic measure as described below:

TECHNIQUE OF SUBDURAL TAPS 1. The child is immobilized and the skull is prepared. 2. The scalp is pulled to form a "Z" tract; the subdural space is entered immediately lateral to the anterior fontanelle with a No. 20 subdural needle directed perpendicularly to the skull. 3. Subdural taps are generally performed bilaterally; if both taps are negative, repeat both 1.5 to 2.0 cm lateral to the fontanelle in the coronal suture. 4. If the fontanelle and sutures are closed, burr holes need to be placed.

ACUTE HEAD TRAUMA IN INFANCY AND CHILDHOOD

733

5. Fifteen ml of fluid per side maximum is removed without aspiration. 6. The needle is removed; pressure and collodion are applied to the skull. 7. The subdural fluid is evaluated (cell count, Gram stain, sugar, protein, bacteriologic culture) and compared with lumbar cerebrospinal fluid obtained immediately after subdural taps unless a lumbar puncture was contraindicated. The protein content of subdural fluid should be at least 40 mg per dl higher than that of the cerebrospinal fluid.

With a sizable accumulation of subdural blood in a child with intracranial hypertension, it is often impossible to remove sufficient blood by tapping the subdural space to provide significant clinical benefit. In such cases, craniotomy and direct operative removal of the hematoma are required. In life-threatening elevation of intracranial pressure that is unresponsive to medical management and subdural taps, ventricular tap can be lifesaving. The technique of ventricular tap is essentially the same as that employed with subdural aspiration, the major difference being the length of the needle used and the angle with which it is advanced: toward the inner canthus of the ipsilateral eye in ventricular tap, perpendicular to the skull in subdural tap.

PROGNOSIS Most children admitted to hospital following head injury associated with loss of consciousness or skull fracture will recover completely within 24 to 48 hours. Others will suffer problems such as post-traumatic epilepsy, motor disability, attentional deficits, or intellectual impairment. It is important to note that in contrast to recovery of neurologic function in adults who have suffered severe head injury, children have been reported to show continuing improvement for more than three years following comparable head traumaY Further, children with signs reflective of severe injury following head trauma have more favorable outcomes than adults manifesting the same signs. 37 Maximal supportive, diagnostic, and therapeutic efforts thus are indicated regardless of how gloomy the initial outlook may appear.

SUMMARY Head trauma in childhood may result in brain injury stemming directly from impact as with contusion, injury derived directly from impact but occurring in delayed fashion as with subdural hemorrhage, or injury occurring as a complication of impact as with bacterial meningitis. History should ascertain relevant particulars in each patient. Examination should focus on pertinent general physical and neurologic signs, with close attention to possible coexisting trauma to the neck, spine, chest, abdomen, and limbs. CT scanning has revolutionized the radiologic assessment of intracranial injury and elucidated greatly the stages of evolution of a variety of post-traumatic intracranial pathologic conditions. Plain radiography con-

734

N. P. ROSMAN, J. HERSKOWITZ, A. P. CARTERANOJ. F. O'CONNOR

tinues to be of greater value than CT scanning in detecting and defining abnormalities of the cranium. With rare exceptions, we feel that any child who is referred for CT scan should first have plain radiographs of the skull. In the first few hours to days after injury, contrast medium enhancement is usually unnecessary; thereafter, it should be used in children in whom an intracranial complication of head trauma is suspected. High yield criteria should be used in all children with head injuries to determine the need for skull radiography, although even a completely negative radiographic assessment does not exclude development of a severe complication of head trauma. Careful observation by parents or other observers is thus mandatory following head injury. Treatment is directed toward urgent, life-threatening factors such as respiratory compromise, shock, acutely raised intracranial pressure, and post-traumatic status epilepticus. Prognosis will depend upon the damage sustained at the time of injury as well as upon the recognition and treatment of associated problems. Because of the child's remarkable capacity to recover from even the most severe head trauma, all children with head injuries should be promptly assessed and actively treated.

REFERENCES 1. Ambrose, J., Gooding, M. R, and Uttley, D.: E. M. I. scan in the management of head injuries. Lancet, 1 :847,1976. 2. Baron, M. A., Bejar, R. L., Sheaff, R. J.: Neurologic manifestations of the battered child syndrome. Pediatrics, 45:1003, 1970. 3. Bell, W. E., and McCormick, W. F.: Increased Intracranial Pressure in Children. Edition 2. Philadelphia, W. B. Saunders Co., 1978. 4. Braakman, R, and Jennett, B.: Depressed skull fracture (non-missile). In Vinken, P. J., and Bruyn, G. W. (eds.): Handbook of Clinical Neurology, Vol. 23. Amsterdam, North-Holland Publishing Company, 1975, p. 403. 5. Caffey, J.: On the theory and practice of shaking infants. Am. J. Dis. Child., 124: 161, 1972. 6. Clasen, R A., Pandolfi, S., and Casey, D.: Furosemide and pentobarbital in cryogenic cerebral injury and edema. Neurology, 24:642, 1974. 7. Committee on Infectious Diseases: Report of the Committee on Infectious Diseases, 18th edition. Evanston, Ill., American Academy of Pediatrics, 1977. 8. Cottrell, J. E., et al.: Furosemide- and mannitol-induced changes in intracranial pressure and serum osmolality and electrolytes. Anesthesiology, 47:28, 1977. 9. Danziger, A., and Price, H.: The evaluation of head trauma by computed tomography. J. Trauma, 19:1,1979. 10. Denny-Brown, D., and Russell, W. R: Experimental cerebral concussion. Brain, 64:93, 1941. 11. Einhorn, A., and Mizrahi, E. M.: Basilar skull fractures in children. The incidence of CNS infection and the use of antibiotics. Am. J. Dis. Child., 132: 1121, 1978. 12. Eyes, B., and Evans, A. F.: Post-traumatic skull radiographs: Time for a reappraisal. Lancet, 2:85, 1978. 13. Franken, E. A., Jr., and Smith, J. A.: Roentgenographic evaluation of infant and childhood trauma. PEDIAT. CLIN. NORTH AM., 22:301, 1975. 14. Gobiet, W.: The influence of various doses of dexamethasone on intracranial pressure in patients with severe head injury. In Pappius and Feindel (eds.): Dynamics of Brain Edema. Berlin, Springer-Verlag, p. 351, 1976. 15. Griffith, J. F., and Dodge, P. R: Transient blindness following head injury in children. New Engl. J. Med., 278:648, 1968. 16. Guthkelch, A. N.: Infantile subdural hematoma and its relationship to whiplash injuries. Br. Med. J., 2:430, 1971. 17. Harwood-Nash, D. C., Hendrick, E. B., and Hudson, A. R: The significance of skull fractures in children. Radiology, 101 :151,1971.

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18. Harwood-Nash, D. C., and Fitz, C. R.: Neuroradiology in Infants and Children. Vol. 2. St. Louis, C. v. Mosby Co., 1976, p. 816. 19. Hill, C.: Extradural hemorrhage in the posterior fossa. Canad. Med. Assoc. J., 85:356, 1961. 20. Hubschmann, 0., et al.: Craniocerebral gunshot injuries in civilian practice-prognostic criteria and surgical management: Experience with 82 cases. J. Trauma, 19:6, 1979. 21. James, H. E., etal.: Treatment of intracranial hypertension. Acta Neurochirurg., 36: 189, 1977. 22. Jamieson, K. G.: Epidural haematoma. In Vinken, P. J., and Bruyn, G. W. (eds.): Handbook of Clinical Neurology, Vol. 24. Amsterdam, North-Holland Publishing Co., 1976, p. 261. 23. Jamieson, K. G.: Posterior fossa haematoma. In Vinken, P. J. and Bruyn, G. W. (eds.): Handbook of Clinical Neurology, Vol. 24. Amsterdam, North-Holland Publishing Co., 1976, p. 343. 24. Jennett, B.: Trauma as a cause of epilepsy in childhood. Dev. Med. Child Neurol., 15:56, 1973. 25. Jennett, B.: Epilepsy After Non-missile Head Injuries. Edition 2. London, William Heinemann Medical Books, Ltd., 1975. 26. Jennett, B.: Post-traumatic epilepsy. In Vinken, P. J., and Bruyn, G. W. (eds.): Handbook of Clinical Neurology, Vol. 24. Amsterdam, North-Holland Publishing Co., 1976, p. 445. 27. Kennedy, D., et al. (eds.): Selection criteria reduce unnecessary skull x-rays. F.D.A. Drug Bull., 8:30, 1978. 28. Kingsley, D., Till, K., and Hoare, R.: Growing fractures of the skull. J. Neurol. Neurosurg. Psychiatry, 41 :312, 1978. 29. Kirkpatrick, J. B., and Di Maio, V.: Civilian gunshot wounds of the brain. J. Neurosurg., 49:185,1978. 30. Macpherson, P., and Graham, D. I.: Correlation between angiographic findings and the ischaemia of head injury. J. Neurol. Neurosurg. Psychiatry, 41 :122, 1978. 31. Marshall, L. F., et al.: Mannitol dose requirements in brain-injured patients. J. Neurosurg., 48:169,1978. 32. Marshall, L. F., et al: Pentobarbital therapy for intracranial hypertension in metabolic coma. Crit. Care Med., 6:1, 1978. 33. McKissock, W., et al.: Extradural haematoma. Observations on 125 cases. Lancet, 2: 167, 1960. 34. Miles, J., and Medlery, A. V.: Posterior fossa subdural haematomas. J. Neurol. Neurosurg. Psychiatry, 37:1373,1974. 35. Milhorat, T. H.: Pediatric Neurosurgery. Philadelphia, F. A. Davis Co., 1978. 36. Ommaya, A. K., and Gennarelli, T. A.: Experimental head injury. In Vinken, P. J., and Bruyn, G. W. (eds.): Handbook of Clinical Neurology, Vol. 23. Amsterdam, NorthHolland Publishing Co., 1975, p. 67. 37. Overgaard, J., et al.: Prognosis after head injury based on early clinical examination. Lancet, 2:631, 1973. 38. Phillips, L. A.: A study of the effect of high yield criteria for emergency room skull radiography. HEW Publication (FDA) 78-8089, 1978. 39. Plum, F., and Posner, J. B.: Diagnosis of Stupor and Coma. Edition 2. Philadelphia, F. A. Davis Co., 1972. 40. Potter, J. M.: The personal factor in the maturation of epileptogenic brain scars: Review and hypothesis. J. Neurol. Neurosurg. Psychiatry, 41 :265, 1978. 41. Ransohoff, J.: Effects of steroids on brain edema. In Reulen and Schilrmann (eds.): Steroids and Brain Edema. New York, Springer-Verlag, 1972, p. 211. 42. Rapport, R. L., and Penry, J. K.: Pharmacologic prophylaxis of post-traumatic epilepsy: A review. Epilepsia, 13:295, 1972. 43. Richardson, F.: Some effects of severe head injury. A follow-up study of children and adolescents after protracted coma. Dev. Med. Child Neurol., 5:471, 1963. 44. Rosman, N. P.: Increased intracranial pressure in childhood. PEDIAT. CLIN. NORTH AM., 21 :483, 1974. 45. Rosman, N. P.: Elevated intracranial pressure. In Swaiman, K. F., and Wright, F. S. (eds.): Practice of Pediatric Neurology. St. LouiS, C. V. Mosby Co., 1975. 46. Rosman, N. P.: Pediatric head injuries. Pediat. Ann., 7:826, 1978. 47. Rottenberg, D. A., Hurwitz, B. J., and Posner, J. B.: The effect of oral glycerol on intraventricular pressure in man. Neurology, 27:600, 1977. 48. Schmitt, B. D., and Kempe, C. H.: The battered child syndrome. In Vinken, P. J., and Bruyn, G. W. (eds.): Handbook of Clinical Neurology, Vol. 23. Amsterdam, NorthHolland Publishing Co., 1975, p. 603. 49. Shapiro, H. M.: Intracranial hypertension: therapeutic and anesthetic considerations. Anesthesiology, 43 :445, 1975.

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50. Shenkin, H. A., and Bouzarth, W. F.: Clinical methods of reducing intracranial pressure. New Engl. J. Med., 282:1465, 1970. 51. Spetzler, R. F., and Wilson, C. B.: Management of recurrent CSF rhinorrhea of the middle and posterior fossa. J. Neurosurg., 49:393, 1978. 52. StOwsand, D., and Bues, E.: Early epilepsy and its prognosis after brain injury in childhood. Zeitschrift fur Neurologie, 198:201, 1970. 53. Walker, A. E.: Pathogenesis and pathophysiology of post-traumatic epilepsy. In Walker, A. E., Caveness, W. F., and Critchley, M. (eds.): The Late Effects of Head Injury, Springfield, Ill., Charles C Thomas, 1969, p. 306. 54. Wright, R. L.: Traumatic hematomas ofthe posterior cranial fossa. J. Neurosurg., 25 :402, 1966. 55. Zelson, C., Lee, S. J., and Pearl, M.: The incidence of skull fractures underlying cephalohematomas in newborn infants. -J. Pediatr., 85:371, 1974.

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