T PEDIATRIC EMERGENCY MEDICINE
0031-3955/92 $0.00 + .20
MANAGEMENT OF PEDIATRIC HEAD INJURY Jamshid Ghajar, MD, PhD, and Robert J. Hariri, MD, PhD
Head injury is the most common cause of traumatic death in approximately 25,000 children annually in the United StatesY In addition, it is a major cause of mental retardation, epilepsy, and physical disability. Despite the frequency of traumatic brain injury, the care and management of these patients continues to challenge clinicians in the critical care environment. The past decade has yielded a better understanding of the pathophysiology of traumatic brain injury. Despite the fact that irreparable cell damage occurs at the initial instant of injury, it is recognized that potentially reversible secondary events contribute to even greater tissue death in the acute posttraumatic period. Nevertheless, significant attention only recently has been devoted to rapid, aggressive, and definitive resuscitation, surgical management, and intensive care of these patients. If one uses a roughly quantitative means of assessing the severity of head injury such as the Glasgow Coma Scale (GCS), children who suffer severe injuries (GCS scores 8
Within first week following neurotrauma with GCS os;; 8
Patient fulfills Brain Death Criteria ICP persistently > 40 mm Hg
ICP generally < 20 mm Hg
Prognosis Dismal prognosis Significant probability of death or major neurologic deficits Low probability of death but with temporary or permanent neurologic deficits Follow institutional protocol for brain death Significant probability of death or major neurologic deficit including persistent vegetative state Low probability of death but with long-term neurologic deficits
in Table 3 can provide appropriate, meaningful information to the members of the patient's family based on data obtained in a systematic manner. Progress can be monitored by improvement in those variables without placing the physician in a difficult position of predicting outcome. True coma (not obeying commands, eyes closed, and not speaking) generally does not exceed more than 2 weeks. Within 2 weeks assessment of the neurotrama patient demonstrates either brain death or indicates some response to external stimuli. Frequently patients open their eyes (thus by definition they are not in a coma) and can be assessed in their ability to follow simple motor commands. A patient's eventual outcome after opening of the eyes can range from a persistent vegetative state to the premorbid condition. Even the best recovery may be associated with personality changes, including mood lability; loss of confidence; and impaired short-term memory, headaches, and subtle cognitive impairments. A persistent vegetative state, in which the patient does not have any useful interaction with the environment, is obviously a disastrous outcome. Generally within 6 months to 1 year after the injury, 90% of the long-term neurologic outcome has been achieved. CLINICAL MANAGEMENT OF PEDIATRIC HEAD INJURY
The child's brain has an age-dependent vulnerability to trauma. Children less than 1 year old have double the mortality compared with those between 1 and 6 years of age and three times more than children
MANAGEMENT OF PEDIATRIC HEAD INJURY
1109
between the ages of 6 and 12.4, 34 This may be due to the increased water content of the poorly unmyelinated brain at birth and an open fontanelle with unfused sutures that persists in the first year. With myelination, closure of the anterior fontanelle and fusion of the cranial sutures the brain can better withstand cerebral trauma. In a study of infants with head injury, 50% of those noted to have a tense anterior fontanelle by palpation had a worse outcome, whereas only 5% with a soft fontanelle did poorly.2 The classification of head injury in children-mild, moderate and severe-can be defined by the level of consciousness after emergency room resuscitation and after the child has been triaged to appropriate care. We routinely obtain CT scan on children with a history of loss of consciousness or with a depressed level of consciousness on admission. Those patients who are alert, have a normal CT, no other injuries, and a responsible parent or guardian who can serve as a reliable observer are discharged from the emergency room with a "head sheet" that instructs parents to bring the child back for any signs of neurologic deterioration. Children who are lethargic or stuporous (can be aroused to open their eyes with a noxious stimulus) are observed closely in the intensive care unit for deterioration. Comatose patients are resuscitated, intubated, and have a ventriculostomy placed for ICP monitoring (Fig. 11). All patients who score GCS 8 or less or CCS 9 or less (see Tables 1 and 2) have ICP monitoring by ventriculostomy (Table 4) and are managed by the ICP management protocol delineated in Figure 12. The head CT scan is usually performed without contrast, and the computer windows adjusted to provide images of soft tissue and bone. The bone window, in conjunction with the initial scout view (a lateral head radiograph on the CT scanner), is more sensitive than a skull radiograph in detecting a fracture, unless the fracture lies in the same axial plane as the CT image. Fractures depressed more than the thickness of the skull are surgically elevated and the dura is inspected for laceration, which if present requires repair to prevent late development of a CSF leak. Sometimes dura can be trapped in a suture or fracture and progressively enlarge, producing a leptomeningeal cyst that needs to be excised operatively, Children less than 3 years old sometimes present not with a skull fracture but with an indented cranium, often called a "ping-pong" fracture, which can be elevated simply in the operating room. Intracranial lesions can be divided into epidural, subdural, subarachnoid, parenchymal, intraventricular hemorrhages and diffuse injury. An expanding epidural hematoma is a life-threatening condition and requires immediate surgical intervention. A comatose child with an epidural clot can rapidly return to the premorbid condition if the hematoma is removed expeditiously; a delay can result in permanent neurologic deficits or death. With the availability and frequency of head CT scans in children who have a normal neurologic examination, numerous nonexpanding epidural hematomas are detected that are managed conservatively and surveyed with follow-up scans. If the
1110
GHAJAR & HARIRI
(Head
r------
Alert
r
CTT)
Post resuscitation Neurological exam
Lethargic or Stuporous
Comatose
lCU
Consider
Discharge
IV: RL Resllsitation in ER - as per ATLS guidelines • IV: Mannitol .2 -.5 gm/kg for acute cerebral herniation • Maintain hemodynamic stability • Arterial Line. Maintain Pa02 100 mm Hg Intubate.Maintain PaC02 35mm Hg Head elevation to 30 degrees Phenytion 15 mg/kg loading then 5 mg/kg/QD maintenance • MS04 0.1 mg/kg/hr for analgesia • Midazolam for amnestic and anxiolytic .04 mg/kg loading O.2ml/kg/hr maintainance • Ventriculostomy for rep monitoring * See ICP management chart
Figure 11. Neurotrauma treatment algorithm.
hematoma is associated with significant mass effect, we favor early evacuation and coagulation of the middle meningeal artery to ensure that reexpansion of the clot does not occur. A subdural hematoma that produces a significant cerebral midline shift should be evacuated. The pathophysiology of a subdural hematoma differs from an epidural hematoma because there is invariably an underlying cortical contusion associated with a subdural hematoma, whereas with an epidural hematoma, underlying primary cortical damage is rare. Subarachnoid hemorrhage virtually always accompanies Table 4. VENTRICULOSTOMY PROTOCOL 1. Drain ventricular CSF to maintaining ICP
0031-3955/92 $0.00 + .20
MANAGEMENT OF PEDIATRIC HEAD INJURY Jamshid Ghajar, MD, PhD, and Robert J. Hariri, MD, PhD
Head injury is the most common cause of traumatic death in approximately 25,000 children annually in the United StatesY In addition, it is a major cause of mental retardation, epilepsy, and physical disability. Despite the frequency of traumatic brain injury, the care and management of these patients continues to challenge clinicians in the critical care environment. The past decade has yielded a better understanding of the pathophysiology of traumatic brain injury. Despite the fact that irreparable cell damage occurs at the initial instant of injury, it is recognized that potentially reversible secondary events contribute to even greater tissue death in the acute posttraumatic period. Nevertheless, significant attention only recently has been devoted to rapid, aggressive, and definitive resuscitation, surgical management, and intensive care of these patients. If one uses a roughly quantitative means of assessing the severity of head injury such as the Glasgow Coma Scale (GCS), children who suffer severe injuries (GCS scores 8
Within first week following neurotrauma with GCS os;; 8
Patient fulfills Brain Death Criteria ICP persistently > 40 mm Hg
ICP generally < 20 mm Hg
Prognosis Dismal prognosis Significant probability of death or major neurologic deficits Low probability of death but with temporary or permanent neurologic deficits Follow institutional protocol for brain death Significant probability of death or major neurologic deficit including persistent vegetative state Low probability of death but with long-term neurologic deficits
in Table 3 can provide appropriate, meaningful information to the members of the patient's family based on data obtained in a systematic manner. Progress can be monitored by improvement in those variables without placing the physician in a difficult position of predicting outcome. True coma (not obeying commands, eyes closed, and not speaking) generally does not exceed more than 2 weeks. Within 2 weeks assessment of the neurotrama patient demonstrates either brain death or indicates some response to external stimuli. Frequently patients open their eyes (thus by definition they are not in a coma) and can be assessed in their ability to follow simple motor commands. A patient's eventual outcome after opening of the eyes can range from a persistent vegetative state to the premorbid condition. Even the best recovery may be associated with personality changes, including mood lability; loss of confidence; and impaired short-term memory, headaches, and subtle cognitive impairments. A persistent vegetative state, in which the patient does not have any useful interaction with the environment, is obviously a disastrous outcome. Generally within 6 months to 1 year after the injury, 90% of the long-term neurologic outcome has been achieved. CLINICAL MANAGEMENT OF PEDIATRIC HEAD INJURY
The child's brain has an age-dependent vulnerability to trauma. Children less than 1 year old have double the mortality compared with those between 1 and 6 years of age and three times more than children
MANAGEMENT OF PEDIATRIC HEAD INJURY
1109
between the ages of 6 and 12.4, 34 This may be due to the increased water content of the poorly unmyelinated brain at birth and an open fontanelle with unfused sutures that persists in the first year. With myelination, closure of the anterior fontanelle and fusion of the cranial sutures the brain can better withstand cerebral trauma. In a study of infants with head injury, 50% of those noted to have a tense anterior fontanelle by palpation had a worse outcome, whereas only 5% with a soft fontanelle did poorly.2 The classification of head injury in children-mild, moderate and severe-can be defined by the level of consciousness after emergency room resuscitation and after the child has been triaged to appropriate care. We routinely obtain CT scan on children with a history of loss of consciousness or with a depressed level of consciousness on admission. Those patients who are alert, have a normal CT, no other injuries, and a responsible parent or guardian who can serve as a reliable observer are discharged from the emergency room with a "head sheet" that instructs parents to bring the child back for any signs of neurologic deterioration. Children who are lethargic or stuporous (can be aroused to open their eyes with a noxious stimulus) are observed closely in the intensive care unit for deterioration. Comatose patients are resuscitated, intubated, and have a ventriculostomy placed for ICP monitoring (Fig. 11). All patients who score GCS 8 or less or CCS 9 or less (see Tables 1 and 2) have ICP monitoring by ventriculostomy (Table 4) and are managed by the ICP management protocol delineated in Figure 12. The head CT scan is usually performed without contrast, and the computer windows adjusted to provide images of soft tissue and bone. The bone window, in conjunction with the initial scout view (a lateral head radiograph on the CT scanner), is more sensitive than a skull radiograph in detecting a fracture, unless the fracture lies in the same axial plane as the CT image. Fractures depressed more than the thickness of the skull are surgically elevated and the dura is inspected for laceration, which if present requires repair to prevent late development of a CSF leak. Sometimes dura can be trapped in a suture or fracture and progressively enlarge, producing a leptomeningeal cyst that needs to be excised operatively, Children less than 3 years old sometimes present not with a skull fracture but with an indented cranium, often called a "ping-pong" fracture, which can be elevated simply in the operating room. Intracranial lesions can be divided into epidural, subdural, subarachnoid, parenchymal, intraventricular hemorrhages and diffuse injury. An expanding epidural hematoma is a life-threatening condition and requires immediate surgical intervention. A comatose child with an epidural clot can rapidly return to the premorbid condition if the hematoma is removed expeditiously; a delay can result in permanent neurologic deficits or death. With the availability and frequency of head CT scans in children who have a normal neurologic examination, numerous nonexpanding epidural hematomas are detected that are managed conservatively and surveyed with follow-up scans. If the
1110
GHAJAR & HARIRI
(Head
r------
Alert
r
CTT)
Post resuscitation Neurological exam
Lethargic or Stuporous
Comatose
lCU
Consider
Discharge
IV: RL Resllsitation in ER - as per ATLS guidelines • IV: Mannitol .2 -.5 gm/kg for acute cerebral herniation • Maintain hemodynamic stability • Arterial Line. Maintain Pa02 100 mm Hg Intubate.Maintain PaC02 35mm Hg Head elevation to 30 degrees Phenytion 15 mg/kg loading then 5 mg/kg/QD maintenance • MS04 0.1 mg/kg/hr for analgesia • Midazolam for amnestic and anxiolytic .04 mg/kg loading O.2ml/kg/hr maintainance • Ventriculostomy for rep monitoring * See ICP management chart
Figure 11. Neurotrauma treatment algorithm.
hematoma is associated with significant mass effect, we favor early evacuation and coagulation of the middle meningeal artery to ensure that reexpansion of the clot does not occur. A subdural hematoma that produces a significant cerebral midline shift should be evacuated. The pathophysiology of a subdural hematoma differs from an epidural hematoma because there is invariably an underlying cortical contusion associated with a subdural hematoma, whereas with an epidural hematoma, underlying primary cortical damage is rare. Subarachnoid hemorrhage virtually always accompanies Table 4. VENTRICULOSTOMY PROTOCOL 1. Drain ventricular CSF to maintaining ICP
