Case Based Pediatrics For Medical Students and Residents
Department of Pediatrics, University of Hawaii John A. Burns School of Medicine
Chapter XVIII.13. Head Trauma and Hemorrhage
Floyd S. Ota, MD
May 2002

Return to Table of Contents

Two days ago, this 6 month old male infant was sitting in an infant carrier which was placed on top of a stroller. The carrier accidentally fell approximately 3 feet onto the ground. He hit his head on the plastic portion of the car seat. There was an immediate cry and no loss of consciousness. His behavior, activity, and feeding pattern were reported as normal. Two days later (today) his mother notes a boggy swelling in the right temporal area of the head and because of this, she brought him to the emergency room for evaluation. He continues to have normal activity and no vomiting.

He has been previously healthy. There is no history of substance use, or child protective services (CPS) involvement in the family.

Exam: VS T 36.9, P 120, R 18, BP 92/50, oxygen saturation 100% in room air. Height, weight and head circumference at the 25th to 50th percentiles. He is alert, active, easily arousable on exam and clean in appearance. He has a 9 by 7 cm swelling over the right temporal/parietal region that is soft, possibly tender, with no palpable bony deformity. No lacerations or wounds are noted. His anterior fontanel is soft and flat. Pupils are 3 mm bilaterally and reactive to light. EOMs are conjugate. There is no hemotympanum, no nasal discharge, and his mucus membranes are moist. His heart, lung, and abdomen exams are normal. Neurologic and extremity exams are normal.

A head CT scan shows a subgaleal hematoma (hematoma under the aponeurosis of Galen), a non-depressed linear skull fracture, and a normal brain. He is discharged home to the care of his parents. He followed up with his pediatrician the next day without sequelae.

Head injuries are the most common cause of traumatic death in children. Head injuries result in about 600,000 visits to the emergency department, and 250,000 hospitalizations annually (1,2). The main causes of head injuries in children overall in descending order are falls, motor vehicle crashes, pedestrian accidents, bicycle injuries, and other injuries (e.g., sports injuries, assault, and non-accidental trauma) (2). Motor vehicle accidents are the most common cause of traumatic death due to head injuries. The diagnostic dilemma for treating head injured children lies in identifying those patients who require more acute attention, and differentiating them from stable patients.

Younger children are at higher risk for sustaining serious head injury. Anatomical considerations that predispose the younger child to head injuries are a large head to body ratio, a relatively weak neck, a thinner skull, and a larger subarachnoid space in which the brain can move freely (2). The pathophysiology of head injuries can be subdivided into two types. The injury directly caused by the mechanical force of the trauma is called primary injury. This type of injury is due to shear force, direct contact, and tissue penetration. Secondary injury is created by the body's response to the primary insult. In secondary injury excitatory neuropeptides, cytokines, free radicals, metabolic and oxygenation insufficiencies cause further tissue damage. Little can be done about primary injury once it has occurred. However, medical management theoretically attempts to minimize the damage caused by secondary injury.

It is important to realize that unlike injuries to other parts of the body, injury to the brain occurs within a confined volume, the intracranial space. The intracranial space is made up of three components; brain volume (90%), blood volume (5%) and cerebral spinal fluid volume (5%). Initially, as the brain swells in response to injury, the increase in brain volume is accommodated by a reduction of cerebral spinal fluid volume, and then blood volume. However, in the finite space of the calvarium, the mass effect caused by acute brain edema and hemorrhage may reach a point at which this volume can no longer be accommodated. Thus, at some point, even the smallest increase in brain volume or hemorrhage produces an exponential increase in intracranial pressure (ICP), at which point, brain perfusion is seriously compromised. This dramatic rise in pressure impedes cerebral perfusion and results in the herniation of brain tissue across the tentorium, falx or through the foramen magnum causing significant morbidity and often death. Intracranial hypertension, or elevated intracranial pressure is harmful as it can decrease cerebral perfusion, inciting further hypoxia and cell death. This relationship between ICP, mean arterial pressure (MAP), and cerebral perfusion pressure (CPP) can be appreciated by the equation CPP=MAP-ICP (1). In normal children ICP is <20 mm Hg, and MAP is 70-80 mm Hg, which provides a normal CPP ranging from 50-60 mm Hg (1). Thus, accordingly an increase in ICP, or decrease in MAP can decrease blood flow into the brain. When CPP is <40 mm Hg, ischemia occurs as proper cerebral blood flow (CBF) cannot be maintained (1). This simplified equation attempts to explain a very complicated pathophysiologic process. Controlled by chemical mediators that produce vasoconstriction and vasodilatation of the blood vessels, CBF is constantly changing to meet the brain's metabolic demands. The most potent chemical mediator is the arterial partial pressure of carbon dioxide (pCO2), which is directly proportional to CBF. The arterial partial pressure of oxygen (pO2) is indirectly proportional to CBF, but it is not as potent a vasoactive mediator as pCO2. In the acute management of the patient with a severe head injury, these values are manipulated via intubation and mechanical ventilation to maximize CPP.

The initial clinical assessment is extremely important in determining the clinical management of a victim with head trauma. The primary survey should begin with the standard ABCs of basic life support and a focused physical exam looking for concurrent life-threatening injuries involving the chest, central nervous system, pelvis, and abdomen. All the while, the patient's mental status is closely monitored. The Glasgow Coma Scale (GCS) has been found to be helpful for this purpose (1). The GCS is a clinical rating scale developed based the patient's clinical assessment in three categories; motor, verbal, and eye opening response. The GCS scale ranges from 3-15. The GCS scale is as follows:

Motor response: 6=normal spontaneous movements, 5=withdraws to touch, 4=withdraws to pain, 3=abnormal extension (decorticate rigidity), 2=abnormal flexion (decerebrate rigidity), 1=none.

Verbal response: 5=oriented, 4=confused, 3=inappropriate words, 2=nonspecific sounds, 1=none.

Eye opening response: 4=spontaneous, 3=to speech, 2=to pain, 1=none (1).

A modified Glasgow Coma Scale for infants was created for pre-verbal children. The GCS is not useful in ruling out serious brain injuries such as hemorrhages since many patients with brain hemorrhages have GCS scores >13, and some even have 15 (normal) GCS scores. Once the patient is clinically stable, a more detailed secondary survey can be carried out.

The majority of head injuries (90%) fall into the minor category. If the head injury has been determined to be mild, a history looking for symptoms of possible intracranial injury should be elicited. This would include questions pertaining to loss of consciousness, headache, amnesia, seizures, nausea, vomiting, or focal neurological defects. Minor head trauma is a difficult clinical dilemma, and multiple studies have shown that no single symptom consistently identifies the presence of an intracranial injury (ICI) in children (3,4). Two prospective studies found that the following clinical findings were commonly associated with intracranial injury in children with minor head trauma: focal neurological deficits, loss of consciousness, amnesia, a GCS less than 15, and altered mental status (3,5). It turns out that a 14 GCS is close to 15, but there is a substantially higher risk of serious head injury if the GCS is 14 compared to 15. Thus, if these clinical findings are present during the assessment, then computed tomography (CT) scanning is indicated. Computed tomography scanning of the head is the diagnostic procedure of choice to determine the presence of acute intracranial injury (6). CT scanning is often easily accessible and a very good test to screen for the presence of acute bleeding and brain swelling. Unfortunately, some children require sedation to perform a CT scan, and thus the risks and benefits of procedural sedation must be weighed. However, the need for procedural sedation is declining with the advanced technology of faster spiral CT scanners. Skull x-rays have a limited role in children with head injuries, since they do not identify intracranial injury. However, these images may be helpful when CT scanning is not available. Plain x-rays can detect a skull fracture, and the presence of a skull fracture was found to be helpful with predicting the presence of intracranial injury (5). However, a normal skull series does not rule out a brain injury. Magnetic resonance imaging has no role in the initial evaluation of an acute head injury since it is time consuming, expensive, and not usually readily available. In minor head injuries, management is almost always observation and parental education. Hospitalization is utilized if there is concern about proper follow up, since most complications will occur within the first 24 hours following the injury (6). Parents should be instructed on what signs to look for and when to return for further care. Separate practice guidelines have been recommended for the management of minor head injuries in children ages 2-20 years and <2 years of age by the American Academy of Pediatrics (6,7).

Skull fractures can occur with even mild trauma. Infants are especially susceptible to linear skull fractures, because of their thinner skull. Half of skull fractures occur from a fall from a height of 4-5 feet, and 70% involve the parietal bone (1). Very often superficial scalp lacerations and hematomas are also present on exam. It is important to mention that in infants, scalp lacerations can cause significant bleeding if left unrecognized. The presence of scalp hematoma has a 95% association with finding an underlying linear skull fracture in infants (8). Thus, diagnostic imaging is recommended for any infant with an obvious scalp hematoma. (7,8). Despite the fact that only close observation is all that is required for a linear skull fracture, proper follow up is important. Rarely, a growing skull fracture can develop. This occurs when a portion of the meninges herniates through the fracture line and does not allow for proper healing. A fluid collection cyst can be produced by the pinched meninges, which is called a leptomeningeal cyst. Leptomeningeal cysts (hence, growing skull fractures) are rare complications, but the clinician should still look for them during follow up weeks after a skull fracture is found.

A subgaleal hematoma will often form around a parietal skull fracture. It is common for these to present several days after the head trauma incident. The infant or young child strikes his/her head during a fall. If a skull fracture is sustained, without a brain injury, the child will appear to be alert and active without signs of brain injury. Bleeding from the skull fracture collects in the subgaleal layer of the scalp. It is initially tense, but over the next few days as the hematoma begins resorption, the hematoma becomes very soft, which is often alarming to parents, prompting them to bring the child to a physician. Skull radiographs frequently identify a small linear fracture beneath the subgaleal hematoma which does not require further diagnostic or therapeutic intervention if the child is doing well clinically. However, radiographs occasionally demonstrate large fractures, comminuted fractures, or multiple fractures which suggest more serious injury and/or non-accidental injury.

A skull fracture that is pushed in a distance equivalent to the thickness of the skull table is called a depressed skull fracture. This is a neurosurgical emergency and must be corrected expeditiously. Lastly, basilar skull fractures (BSF) may occur from head trauma, and can be diagnosed by clinical exam. Physical exam findings associated with a BSF include: blood in the mastoid air space (Battle's sign which is bruising over the mastoid process), blood collection in the periorbital space (Raccoon eyes), hemotympanum, and CSF rhinorrhea. BSF were found to be associated with the presence of ICI (5). Thus, radiographic imaging should be performed if these clinical signs are found. A small increase in the risk for meningitis is associated with a BSF due to the break in protective covering that the meninges provide. This risk is small and prophylactic antibiotics are not routinely recommended. However, this needs to be considered in the febrile child with a recent history of a BSF during follow up care.

The most mild type of brain injury is a concussion. A concussion is defined as, "a trauma induced alteration of mental status that may or may not involve a loss of consciousness" (1). Very often, confusion and/or amnesia may accompany the event. In concussions, CT scans are normal and close observation is all that is required. The "Second Impact Syndrome," is characterized by rapid death due to a second concussion prior to a return to baseline functioning after an initial one. Sudden death is thought to occur due to a rapid rise in ICP from local vasospasm and edema (9). This has been reported to occur in adolescent athletes in contact sports, and the appropriate time to return to activity after sustaining a concussion is under much debate. Practice guidelines for the return of activity after sustaining a concussion have been recommended in the literature (10).

An epidural hematoma (EDH) can develop if blood collects in the potential space between the dura and the inner table of the skull. Very often the blood is arterial originating from the middle meningeal artery in association with a parietal skull fracture. However, in younger children, 20% of epidural hematomas are due to venous blood (1). The classic clinical coarse is that of a child who sustains a head injury and may have been rendered unconscious. He may then have the "classic" lucid interval at which time he may be able to interact with the examiner. This is because, the initial brain injury itself is only a concussion. Subsequent middle meningeal bleeding causing the hematoma results in ensuing decompensation from the expanding blood collection, causing increased intracranial pressure and a reduction in cerebral perfusion (a secondary injury). An epidural hematoma is best diagnosed by CT scan, which will show a lenticular (football shaped) hyperdense (white) hemorrhage along the skull table. EDH can cause a significant increase in ICP, illustrated by a midline shift and small ventricles on CT scan. This is a neurosurgical emergency, and craniotomy with evacuation of the hematoma can be life saving. If neurosurgical intervention is early and successful, EDH has a good prognosis since the initial brain injury was only a concussion in most instances (i.e., the brain itself is not significantly injured in an EDH, since the bleeding originates from outside the brain parenchyma).

A subdural hematoma (SDH) is the accumulation of blood in the subdural space. This is most often due to venous blood from the bridging veins that traverse this space. Very often a SDH is created by acceleration-deceleration injury in which the brain parenchyma is damaged from the surface of the calvarium. CT scanning of these lesions will show a crescent shaped hyperdense (white) hemorrhage. The majority of SDH are managed medically, and observation with supportive care is all that is required. This is usually not a neurosurgical emergency, since evacuation of the clot will not usually reverse the significant primary damage inflicted on the brain parenchyma. However, neurosurgical intervention may be warranted when a significant mass effect is present, and the patient would benefit from an acute reduction in ICP. When a child presents with unexplained vomiting, lethargy, and/or head trauma, non-accidental injury must be included in the differential diagnosis. Especially when subdural hematomas are found, the possibility for child abuse must be explored. Associated findings of non-accidental trauma are failure to thrive, retinal hemorrhages, intra-abdominal injuries, and various fractures of different ages. In one retrospective review, cases of acute head injury caused by child abuse were often initially misdiagnosed if the patient was well appearing, Caucasian, and living with both biological parents (11). Thus, the examining clinician should have a low threshold to perform a skeletal survey and attain ophthalmology consultation for suspicious cases of head injuries.

This type of acute subdural hematoma is very different from the type of subacute subdural hematoma found in the elderly. Acute subdural hematoma is associated with substantial brain parenchymal injury. Subacute subdural hematoma in the elderly results from a slow bleed from bridging brains often due to minor head trauma. As the hematoma expands, ICP increases and cerebral perfusion is compromised. If the hematoma is identified and evacuated early, the brain is preserved with little injury. The difference between acute subdural hematoma (usually a poor prognosis) should be contrasted with subacute subdural in the elderly (usually a good prognosis). The latter is more similar to an epidural hematoma (usually a good prognosis as well).

The concept of primary versus secondary injury is important in understanding the prognosis. Most epidural hematomas have mild primary injury, but have the potential for severe secondary ischemic injury if failure to evacuate the hematoma in a timely evacuation leads to excessive ICP increase and brain ischemia/infarction. Compare this to an acute subdural in which case, there is substantial primary brain injury (damage) which cannot be reversed with evacuation of the hematoma.

Sometimes a subarachnoid hematoma and an intracerebral contusion can accompany a subdural hematoma. Subarachnoid blood can be distributed widely throughout the subarachnoid space, and its symptoms can sometimes mimic meningitis. On CT scan hyperdense blood collections are found along the falx, and in the basilar cisterns. Intracerebral contusions are actual injury within the brain parenchyma. Due to tissue edema, these lesions are at high risk for producing a mass effect and increased ICP. In this type of injury, the GCS is often low, and focal neurologic symptoms, loss of consciousness (LOC), and visual changes are often present. CT scan shows a mixture of hypo and hyper dense lesions within the brain parenchyma. Secondary injury may further complicate the clinical picture by producing infarcts due to local vasospasm. Medical and neurosurgical management are often required, and the prognosis is usually poor.

In moderate to severe head injuries, medical and surgical management is aggressive and complex. Patients often present in an obtunded or combative state. Late clinical findings include unequal and non-reactive pupils, focal neurologic findings, abnormal posturing, and Cushing's triad (hypertension, bradycardia, and irregular respirations). These clinical findings are usually indicative of severe injury and probable brain herniation. These clinical signs require expeditious medical management, and close monitoring in the intensive care unit. Expeditious CT scanning to determine the extent of brain injury is required. Neurosurgical consultation is required because the only way to accurately access and monitor ICP is to measure it with a direct device such a Richmond bolt or a ventriculostomy. This device, placed by the neurosurgeon, can directly monitor acute changes in ICP. The targeted value for adequate CPP is an ICP <20 mm Hg in the presence of a normal systemic arterial blood pressure. The two physiologic parameters that must be avoided are hypoxia and hypotension. The brain is an obligate aerobic organ and systemic hypoxia leads to increased CNS morbidity. Furthermore, maintaining adequate MAP is critical to maintaining proper CPP.

Monitoring and maintaining the intravascular volume status is crucial. Intravascular volume may be decreased due to capillary leak, an acute bleeding process, or overzealous use of hyperosmotic agents. Very often, vasopressor agents such as dopamine, dobutamine, or epinephrine may be required to maintain proper MAP. The head of the bed should be elevated to 30 degrees to facilitate venous drainage. Sedation and analgesia may aid to decrease dramatic shifts in ICP due to generalized motor activity and anxiety. If these pharmacological interventions fail to adequately minimize changes in ICP, paralytic agents may also be added. If the patient has seizure activity, benzodiazepines or fosphenytoin can be used. Fosphenytoin for seizure prophylaxis may be indicated in the presence of an obvious parenchymal injury. Manipulation of pCO2 and pO2 values via intubation and mechanical ventilation may be useful to optimize CPP. However, this is controversial and recommendations are evolving. While moderate hyperventilation was an accepted treatment modality (with the targeted pCO2 in the 30-35 mmHg range) to reduce ICP, this is controversial since it may reduce net cerebral perfusion by vasoconstricting the cerebral arteries. Perhaps hyperventilation should be reserved for impending brain herniation only.

Osmotic agents such as mannitol or 3% saline are given intravenously to achieve a hyperosmolar intravascular compartment. The hyperosmolarity of the intravascular compartment draws free-water from the interstitial space potentially lowering intracranial pressure and thus improving cerebral blood flow (1,12). Serum electrolytes, and serum osmolarity must be closely monitored. Hyponatremia can result from the inappropriate release of anti-diuretic hormone (SIADH), and hypernatremia may result from diabetes insipidus, dehydration and osmotic diuresis due to the use of hyperosmolar medications. Mannitol and hyperventilation have not been shown to be of clear benefit in the long-term management of increased ICP, and their benefits appear to be primarily helpful in the acute setting dealing with impending brain herniation (1). Despite aggressive attempts at medical management, severe head injuries may continue to progress to a level of refractory intracranial hypertension leading to significant morbidity and/or death.

The prognosis for minor head injuries is very good. Minor effects of the injury that may persist include headache, concentration problems, and hesitation to return to normal activities. These typically resolve and the patient will return to baseline functioning with time (13). For children who survive major head injuries, significant morbidity is common. However, when compared with adults, children with a GCS of <8 often have better outcomes (12). Intensive rehabilitation therapy may be required long after hospitalization and the acute phase is complete. Prognosis may be poor, and for some, a persistent vegetative state may be the result. Head injuries are a major cause of morbidity and mortality in children, and only through primary injury prevention will this problem be decreased.


1. True/False: Epidural hematomas have a crescent shaped mass on CT scan

2. True/False: Epidural hematomas are mostly produced by venous blood.

3. True/False: The prognosis for epidural and subdural hematomas are about the same as long as the hematomas have been evacuated early.

4. True/False: Since epidural hematoma is always a neurosurgical emergency and subdural hematoma is less often a neurosurgical emergency, epidural hematomas are more serious (i.e., the prognosis is poorer) than subdural hematoma.

5. True/False: Infants are at low risk for having intracranial injuries.

6. True/False: Hypotension and hypoxia are two monitoring parameters that are extremely important to avoid in a child with a moderate to severe head injury.

7. True/False: The equation to calculate cerebral perfusion pressure is: CPP=MAP-ICP.

8. True/False: Hypernatremia can occur secondary to inappropriate anti-diuretic hormone release in moderate to severe head injuries.

9. True/False: A 4 year old male child fell and hit his head on the carpet about 5 hours ago. There is no reported history of loss of consciousness or vomiting. His PE is normal, and he is acting appropriately at the time of the visit. A CT scan should be ordered to assess this child for intracranial injury even though the risk of serious injury is remote.

10. True/False: A patient has a GCS of 9 if he can open his eyes to a noxious stimuli, has inappropriate speech, and flexes his extremities to pain.

Related x-rays

Yamamoto LG. Intracranial Hypertension and Brain Herniation Syndromes. In: Yamamoto LG, Inaba AS, DiMauro R. Radiology Cases In Pediatric Emergency Medicine, 1996, volume 5, case 6. Available online at:

Young LL. Intracranial Hemorrhage in Children. In: Yamamoto LG, Inaba AS, DiMauro R. Radiology Cases In Pediatric Emergency Medicine, 1996, volume 5, case 7. Available online at:

Yamamoto LG. Infant Skull Fractures. In: Yamamoto LG, Inaba AS, DiMauro R. Radiology Cases In Pediatric Emergency Medicine, 1996, volume 5, case 9. Available online at:

Yamamoto LG. Lethargy and Vomiting Following Child Abuse. In: Yamamoto LG, Inaba AS, DiMauro R. Radiology Cases In Pediatric Emergency Medicine, 1996, volume 5, case 10. Available online at:

Newton-Weaver RO. A Growing Skull Fracture. In: Yamamoto LG, Inaba AS, DiMauro R. Radiology Cases In Pediatric Emergency Medicine, 2002, volume 7, case 2. Available online at:

Temple TLHH, Yamamoto LG. Skull Fractures. In: Yamamoto LG, Inaba AS, DiMauro R. Radiology Cases In Pediatric Emergency Medicine, 2002, volume 7, case 15. Available online at:


1. Greenes DS, Madsen JR. Chapter 105-Neurotrauma. In: Fleisher GR, Ludwig S (eds). Textbook of Pediatric Emergency Medicine, Fourth edition. 2000, Philadelphia: Lippincott Williams and Wilkins, pp. 1271-1296.

2. Zuckerman GB, Conway EE. Accidental Head Injury. Pediatr Ann 1997;26(10):621-631.

3. Dietrich AM, Bowmen MJ, Ginn-Pease ME, Kosnik E, King DR. Pediatric Head Injuries: Can Clinical Factors Reliably Predict an Abnormality of Computed Tomography? Ann Emerg Med 1993;22(10):1535-1540.

4. Greenes DS, Schutzman SA. Clinical Indicators of Intracranial Injury in Head-injured Infants. Pediatrics 1999;104(4):861-867.

5. Quayle KS, Jaffe DM, Kuppermann N, et al. Diagnostic Testing for Acute Head Injury in Children: When are Head Computed Tomography and Skull Radiographs Indicated? Pediatrics 1997;99(5):e11.

6. AAP Committee on Quality Improvement. The Management of Minor Closed Head Injury in Children. Pediatrics 1999;104(6):1407-1415.

7. Schutzman SA, Barnes P, Duhaime AC, et al. Evaluation and Management of Children Younger than Two Years Old with Apparently Minor Head Trauma: Proposed Guidelines. Pediatrics 2001;107(5):983-993.

8. Greenes DS, Schutzman SA. Occult Intracranial Injuries in Infants. Ann Emerg Med 1998;32(6):680-686.

9. McCrory PR, Berkovic SF. Second Impact Syndrome. Neurology 1998;50:677-683.

10. Quality Standards Subcommittee. Practice Parameter: The management of concussion in sports (Summary Statement) Neurology 1997;48:581-585.

11. Jenny C, Hymel KP, Ritzen V, et al. Analysis of Missed Cases of Abusive Head Trauma. JAMA 1999;281(5):621-626.

12. Allen AM, Boyer R, Cherny WB, et al. Chapter 24-Head and Spinal Cord Injuries. In: Rogers MC (ed). Textbook of Pediatric Intensive Care, third edition. 1996, Baltimore: Williams and Wilkins, pp. 809-857.

13. Bijur PE, Haslum M, Golding J. Cognitive and Behavioral Sequelae of Mild Head Injury in Children. Pediatrics 1990;86(3):337-344.

14. Ghajar J, Hariri RJ. Management of Pediatric Head Injury. Pediatr Clin North Am 1992;39(5):1093-1125.

Answers to questions

1. False. Epidural hematomas are a neurosurgical emergency and have a lenticular (lens or football shaped, also called biconvex) shape on CT scan.

2. False. Only 20% of epidural hematomas are produced by venous blood in children.

3. False. Acute subdural hematoma is associated with substantial brain parenchymal injury so its prognosis is poor compared to epidural hematoma.

4. False. Epidural hematoma is a neurosurgical emergency because its prognosis is dramatically better with early evacuation, while subdural hematoma is less of an emergency because the prognosis is already poor even with hematoma evacuation.

5. False. Infants are at higher risk for sustaining serious head injury. Anatomical considerations that predispose the younger child to head injuries are a large head to body ratio, a relatively weak neck, a thinner skull, and a larger subarachnoid space in which the brain can move freely.

6. True.

7. True.

8. False. Hyponatremia occurs with SIADH. Free-water is retained in the collecting tubules due to anti-diuretic hormone causing a dilutional effect of the serum sodium. Hypernatremia is usually caused by the use of hyperosmotic agents such as mannitol or diabetes insipidus.

9. False. In well appearing children 2-18 years of age with no loss of consciousness and a normal neurological exam, no imaging studies are required. Close observation and parental education is all that is needed (6).

10. True. GCS=9: motor=4, verbal=3, and eye opening=2.

Return to Table of Contents

University of Hawaii Department of Pediatrics Home Page