eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Critical Care

Head Trauma: Treatment & Medication

Author: Arabela Stock, MD, Consulting Staff, Department of Pediatrics, Divisions of Critical Care and Pulmonology, Florida Pediatric Association
Coauthor(s): Jagvir Singh, MD, Director, Division of Pediatric Emergency Medicine, Lutheran General Hospital of Park Ridge
Contributor Information and Disclosures

Updated: Jun 1, 2009

Treatment

Medical Care

The goal of medical care of patients with head trauma is to recognize and treat life-threatening conditions and to eliminate or minimize the role of secondary injury. Guidelines for the treatment of patients with head trauma have been established.10

Patients with severe head trauma are at increased risk of developing cerebral edema, respiratory failure, and herniation secondary to the increased intracranial pressure (ICP); therefore, frequent serial assessments of the neurologic status must be performed.

The Brain Trauma Foundation has developed guidelines regarding the medical management of patients with severe head injury. These guidelines suggest that cardiopulmonary resuscitation should be the foundation upon which treatment of intracranial hypertension must be based. They also state that, in the absence of any obvious signs of increased ICP, no prophylactic treatment should be initiated because this may directly interfere with the optimal resuscitation process.

  • Airway management
    • A stable airway should be obtained to provide adequate oxygenation and ventilation. If endotracheal intubation is required, adequate sedation and paralysis must be assured to avoid further increase in ICP. Rapid sequence induction and endotracheal intubation are generally recommended. Stabilization of the cervical spine should be achieved in every patient with severe head trauma. Nasal intubation or nasogastric tube placement should be avoided, especially for patients in whom basilar skull fracture is suspected.
    • Breathing may be impaired because of neurological or thoracic injuries. Patients with significant head injury and altered mentation should be supplemented with 100% oxygen and should be supported with positive pressure ventilation.
    • Endotracheal intubation should be performed in cases in which the patient has difficulty maintaining the airway because of large secretions, poor gag reflex, coma, or the need prolonged ventilatory support.
    • Premedication for rapid sequence induction (RSI) includes atropine (0.02 mg/kg for children younger than 8 y) to blunt the effect of vagal stimulation and decrease the secretions. Lidocaine (1-2 mg/kg) may be used to decrease airway stimulation during intubation and prevent an increase in ICP. Thiopental (4-7 mg/kg), etomidate (0.3 mg/kg), or midazolam (0.1 mg/kg) have been successfully used to sedate the patient for intubation. Ketamine is contraindicated in patients with significant head and eye injuries because it may increase ICP and intraocular pressure (IOP). Succinylcholine, a depolarizing paralytic agent, may be used in older children in doses of 1-1.5 mg/kg. It acts rapidly and lasts for a short duration. Succinylcholine is contraindicated in neuromuscular disorders. Nondepolarizing agents including rocuronium, pancuronium, and vecuronium are commonly used in young children.
  • Cardiovascular management
    • Achieving normotension and euvolemia is the goal in cardiovascular management. Cerebral perfusion pressure (CPP), defined as the mean arterial blood pressure (MAP) minus the ICP (CPP = MAP - ICP), is the physiologic variable that defines the pressure gradient driving the cerebral blood flow (CBF) and metabolite delivery; it is therefore closely related to ischemia. Several clinical studies suggest that maintaining CPP at 70-80 mm Hg may be the critical threshold.
    • Adequate volume resuscitation with isotonic solutions should be conducted to maintain adequate filling pressures, normal cardiac output, and ultimately normotension (MAP >90 mm Hg). More recent adult and pediatric studies have shown that the use of hypertonic solution in the resuscitation process is superior to that of lactated Ringer solution or isotonic sodium chloride solution. Patients who have received hypertonic sodium chloride solution have improved blood pressure response, overall decreased fluid requirement, fewer interventions in controlling the ICP, fewer complications, and improved survival.
    • Hypertension, if present, could represent a compensatory mechanism in response to the increased ICP; thus, reflex treatment of it may significantly compromise the cerebral perfusion. When normotension is desired in the presence of intracranial or intracerebral hemorrhage following surgical evacuation, calcium channel blockers or beta-blockers are the drugs of choice instead of direct vasodilators to avoid sudden hypotension.
    • Continuous cardiac monitoring should be performed because of the high incidence of ventricular dysrhythmias present in patients with head trauma and in those in whom cardiac contusion is suspected.
  • Increased ICP and cerebral perfusion management
    • Medical management of increased ICP includes elevating the head end of the bed to 30° and maintaining head and neck in midline position. Sedation and paralysis are used to prevent agitation and increased muscular activity that may increase the ICP. If neuromuscular blockers are used, monitoring the ICP and having an electroencephalogram in place is necessary.
    • The use of loop or osmotic diuretics (eg, furosemide, mannitol) is directed mostly at decreasing CSF production and improving cerebral compliance and CBF by decreasing the cerebral blood volume (CBV). The effect on the reduction of cerebral edema remains unproved. They are also used to maintain euvolemia.
    • Hyperventilation should be used carefully for treating acute ICP elevations. Studies have shown that prolonged prophylactic use of hyperventilation in head trauma patients is associated with negative outcome. CBF is known to be diminished in the first 24 hours in patients with severe traumatic brain injury, with absolute values close to those of ischemia. Hyperventilation decreases CBF. It also potentially leads to the loss of autoregulation. This may cause further ischemic injury and does not produce a consistent reduction in ICP. Therefore, mild hyperventilation with PaCO2 level of 30-35 mm Hg is tolerated better over a longer period with less deleterious effect.
    • CSF drainage by extraventricular drains improves the ICP in these patients and provides continuous ICP monitoring.
    • Corticosteroids have no effect in decreasing the cerebral edema associated with head trauma and are not currently recommended. However, in the presence of head trauma and spinal cord injury, prompt use of methylprednisolone as a continuous infusion may improve the outcome of spinal injury.
    • Barbiturate therapy lowers the ICP and exerts cerebral protection through several mechanisms: alterations in vascular tone, inhibition of free radical–mediated lipid peroxidation, and suppression of metabolism. By lowering the metabolic demands, it decreases the CBF and related CBV, providing beneficial effects on the ICP and global cerebral perfusion. However, several studies have shown that barbiturate therapy does not improve outcome when compared to mannitol as empiric coma therapy or when used as prophylactic treatment of ICP.
    • The only patients to respond favorably to barbiturate ICP control seem to be those in whom the cerebrovascular autoregulatory response is preserved. Therefore, their use should be reserved only for intractable increased ICP when all conventional medical therapies have failed. The goal of barbiturate therapy should be directed to achieve electroencephalographic burst suppression because maximal reduction in CBF and metabolism occurs at this level. The main side effect remains hypotension and cardiovascular toxicity. Hence, when used, invasive hemodynamic monitoring is generally recommended.
  • Bleeding management: Disseminated intravascular coagulopathy is present in one third of head trauma patients and requires aggressive management and correction with replacement factors in order to decrease the risk of further intracranial bleeding and allow surgical intervention when necessary.
  • Seizure management: Posttraumatic seizures present in 10% of pediatric patients with head trauma may affect the outcome adversely by increasing the ICP, increasing the metabolic demands of the brain, and causing hypoxia and/or hypoventilation in a spontaneously breathing patient. Short-acting benzodiazepines (eg, lorazepam, diazepam) may be used to control the seizure, and phenytoin or phenobarbital should be used for maintenance anticonvulsant.

Surgical Care

  • Surgical decompression is required in the presence of a rapidly expanding epidural or subdural hematoma that causes an increase in ICP and focal compression.
  • The craniotomy and surgical drainage of an epidural hematoma and repair of vessels should be done immediately if signs of increased ICP, altered mentation, focal neurologic signs, pupillary changes, or a midline shift are present.
  • Conservative management with close monitoring in a pediatric ICU (PICU) is acceptable if no focal neurologic signs, altered mentation, or pressure effects with midline shift are present and the hematoma is less than 2 cm.
  • Patients with subdural hematoma with midline shift or altered mental status should have the hematoma emergently drained.
  • Patients with small subdural hematoma with no midline shift or pressure effects should be managed conservatively with close monitoring.
  • Surgical drainage of subdural hematoma is not required in most cases.
  • Most patients with penetrating injuries require surgical debridement and evacuation of the hematoma and receive prophylactic antibiotics, as well as anticonvulsants.
  • Depressed skull fractures require surgical elevation if the depth of the depression is thicker than the calvaria, if the depression is greater than 1 cm, and if bony fragments are causing the compression against the brain tissue.

Consultations

Diet

  • Nutritional support is directed at avoiding hypoglycemia or hyperglycemia and providing enough calories to prevent catabolism and a negative nitrogen balance.
  • Either the enteral or the parenteral route can be used, depending on the clinical status of the patient.

Activity

  • Elevation of the head to 30° and maintaining midline position continues to be recommended because it improves the venous drainage and decreases the ICP without affecting the CBF.
  • A cervical spine collar should be used until clearance of the spine is achieved.

Medication

Medical therapy is directed at controlling the intracranial pressure (ICP) with sedatives and neuromuscular blockers, diuretics, lidocaine, and anticonvulsants.

Nondepolarizing neuromuscular blockers

These are used in combination with a sedative as part of the rapid sequence intubation process or to achieve control of the ICP.


Vecuronium (Norcuron)

Used to facilitate endotracheal intubation and provide neuromuscular relaxation during intubation and mechanical ventilation. Used as an adjunct to a sedative or hypnotic agent.

Adult

0.1 mg/kg/dose IV

Pediatric

Loading dose: 0.08-0.1 mg/kg/dose IV
Maintenance: 0.05-0.1 mg/kg/dose IV q1h prn; alternatively, 0.1 mg/kg/h IV as continuous infusion

When vecuronium is used concurrently with inhalational anesthetics, neuromuscular blockade is enhanced; renal or hepatic failure as well as concomitant administration of steroids may result in prolonged blockade despite withdrawal of the agent

Documented hypersensitivity; myasthenia gravis or related syndromes

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Smaller dose should be used in patients with myasthenia gravis, and the effect should be titrated with a peripheral nerve stimulator

Barbiturates

These are used as an adjunct for intubation in patients with head trauma and in the management of elevated ICP. They may also be used as anticonvulsants.


Thiopental (Pentothal Sodium)

DOC for endotracheal intubation of patients with head injury. Also decreases the ICP.
Facilitates transmission of impulses from thalamus to cortex of brain, resulting in an imbalance in central inhibitory and facilitatory mechanisms.

Adult

75-250 mg/dose IV, repeat prn

Pediatric

Induction: 4-7 mg/kg/dose IV
Maintenance: 1 mg/kg IV prn
Acute rises in ICP: 1.5-5 mg/kg/dose IV

Coadministration with CNS depressants, salicylates, and sulfisoxazole increases toxicity

Documented hypersensitivity; porphyria; severe hypovolemia; unstable hemodynamics; lack of familiarity with drug; inability to manage airway

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause myocardial depression, decreased cardiac output, and hypotension; caution in hepatic or renal insufficiency, asthma, severe cardiovascular disease, unstable aneurysm, hypotension, and laryngospasm or bronchospasm


Pentobarbital (Nembutal)

Short-acting barbiturate with sedative, hypnotic, and anticonvulsant properties. May be used in high dosage to induce barbiturate coma for treatment of refractory increased ICP.

Adult

Pediatric

Pentobarbital coma:
Loading dose: 10-15 mg/kg/dose IV over 1-2 h
Maintenance: 1 mg/kg/h IV; may increase to 2-3 mg/kg/h until burst suppression is shown on EEG

Concomitant use with alcohol may produce additive CNS effects and fatality; chloramphenicol may inhibit pentobarbital metabolism; pentobarbital may enhance chloramphenicol metabolism; MAOIs may enhance sedative effects of barbiturates; valproic acid appears to decrease barbiturate metabolism, increasing toxicity; barbiturates can decrease effects of anticoagulants (patients may require dosage adjustments if barbiturates are added to or withdrawn from the regimen); barbiturates may decrease corticosteroid and digitoxin effects through induction of hepatic microsomal enzymes, which increase metabolism; barbiturates decrease theophylline levels and may decrease effects; pentobarbital may decrease verapamil bioavailability

Documented hypersensitivity; liver failure

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Rapid and prolonged IV administration may cause hypotension, respiratory depression, apnea, bronchospasm, and laryngospasm; caution in hypovolemic shock, respiratory dysfunction, renal dysfunction, and congestive heart failure


Phenobarbital (Luminal, Solfoton)

Used for seizure control in patients with head trauma.

Adult

300-800 mg, followed by 120-240 mg/dose at 20-min intervals until seizures are controlled or total dose of 1-2 g is administered

Pediatric

Loading dose: 15-20 mg/kg/dose IV in single or divided doses
Maintenance: 5 mg/kg/d PO/IV divided bid

May decrease effects of chloramphenicol, digitoxin, corticosteroids, carbamazepine, theophylline, verapamil, metronidazole, and anticoagulants (patients stabilized with anticoagulants may require dosage adjustments if medications are added to or withdrawn from their regimen); coadministration with alcohol may produce additive CNS effects and death; chloramphenicol, valproic acid, and MAOIs may increase phenobarbital toxicity; rifampin may decrease phenobarbital effects

Documented hypersensitivity; severe respiratory disease; marked impairment of liver function; nephritis

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Monitor respiratory and cardiac function during loading dose; may cause drowsiness and impaired ability to perform tasks requiring alertness; caution in myasthenia gravis and myxedema

Benzodiazepines

These agents may be used to obtain immediate control of seizure activity or as adjuncts to narcotics and neuromuscular blockers to control the ICP. Prolonged use of these drugs may alter neurologic examination findings.


Midazolam (Versed)

Short-acting benzodiazepine with rapid onset of action. Useful in treating increased ICP.

Adult

Pediatric

0.05-0.1 mg/kg/dose IV; dose may be repeated prn; not to exceed a cumulative dose of 6 mg for infants and 10 mg for children

Sedative effects of midazolam may be antagonized by theophyllines; narcotics and erythromycin may accentuate sedative effects of midazolam because of decreased clearance

Documented hypersensitivity; uncontrolled pain; preexisting hypotension; narrow-angle glaucoma

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Careful monitoring of cardiorespiratory status during administration; caution in congestive heart failure, pulmonary disease, renal impairment, and hepatic failure


Lorazepam (Ativan)

Long-acting benzodiazepine, used as anticonvulsant for immediate control of seizure activity.

Adult

4 mg/dose IV slowly over 2-5 min and repeat in 10-15 min prn; not to exceed a cumulative dose of 8 mg/12 h

Pediatric

0.05-0.1 mg/kg/dose IV over 2-5 min; may be repeated in 10-15 min

Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAOIs

Documented hypersensitivity; CNS depression; hypotension; narrow-angle glaucoma; uncontrolled pain

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Cardiorespiratory monitoring during administration is required; long-term use requires liver function and CBC monitoring; caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease

Anticonvulsants

These agents are recommended as a prophylactic measure for patients at increased risk for seizure activity following head trauma. No proof exists of a beneficial effect in seizure prevention after 1 week following head trauma. They are also used for immediate control of seizures.


Phenytoin (Dilantin)

May act in motor cortex where may inhibit spread of seizure activity. Activity of brainstem centers responsible for tonic phase of grand mal seizures may also be inhibited. Is preferred to phenobarbital to control seizures because it does not cause as much CNS depression.

Adult

Loading dose for status epilepticus: 15-20 mg/kg PO/IV once or in divided doses, followed by 100-150 mg/dose at 30-min intervals
Initial maintenance dose (administered 12 h after loading dose): 100 mg (if administering oral susp, use dose of 125 mg) PO/IV tid
Maintenance: 300-400 mg/d PO/IV divided tid or qd/bid if using ER; increase to 600 mg/d (625 mg/d for PO susp) may be necessary; not to exceed 1500 mg/24 h
Rate of IV infusion must not exceed 50 mg/min to avoid hypotension and arrhythmias

Pediatric

Loading dose: 15-20 mg/kg PO/IV once or in divided doses
Initial maintenance dose (administered 12 h after loading dose): 5 mg/kg/d PO/IV divided bid/tid
Maintenance: 4-8 mg/kg PO/IV divided bid/tid; children > 6 y may require minimum adult dose (300 mg/d); not to exceed 300 mg/d

Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole, phenylbutazone, succinimides, sulfonamides, omeprazole, phenacemide, disulfiram, ethanol (acute ingestion), trimethoprim, and valproic acid may increase phenytoin toxicity; phenytoin effects may decrease when taken concurrently with barbiturates, diazoxide, ethanol (long-term ingestion), rifampin, antacids, charcoal, carbamazepine, theophylline, and sucralfate; phenytoin may decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, quinidine, theophylline, methadone, metyrapone, mexiletine, PO contraceptives, and valproic acid; continuous tube feeding decreases the bioavailability of phenytoin

Documented hypersensitivity; sinoatrial block; second- and third-degree AV block; sinus bradycardia; Adams-Stokes syndrome

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Perform blood counts and urinalyses when therapy is initiated; discontinue use if a rash appears and do not resume use if rash is exfoliative, bullous, or purpuric; rapid IV infusion may result in death from cardiac arrest, marked by QRS widening; caution in acute intermittent porphyria and diabetes (may elevate blood sugars); discontinue use if hepatic dysfunction occurs

Diuretics

These may have a beneficial effect in lowering the ICP by decreasing the CSF production, excreting more water over solute and decreasing blood viscosity, with subsequent improvement of CBF.


Furosemide (Lasix)

A loop diuretic helpful in decreasing the ICP via 2 mechanisms. One influences CSF formation by affecting the sodium-water movement across the blood-brain barrier; the other mechanism is the preferential excretion of water over solute in the distal tubule.
Mostly useful when used in combination with mannitol, especially when the latter is administered 15 min before furosemide.

Adult

20-80 mg/d IV/IM; may increase dose; not to exceed 600 mg/d

Pediatric

1-2 mg/kg/dose IV q6-12h

Metformin decreases furosemide concentrations; furosemide interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides and furosemide; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently with this medication; increased plasma lithium levels and toxicity are possible when taken concurrently with this medication

Documented hypersensitivity; hepatic coma, anuria, and severe electrolyte depletion

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid hypotension due to large-volume depletion; requires serum electrolyte monitoring


Mannitol (Osmitrol)

Osmotic diuretic, which lowers the blood viscosity and produces cerebral vasoconstriction with normal CBF. ICP decrease occurs subsequent to a decrease in CBV.

Adult

1.5-2 g/kg IV as 20% solution (7.5-10 mL/kg) or as 15% solution (10-13 mL/kg) over a period as short as 30 min

Pediatric

0.5-1 g/kg/dose IV initial dose
0.25-0.5 g/kg/dose IV q4-6h

May decrease serum lithium levels

Documented hypersensitivity; anuria; severe pulmonary congestion; progressive renal damage; severe dehydration; active intracranial bleeding; progressive heart failure

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Carefully evaluate cardiovascular status before rapid administration of mannitol because a sudden increase in extracellular fluid may lead to fulminating CHF; avoid pseudoagglutination, when blood is administered simultaneously, add at least 20 mEq of sodium chloride to each liter of mannitol solution; do not administer electrolyte-free mannitol solutions with blood; If used every 4-6 h, serum osmolarity should be monitored and dose held if osmolarity exceeds 320 mOsm/kg

Anesthetics

These agents may be used to blunt ICP elevation during endotracheal intubation process or during airway manipulation such as suctioning.


Lidocaine 1% (Xylocaine)

Used with good results in controlling the ICP in patients with head trauma.

Adult

Pediatric

1-1.5 mg/kg/dose IV

Coadministration with cimetidine or beta-blockers increases toxicity of lidocaine; coadministration with procainamide and tocainide may result in additive cardiodepressant action; may increase effects of succinylcholine

Documented hypersensitivity; Adams-Stokes syndrome (avoid); Wolf-Parkinson-White syndrome (avoid); severe sinoatrial, (AV), or intraventricular block if artificial pacemaker not in place (avoid)

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in heart failure, hepatic disease, hypoxia, hypovolemia or shock, respiratory-depression, and bradycardia; may increase risk of CNS and cardiac adverse effects in elderly patients; high plasma concentrations can cause seizures, heart block, and AV conduction abnormalities

More on Head Trauma

Overview: Head Trauma
Differential Diagnoses & Workup: Head Trauma
Treatment & Medication: Head Trauma
Follow-up: Head Trauma
Multimedia: Head Trauma
References
Further Reading

References

  1. Cakmakci H. Essentials of trauma: head and spine. Pediatr Radiol. Jun 2009;39 Suppl 3:391-405. [Medline].

  2. [Best Evidence] Yeates KO, Taylor HG, Rusin J, et al. Longitudinal trajectories of postconcussive symptoms in children with mild traumatic brain injuries and their relationship to acute clinical status. Pediatrics. Mar 2009;123(3):735-43. [Medline].

  3. Iranmanesh F. Outcome of head trauma in children. Indian J Pediatr. May 27 2009;[Medline].

  4. Garcia Garcia JJ, Manrique Martinez I, Trenchs Sainz de la Maza V, et al. [Registry of mild craniocerebral trauma: Multicentre study from the Spanish Association of Pediatric emergencies.]. An Pediatr (Barc). May 21 2009;[Medline].

  5. Mackerle Z, Gal P. Unusual penetrating head injury in children: personal experience and review of the literature. Childs Nerv Syst. May 19 2009;[Medline].

  6. Allard RH, van Merkesteyn JP, Baart JA. [Child abuse]. Ned Tijdschr Tandheelkd. Apr 2009;116(4):186-91. [Medline].

  7. Rangarajan N, Kamalakkannan SB, Hasija V, et al. Finite element model of ocular injury in abusive head trauma. J AAPOS. May 4 2009;[Medline].

  8. Trenchs V, Curcoy AI, Castillo M, et al. Minor head trauma and linear skull fracture in infants: cranial ultrasound or computed tomography?. Eur J Emerg Med. Jun 2009;16(3):150-2. [Medline].

  9. Ringl H, Schernthaner R, Philipp MO, et al. Three-dimensional fracture visualisation of multidetector CT of the skull base in trauma patients: comparison of three reconstruction algorithms. Eur Radiol. May 14 2009;[Medline].

  10. [Guideline] Davis PC, Seidenwurm DJ, Brunberg JA, et al. Head trauma. American College of Radiology (ACR). 2006.

  11. [Guideline] Kellogg ND. Evaluation of suspected child physical abuse. Pediatrics. Jun 2007;119(6):1232-41. [Medline][Full Text].

  12. Alberico AM, Ward JD, Choi SC, et al. Outcome after severe head injury. Relationship to mass lesions, diffuse injury, and ICP course in pediatric and adult patients. J Neurosurg. Nov 1987;67(5):648-56. [Medline].

  13. Allen EM, Boyer R, Cherny WB. Head and Spinal Cord Injury. In: Rogers MC, Nichols DG, eds. Text Book of Pediatric Intensive Care. 3rd ed. Baltimore, MD: Lippincott, Williams & Wilkins; 1996:809-57.

  14. [Guideline] Chang BS, Lowenstein DH. Practice parameter: antiepileptic drug prophylaxis in severe traumatic brain injury: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. Jan 14 2003;60(1):10-6. [Medline][Full Text].

  15. Dias MS. Traumatic brain and spinal cord injury. Pediatr Clin North Am. Apr 2004;51(2):271-303.

  16. Dietrich AM, Bowman MJ, Ginn-Pease ME, et al. Pediatric head injuries: can clinical factors reliably predict an abnormality on computed tomography?. Ann Emerg Med. Oct 1993;22(10):1535-40. [Medline].

  17. Dikmen S, Machamer J, Temkin N, McLean A. Neuropsychological recovery in patients with moderate to severe head injury: 2 year follow-up. J Clin Exp Neuropsychol. Aug 1990;12(4):507-19. [Medline].

  18. Doberstein CE, Hovda DA, Becker DP. Clinical considerations in the reduction of secondary brain injury. Ann Emerg Med. Jun 1993;22(6):993-7. [Medline].

  19. Dolan M. Head Trauma. In: Pediatric Emergency Medicine. St. Louis, MO: Mosby-Year Book; 1997:236-51.

  20. Duhaime AC, Gennarelli TA, Thibault LE, et al. The shaken baby syndrome. A clinical, pathological, and biomechanical study. J Neurosurg. Mar 1987;66(3):409-15. [Medline].

  21. Fessler RD, Diaz FG. The management of cerebral perfusion pressure and intracranial pressure after severe head injury. Ann Emerg Med. Jun 1993;22(6):998-1003. [Medline].

  22. Ford EG, Jennings LM, Andrassy RJ. Steroid administration potentiates urinary nitrogen losses in head- injured children. J Trauma. Sep 1987;27(9):1074-7. [Medline].

  23. Ghajar J, Hariri RJ, Narayan RK, et al. Survey of critical care management of comatose, head-injured patients in the United States. Crit Care Med. Mar 1995;23(3):560-7. [Medline].

  24. Goldman H, Morehead M, Murphy S. Use of adrenocorticotrophic hormone analog to minimize brain injury. Ann Emerg Med. Jun 1993;22(6):1035-40. [Medline].

  25. Greenes DS. Neurotrauma. In: Textbook of Pediatric Emergency Medicine. 5th ed. 2006:1361-88.

  26. Haas DC, Lourie H. Trauma-triggered migraine: an explanation for common neurological attacks after mild head injury. Review of the literature. J Neurosurg. Feb 1988;68(2):181-8. [Medline].

  27. Kadish HA, Schunk JE. Pediatric basilar skull fracture: do children with normal neurologic findings and no intracranial injury require hospitalization?. Ann Emerg Med. Jul 1995;26(1):37-41. [Medline].

  28. Kraus JF, Rock A, Hemyari P. Brain injuries among infants, children, adolescents, and young adults. Am J Dis Child. Jun 1990;144(6):684-91. [Medline].

  29. Lewis RJ, Yee L, Inkelis SH, Gilmore D. Clinical predictors of post-traumatic seizures in children with head trauma. Ann Emerg Med. Jul 1993;22(7):1114-8. [Medline].

  30. Marion DW, Spiegel TP. Changes in the management of severe traumatic brain injury: 1991-1997. Crit Care Med. Jan 2000;28(1):16-8. [Medline].

  31. Masters SJ, McClean PM, Arcarese JS, et al. Skull x-ray examinations after head trauma. Recommendations by a multidisciplinary panel and validation study. N Engl J Med. Jan 8 1987;316(2):84-91. [Medline].

  32. McAllister JD, Gnauck. Rapid Sequence Intubation Of The Pediatric Patient. Peditric Clinics of N Am. 1999;46:1249-1284.

  33. Muizelaar JP, Marmarou A, DeSalles AA, et al. Cerebral blood flow and metabolism in severely head-injured children. Part 1: Relationship with GCS score, outcome, ICP, and PVI. J Neurosurg. Jul 1989;71(1):63-71. [Medline].

  34. Muizelaar JP, Marmarou A, Ward JD, et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurg. Nov 1991;75(5):731-9. [Medline].

  35. Povlishock JT. Pathobiology of traumatically induced axonal injury in animals and man. Ann Emerg Med. Jun 1993;22(6):980-6. [Medline].

  36. Rosenthal M. Mild traumatic brain injury syndrome. Ann Emerg Med. Jun 1993;22(6):1048-51. [Medline].

  37. Rosner MJ. Introduction to cerebral perfusion pressure management. Neurosurg Clin N Am. Oct 1995;6(4):761-73. [Medline].

  38. Rosner MJ, Rosner SD, Johnson AH. Cerebral perfusion pressure: management protocol and clinical results. J Neurosurg. Dec 1995;83(6):949-62. [Medline].

  39. Siesjo BK. Basic mechanisms of traumatic brain damage. Ann Emerg Med. Jun 1993;22(6):959-69. [Medline].

  40. Simma B, Burger R, Falk M, Sacher P, Fanconi S. A prospective, randomized, and controlled study of fluid management in children with severe head injury: lactated Ringer's solution versus hypertonic saline. Crit Care Med. Jul 1998;26(7):1265-70. [Medline].

  41. Temkin NR, Dikmen SS, Wilensky AJ, et al. A randomized, double-blind study of phenytoin for the prevention of post-traumatic seizures. N Engl J Med. Aug 23 1990;323(8):497-502. [Medline].

  42. Tepas JJ 3d, Mollitt DL, Talbert JL, Bryant M. The pediatric trauma score as a predictor of injury severity in the injured child. J Pediatr Surg. Jan 1987;22(1):14-8. [Medline].

  43. Thiessen ML, Woolridge DP. Pediatric Minor Closed Head Injury. Pediatric Clinics of North America. 2006;53:1-26.

  44. Tietjen CS, Hurn PD, Ulatowski JA, Kirsch JR. Treatment modalities for hypertensive patients with intracranial pathology: options and risks. Crit Care Med. Feb 1996;24(2):311-22. [Medline].

Keywords

head trauma, head injury, brain trauma, brain injury, primary head trauma, secondary head trauma, intracranial pressure, ICP, hypotension, hypoxia, hypercapnia, traumatic brain injury, scalp injury, skull fracture, basilar skull fracture, concussion, contusion, intracranial hemorrhage, subarachnoid hemorrhage, epidural hematoma, subdural hematoma, intraventricular hemorrhage, penetrating injuries, diffuse axonal injury, skull fracture, Battle sign, raccoon eyes, birth trauma, seizures, respiratory distress, shaken baby syndrome, spinal cord injury, paralysis, accidents, falls, assaults, recreational activities, child abuse, seizure disorder, attention deficit disorder, treatment, diagnosis

Contributor Information and Disclosures

Author

Arabela Stock, MD, Consulting Staff, Department of Pediatrics, Divisions of Critical Care and Pulmonology, Florida Pediatric Association
Arabela Stock, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians
Disclosure: Nothing to disclose.

Coauthor(s)

Jagvir Singh, MD, Director, Division of Pediatric Emergency Medicine, Lutheran General Hospital of Park Ridge
Jagvir Singh, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Medical Editor

G Patricia Cantwell, MD, Associate Clinical Professor, Department of Pediatrics, University of Miami; Director of Pediatric Critical Care Medicine, Miller School of Medicine, Jackson Children's Hospital
G Patricia Cantwell, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians, American Heart Association, American Trauma Society, National Association of EMS Physicians, Society of Critical Care Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Barry J Evans, MD, Assistant Professor of Pediatrics, Temple University Medical School; Director of Pediatric Critical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's Medical Center
Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital
Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians
Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

Chief Editor

Timothy E Corden, MD, Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin
Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.