Head Trauma

Head Trauma

 Trauma is a leading cause of death in children older than 1 year in the United States, with head trauma representing 80% or more of the injuries. Approximately 5% of head trauma victims die at the site of the accident. Head trauma has a high emotional, psychosocial, and economic impact as these patients often have comparatively long hospital stays, and 5-10% require discharge to a long-term care facility.

The anatomical differences of the child's brain render it more susceptible than an adult's to certain type of injuries following head trauma. The head is larger in proportion to the body surface area, and stability is dependent on the ligamentous rather than bony structure. The pediatric brain has a higher water content, 88% vs 77% in adult, which makes the brain softer and more prone to acceleration-deceleration injury. The water content is inversely related to the myelinization process. The unmyelinated brain is more susceptible to shear injuries. Infants and young children tolerate intracranial pressure (ICP) increases better because of open sutures .

Pathophysiology: Primary and secondary injuries are described with head trauma, and their presence affect. the outcome of these patients.

The primary injury occurs at the time of impact, either by a direct injury to the brain parenchyma or by an injury to the long white-matter tracts through acceleration-deceleration forces. Direct injury to the brain parenchyma occurs as the brain is impacted on the bony protuberances of the calvarium or by penetration of the brain by bony fragments or a foreign body. In children, the compliant skull is easily deformed, and impacts on the brain at the time of the insult result in a coup injury, as opposed to adults, in whom the brain is forced against the bony protuberances opposite the point of the impact, resulting in a countercoup injury. Intracranial hemorrhage also may result from shearing or laceration of vascular structures. Acceleration-deceleration forces cause shearing of the long white-matter tracts, leading to axonal disruption and secondary cell death.

The secondary injury is represented by systemic and intracranial events that occur in response to the primary injury and further contribute to neuronal damage and cell death.

The systemic events are hypotension, hypoxia, and hypercapnia and may occur as a direct result of primary injury to the CNS or could result from associated injuries in a person with multiple traumas.

The intracranial events are a series of inflammatory changes and pathophysiologic perturbations that occur immediately after the primary injury and continue over time. Their presence adds to the adverse outcome of the head trauma patient. The inflammatory events are the result of a cascade of biomolecular changes triggered by the initial insult leading to microcirculatory disruption and neuronal disintegration. A series of factors such as free radicals, free iron, and excitatory neurotransmitters (glutamate, aspartate) are the result of these inflammatory events, and their presence contributes to the negative outcome. The pathophysiologic events, are cerebral edema, ICP, hyperemia, and ischemia.

The brain has minimal ability to store energy thus it is dependent on aerobic metabolism. The delivery of oxygen and metabolic substrate to the brain is maintained by a constant supply of blood known as cerebral blood flow. Cerebral blood flow (CBF) defined as the amount of blood in transit through the brain at one given point in time is estimated to be in a normal adult 50/ml/100g/min, and is known to be much higher in children. The minimum amount necessary to prevent ischemia however remains unknown. CBF is influenced by mean arterial blood pressure (MAP), ICP, viscosity of the blood, metabolic products, and the diameter of brain vessels. CBF should not be confused with cerebral blood volume (CBV), which represents the amount of blood present in the brain vasculature. CBV is the major contributor to the ICP and is dependent on the diameter of intracranial vessels. When CBV is increased, the pressure gradient across the compartment is decreased, and the CBF is decreased.

The brain has the capacity of maintaining constant blood flow, through a mechanism known as autoregulation. This occurs over a wide range of blood pressures through changes in cerebral resistance in response to fluctuations in MAP pressure. It is established that the CBF is maintained between a MAP of 60-150 mmHg. At 60 mmHg the cerebral vasculature is maximally dilated and at 150 mmHg is maximally constricted. Fluctuations past this range will lead to alterations in CBF and contribute to ischemia or disruption of the blood-brain barrier. Several mechanisms are known to affect autoregulation of CBF, and they can be divided in metabolic products and arterial blood gas content, myogenic, neurogenic, and endothelium-dependent factors. Their effect is not fully known and their mechanism of action is still under experimental investigation.

CBF is closely linked to cerebral metabolism. Although the mechanism of coupling is not clearly defined it is suspected to involve vasodilators released from neurons. Several factors have been implicated such as adenosine and free radicals. Pathophysiologic states such as fever, seizure activity known to increase the metabolic activity will lead to an increase in CBF.

CBF can be altered by changes in the partial pressure of oxygen or carbon dioxide. Alteration in the partial pressure of oxygen acts on the vascular smooth muscle through mechanisms that remained unclear. Hypoxia causes vasodilatation with significant increase in CBF. Increases in oxygen pressure cause vasoconstriction but to a lesser degree than hypoxia. Hypercarbia increases CBF up to 350% of normal, hypocapnia produces a decrease in blood flow. The mechanism appears to involve alteration in tissue pH that leads to changes in arteriolar diameter. This mechanism is preserved even when autoregulation is lost.

The myogenic mechanism was considered for a long time to be the most important in the autoregulation process. It was thought that the changes in the actin-myosin complex lead to rapid changes in the vasculature diameter thus affecting the CBF. Currently it has been shown that it mostly causes dampening of arterial pulsation and has little direct effect on cerebral autoregulation.

The neurogenic mechanism is represented by the effect of the sympathetic system on the cerebral vasculature. The sympathetic nervous system shifts autoregulation towards higher pressures whereas sympathetic blockade shifts it downwards.

Recent studies identified nitric oxide as one of the factors affecting cerebral autoregulation by producing relaxation of cerebral vessels. It is present in several conditions such as ischemia, hypoxia, and stroke. Nitric oxide has been shown to be generated by different cells at rest but also under direct stimulation by factors like cytokines.

Traumatic brain injury may lead to loss of autoregulation through alterations of the described mechanisms. These mechanisms represent the foundation upon which the medical management of increased ICP and cerebral perfusion pressure is based in patients with traumatic brain injury.

Frequency:

Mortality/Morbidity: The overall outcome for children with head injuries is better than that of adults with the same injury score. Recovery in children takes longer, from months to, sometimes, years, whereas adults reach maximum recovery by about 6 months following the injury. Outcome assessment based on Glasgow Coma Scale (GCS) could be used as an early predictor but has limitations regarding long-term outcome. Victims of multiple organ injuries, including head trauma, generally have a far worse outcome than those with isolated head injury alone.

Race: African American adolescent boys account for most of the firearms-related CNS injuries in pediatric population.

Sex: Males are twice as likely to sustain head injuries than females and have 4 times the risk of fatal trauma.

Age: The distribution of head trauma is relatively stable throughout childhood. An increase in the incidence of head trauma was identified in 2 age groups.

History: Head trauma patients may experience one or a combination of primary injuries, depending on the degree and mechanism of trauma. Specific types of primary injury include scalp injury, skull fracture, basilar skull fracture, concussion, contusion, intracranial hemorrhage, subarachnoid hemorrhage, epidural hematoma, subdural hematoma, intraventricular hemorrhage, subarachnoid hemorrhage, penetrating injuries, and diffuse axonal injury.

Physical: Head trauma patients often have multiple organ injuries. Assessment of patients with severe head injuries involves a primary and a secondary survey. The primary survey is a focused physical exam directed at identifying and treating life-threatening conditions present in a trauma patient and by this, preventing secondary brain injury. The secondary survey of patients with head trauma is a detailed examination and assessment of the system with the goal of identifying all traumatic injuries and directing further treatment.

Causes: Most head injuries occur secondary to motor vehicle accidents, falls, assaults, recreational activities, and child abuse. The percentage of each contributing factor differs between studies, and the distribution varies according to age group and sex. Few factors such as seizure disorder, attention deficit disorder, and alcohol and drug use enhance the vulnerability of the child or adolescent to this type of trauma. Infants and young children are more vulnerable to abuse because of their dependency on adults.

Lab Studies:

Imaging Studies:

Other Tests:

Procedures:

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. Patients with severe head trauma are at increased risk of developing cerebral edema, respiratory failure, and herniation secondary to the increased 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 as this may directly interfere with the optimal resuscitation process.

Surgical Care:

Consultations:

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

Activity:

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

Drug Category: 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.
Drug Name
Vecuronium (Norcuron) -- Used to facilitate endotracheal intubation and provide neuromuscular relaxation during the intubation and mechanical ventilation. Used as an adjunct to a sedative or hypnotic agent.
Adult Dose 0.1 mg/kg/dose IV
Pediatric Dose 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
Contraindications Documented hypersensitivity; myasthenia gravis or related syndromes
Interactions 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
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Smaller dose should be used in patients with myasthenia gravis and the effect titrated with a peripheral nerve stimulator
Drug Category: Barbiturates -- These are used as an adjunct for intubation in patients with head trauma and in the management of elevated ICP. They also may be used as anticonvulsants.
Drug Name
Thiopental (Pentothal Sodium) -- DOC for endotracheal intubation of patients with head injury. Also decreases the ICP.
Facilitates, transmission or impulses from thalamus to cortex of brain, resulting in an imbalance in central inhibitory and facilitatory mechanisms.
Adult Dose 75-250 mg/dose IV, repeat prn
Pediatric Dose Induction: 4-6 mg/kg/dose IV
Maintenance: 1 mg/kg IV prn

1.5-5 mg/kg/dose IV is used to treat acute rises in the ICP
Contraindications Documented hypersensitivity; porphyria; presence of severe hypovolemia or unstable hemodynamics; lack of familiarity with drug; inability to manage airway
Interactions Coadministration with CNS depressants, salicylates, sulfisoxazole, increases toxicity
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions May cause myocardial depression, decreased cardiac output, and hypotension; caution in hepatic or renal insufficiency, asthma, severe cardiovascular disease, unstable aneurysm, hypotension, laryngospasm or bronchospasm
Drug Name
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.
Pediatric Dose 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
Contraindications Documented hypersensitivity; liver failure
Interactions 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 added to or withdrawn from 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
Pregnancy D - Unsafe in pregnancy
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
Drug Name
Phenobarbital (Luminal, Solfoton) -- Used for seizure control in patients with head trauma .
Adult Dose 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 Dose Loading dose: 15-20 mg/kg/dose IV in single or divided doses
Maintenance: 5 mg/kg/d PO/IV divided bid
Contraindications Documented hypersensitivity; severe respiratory disease, marked impairment of liver function, and nephritis
Interactions May decrease effects of chloramphenicol, digitoxin, corticosteroids, carbamazepine, theophylline, verapamil, metronidazole, and anticoagulants (patients stabilized with anticoagulants may require dosage adjustments if 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
Pregnancy D - Unsafe in pregnancy
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
Drug Category: Benzodiazepines -- 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.
Drug Name
Midazolam (Versed) -- Short-acting benzodiazepine with rapid onset of action. Useful in treating increased ICP.
Pediatric Dose 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
Contraindications Documented hypersensitivity; uncontrolled pain; preexisting hypotension, narrow-angle glaucoma
Interactions Sedative effects of midazolam may be antagonized by theophyllines; narcotics and erythromycin may accentuate sedative effects of midazolam because of decreased clearance
Pregnancy D - Unsafe in pregnancy
Precautions Careful monitoring of cardiorespiratory status during administration; caution in congestive heart failure, pulmonary disease, renal impairment, and hepatic failure
Drug Name
Lorazepam (Ativan) -- Long-acting benzodiazepine, used as anticonvulsant for immediate control of seizure activity.
Adult Dose 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 Dose 0.05-0.1 mg/kg/dose IV over 2-5 min; may be repeated in 10-15 min
Contraindications Documented hypersensitivity; preexisting CNS depression, hypotension, and narrow-angle glaucoma; uncontrolled pain
Interactions Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAOIs
Pregnancy D - Unsafe in pregnancy
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
Drug Category: Anticonvulsants -- 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 also are used for immediate control of seizures.
Drug Name
Phenytoin (Dilantin) -- May act in motor cortex where may inhibit spread of seizure activity. Activity of brain stem centers responsible for tonic phase of grand mal seizures also may be inhibited. Is preferred to phenobarbital to control seizures because it does not cause as much CNS depression.
Adult Dose 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 (use 125 mg for oral susp) IV/PO 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 oral susp) may be necessary; do not exceed 1500 mg/24h

Rate of IV infusion must not exceed 50 mg/min to avoid hypotension and arrhythmias
Pediatric Dose 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

>6 years: May require minimum adult dose (300 mg/d); not to exceed 300 mg/d
Contraindications Documented hypersensitivity; sinoatrial block, second- and third-degree AV block, sinus bradycardia, or Adams-Stokes syndrome
Interactions 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 (chronic 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, oral contraceptives, valproic acid

Continuous tube feeding decreases the bioavailability of phenytoin
Pregnancy D - Unsafe in pregnancy
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
Drug Category: 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 cerebral blood flow.
Drug Name
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 Dose 20-80 mg/d IV/IM; may increase dose; not to exceed 600 mg/d
Pediatric Dose 1-2 mg/kg/dose IV q6-12h
Contraindications Documented hypersensitivity; hepatic coma, anuria, and severe electrolyte depletion
Interactions 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
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Avoid hypotension due to large volume depletion; requires serum electrolyte monitoring
Drug Name
Mannitol (Osmitrol) -- Osmotic diuretic, which lowers the blood viscosity and produces cerebral vasoconstriction with normal cerebral blood flow. ICP decrease occurs subsequent to a decrease in cerebral blood volume.
Adult Dose 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 Dose 0.5-1 g/kg/dose IV initial dose
0.25-0.5 g/kg/dose IV q4-6h
Contraindications Documented hypersensitivity; anuria, severe pulmonary congestion, progressive renal damage, severe dehydration, active intracranial bleeding, and progressive heart failure
Interactions May decrease serum lithium levels
Pregnancy C - Safety for use during pregnancy has not been established.
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 given simultaneously, add at least 20 mEq of sodium chloride to each liter of mannitol solution; do not give 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
Drug Category: Anesthetics -- May be used to blunt intracranial pressure elevation during endotracheal intubation process or during airway manipulation such as suctioning.
Drug Name
Lidocaine 1% (Xylocaine) -- Used with good results in controlling the ICP in patients with head trauma.
Pediatric Dose 1-1.5 mg/kg/dose IV
Contraindications Documented hypersensitivity to amide-type local anesthetics; avoid in Adams-Stokes syndrome and Wolf-Parkinson-White syndrome; avoid in severe sinoatrial, atrioventricular (AV), or intraventricular block, if artificial pacemaker not in place
Interactions 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
Pregnancy B - Usually safe but benefits must outweigh the risks.
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

Further Inpatient Care:

Further Outpatient Care:

In/Out Patient Meds:

Transfer:

Deterrence/Prevention:

Complications:

Prognosis:

Patient Education:

Medical/Legal Pitfalls:

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Constructed by Dr N.A. Nematallah Consultant in perioperative medicine and intensive therapy, Al Razi Orthopedic Hospital , State of Kuwait, email : razianesth@freeservers.com