Head Trauma

Dr: Zohair AlAseriFRCPc, Emergency MedicineFRCPc, Critical Care Medicine FCEM UKChairman, Department of Emergency Medicine King khalid University Hospital, Riyadh, KSA.

Head Trauma

35 year old male involved in motor vehicle collision

Presented with GCS of 8

And BP of 85/32, HR of 140

What is your 1st line of treatment

1—intubate

2---IV fluid

3---CT scan to exclude intracranial bleed

4---hypervetilation

Head Trauma


Presented with GCS of 8, smell of ethanol

And BP of 85/32, HR of 140

What is most likely cause of his hypotension

1---sever head trauma

2---hypovolemia

3---intoxication

Head Trauma

Minor head trauma (Glasgow Coma Scale [GCS] score of 14 to 15)

or presence of any intracranial contusion, hematoma, or laceration

Moderate head injuries (GCS of 9 to 13)

Severe head injuries (GCS of 8 or less)

•External physical signs not always present in the patient who has sustained serious underlying traumatic brain injury (TBI).

Head Trauma

• The normal pressure exerted by the CSF is 65 to 195 mm H2O or 5 to 15 mm Hg.

Cerebral Hemodynamics Blood-Brain Barrier.

Head Trauma

The blood-brain barrier (BBB) maintains the microenvironment of the brain tissue.

Extracellular ion and neurotransmitter concentrations are regulated by movement across BBB.

The brain has an extremely high metabolic rate, using approximately 20% of the entire oxygen volume consumed by the body So it requires about 15% of the total cardiac output.


Head Trauma

The brain has an extremely high metabolic rate

using approximately 20% of the entire oxygen volume consumed by the body

it requires about 15% of the total cardiac output.


Head Trauma

Hypertension, alkalosis, and hypocarbia promote cerebral vasoconstriction

hypotension, acidosis, and hypercarbia cause cerebral vasodilation.


Head Trauma

increased brain swelling and mass effect.

Over time, injured vessels lose their responsiveness to hypocarbia

become vasodilated.

Cerebral Hemodynamics Pco2

Head Trauma

Low Po2 ----- cerebral vessels dilate

vasogenic edema.

Cerebral Hemodynamics

Po2

Head Trauma

So hypoxia should be treated

CPP is estimated as MAP minus ICP. CBF remains constant when CPP is 50 to 160 mm Hg.

If CPP falls below 40 mm Hg, the autoregulation of CBF is lost----ischemia

Cerebral Perfusion Pressure & BP

Head Trauma

So hypotension & increased ICP should be controlled

Primary ---- damage that occurs at the time of head trauma.

it causes permanent mechanical cellular disruption and microvascular injury.

Head Trauma

Primary and Secondary Brain Injury

Secondary brain injury results from intracellular and extracellular derangements

All currently used acute therapies for TBI are directed at reversing or preventing secondary injury.

Head Trauma

Secondary Brain Injury

Influence the outcome

Common secondary systemic insults in trauma patients include

HypotensionHypoxiaAnemia. hypercarbia, hyperthermia, coagulopathy, and

seizures.

Head Trauma


Hypotension doubles the mortality

Hypoxia, defined as a Po2 less than 60 mm Hg

Anemia When anemia (hematocrit less than 30%) occurs in patients with severe head injury, the mortality rate increases

Brain Trauma Foundation, American Association of Neurological Surgeons, Joint Section on Neurotrauma and Critical Care : Guidelines for the management of severe traumatic brain injury. J

Neurotrauma 2000; 17:471.

Head Trauma


All Bad

Contributing events in the pathophysiology of secondary brain injury.

Hallmark of brain insult

Causes hypoxic Hypotension intoxication consumed before the injury.

Head Trauma

Altered Levels of Consciousness


Presented with GCS of 8, smell of ethanol

And BP of 170/32, HR of 40 and bouts of irregular breathing

Your next action will be

1—consult NS

2—admit for evaluation

3—manitol

4---atropine

Progressive hypertension associated with bradycardia and diminished respiratory effort

D/T acute, potentially lethal rises in ICP.

Head Trauma

Cushing's Reflex

Head Trauma

Cushing's Reflex

The full triad of hypertension, bradycardia, and respiratory irregularity is seen in only one third of cases of life-threatening increased ICP.

TriadHow frequent is seen in cushing reflex

When increasing ICP cannot be controlled, the intracranial contents shift and herniate through the cranial foramen.

Herniation can occur within minutes to days mortality approaches 100% without rapid

implementation of temporizing emergency measures and definitive neurosurgical therapy.

Head Trauma

Cerebral Herniation

The most common

a form of transtentorial herniation.

hematomas in the lateral middle fossa or the temporal lobe.

Head Trauma

Uncal Cerebral Herniation

Third cranial nerve is compressed; ipsilateral anisocoria, ptosis, impaired extraocular movements, and a sluggish pupillary light reflex

As the herniation progresses, compression of the ipsilateral oculomotor nerve eventually causes ipsilateral pupillary dilation and nonreactivity.


Head Trauma

Contralateral Babinski's Contralateral hemiparesis Decerebrate posturing eventually occurs; LOS & change in respiratory pattern, and cv system. Herniation that is uncontrolled progresses rapidly to

brainstem failure, cardiovascular collapse, and death.

Head Trauma


When hemiparesis is detected ipsilateral to the dilated pupil and the mass lesion, it causes false-localizing motor findings

Kernohan's notch syndrome

mechanism comorbid factors. Past medical history, Medications level of consciousness, course Witnessed posttraumatic seizures apnea

Head Trauma

CLINICAL FEATURES, History

Identification of life-threatening injuries and of neurologic changes in the immediate posttrauma period.

mental status GCS pupillary size Responsiveness motor strength and symmetry. neurologic assessment in the immediate

posttrauma period serves as a baseline

Head Trauma

Acute Neurologic General Examination

The GCS assesses a patient's best eye, verbal, and motor responsiveness.

limitations. Hypoxia, hypotension, and intoxication can falsely

lower the initial GCS. Intubation Periorbital edema Extremity fractures

Decisions on continued resuscitation should not be based on the initial GCS

Head Trauma

Glasgow Coma Scale

must be done early A large fixed pupil suggests herniation

syndromeLimitations:Traumatic mydriasis, resulting from direct injury to

the eye and periorbital struc-tures, may confuse the assessment of the pupillary responsiveness.

Atropine///???

Head Trauma

Pupillary Examination

A false-localizing motor examination

Kernohan's notch syndrome occult extremity trauma spinal cord injury nerve root injury

motor movement should be elicited by application of noxious stimuli.

Head Trauma

Motor Examination: Posturing

Decorticate posturing

implies injury above the midbrain.

Decerebrate posturing is the result of a more caudal

injury and therefore is associated with a worse prognosis.

Head Trauma

Motor Examination: Posturing

Respiratory pattern Pupillary size Eye movements The oculocephalic response The oculovestibular response (cold water calorics) (CN) examination is often limited to the pupillary

responses (CN III), Gag reflex (CNs IX and X) Corneal reflex (CNs V and VII). Facial symmetry (CN VII) with noxious stimuli.

Head Trauma

Brainstem Function

Cranial nerve deficits

Blood in ear canal

Hemotympanum

Rhinorrhea

Otorrhea

Battle's sign (retroauricular hematoma)

Raccoon sign (periorbital ecchymosis)

Facial paralysis

Decreased auditory acuity

Dizziness

Tinnitus

Nystagmus

Clinical Characteristics of Basilar Skull Fractures

initial motor activity pupillary responsiveness Age premorbid condition secondary systemic insult The prognosis cannot be reliably predicted

by the initial GCS or initial CT scan.

Head Trauma

Clinical prognostic indicators

complete blood count Electrolytes Glucose coagulation studies. ECG

Head Trauma

MANAGEMENT, Laboratory Tests

non–contrast-enhanced head CT scan.

Emergency management decisions are strongly influenced by these acute CT scan findings.

MRI is better than CT in detecting posttraumatic ischemic infarctions subacute nonhemorrhagic lesions contusions axonal shear injury lesions in the brainstem or posterior fossa

Head Trauma

MANAGEMENT, Neuroimaging

The goals of the out-of-hospital management are necessary airway interventions to prevent hypoxia

establishing intravenous (IV) access to treat trauma-related hypotension.

GCS pupillary responsiveness and size level of consciousness motor strength and symmetry.

Head Trauma

MANAGEMENT Out-of-Hospital Care

All head-injured patients should have a cardiac monitor as they are transported from the accident scene.

Head Trauma

MANAGEMENT

Rapid sequence intubation (RSI) a brief neurologic examination before RSI

Lidocaine (1.5 to 2 mg/kg IV push) may help as premedication

Head Trauma

MANAGEMENT, Airway

Thiopental may also be effective but should not be used in hypotensive patients.

Etomidate (0.3 mg/kg IV)

a short-acting sedative-hypnotic agent beneficial effects on ICP by reducing CBF

and metabolism. minimal adverse effects on blood pressure

Head Trauma

MANAGEMENT, Airway

Combinations of ketamine-midazolam or ketamine-sufentanil have recently been shown to be comparable in maintaining ICP and CPP in patients with severe head injury receiving mechanical ventilation

Bourgoin A , Albanese J , Wereszczynski N , et al: Safety of sedation with ketamine in severe head injury patients : Comparison with sufentanil . Crit Care Med 2003 ; 31 : 711–717

MANAGEMENT, Airway

Head Trauma

Propofol : the preferred sedating agent based on its short duration of action, facilitating serial neurologic evaluations.

Propofol-induced hypotension may occur, and it should be titrated carefully

McKeage K , Perry CM : Propofol : A review of its use in intensive care sedation of adults . CNS Drugs 2003 ; 17 : 235–272

MANAGEMENT, Airway

Head Trauma

rarely caused by head injury in adult

spinal cord injury, neurogenic hypotension may occur.

fluids do not produce clinically significant increases in ICP;

SO should never be withheld in the head trauma patient with hypovolemic hypotension for fear of increasing cerebral edema and ICP

normal saline or lactated Ringer's solution or hypertonic saline

Head Trauma

MANAGEMENT, Hypotension

Ract C , Vigue B : Comparison of the cerebral effects of dopamine and norepinephrine in severely head-injured patients . Intensive Care Med 2001 ; 27 : 101–106

Steiner LA , Johnston AJ , Czosnyka M , et al: Direct comparison of cerebrovascular effects of norepinephrine and dopamine in head-injured patients . Crit Care Med 2004 ; 32 : 1049–1054

Johnston AJ , Steiner LA , Chatfield DA , et al: Effect of cerebral perfusion pressure augmentation with dopamine and norepinephrine on global and focal brain oxygenation after traumatic brain injury . Intensive Care Med 2004 ; 30 : 791–797

Head Trauma

MANAGEMENT, Hypotension

Vasopressor of choice if fluid is not doingthe job

Norepinephrine

There is no real preference for one analgesic agent over another

The key factor is that arterial hypotension secondary to excessive doses of a sedative/analgesic should be avoided and is more likely to occur in patients with underlying hypovolemia.

Head Trauma

MANAGEMENT, analgesia

only in patients demonstrating neurologic deterioration.

onset of action is within 30 seconds peaks within 8 minutes after the Pco2 drops to the

desired range. Pco2 should not fall below 25 mm Hg

Head Trauma

MANAGEMENT, Hyperventilation

For increased ICP Mannitol (0.25 to 1 g/kg) works within minutes peak about 60 minutes after bolus

administration. The ICP-lowering effects of a single bolus

may last for 6 to 8 hours.

Head Trauma

MANAGEMENT, Mannitol

It is an effective volume expander It also promotes CBF by reducing blood viscosity and

microcirculatory resistance. It is an effective free radical scavenger,

Limitation renal failure or hypotension if given in large doses. paradoxical effect of increased bleeding into a traumatic

lesion by decompressing the tamponade effect of a hematoma.

Head Trauma

MANAGEMENT, Mannitol

also improves hemodynamics by plasma volume expansion,

reduction of vasospasm by increasing vessel diameter, and reduction of the posttraumatic inflammatory response.

Concerns osmotic demyelinization syndrome acute renal failure Coagulopathies Hypernatremia red blood cell lysis.

Head Trauma

MANAGEMENT, Hypertonic Saline

If other methods unsuccessful, it may be added in the hemodynamically stable patient.

Pentobarbital is the barbiturate most often used

Head Trauma

MANAGEMENT, Barbiturates

No evidence indicates that steroids are of benefit in head injury.

Head Trauma

MANAGEMENT, Steroids

Initial resuscitation of patient with severe head injury: treatment options

common in the acute or subacute period. Acute posttraumatic seizures are usually brief

After the acute seizure, the patient often has no additional seizure activity.

In the subacute period, 24 to 48 hours after trauma, seizures are caused by worsening cerebral edema, small hemorrhages, or penetrating injuries.

Head Trauma

COMPLICATIONS AFTER HEAD INJURY

Neurologic Complications Seizures

Depressed skull fracture

Paralyzed and intubated patient

Seizure at the time of injury

Seizure at emergency department presentation

Penetrating brain injury

Severe head injury (Glasgow Coma Scale score ≤8)

Acute subdural hematoma

Acute epidural hematoma

Acute intracranial hemorrhage

Prior history of seizures

Indications for Acute Seizure prophylaxis

Head Trauma MANAGEMENT, Seizure Prophylaxis

immediate posttrauma seizures ---no predictive value for future epilepsy

early seizures can cause Hypoxia Hypercarbia release of excitatory neurotransmitters increased ICP

Head Trauma

MANAGEMENT, Seizure Prophylaxis

Lorazepam (0.05 to 0.15 mg/kg IV, over 2 to 5 minutes up to a total of 4 mg) has been found to be most effective at aborting status epilepticus

Diazepam (0.1 mg/kg, up to 5 mg IV, every 10 minutes up to a total of 20 mg) is an alternative.

For long-term anticonvulsant activity, phenytoin (13 to 18 mg/kg IV) or fosphenytoin (13 to 18 phenytoin equivalents/kg) can be given.

Head Trauma


In a review published in the Cochrane database, the use of antiepileptic drugs reduced the risk of early seizures by 66%.

all paralyzed head-injured patients should have prophylactic anticonvulsant & Continuous electroencephalographic monitoring

Head Trauma


Infection may occur as a complication of penetrating head injury open skull fractures complicated scalp lacerations.

Not indicated in BSF

Head Trauma

MANAGEMENT, Antibiotic Prophylaxis

Severely head-injured patients require admission to an institution capable of intensive neurosurgical care and acute neurosurgical intervention.

Head Trauma

MANAGEMENT, Transfer

In patients with a CSF leak after basilar fracture, early meningitis,within 3 days of injury)

PneumococciCeftriaxone or cefotaxime Vancomycin if a high regional

pneumococcal resistance exists. Gram-negative------more than 3 days after trauma A third-generation cephalosporin, with nafcillin or

vancomycin added to ensure coverage of Staphylococcus aureus.

Prophylactic antibiotics are not currently recommended

Lapointe M, et al: Basic principles of antimicrobial therapy of CNS infections. In: Cooper PR, Golfinos JG, ed. Head Injury, 4th ed.. New York: McGraw-

Hill; 2000:483.

Head Trauma COMPLICATIONS AFTER HEAD INJURY

Meningitis after Basilar Fractures

CT. A ring pattern The treatment is usually operative drainage. The patient with cerebritis may respond to IV

antibiotics. Common organisms are S. aureus and gram-

negative aerobes Cranial Osteomyelitis with penetrating injury to

the skull.

Brain Abscess

Head Trauma


DIC The injured brain is a source of tissue thromboplastin that

activates the extrinsic clotting system. Neurogenic Pulmonary Edema

Medical Complications

Head Trauma


Cardiac Dysfunction can be life threatening and require aggressive therapy. cardiac dysrhythmia after head injury is supraventricular

tachycardia, diffuse large upright or inverted T waves, prolonged QT intervals, ST segment depression or elevation, and U waves.

Dysrhythmias in head-injured patients often resolve as ICP is reduced. Standard ACLS

Medical Complications

Head Trauma


All types of head injuries with cranial hematoma should be admitted initially to critical care area with neurosurgical consultation.

The mortality from isolated traumatic intracerebellar hematoma is very high.

Head Trauma

Severe and Moderate Head Injuries

▪

All patients with severe or moderate head injury require serial neurologic examinations

▪

Acute herniation syndrome manifested by neurologic deterioration should initially be managed with short-term hyperventilation, to a Pco2 of 30 to 35 mm Hg, with monitoring and then surgical intervention as soon as possible.

Long-term hyperventilation is not indicated. Mannitol should be used only in patients with increasing ICPs or acute neurologic deterioration.

▪ Secondary systemic insults such as hypoxia and hypotension worsen

neurologic outcome after severe and moderate head trauma and should be corrected as soon as detected

For adult patients, hypotension in the presence of isolated severe head injury is a preterminal event. Hypotension usually results from comorbidity, and its cause should be sought and treated.

The Glasgow Coma Scale is a useful clinical tool for following head-injured patients' neurologic status, but because of its limitations, the initial GCS in the emergency department cannot reliably predict prognosis after acute head injury.

Head-injured patients who have been chemically paralyzed do not have clinical manifestations of seizures; anticonvulsants should be given prophylactically.

Most “talk and deteriorate” patients who present with moderate head injury have subdural or epidural hematomas. Early detection, CT scan, and expedient surgical intervention are the keys to a good outcome.


Minor Head Trauma

▪

The decision to perform CT scans on patients with minor head trauma should be individualized but based on consideration of high- and moderate-risk criteria.

Moderate Head Trauma

a postresuscitation GCS of 9 to 13.

patients must be vigilantly monitored to avoid hypoxia and hypotension and other second-ary systemic insults that could worsen neurologic outcome.

Moderate Head Trauma

A wide variety change in consciousness Headache posttraumatic seizures Vomiting posttraumatic amnesia. Focal neurologic deficits may be present.

Moderate Head Trauma Clinical Features and Acute Management

“talk and deteriorate” patient. These patients speak after their head injury but deteriorate to a status of a severe head injury within 48 hours.

Approximately 75% of these patients have sustained subdural or epidural hematomas.

Successful management of moderately head-injured patients involves close clinical observation for changing mental status or focal neurologic findings, early CT


Approximately 40% of moderately head-injured patients have an abnormal CT scan, and 10% lapse into coma


CT head scan is required only for minor-head injurypatients with any one of the following findings. Minor head injury patients presentwith a GCS score of 13 to 15 after witnessed loss of consciousness, amnesia, or confusion.

All patients with moderate head injury should be admitted for observation, even with an apparently normal CT scan.

Ninety percent of patients improve over the first few days after injury.

repeated CT scan is indicated if the patient's condition deteriorates or fails to improve over the first 48 hours after trauma.

Moderate Head Trauma Disposition

mortality 20%, MRI has prognostic value during

subsequent care (NOT IN ED) and assists in directing the future rehabilitation of these patients.

Moderate Head Trauma Complications

Minor Head Trauma

Minor head trauma is defined as isolated head injury producing a GCS of 14 to 15

Minor Head Trauma Clinical and Historical Features

The most common complaint after minor head trauma is headache.

nausea and emesis. Occasionally, patients may complain of

disorientation, confusion, or amnesia after the injury, but these symptoms are usually transient.

the incidence of intracranial lesions may be increased by a factor of 5 compared with patients who have not sustained an LOC

Minor Head Trauma Clinical and Historical Features

Servadei F, Teasdale G, Merry G: Defining acute mild head injury in adults: A proposal based on prognostic factors, diagnosis and management. J Neurotrauma 2001; 18:657

Neurosurgical literature often advocates CT scanning of all patients with minor head trauma with a history of LOC (duration not clearly defined) or with amnesia for the traumatic event.

MRI is more sensitive than CT for detecting diffuse axonal injury, ischemia after TBI, and some hemorrhagic lesions, especially those located at the base of the skull or in the posterior fossa.

Minor Head Trauma Imaging Studies

Most patients with low-risk minor head trauma can be discharged from the emergency department after a normal examination and observation of 4 to 6 hours.

Patients should be discharged with instructions describing the signs and symptoms of delayed complications of head injury,

Minor Head Trauma Disposition

Concussion

A concussion is a temporary and brief interruption of neurologic function after minor head trauma, which may involve LOC. Acute CT or MRI abnormalities are not usually found after concussions

Functional imaging (i.e., PET) shows abnormal glucose uptake and CBF when concussed patients perform spatial working memory tasks.

Headache Confusion Amnesia of variable duration and intensity.

Concussion

Concussion The second impact syndrome

Occurs when an athlete sustains a second concussion before being completely asymptomatic from the first and then experiences a rapid, usually fatal, neurologic decline.

All current recommendations for return to play after a sports-related concussion state that players with concussion should not return to play for at least 1 week after they have become asymptomatic.

symptoms may persistent for days to months after a concussion and are termed the postconcussive syndrome (PCS).

The duration of PCS was related to the number of initial complaints, with 50% of patients with three symptoms remaining symptomatic at 6 months after injury.[76]

Concussion Postconcussive

most common complaints are headache, confusion, and amnesia for the traumatic event.

Concussion Clinical Features

Emergency department patients who have a sports-related concussion should probably not be allowed to return to play; follow-up at 1 week determines the duration of symptoms and when the patient can safely return to sports.

Concussion Disposition

PEDIATRIC HEAD INJURIES

In head-injured children younger than 1 year, as many as 66% of all injuries and 95% of severe injuries may be nonaccidental.

PEDIATRIC HEAD INJURIES Pathophysiology

Until the cranial sutures close, children's skulls are more distensible than those of adults. As a result, young children may often sustain less TBI after head trauma than adults with comparable nonfatal mechanisms of injury.

Very young children (younger than 1 year) have higher mortality after head trauma than older children with the same severity of injury.

Many factors contribute to this. delayed Medical attention nonaccidental injuries. language and comprehension accurate formal neurologic examination

Children have fewer traumatic mass lesions, fewer hemorrhagic contusions, more diffuse brain swelling, and more diffuse axonal injury.

Of head-injured patients younger than 20 who talk and deteriorate, 39% have brain swelling only (i.e., no mass lesions), whereas 87% of patients older than 40 who talk and deteriorate have mass lesions.

PEDIATRIC HEAD INJURIESClinical Features

As with adults, an accurate description of the mechanism of injury, the appearance of the child immediately before and after the injury, and subsequent events can provide useful information to assist in the evaluation and management of the acutely head-injured child.

In principle, the acute neurologic assessment of the head-injured child is the same as that of adults.

the GCS is difficult to apply to children younger than 5 years. Modified scales

no universally accepted coma scale exists for children. Mental status changes, which may be the first symptom of head

injury, are difficult to evaluate in children


Infants appear at especially high risk for posttraumatic seizures.

Most seizures occur within the first 24 hours and do not predict seizures later in the posttraumatic period.

acute prophylaxis with phenytoin is recommended in severely head-injured children to prevent early posttraumatic seizures.

Mazzola CA, Adelson PD: Critical care management of head trauma in children. Crit Care Med 2002; 30(11 Suppl):S393.

Concussive injuries in children produce two unique clinical circumstances.

Many children experience a brief impact seizure at the time of relatively minor head injury. By the time the child is evaluated, he or she is at baseline neurologic function. Impact seizures do not appear to predict subsequent early posttraumatic seizures.

Postconcussive blindness, another serious complication of concussive injuries in children, is usually associated with impact to the back of the head.

Children experience a temporary loss of vision that can persist from minutes to hours before normal vision returns.


The clinical presentation of posttraumatic intracranial lesions in infants can be extremely subtle, especially in those younger than 6 months.

Most authorities suggest that all head-injured infants and toddlers younger than 2 years should be considered at least at moderate risk for intracranial lesions, unless the injury was trivial

Inflicted head injury is the most common cause of head injury deaths in infants.

??? Child abuse


As with adults

PEDIATRIC HEAD INJURIESDiagnosis and Management

In children, unlike adults, hypovolemic hypotension can occur because of head trauma.

Hypotension from intracranial bleeding can occur in children younger than 1 year with a large linear skull fracture and an underlying large epidural hematoma.

The intracranial blood can seep through the fracture and produce a large galeal or subperiosteal hematoma.

Hypotension from intracranial bleeding can also occur in a child with hydrocephalus and a functioning shunt. Blood may accumulate without much evidence of increased ICP.

Scalp lacerations can also produce significant hemorrhage and subsequent hypotension.


In infants, a bulging fontanelle suggests elevated ICP. Other signs of elevated ICP include bradycardia, papilledema, declining level of consciousness, and seizures.

When increased ICP is suggested by physical examination, methods to reduce ICP should be initiated. As with adults, acute hyperventilation has immediate effects but is never indicated for prophylaxis or for prolonged management of increased ICP.


One clinical sign of potential brain injury in children younger than 2 is the presence of a scalp hematoma, especially a large parietal scalp hematoma.

scalp hematomas were present in 93% of children 2 years old or younger who had brain injuries.

Greens DS, Schutzman SA: Occult intracranial injury in infants. Ann Emerg Med 1998; 32:680. Greenes DS, Schutzman SA: Clinical indicators of intracranial injury in head-injured infants. Pediatrics 1999; 104:861. Greenes DS, Schutzman SA: Clinical significance of scalp abnormalities in asymptomatic head injured infants. Pediatr Emerg Care 2000; 17:88.


It should also be strongly considered in pediatric patients with minor head trauma who have history of vomiting, abnormal mental status or lethargy, clinical signs of a skull fracture, obvious scalp hematomas in children 2 years old or younger, and increasing headache.


The use of skull radiographs in the diagnostic workup of head-injured children is controversial but may be appropriate under some circumstances.

As with adults, when a CT scan is indicated, skull radiographs are not necessary.

Parietal skull fractures are the most common.


In older children, skull films are rarely useful

Ping-pong fractures occur with concentrated forces that indent the skull. These fractures are unique to infants and appear as multiple indentations in the skull with no significant bone discontinuity.

Skull fractures are common in children who have sustained deep scalp lacerations or who have a large scalp hematoma.


Leptomeningeal cysts or growing skull fractures are delayed complications of linear skull fractures in infancy. If a tear in the dura accompanies the linear fracture, the meninges may fill with CSF and prolapse through the fracture margins, thus preventing fracture healing.


The immature brain has increased susceptibility to permanent injury because of incomplete myelination.


PENETRATING HEAD INJURIES

If the presenting GCS is less than 5, mortality approaches 100%. If the presenting GCS is greater than 8 and the pupils are reactive, survival approaches 75%.

Kaufman HH, et al: Civilian gunshot wounds to the head. Neurosurgery 1993; 32:962.

Tangential wounds are caused by an impact that occurs at an oblique angle to the skull.

Perforating wounds are usually caused by high-velocity projectiles, which cause through-and-through injuries of the brain with an entrance and an exit wound.

Penetrating missile wounds are produced with moderate- to high-velocity projectiles discharged at close range.

PENETRATING HEAD INJURIES Pathophysiology

GCS Pupillary responsiveness. ICP rises

PENETRATING HEAD INJURIES Clinical Features

IV antibiotics Anticonvulsants should be given in the acute

setting Pneumocephalus is common object should be left in place to be removed at

surgery.

PENETRATING HEAD INJURIES Management

SPECIFIC INJURIES

are extremely common significant bleeding direct digital compression lidocaine with epinephrine ligation of identified bleeding vessels. Wond management If the galea is lacerated, quick closure If the avulsion remains attached to the rest of the scalp by a tissue

bridge, it should be reattached to the surrounding tissue. If the avulsion is completely detached from the scalp, it should be

treated as any other amputated part and reimplanted as soon as possible.

Scalp Wounds

presence of a skull fracture after trauma increases the likelihood of having a TBI

Clinically significant skull fractures (1) result in intracranial air (2) overlying scalp laceration (open skull fracture), (3)depressed (4) overlie a major dural venous sinus or the middle

meningeal artery.

Skull Fractures

SPECIFIC INJURIES

goes through the entire thickness of the skull. clinically important if they cross the middle meningeal

groove or major venous dural sinuses; Sutural diastasis is the traumatic disruption of a cranial

suture. Comminuted skull fractures are multiple linear fractures

that radiate from the impact site.

A linear vault fracture substantially increases the risk of intracranial injury.

Linear FracturesSPECIFIC INJURIES

underlying brain injury and complications A CT scan is indicated for patients with a

history or physical examination that suggests a depressed skull fracture.

Depressed skull fractures may increase the risk for developing seizures.

prophylaxis for posttraumatic seizures,

Depressed Fractures

SPECIFIC INJURIES

linear fractures at the base of the skull. The fracture usually occurs through the temporal bone, with

bleeding into the middle ear producing hemotympanum. Often the fracture has caused a dural tear, which produces

a communication between the subarachnoid space, the paranasal sinuses, and the middle ear.

TBI must be ruled out. CT scan If a patient with a previously diagnosed CSF leak returns to

the emergency department later with fever, the diagnosis of meningitis should be strongly suspected and appropriate workup (i.e., lumbar puncture) and antibiotic treatment initiated immediately.

SPECIFIC INJURIES

Basilar Fractures

Cranial nerve deficits

Blood in ear canal

Hemotympanum

Rhinorrhea

Otorrhea

Battle's sign (retroauricular hematoma)

Raccoon sign (periorbital ecchymosis)

Facial paralysis

Decreased auditory acuity

Dizziness

Tinnitus

Nystagmus

Clinical Characteristics of Basilar Skull Fractures

A skull fracture is open when a scalp laceration overlies a fracture.

If the fracture has disrupted the dura, a communication exists between the external environment and the brain.

A fracture that disrupts the paranasal sinuses or the middle ear structures is also considered open.

An open skull fracture requires careful irrigation and debridement.

Blind probing of the wound should be avoided because it can introduce contaminants into the wound and can further depress comminuted fracture pieces.

Open Fractures

SPECIFIC INJURIES

Diffuse Axonal Injury DAI is described as coma beginning immediately at the time of

trauma and persisting for at least 6 hours.

No specific acute focal traumatic lesions are noted on a head CT scan.

Occasionally, small petechial hemorrhages in proximity to the third ventricle and within the white matter of the corpus callosum or within the internal capsule of the brainstem are detected.

Recovery depends on the reversal or correction of structural and physiologic abnormalities.

SPECIFIC INJURIES

The severity of the injury is determined by the clinical course.

SPECIFIC INJURIES

Diffuse Axonal Injury

in coma for 6 to 24 hours. About a third of patients with mild DAI

demonstrate decorticate or decerebrate posturing, but by 24 hours they are following commands

The mortality is 15%

Mild DAI

SPECIFIC INJURIES

is the most common clinical picture. Patients with moderate DAI are in coma for

longer than 24 hours.

Patients may exhibit transient decortication or decerebration but eventually recover purposeful movements.

On awakening, patients have prolonged severe posttraumatic amnesia and moderate to severe persistent cognitive deficits.

Almost 25% die of complications of prolonged coma.

Moderate DAI

SPECIFIC INJURIES

demonstrate persistent brainstem dysfunction (posturing)

autonomic dysfunction (e.g., hypertension, hyperpyrexia).

Diffuse brain swelling subsequent to injury causes intracranial hypertension.

Herniation syndrome can occur if elevated ICP does not respond to medical or surgical intervention.

Some patients eventually awaken are severely disabled. Some remain in a persistent vegetative state, but most with severe DAI die from their head injury

Severe DAI

SPECIFIC INJURIES

Contusions

Contusions are bruises on the surface of the brain usually caused by impact injury.

coup injury If the contusion occurs on the same side as the impact injury

contrecoup injury if it occurs on the opposite side

Often, subarachnoid blood is found

Some time local mass effect with Compression of the underlying tissue

brief LOC

posttraumatic confusion and obtundation may be prolonged.

If occur near the sensorimotor cortex, focal neurologic deficits may be present.

In CT. heterogeneous and irregular Often the surrounding edematous tissue appears hypodense. By days 3 and 4, the blood located within the contusions has

begun to degrade.

Contusions

Epidural Hematoma blood clots that form between the inner table of the skull

and the dura. Eighty percent are associated with skull fractures across

the middle meningeal artery or across a dural sinus and are therefore located in the temporoparietal region.

arterial usually unilateral 20% other intracranial lesions

rare in elderly decreased level of consciousness followed by a “lucid”

interval. 30% of patients with EDHs present classically.

If the patient is not in coma when the diagnosis is established and if the condition is rapidly treated, the mortality is nearly zero.

If the patient is in coma, the mortality from EDH is about 20%.

If it is rapidly detected and evacuated, the functional outcome is excellent.

Epidural Hematoma

On CT appears hyperdense, biconvex, ovoid, and lenticular. does not usually extend beyond the dural attachments at

the suture lines. The most common site is the temporal region.

Epidural Hematoma

blood clots that form between the dura and the brain.

In brain atrophy, such as elderly patients.

SDHs are more common than EDHs The slow bleeding of venous structures

delays the development of clinical signs and symptoms and can cause ischemia and damage.

Subdural Hematoma

Acute SDHs are symptomatic within 24 hours after trauma.

Between 50% and 70% have a lucid interval after injury, followed by declining mental status.

In most patients the optimal treatment for acute SDHs is surgical evacuation.

On CT appears hyperdense and crescent shaped and

lies between the calvaria and the cortex. often extend beyond the suture lines

Subdural Hematoma

A subacute SDH is symptomatic between 24 hours and 2 weeks after injury.

It may appear hypodense or isodense on CT scans.

Contrast increases detection of isodense lesions.

Most patients with subacute SDH require surgical evacuation of the lesion.

Subdural Hematoma

A chronic SDH becomes symptomatic 2 weeks or more after trauma.

On CT appear isodense or hypodense to brain

parenchyma.

Contrast may increase the likelihood of identifying a chronic SDH that has become isodense.

If they become symptomatic, chronic SDHs require surgical evacuation.

Subdural Hematoma

Subdural Hematoma

Prognosis Does not depend on the size of the hematoma Depends on the degree of brain injury

In children the presence of an SDH should prompt consideration of child abuse.

Subdural Hygroma

A subdural hygroma (SDHG) is a collection of clear, xanthochromic blood-tinged fluid in the dural space.

10% of cases of severe head injury.

SDHG cannot be distinguished from other mass lesions.

On CT scans, SDHGs appear crescent shaped in the extraaxial space.

Bilateral SDHGs are common. If asymptomatic, observation is reasonable management. Otherwise, they

must be surgically evacuated. Mortality varies from 12% to 28% and appears to depend on the severity of

other intracranial injury

Traumatic Subarachnoid Hemorrhage

blood within the CSF and meningeal intima and probably results from tears of small subarachnoid vessels.

TSAH with no other brain injury does not generally carry a poor prognosis.

cerebral vasospasm is a serious complication common, occurring about 48 hours after injury and

persisting for up to 2 weeks. CCB (e.g., nimodipine, nicardipine) have been used

to prevent or reduce vasospasm after TSAH.

Barket FG, Ogilvy CS: Efficacy of prophylactic nimodipine for delayed ischemic deficit after SAH: A metaanalysis. J Neurosurg 1996; 84:405.

Intracerebral Hematoma

formed deep within the brain tissue

85% are in the frontal and temporal lobes.

Often is not seen in CT for several hours or days On CT scan an ICH appears as well-defined

hyperdense homogeneous areas of hemorrhage

ICHs that bleed into the ventricles or cerebellum also carry a high mortality rate.

Rare

Direct blow to the suboccipital area.

The mortality from isolated traumatic intracerebellar hematoma is very high.

Traumatic Intracerebellar Hematoma

Anterior view of transtentorial herniation caused by large epidural hematoma. Skull fracture overlies hematoma.


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All patients with severe or moderate head injury require serial neurologic examinations while in the emergency department to allow early detection of herniation syndrome related to expanding traumatic mass lesions or increasing cerebral edema.

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Acute herniation syndrome manifested by neurologic deterioration should initially be managed with short-term hyperventilation, to a Pco2 of 30 to 35 mm Hg, with monitoring and then surgical intervention as soon as possible. Long-term hyperventilation is not indicated. Mannitol should be used only in patients with increasing ICPs or acute neurologic deterioration.

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Secondary systemic insults such as hypoxia and hypotension worsen neurologic outcome after severe and moderate head trauma and should be corrected as soon as detected in the out-of-hospital or emergency department setting.

For adult patients, hypotension in the presence of isolated severe head injury is a preterminal event. Hypotension usually results from comorbidity, and its cause should be sought and treated.

The Glasgow Coma Scale is a useful clinical tool for following head-injured patients' neurologic status, but because of its limitations, the initial GCS in the emergency department cannot reliably predict prognosis after acute head injury.

Head-injured patients who have been chemically paralyzed do not have clinical manifestations of seizures; anticonvulsants should be given prophylactically.

Most “talk and deteriorate” patients who present with moderate head injury have subdural or epidural hematomas. Early detection, CT scan, and expedient surgical intervention are the keys to a good outcome.


Minor Head Trauma

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Risk stratification of patients with minor head injury into low-risk and high-risk categories can help direct the emergency physician to an appropriate diagnostic workup.

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The decision to perform CT scans on patients with minor head trauma should be individualized but based on consideration of high- and moderate-risk criteria.

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Alcohol can affect the GCS and significantly obscure the neurologic examination. Intoxicated patients should be considered at high risk.

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Most patients with minor head trauma can be discharged from the emergency department after a period of observation but require a competent observer.

Patients sustaining a concussion are at risk for prolonged and substantial morbidity. Athletes should not be allowed to return immediately to sports activities because of the potential risk of second impact syndrome. All current recommendations for return to play after a sports-related concussion state that players with concussion should not return to play for at least 1 week after they have become asymptomatic. This period is usually increased to at least a symptom-free month if an LOC or prolonged posttraumatic amnesia occurred at the time of concussion.

Minor Head Trauma

Pediatric Head Injuries

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Children with severe head trauma have fewer intracranial lesions than adults but more edema. In children, increasing edema alone can cause talk and deteriorate or other significant neurologic decline.

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Skull fractures have more clinical significance in children than in adults.

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In children, unlike adults, hypovolemic hypotension can occur because of head injury, especially those younger than 1 year.

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In very young children, head injury is often caused by nonaccidental causes. Child abuse should be suspected in young children with head trauma, especially those younger than 2 years.

Penetrating Head Injuries

▪ Tangential gunshot wounds are associated with a high frequency of intracranial traumatic lesions; CT scanning should be performed.

▪ Anticonvulsant prophylaxis and antibiotics should be given to a patient with penetrating head injuries.

▪ The clinical outcome after gunshot wounds to the head can be predicted by the initial clinical presentation and the missile path through the brain.

Contusions: Are bruises on the surface of the brain, usually caused by impact injury.

Epidural Hematoma (EDHs): Are blood clots that form between the inner table of the skull and the dura.

Subdural Hematoma (SDHs): are blood clots that form between the dura and the brain.

Head Trauma

Traumatic Subarachnoid Hemorrhage (TSAH): is defined as blood within the CSF and meningeal intima.

Intracerebral Hematoma (ICHs): are formed deep within the brain tissue

All types of head injuries with cranial hematoma should be admitted initially to critical care area with neurosurgical consultation.

Head Trauma

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Head Trauma