HEAD TRAUMA

Vicheryl M. Lopez

Head Trauma
Or Head injury refers to trauma to the head y This may or may not include injury to the brain y Incidence:300 per 100,000 per year (0.3% of the population) y Mortality: 25 per 100,000 in North America and 9 per 100,000 in Britain
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Motor Response (M) Obeys commands 6 Localizes to pain 5

Verbal Response (V) Oriented 5 Confused 4

Eye-Opening Response (E) Opens spontaneously 4

Glasgow Coma Opens to speech Scale (GCS) Score 3

Opens to pain 2 No eye opening 1

Withdraws from pain Inappropriate 4 words 3 Flexor posturing 3 Extensor posturing 2 No movement 1
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Unintelligible sounds 2 No sounds 1

the three scores to obtain the Glasgow Coma Scale score, which can range from 3 to 15. Add "T" after the GCS if intubated and no verbal score is possible. For these patients, the GCS can range from 2T to 10T.

Scalp Injury
Blunt or penetrating trauma to the head can cause injury to the densely vascularized scalp, and significant blood loss can occur. y Direct pressure initially controls the bleeding, allowing close inspection of the injury. y If a simple laceration is found, it should be copiously irrigated and closed primarily. y If the laceration is short, a single-layer percutaneous suture closure will suffice.
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If the laceration is long or has multiple arms, the patient may need dbridement and closure in the operating room, with its superior lighting and wider selection of instruments and suture materials. y Careful reapproximation of the galea will provide a more secure closure and better hemostasis. y Blunt trauma can also cause crush injury with subsequent tissue necrosis. These wounds require dbridement and consideration of advancement flaps to cover the defect.
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Skull Fractures
Characterization may be done using skull xrays or head CT 1. A closed fracture is covered by intact skin.  Closed skull fractures do not normally require specific treatment. 2. An open, or compound, fracture is associated with disrupted overlying skin.  require repair of the scalp.
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The fracture lines may be single (linear); multiple and radiating from a point (stellate); or multiple, creating fragments of bone (comminuted).

Depressed skull fracture  may result from a focal injury of significant force  inner and outer cortices of the skull are disrupted, and a fragment of bone is pressed in toward the brain in relation to adjacent intact skull.  The fragment may overlap the edge of intact bone, or may plunge completely below the level of adjacent normal skull.  The inner cortex of the bone fragments often has multiple sharp edges that can lacerate dura, brain, and vessels.
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Craniotomy is required to elevate the fracture, repair dural disruption, and obtain hemostasis in these cases. y Fractures overlying dural venous sinuses require restraint. y Surgical exploration can lead to lifethreatening hemorrhage from the lacerated sinus.
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Bone-window axial head CT of a patient who presented aphasic after being struck with the bottom of a beer bottle. CT demonstrates a depressed skull fracture in the left posterior temporoparietal area

Brain-window axial head CT demonstrating intraparenchymal hematoma caused by laceration of cortical vessels by the edge of the fractured bone. Arrowhead indicates traumatic subarachnoid hemorrhage in the sylvian fissure.

Fractures of the skull base

generally apparent on routine head CT, but should be evaluated with dedicated fine-slice coronal-section CT scan to document and delineate the extent of the fracture and involved structures. y If asymptomatic, they require no treatment. y Symptoms from skull base fractures include cranial nerve deficits and CSF leaks.
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Fracture of the temporal bone

damage the facial or vestibulocochlear nerve, resulting in vertigo, ipsilateral deafness, or facial paralysis. y A communication may be formed between the subarachnoid space and the middle ear, allowing CSF drainage into the pharynx via the eustachian tube or from the ear (otorrhea). y Extravasation of blood results in ecchymosis behind the ear, known as Battle's sign.
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Fracture of the anterior skull base

can result:  anosmia (loss of smell from damage to the olfactory nerve),  CSF drainage from the nose (rhinorrhea),  or periorbital ecchymoses, known as raccoon eyes.
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Closed Head Injury

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most common type of TBI, and a significant cause of morbidity and mortality in the United States

2 important factors that affect the outcome in CHI and TBI in general 1. primary injury  immediate injury to neurons from transmission of the force of impact.  The long, delicate axons of the neurons can shear as the different areas of the brain through which they pass accelerate and decelerate at different speeds.  Prevention strategies: wearing helmets
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2. secondary injury  Subsequent neuronal damage due to the sequelae of trauma  Mechanisms of secondary injury: Hypoxia, hypotension, hydrocephalus, intracranial hypertension, and intracranial hematoma

Initial Assessment
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ABCDs of resuscitation, Hypoxia and hypotension worsen outcome in TBI (due to secondary injury), so cardiopulmonary stabilization is critical. Patients who cannot follow commands require intubation for airway protection and ventilatory control. The fourth element, assessment of the D, for disability, is undertaken next. Motor activity, speech, and eye opening can be assessed in a few seconds and a GCS assigned

Medical Management
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Closed head injury : 17-mg/kg phenytoin loading dose, followed by 1 week of therapeutic maintenance phenytoin, typically 300 to 400 mg/d, shown to decrease the incidence of early posttraumatic seizures. Blood glucose levels should be closely monitored by free blood sugar checks and controlled with sliding scale insulin. Fevers should also be evaluated and controlled with antipyretics, as well as source-directed therapy when possible. Hyperglycemia and hyperthermia are toxic to injured neurons, and so contribute to secondary injury.

Classification
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mild head injury GCS is 13 to 15 Asymptomatic who have only headache, dizziness, or scalp lacerations or abrasions; who did not lose consciousness have a low risk for intracranial injury and may be discharged home without a head CT scan.

2.  

moderate head injury GCS is 9 to 12 history of altered or lost consciousness, amnesia, progressive headache, skull or facial fracture, vomiting, or seizure have a moderate risk for intracranial injury and should undergo prompt head CT. If the CT is normal, and the neurologic exam has returned to baseline (excluding amnesia of the event), then the patient can be discharged to the care of a responsible adult, again with printed criteria for returning to the ER. Otherwise the patient must be admitted for a 24-hour observation period.

3. severe head injury  GCS is 3 to 8  with depressed consciousness, focal neurologic deficits, penetrating injury, depressed skull fracture, or changing neurologic exam have a high risk for intracranial injury  should undergo immediate head CT and admission for observation or intervention as needed

Concussion
neuronal dysfunction after nonpenetrating head trauma y The head CT is normal, and deficits resolve over minutes to hours. y Definitions vary; some require transient loss of consciousness, while others include patients with any alteration of mental status. y Memory difficulties, especially amnesia of the event, are very common.
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Concussions may be graded. One method is the Colorado Medical Society system. 1. grade 1  Head trauma patients with confusion 2. grade 2  patients with amnesia 3. grade 3  patients who lose consciousness

secondsecond-impact syndrome
Studies have shown that the brain remains in a hypermetabolic state for up to a week after injury. y The brain is also much more susceptible to injury from even minor head trauma in the first 1 to 2 weeks after concussion. y Patients should be informed that even after mild head injury they might experience memory difficulties or persistent headaches.
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Contusion
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bruise of the brain, and occurs when the force from trauma is sufficient to cause breakdown of small vessels, and extravasation of blood into the brain. The frontal, occipital, and temporal poles are most often involved. The brain sustains injury as it moves in relation to rough bony surfaces rarely cause significant mass effect as they represent small amounts of blood in injured parenchyma rather than coherent blood clots.

Edema may develop around a contusion, causing mass effect. y Contusions may also enlarge, or develop a true hematoma, especially during the first 24 hours. y Contusions may also be seen in brain tissue opposite the site of impact. This is known as a contrecoup injury. y These contusions result from deceleration of the brain against the skull.
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Severe bilateral contusions in the basal aspect of the frontal lobes, caused by the brain moving over the rough, irregular skull base during sudden cranial acceleration.

Causes
Often caused by a blow to the head, contusions commonly occur in coup or contre-coup injuries y In coup injuries, the brain is injured directly under the area of impact, while in contrecoup injuries it is injured on the side opposite the impact.
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Signs and symptoms

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Contusion can present with weakness, lack of motor coordination, numbness, aphasia, and memory and cognitive problems.

Treatment
Since cerebral swelling presents a danger to the patient, treatment of cerebral contusion aims to prevent swelling. y Measures to avoid swelling include:  prevention of hypotension (low blood pressure), hyponatremia (insufficient sodium), and hypercapnia(excess carbon dioxide in the blood).
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Diffuse Axonal Injury

caused by damage to axons throughout the brain, due to rotational acceleration and then deceleration. y Axons may be completely disrupted and then retract, forming axon balls. y Small hemorrhages can be seen in more severe cases, especially on MRI. y Hemorrhage is classically seen in the corpus callosum and the dorsolateral midbrain.
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one of the most common and devastating types of traumatic brain injury, meaning that damage occurs over a more widespread area than in focal brain injury. refers to extensive lesions in white matter tracts, is one of the major causes of unconsciousness and persistent vegetative state after head trauma. The outcome is frequently coma, with over 90% of patients with severe DAI never regaining consciousness. Those who do wake up often remain significantly impaired.

Diagnosis and treatment

difficult to detect since it does not show up well on CT scans or with other macroscopic imaging techniques, though it shows up microscopically has more microscopic injury than macroscopic injury and is difficult to detect with CT and MRI, but its presence can be inferred when small bleeds are visible in the corpus callosumor the cerebral cortex MRI is more useful than CT for detecting characteristics of diffuse axonal injury in the subacute and chronic time frames.

Newer studies such as Diffusion Tensor Imaging are able to demonstrate the degree of white matter fiber tract injury even when the standard MRI is negative. Since axonal damage in DAI is largely a result of secondary biochemical cascades, it has a delayed onset, so a person with DAI who initially appears well may deteriorate later. Thus injury is frequently more severe than is realized, and medical professionals should suspect DAI in any patients whose CT scans appear normal but who have symptoms like unconsciousness

1. 2.

3.

MRI is more sensitive than CT scans,but MRI may also miss DAI, because it identifies the injury using signs of edema, which may not be present. DAI is classified into grades based on severity of the injury: In Grade I, widespread axonal damage is present but no focal abnormalities are seen. In Grade II, damage found in Grade I is present in addition to focal abnormalities, especially in the corpus callosum. Grade III damage encompasses both Grades I and II plus rostral brain stem injury and often tears in the tissue.

DAI currently lacks a specific treatment beyond what is done for any type of head injury, including stabilizing the patient and trying to limit increases in intracranial pressure(ICP).

Potential Treatments
Polyethylene glycol  acts as a membrane sealant, and may serve to prevent the aforementioned devastating calcium influx.  Rats treated with polyethylene glycol immediately following DAI induction showed no cytotoxic edema on diffusion weighted MRI 7 days later unlike controls
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Susceptibility weighted image (SWI) of diffuse axonal injury in trauma

Penetrating Injury
Complex and must be evaluated individually y The two main subtypes: 1. missile injury (e.g., due to bullets or fragmentation devices) and 2. nonmissile injury (e.g., due to knives or ice picks
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If available, skull x-rays and CT scans are useful in assessing the nature of the injury. Cerebral angiography must be considered if the object passes near a major artery or dural venous sinus. Operative exploration is necessary to remove any object extending out of the cranium, as well as for dbridement, irrigation, hemostasis, and definitive closure.

Small objects contained within brain parenchyma are often left in place to avoid iatrogenic secondary brain injury. Antibiotics are given to decrease the chances of meningitis or abscess formation. High-velocity missile injuries (from high-powered hunting rifles or military weapons) are especially deadly, because the associated shock wave causes cavitary tissue destruction of an area that is much larger than the projectile itself. Projectiles that penetrate both hemispheres or traverse the ventricles are almost universally fatal.

Intracranial hemorrhage
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a hemorrhage, or bleeding, within the skull.

Causes
Intracranial bleeding occurs when a blood vessel within the skull is ruptured or leaks y physical trauma (as occurs in head injury) y or nontraumatic causes (as occurs in hemorrhagic stroke) such as a ruptured aneurysm. y Anticoagulant therapy, as well as disorders with blood clotting can heighten the risk that an intracranial hemorrhage will occur.
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Prognosis
a serious medical emergency because the buildup of blood within the skull can lead to increases in intracranial pressure, which can crush delicate brain tissue or limit its blood supply. y Severe increases in intracranial pressure can cause potentially deadly brain herniation, in which parts of the brain are squeezed past structures in the skull.
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Diagnosis
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CT scan (computed tomography) is the definitive tool for accurate diagnosis of an intracranial hemorrhage

Classification
Types of intracranial hemorrhage are roughly grouped into intra-axial and extra-axial. y The hemorrhage is considered a focal brain injury; that is, it occurs in a localized spot rather than causing diffuse damage over a wider area.
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IntraIntra-axial hemorrhage
bleeding within the brain itself, or cerebral hemorrhage. y Category: 1. intraparenchymal hemorrhage, or bleeding within the brain tissue, and 2. intraventricular hemorrhage, bleeding within the brain's ventricles (particularly of premature infants) y more dangerous and harder to treat than extra-axial bleeds.
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ExtraExtra-axial hemorrhage
bleeding that occurs within the skull but outside of the brain tissue y Three subtypes: 1. Epidural hematoma 2. Subdural hematoma and 3. Subarachnoid hemorrhage:
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1. Epidural hematoma

rapidly accumulating hematoma between the dura mater and the cranium patients have a history of head trauma with loss of consciousness, then a lucid period, followed by loss of consciousness. clinical onset occurs over minutes to hours. associated with lacerations of the middle meningeal artery A "lenticular", or convex, lens-shaped extracerebral hemorrhage will likely be visible on a CT scan of the head. Although death is a potential complication, the prognosis is good when this injury is recognized and treated

The dura mater also covers the spine, so epidural bleeds may also occur in the spinal column. y The condition is present in one to three percent of head injuries y Between 15 and 20% of patients with epidural hematomas die of the injury
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Large epidural hematoma with midline shift. This is an obvious indication for operative decompression.

Signs and symptoms

rapid because it is usually from arteries, which are high pressure. Epidural bleeds from arteries can grow until they reach their peak size at six to eight hours post injury, spilling from 25 to 75 cubic centimeters of blood into the intracranial space As the hematoma expands, it strips the dura from the inside of the skull, causing an intense headache.

Epidural bleeds can become large and raise intracranial pressure, causing the brain to shift, lose blood supply, or be crushed against the skull. y Larger hematomas cause more damage. y Epidural bleeds can quickly expand and compress the brain stem, causing unconsciousness, abnormal posturing, and abnormal pupil responses to light.
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CT scans and MRIs, epidural hematomas convex in shape because their expansion stops at skull's sutures, where the dura mater is tightly attached to the skull. Thus they expand inward toward the brain rather than along the inside of the skull, as occurs in subdural hematoma. The lens like shape of the hematoma leads the appearance of these bleeds to be called "lentiform". May occur in combination with subdural hematomas, or either may occur alone. CT scans reveal subdural or epidural hematomas in 20% of unconscious patients.

Hematoma type Location

Epidural

Subdural

Between the skull and the dura

Between the dura and the arachnoid

Involved vessel Symptoms

Middle meningeal artery Lucid interval followed by unconsciousness

Bridging veins

Gradually increasing headache and confusion

Appearance on CT

Biconvex

Crescent-shaped

Causes

usually traumatic, although spontaneous hemorrhage is known to occur. result from acceleration-deceleration trauma and transverse forces. 10% of epidural bleeds-venous; usually due to shearing injury from rotational or linear forces, caused when tissues of different densities slide over one another. commonly results from a blow to the side of the head. The pterion region which overlies the middle meningeal artery is relatively weak and prone to injury. Epidural hematoma is usually found on the same side of the brain that was impacted by the blow, but on very rare occasions it can be due to a contrecoup injury

Treatment
As with other types of intracranial hematomas, the blood may be aspirated surgically to remove the mass and reduce the pressure it puts on the brain. The hematoma is neurosurgically evacuated through a burr hole or craniotomy. The diagnosis of epidural hematoma requires a patient to be cared for in a facility with a neurosurgeon on call to decompress the hematoma if necessary and stop the bleed by ligating the injured vessel branches.

Prognosis
In TBI patients with epidural hematomas, prognosis is better if there was a lucid interval (a period of consciousness before coma returns) than if the patient was comatose from the time of injury. y Unlike most forms of TBI, people with epidural hematoma and a Glasgow Coma Score of 3 (the lowest score) are expected to make a good outcome if they can receive surgery quickly
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2. Subdural hematoma

occurs when there is tearing of the bridging vein between the cerebral cortex and a draining venous sinus. may be caused by arterial lacerations on the brain surface. usually associated with cerebral cortex injury as well and hence the prognosis is not as good as extra dural hematomas. Clinical features depend on the site of injury and severity of injury. Patients may have a history of loss of consciousness but they recover and do not relapse.

Clinical onset occurs over hours. y A crescent shaped hemorrhage compressing the brain will be noted on CT of the head. y Craniotomy and surgical evacuation is required if there is significant pressure effect on the brain.
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Complications:  focal neurologic deficits depending on the site of hematoma and brain injury,  increased intra cranial pressure leading to herniation of brain and  ischemia due to reduced blood supply and seizures.
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CT scan of a patient with a subdural hematoma. In addition, there is air in the subarachnoid space and the ventricles.

Head CT scan of an elderly patient with progressing left hemiplegia and lethargy, demonstrating an acute-on-chronic subdural hematoma. History revealed that the patient sustained a fall 4 weeks prior to presentation. Arrowheads outline the hematoma. The acute component is slightly denser, and is seen as the hyperdense area in the dependent portion

Classification
ACUTE  develop after

high speed acceleration or deceleration injuries and are increasingly severe with larger hematomas.  most severe if associated with cerebral contusions  usually venous and therefore slower than the usually arterial bleeding of an epidural hemorrhage.  high mortality rate, higher even than epidural hematomas and diffuse brain injuries, because the force (acceleration/deceleration) required to cause them cause other severe injuries as well.  The mortality rate:60 to 80%.

subacute, and y CHRONIC  develop over the period of days to weeks, often after minor head trauma, though such a cause is not identifiable in 50% of patients.  may not be discovered until they present clinically months or years after a head injury.  The bleeding is slow, probably from repeated minor bleeds, and usually stops by itself.  Since these bleeds progress slowly, they present the chance of being stopped before they cause significant damage.  common in the elderly
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Signs and symptoms

Symptoms of subdural hemorrhage have a slower onset than those of epidural hemorrhages because the lower pressure veins bleed more slowly than arteries y Therefore, signs and symptoms may show up in minutes, if not immediately but can be delayed as much as 2 weeks. y If the bleeds are large enough to put pressure on the brain, signs of increased ICP or damage to part of the brain will be present.
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Other signs and symptoms of subdural hematoma can include any combination of the following:  A history of recent head injury  Loss of consciousness or fluctuating levels of consciousnes  Irritability  Seizures  Pain  Numbness  Headache(either constant or fluctuating)  Dizziness

 Disorientation  Amnesia  Weakness

or lethargy  Nausea or vomiting  Loss of appetite  Personality changes  Inability to speak or slurred speech  Ataxia, or difficulty walking  Altered breathing patterns  Blurred Vision  Deviated gaze, or abnormal movement of the eyes

Causes
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most often caused by head injury, when rapidly changing velocities within the skull may stretch and tear small bridging veins. result from shearing injuries due to various rotational or linear forces. classic finding in shaken baby syndrome in which similar shearing forces classically cause intraand pre-retinal hemorrhages. also commonly seen in the elderly and in alcoholics, who have evidence of cerebral atrophy

Cerebral atrophy increases the length the bridging veins have to traverse between the two meningeal layers, hence increasing the likelihood of shearing forces causing a tear. y It is also more common in patients on anticoagulants, especially aspirin and warfarin. Patients on these medications can have a subdural hematoma with a minor injury.
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Risk factors
very young or very old age.  As the brain shrinks with age, the

subdural space enlarges and the veins that traverse the space must travel over a wider distance, making them more vulnerable to tears. This and the fact that the elderly have more brittle veins make chronic subdural bleeds more common in older patients.  Infants, too, have larger subdural spaces and are more predisposed to subdural bleeds than are young adults.For this reason, subdural hematoma is a common finding in shaken baby syndrome.

 In

juveniles, an arachnoid cyst is a risk factor for a subdural hematoma. Other risk factors for subdural bleeds include taking blood thinners (anticoagulants), long-term alcohol abuse, and dementia

Pathophysiology
Collected blood from the subdural bleed may draw in water due to osmosis, causing it to expand, which may compress brain tissue and cause new bleeds by tearing other blood vessels.The collected blood may even develop its own membrane. In some subdural bleeds, the arachnoid layer of the meninges is torn, and cerebrospinal fluid (CSF) and blood both expand in the intracranial space, increasing pressure.

Substances that cause vasoconstriction may be released from the collected material in a subdural hematoma, causing further ischemia under the site by restricting blood flow to the brain. y When the brain is denied adequate blood flow, a biochemical cascade known as the ischemic cascade is unleashed, and may ultimately lead to brain cell death. y The body gradually reabsorbs the clot and replaces it with granulation tissue.
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Diagnosis

Subdural hematomas occur most often around the tops and sides of the frontal and parietal lobes They also occur in the posterior cranial fossa, and near the falx cerebri and tentorium cerebelli Unlike epidural hematomas, which cannot expand past the sutures of the skull, subdural hematomas can expand along the inside of the skull, creating a concave shape that follows the curve of the brain, stopping only at the dural reflections like the tentorium cerebelli and falx cerebri.

A subdural hematoma demonstrated by CT

Treatment
depends on its size and rate of growth Small subdural hematomas-careful monitoring until the body heals itself inserting a temporary small catheter through a hole drilled through the skull and sucking out the hematoma; this procedure can be done at the bedside. Large or symptomatic hematomas- require a craniotomy, the surgical opening of the skull.