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1. Introduction Head injury is physical injury to brain tissue that temporarily or permanently impairs brain function.

Loss of consciousness does not need to occur. The severity of head injuries is most commonly classified by the initial post-resuscitation of Glasgow Coma Scale (GCS) score, which generates a numerical summed score for eye, motor, and verbal abilities. Traditionally, a score of 13-15 indicates mild injury, a score of 9-12 indicates moderate injury, and a score of 8 or less indicates severe injury. Head injury is classified as either closed or open (penetrating). A closed head injury means you received a hard blow to the head from striking an object, but the object did not break the skull. While an open, or penetrating, head injury means you were hit with an object that broke the skull and entered the brain. This usually happens when you move at high speed, such as going through the windshield during a car accident. It can also happen from a gunshot to the head. 2. Classification 2.1 Hematoma Hematomas (collections of blood in or around the brain) can occur with open or closed injuries and may be epidural, subdural, or intracerebral. Subarachnoid hemorrhage is common in head injury, although the appearance on CT scan is not usually the same as aneurysmal Subarachnoid hemorrhage. 2.2 Subdural hematoma Subdural hematomas are collections of blood between the dura mater and the piaarachnoid mater. Acute subdural hematomas arise from laceration of cortical veins or avulsion of bridging veins between the cortex and dural sinuses. They often occur with head trauma from falls and motor vehicle crashes. Compression of the brain by the hematoma and swelling of the brain due to edema or hyperemia (increased blood flow due to engorged blood vessels) can increase ICP. When these processes both occur, mortality and morbidity can be high. A chronic subdural hematoma may appear and produce symptoms gradually over several weeks after trauma.These hematomas occur more often in elderly patients (especially in those taking antiplatelet or anticoagulant drugs, or in those with brain atrophy). Elderly patients may consider the head injury relatively trivial or may have even forgotten it.

2.3 Epidural hematoma With an epidural hematoma, the bleeding is located between the dura mater and the skull. This is often present along the side of the head where the middle meningeal artery runs in a groove along the temporal bone. This bone is relatively thin and offers less protection of the skull. As the bleeding continues, the hematoma expands. There is little space in the skull for the hematoma to grow and as it expands, the adjacent brain tissue is compressed. As the pressure increases, the whole brain begins to shift and becomes compressed against the bones of the skull. The pressure tends to build quickly because the septae that attach the dura to the skull bones create small spaces that trap blood. 2.4 Subarachnoid bleed Subarachnoid bleeding occurs in the space beneath the arachnoid layer where the CSF is located. Often there is intense headache and vomiting with subarachnoid bleeding. Because this space connects with the spinal canal, pressure build-up tends not to occur. However, this injury often occurs in combination with the other types of bleeding in the brain, and the symptoms can be compounded. 2.5 Intracerebral bleed Intracerebral bleeding occurs within the brain tissue itself. Sometimes the amount of bleeding is small, but like bruising in any other part of the body, swelling or edema may occur over a period of time, causing a progressive decrease in the level of consciousness and other symptoms of head injury. 2.6 Skull fracture The bones of the skull are classified as flat bones, meaning that they do not have an inside marrow. It takes a significant amount of force to break the skull, and the skull does not absorb any of that impact. It is often transmitted directly to the brain. Skull fractures are described by which bone is broken, whether there is an associated laceration of the scalp, and whether the bone is depressed and potentially pushed into the brain tissue. 2.7 Concussion Concussion is defined as a transient and reversible post traumatic alteration in mental status (eg, loss of consciousness or memory) lasting from seconds to minutes and, by arbitrary definition, < 6 h. Gross structural brain lesions and serious neurologic residual are not part of concussion, although temporary disability can occur due to symptoms,

such as nausea, headache, dizziness, and memory disturbance (post concussion syndrome). 2.8 Brain contusions Contusions (bruises of the brain) can occur with open or closed injuries and can impair a wide range of brain functions, depending on contusion size and location. Larger contusions may cause brain edema and increased intracranial pressure (ICP). Contusions may enlarge in the hours and days following the initial injury and cause neurologic deterioration. 2.9 Diffuse axonal injury Diffuse axonal injury (DAI) occurs when deceleration causes shear-type forces that result in generalized, widespread disruption of axonal fibers and myelin sheaths. A few DAI lesions may also result from minor head injury. Gross structural lesions are not part of DAI, but small petechial hemorrhages in the white matter are often observed on CT scan and on histopathologic examination. DAI is sometimes defined clinically as a loss of consciousness lasting > 6 h in the absence of a specific focal lesion. Edema from the injury often increases ICP, leading to various manifestations. DAI is typically the underlying injury in shaken baby syndrome. Common Types of Traumatic Brain Injury
Disorder
Acute subdural hematoma

Clinical Findings
Typically, acute neurologic

Diagnosis
CT: Hyperdensity in subdural

dysfunction, which may be focal, space, classically crescent-shaped nonfocal, or both Patients with small hematomas may have normal function Basilar skull fracture Leakage of CSF from the nose or CT: Usually visible ear Blood behind the tympanic membrane (hemotympanum) or in the external ear Ecchymosis behind the ear (Battle's sign) or around the eye (raccoon eyes) Brain contusion Widely variable degrees of CT: Hyperdensities resulting from Degree of midline shift important

neurologic dysfunction or normal punctate hemorrhages of varied function Concussion sizes

Transient mental status alteration Based on clinical findings (eg, loss of consciousness or memory) lasting < 6 h CT or MRI: Clinical abnormalities not explained by lesions in brain parenchyma

Chronic subdural hematoma

Gradual headache, somnolence, confusion, sometimes with focal deficits or seizures

CT: Hypodensity in subdural space (abnormality is isodense during subacute transition from hyperdense to hypodense)

Diffuse axonal injury

Loss of consciousness lasting > 6 Based on clinical findings h but may not have focal deficits or motor posturing CT: At first, may be normal or show small hyperdensities (microhemorrhages) in corpus callosum, centrum semiovale, basal ganglia, or brain stem MRI: Often abnormal

Epidural hematoma

Headache, impaired consciousness within hours, sometimes with a lucid interval Herniation typically causing contralateral hemiparesis and ipsilateral pupillary dilation

CT: Hyperdensity in epidural space, classically lenticularshaped and located over the middle meningeal artery (temporal fossa) due to a temporal bone fracture

Subarachnoid hemorrhage

Typically, normal function Occasionally, acute neurologic dysfunction

CT: Hyperdensity within subarachnoid space on the surface of the brain; often outlining sulci

3. Etiology By definition, trauma is required to cause a head injury, but that trauma does not necessarily need to be violent. Falling down a few steps or falling into a hard object may

be enough to cause damage. Motor vehicle crashes account for more than 50% of traumatic brain injuries, with sports related injuries mostly football adding another 20%. Almost 80% of head injuries occur in males. 3.1 Penetrating trauma Missiles such as bullets or sharp instruments (such as knives, screwdrivers, or ice picks) may penetrate the skull. The result is called a penetrating head injury. Penetrating injuries often require surgery to remove debris from the brain tissue. The initial injury itself may cause immediate death, especially if from a high-energy missile such as a bullet. 3.2 Blunt head trauma These injuries may be from a direct blow (a club or large missile) or from a rapid deceleration force (a fall or striking the windshield in a car accident). 4. Pathophysiology Brain function may be immediately impaired by direct damage (crush, laceration) of brain tissue. Further damage may occur shortly from the cascade of events triggered by the initial injury. Head injury of any sort can produce cerebral edema and decrease brain blood flow. The cranial vault is fixed in size (constrained by the skull) and filled by CSF and minimally compressible brain tissue, consequently, any swelling from edema or an intracranial hematoma has nowhere to expand and thus increases ICP. Cerebral blood flow is proportional to the cerebral perfusion pressure (CPP), which is the difference between mean arterial pressure (MAP) and mean ICP. Thus, as ICP increases, CPP decreases. When CCP falls below 50 mm Hg, the brain may become ischemic. Ischemia and edema may trigger various secondary mechanisms of injury (eg, release of excitatory neurotransmitters, intracellular Ca, free radicals, and cytokines), causing further cell damage, further edema, and further increases in ICP. Systemic complications from trauma (eg, hypotension, hypoxia) can also contribute to cerebral ischemia and are often called secondary brain insults. Excessive ICP initially causes global cerebral dysfunction. If excessive ICP is unrelieved, it can push brain tissue across the tentorium or through the foramen magnum, causing herniation and increased morbidity and mortality. 5. Symptoms

Signs and symptoms of head injuries vary with the type and severity of the injury. Symptoms can vary from almost none to loss of consciousness and coma. As well, the symptoms may not necessarily occur immediately at the time of injury. While a brain injury occurs at the time of trauma, it may take time for enough swelling or bleeding to occur to cause symptoms that are recognizable. Minor blunt head injuries may involve only symptoms of being "dazed" or brief loss of consciousness. They may result in headaches or blurring of vision or nausea and vomiting.There may be longer lasting subtle symptoms including, irritability, difficulty concentrating, insomnia, and difficulty tolerating bright light and loud sounds. These post concussion symptoms may last for a prolonged period of time. Severe blunt head trauma involves a loss of consciousness lasting from several minutes to many days or longer. Seizures may result. The person may suffer from severe and sometimes permanent neurological deficits or may die. Neurological deficits from head trauma resemble those seen in stroke and include paralysis, seizures, or difficulty with speaking, seeing, hearing, walking, or understanding. While in penetrating trauma may cause immediate, severe symptoms or only minor symptoms despite a potentially life-threatening injury. Death may follow from the initial injury. Any of the signs of serious blunt head trauma may result. 6. Diagnosis The physician or health care practitioner will take a history of the events. The information may be provided by the patient, people who witnessed the event, emergency medical personnel, and if applicable, the police. The circumstances are very important since it is important to find out the severity and intensity of the trauma sustained by the head. If the patient is not fully awake, the examination will initially try to determine the level of coma using the Glasgow Coma Scale (GCS) which number is useful in tracking whether the patient is improving or declining in function over time. If no other injuries are found on examining the body, attention will be paid to the head and the neurologic exam. The health care practitioner will examine the patient for evidence of a basilar skull fracture, in which an injury has occurred to the bones that support the brain. Signs of this type of fracture include bruising of around the eyes (called raccoon eyes), bruising behind the ear (Battle's sign), bleeding from the ear canal, or CSF leaking from the ear or

nose. The neurologic exam may include evaluation of the cranial nerves. If the neck is not injured, the exam may include evaluation of muscle tone and strength of the arms and legs; sensation in the extremities including light touch, pain, and vibration; coordination; and walking. It is important to remember that injuries to other parts of the body may also be present, and the evaluation of the head injury may occur at the same time as the evaluation of other injuries. Imaging should always be done in patients with more than transiently impaired consciousness, GCS score < 15, focal neurologic findings, persistent vomiting, seizures, a history of loss of consciousness or clinically suspected fractures. However, a case can be made for obtaining a CT scan of the head in all patients with more than a trivial head injury, because the clinical and medicolegal consequences of missing a hematoma are severe. MRI may be useful later in the clinical course to detect more subtle contusions and DAI. It is usually more sensitive than CT for the diagnosis of very small acute or isodense subacute and isodense chronic subdural hematomas. Preliminary, unconfirmed evidence suggests that certain MRI findings predict prognosis. 7. Treatment Multiple noncranial injuries, which are likely with motor vehicle crashes and falls, often require simultaneous treatment. At the injury scene, a clear airway is secured and external bleeding is controlled before the patient is moved. Particular care is taken to avoid displacement of the spine or other bones to protect the spinal cord and blood vessels. Proper immobilization should be maintained with a cervical collar and long spine board until stability of the entire spine has been established by appropriate examination and imaging. After the initial rapid neurologic assessment, pain should be relieved with a short-acting opioid. In the hospital, after quick initial evaluation, neurologic findings (GCS and pupillary reaction), BP, pulse, and temperature should be recorded frequently for several hours because any deterioration demands prompt attention. Serial GCS and CT results stratify injury severity.

7.1 Mild injury

Injury is mild (by GCS score) in 80% of patients who have head injury and present to an emergency department. If there is brief or no loss of consciousness and if patients have stable vital signs, a normal head CT scan, and normal mental and neurologic function, they may be discharged home provided family members or friends can observe them closely for an additional 24 h. These observers are instructed to return patients to the hospital if any of the following develop: decreased level of consciousness, focal neurologic deficits, worsening headache, vomiting, or deterioration of mental function. Patients who have had loss of consciousness or have any abnormalities in mental or neurologic function and cannot be observed closely after discharge are generally observed in the emergency department or overnight in the hospital and follow-up CT is done in 4 to 8 h. Patients who have no neurologic changes but minor abnormalities on head CT (eg, small contusions, small subdural hematomas with no mass effect, or punctuate or small traumatic subarachnoid hemorrhage) may need only a follow-up CT within 24 h. With a stable CT and normal neurologic examination results, these patients may be discharged home. 7.2 Moderate and severe injury Injury is moderate in 10% of patients who have head injury and present to an emergency department. They often do not require intubation and mechanical ventilation (unless other injuries are present) or ICP monitoring. However, because deterioration is possible, these patients should be admitted and observed even if head CT is normal. Injury is severe in 10% of patients who have head injury and present to an emergency department. They are admitted to a critical care unit. Because airway protective reflexes are usually impaired and ICP may be increased, patients are intubated endotracheally while measures are taken to avoid increasing ICP. Close monitoring using the GCS and pupillary response should continue, and CT scan is repeated, particularly if there is an unexplained ICP rise. Osmotic diuretics (eg, mannitol) may be given IV to lower ICP and maintain serum osmolality. 7.3 Surgery

Intracranial hematomas may require urgent surgical evacuation to prevent or treat brain shift, compression, and herniation; hence, early neurosurgical consultation is mandatory. However, not all hematomas require surgical removal. Small intracerebral hematomas rarely require surgery. Patients with small subdural hematomas can often be treated without surgery. Factors that suggest a need for surgery include a midline brain shift of > 5 mm, compression of the basal cisterns, and worsening neurologic examination findings. Chronic subdural hematomas may require surgical drainage but much less urgently than acute subdural hematomas. Large or arterial epidural hematomas are treated surgically, but small epidural hematomas that are thought to be venous in origin can be followed with serial CT scans. 7.4 Rehabilitation When neurologic deficits persist, rehabilitation is needed. Rehabilitation is best provided through a team approach that combines physical, occupational, and speech therapy, skillbuilding activities, and counseling to meet the patient's social and emotional needs. Brain injury support groups may provide assistance to the families of brain-injured patients. 8. Prognosis Adults with severe head injury who are treated have a mortality rate of about 25 to 33%. Mortality is lower with higher GCS scores. Mortality rates are lower in children 5 yr (10% with a GCS score of 5 to 7). Children overall do better than adults with a comparable injury. The vast majority of patients with mild head injury retain good neurologic function. With moderate or severe head injury, the prognosis is not as good but is much better than is generally believed. There are indications for head injury outcome:

Good recovery (return to previous level of function) Moderate disability (capable of self-care) Severe disability (incapable of self-care) Vegetative (no cognitive function) Death

Over 50% of adults with severe head injury have a good recovery or moderate disability. Occurrence and duration of coma after a head injury are strong predictors of disability. Of patients whose coma exceeds 24 h, 50% have major persistent neurologic sequelae, and 2 to 6% remain in a persistent vegetative state at 6 mo. In adults with severe head injury, recovery occurs most rapidly within the initial 6 mo. Smaller improvements continue for perhaps as long as several years. Children have a better immediate recovery from head injury regardless of severity and continue to improve for a longer period of time. Cognitive deficits, with impaired concentration, attention, and memory, and various personality changes are a more common cause of disability in social relations and employment than are focal motor or sensory impairments. Posttraumatic anosmia and acute traumatic blindness seldom resolve after 3 to 4 mo. Hemiparesis and aphasia usually resolve at least partially, except in the elderly. 9. Prevention In sporting activities, the use of a helmet may help minimize the risk of injury; similarly, wearing a helmet while riding a motorcycle or bicycle helps minimize the risk of brain injury. Seatbelts can help prevent a head injury during a car crash. Since alcohol is a risk factor for falls and other injuries, it should be used responsibly. Falls are a concern in the elderly. Homes can be made less fall-prone by installing assist devices on walls and in bathrooms. Loose floor coverings such as area rugs should be avoided, since walking from one floor covering to another increases the risk of falls. If needed, canes and walkers may be helpful as walking assistive devices.

References

Brain Traumatic Injury. The Merck Manual of Diagnosis and Therapy website. Available from:http://www.merckmanuals.com/professional/sec21/ch310/ch310a.html [Accessed 10 April 2011] Benjamin, C. 2010. Head Injury, Medicinenet website, Available from :

http://www.medicinenet.com/head_injury/article.htm [Accessed 11 April 2011] David , A. 2009. Head Injury, Emedicine website, Avalaible from :

http://emedicine.medscape.com/article/1163653-overview [Accessed 11 April 2011] Kumar P, Clark M. 2002. Clinical Medicine 5th Edition. Head Injury. WB Saunders. P 1175-1176 Tortora G, Derrickson B. 2006. Principles of Anatomy and physiology 11th Edition. The Brain and Cranial Nerves. John Wiley & sons,Inc. P 496

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