Head Trauma Scalp injury Skull fractures Closed head injury

Head Trauma Scalp injury Skull fractures Closed head injury

Head Trauma

Trauma is the leading cause of death in children and young adults; however. incidences of death and disability from trauma have been slowly decreasing. This is partly attributable to increased awareness of the importance of using seat belts and bicycle and motorcycle helmets. However, trauma remains a major cause of morbidity and mortality, and can affect every major organ system in the body. The three main areas of neurosurgic interest in trauma are TBI, spine and spinal cord injury (SCI), and peripheral nerve injury.

Head Trauma
Glasgow Coma Scale (GCS)Score
Motor Response (M) Verbal Response (V) Eye-Opening Response(E

Eye opening response E
Verbal response V
Motor response M
open spontaneously 4
oriented 5
Obeys commands 6
opens to speech 3
confused 4

Localize to pain  5

opens to pain 2
inappropriate words 3
Withdraws from pain4
no eye opening 1
unintelligible sounds 2
flexor posturing  3

no sound 1
extensor posturing 2

no movement  1

The initial assessment of the trauma patient includes the pri­mary survey, resuscitation, secondary survey, and definitive care. Neurosurgical evaluation begins during the primary survey with the determination of the GCS score (usually referred to simply as the GCS) for the patient The GCS is determined by adding the scores of the best responses of the patient in each of the three categories. The motor score ranges from I to 6, verbal from 1 to 5, and eyes from 1 to 4. The GCS therefore ranges from 3 to IS

Scalp Injury

Blunt or penetrating trauma to the head can cause injury to the densely vascularized scalp, and significant blood loss can occur. Direct pressure initially controls the bleeding, allowing close  inspection of the injury. If a simple laceration is found,it should be copiously irrigated and closed primarily. If the laceration is short, a single-layer percutaneous suture closure will suffice. If the laceration is long or has multiple arms, the patient may need debridement and closure in the operating room. with its superior lighting and wider selection of instruments and suture materials. Careful reap­proximation of the galea will provide a more secure closure and better haemostasis. Blunt trauma can also cause crush injury with subsequent tissue necrosis. These wounds require debridement and consideration of advancement flaps to cover the defect

Skull Fractures

The usual classification system for bone fractures may be applied­  to the skull. Characterization may be done using skull x-rays or head CT- A closed fracture is covered by intact skin. An open, or compound, fracture is associated with disrupted overlying skin
hemostasis in these cases . Fractures overlying dural ve­nous sinuses require restraint. Surgical exploration can lead to life­ threatening hemorrhage from the lacerated sinus.

Fractures of the skull base

 Are common in head-injured patients
and they indicate significant impacts. They are 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. If asymptomatic, they require no treatment. Symptoms from skull base fractures include cranial nerve deficits and CSF leaks. A fracture of the temporal bone, for instance, can damage the facial or vestibulocochlear nerve, resulting in vertigo, ipsilateral deafness, or facial paralysis. 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). Extravasation of blood results in ecchymosis behind the ear, known as Battle's sign. A fracture of the anterior skull base can result in anosmia (loss of smell from damage to the olfactory nerve), CSF drainage from the nose (rhinorrhea), or Periorbital ecchymoses, known as raccoon eyes.
Copious clear drainage from the nose or ear makes the diagnosis
of CSF leakage obvious. Often, however, the drainage may be dis­ colored with blood or small in volume if some drains into the throat. The halo test can help differentiate. Allow a drop of the fluid to fall
'on an absorbent surface such as a facial tissue. If blood is mixed
with CSF, the drop will form a double ring, with a darker center
-spot containing blood components surrounded by a light halo of CSF. If this is indeterminate, the fluid can be sent to the lab for beta­ transferrin testing. Beta-transferrin testing will only be positive if CSF is present.
Many CSF leaks will heal with elevation of the head of the bed for several days. A lumbar drain can augment this. A lumbar drain is a catheter placed in the lumbar CSF cistern to decompress the cranial vault and allow the defect to heal by eliminating normal by­ drostatic pressure. There is no proven efficacy of antibiotic coverage for preventing meningitis in patients with CSF leaks.

Traumatic cranial neuropathies management

 Are generally managed conservatively, with documentation of the extent of impairment and signs of recovery. Patients with traumatic facial nerve palsies may benefit from a course of steroids, although their benefit is unproven. Pa­tients with facial nerve palsy of abrupt onset, who do not respond to steroids within 48 to 72 hours may be considered for surgical ­ decompression of the petrous portion of the facial nerve. Patients may also present with delayed-onset facial nerve palsy. Again, steroids are employed and surgery is considered, with mixed results.

Closed Head Injury
Closed head injury (CHI) is the most common type of TBl, and a significant cause of morbidity and mortality in the United States. There are two important factors that affect the outcome in CHI and TBI in general. The initial impact causes the primary injury, defined as the immediate injury to neurons from transmission of the force of impact. The long, delicate axons of these neurons can shear as the different areas of the brain through which they pass accelerate and decelerate at different speeds. Prevention strategies, such as wearing helmets, remain the best means to decrease disability from primary injury. Subsequent neuronal damage due to the sequelae of trauma is referred to as secondary injury. Hypoxia. hypotension. hydro­cephalus, intracranial hypertension, and intracranial hematoma all mechanisms of secondary injury. The focus of basic research into brain trauma, critical care medicine, and neurosurgical intervention is to decrease the effects of secondary injury.

The Brain Trauma Foundation released, with the approval of the American Association of Neurological Surgeons, an updated summary of management recommendations for brain-injured patients in 2000. The guidelines standardize the care of these patients with the hope of improving outcomes. Some of the common patterns of CHI, including concussion, contusion, and diffuse axonal injury, are discussed below.

Initial Assessment

. The initial evaluation of a trauma pa­tient remains the same whether or not the primary surveyor sus­pects head injury. The first three elements of the ABCDs of resus­citation, airway, breathing, and circulation, must first be assessed and stabilized. 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.

An efficient way for the primary surveyor to assess disability and
ascertain the status of the three components of the GCS follows. Approach the patient and enter his or her field of view. Observe whether the patient visually orients to you. Clearly command: "Tell me your name." Then ask the patient to lift up two fingers on each side sequentially, and wiggle the toes. A patient not responsive to these prompts should be assessed for response to deep central painful stimulus, with a firm, twisting pinch of the sensitive skin above the clavicle. Watch for eye opening and movement of the extremities, whether purposeful or reflex. Assess the verbal response. The motor, verbal, and eye-opening scores may be correctly assigned using this rapid examination, and an initial assessment of the probability of significant head injury made. Also take note of any external signs of head injury, including bleeding from the scalp, nose, or ear, or deformation of the skull or face.

Medical Management

. Several medical steps may be taken to minimize secondary neuronal injury and the systemic conse­quences of head injury. Patients with a documented closed head injury should receive a 17-mglkg phenytoin loading dose, followed by 1 week of therapeutic maintenance phenytoin, typically 300 to400 mgld. Phenytoin prophylaxis has been shown to decrease the
incidence of early post traumatic seizures. There is no evidence to support longer-term use of prophylactic antiepileptic agents. 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 10 secondary injury. Head-injured patients have an increased prevalence of peptic ulcer­ ation and gastrointestinal (01) bleeding. Peptic ulcers occurring in patients with head injury or high ICP are referred to as Cushing's ulcers, and may be related to hypergastrinemia. Ulcer prophylaxis should be used. Compression stockings or athrombic pumps should be used when the patient cannot be mobilized rapidly.

Classification of head injury

. Head injury can be classified as mild, moder­ate, or severe. For patients with a history of head trauma, classifica­tion is as follows: Severe head injury if the GCS is 3 to 8
 Moderate head injury if the GCS is 9 to 12
 Mild head injury if the GCS is13 to 15
. Many people present to emergency rooms and trauma bays
with a history of head trauma, so a triage system must be employed to maximize resource utilization while minimizing the chance of missing occult or progressing injuries.

Management of Head trauma

Patients who are asymptomatic; who have only
headache, dizziness, or scalp lacerations or abrasions; or who did not lose consciousness have a low risk for intracranial injury and
may be discharged home without a head CT scan ,Head-injured
patients who are discharged should be sent home with reliable family or friends who can observe the patient for the first post injury day

Printed discharge instructions, which describe monitoring for confusion, persistent nausea, weakness, or speech difficulty, should be given to the care taker
The patient should return to the emergency department for evaluation of such symptoms.Patients with a 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 scanning. 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
Patients with depressed consciousness, focal neurologic deficits
penetrating injury, depressed skull fracture, or changing neurologic exam have a high risk for intracranial injury. These patients should
undergo immediate head CT and admission for observation or intervention as needed.

Brain concussion or postconcussion pc

 A concussion is temporary neuronal dysfunc­tion after non penetrating head trauma. the head CT is normal, and deficits resolve over minutes to hours. Definitions Way; some re­quire transient loss of consciousness, while others include patients with any alteration of mental status. Memory difficulties, especially amnesia of the event. are very common. Concussions may be graded. One method is the Colorado Medical Society system. Head trauma patients with confusion only are grade 1, patients with amnesia are grade 2, and patients who lose consciousness are grade 3. Studies have shown that the brain remains in a hypermetabolic state for up to a week after injury. The brain is also much more susceptible to injury from even minor head trauma in the first I to 2 weeks after concussion. This is known as second-impact syndrome, and patients should be informed that even after mild head injury they might experience memory difficulties or persistent headaches.

Brain contusion

A contusion is a 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 contused areas appear bright on CT scan,  The frontal, occipi­tal, and temporal pole are most often involved. The brain sustains injury as it moves in relation to rough bony surfaces. Contusions themselves 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. Contusions may also enlarge, or develop a true hematoma, especially during the first 24 hours. Contusions may also be seen in brain tissue opposite the site of impact. This is known as a contre-coup injury. These contusions result from deceleration of the brain against the skull.

Diffuse Axonal brain injury

. Diffuse axonal injury is caused by damage to axons throughout the brain, due to rotational acceleration and then deceleration. Axons may be completely disrupted and then retract, forming axon balls. Small hemorrhages can be seen in more severe cases, especially on MRI. Hemorrhage is classically seen in
the corpus callosum and the dorsolateral midbrain.

Penetrating brain Injury

. These are complex and must be evalu­ated individually. The two main subtypes are missile injury (e.g  due to bullets or fragmentation devices) and non missile injury (e.g., due to knives or ice picks). Some general principles do apply. 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 debridement, 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.

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