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G Management of skull fractures

Classification

Linear, stellate , or comminuted describe skull fractures, depending on the complexity of the fracture line.

Depressed fractures are those in which a portion of the vault is displaced inward.

Compound fractures are present if the overlying scalp is lacerated.

Basilar fractures traverse the base of the skull.

Operative intervention

Depressed skull fractures may be associated with dural tear and underlying brain damage. Depressed skull fractures larger than 1 cm or the width of the skull in depth are usually surgically elevated.

Epilepsy is due to the immediate neuronal injury that occurs at the time of the depressed skull fracture injury.

Elevation of depressed skull fracture does not affect the incidence of post-traumatic epilepsy.

Compound fractures require a thorough debridement and closure to prevent subsequent infection.

Multiple skull fragments (comminuted) can frequently be reapproximated to reconstruct normal skull contour by use of nylon suture or small plating techniques.

Failure to remove all bone fragments and debride underlying brain of contaminated material (e.g., skin, hair, foreign bodies) may lead to subsequent development of brain abscess.

H Management of CSF

Leaks of CSF, if mixed with blood, can be diagnosed by the ring (halo) sign: If drops of CSF mixed with blood are placed on gauze, a lighter halo forms around a central bloodier area.

Most post -traumatic CSF fistulas close spontaneously with conservative management, which includes elevating the head to reduce both the ICP and the CSF leakage.

Post -traumatic rhinorrhea frequently results from a fracture of the cribriform plate, with associated dural defect.

Post -traumatic otorrhea is associated with fracture of the mastoid air cells and associated dural tear (Fig. 27 -3).

More than 95% of all patients with rhinorrhea or otorrhea due to basal skull fracture and dural tear will resolve with head of bed elevation at 45 degrees.

In some cases, a lumbar CSF drain is placed for continuous CSF drainage to promote fistula healing.

If lumbar drainage fails, craniotomy with closure of the dural defect may be necessary to resolve the leak.

Speed of acceleration or deceleration

Hyperextension versus hyperflexion

Underlying abnormalities in the spinal column secondary to degenerative disease (e.g., disc disease)

The patient's age and associated systemic injuries

D The aims of neurosurgical intervention

Primary focus is on the ABCs of trauma resuscitation (see V C 1 a)

SCI problems include hyperventilation secondary to SCI

Hypotension secondary to neurogenic shock

Additional aims of specific neurosurgical intervention are:

Restoration of bony alignment

Preservation of neuronal function

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E Initial management

Immobilization of the spine in the field before the patient is transferred to the hospital.

An estimated 4%–25% of patients still suffer some improper manipulation of the spine before they arrive at a trauma center.

Patients assumed to have cervical spine injury should be assumed to have more than one focus of spinal injury (i.e., use total spine precautions).

Patients should be in a hard cervical collar and on a spine board.

The use of transfer techniques such as log -rolling and scoop stretchers ensures that full spinal precautions are being maintained.

Stabilization

A patient may have a complete SCI and not feel pain associated with a broken limb or with an internal hemorrhage.

Vital signs and observation of the patient's overall hemodynamic status are very important in SCIs.

Patients with high cervical or high thoracic SCIs may go into neurogenic shock secondary to interruption of the sympathetic pathways.

These patients will develop hypotension in association with bradycardia, secondary to unopposed vagal tone.

Patients often require volume resuscitation and may need pressor agents as well.

Methylprednisolone is now shown in a national cooperative double -blind randomized study to be effective in the treatment of SCI.

Methylprednisolone in high doses should be administered shortly after the diagnosis of an SCI.

It must be administered within 8 hours of the time of SCI to be effective and must be given for 24 hours. Some data suggest that a 48 -hour regimen may be beneficial if treatment is started with more than 8 hours' delay after the initial injury.

Other agents currently under investigation for SCI resuscitation include G M1-gangliosides, glutamate receptor inhibitors, and antioxidants.

Neurologic evaluation

Information obtained from paramedics and emergency medical personnel is important to determine whether the patient ever exhibited motor function.

Motor function must be assessed in all four extremities.

A thorough sensory evaluation needs to be done and a determination made as to whether hemianesthesia exists.

It is important to determine whether hemianesthesia involves the face (not SCI) or just the arms and legs.

The sensory level should be measured, and a determination as to where the sensory level exists should be made rapidly.

The best way to determine a sensory level is to use a sharp pin and mark the level of a pinprick test result.

Reflexes

It is important to make a quick determination of reflexes and to obtain truncal reflexes.

Abdominal reflexes, cremasteric reflexes, and sphincteric reflexes, such as the bulbocavernosus and anal twitch, must also be assessed.

Sacral reflexes are important because of sparing of the sacral segment of the cord. Prognosis for recovery is better if the patient exhibits sacral sparing.

SCIs are classified as complete or incomplete.

Complete SCIs are those injuries with no motor or sensory function below the level of the injury. This is usually a dismal prognosis; 1% of patients exhibit significant recovery if the SCI remains complete for 24 hours.

Incomplete SCIs are important because rapid surgical intervention can help to restore function in these patients. Examples of incomplete SCIs include specific SCI syndromes:

Central cord injury. Results from a concussive blow to the cord. Deficits in the upper extremities are greater than in the lower extremities. Sensory function is usually

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more affected than motor function, and peripheral musculature (e.g., the hands) is usually more severely affected than proximal musculature (e.g., the shoulders).

Anterior SCI usually involves damage to the anterior spinal artery, resulting in infarction or ischemia of the anterior two thirds of the cord. This results in significant muscle weakness. There is a loss of some spinothalamic function; the hallmark is preservation of the posterior column function with intact light touch, position sense, and vibration.

Brown -Séquard syndrome typically occurs from hemisection of the cord, which usually results from penetrating trauma to the spinal cord. The hallmark is ipsilateral loss of motor function, light touch, and vibration with a contralateral loss of pain and temperature.

Radiographic studies. Any patient with an injury above the clavicle should be considered to have a cervical cord injury.

Common practice in the emergency department is to obtain a lateral cervical spinal radiograph as a first assessment of spinal cord alignment. The film must permit evaluation of the C-7/T -1 junction.

Evaluation of the entire cervical, thoracic, and lumbosacral spine may be required.

Any patient with an SCI requires full radiographic assessment (often CT scan) through the area of abnormalities identified in spinal films.

Once bony abnormalities have been identified with plain radiographs and CT scan (Fig. 27 -4), an additional evaluation may be necessary. MRI is increasingly becoming the second study of choice. MRI can reveal intramedullary abnormalities (contusion or intramedullary hematoma) and extra-axial abnormalities (e.g., an epidural hematoma or ruptured intervertebral disc).

In patients with contraindications to MRI (e.g., cardiac pacemaker, prosthetic metal devices), a full myelographic study of the spine may be necessary.

Treatment

Immobilization. The patient should not undergo any undue manipulation of the spine if an SCI is suspected.

FIGURE 27-4 CT scan, axial view, C-5 level. Note the midline fracture through the C-5 body and spinous process base.

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The patient should be immobilized in a hard cervical collar as well as on a rigid spine board until the level of SCI has been fully revealed.

If the patient requires closed reduction, traction is often successful.

In the past, Gardner -Wells tongs were used almost exclusively for traction.

More recently, lighter halo rings have been applied to the patient and used for traction.

Patients who have highly unstable cervical cord injuries or cervical-thoracic cord injuries often will require immobilization in a halo device until definitive reduction can be accomplished.

Open reduction and fixation. In the last two decades, there has been an increasing trend toward aggressive surgical reduction and fixation for unstable vertebral injuries.

Patients who undergo definitive surgical reduction and fixation can be more quickly mobilized and rehabilitated. This is translated into decreased mortality and morbidity from complications secondary to SCI.

Indications for acute surgical intervention. Immediate surgical intervention is required in patients with incomplete SCI and in patients who exhibit progressive neurologic deterioration with myelographic evidence of a block or an MRI scan suggestive of external compression.

For most SCI patients, surgery is required under more subacute conditions. These patients need extensive stabilization in the intensive care unit and then later undergo definitive reduction and fixation.

Epidural hematoma is a collection of blood between the bone and dura, usually of arterial origin, caused by laceration of the middle meningeal artery with an associated fracture of temporal bone. Less common etiologies include bleeding from the middle meningeal vein, venous sinus, or skull diploe.

Diagnosis

Between 10% and 15% of patients present with a lucid interval. That is, the patient is knocked out immediately after injury (concussion effect), then quickly regains consciousness but has a headache, and then slowly loses consciousness (over minutes to hours) again as the epidural hematoma expands and creates mass effect and elevated ICP.

Unenhanced CT has a characteristic appearance of lenticular (or lens -shaped) high density adjacent to bone.

Treatment

Very small epidural hematomas without evidence of significant mass effect and without clinical deficits can be followed up with serial CT scans and close clinical observation. If the hematomas do not expand or produce deficits, then they can be managed conservatively.

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Epidural hematomas that are associated with neurologic deficits or that produce significant mass effect must be evacuated, and the lacerated blood vessel must be identified and ligated.

SDH is a collection of acute or chronic blood that accumulates between the dura and the pia arachnoid.

Usually, SDH is from disrupted bridging veins between the dura and the cortical surface. Often, the blood accumulates very slowly over days or even weeks after a trauma often perceived as trivial, especially in the elderly. Many times, a clot will begin lysing and become enveloped by a membrane of fibrous tissues and delicate capillaries, leading to what is called a chronic SDH.

Diagnosis

Acute SDH presents as an evolving and expanding mass lesion. Often, there is deteriorating mental status with worsening focal deficits.

Chronic SDH is often a subtle, slow, progressive deterioration (e.g., headache, hemiparesis, hemianopsia) over weeks or months, which often presents as dementia, typically in the elderly patient. Chronic SDH is called the “great impersonator” because its clinical manifestations are legion.

CT scan is the diagnostic method of choice.

Acute SDH appears as a hyperdense lesion that shifts and compresses adjacent brain. It is often associated with an underlying contusion. Typically, it is not lenticular shaped; usually, the collection hugs the contour of the adjacent cerebral hemisphere.

Chronic SDH is present bilaterally 50% of the time. It is usually a hypodense or isodense collection associated with shift and compression. Isodense hematomas can be detected with contrast-enhanced CT scan.

Treatment

Acute SDH with decreased mentation or focal neurologic symptoms usually requires craniotomy and surgical evacuation of the dense clot.

Chronic SDH can often be treated initially with burr hole drainage of the lysed, liquefied clot; reaccumulation can require craniotomy for definitive drainage or subdural peritoneal shunt.

SAH may be spontaneous (e.g., aneurysm or arteriovenous malformation). The most common cause of SAH is trauma. Usually, there is a diffuse collection of blood in the subarachnoid space, which is normally filled with CSF and bathes the cerebral vessels.

Spontaneous SAH due to aneurysm rupture is usually associated with sudden onset of severe headache, often associated with nausea, vomiting, stiff neck, photophobia, decreased mentation, and a history of earlier severe so-called herald headaches (i.e., heralding a catastrophic SAH; “sentinel bleed”). Certain types of aneurysms are associated with specific neurologic findings.

Posterior communicating artery aneurysm is associated with third nerve palsy.

Internal carotid–ophthalmic aneurysm is associated with monocular visual field cut.

Diagnosis. CT scan demonstrates nearly 90% of all SAH.

If the CT scan is negative and shows no mass effect, then it is safe to proceed with lumbar puncture to establish diagnosis of SAH.

If CT or lumbar puncture is positive , an angiogram will be needed to determine the following (Fig. 27 -5):

Is there one aneurysm or more than one ? Fifteen percent of patients have multiple aneurysms.

If there are multiple aneurysms, which aneurysm is the one that most likely ruptured? There appears to be a correlation between aneurysm size and risk of rupture.

What is the exact orientation of the aneurysm? How can it be approached surgically ? Does it possess a “clippable” neck?

Is there an abnormality ? Fifteen percent of patients do not exhibit an angiographically identifiable source of SAH.

Common aneurysms. Berry aneurysms can occur at almost any junction point of any artery or any point along a vessel that receives an unusually strong stream of arterial blood. However, there are some very common aneurysms.

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