Download Cranial Trauma

CRANIAL TRAUMA
Brain injury is associated with more deaths from trauma than injury to any other region of the
body. There are approximately 150,000 deaths from all injuries per year in the United States, of
which 75,000 are estimated to be from brain injury. About 370,000 patients are hospitalized and
approximately 2,000,000 are medically attended for head injury. The overall incidence
eliminating the ten highest and lowest reported rates is about 200/100,000 population per year.
Brain injury incidence is higher in young people showing a peak incidence in young adults aged
15-24 with secondary peaks in infants and the elderly between the ages of 70-80. Males
outnumber females 2 to 1 in most studies except the very young where the incidence is the same
in males and females. The external causes of brain injury may vary relative to the geographic
area (city vs. state wide). About half are related to transport (motor vehicle, bicycles,
motorcycles, etc., pedestrian injuries). Falls are second and sports, assaults, gunshot wounds
account for most of the remainder. In some cities gunshot wounds may account for 50%.
Classification of injuries: Primary head injuries include skull fractures, focal injuries and
diffuse brain injures. Skull fracture may occur without brain damage, but focal or diffuse brain
injury is often present. These occur as primary damage at the moment of injury in the form of
contusions, lacerations, diffuse axonal injury or secondary damage initiated by, but not present
at, time of injury. These include intracranial hemorrhage, brain swelling, raised intracranial
pressure, hypoxic brain damage and infection.
Focal Injuries
Cerebral contusions are areas of infarctions, hemorrhage, or edema within brain tissue. The
gyral crest is maximally involved with variable effects to the subjacent white matter. These are
found in 20-40% of head injured patients studied by CT.
Contusions and lacerations occur more frequently in the frontal and temporal poles where the
brain is restricted by the frontal and temporal skull base near the sphenoid ridge. They occur
beneath the fracture sites or beneath the site of trauma (coup injuries) and/or opposite the point
of injury (contra-coup injuries). Hemorrhagic contusions may be relatively minor in appearance
on initial CT scan. Over time (hours to days), the patient may develop progressive neurological
deterioration. In
such instances, subsequent CT scan may reveal evolution of the contusion into a frank
intracerebral hematoma, so called delayed traumatic intracerebral hematoma (DTIC).
Epidural hematomas occur in 5-15% of fatal injuries. They are usually caused from bleeding
from a meningeal artery - most often the middle meningeal artery.
Occasionally they result from tears in the capital or transverse sinuses with slower onset of
symptoms. 85% of epidural hematoma patients have a skull fracture. The patient may have a
lucid interval between injury and coma, but this interval may occur with all conditions listed
below seventy to eighty percent are in the temporal fossa, but they can occur at any location. If
the patient is comatose from the onset, other types of brain damage are present.
Subdural hematoma results from tearing and stretching of parasagittal bridging veins resulting
from rapid acceleration of the brain. They are more common from falls and assaults than
vehicular accidents. Arterial bleeding may account for 30% of these hematomas. Subdural
hematomas can occur in "pure" form, but many are associated with contusions and diffuse brain
injury.
Intracerebral hematoma: In closed head trauma, the causes and mechanisms are much the
same as for contusions. They are most common in the frontal and temporal poles and they are
often associated with extracerebral hematoma. Linear fractures occur in 10-50 % of cases.
Diffuse Brain Injury
These are associated with widespread disruption of neurological function, without obviously
visible brain lesions on imaging studies. They are caused by inertial or acceleration effects of
the forces applied to the head. Rotational acceleration is thought to be the primary mechanism
causing diffuse brain injuries can be further classified as:
Mild concussion: There is temporary disturbance of neurological function without loss of
consciousness, usually with mild contusion and disorientation. The patient may not come to
medical attention and may have amnesia of five to ten minutes.
Classical cerebral concussion: There is temporary: reversible loss of consciousness lasting less
than six hours. The patient always has some retrograde amnesia and post traumatic amnesia.
Patients should be observed for subsequent development of intracranial hematoma.
Diffuse axonal injury (DAI): This is pathologically characterized by axonal damage or actual
tissue tears and small blood vessel tears. Axons form "retraction balls' which later appear as
diffuse astrocytosis and demyelination. Diffuse axonal injury can be further classified into mild,
moderate and severe with corresponding difference, of duration of corna, neurological findings,
and degree of recovery:
Evaluation of closed head trauma The history of an accident, nature of and circumstances of
injury and condition after an accident will aid in further evaluation of patient and subsequent
management.
The initial neurological evaluation is brief to assess the level of consciousness and the presence
of focal neurological deficits. A useful and now widely used scale of measurement is the
Glasgow Coma scale. (See: Neurological Exam). This is used to triage patients and to grade the
clinical course during treatment. For instance, with patients unable to speak or follow
commands, the incidence of intracranial mass lesions requiring surgery ranges from 40%-60%.
After initial examination, a thorough examination is required. Often in major head trauma, other
organ systems can be severely injured. In these cases there is a need to treat multiple systems
simultaneously. Immobilization of the spine may be indicated since 5%-10% of head injury
patients have an associated spine or spinal cord injury. Thoracic, abdominal and skeletal injuries
must be identified and managed.
Airway maintenance is of primary importance. The oropharynx must be cleared of debris or
secretions. Intubation may be requited with cure not to extend the neck if cervical spinal
assessment has not been done.
Hypotension is hardly ever a result of intracranial bleeding unless, the medulla is already
compromised. In open head injuries, blood loss from scalp laceration can be significant,
particularly in infants and children. But, in the usual setting, other causes of shock mast be
sought. Hypotension, however, can result from spinal injury by disrupting sympathetic tone to
the peripheral vasculature.
Physical examination: It is impossible to outline an exam appropriate for all patients because
of the enormous variations in individual injuries. Some with minor head trauma are awake and
cooperative; others with multisystem, major trauma are comatose and require examination by
many physicians simultaneously. The order and priority of examination is unique to each
situation.
Inspection of cranium: Areas of scalp confusion and swelling may overlie sites of linear or
depressed fractures.
Evidence of basilar fracture.
a.
b.
c.
d.
Raccoon eyes: blood staining of periorbital tissue.
Battle's sign: ecchymosis around mastoid, air sinuses
Drainage of CSF from nose or ear (rhinorrhea or otorrhea, respectively).
Hemotympanrrm or laceration of external auditory canal.
Facial fracture. LeFort fracture: palpate stability of facial bones and orbital rims. Palpation of
mandible.
Orbital injury. Inspection of globe. Note presence of proptosis or edema of conjunctiva.
Auscultation of neck and eye or head for bruits may reveal carotid cavernous fistula or carotid
artery injury such as a traumatic dissection or pseudoaneurysm.
Neurological examination: The initial exam serves as a baseline for future assessment of
improvement or deterioration and must be well documented.
Level of consciousness. The Glasgow Coma Scale (GCS) is used for standardized numerical
assessments useful for following the individual patient and making comparisons with
information from institutions treating head trauma. It provides a qualitative measure of
neurological injury-severity based on eye opening, verbal responsiveness, and motor response.
A mild injury is GCS of 13 to 15, moderate 8-12,
EYE OPENING
Spontaneous
To verbal command
To pain
None
GLASGOW COMA SCALE
4
3
2
1
BEST MOTOR RESPONSE
Obeys verbal commands
Localizes pain
Withdrawal
Flexion/abnormal (decorticate)
Extension (decerebrate)
None
6
5
4
3
2
1
BEST VERBAL RESPONSE
Oriented, conversing
Disoriented, conversing
Inappropriate words
Incomprehensible sounds
None
5
4
3
2
1
Total
3-15
In patients who are communicating, a more detailed exam of orientation is appropriate
Cranial Nerve Exam. Pupil reaction to light is most important. Pupillary inequality may signal
partial or complete III N palsy as a result of an ipsilateral compression by the uncus into the
tentorial notch. Rarely, it may result from contralateral herniation. In either case, the finding is
of extreme importance requiring urgent diagnosis and treatment to prevent further effects of
herniation. Rarely optic nerve compression or transaction may produce this finding. Pupillary
size reflects levels of damage to the brain stem. Damage to diencephalons or pons causes small,
but reactive pupils. Damage to the tegmentum of mid brain or third cranial nerves result in
dilated fixed pupils. Mid position, non-reactive pupils may occur with more diffuse mid brain
injury. Drugs or drops which may after pupillary size should be avoided in the setting of acute
trauma as this will effect the ability to appropriately monitor the patients neurological exam.
Funduscopic exam. Examine for retinal or pre-retinal hemorrhage. Papilledema is
rarely seen soon after trauma.
Corneal reflexes tests fifth cranial nerve sensation and integrity of brain stem
connections to the seventh cranial nerve.
Facial nerve. Complete paralysis usually indicates peripheral injury. Partial paralysis
may indicate a variety of central causes i.e. cortical through brain stern.
Olfactory nerve function may be lost after blunt injury. This is often due to damage to
the nerves at the cribriform plate.
It is rare for the remaining lower cranial nerves to be impaired in awake patients; but they
should be tested when possible.
With deeply comatose patients oculocephalic reflexes may be appropriate to test. In the absence
of cervical spine injury, “dolls eye maneuver" can be done. The eyes deviate from the direction
of head motion and rapidly return to neutral. With a unilateral mid brain lesion, the ipsilateral
eye will not adduct, but the eyes contralateral to the lesion deviates away from the directions of
head motion. With lesions of the mid pons there is no reflex. Ice water caloric testing may be
used to assess the same reflexes, but this test consumes more time.
Motor exam: Assesses functions of motor tracts from the brain through the spinal cord. In the
awake patient, a complete exam is possible. In comatose or uncooperative patients responses to
noxious stimuli are required to identify posturing responses as distinct from voluntary.
Decorticate posturing (flexion of elbows, wrists, and fingers and extension of lower extremities
may be seen with lesions above the mid brain. Decerebrate posturing (extension, adduction and
pronation of upper extremities and extension of lower extremities with foot plantar flexed) is
seen with lesions below the upper mid brain and above the vestibular nuclei.
Sensory loss can be partially assessed in comatose patients when testing for motor responses. If
spinal cord injury is suspected, rectal exam should be done to assess rectal tone and the
bulbocavernosus reflex. Sensory exam in the awake patient should assess pin and touch in the
major dermatomes of the spinal cord as well as posterior column function (vibration, and joint
position).
Reflexes: Test deep tendon reflexes of four extremities and plantar reflexes. In the absence of
reflexes, spinal cord injury may be suspected. Anal wink and bulhocavernosus reflex should be
tested.
Brain Herniation may occur under the falx, through the tentorial notch either on one or both
sides, or through the foramen magnum. At the time of initial evaluation, one or all may have
occurred but in the less severely injured patient, careful and frequent assessment is demanded
for early detection.
Central herniation results from diffuse bilateral supratentorial swelling or mass effect with
downward displacement of all supratentorial structures with progressive loss of brain function in
a rostro caudal direction. Changes in mental status progress with increasing (drowsiness to
confusion to agitation to coma. Breathing “irregularities" with pauses, small but reactive pupils,
increased muscle tone, Babinski signs and posturing then occur. If therapy is unsuccessful,
continued mid-brain function is lost with eventual loss of all brainstem function and death.
Uncal, or lateral herniation, occurs from lesions (such as hematomas) or swelling causing the
medial edge of the temporal lobe (uncus) to herniate over and through the tentorial notch.
Dilation of the ipsilateral pupil is an early sign and may occur with or without alteration in
mental status initially. Progression of herniation may produce complete third cranial nerve
palsy associated with contralateral motor paresis and loss of consciousness from mid-brain
compression. Occasionally, ipsilateral hemiparesis will occur from compression of the opposite
cerebral peduncle against the contralateral tentorial edge (Kernohan’s notch phenomenon). If
not treated successfully, progressive loss of midbrain function continues as in central herniation.
Cerebellar tonsil herniation through the foramen magnum usually occurs from lesions within
the posterior fossa. Depression of consciousness, alteration of respiratory rhythm, dysconjugate
gaze and vertical nystagmus may signal its beginning and respiratory arrest the end.
Clinical assessment including radiographic studies: After one has obtained the history and
accomplished the necessary physical and neurological exanimation and resuscitation measures a
decision regarding likelihood of significant intracranial injury is made. Patients can be placed in
low, moderate, and high risk groups based on physical findings and neurological examination.
Low risk: Asymptomatic, and/or headache, dizziness, scalp hematoma,
scalp laceration, contusion or abrasion and absence of the moderate or high risk criteria.
Moderate risk: Change of consciousness, at or subsequent to injury, increasing headache,
alcohol or drug ingestion, inadequate history, age <2, vomiting, amnesia, signs of basilar
fracture, possible skull penetration or depressed fracture.
High risk: Depressed level of consciousness not clue to alcohol, drugs; or other causes
(metabolic, seizures). Focal neurological signs, decreasing level of consciousness, and obvious
penetrating skull injury or depressed fracture.
Further management of these groups.
Low Risk: Observation and discharged with head sheet (instruction on careful observation at
home) to watch for moderate or high risk signs.
Moderate Risk: Extended observation in hospital setting. Many of these patients will need CT
scanning.
High Risk. All should have emergency CT scan and neurosurgical consultation.
Radiographic evaluation: current imaging modalities are skull x-rays,
computed tomography (CT); magnetic resonance imaging (MRI), and cerebral angiography.
CT scan is the primary imaging modality for initial diagnosis and management. It is quickly
available, safe, fast and can be performed on patients with serious and multiple injuries. It can
demonstrate hematomas, subarachnoid blood, contusion, cerebral swelling, ventricular and
subarachnoid cistern compressions. Fractures of the skull can be seen well with the use of boric
windows on CT. Immediate decisions regarding surgical treatment can be made.
MRI is rarely used at present for emergency evaluation of intracranial
trauma. It takes much longer, is cumbersome to use with resuscitation equipment, and may be
contraindicated in patients with implanted metal devices. However, its multiplanar capacities
demonstrate pathology more accurately, particularly in brain stem and posterior fossa. Its brain
use is in assessment of patients in subacute stage of injury.
Skull x-rays: Routine use of skull x-rays is controversial. They affect management in only
0.4% to 2% of patients. A linear fracture implies that great force to skull occurred. 213 of
patients hospitalized with skull-fracture have significant intracranial injury. Therefore, the use
of skull x-rays is dictated by risk assessment of injured patient (see above). In most instances,
CT provides adequate information regarding skull fractures as, well as superior imaging of the
intracranial contents, and therefore skull films are not needed.
Spine films. It the nature of injury and other risk factors are present, cervical spine films should
be made. The cranio-cervical juncture to C7 must be visualized. Special techniques such as a
swimmer’s view may be required to visualize lower cervical spine. If inadequate visualization is
possible with plain x-rays, then spine CT may be required, but plain x-rays are still the imaging
modality of choice to screen for fractures. Similarly, thoracic and lumbar spine films are
indicated depending on history, mechanism of injury and mental status of patient.
Management
Pre hospital: Airway maintenance of utmost importance: Thirty percent of severely head
injured patients are hypoxemic in ER. Oral or nasopharyngeal airways or intubation is required
without extension of neck if possible. Hypotension is associated with increased morbidity and
mortality. It is usually due to extracranial causes. At present isotonic saline or Ringers lactate
solution are the fluids most often used initially,
Scalp injuries: Scalp lacerations may cause significant blood toss if multiple or large.
Hemostasis is obtained by pressure or clamping of obvious arterial bleeders. Repair is done after
thorough cleaning and inspection for foreign material, underlying fractures. Scalp avulsion may
require scalp flap or skin grafting.
Linear skull fractures: Require no treatment, but indicate high probability of intracranial
injury and therefore, a CT scan of the head should be obtained.
Depressed skull fracture: Best assessed by CT scan and skull x-rays. Elevation required
depending on depth-, and location of depression. In infants and children a depression of a few
millimeters may be left alone. Surgical repair of depression over major venous sinuses may be
best avoided because of severe blood loss if the sinus is tamponaded by fragment removed
surgically. Though there is little evidence that elevation of closed depressed fracture affects
neurological outcome, or alters the incidence of seizures, they are usually elevated to correct
cosmetic defects.
Compound skull fractures: Require elevation and debridement and closure of dura it torn.
Bone fragments can be replaced unless there is severe contamination of the wound or the injury
is old and infected.
Basilar skull fractures: Suspected on clinical grounds CSF rhinorrhea or otorrhea occur in 511 %. Fracture of the ethmoid plate, orbital plate or sphenoid sinus usually cause rhinorrhea and
fracture of petrous portion of temporal bone usually causes otorrhea. Most CSF leaks (80%) will
cease within one week.
Imaging of anterior cranial fossa or temporal bone by tomography or CT with the use of
intrathecal contrast media are sometimes required to demonstrate site of CSF leak. Controversy
exists over tinning and necessity of surgical repair. Some advocate repair in all patients since
development of meningitis later is not uncommon. Others recommend-repair only if leaks
persist more than a week.
Repair is accomplished by either intracranial or extracranial approaches. Endoscopic
transnasal/trans-sinus routes of repair performed in conjunction with otolaryngologist may be
indicated in certain cases In the absence of meningitis the use of antibiotics is not indicated.
Epidural hematoma: Incidence 1 % to 2% of patients admitted for head injury. Clinical
presentation can vary from never unconscious to unconscious at all times, initially conscious
and subsequent unconscious, initially unconscious and subsequent conscious or initially
unconscious, lucid, then unconscious. Depends on severity of initial trauma. Only one-third
have classic "lucid" interval. Symptoms progress rapidly usually within 6hours. May be
delayed, however. Signs and symptoms are as described in the herniation syndrome section,
usually lateral herniation. CT scan is the best diagnostic study, but if not possible and the
patient's condition dictates immediate surgery, a burr note should be made over the temporal
area ipsilateral to the dilated pupil, or area of contusion or fracture. If found, partial evacuation
immediately decreases intracranial pressure (ICP) and is followed by craniotomy or
craniectomy to remove all clot and control bleeding site. If nothing is found, frontal and parietal
burr holes can be placed on one or both sides. In most cases, CT scan can be done and the
surgical flap tailored appropriately. Delay in diagnosis is the main cause of mortality and
morbidity. Mortality varies from 5%-43%. Mortality is less in younger patients. Additional
brain-injury (subdural hematoma, intracerebral hematoma or contusion) triples the mortality.
Acute subdural hematoma: About one-third are "simple" subdural hematomas and the rest are
associated with cerebral contusion, intracerebral hematoma and/or diffuse axonal injury.
Patients on anticoagulation have increased risk following trauma. The spectrum of clinical
presentation is similar to extradural hematoma (see above). One third to one-half of patients
have pupillary inequality, half have hemiparesis and other findings of herniation. CT scanning is
the diagnostic.-procedure of choice disclosing the presence of clot, degree of shift and intraaxial lesions.
If the subdural is less than 1 cm thick, it may be observed, but it must be followed by repeat
scans. Comatose patients with thin hematomas probably have parenchymal damage and need to
be aggressively monitored with imaging or ICP monitoring.
Subdural hematoma > 1 cm or with significant mass effect requires operative treatment usually
with a large craniotomy flap over the appropriate area and removal of as much clot as possible.
Associated
"burst" injuries of frontal or temporal poles, may be resected at same time. Burr holes may be
used to search for clot if a CT scan was not done, but adequate removal is rarely possible.
Comatose patients treated within four hours fare better than those treated later with 30%, vs.
90% mortality. Also, patients over 65, those injured in motorcycle accidents, and those with ICP
>45 post-operatively fare worse.
Chronic subdural hematoma. Subdural hematoma detected after the acute injury.
Three-fours are over 50 years of age. Over age 70, the incidence increases sharply to
7.4/100,000/yr. History of trauma is obtained in only 50% to 75% of patients and may be mild.
Contributing factors are alcoholism and seizures. CT and MR scans are the best diagnostic
modalities. Chronic subdural hematomas may be bilateral so no midline shift is evident. Some
are isodense on CT and the scan can easily be misinterpreted. Cerebral angiography is very
accurate, but rarely required today. Depending on their size, chronic subdural hematomas may
be managed operatively or medically.
Treatment of chronic subdural hematomas:
Operative
Burr hole. Bulk of hematoma is drained rapidly and the drain is attached to closed drainage
system-for next 24-48hrs.
Crainotomy is occasionally required for solid, organized or loculated chronic subdural
hematomas.
Subdural-peritoneal or subdural atrial shunt occasionally is required, particularly in pediatric
patients.
Medical: For asymptomatic or mildly symptomatic collections,
rest, is successful. Serial CT scans required to assess resolution.
use of low dose steroids,
Cerebral contusions and hematoma. Management is often not clear cut. CT scans are
required to assess the size and extent. Some require lop monitoring and appropriate management
of ventilation and osmotic agents. Frontal and temporal pole contusions may require removal on
one or both sides. Sudden herniation may occur 1-2 weeks after injury because of delayed
enlargement, necrosis and swelling
Hematomas of posterior fossa are relatively uncommon when compared to supratentorial
space. Incidence reported from 3%-13% of all extradural hematomas and 1% of subdural
hematomas. Occipital skull fracture is found in two-thirds or more. Headache and stiff neck are
the most common symptoms. Cerebellar signs are seen in less than half and may be confused
with lesions elsewhere. Many patients may die undiagnosed. CT scan is the best imaging study,
but may require special positioning and more frequent cuts to detect Hydrocephalus is present in
one-third of patients and supratentorial lesions in about one-half. Surgical removal is, required
and with extradural hematomas the clot may extend above the transverse sinus requiring
exploration above it. Mortality is reported front 15% to 24% for extradural hematomas and
42%-70% for subdural hematomas.
Gunshot injuries: Approximately 70% of patients die at the scene of injury. Injury severity is
dependent on size and type of missile and velocity of injury. Flaccid patients all die.
Decerebrate patients have a mortality of 95%-97%. CT scan is the best initial study for
detection of bone fragments, course of missile, hemorrhage and swelling. For viable patients,
surgery is required to remove hematoma, nonviable brain, missiles and bone fragments when
feasible, and to repair and close the dura and scalp. Depending on the severity of injury, surgery
may be done through a small craniectomy or it may require a large flap to deal with extensive
bilateral brain damage. Retained bone-fragments may cause delayed abscess formation
requiring further surgery.
Medical Management of Severe Head Injuries: The basic goals are to maintain normal blood
pressure, adequate arterial oxygenation, control body temperature (hypothermia worsens
outcome) and fluid and electrolyte balance.
Management of Raised ICP: Control of elevated intracranial pressure is the most important
treatment modality for head injured patient. Approximately 40% of patients with loss of
consciousness will develop intracranial hypertension at some point during treatment and its
level is a strong predictor of outcome. Upper limits of normal in adults and older children is 1015 mmHg, children 3-7 mmHg and infants 1.5 6 mmHg. Cerebral blood flow in the critical
parameter for brain survival and depends on cerebral perfusion pressure (CPP) which is defined
as: CPP=MAPBICP. MAP is mean arterial pressure; ICP is intracranial pressure. Therefore,
careful control of systemic blood pressure and ICP is vital in severe head injury. One episode of
hypotension (SRP=90) after injury increases mortality 50% compared to 27% without. Hypoxia
also plays a significant role. Treatment of small rises in ICP may prevent later uncontrollable
elevations of ICP. The goal of therapy is to keep ICP below 15-20 mmHg and maintain CPP
above 50 mmHg.
Patient position: Elevate head 30-35° and prevent venous outflow obstruction in the neck by
maintaining a neutral plane of the head and thorax. There is no neck compression by external
object; such as a cervical collar or tape.
Anticonvulsants are usually given to prevent post traumatic seizures which may raise ICP in
obtunded or comatose patients, even if pharmacologically paralyzed.
Fluids usually are isotonic at 75-150 cc/hr in adults. In multi-injured patients, more complicated
management is required.
Antacid or H2 antagonists are given to any patient on steroids. They help prevent stress ulcers
also.
Corticosteriods: There is no clear evidence of benefit of these agents on outcome in head injury,
but they appear to provide a small benefit for patients with spinal cord injury. Corticosteroid
increase complications of infection, hyperglycemia aseptic necrosis.
Intubation is usually required if the GCS is 7 and for any evidence of respiratory distress.
ICP monitor is usually used if GCS is < or = 8. The patient should have undergone: full
evaluation for systemic trauma, have IV access, a central venous line, arterial blood gases; and
appropriate scans or films of the head and other systemic injuries. If the CT scan shows a
surgical lesion, the patient is taken to the operating room and ICP monitors are installed at the
end of the procedure if appropriate. If the CT does not indicate surgery, an ICP monitor is
placed in the ICU. There are various types of monitors. An intraventricular catheter is most
accurate and allows removal of CSF which may help control ICP. It may be difficult to insert if
the lateral ventricles are small. It can become occluded and dive erroneous information. There is
slightly higher risk of causing hemorrhage at the site of insertion. Other types are: subarachnoid
screw (bolt), subdural, epidural, and intraparenchyrnal (Camino fiberoptics). All monitoring
devices have problems with maintenance of accuracy and may become infected with prolonged
use.
Measures to reduce ICP:
Hyperventilation reduces PCO2 to 25-30 mmHg, which causes vasoconstriction and reduces
intracranial blood volume. It will decrease ICP 25% to 30% in most patients. It will lose its
effect with repeated prolonged use and can worsen ischemia in area of impaired perfusion
Hyperventilation should only be used in the setting of acute herniation, but otherwise should be
avoided because of the potential to cause further injury to the brain.
Mannitol is used if ICP remains elevated above 16 mmHg for 10 minutes with patient at rest. It
is given in doses of 0.25 gm/Kg every 4-6 hours. Serum hyperosmolarity caused by this agent
is thought to reduce cerebral edema. However, the mechanism of action is uncertain. Mannitol
may also have a rheological benefit that enhances blood flow. Serum osmolarity can also be
increased by administration of hypertonic saline.
Furosemide is sometimes used with mannitol. It is less reliable when used alone. It may
exacerbate the dehydrating effects of mannitol and induce hypokalemia.
Barbituate coma is sometimes used in patients with uncontrollable elevations in ICP.
Improvements in the outcome of patients has not been clearly demonstrated. The risk of
hypertension is greater, particularly with the prior existence of cardiovascular compromise. Its
use requires extraordinarily close observation and monitoring capability
Decompressive craniectomy with the removal of a large portion of the frontotemporal skull is
sometimes done if ICP is not controlled by the measures outlined above in patients with no
demonstrated extra- or intracerebral lesion that could be removed. A wide dural opening may be
required. Recovery in 41% of patients has been reported.
SPINE AND SPINAL CORD TRAUMA
The evaluation and treatment of trauma to the spine, spinal cord and nerve roots demands a
systemic approach which is integrated into the overall management of the traumatized patient.
Issues of particular relevance to the spine are those of neurological injury and spinal stability.
The most common cause of cervical spine injury is vehicular accidents, followed by falls, diving
accidents and gunshot wounds. Thoracolumbar injuries are caused by essentially the same
mechanisms excepting diving. Spine and spinal cord injuries, like other forms of trauma, tend to
occur in young adults. Males predominate, with a ratio
approximating 2:1 inmost series. Neurological injury occurs in up to 70% of cases of cervical
spine injury.
Initial Approach: All patients presenting with significant trauma or with spine pain or
tenderness should be presumed to have an unstable injury. The initial priorities are the ABC's of
trauma management (airway, breathing, circulation). During respiratory and hemodynamic
stabilization, the spine must be immobilized to minimize the risks of compounding neurologic
injury. If endotracheal intubation is required, the cervical region should be manually stabilized
and extension should not be performed.
Hemodynamic stabilization is an early priority as tissue per fusion and oxygenation are critical
to minimize secondary neurological injury. Ventilatory assistance may be required in patients
with high cervical cord lesions even when they initially appear to be moving air satisfactorily.
Systolic blood pressure should be maintained above 90mm Hg. Some quadriplegic patients may
demonstrate mild to moderate hypotension associated with relative bradycardia. This is
secondary to interruption of syrmpathetic outflow. Care must be taken in these cases to avoid
over-hydration and pulmonary edema.
During the primary assessment, an awake patient should be questioned about spine pain or
tenderness. A lateral cervical spine film should be performed early during the course of
evaluation. Later, anteroposterior- films, an open mouth view of the odontoid and oblique
cervical spine films should be obtained. A-P and lateral films of the thoracic and lumbar spine
are requested if there is pain, tenderness or deformity affecting there regions, if the patient is
unconscious after major trauma (e.g. a vehicular accident) or if neurological abnormalities are
noted on examination.
A neurological examination should be performed on any patient suspected of having a spinal
injury. This should consist of an assessment of level of consciousness, a brief evaluation of
cranial nerve and brainstem function, a motor examination of all major muscle groups (proximal
and distal in the upper and lower extremities), a sensory evaluation (screen with light touch and
pinprick), reflex testing and a rectal examination to gauge sphincter function and sacral
sensation.
Plain radiographs are quite useful in detecting spinal fractures or dislocations. Instability can be
more difficult to be certain about on plain films. As a general rule, acute subluxations of more
than 3.5mm in the cervical and thoracic spine and 4.5mm in the lumbar spine are considered
unstable. Angulations also suggest instability (e.g. relative angulation 11 degrees in the cervical
spine). Fractures involving more than one column are generally unstable, and patients, with a
neurological deficit after trauma should be considered unstable even if early radiographs do not
suggest instability. Flexion extension films of the cervical spine are used to evaluate stability in
a more dynamic way. These studies should only be performed on an awake, cooperative patient
with no evidence of spinal cord injury and only if no other indication of acute instability exists.
Computed tomography and/or MRI are useful adjuncts to the plain film evaluation of patients
with spine or spinal cord injury. Each has advantages and disadvantages. Bony detail is best
seen with CT, but soft tissue structures such as the spinal cord, ligaments and discs and
hematomas are not well seen. MRI demonstrates soft tissue changes well facilitating the
diagnosis of conditions such as traumatic disc herniation, traumatic cord disruption, or
hematomyelia to be made. Myelography is occasionally utilized when MRI is not available of
is not feasible.
After a significant spinal injury is detected, therapy is directed at restoration or maintenance of
spinal alignment, treatment of any associated life-threatening injuries and treatment of
neurological injury. It should be remembered that 4-17% of patients with a spinal fracture will
have a noncontiguous injury of which as many as 20% will be unstable.
Early stabilization and reduction' of cervical spine-fractures is often achieved with the
application of skull tongs and traction. The appropriate amount of weight to apply is dependent
on the typo and level of fracture. Significant neurological injury can occur with over distraction.
Definitive treatment of cervical fractures may range from simple immobilization in an orthosis
to operative decompression and stabilization.
Thoracolumbar injuries are usually managed early on with recumbent therapy. The patients are
log rolled to prevent skin breakdown. Stable injuries may be managed in an orthosis while
unstable fractures are most often treated with open reduction and internal fixation.
Spinal cord injury is most commonly encountered in. the context of cervical-spine facture or
ligamentous injury. Injuries to the thoracolumbar spine affecting the distal cord or conus are
next most frequent. The term “complete" implies that there is no neurologic function (except
reflex action) below the level of injury. Incomplete injuries demonstrate patterns of partial
spinal cord dysfunction with preserved function distal to the level of injury.
The clinical patterns are determined by the part of the spinal cord (and/or nerve roots) that is
injured as well as the anatomic arrangement of the cord itself. Example of patterns of partial
cord injury include: the anterior cord syndrome, the central cord syndrome, posterior cord
syndrome and the Brown-Sequard (or cord hemisection) syndrome. Although patients often
present with features on examination consistent with these described syndromes, it is not
unusual to see mixed patterns.
SYNDROME
Anterior Cord Syndrome
MOTOR DEFICIT
Bilateral LE plegia
Central Cord Syndrome
Bilateral UE plegia; LE
weakness less, esp. distal
Ipsilateral motor loss
Brown-Sequard Syndrome
SENSORY DEFICIT
Bilateral LE pain and
temperature
Sensory loss in UE’s.
Relative preservation distally.
Ipsilateral vibratory and
Posterior Cord Syndrome
(rare)
Mild or none
propioceptive loss.
Contralateral pain and
temperature loss.
Bilateral vibratory and
position sense loss
The early therapy of cord injury is directed toward the prevention of secondary damage to the
already traumatized cord. As stated above, the restoration of normal oxygenation, ventilation
and perfusion are instrumental in minimizing neurological morbidity. Immobilizing unstable
spinal segments will prevent additional mechanical injury. Steroids (specifically
methylprednisolone) have been demonstrated to improve neurological outcome after nonpenetrating cord injury in randomized, prospective, double-blind, multicenter clinical trials
(North American Spinal Cord Injury Study NASCIS II & III). For benefit, it appears that
steroids must be administered within 8 hours of injury. In fact, after eight hours steroids may be
detrimental. The dose of methylprednisolone recommended is specific: 30 mg/kg IV bolus
administered every 15 minutes followed 45 minutes later by 5.4 mg/kg/hr continuous IV
infusion. The infusion should be continued for 23 hours if initiated within 3 hours of the injury,
and for 48 hours it initiated 3-8 hours after the injury. At present there are no other
pharmacotherapeutic agents of proven benefit in spinal cord injury although a randomized.
Timing of operation: The timing of operative intervention is usually semi-elective for patients
without neurological involvement, being determined in part by the status of any concurrent
injuries. Patients manifesting neurological deficits present a more difficult problem. Most
surgeons would agree that emergent intervention should be undertaken when there is
progression of a neurological deficit in the context of a compressive lesion. On the other hand,
there is some question as to the optimal timing of surgery for patients with stable or improving
deficits. Most neurosurgeons postpone operative intervention for a few days if there is
improvement in function as there is some evidence that the risk of worsening after early surgery
is greater than when surgery is delayed a few days. Patients with deficits which are truly
complete for more than 24 hours have virtually no potential for the recovery of useful motor
function. For this reason, some surgeons have advocated an aggressive approach to
decompression in patients who are seen very soon after injury with what appears to be a
complete lesion. Otherwise, the timing of surgical stabilization in patients with complete cord
lesions is in accordance with their overall medical condition.
Indications for Surgery: The indications for surgical intervention in the context of spinal
trauma relate to the goals of restoring spinal alignment and stability and providing an optimal
situation for neurological recovery. If these goals cannot be achieved by alternative means or if
operation is the best way to achieve these goals, then surgery should be considered. The risks of
operative intervention must then be examined in the context of the patient's condition.
Advances in the ability to provide rigid internal fixation for unstable segments during the Weeks
or months required for the development of bony stability has increased the role of surgery in the
treatment of spinal trauma.
CERVICAL SPINE INJURY.
Upper Cervical Spine and Craniocervical Junction: Fractures and dislocations of this region
of the spine with associated cord injury are not uncommon in autopsy series examining
vehicular fatalities. On the other hand, most patients seen clinically with fractures in this region
are neurologically intact or have minor deficits. This is not surprising in view of the fact that the
neural outflow to the diaphragm exits at levels C3-C5 of the spinal cord. Traumatic injury to the
cord above this level is not associated with survival unless respiration can be maintained.
Nonetheless, increasing numbers of cases of survivors from such devastating injuries are being
reported presumably a result of improvements in pre-hospital emergency care.
Condyle fracture: Fractures of the occipital condyles are relatively uncommon injuries and are
frequently found in association with fractures of the atlas (e.g. Jefferson fractures). They are
most commonly associated with occipitocervical pain rather than neurological symptoms
although lower cranial nerve palsies have been reported. When seen in isolation, these fractures
are often treatable in a hard collar.
Craniocervical Dislocation: This lesion is rarely encountered in a living patient but should be
looked for especially after high speed vehicular injury or pedestrian/vehicle accidents. It will be
manifest on plain lateral radiographs as an increased distance between the clivus and the tip of
the dens, or as a displacement either forward or back of the skull relative to the upper cervical
spine. Cervical traction is contra indicated as it may worsen distraction and medullary injury.
Survivors of this injury will generally require surgical stabilization.
C1 Fractures: Fractures of the atlas account for approximately 5-10% of cervical spine injuries.
They are most commonly the result of axial loading mechanisms. The so-called Jefferson
fracture involves a disruption of the C1 ring with expansion of the spinal canal. The ring is
fractured in two or more sites. Neurological injuries are rare in this setting and treatment with
immobilization for 3 months in a halo vest is generally sufficient. Unilateral fractures of the
lateral mass or posterior arch fractures are also occasionally seen. C1 fractures are commonly
seen in combination with C2 fractures (e.g. 41% of Jefferson fractures).
Axis injuries: The anatomy of the second cervical vertebra is unique leading to number of
unique patterns of injury. Fractures of the odontoid process are relatively common injuries.
They have been classified by Anderson and D'Alonzo according to the site of the fracture line.
Type I fractures are avulsions, of a portion of the tip of the odontoid by the alar ligament. These
are uncommon fractures and are generally thought to be stable. They are usually treated in a
hard collar. Type II fractures, the most common, involve a fracture through the base of the
odontoid process at its junction with the C2 body. These lesions are most commonly related
with a halo orthosis but the nonunion rate has been reported to be in the range of 25-63 % in
some series. This is thought to be related to a relative lack of blood supply to the distal
odontoid. Patients who go to nonunion or patients at high risk of doing so are treated surgically.
The options in these cases include anterior odontoid screw fixation, posterior articular C1-C2
screw fixation or a variety of atlantoaxial fusion techniques. The fracture line in Type III
fractures passes into the axis body. These fractures generally heal well when treated in a halo.
Traumatic spondylolisthesis of C2, also called Hangman’s fracture is another common injury
pattern. These lesions involve a fracture through the pedicles of C2. These fractures are often
seen without neurological injury because the spinal canal is expanded by the injury. There may
be disruption of ligamentous structures rendering these injuries unstable. Most commonly these
fractures are treated in a halo vest; some may be successfully immobilized in a cervical collar or
other orthosis.
Subaxial injuries: Fractures and dislocations to cervical vertebrae below C2 are generally
considered together since vertebral anatomy is similar from level to level and fracture patterns
are likewise similar. The most common levels to be injured are C5 and C6. Some of the more
common injury patterns include unilateral and bilateral locked teardrop fracture, burst fracture,
hyperflexion injury and clay shoveler's fracture.
Unilateral locked facets: Unilateral locked facets results from a flexion-rotation type of
mechanism. In this injury, the facet joint, at one level are dislocated such that the inferior
articular process of the upper vertebra locks anterior to the superior process of the lower
vertebra. Plain radiographs demonstrate a characteristic appearance. On the lateral projection
there is anterolisthesis of the upper vertebra measuring 25% of the A-P dimension of the body.
There is also a rotary component such that on a given lateral film either the segment of the spine
above or below the dislocation will appear rotated. Similarly, a mal-alignment of the spinous
processes will be seen in the A-P projection. Unilateral locked facets may or may not be
associated with cord injury. The initial management of these unstable injuries is skull tongs
traction with an attempt at reduction. When closed reduction is accomplished, most surgeons
recommend halo immobilization. Failure at closed reduction is usually considered an indication
for operative reduction in which the facets are drilled until they can be realigned under direct
vision. Fusion and internal fixation by a variety of methods is then employed.
Bilateral locked facets: Bilateral locked facets occurs via a hyperflexion mechanism in which
the posterior ligaments are disrupted sufficiently to: allow both facet complexes to dislocate.
These injuries are commonly associated with neurological involvement. Plain lateral
radiographs demonstrate a subluxation of 50% or more of the vertebral body, often with an
angular deformity. These Injuries are highly unstable. They, can frequently be reduced by
closed techniques, but surgical stabilization is generally advocated.
Teardrop Fracture: Teardrop fractures are hyperflexion injuries characterized by a small chip
of bone ("teardrop") off of the anterior inferior aspect of the vertebral body. Patients frequently,
but not always, have severe neurological injury. Treatment includes: management in a halo
orthosis or surgical stabilization and fusion. A more severe injury with flexion and axial loading
is the burst fracture. These fractures have failure of the anterior and middle columns often with
retropulsion of bone into the canal. These fractures are often treated
surgically if neurologically incomplete. Immobilization in a halo may be reasonable for patients
with complete quadriplegia. Minor teardrop fractures may be managed by immobilization of the
patient's cervical spine with a Philadelphia collar.
Burst Fracture: These fractures are the result of axial compressive forces and are similar to the
lesions seen in the thoracolumbar spine (sec below). Neurological injury is common and
surgical decompression via an anterior cervical procedure (e.g. trough corpectorny) in often
required in incomplete lesions. These fractures are unstable but will often heal in a halo if spinal
cord compression Is not an issue .
Clay Shoveler's Fracture: Classically, the clay shoveler’s fracture is an avulsion of the
spinous process of C7, though any spinous process fracture without other injury is often labeled
by this term. Presently, the most common mechanism is a direct blow to the posterior elements.
These are stable injuries though they may be painful. Care must be taken to rule out less
obvious, but more serious ligamentous or bony injury. This last point is especially true when
such fractures involve the spinous processes of levels above C6.
THORACIC AND LUMBAR SPINE INJURY
Fractures of thoracic and lumbar level, tend to occur in a younger population. They are most
often the result of vehicular accidents, industrial accidents, falls and suicide attempts. The
thoracolumbar junction is the most common level injured. This is because it is a transitional
zone between the relatively rigid thoracic region and the flexible lumbar spine. It is also a
transitional area between the thoracic kyphosis and the lumbar lordosis. Fractures in the lumbar
area often occur when the physiological range of motion is exceeded. Fractures to the upper
thoracic spine require considerable violence because of the stabilizing influence of the ribs.
Because of the increased levels of force required to injure the thoracic and lumbar spine, one
should have a heightened level of suspicion in looking for associated visceral and soft tissue
injuries. Lap belt injuries to the lumbar region (e.g. 'Chance fractures') are an example of
fractures often associated with small bowel injury.
Fracture Classifications: A number of classification schemes for thoracic and lumbar fractures
have been developed, primarily to distinguish between fractures which can be considered stable
vs. unstable. Different schemes have emphasized different aspects of the problem. Some are
mechanistic, describing fracture in terms of the probable forces; involved in their generation,
e.g. flexion, flexion compression, translation etc. Other systems have focused on the supporting
columns of the spine (either a 2 column or 3 column concept). Still others have described
fractures in terms of pathoanatomic descriptions. A complete discussion of these various
systems is beyond the scope of this review although some explanation of the 3 column concept
of the spine described by Denis is useful to provide a simple means of predicting stability for
these injuries.
Denis conceptualized the spine as consisting of three osteo-ligamentous columns each
contributing to spinal stability. The anterior column consists of the anterior half of the vertebral
body and the associated discs and ligaments. The middle column is the posterior aspect of the
vertebral bodies and discs along with the posterior longitudinal ligament. The posterior column
is the posterior elements (pedicles, spinous processes and laminae) and their associated
ligaments. Fractures associated with failure of two or three columns are considered unstable.
For example, burst fractures involve failure of the anterior and middle columns.
SPECIFIC FRACTURF PATTERNS IN THORACOLUMBAR INJURIES
Anterior Wedge Compression Fractures: These fractures are probably the most common
affecting the thoracic spine. The anterior column fails in compression while the middle and
posterior columns remain intact. There is usually less than a 50% loss of anterior vertebral
height. Because ligamentous structures are preserved and because of the stabilizing effect of the
rib cage, these fractures tend to be sable. Treatment is most often symptomatic. Analgesics are
given for pain and bed rest is prescribed until the acute pain has subsided. Subsequently
symptomatic patients are mobilized in an orthosis. Wedge compression fractures are frequently
seen in the context of osteoporosis secondary to neoplastic vertebral involvement must be
excluded.
Anterior Wedge Compression Fractures with Posterior Disruption: Compression fractures
with failure of the posterior column in tension may occur with injuries of greater force. These
fractures are commonly seen in the lumbar spine. In these cases there is usually disruption of
the facet capsules, the ligaments flavum and other posterior ligamentous structures. The
tendency for these lesions to develop a kyphotic deformity generally necessitates early operative
stabilization.
Flexion-Distraction Injuries: The classical form of this type of injury is the lap belt fracture
such as that described by Chance in 1948. In these injuries all three columns fail in tension as
could occur when the body is forcibly stretched over a lap belt in a vehicular accident. These are
unstable injuries and most require operative intervention, often with posterior compression
instrumentation.
Burst Fracture: This is probably the most common pattern of fracture at the thoracolumbar
junction. These lesions are the result of axial loading such that the vertebral body fails in
compression at both the anterior and middle columns. There is generally retropulsion of bone
into the canal and significant risk of neurological injury. Plain radiographs demonstrate loss of
vertebral height, widening of the inter-pedicular distance and occasionally evidence of bony
retropulsion into the canal. Plain films give a very poor estimate of canal encroachment
however and additional study with CT or MRI is usually required. Involvement of the posterior
elements will result in these fractures being considered "unstable" although some burst fractures
may demonstrate the development of progressive deformity even when the posterior column
appears intact. The thresholds for surgical intervention in burst fractures are somewhat
controversial though most surgeons would consider operative de compression and fixation when
there is > 50% canal compromise, and/or 30% loss of height when there is evidence of neural
compression and a deficit, when there is posterior element involvement or when there is
excessive angulation.
Translational Injuries: These fractures result from shear forces acting to displace the vertebral
body interiorly, posteriorly or laterally. The nature of these injuries is such that neurologic
injury is extremely common. When these lesions are seen in the thoracic region, the incidence
of complete paraplegia is about 80%. Reduction and stabilization is often difficult for these
highly unstable fractures.