Initial Evaluation and Management of CNS Injury: The Problem, Relevant Anatomy/Pathophysiology, Management Principles

Upon arrival at the emergency department, the same protocols of transfer and patient handling should be followed carefully. Triaging the patient upon arrival is an integral part of the initial assessment, especially in a multicasualty situation. Head injuries can be classified according to the GCS score as minor (GCS score ≥14), moderate (GCS score ≤13 and ≥9), and severe (GCS score ≤8). All patients with severe head injuries should arrive in the emergency department intubated and ventilated. If a patient with severe or moderate head injury arrives with an unprotected airway, institute immediate measures for transfer to the resuscitation area. A patient whose condition is deteriorating should also receive care in the resuscitation area.

ATLS protocols should be followed as for any trauma patient. Airway management and support of breathing with protection of the whole spine should be instituted or continued. Maintenance of adequate mean BP in order to sustain an adequate CPP is also important. No consensus has been reached on the type of fluids that should be administered to such patients, but the majority of health care professionals give colloids initially. ^[10]

Examination of a patient with a head injury should be as thorough as for any other patient and should take into consideration the clinical state of the patient and the particular aspects of the accident. ^[11] Look especially for features indicating skull base fracture, as follows:

• Raccoon eyes

• Battle sign (after 8-12 h)

• CSF rhinorrhea or otorrhea

• Hemotympanum

With facial fractures, auscultate the carotids for bruit, indicating possible carotid dissection.

A full neurological examination should follow. Look especially for the following:

• Visual acuity in an alert patient

• Pupillary light reflexes, both direct and consensual

• Retinal detachment or hemorrhages or papilledema

• Spinal tenderness and, if the patient is cooperative, limb movements

• Motor weaknesses, if possible, and gross sensory deficits

• Reflexes, plantar response

Do not forget to reassess patients at frequent intervals because their neurological condition can change rapidly.

Minor head injuries

After taking the history and performing the initial examination of patients with minor head injuries (ie, GCS score ≥14), assess whether a skull radiograph is indicated. Indications for skull radiographs are as follows:

• History of loss of consciousness or amnesia

• Scalp laceration (to bone or > 5 cm)

• Violent mechanism of injury

• Persisting headache and/or vomiting

• Significant maxillofacial injuries

If the radiographic findings are unremarkable, the patient can be discharged home with head injury instructions. However, the patient should be admitted if any difficulties in assessment occur, as in the following:

• Possible drug or alcohol use

• Epilepsy

• Attempted suicide

• Preexisting neurological conditions (eg, Parkinson disease, Alzheimer disease)

• Patient treated with warfarin or who has coagulation disorder

• Lack of responsible adult to supervise

• Any uncertainty in diagnosis

If the x-ray film reveals CNS injury, as shown in the images below, admit the patient to the hospital and, ideally, have a CT scan of the head performed.

The likelihood of intracranial pathology after head injury increases considerably with impairment of consciousness and the presence of a skull fracture. See the image below.

Moderate head injuries

All patients with moderate head injury (GCS score ≤13 and ≥9) should undergo CT scan of the head and should be admitted to the hospital. If the CT scan findings reveal CNS injury, referral to the neurosurgical unit is imperative. If the CT scan findings are unremarkable, the patient must be admitted for observation. A patient with a moderate head injury and normal CT scan findings should improve within hours of admission. If no improvement is noticed, the CT scan should be repeated.

When admitting patients with minor or moderate head injuries without intracranial pathology, the following guidelines apply:

• Neurological observations should be performed every 2 hours. The patient should take nothing by mouth until alert.

• Start intravenous administration of 0.9% sodium chloride solution (plus 20 mmol of potassium chloride if the patient is vomiting).

• Mild analgesics (eg, paracetamol, codeine phosphate) and antiemetics can be prescribed if necessary. Avoid phenothiazines because they can lower the seizure threshold.

Severe head injuries

After stabilization, patients with severe head injuries (GCS score ≤8) should undergo a CT scan of the head. Neurosurgical referral is imperative for management of intracranial pathology and ICP. Take immediate measures to lower the ICP. If the CT scan findings indicate diffuse brain injury and/or intracranial pathology, simple measures can be taken to lower the ICP until transfer to the neurosurgical unit, as follows ^[11] :

• The head should be elevated (30-45°). Keep the neck straight, and avoid constriction of venous return.

• Maintain normovolemia and normal BP (mean BP >90 mm Hg).

• Ventilate to normocapnia and avoid hypocapnia (PCO₂ >3.5 kPa).

• Use light sedation and analgesia (eg, codeine phosphate at 30-60 mg IM q4h).

• Consider administration of mannitol (1 g/kg IV immediately), but contact the neurosurgical registrar first.

Emergency surgical treatment

Emergency surgical treatment in the emergency department should not be necessary in areas of well-established neurosurgical care. However, if immediate neurosurgical care is not available, making exploratory burr holes may be necessary. CT scan facilities are not likely to be available; therefore, clinical acumen is very important under these circumstances. Burr holes are made primarily for diagnostic purposes because most acute hematomas are too congealed to be removed through the hole and the most common intracranial hematoma is subdural rather than extradural. However, making burr holes can help achieve modest decompression, and ideally, the physician should be prepared to proceed to a full trauma craniotomy. In any case, no such procedure should be undertaken unless it has been authorized by the referring neurosurgical unit.

Criteria for exploratory burr holes are as follows:

• No CT scan facilities are immediately available.

• No neurosurgical referral center is immediately available.

• The patient is deteriorating rapidly, with one pupil fixed and dilated, and the patient does not respond to mannitol.

• The patient is dying from brain stem herniation.

Place burr holes along the possible line of a trauma craniotomy and on the side of the dilating pupil or the pupil that dilated first (if known). Start just in front of the ear (1-1.5 cm) and above the zygomatic arch. If no hematoma is encountered, consider opening the dura, especially if a bluish discoloration suggests a subdural hematoma.

Spinal injuries

The vast majority (>70% in adults and >60% in children) of spinal injuries involve the cervical spine, the most mobile part of the vertebral column. In children, the upper cervical spine (between C2 and the occiput) is more commonly injured, while in adults, the middle-to-lower cervical spine is the most common casualty. Because of the likelihood of spinal injury, any patient who incurs trauma should be treated as having potential spinal injury until radiographic and clinical evidence indicates otherwise. Immediate immobilization of the cervical spine in the appropriate collar and immediate immobilization of the rest of the spine on a spinal board is appropriate.

Imaging of the spine should include at least plain x-ray films of the cervical spine (anteroposterior and lateral, a peg view, and with the C7-T1 junction visible). When a spinal injury is strongly suggested, that is, due to the mode of injury or because of indicative findings on the x-ray film, a CT scan of the spine should be performed next.

Management

Upon arrival at the emergency department, the patient should have been placed on a protective spinal board. Full clinical examination and assessment should follow initial stabilization. Beware of neck extension if intubation is needed. Check palpable steps over the whole spine during the secondary survey. Check for clinical signs of cord injury. Do not forget the bladder (catheterization may be necessary). Be aware of the possibility of spinal shock, that is, hypotension due to loss of sympathetic tone that is associated with bradycardia. Fluid administration to correct imbalances, with or without added pressor agents, is necessary to maintain a mean arterial pressure greater than 90 mm Hg (dopamine is the agent of choice), but do not overload because this can lead to heart failure. Also be aware that lack of tachycardia can mask a true fluid loss.

Plain lateral x-ray films of the cervical spine, as shown below, should be the least of the investigations performed. Examine for alignment, soft tissue swelling, steps, or fractures. If clinical or radiological evidence of a spinal injury is present, the immediate management of the patient following stabilization includes analgesia, full imaging, and consultation with spinal surgeons.

An absence of radiological evidence confirming a spinal injury should not lead to a relaxation of precautions until the patient is lucid and cooperative enough to move all limbs and report any areas of excessive tenderness. Spinal cord injury without radiographic abnormality (ie, SCIWORA) occurs in approximately 2-4% of spinal injuries.

Common types of injury

• Atlantooccipital dislocation: These are almost universally fatal, but prompt recognition and stabilization can be very important.

• Atlas fractures: Depending on the type, most are treated conservatively.

• Axis fractures: These are difficult to treat due to high nonunion rates, but most require some form of internal fixation.

• C3-T1 injuries: Early reduction and alignment are important. Decompression of the spinal cord is advocated for patients with incomplete injuries.

Use of steroids in spinal cord injury (methylprednisolone)

The National Acute Spinal Cord Injury Studies (NASCIS) I and II published in the 1990s demonstrated significant benefit in administering high doses of methylprednisolone early after a spinal cord injury (within 8 h). The dose is 30 mg/kg IV over 15 minutes, followed by 5.4 mg/kg/h via continuous intravenous infusion over 24 hours.

The NASCIS I and II trials have received significant criticism with regards to both their design and the possible benefit-to-risk ratio. Most experts and authorities in spinal injury would not advise the routine use of steroids in spinal cord injury. The recent evidence from the CRASH trial in head injuries further reinforced this view. Management of spinal injuries, however, should always be guided by local guidelines.

Steroids are not routinely recommended for severe head injury patients. Initial enthusiasm in the 1960s, generated by positive laboratory study findings, never translated into meaningful improvement in outcomes. Consequently, guidelines do not recommend the use of steroids in severe head injury patients. ^[7] However, the validity of the evidence used to reach these conclusions has been questioned, ^[12] and the use of corticosteroids in all grades of severity of head injury has recently been explored in a large, randomized international trial (ie, the CRASH trial) supported by the Medical Research Council. This study was halted 6 months early because no specific benefit was noted in patients receiving steroids, while a slight increase in comorbidity was noted. ^[12]

Fluid replacement

Intravenous fluid replacement is an integral part in the resuscitation process. The age of the patient and the presence of other injuries that can result in severe hypovolemia, such as vascular injuries, intra-abdominal hemorrhages, or pelvic fractures, are of vital importance. Special care should also be taken in the presence of severe spinal injury (paraplegia or tetraplegia), which can result in spinal shock due to lack of sympathetic outflow. This can last 8-12 hours and is manifested with severe hypotension not associated with tachycardia, sweating, or peripheral vasoconstriction. Attempting to support the blood pressure with large volumes of fluids can lead to significant problems when the spinal shock recedes and sympathetic tone returns. The excessive fluid load can result in heart failure and, in the case of brain injury, aggravate brain edema.

There is no evidence on the best replacement fluid for patients with brain injury. Published guidelines do not support any specific fluid, but isotonic crystalloid solutions (eg, sodium chloride) are generally recommended. Hypotonic solutions (eg, Ringers lactate or dextrose/saline) should be avoided though, ^[13] except in children, in whom dextrose/saline is routinely used. In cases of severe hypovolemia due to trauma, rapid volume replacement with colloids or human albumin is not contraindicated. In general, fluid resuscitation should be guided by the coexistent trauma and aim to maintain a brain injury patient in a euvolemic state. The concept of “running patients dry” is considered obsolete. ^[14] Such an approach can compromise the cerebral blood flow and adversely affect outcome.

There is an ongoing controversy on the value of early mannitol administration in suspected brain injury. ^[15] The original perception that mannitol works by “dehydrating” the brain and thus reducing the intracranial pressure (ICP) has been refuted and it is now known that its main effect is rheologic. By decreasing blood viscosity, mannitol increases cerebral blood flow, resulting in partial reactive vasoconstriction of arterioles and reduction in ICP. Even when it does not achieve any significant ICP reduction, mannitol can still increase cerebral blood flow by almost 30%. ^[16] Moreover, the timing and rate of mannitol administration as well as the specific indications for its administration have never been subjected to a randomized trial.

In the United States, all severe head injury patients with abnormal pupillary signs routinely receive 100 mL of mannitol 20% upon arrival in the emergency department. Traditionally most neurosurgeons in the United Kingdom would recommend administering 1 g/kg mannitol 20% as a bolus infusion. The published guidelines also indicate that plasma osmolality should be kept at less than 320 mOsm. In the acute situation, this is less of a concern, but it should always be kept in mind, as occasionally these patients remain in the resuscitation area for long periods. If mannitol is administered to a patient, he or she should be catheterized.

It is likely, however, that much higher doses than those recommended above are actually required. Recent evidence from 2 randomized trials from the same group ^{[17, 18]} has demonstrated significantly improved recovery rates of severe head injury patients who received upon arrival and before CT scanning an initial bolus infusion of mannitol 20% at 0.6-0.7 g/kg. After CT scanning confirmed the presence of acute subdural hematoma or intracerebral contusions, those patients who had normal pupils received a further 0.6-0.7 g/kg, while those with unequal pupils received a further 1-1.4 g/kg. In both groups of patients, concomitant administration of saline was used to correct the diuretic effect of the mannitol and maintain euvolemia. Although not all questions have been resolved by these studies, they support the early and aggressive use of mannitol in brain injury patients.

Hypertonic solutions have recently gained popularity in the treatment of trauma patients. ^[19] There is some evidence that hypertonic saline can be used as an alternative to mannitol, especially in children. ^[20] Infusions of 3% sodium chloride solution have been shown to reduce ICP and improve outcomes in children ^[21] but not in adults. ^[22] In a recent meta-analysis ^[23] of 5 randomized clinical trials, hypertonic sodium solutions were found to be more effective than mannitol in controlling episodes of elevated ICP. No evidence to support better clinical outcome is currently available, and a large randomized trial is warranted.

Anticonvulsant therapy

Anticonvulsants are also not recommended routinely in brain injury patients who are not having seizures. ^[24] Immediate (on impact) seizure activity is commonly reported, especially in children. It can last from a few seconds to a minute and is not considered true epilepsy. ^[25] It is now thought to be a brief functional decerebration that results from loss of cortical inhibition. The recovery phase is usually brief and the risk of later seizures is not increased. No anticonvulsants are indicated in this case.

Certain types of severe head injury can result in an increased risk (>60%) of early epilepsy (first 7 d), as follows:

• Acute subdural

• Penetrating injuries

• Cortical contusions

• History of significant alcohol abuse

• Epilepsy in the first 24 hours

In these patients, randomized control trials have demonstrated benefit from prophylactic administration of anticonvulsants (phenytoin or carbamazepine) for 1 week. ^{[24, 26]} After this period, if no further seizures have occurred, anticonvulsants should be tapered off, as there is no significant advantage in continuing and late epilepsy is not prevented. ^[26]

If the patient is having seizures upon or immediately after arrival, anticonvulsants should be administered after immediate control with diazepam or lorazepam (preferably) has been achieved. A recent meta-analysis of 47 controlled trials on seizure prevention supported the use of phenytoin as the agent of choice in traumatic brain injury. ^[27] It is also very important to realize that seizures adversely compromise the oxygenation of any severe head injury patient. Immediate airway support and early control is, therefore, imperative.

It is crucial to achieve and maintain adequate plasma levels of anticonvulsants in a brain injury patient. For phenytoin, an intravenous loading dose of 18 mg/kg is recommended for adults and 20 mg/kg for children. Slow administration (over 30 min), preferably with an intravenous pump, is recommended. It is also important to remember, however, that after control of seizures has been macroscopically achieved, an unusually prolonged postictal state may actually be poorly controlled seizures (ie, status epilepticus). If adequate anticonvulsants have been administered (ideally, if electroencephalography has excluded status epilepticus), then other causes should be explored.

Hyperoxia and brain injury

Some emerging evidence indicates that the early application of high inspired oxygen concentrations may be of benefit in adult brain injury. ^[13] Management of severe head injuries with more emphasis in brain tissue oxygen monitoring has also demonstrated some encouraging results, which may have the same physiological basis. ^[14]