Chapter 50: Traumatic Brain and Spinal Cord Injury

Introduction

Traumatic brain injury (TBI) is the leading cause of death in the early decades of life. The estimated number of deaths is 50,000 with 40% of survivors with disability after the injury.¹ The estimated incidence is 17.5 to 24.6 deaths per 100,000 population.^2,3 Men are more likely to suffer TBI compared to women and the majority of injuries are due to falls.

Injury Types

In TBI injuries are classified as primary and secondary. Primary injury (Table 50–1) happens at the time of impact and secondary injury occurs later due to oxygen deprivation to the brain and the cascade of events set off by ischemia and reperfusion leading to further injury. The target of management focuses more on prevention and treatment of secondary brain injury.

In primary injury, depending upon the mechanism of trauma, fractures of the skull can be open or closed, depressed or nondepressed, and linear or comminuted. Most of these fractures are evident on clinical exam but radiography is required for accurate diagnosis. Both plain skull X-ray and computed tomography (CT) scan can be used for skull fractures, although plain radiologic films are better for linear calvarial fractures tangential to the axial plane. Multislice CT, alternatively, can delineate skull fractures better than plain CT scans. Fractures can result in neurologic deficits related to underlying brain injury, cerebral spinal fluid (CSF) leak (suggesting dural laceration) such as otorrhea or rhinorrhea, pituitary gland shearing injuries, and cranial nerve (CN) injuries. Depending on the fracture location, different CNs can be involved. Temporal bone fractures cause facial or acoustic nerve injuries, anterior fossa basal skull fracture can cause olfactory and optic nerve injuries, and clival fractures can cause abducens nerve injuries. Postauricular ecchymosis (Battle's sign) and periorbital ecchymosis (raccoon's eye) may be seen in basal skull fractures.

Most skull fractures are managed conservatively and prophylactic antibiotic use is controversial. Operative or endovascular treatment is indicated in traumatic aneurysms, carotid-cavernous fistula, CSF fistula, abscess management and for CN decompression.

Depending on the type of injury, different types of hemorrhage can occur in TBI as follows:

1. Epidural: Bleeding between dura and skull, usually from disrupted meningeal artery laceration. The mean age of patients with epidural hemorrhage (EDH) is between 20 and 30 years. About 70% to 90% of EDH is associated with skull fracture and in 36% of cases there was found to be a bleeding artery. Diffuse bone bleeding and venous bleeding (middle meningeal vein, diploic veins and dural venous sinuses) also cause EDH. The most common location is temporal because the bone is relatively thin and more vulnerable to fracture. It appears as a lentiform shape on CT scan and usually stops at the suture lines where the dura is adherent (Figure 50–1).

2. Subdural: Occurs between the dura and the arachnoid space and is caused by disruption of bridging veins due to acceleration, deceleration, and rotational shearing forces. Frontal and parietal convexities are common places for subdural hemorrhage (SDH). The skull suture lines do not limit the bleeding, so on CT scan it can appear as crescent shape, conforming to the brain surface and traversing suture lines. Acute SDH appears hyperdense on CT scan but can have low-attenuation areas representing hyperacute or active hemorrhage. The incidence of SDH after TBI is approximately 11% with most due to motor vehicle accidents (MVAs) in young people and falls in the elderly. Up to 80% of patients with acute SDH may present with a Glasgow Coma Scale (GCS) less than 8 and pupillary abnormalities are seen in 50% of these patients (Figure 50–2).

3. Subarachnoid: Occurs in the space surrounding the brain and blood vessels. Trauma is the most common reason and occurs due to crushed or ruptured small vessels. Bleeding is common on the cortical surface but occasionally in the basal cisterns. Complications of SAH include hydrocephalus, seizures, and cerebral vasospasm, the latter an independent predictor of mortality in severe TBI (Figure 50–3).⁴

4. Intraparenchymal or intracerebral: Bleeding occurs in the parenchyma of the brain. This can vary from contusions to large hematomas in superficial or deep brain areas. Coup injuries are contusions present at the site of impact. For example, an occipital impact may cause frontal contusions. The coup/countercoup phenomenon can also be seen with subdural hematomas, indicating acceleration–deceleration forces. The inferior frontal and temporal areas are most vulnerable to contusion formation due to ridging of the orbital roof and floor of the temporal fossa.⁴

Primary injury causes direct trauma to tissue leading to symptoms. Primary injury to the brain can be due to acceleration, deceleration, or rotational forces. Linear forces cause more superficial grey-matter injuries, while rotational forces cause deeper white-matter injuries leading to diffuse axonal injuries.

Secondary injury occurs due to deprivation of oxygen to the brain, which in turn sets off a cascade of biochemical/molecular events leading to further damage to brain. There are complex cellular and molecular changes including glutamate excitotoxic effects, oxidative stress, metabolic derangements, and inflammatory changes that play a major role in its pathogenesis.⁵ Progressive neuronal necrosis and apoptosis may result.

At the beginning of the injury, huge depolarization of neurons and glial cells lead to influx of calcium into the brain cells. This increases oxygen-free radical reactions producing nitric oxide and excitatory amino acids such as glutamate. Glutamate is believed to promote cell death and dysfunction. Mitochondrial influx of calcium causes swelling and loss of ATP generation. As cellular membranes depend on ATP for their integrity, the inability to produce ATP leads to cell wall disruption and cell death.

Apart from the direct compromise of the cranium and outer layers of brain in TBI, disruption of blood brain barrier (BBB) contributes to loss of cerebral autoregulation. Cerebral autoregulation is the maintenance of cerebral blood flow (CBF) over a wide range of blood pressures of which cerebral perfusion pressure (CPP) is an important component. CPP is defined as the difference between mean arterial pressure (MAP) and intracranial pressure (ICP). In TBI, loss of autoregulation results in the inability to maintain adequate cerebral perfusion at CPP below 50. Loss of the BBB causes vasogenic edema from leaking, dilated blood vessels. In the brain, the edema resulting from cellular swelling is called cytotoxic edema.

According to the Monroe–Kellie principle, the cranium has fixed space and is occupied predominantly by brain tissue, CSF, and blood. Any increase in the volume in the cranium will lead to an increase in ICP, unless it is offset by a decrease in the volume of any one of the contents of the cranium. Therefore, intracranial hemorrhage and brain swelling, which increase intracranial mass, cause ICP increase and further brain damage.

In conclusion, production of oxygen-free radicals and calcium ion influx leads to widespread neuronal injury due to oxidation and enhanced enzymatic activity. Shearing of axons causes neurofilament disruption and increases permeability to calcium ions. Calpains are enzymes, which target the cytoskeleton of axons. Apoptosis ensues during TBI and there is proliferation of glial cells and astrocytes.⁶

Diffuse axonal injury is an acceleration–deceleration and rotational injury leading to shearing and disruption of the white-matter axonal transport system pathways. Both functional and anatomic injury can lead to unconsciousness in a patient not explained by other primary injuries (Figures 50–4a and 50–4b).

Injury Severity

The severity of injury determines the outcome of patients with TBI. The GCS (Table 50–2) is the most common tool used to grade severity of TBI at the time of initial injury. It uses 3 parameters—eye opening, motor response, and verbal response—for injury assessment.

A GCS score of 13 to 15 is considered mild TBI, 9 to 12 is moderate TBI, and 3 to 8 is severe TBI (patient in coma). About 70% to 90% of TBI cases are in the mild category. The GCS scoring system is limited when patients are intubated, aphasic, or aphonic as the verbal and eye variables are hard to measure. Other scales have been developed to account for respiratory or pupillary abnormalities.⁷ These scales are not as widely used as the GCS.

Neuroimaging can also be used to predict injury severity. Presence of midline shifts, Intracerebral hemorrhage (ICH), SAH, and extra-axial hematomas on CT scan are poor prognostic markers. CT scan grading systems have been used for grading injury on initial presentation. The Marshall (Table 50–3) score is an example.^8,9

Imaging

Imaging can provide important information regarding severity of injury. The goal of initial imaging is to rapidly diagnose life-threatening injuries in TBI and to treat them in a timely manner.

CT scan is a widely used modality and often the first one to be used in TBI, as it is fast and sensitive. Newer multi-row-detector CT is even faster and can scan a head within seconds. CT scan provides either 2D or 3D reformatted images. CT scans are useful for diagnosing and differentiating different types of brain hemorrhage, hydrocephalus, and mass effect.

In SDH, as mentioned earlier, the bleed can spread beyond skull suture lines and on CT scan blood can appear as crescent-shaped hyperdense in acute stage. Epidural hematomas appear as a lens-shaped hyperdensity not extending beyond suture margins. Subarachnoid hemorrhage usually conforms to the sulcal space of the brain and CT angiography helps in determining aneurysm or vascular malformation as the cause of the bleed.

If hemorrhagic, contusions can be seen on CT scan and if these small hemorrhages coalesce, they can appear as a hematoma. Small hemorrhages (also called Duret hemorrhages) can be seen in the central pons as a consequence of severe uncal herniation and brainstem compression.

CT angiography is useful for assessing vascular injuries such as aneurysm, pseudoaneurysm, dissection, or thrombus, especially in the face of basilar skull fracture or those crossing a venous sinus. CT perfusion scanning evaluates time to peak (contrast) density, mean transit time, cerebral blood volume, and CBF. Normal CBF is 50 mL/100 g/min (of brain tissue). This modality helps in differentiating between ischemia and infarction, CBF measure 10 to 22 mL/100 g/min and less than 10 mL/100 g/min, respectively.

Magnetic resonance imaging (MRI) evaluates the movement of protons in the tissue when a magnetic field is applied. MR is sensitive in detecting subacute hemorrhage and depending on the appearance of blood on T1 and T2 weighted images, it can detect the timeline of the bleed. Gradient Recalled Echo is a modality of MR that provides information about blood or its degradation products, which appears as a low-intensity signal.

MR angiography is an alternative to CT angiography for characterizing major arterial or venous vascular injuries and can be done with or without contrast. Catheter angiography is the gold standard for diagnosing and treating vascular injuries. Due to long acquisition times, MR imaging may be problematic in critically ill, intubated trauma patients.¹⁰

Management

Prehospital Management

Management of TBI starts with basic resuscitation efforts. Supplemental oxygen to correct hypoxemia is essential. Hypoxemia should be avoided as it leads to an increase in severe disability and mortality.¹¹ If needed, the airway should be secured in the field. Volume resuscitation should begin prior to reaching the hospital. Hypertonic solutions such as hypertonic saline (HS) solutions are anti-inflammatory and immunomodulatory.¹² They can be used in case of suspected high ICP.

There is no role for prophylactic hyperventilation that should only be used as a brief temporizing measure when there are visible signs of herniation such as dilated and unreactive pupils, asymmetric pupils, extensor posturing, or no response or decline of 2 or more points from the baseline GCS.

Hospital Management

General Principles—

Care should be taken to avoid hypoxemia and hypotension at all costs in TBI patients. Patients with oxygen saturations less than 60% have a 50% incidence of mortality or severe disability. Correction of hypotension improves outcomes. Although a systolic blood pressure value cutoff of 90 is normally targeted, the best systolic blood pressure for optimal outcomes is unknown.

Patients with concussion should be managed based on the severity of the concussion. Patients with mild TBI may be discharged home after a brief observation without any follow-up CT scan or imaging. The only exception is EDH as these patients may have a lucid interval and then rapidly progress to coma and death. Normally, analgesics (avoiding opioids) for headache and meclizine or vestibular exercises for dizziness are sufficient, along with appropriate rest. Some may have a seizure that may be mistaken for a more severe brain injury.

For severe TBI, management is based mainly on treatment of ICP/CPP derangements. Both mannitol and HS can be used to lower ICP. If patients have signs of high ICP such as transtentorial herniation or deteriorating mental status, ICP monitoring is advised for goal directed ICP treatment. Mannitol expands plasma volume and improves blood viscosity and improves oxygen delivery often reducing ICP within a few minutes. The osmotic effect starts within a few minutes and may last for a few hours as a gradient is established between plasma and cells. Mannitol can be given as an intravenous infusion or as a bolus in dosages of 0.25 g/kg to 1 g/kg. HS acts by mobilization of water from the brain across the BBB due to its high osmolality. It also improves plasma volume and hence blood flow. As with mannitol, it can also be given as intravenous infusion or bolus. HS comes in different concentrations ranging from 1.5% to 23.4%. As of this writing, there has been no consensus on the dosing and method of administration. Serum osmolality and serum sodium (Na) levels should be periodically checked, with a goal of not exceeding 320 mOsm/kg and Na of 155, respectively; there is potential for acute kidney injury if these levels are exceeded.

Hyperventilation reduces CO₂ and causes cerebral vasoconstriction, decreasing ICP. Hyperventilation is to be avoided in patients with TBI in the first hours (24-48 hours) as the CBF is decreased. It should only be used as a short-term temporizing measure to delay impending herniation.¹³

Currently, the indications for measuring ICP are GCS less than 8, an abnormal CT scan showing evidence of mass effect in the presence of SDH, EDH, or brain swelling. If the CT scan is normal but injury is severe then monitoring is indicated in patients who have 2 or more of the following:

1. Age above 40 years of age

2. Systolic blood pressure below 90

3. Unilateral or bilateral posturing

Measurement of ICP is useful for prognosis and helpful in guiding therapy. Patients in whom ICP responds to treatment do better than patients who fail to respond, while ICP elevations have been associated with poorer outcomes. The currently proposed threshold to initiate treatment for ICP is 20 to 25 mm Hg.

The devices to monitor ICP range from invasive to less invasive. The gold standard and most accurate ICP monitor is an external ventricular drain (EVD) attached to an external strain gauge pressure transducer. Although being most invasive, EVD confers the benefit of CSF drainage to manage ICP. The risk of hemorrhage is about 0.5% and infection is about 8% with these catheters. Internal transducer devices consisting of a fiber-optic cable or strain-gauge wire can be placed in the brain parenchyma. They are largely accurate but unable to be calibrated once inserted in the parenchyma and are subject to varying degrees of drift after several days of monitoring. Parenchymal devices are also helpful in cases where intraventricular drain insertion is unsuccessful or when the ventricles are collapsed around the catheter. Subdural, subarachnoid, or epidural space transducers are fluid-coupled systems placed through a hollow bolt in the cranium but are less accurate and are now rarely used.

CPP, the difference between MAP and ICP, is a primary determinant of CBF (along with cerebrovascular resistance). Patients with TBI should be targeted for CPP between 60 and 70 mm Hg. CPP less than 50 mm Hg should be avoided and aggressively treated as patient outcomes are poor. In the same manner, higher CPP should be avoided, as there is an increased risk of acute lung injury, which is thought to be due to increased fluid and inotrope usage.

Besides monitoring and treating ICP/CPP, there are other parameters that can be monitored. These include brain tissue oxygen tension (PtiO₂), jugular venous oximetry, near infrared spectroscopy, cerebral microdialysis, CBF assessment, and continuous electroencephalography. Among these parameters, PiO₂ is the most commonly used due to wider commercial availability. TBI patients with optimal ICP/CPP may still have cerebral hypoxia in pericontusional areas according to PtiO₂ measurements. Patients who have PtiO₂ less than 15 for increased duration have been shown to have poor outcomes and increased mortality. Use of PtiO₂ along with use of ICP-based treatment/CPP-based treatment may improve outcomes as compared to only ICP-based management/CPP-based management.¹⁴

TBI patients may need sedation or analgesia or both for comfort and pain relief. Analgesics such as morphine, fentanyl, or sufentanil provide pain relief, but have minimal effect on ICP. Sedative agents commonly used include propofol and midazolam. The long-term use of propofol or midazolam does not result in significant differences in ICP, CPP, or MAP. In general, sedation decreases ICP in patients with TBI. Propofol infusion may have some side effects such as hypertriglyceridemia (if patients are on TPN, the lipid should be reduced) and the propofol infusion syndrome (rare but usually fatal), especially if used in doses of more than 4 mg/kg/h for more than 48 hours. Barbiturates such as pentobarbital can be used in patients with elevated ICP. For pentobarbital, the following dosing regimen can be used: loading dose 10 mg/kg over 30 min; 5 mg/kg/h for 3 doses; and maintenance of 1 mg/kg/h (see Table 50–4).

Other medications that are used include ketamine and etomidate. The use of any specific analgesics or sedatives, however, has not shown to improve outcome after TBI.¹⁵

Use of prophylactic hypothermia in patients with TBI has not shown statistically significant mortality benefit,¹³ although hypothermia can be used for the management of high ICP.

Patients with TBI and spinal cord injury are at high risk of venous thromboembolism (VTE). The risk ranges from 5% to 6% in patients with spinal cord injury and 3% to 5% in TBI.¹⁶ Currently, the recommendations are to add mechanical thromboprophylaxis to pharmacologic thromboprophylaxis in patients with TBI. When the decision to employ pharmacologic thromboprophylaxis is made after TBI or spinal injury, intravenous unfractionated heparin is the first choice due to the short half-life and rapid reversibility. Low-molecular-weight heparin (LMWH) is an option if the bleeding risks are assessed to be low, but LMWH is avoided in renal failure due to bioaccumulation. There is no data about the timing of VTE prophylaxis, but the sooner it can be safely started, the better. Our protocol is to commence chemoprophylaxis 24 hours after the last stable (no increase in hemorrhage) CT.

Patients with TBI should be started early on nutritional support. Early nutrition support may reduce infectious complications and mortality. If possible enteral nutrition should be started 24 to 48 hours following admission with the aim of reaching goal within 5-7 days.

Post-traumatic seizures (PTS) can occur in patients with TBI with an incidence of 4% to 25% within the first 7 days of injury. Risk factors for PTS after TBI are as follows: GCS less than 10; epidural, subdural, or intracerebral hematoma; cerebral contusion; depressed skull fracture; penetrating head injury; and seizures within the first 24 hours of injury.

Anticonvulsants can be used to decrease the incidence of early PTS during the first week of TBI. They are not recommended for long-term use to prevent late onset PTS. Phenytoin or valproate can be used for seizure prophylaxis. The use of steroids in TBI is not recommended and may be even harmful.

Surgical Management

Surgical options are considered using the following criteria.

Epidural—If EDH volume is more than 30 cm³, it should be evacuated regardless of the GCS score. Patients with anisocoria and coma should undergo hematoma evacuation as soon as possible. Patients can be managed nonoperatively, if they meet all of the following criteria: EDH volume is less than 30 cm³; thickness is less than 15 mm; midline shift is less than 5 mm; GCS is more than 8; and no focal neurologic deficit.¹⁷

Subdural—Patients with acute traumatic SDH with GCS less than 9 should have ICP monitoring. These patients can be watched nonoperatively if the SDH thickness is less than 10 mm and midline shift is less than 5. If the GCS decreases by 2 points from the time of admission and/or they have asymmetrical or fixed and dilated pupils and/or their ICP rises above 20, they should be taken to operating room (OR). Patients with a hematoma thickness more than 10 mm or midline shift more than 5 mm should be operated upon irrespective of the GCS score. Surgery should be conducted sooner rather than later to improve outcomes.¹⁸

Parenchymal Lesions—Patients with TBI can have either focal or diffuse parenchymal lesions. Diffuse or nonfocal injuries include cerebral edema or diffuse injury. Focal lesions include contusions, ICH, delayed traumatic ICH (DTICH), and infarctions. DTICH is defined as ICH, which was not initially present on admission CT scan but developed subsequently, mostly in the region of contusions.

Patients with parenchymal lesions should be operated on in the following situations: deteriorating neurologic exam as evidenced by a decrease in GCS by 2 points; refractory ICP; signs of mass effect on CT scan such as basal cistern obliteration; GCS of 6 to 8 and fronto-temporal lesion of more than 20 cm³ with midline shift more than 5 mm and/or cisternal obliteration on CT scan; any patient with a lesion volume more than 50 cm³.

Patients who do not meet the aforementioned criteria and who have their ICP controlled medically can be monitored with serial exams and CT scans. Patients who have diffuse cerebral swelling and difficult to control ICP, can undergo decompressive craniectomy. Others may have focal decompression and lesion resection.¹⁹

Traumatic Posterior Fossa Mass Lesions—Patients with lesions in the posterior fossa leading to neurologic dysfunction or deterioration require emergent craniotomy as they have a tendency to worsen rapidly. If CT scans show signs of a mass effect such as distortion or compression of the fourth ventricle or hydrocephalus, suboccipital craniotomy should be performed.²⁰

Depressed Skull Fractures—Patients with depressed skull fractures may have dural penetration, hematoma formation, and wound contamination. The fracture can involve frontal sinuses and also major cosmetic defects. Surgery may be warranted if any of the aforementioned is present. It is also recommended to operate if the bone is depressed the full thickness of the cranium, or if CSF leak or brain parenchyma is present in the open fractures.²¹

Outcomes

Patients after TBI may follow basic functions of emergence of consciousness, recovery of neuropsychologic functions, and return of functional capacity, or they can progress to coma and further deterioration leading to brain death (Table 50–5).²²

Introduction

Traumatic spinal cord injury (TSCI) predominantly affects the young adult (age < 40 years). Annually there are 15 to 40 cases per million. MVA account for the majority (40%-50%) of TSCI. Falls (20%) and violence (14%) account for the rest. The level of injury also determines an individual's functionality. Injuries below T1 are likely to result in independent function, while injury above C6 requires almost complete dependency.²³

Facial fractures and TBI are not associated with an increased risk of TSCI.²⁴ Underlying spinal disease such as osteoporosis, rheumatoid arthritis, or ankylosing spondylitis (AS) can predispose to TSCI.

Spinal Cord Anatomy

The spinal cord extends from the medulla in the cervical region to the lumbosacral area. The spinal canal contains the spinal cord, CSF, epidural fat and vessels, and dura mater. On cross-section, the spinal cord fills about 50% of the spinal canal. The corticospinal tracts originating from cerebral cortex (upper motor neuron) cross over to the contralateral side in the medulla and form the lateral corticospinal tract. The corticospinal tract makes synapsis with the lower motor neurons in ventral spinal cord. The sensory input originates in the dorsal grey-matter neurons. Fibers carrying pain and temperature cross over immediately in the spinal cord and ascend up as lateral spinothalamic tracts. Proprioception and vibratory sensation ascend ipsilaterally in the funiculus gracilis and funiculus cuneatus. At the level of L1-L2, there is the conus medullaris, below which the spinal canal is filled by motor and sensory neurons forming the cauda equina.

Pathophysiology

A number of processes occur during spinal cord injury. Primary injury occurs at the time of direct impact to the spinal cord and secondary injury as a cascade of events after the moment of impact. Primary injury can happen due to extension, flexion, or rotation of the spinal cord. It happens when the above movements occur beyond the normal movement capacity of the vertebral column. Most of the information regarding the pathophysiology is derived from animal models and it is still not known how much intact spinal cord is required for neuronal function.

Proposed mechanisms of TSCI include the following:

1. Vascular abnormalities: Most of the impact is due to disruption of the microvasculature. Larger vessels are rarely injured. As the grey matter is highly metabolic, it is more vulnerable to ischemia and gets injured earlier. Further, there may be loss of autoregulation (the ability to maintain blood flow at various pressures) that can lead to further insults to the spinal cord, if the blood pressure varies due to other injuries. Paradoxically, to maintain perfusion to the spinal cord, maintenance of higher pressures may lead to reperfusion injury.

2. Free radicals: Free radicals such as superoxide are produced due to ischemia and these free radicals react with cell membranes causing lipid peroxidation, damaging cell membranes. Superoxides also damage mitochondrial DNA and associated enzymes, inhibiting sodium-potassium ATPase. All this leads to generation of toxic metabolites such as malonyldialdehyde, leading to cell death.

3. Excitotoxic glutamate and electrolyte imbalance: Glutamate accumulates due to ischemia in cells. It acts on N-methyl-D-aspartate receptors and opens calcium channels. The huge influx of calcium causes activation of lethal enzymes. The loss of ATP also leads to an increase in sodium and water within the cell bodies. It is also thought to lead to cell death especially in axonal and glial components of the white matter.

4. Inflammation: At the site of injury in spinal cord, the inflammatory cells secrete lytic enzymes and cytokines such as TNF-α, interleukins, and interferons. These lead to further cell damage.²⁵

Histologically, the spinal cord develops microhemorrhages within 30 minutes of trauma beginning anteriorly and moving posteriorly over the next 1 hour. These microhemorrhages coalesce and necrosis of the spinal cord extend beyond the initial impact of the injury. Edema begins within 6 hours of injury, maximizing in 48 to 72 hours.²⁶

Neurologic Injury Classification and Clinical Presentation

The American Spinal Injury Association (ASIA) classifies spinal cord injury based on the sensory and motor impairments in the spinal cord after TSCI. It assesses different dermatomes for light touch and pin prick sensation and 10 key muscle movements to establish the grading of TSCI. The maximum score is 100. Any sensory or motor response at the S4-S5 level indicates incomplete spinal cord injury. If both are absent then barring exception of injury at that level, it signifies complete cord paralysis. Preservation of perianal sensation, rectal tone, or great toe flexion means intact S2-S5 and is called sacral sparing. “Spinal shock” is the loss of all muscle tone and reflexes. If the S2-S5 reflexes have not returned within 24 hours, the injury is called complete spinal cord injury (ASIA class A), which is associated with a poor prognosis and poor spinal cord function recovery (Figure 50–5).

Incomplete Spinal Cord Syndromes

Central Cord Syndrome

Patients' central grey matter is affected with sparing of the surrounding outer spinal cord. Clinically, patients are often tetraparetic with sacral sparing; upper extremity function is often affected more than that of the lower extremities.

Anterior Cord Syndrome

Occurs due to injury of the anterior spinal artery affecting the anterior two-thirds of the spinal cord. Patients have both motor and sensory loss (pain, temperature). Proprioception is preserved due to sparing of the posterior spinal cord.

Posterior Cord Syndrome

A rare syndrome where there is loss of proprioception in an otherwise normal functioning spinal cord.

Brown-Sequard Syndrome

Injury to one side of the spinal cord leads to ipsilateral motor function and proprioception loss with contralateral pain and temperature loss. This syndrome usually occurs after penetrating spinal cord injury.²⁶

Prehospital Management

Emergency medical personnel are often the first responders for suspected spinal cord injury. Three percent to 25% of patients can have TSCI after primary trauma during transport or early management. Patients with suspected cervical TSCI should have their spine secured using a rigid cervical collar and immobilization, which may include a backboard with straps. Patients who are awake and fully oriented (without intoxication) with no complaints of neck pain or tenderness and no neurologic deficit or distracting injuries do not need immobilization as is the case with patients with penetrating spinal injury. After initial resuscitation and, if necessary, spine immobilization, patients should be taken to the nearest medical center equipped to handle such injuries. Delay in transport leads to increased costs and less favorable outcomes.²⁷

Hospital Management

Radiography

Once the patient is safely transported to a hospital and undergoes initial resuscitation and clinical examination, the full extent of their spinal injury is assessed by different diagnostic modalities. The following scenarios guide which patient needs radiographic evaluation.

Awake, Asymptomatic Patient—Fully awake, oriented nonintoxicated patients with no neck pain or tenderness, who have no motor or sensory deficit and no major other injuries (which prevent full evaluation), need not have any imaging study.

Awake, Symptomatic Patient—These patients should have good-quality CT scans of the cervical spine. If that is not available, then 3-view cervical spine series (anteroposterior, lateral, and odontoid) should be taken. If there are no radiographic abnormalities and patient is still symptomatic, cervical immobilization can be discontinued in following situations: when the patient is asymptomatic; if dynamic flexion/extension of cervical radiographs are normal; if spine MRI done within 48 hours is normal; at the physician's discretion.

Obtunded Patient—These patients should undergo radiologic imaging. Thin-cut CT with axial, coronal, and sagittal reconstructions, making sure to visualize both bone and soft-tissue imaging, can be used in the decision to remove cervical spine immobilization, especially if such patients are not expected to regain consciousness within 24 hours. Flexion/extension imaging should not be attempted. High clinical suspicion of TSCI should prompt expert clinical consult. MRI in TSCI has an added benefit of providing information regarding soft-tissue/ligamentous injury in the cervical spine.

Management

General Management

Patients with TSCI frequently have respiratory and cardiovascular dysfunction. Patients have reduced vital and inspiratory capacity. They may have frequent hypoxemia, which may exacerbate cord ischemia. Hypotension is frequent after TSCI and may be due to hypovolemia or neurogenic shock. Neurogenic shock is the sudden loss of sympathetic tone as a result of injury to the cervical and upper thoracic spinal cord. Neurogenic shock is manifested by hypotension and bradycardia. Patients who were aggressively managed with close monitoring of vital signs such as blood pressure and oxygen saturation had improved outcomes. Intensive care unit monitoring is recommended in such cases. Hypoxemia should be treated with supplemental oxygen as necessary. The mean arterial blood pressure should be maintained between 85 and 90 mm Hg for the first 7 days of injury. Vasopressors can be used if required for that purpose.²⁷

Pharmacotherapy

Use of steroids such as methylprednisolone is associated with complications such as wound infection, hyperglycemia, and even death and is not recommended according to recent guidelines. GM-1 ganglioside (GM) is a natural compound thought to have antiexcitatory properties and neuronal regeneration. Patients receiving GM initially showed improvement in neurologic recovery, which was subsequently lost. It is, therefore, also not recommended to use in acute TSCI. Other agents studied have not been shown to improve outcomes.²⁷

Nutrition

Patients with TSCI have a catabolic state due to the intense reaction of the body to trauma. This leads to breakdown of muscle mass and loss of proteins, immunosuppression, and loss of gastrointestinal barrier breakdown. It makes intuitive sense to start feeding sooner than later. Although early nutrition in these patients have not shown to improve neurologic outcome, nutritional support within the first 72 hours of injury is recommended.²⁸

Deep Vein Thrombosis and Thromboprophylaxis

Patients with TSCI have an increased incidence of deep vein thrombosis (DVT) (10%-18%) and the majority occur within the first 3 months of injury. Patients with TSCI should be started on both pharmacologic and mechanical DVT thromboprophylaxis. Low dose heparin, low-molecular-weight heparin or oral anticoagulation can be used but not alone. Mechanical thromboprophylaxis including rotating beds, pneumatic compression stockings, or electrical stimulation should be used additionally. Prophylaxis should be continued for 3 months and then discontinued. Inferior vena cava filters are not recommended unless anticoagulation is contraindicated or the patient has developed DVT or pulmonary embolism while receiving pharmacologic prophylaxis. Ultrasound Doppler studies should be used for diagnosis of DVT.²⁹

Management of Specific Injuries

Occipital condyle fractures are rare injuries that should be suspected in patients with high impact trauma, lower CN deficits, and loss of consciousness and neck pain. CT scan is recommended for fracture evaluation. External cervical immobilization is recommended for all types. If bilateral, more rigid immobilization with a halo device is recommended. Surgery (occipitocervical stabilization and fusion) is done in cases with associated atlanto-occipital ligament injury or instability.³⁰

Atlanto-occipital dislocation (AOD) is frequently missed and should be suspected in patients with TBI. The condyle-C1 interval should be measured on CT scan for its diagnosis (mostly in pediatric patients). A lateral cervical radiograph showing basion-axial interval-basion dental interval can also demonstrate this injury. Presence of upper cervical prevertebral soft-tissue swelling raises suspicion of AOD. Patients with these injuries often have or may develop neurologic deficits. These injuries should always be treated surgically with internal fixation and fusion.³¹

Isolated atlas fractures can be diagnosed with plain radiography (open mouth radiograph) or CT. They can be of 3 types, anterior or posterior arch fractures (Landell type 1), burst fractures (Landell type 2), and lateral mass fractures (Landell type 3) (Figures 50–6a and 50–6b).

MRI can assess whether the transverse atlantal ligament is intact or not, which will determine if the fracture is stable or not. In general, type 1 and type 3 fractures are considered stable and may be treated with collar or halo. Type 2 fractures may need surgical stabilization and fusion.³²

C2 dens fracture: Forceful flexion-extension of the head in the sagittal plane may result in fracture of the odontoid process (dens). Three types of fractures are identified; type 1 fracture occurs above the transverse ligament and is stable. Type 2 fracture results in complete disruption of the base of dens and is unstable, requiring surgical management. Type 2 has been further divided into types 2A, 2B, and 2C depending on whether it is nondisplaced, displaced amenable to anterior fixation, and displaced or communicated amenable to posterior fixation/fusion, respectively. Type 3 fractures involve the extension of fracture through the body of C2 and are considered mechanically unstable.³³

Subaxial cervical spinal injuries can include burst fractures, unilateral or bilateral facet dislocation, and other bony injuries. Patients with these injuries can be managed with external or internal immobilization/fixation. The goal is to restore alignment and decompress the spinal canal. Both anterior and posterior approaches are good surgical options. For patients with incomplete spinal cord injuries and canal compromise, surgical decompression within 24 hours of injury is recommended.³⁴ Patients who have AS should undergo thorough investigation with CT scan or MRI, even in minor trauma. AS patients requiring surgery should have either posterior fixation or combined anterior and posterior fixation but not stand-alone anterior fixation due to high failure rates.³⁵

Acute traumatic central cord syndrome (CCS) is a clinical entity that is suspected when upper extremities are weaker than lower extremities and is most commonly associated with cervical spondylotic disease or ossification of the posterior longitudinal ligament. Patients to be diagnosed with CCS should have 10 points lower on the ASIA classification motor score in the upper extremities as compared to lower extremities. CCS is thought to be due to disruption of the corticospinal tract. It can be associated with other injuries such as fractures and dislocations. Surgical decompression is considered advisable in many circumstances.³⁶

Vertebral artery injuries (VAI) (nonpenetrating cervical trauma) are usually seen in patients with fractures through the foramen transversarium, facet fracture-dislocation, or vertebral subluxation. The modified Denver screening criteria in patients with blunt cervicovertebral injury should prompt VAI evaluation. CT angiography is a good, quick screening tool (Figures 50–7a and 50–7b).

Angiography or MRI may also be used for diagnosis. Symptomatic patients may be treated with antiplatelet therapy, depending on their risk-benefit ratio. Asymptomatic VAI need not be treated.³⁷