Tuesday, February 1, 2022

Spinal Cord Injury, Traumatic Case File

Posted By: Medical Group - 2/01/2022 Post Author : Medical Group Post Date : Tuesday, February 1, 2022 Post Time : 2/01/2022
Spinal Cord Injury, Traumatic Case File
Eugene C. Toy, MD, Ericka Simpson, MD, Pedro Mancias, MD, Erin E. Furr-Stimming, MD

CASE 7
A 13-year-old right-handed adolescent boy is brought to the emergency room (ER) following a moderate speed motor vehicle accident (MVA). The patient was an unrestrained front-seat passenger but was not ejected during the head-on collision (~ 35-40 mph). According to the paramedics accompanying the patient, there was significant front-end damage to the car, and the patient’s head appeared to have impacted the windshield. On arrival at the scene, approximately 4 minutes after the accident, the patient was found to be unresponsive with flaccid muscle tone, bradycardia, and inadequate respiratory effort. His cervical spine was immobilized, he was intubated to maintain adequate ventilation, and he was transported to the ER secured to a rigid backboard. On examination, he is afebrile with irregular respiratory effort, requiring mechanical ventilator support. Noxious stimulation of his face produces some grimacing, but there is no response to such stimulation of the extremities. There is a large contusion over his forehead but no other external signs of trauma. On neurologic examination, his pupils are equally reactive to light, and he has a brisk corneal reflex bilaterally, but there is no gag reflex. His muscle tone is significantly decreased in all four extremities, and he is areflexic throughout, including his superficial abdominal reflexes. His rectal sphincter is patulous, and there is no anal wink. According to the patient’s father, the child was healthy and neurodevelopmentally normal prior to this accident. He is on no medications and has no known allergies.

 What is the most likely diagnosis?
 What is the next diagnostic step?
 What is the next step in therapy?


ANSWERS TO CASE 7:
Spinal Cord Injury, Traumatic                                        

Summary: This 13-year-old adolescent boy presents to the ER significantly obtunded with flaccid quadriparesis and agonal respirations following a head-on MVA in which he was an unrestrained passenger. He is now intubated, and his cervical spine is immobilized. He was previously healthy and is on no medications.
  • Most likely diagnosis: High cervical spine injury and traumatic brain injury (TBI).
  • Next diagnostic step: Magnetic resonance imaging (MRI) of the brain and spine.
  • Next step in therapy: Maintain oxygenation and perfusion pressure in a critical care setting.

ANALYSIS
Objectives
  1. Understand the initial management of acute spinal cord injury.
  2. Know the different types of spinal cord syndromes.
  3. Describe the usefulness of different imaging modalities for evaluating spinal cord injury and the importance of the patient’s age.
  4. Be aware of the role of steroids, surgical intervention, and rehabilitation in spinal cord injury.

Considerations

This 13-year-old adolescent boy brought to the ER following a significant MVA has findings worrisome for traumatic injury to both his brain and spinal cord. This case focuses on considerations for evaluating and managing the latter. Significant findings on the patient’s examination include flaccid quadriparesis (suggesting interruption of the corticospinal tracts in the upper cervical region), failure to grimace or otherwise respond to painful stimulation of any of his four extremities (suggesting interruption of ascending sensory tracts in the upper cervical region), preservation of pupillary light reflex and corneal reflex (indicating that the brainstem is intact above the pontomedullary junction), and poor respiratory function and absence of gag (indicative of injury to the upper cervical cord as well as the lower brainstem). These findings point to a complete or nearly complete acute spinal cord injury at a high cervical level, with ascending spinal shock also affecting the lower brainstem.


APPROACH TO:
Traumatic Spinal Cord Injury                                        

EPIDEMIOLOGY

There are approximately 40 new cases per million per year of traumatic spinal cord injury in the United States. The peak age-related incidence occurs between 15 and 25 years and is more common in males than females, with a ratio of 3 to 4:1. Approximately 5% of all spinal cord injuries occur between birth and 16 years, and these pediatric patients require special consideration discussed as follows. Neonatal (birth-related) spinal cord injury complicates approximately 1 of every 60,000 births and carries a 50% mortality rate. In childhood, the most common causes of spinal cord injury prior to 10 years of age are MVAs and falls, whereas in individuals older than 10 years, MVAs and sports-related injuries are the most common. With regard to MVAs, children younger than 13 years should be restrained passengers in the backseat only to avoid potential injury from air bag deployment. Younger children can sustain
significant and often fatal cervical spinal cord injuries from passenger side air bags. The rate of nontraumatic spinal cord injury is at least threefold higher than traumatic cases, although the epidemiologic data are not as complete in this regard.


TYPES OF SPINAL CORD INJURIES

Spinal cord injuries can be complete or incomplete. Complete spinal cord injuries present with complete loss of sensation and motor strength below the level of injury. Patients can also present with incomplete lesions of the spinal cord. For example, hemisection produces the classic Brown-Séquard syndrome with ipsilateral loss of motor function, fine touch, and vibration sensations starting at the level of the injury, but contralateral loss of pain and temperature one or two levels below the level of the lesion. This is a result of fibers in the dorsal column remaining ipsilateral to the brainstem while fibers in the spinothalamic tract synapse and cross within one or two spinal levels then travel contralaterally. Trauma is the most common cause of the Brown-Séquard syndrome, which rarely presents as a pure unilateral injury. Anterior cord syndrome is usually caused by either a traumatic or a vascular insult to the anterior two-thirds of the spinal cord. This results in a bilateral loss of spinothalamic tract function (loss of pain and temperature sensations) as well as bilateral loss of corticospinal tracts function (weakness) with preservation of dorsal column function, such as fine touch, proprioception, and vibration.

Central cord syndrome is caused by injury to the structures around the spinal central canal. Although this can occur acutely with trauma (particularly flexion-extension injury in athletes and patients with cervical spondylosis), it more commonly occurs with chronic processes such as intra-axial neoplasms or dilation of the central canal (referred to as syringomyelia). Clinically, this typically presents with a bilateral loss of pain and temperature sensation in the upper extremities (spinothalamic tract function) as well as weakness in the same distribution (corticospinal tract function) but with preservation of fine touch (dorsal column). Anatomically, this is because the spinothalamic tract decussates immediately anterior to the central canal. Also, motor fibers traveling to the legs (fasciculus gracilis) tend to run more laterally in the spinal cord than fibers supplying the arms (fasciculus cuneatus) and are therefore relatively spared.


INITIAL MANAGEMENT OF SPINAL CORD INJURIES
Management of acute spinal cord injury follows the basic principle of ABCD: airway, breathing, circulation, and disability. Once the airway is secured and the patient is hemodynamically stable, the management is focused on preventing additional damage and disability. This begins in the field, with the first responders immobilizing the spine in a neutral position using rigid collars and backboards. Further injury can occur because of impingement of bony matter onto the cord, excessive movement of the cord as a result of spinal instability, compression of the cord by hemorrhage, or cord ischemia caused by hypotension. Given the disproportionately large head size in children relative to the trunk, it is often necessary to elevate the torso to achieve a neutral position for the neck.

In the ER, once stabilization of airway, breathing, and circulation has been confirmed, a neurologic examination is performed to assess the clinical level of injury. In this patient, there are several findings pointing to an extensive and likely complete high cervical spinal cord injury. The complete loss of motor and sensory function of the upper and lower extremities, respiratory difficulties, and preservation of cranial nerve reflexes are consistent with this localization (because the upper extremity is innervated by spinal nerves from C5 to T1 and the phrenic nerve arises from C3 to C5).

Superficial abdominal reflexes are elicited by scratching the skin in all four quadrants around the umbilicus and watching for contraction of the underlying abdominal musculature. Stimulating above the umbilicus tests spinal levels T8 to T10, whereas stimulating below the umbilicus tests approximately T10 to T12. In addition to loss of motor and sensory function below the level of the lesion, spinal cord transection also results in loss of autonomic function, which can produce spinal shock. The acute loss of descending sympathetic tone produces decreased systemic vascular resistance, which can result in hypotension. If vagal output is intact, its unopposed influence can further lower vascular resistance and result in a paradoxical bradycardia. In the context of spinal shock, aggressive fluid resuscitation is necessary to maintain perfusion pressure and prevent cord ischemia. The complete absence of deep tendon reflexes, superficial cutaneous reflexes, and rectal tone also suggests the presence of spinal shock. It is important to remember that, as the inflammatory response to the injury develops and edema occurs, the apparent clinical level of the injury can rise to higher spinal levels or into the brainstem.

Once the patient has been stabilized and an expedited neurologic examination has been performed, the appropriate imaging modality must be selected. In blunt trauma of patients older than 9 years, no spine imaging is necessary if they are alert, conversant, nonintoxicated, and have a normal neurologic examination without cervical tenderness. If patients are younger than 9 years, imaging is recommended and should be interpreted by a radiologist accustomed to reviewing spine studies of young children. Bony structures can also be well imaged using a helical computed tomography (CT) scanner. Visualizing the spinal cord itself is best accomplished using an MRI. Children younger than 9 years can develop spinal cord injury without radiographic abnormality (SCIWORA). Given the greater mobility and flexibility of the pediatric spine relative to that found in adults, bony elements can be displaced into the spinal cord and then revert to their normal position. When this occurs, the patient will clinically appear to have a traumatic myelopathy (spinal cord injury) on neurologic examination, but no bony or ligamentous damage is seen with plain films or CT scans. An MRI, however, can demonstrate damage to the spinal ligaments, injury to the spinal cord, or both.


THE ROLE OF SURGERY AND STEROIDS

The principal goal in managing acute spinal cord injury is to prevent secondary injury. Although the initial traumatic event can produce major damage, subsequent inflammation, edema, and ischemia can lead to significant worsening of this primary insult. Surgical intervention to stabilize the spine, remove bony matter, evacuate hemorrhage, and decompress the spinal canal has been evaluated, particularly in adult patients, and it remains controversial with little data available in children. Animal work has supported the use of early decompression within the first 8 hours in order to improve outcome. There are no evidence-based guidelines at this point. Significant compromise of the spinal canal and fixation of a very unstable spine that is not amenable to closed reduction are considered the principal indications for early surgery in traumatic spinal cord injury at this point.

Because inflammation plays a major role in mediating secondary injury, administration of corticosteroids has been studied in acute spinal cord injury. Certainly, the benefits of steroids in subacute spinal cord injury, such as cord compression by tumor, are well established. However, this subject remains a matter of controversy, and limited evidence indicates that intravenous methylprednisolone can lead to improvements in motor scores for adult patients with acute spinal cord injury if administered within 8 hours of injury and continued for 24 to 48 hours. Continuing steroid therapy beyond this period has not been shown to improve outcomes and may increase side effects such as infections and wound dehiscence. The American Association of Neurological Surgeons and Congress of Neurological Surgeons currently do not recommend using steroid therapy with the current level of evidence and list it as a treatment option in adults with closed spinal cord injury rather than a treatment recommendation. Steroid therapy has been shown to worsen outcomes in TBI and in patients with polytrauma and penetrating injuries, and therefore it is contraindicated in these cases.


MEDICAL COMPLICATIONS OF SPINAL CORD INJURY

Spinal cord injury can be complicated by a host of medical issues during hospitalization. This is due to a combination of sympathetic dysregulation, pain, and immobility. Because there are no widely available therapies for spinal cord injury, supportive therapy during the acute phase and mitigating medical complications is of utmost importance. Pressure sores can develop over the course of hours and have serious mortality and morbidity implications. To avoid pressure sores, backboards should be used only for transport and discontinued as soon as the spine is stabilized. Frequent turning and rolling every 2 to 3 hours should follow.

Patients can develop urinary distention and loss of urinary control, leading to urinary stasis and overflow incontinence. This should be avoided by inserting an indwelling Foley catheter in the acute period followed by intermittent catheterization thereafter. Gastrointestinal complications include stress ulcers and paralytic ileus. Prophylactic proton pump inhibitors or H2-receptor blockers can lower the risk of stress ulcers. Prophylactic stool softeners and monitoring stool output are important as well. Patients may have sympathetic dysregulation manifesting as bradycardia, hypotension, and hypo- or hyperthermia. These should be monitored closely and treated as needed with intravenous (IV) fluids, vasopressors, cooling or warming blankets, and antipyretic agents as needed.


Long-Term Care and Rehabilitation

Maximizing long-term neurologic outcome for survivors of acute spinal cord injury requires an intensive team-based approach to rehabilitation. Important issues to be addressed include development of an appropriate bowel and bladder care program, maintenance of skin integrity, and management of persistent autonomic dysreflexia. As spinal shock subsides and spasticity begins to develop over the course of 1 to 6 weeks, prevention of contractures with preservation of functional position of the joints becomes crucial. Psychological and cognitive rehabilitation is also vital, both in terms of adjusting to life after the injury and dealing with concurrent head trauma. In general, patients will spend a significant period of time in an inpatient rehabilitation setting, followed by a transitional outpatient program. Even after this period, however, the patient should continue to be evaluated by a physical medicine and rehabilitation specialist at least yearly to maximize adaptation and function.


COMPREHENSION QUESTIONS

7.1 Currently, which of the following is the best strategy for preventing further damage in patients with acute spinal cord injury?
A. High-dose corticosteroids
B. Immediate exploratory surgery
C. Maintenance of oxygenation and spinal cord perfusion
D. Intravenous diuretic therapy

7.2 A patient is brought to the ER following an MVA. On examination, he or she has weakness of the left arm and leg and loss of fine touch on the left with loss of pain and temperature sensation on the right. This clinical picture is most consistent with which of the following?
A. A complete cord syndrome
B. A central cord syndrome
C. An anterior spinal cord syndrome
D. A left spinal cord hemisection syndrome
E. A right spinal cord hemisection syndrome

7.3 A 5-year-old boy is brought to the ER following a fall from approximately 4 ft. He is now alert, moving all his extremities, and responding to touch on all four extremities, but he is somewhat irritable and has a large laceration on his chin. Which of the following is true regarding evaluating the child’s spine?
A. As he is moving all extremities and appears to have intact sensation, no further spinal evaluation needs to be performed.
B. Given the child’s age, spinal imaging should be performed.
C. Imaging should only be performed if cervical spine tenderness can be demonstrated.
D. Spinal imaging should be arranged as an outpatient.


ANSWERS

7.1 C. The most important aspect of initial management is to avoid spinal cord ischemia.

7.2 D. This patient has the classic findings of a left cord hemisection (Brown-Séquard) syndrome with ipsilateral weakness, ipsilateral loss of fine touch, and contralateral loss of pain, and temperature sensation.

7.3 B. Children younger than 9 years who experience blunt trauma or falls should have their spine imaged because clinical criteria can still miss injuries. Even if this child were older, the presence of a distracting injury (the large chin laceration) can mask cervical tenderness.

    CLINICAL PEARLS    

▶ After ensuring hemodynamic stability by securing airway, breathing, and circulation, the most important step in the emergency care of patients with spinal cord injury is stabilization of the spine. The next step is to maintain spinal cord perfusion pressure.
▶ The most common cause of spinal cord injury in the pediatric and adult population is MVA.
▶ Traumatic brain injury commonly accompanies traumatic spinal cord injury, including hemorrhage, ischemia, or diffuse axonal injury.
▶ Superficial abdominal reflexes are elicited by scratching the skin in all four quadrants around the umbilicus and watching for contraction of the underlying abdominal musculature. Stimulating above the umbilicus tests spinal levels T8 to T10, whereas stimulating below the umbilicus tests approximately T10 to T12.
▶ Medical complications of spinal cord injury include sympathetic instability, urinary retention, stress ulcers, and paralytic ileus. These complications can lead to significant morbidity and mortality if not monitored closely.


REFERENCES

Bracken MB. Steroids for acute spinal cord injury. Cochrane database Syst Rev. 2012;1:CD001046. 

Congress of Neurological Surgeons. Management of pediatric cervical spine and spinal cord injuries. Neurosurgery. 2002;50(suppl 3):S85-S99. 

Devivo MJ. Epidemiology of traumatic spinal cord injury: trends and future implications. Spinal Cord. 2012;50(5):365-372. 

Eleraky M, Theodore N, Adams M, Rekate HL, Sonntag VK. Pediatric cervical spine injuries: report of 102 cases and review of the literature. J Neurosurg. 2000;92(suppl 1):12-17. 

Heary RF, Vaccaro AR, Mesa JJ, et al. Steroids and gunshot wounds to the spine. Neurosurgery. 1997; 41(3):576-583; discussion 583-584. http://www.ncbi.nlm.nih.gov/pubmed/9310974. Accessed September 26, 2016. 

Hugenholtz H, Cass DE, Dvorak MF, et al. High-dose methylprednisolone for acute closed spinal cord injury—only a treatment option. Can J Neurol Sci. 2002;29(3):227-235. http://www.ncbi.nlm.nih.gov/pubmed/12195611. Accessed September 26, 2016. 

Hurlbert RJ, Hadley MN, Walters BC, et al. Pharmacological therapy for acute spinal cord injury. Neurosurgery. 2013;72(suppl 2):93-105. 

Jia X, Kowalski RG, Sciubba DM, Geocadin RG. Critical care of traumatic spinal cord injury. J Intensive Care Med. 2013;28(1):12-23. 

McDonald J, Sadowsky C. Spinal cord injury. Lancet. 2002;359:417-425. 

Roberts I, Yates D, Sandercock P, et al. Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo-controlled trial. Lancet. 2004;364(9442):1321-1328. 

Saveika J, Thorogood C. Airbag-mediated pediatric atlanto-occipital dislocation. Am J Phys Med Rehabil. 2006;85:1007-1010. 

Thuret S, Moon L, Gage F. Therapeutic interventions after spinal cord injury. Nat Rev Neurosci. 2006;7:628-643. 

Tsutsumi S, Ueta T, Shiba K, Yamamoto S, Takagishi K. Effects of the Second National Acute Spinal Cord Injury Study of high-dose methylprednisolone therapy on acute cervical spinal cord injury-results in spinal injuries center. Spine. 2006;31(26):2992-2996.

0 comments:

Post a Comment

Note: Only a member of this blog may post a comment.