CONTENTS
- Rapid Reference 🚀
- Epidemiology
- Physiology
- Clinical presentation
- Imaging
- Management
- Podcast
- Questions & discussion
- Pitfalls
common causes of spinal cord trauma (33896529)
- Motor vehicle collisions, especially among the young (~40%).
- Falls, especially among the elderly (~30%).
- Violence including assaults and gunshot wounds (~15%).
- Sports injuries (~10%).
relationship to traumatic brain injury (TBI)
- 5-10% of patients with traumatic brain injury also have spinal cord injury.
- About half of patients with spinal cord injury also have traumatic brain injury.
anatomy of spinal cord injury
- Most injuries affect the cervical spine, which is the most mobile and vulnerable.(29613899)
primary versus secondary injury
- The concepts of primary versus secondary injury are the same as for traumatic brain injury (TBI). (as discussed further here 📖 )
- Primary injury results from direct mechanical trauma at the time of injury (e.g., shearing of neurons). This is generally irreversible.
- Secondary injury results from a cascade of pathologic consequences following the initial insult (e.g., hypotension, hypoxemia, inflammation, edema, microhemorrhages, microthrombosis, oxidative damage, intracellular hypercalcemia, glutamate excitotoxicity). Critical care of the patient with spinal cord injury focuses on minimizing secondary injury.
time course
- Spinal cord edema often increases over 3-6 days following the initial injury. Gradual improvement may then occur over the course of weeks.(29613899)
neuroanatomy of the autonomic nervous system
- The sympathetic nervous system serving the heart arises from T1-T6, whereas parasympathetic innervation of the heart arises from the vagus nerve (figure below). Therefore, spinal cord damage above the T6 level will cause a selective deficit of sympathetic innervation of the heart (causing the heart to receive unopposed parasympathetic activity from the vagus nerve).
- Cell bodies of the preganglionic sympathetic neurons are located in the intermediolateral cell column from T1 to L2/L3 (figure below). Cell bodies for preganglionic parasympathetic neurons lie in cranial nuclei (CN3, 7, 9, 10) as well as sacral parasympathetic nuclei which are located in the mid-grey matter (in a location similar to the intermediolateral cell column).
movements related to various spinal levels
- C5
- Elbow flexion.
- Shoulder flexion, extension, abduction, adduction, internal/external rotation
- C6
- Wrist flexion.
- Elbow pronation.
- C7
- Elbow extension (triceps).
- Finger: Flexion at proximal joint, extension
- Thumb: Flexion, extension, and abduction in plane of thumb
- C8
- Finger flexion at MCP joint.
- Thumb: Opposition, adduction and abduction perpendicular to palm
- T1
- Abduction of the 2nd and 5th fingers.
- L2
- Hip flexion.
- L3
- Knee extension.
- Hip external rotation.
- L4
- Foot dorsiflexion.
- Hip extension, abduction, internal rotation
- Knee flexion
- Toe: MP and IP extension
- L5
- Great toe dorsiflexion (movement towards the shin).
- S1
- Foot plantar flexion.
terminology to describe spinal cord injury
- The neurological level of injury is defined as the lowest segment with antigravity muscle strength (3/5 strength or better) and intact sensation (to light touch and pinprick).(29613899) This may not correlate exactly with the anatomic level of injury.
- Injury is complete if all function is lost below the spinal level. Alternatively, injury is incomplete if some function is preserved below the level of injury.(29613899)
what is spinal shock?
- Spinal shock refers to reversible impairment in spinal cord function occurring within hours of injury. This shouldn't be confused with neurogenic shock (which is a distinct entity, as discussed further below 📖).(29613899)
- Spinal shock often causes transient loss of all function below the level of injury (causing flaccid paralysis and areflexia). This may cause patients to appear more severely injured than they actually are.
- Four stages of spinal shock have been proposed, as described below. An individual patient may not precisely follow these stages. Additionally, this model refers to complete spinal cord injury, so it may not apply to partial injuries. Nonetheless, the stages can provide a useful rubric to help understand spinal shock.(15037862)
phase #1 (0-1 day) – areflexia/hyporeflexia
- There is a loss of deep tendon reflexes, as well as cutaneous reflexes.
- A delayed plantar response is the first reflex to return, occurring within hours of injury. (Unusually strong stimulation of the sole of the foot results in delayed plantar flexion of the toes.)
- Neurogenic shock may occur.
phase #2 (1-3 days) – initial reflex return
- Cutaneous reflexes return (e.g., bulbocavernosus reflex, anal wink reflex, and cremasteric reflex).
- Deep tendon reflexes may remain absent.
phase #3 (4-30 days) – early hyperreflexia
- Deep tendon reflexes reappear.
- The Babinski sign appears (pathological dorsiflexion of the toes).
- Vasovagal hypotension and bradyarrhythmias generally resolve after 3-6 weeks, although orthostatic hypotension may persist for longer.
- Autonomic dysreflexia 📖 may begin to emerge.
phase #4 (1-12+ months) – spasticity/hyperreflexia
- Cutaneous reflexes, deep tendon reflexes, and the Babinski sign become hyperactive.
- Orthostatic hypotension often resolves.
- Autonomic dysreflexia 📖 becomes more common (and may persist indefinitely).
CT scan
- CT scanning is generally the front-line investigation, due to speed and availability.
- If there is a C-spine injury, consider imaging the thoracic and lumbar spine to exclude occult injuries (which may be masked by the C-spine injury).(Nelson, 2020)
- The addition of a CT angiogram may be considered to exclude cervical artery dissection (the precise indications are discussed further here 📖).
MRI
- MRI is the gold standard for spinal imaging.
- MRI provides additional information about:
- Ligamentous injury.
- Hematoma.
- Spinal cord edema.
anatomy & physiology
- Neuroanatomy of respiratory muscles:(29613899)
- Diaphragm: C3-C5.
- Sternocleidomastoids and trapezius: Cranial Nerve XI.
- Scalenes: C3-C8.
- External & internal intercostals: T1-T11.
- Abdominal muscles: T7-L2.
- General principles:
- The degree of respiratory dysfunction depends on the spinal level, as well as the completeness of the injury. For example, a complete injury at C2 or C3 will invariably cause respiratory failure.
- During normal breathing at rest, inhalation is an active process whereas exhalation is passive. However, coughing requires active exhalation, which involves the external intercostal muscles (T1-T11) and abdominal muscles (T7-L2). Patients with a thoracic spine injury may have preserved inspiration (allowing them to breathe), yet they may still have an impaired ability to cough.
- Some rough generalizations:
- Lesions at C2-C6 may cause 80-95% reduction in vital capacity with absent/impaired cough.(Shutter 2019)
- Lesions at C7-T4 may cause 30-50% reduction in vital capacity with impaired cough.(Shutter 2019)
- Increased bronchial mucus hypersecretion may occur in some patients, perhaps related to unopposed vagal output (since sympathetic output is interrupted).(Torbey, 2019)
clinical management
- Respiratory function should be monitored carefully.
- Ongoing spinal cord edema over time may cause a progressive neuromuscular weakness, leading to delayed respiratory failure.
- Patients with preserved inspiratory strength but impaired cough may develop delayed respiratory failure due to the accumulation of secretions. Delayed respiratory failure may also reflect muscle fatigue, if some remaining muscle groups are compensating for other paralyzed muscles.(29613899)
- Analgesia should be provided to allow for comfortable breathing and coughing, while avoiding respiratory suppression (e.g., with the use of multimodal analgesia 📖).
- Various techniques for secretion clearance may be helpful, depending on available therapies (e.g., an insufflation-exsufflation cough assist device).
- Mechanical ventilation:
- Intubation may be required for management of respiratory failure, or management of impaired mental status due to concomitant traumatic brain injury.
- Noninvasive ventilation has a very limited role in the management of respiratory failure due to acute spinal cord injury.(29613899)
- Respiratory failure due to spinal cord injury usually isn't rapidly reversible. Consequently, for many patients early tracheostomy may shorten ICU stay and reduce laryngotracheal complications.(29651626)
- Two prospective studies found that higher MAP goals (>85 mm) improved outcomes.(33896529)
- The optimal duration of MAP augmentation is unclear, ranging from 5-7 days after injury.(33896529; 34966774)
- Norepinephrine is generally utilized. However, for patients with neurogenic shock and bradycardia, the use of epinephrine could be considered as well.
anatomy & physiology
- Neurogenic shock occurs in up to 90% of patients with complete lesions above the T6 level. With partial lesions, the risk is lower.
- Parasympathetic innervation of the heart and blood vessels comes from the vagus nerve.
- Sympathetic innervation of the heart and blood vessels comes from the thoracic spinal cord.
- Spinal cord lesions above T6 cause selective removal of sympathetic tone, causing bradycardia and vasodilation. Patients may actually have elevated vagal output.(O'Phelan 2022)
- This tends to occur in the acute phase following injury (i.e., the first two weeks).(Jankovic 2022)
- Neurogenic shock may occasionally occur with acute nontraumatic myelopathies as well.(33522735)
clinical findings
- The hallmark of neurogenic shock is hypotension plus bradycardia (although the heart rate may also be inappropriately normal). Pulse pressure may be widened due to peripheral vasodilation that reduces the systemic vascular resistance.
- Cutaneous vasodilation is problematic:
- (1) Patients may not appear to be shocked (they may feel warm).
- (2) Cutaneous vasodilation may cause hypothermia.
- Priapism may result from unopposed parasympathetic activation.
differential diagnosis includes:
- Hemorrhagic shock.
- Pericardial tamponade.
- Tension pneumothorax.
- (For the complete approach to undifferentiated shock, see this chapter: 📖)
management
- The mainstay of therapy is vasopressors +/- inotropes (e.g., norepinephrine or epinephrine), with a goal of restoring a reasonable blood pressure and heart rate.
- More on blood pressure targets above.📖
- Bradycardia may cause impaired systemic perfusion, even in patients with adequate blood pressure (discussed further in the bradycardia chapter here 📖). Thus, it may be reasonable to target both an adequate blood pressure and normalization of the heart rate (e.g., heart rate > ~60 b/m).
- Vasopressors with more chronotropy might be needed to achieve this (e.g., epinephrine monotherapy, or a combination of norepinephrine plus dobutamine; more discussion of pressors here 📖).
- Occasionally, anticholinergics (atropine or glycopyrrolate) may be needed to counteract excess parasympathetic activity (more on this in the section below).(Louis 2021)
physiology
- A spinal cord lesion above T6 disrupts sympathetic innervation of the heart, leaving the autonomic control of the heart solely under the control of the vagus nerve.
- This is anatomically identical to the lesions which cause neurogenic shock. There may be some clinical overlap between these two entities.
clinical manifestation
- Patients may experience exaggerated vagal responses, which may be life-threatening. This tends to occur during the first two weeks following injury (similar to neurogenic shock).
- Common triggers include suctioning or even just turning.
- Clinical consequences may include:
- Bradycardia.
- Sinus pauses, intermittent heart blocks, asystolic cardiac arrest.
management
- Atropine or glycopyrrolate are front-line therapies, to inhibit vagus nerve signaling.(O'Phelan 2022)
- Some patients may benefit from prophylactic glycopyrrolate prior to suctioning.
- If ineffective, other options may include oral theophylline 📖 or oral albuterol.(24458037)
- Temporary pacing may be rarely required.(21817987) This is the definitive therapy, with the drawback of being more invasive.
- (More on the general management of bradycardia here: 📖)
physiology
- Autonomic dysreflexia may occur in patients with C-spine or high T-spine injuries (above T6).(Nelson, 2020; Louis 2021)
- In the absence of regulation from higher brain centers, the distal sympathetic nervous system becomes dysregulated and hyperresponsive. A stimulus below the level of spinal dysfunction leads to hyperactivation of the sympathetic nervous system (causing hypertension due to vasoconstriction).
- Triggered by hypertension, a carotid baroreceptor reflex leads to increased parasympathetic output to preserved components of the spinal cord (above the level of spinal cord injury). Since parasympathetic output to the visceral organs occurs largely via the cranial nerves, this will be preserved even in high C-spine injuries (figure below).
clinical features
- Autonomic dysreflexia usually occurs in the subacute/chronic period, but it may occur as early as 1-4 weeks following injury.(15037862)
- An episode of autonomic dysreflexia is triggered by stimuli below the level of the spinal cord lesion (e.g., surgical procedures, bowel distension, pressure ulceration, or especially bladder distension).
- ⚠️ Due to lack of sensation, patients may be unaware of these triggers.
- Episodic severe hypertension is the hallmark finding.
- Severe hypertension may lead to Posterior Reversible Encephalopathy Syndrome (PRES) or intracranial hemorrhage, if untreated.
- Headache often occurs.
- Exaggerated parasympathetic activation occurs above the level of cord lesion. This causes:
- Cutaneous flushing.
- Sweating.
- Nasal congestion; oral and respiratory secretions.
- Pupillary contraction, blurred vision.
- Exaggerated sympathetic activation occurs below the level of cord lesion, causing:
- Pale, cool limbs.
- Piloerection.
- Heart rate is variable. Generally baroreceptor-mediated bradycardia occurs, but tachycardia may also occur.(31996626)
management
- (1) Removal & avoidance of triggers, e.g.:
- Inspect the skin for pressure ulcerations, sources of pain, or tight clothing.
- Management of bladder spasm, urinary retention, or Foley catheter occlusion.
- Aggressive bowel regimen, management of fecal impaction if present (however, blood pressure should be controlled prior to disimpaction).
- (2) Treatment of hypertension:
- Sitting upright can be beneficial.
- Vasodilators may be needed to prevent dangerous hypertension (e.g., nitrates, hydralazine, dihydropyridine calcium channel blockers that don't affect the AV node, alpha-adrenergic blockers such as prazosin).(31996626) Beta-blockers should be avoided, as these could exacerbate reflex bradycardia. For management of a single episode, short-acting medications are preferred. Low doses should initially be used, as patients may be very sensitive to antihypertensives.(29613899)
- For patients with repeated episodes, ongoing use of vasodilators might be reasonable (e.g., alpha-blockers such as prazosin 0.5-1 mg PO BID/TID).(Nelson, 2020) However, this may increase the risk of orthostatic hypotension.
- Orthostatic hypotension may result from impaired sympathetic output among patients with spinal injury involving the cervical or upper thoracic spine (C2-T6).
- This often resolves over ~4 months following injury.(15037862)
- Enteral midodrine may be useful for management.(Kumar, 2018)
neurogenic bladder
- Physiology:
- Initially following spinal cord injury, spinal cord shock often causes the bladder to be flaccid, with urinary retention. This usually lasts for 6-12 weeks, but can persist for up to a year.(Jankovic, 2022)
- Subsequent to resolution of spinal shock, various patterns of bladder dysfunction may emerge:
- If the injury is above the sacral spinal cord, an upper motor neuron lesion occurs leading to spastic bladder.
- If the injury is within the sacral spinal cord or cauda equina, a lower motor neuron injury occurs, leading to a flaccid bladder with urinary retention.
- Dyssynchrony between the detrusor and external sphincter may cause incomplete emptying of the bladder.
- Inpatient management:
- Postvoid residual volume should be monitored.
- Intermittent or indwelling catheterization may be needed.
constipation
- Physiology:
- Transient ileus is seen in up to 10% of patients with cervical or thoracic injuries.(Torbey, 2019)
- Fecal impaction is common, occurring in up to half of patients.
- Management:
- Aggressive bowel regimen including stimulant laxatives (e.g., senna, bisacodyl, sodium picosulfate).
- Rectal stimulation or suppositories may be helpful.
- Avoid opioids as able.
- Spinal cord injury patients have an extremely high risk of venous thromboembolic disease, with major venous thromboemboli in 15% of patients – even if DVT prophylaxis is applied properly. (Shutter 2019)
- 🛑 Prophylactic IVC filter placement in trauma patients hasn't been shown to affect the rates of symptomatic PE or mortality, so this is not recommended.(33896529)
- DVT prophylaxis should be initiated as soon as it is safe to do so, and within <72 hours of injury.(33896529) For patients undergoing surgery, DVT prophylaxis can usually be started within 24 hours after surgery – but this decision should be made jointly with the surgical team.(Kumar, 2018)
- There is no level I or II evidence that steroid is beneficial.
- Historically, trials have investigated the use of massive doses of steroid (e.g., gram doses of methylprednisolone). These have been found to cause harm.
- Interventions may include external fixation, or internal reduction and fixation.
- Earlier intervention may improve neurological outcomes by decompressing the spinal cord and thereby improving perfusion.
- Neurosurgery and/or orthopedic surgery should be consulted immediately to determine the appropriate procedure and timing (issues beyond the scope of this chapter). Hospitals vary regarding which service covers spinal trauma.
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- Don't forget to obtain appropriate imaging to evaluate for cervical artery dissection in patients with indications for this.
- Guidelines recommend maintaining a MAP of >85-90 mm. Don't delay vasopressor initiation among patients with marked hypotension, particularly in the context of neurogenic shock. Vasopressors may be initiated rapidly, with simultaneous fluid resuscitation and evaluation for other causes of shock (e.g., hemorrhage, tension pneumothorax, pericardial tamponade).
Guide to emoji hyperlinks
- = Link to online calculator.
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- = Link to FOAMed site with related information.
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Going further
- The American Spinal Injury Association (ASIA) impairment scale.🌊
References
- 15037862 Ditunno JF, Little JW, Tessler A, Burns AS. Spinal shock revisited: a four-phase model. Spinal Cord. 2004 Jul;42(7):383-95. doi: 10.1038/sj.sc.3101603 [PubMed]
- 29613899 Rabinstein AA. Traumatic Spinal Cord Injury. Continuum (Minneap Minn). 2018 Apr;24(2, Spinal Cord Disorders):551-566. doi: 10.1212/CON.0000000000000581 [PubMed]
- Kumar, M., Kofke, W.A., Levine, J. M., & Schuster J. (2018). Neurocritical Care Management of the Neurosurgical Patient (1st ed.). Elsevier.
- 29651626 Shank CD, Walters BC, Hadley MN. Current Topics in the Management of Acute Traumatic Spinal Cord Injury. Neurocrit Care. 2019 Apr;30(2):261-271. doi: 10.1007/s12028-018-0537-5 [PubMed]
- 31363857 Karsy M, Hawryluk G. Modern Medical Management of Spinal Cord Injury. Curr Neurol Neurosci Rep. 2019 Jul 30;19(9):65. doi: 10.1007/s11910-019-0984-1 [PubMed]
- Shutter, L. A., Molyneaux, B. J.(2019). Neurocritical care. Oxford University press.
- Wijdicks E.F.M., Findlay, J. Y., Freeman, W. D., Sen A. (2019). Mayo Clinic critical and Neurocritical Care Board Review. Oxford University Press.
- Torbey, M. T. (2019). Neurocritical Care (2nd ed.). Cambridge University Press.
- 31996626 Rabinstein AA. Autonomic Hyperactivity. Continuum (Minneap Minn). 2020 Feb;26(1):138-153. doi: 10.1212/CON.0000000000000811 [PubMed]
- Nelson, S. E., & Nyquist, P. A.(2020). Neurointensive Care Unit: Clinical Practice and Organization (Current Clinical Neurology) (1st ed. 2020 ed.). Springer.
- Jallo, J. I., & Urtecho, J. S. (2021). The Jefferson Manual for Neurocritical Care. Georg Thieme Verlag.
- Louis ED, Mayer SA, Noble JM. (2021). Merritt’s Neurology (Fourteenth). LWW.
- 33896529 Eli I, Lerner DP, Ghogawala Z. Acute Traumatic Spinal Cord Injury. Neurol Clin. 2021 May;39(2):471-488. doi: 10.1016/j.ncl.2021.02.004 [PubMed]
- 34010969 Huang KT, Lu Y. Traumatic Spinal Cord Disorders: Current Topics and Future Directions. Semin Neurol. 2021 Jun;41(3):247-255. doi: 10.1055/s-0041-1725125 [PubMed]
- 34966774 Wang TY, Park C, Zhang H, Rahimpour S, Murphy KR, Goodwin CR, Karikari IO, Than KD, Shaffrey CI, Foster N, Abd-El-Barr MM. Management of Acute Traumatic Spinal Cord Injury: A Review of the Literature. Front Surg. 2021 Dec 13;8:698736. doi: 10.3389/fsurg.2021.698736 [PubMed]
- Jankovic, J., Mazziotta, J. C., Pomeroy, S. L., & Newman, J. N. (2022). Bradley and Daroff’s Neurology in Clinical Practice, 2-Volume Set (Bradley’s Neurology in Clinical Practice) (8th ed.). Elsevier.
- Dangayach N, Classen J, O'Phelan K (2022): Neurologic Intensive Care: Brain, acute spinal cord injury, and neuromuscular disease. Presentation at the American Academy of Neurology Conference, Seattle 2022.