Spinal shock

I. What every physician needs to know.

Spinal shock refers to a clinical syndrome characterized by the loss of reflex, motor and sensory function below the level of a spinal cord injury (SCI). In some instances (possibly when lesion is T6 or higher), this syndrome is associated with loss of autonomic tone leading to hypotension, hypothermia and illeus.

When present, the neurogenic hypotension secondary to spinal shock is associated with lack of reflex tachycardia. Spinal shock usually develops suddenly or within a few hours and it is not necessarily associated with hypotension resulting in shock.

II. Diagnostic Confirmation: Are you sure your patient has spinal shock?

  • Spinal shock: Sudden and temporary loss of reflex, motor and sensory function below a spinal cord level.

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  • Neurogenic shock: Hypotension with lack of reflex, tachycardia associated with spinal shock when injury level is above T6.

A. History Part I: Pattern Recognition:

The typical presentation is that of a young individual brought in by ambulance to the emergency department after sustaining a traumatic injury; in this example, injury is secondary to multiple gun shot wounds to chest and abdomen. Patient has a blood pressure of 62/35, pulse of 86, respiratory rate of 32, temperature of 36.1 Celsius. Glasgow Coma Scale (GCS) 13/15. On further exam, the patient has no breath sounds on the right hemithorax, tense abdomen, flaccid lower extremities, and no rectal tone.

Even though the scenario described above is the most commonly seen, the patient with pure spinal shock secondary to spinal cord injury (SCI) presents with hypotension, normal heart rate or bradycardia, hypothermia, flaccid paralysis, areflexia, loss of sensation, urinary bladder incontinence and intestinal ileus.

B. History Part 2: Prevalence:

Based on data extracted from the National Spinal Cord Injury Database (NSCID), spinal cord injury affects predominantly productive young adults, 55% of cases are between 16 and 30 years of age, and 81% are male. Motor vehicle accidents account for 38.5% of cases, followed by intentional injuries (GSW and assault) 24.5%, falls 21.8% and sports related injuries 7.2%. There is an average of 11,000 new cases per year and currently more than 200,000 SCI victims living in the United States, with an estimated total annual cost of more than $5 billion.

Neurogenic hypotension secondary to spinal shock occurs in 20-30% of all SCI, most commonly associated with high cervical lesions and complete to near complete SCI.

C. History Part 3: Competing diagnoses that can mimic spinal shock.

As most patients presenting with SCI and spinal shock have also suffered significant trauma and are at risk for hypovolemic shock as well as for “obstructive”/”mechanical” shock (cardiac tamponade, tension pneumothorax), efforts should be made to rule-out and treat all these reversible causes of shock. Risk factors for these kinds of injuries include intoxication which will interfere with the neurologic exam as some will be non-cooperative or obtunded. With the presence of distracting injuries, ruling out other central nervous system (CNS) lesions which could be causing the neurologic deficits will be difficult.

Spinal shock presents usually with a sudden onset (frequently associated with trauma or less likely, vascular lesions), however other non-traumatic lesions could lead to presentations similar to those of spinal shock but may be with a more insidious onset (malignancy, infections, vascular lesions, CNS demyelinating/ degenerative diseases, etc.).

D. Physical Examination Findings.

There are several ways to classify SCI and to describe physical findings.

1. One way to approach it is based on temporal findings which are seen in spinal shock (not necessarily in complete SCI), with 4 different evolving phases as described by Ditummo, et.al.:

  • Phase 1 (0-1 day), areflexia/hyporeflexia (muscle flaccid and paralyzed)

  • Phase 2 (1-3 days), initial reflex return (return of cutaneous reflexes with DTR still absent)

  • Phase 3 (1-4 weeks), initial hyper-reflexia (DTR reappear, may present vaso-vagal hypotension and brady-arrythmias)

  • Phase 4 (1-12 months), final hyper-reflexia (DTR disappear, spasticity, sometimes orthostatic hypotension versus malignant hypertension of autonomic dysreflexia).

2. Another approach is based on anatomical lesion: complete versus incomplete (90% of all lesions) and the latter with the following subgroups: central cord syndrome, anterior cord syndrome and Brown-Sequard syndrome (90% of all incomplete SCI can be classified as one of these 3 syndromes); as well as the level of lesion (cervical, thoracic, lumbosacral).

3. Complete SCI: Characterized by complete loss of motor power and sensation distal to the site of the lesion. Important to rule out sacral sparing (perianal sensation, normal rectal tone, flexor toe movement) as it indicates partial SCI.

4. Spinal shock: Mimics complete SCI but is temporary and caused by concussion of spinal cord secondary to traumatic lesions (see evolving phases above). A complete SCI will remain unchanged after the resolution of the spinal shock.

5. Central cord syndrome: Most common, often seen in elderly people with cervical degenerative joint disease (DJD). Characterized by greater neurologic deficit in upper extremities than in lower extremities. Variable severity and prognosis.

6. Brown-Sequard syndrome: Also known as hemisection of the spinal cord. Characterized by ipsilateral motor deficit with contralateral sensory hypoesthesia distal to the level of injury. All patients maintain bladder and bowel function.

7. Anterior cord syndrome: Characterized by paralysis and hyperalgesia below the level of injury with preservation of posterior column function. Variable degrees of recovery are seen within first 24 hours.

Also, impact on respiratory function and swallowing function will depend on level of injury. Eighty-four percent of high injuries (C1-4) will develop respiratory complications while hospitalized including intubation (74 % of complete high SCI) and tracheostomy (69% overall), pneumonia, atelectasis (most commonly seen in lower cervical spine lesions). Swallow evaluation is necessary as this function can be impaired in high level injuries.

E. What diagnostic tests should be performed?

  • Magnetic resonance imaging of the spine

  • Computed tomography of the spine

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

No laboratory tests are needed to establish diagnosis as it is a clinical diagnosis supported by imaging studies.

Currently under research is the use of lumbar puncture with measurement of inflammation markers to determine diagnosis and prognosis.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Radiographic evaluation (X-ray)

Helpful in diagnosis of bony lesions but will not assess spinal cord directly. It is fast and can be done bedside, however is frequently limited due to difficulties in positioning, lack of cooperation, etc. An abnormal X-ray associated with neurologic deficits should prompt neurosurgical evaluation even while awaiting further imaging.

Computed tomography (CT)

Improved fracture detection rate, spinal canal evaluation and paraspinal soft tissue assessment with reduced manipulation of patient but still not ideal for evaluation of spinal cord.

Magnetic resonance imaging (MRI)

Modality of choice. Its advantages include the direct evaluation of non-osseous structures including disk herniation, filamentous injury, bone compression, epidural and subdural hemorrhage, vertebral artery occlusion, as well as identifying different patterns of SCI (hemorrhage, edema, contusion, mixed patterns). Hence, it can assess potentially surgically correctable lesions and provide a prognosis evaluation. However, the disadvantages are the many contraindications for the study (pace maker, CNS aneurismal clips, ferromagnetic foreign bodies), patients should be stable enough to perform a study that is at least 30 minutes in duration.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.

Most patients who sustained a SCI will require a sequential approach to evaluate both osseous and non-osseous structures and a high number of plain X-rays are non-diagnostic or at least will warrant further evaluation. It is reasonable to say that in patients with suspected SCI or spinal shock a CT and MRI of the area will be needed and plain X-ray could be avoided as it is a “wasted study”.

III. Default Management.


A. Immediate management.

As most SCIs result from trauma, the immediate management will be guided by ABCDEs surveys. A: airway management with cervical spine immobilization; B: breathing with ventilation; C: circulation with hemorrhage control; D: disability with neurologic evaluation; E: exposure and environmental control. As most patients are trauma patients, most immediate management will be ruled out by the Advanced Trauma Life Support (ATLS) guidelines (ABCDEs), however, these are beyond the scope of this chapter, so we will only focus on what attends to SCI patients.

  • Spinal cord stabilization/immobilization: should be implemented during pre-hospital care to avoid further injuries.

  • Airway management: if needed.

  • Treatment of shock: as described above, shock is unlikely pure so initially administer IV crystalloid for fluid resuscitation (10-20ml/Kg), treat obvious causes of shock (tamponade, pneumothorax, control hemorrhage)

  • Vasopressors: if fluid resuscitation is inadequate to assure organ perfusion, inotropic agents such as dopamine 2.5-20.0µg/kg per min and dobutamine 2.0-20.0µg/kg per min may be added to improve cardiac output and perfusion pressure. The doses should be titrated to the appropriate clinical response. Avoid phenylephrine and norepinephrine as these drugs can worsen bradycardia. Atropin 0.5-1mg can be used for extreme bradycardia.

  • Steroids: at present, there is insufficient evidence to support the routine use of steroids in SCI.

  • Neurosurgery consult: immediate surgery is recommended when certain injuries are demonstrated by MRI; these include impingement of spinal cord caused by foreign body, herniated discs, bony fracture fragments or epidural hematoma.

Later surgery can be considered or be necessary to stabilize bony injuries or to reduce spinal dislocations.

B. Physical Examination Tips to Guide Management.

Immediate management will be ruled by the presence of hypotension and shock, and tips for utilizations of pressors, inotropes and atropine are described above.

The appearance of anal wink and/or bulbo-cavernosus reflexes indicate the resolution of the phase 1 of spinal shock and will be consistent with the absence of complete SCI. Rehabilitation should be initiated as soon as feasible (based on comorbidities).

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

  • Acute stage: hemodynamic monitoring with pulmonary artery catheter could be considered but is not necessary in most cases.

  • Subacute/chronic stages: electrophysiological measurements, such as electromyography (EMG), motor- evoked potentials and surface EMG, provide objective data on spinal conductivity and muscle function which can lead towards optimal therapy.

D. Long-term management.

SCI has a devastating impact on patients and their families; emotionally. psychologically and economically. Long-term care should focus on trying to rehabilitate these patients and insert them back in society.

Rehabilitation should be directed as a multisystem and multidisciplinary approach focusing on: functional potential, upper extremity function, ambulation, general autonomic function, colon and rectal function, lower urinary tract function, sexual function, pain management, spasticity, depression, quality of life and participation.

E. Common Pitfalls and Side-Effects of Management

No specific considerations.

IV. Management with Co-Morbidities


A. Renal Insufficiency.

No significant changes in management except for patient with End Stage Renal Disease (ESRD) in hemodialysis that will need closer monitoring with IVF administration.

B. Liver Insufficiency.

No change in standard management.

C. Systolic and Diastolic Heart Failure

As described above, patients may need aggressive IVF resuscitation if spinal shock is associated with hemorrhagic shock, so close monitoring of intravascular volume status is warranted. Also practice caution when choosing vasoactive drugs.

D. Coronary Artery Disease or Peripheral Vascular Disease

When in need of vasoactive drug try to avoid vasopressin or phenylephrine, however if in need of peripheral vasopressor, perform close monitoring of patient. Consider checking troponin levels and measuring peripheral Doppler pulses if appropriate for your individual patient. There is no official consensus on this subject.

E. Diabetes or other Endocrine issues

Consider glycemic control in patients receiving steroids (however routine use is no longer recommended).

F. Malignancy

If spinal shock is thought to be associated with a pathological fracture and not trauma, may need to do further cancer screening or work-up.

G. Immunosuppression (HIV, chronic steroids, etc).

No change to standard management.

H. Primary Lung Disease (COPD, Asthma, ILD)

Early respiratory therapy, especially if patient presenting with a high level lesion which will place him/her at risk for pulmonary complications.

I. Gastrointestinal or Nutrition Issues

If cervical lesion, consider swallow evaluation before initiation of oral/enteral nutrition. As with any other chronic disease (as SCI will end up being) optimal nutritional status is warranted.

J. Hematologic or Coagulation Issues

No change to standard management.

K. Dementia or Psychiatric Illness/Treatment

No change to standard management.

V. Transitions of Care

A. Sign-out considerations While Hospitalized.

Stress importance of spinal cord immobilization and discuss preferred pressor therapy if patient becomes hypotensive. Also, remind cross-cover physician that patient is at risk (due to recent trauma) of different types of shock, not just spinal shock, and will need regular assessment or any time clinical status changes. Don’t assume hypotension is solely spinal shock.

B. Anticipated Length of Stay.

Variable. Will depend on associated injuries, comorbidities and developing of complications during hospital stay (more common with higher lesions).

C. When is the Patient Ready for Discharge.

Often patients will be discharged to an acute or subacute rehabilitation facility whenever shock resolved.

D. Arranging for Clinic Follow-up


1. When should clinic follow up be arranged and with whom.

Patient will likely be discharged to a rehabilitation facility, and follow-up will depend on several factors including: whether surgery was performed or not, urinary complications, presence of tracheostomy, etc. Most patients will need a primary care provider regardless of the need for a specialist.

2. What tests should be conducted prior to discharge to enable best clinic first visit.


3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.


E. Placement Considerations.

Most patients will need placement in an acute or subacute rehabilitation facility.

F. Prognosis and Patient Counseling.

Most patients will attain sufficient independence to live outside a high-level care environment. This statement is true with the exception of patients who sustained high lesions (C5 and higher).

VI. Patient Safety and Quality Measures

A. Core Indicator Standards and Documentation.

SCI is not one of the diagnoses included in the Joint Commission on Accreditation of Heathcare Organizations (JCHCO) Core Measure sets. However it is important to document a complete neurologic exam daily including presence or absence of reflexes (anal wink, cremasteric, deep tendon reflexes (DTR), cutaneous reflexes, rectal tone, etc.), motor strength and tone, and sensory deficit level. Also document if spinal immobilization is needed, presence of pressure ulcers, nutrition and when rehabilitation was initiated.

B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

  • Prevent pressure ulcers

  • Initiate deep vein thrombosis (DVT) prophylaxis

  • Consider proton pump inhibitors if high dose steroids are being used

  • Incentive spirometry if patient is not intubated

  • If a patient is intubated perform ventilator acquired pneumonia (VAP) prophylaxis

  • Glycemic control if using high dose steroids

What's the evidence?

Alexander, MS, Anderson, KD, Biering-Sorensen, F. “Outcome measures in spinal cord injury: recent assessments and recommendations for future directions”. Spinal Cord. vol. 47. 2009. pp. 582-591.

Ditunno, JF, Little, JW, Tessler, A, Burns, AS. “Spinal Shock revisited: a four-phase model”. Spinal Cord. vol. 42. 2004. pp. 383-395.

Berney, S, Bragge, P, Granger, C, Opdam, H, Denehy, L. “The acute respiratory management of spinal cord injury in the first 6 weeks after injury: a systematic review”. Spinal Cord. vol. 49. 2011. pp. 17-29.

Atkinson, PP, Atkinson, J. “Spinal Sock”. Mayo Clin Proc. vol. 71. 1996. pp. 384-389.

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