Spinal Shock

Description

Spinal shock describes the transient loss of spinal cord function distal to a complete or incomplete acute spinal cord injury (SCI). It may last several weeks, and possibly months.
A low systemic vascular resistance (SVR) state (with hypotension) and bradycardia often coexist with acute SCI. These hemodynamic perturbations are known as neurogenic shock (a separate entity from spinal shock).
The presence of spinal shock is important in the determination of injury levels and prognosis; and it may confound the accurate assessment of neurological status in the post injury period.
In the immediate/acute post injury period, priority should be to reduce secondary injury and prevent an incomplete injury from progressing. In later months, when patients are likely to present for urological and other procedures, special attention to avoid complications of hyperreflexive responses may be required.

Epidemiology

Incidence

In the US, the incidence of SCI is ~12,000 cases per year (1).

Morbidity

Hypotension is associated with progression of secondary neurologic injury (1).

Physiology/Pathophysiology

The exact definition/model of spinal shock is controversial (2). It is commonly considered to be a transient physiological interruption of spinal cord function caudal to the injury that results in areflexia, flaccid paralysis, loss of sensation, and loss of temperature regulation. Four phases have been proposed:
- Phase 1 (0–24 hours post injury). Absent deep tendon reflexes (DTRs) and flaccid muscles that are largely due to a loss of supraspinal excitatory input. Impaired sympathetic innervation also occurs during this phase.
- Phase 2 (1–3 days post injury). Initial reflex return via supersensitivity to neurotransmitters.
- Phase 3 (4 days to 1 month post injury). Early hyperreflexia via replacement synapse growth; most DTRs reappear and acute hemodynamic perturbations improve during this phase.
- Phase 4 (1–12 months post injury). Spasticity and hyperreflexia via continued synapse growth (axon-length-dependent timeframe) (2).

Anesthetic GOALS/GUIDING Principles

SCI interferes with the ability of the spinal cord to autoregulate its blood flow, so perfusion becomes more pressure dependent (1). Additionally, concomitant injuries and neurogenic shock may compound hemodynamic perturbations. Secondary ischemic SCI is likely mitigated with supportive measures.
- Maintain mean arterial BP in the high-normal range (> 90 mm Hg) (1) [B]. Based on studies in traumatic brain injury, blood pressure support is usually continued for the first 7 days after injury (1) [C].
- Avoid hypoxia (paO₂60 mm Hg) (1) [C].
- Avoid acute anemia (1) [C].
Special precautions during airway management may be required; discuss the cervical spine stability/clearance status with the spine surgeon.
Succinylcholine should be avoided after 48–72 hours of denervation states, as described below (3) [C].

Symptoms

Inquire about motor and sensory function and the presence of dyspnea and/or increased work of breathing.
In the chronic SCI patient, inquire about hyperreflexia symptoms (e.g., headache or blurred vision with bowel/bladder distention).

History

Elicit the time and mechanism of SCI, level of cord injury, and rule out concomitant hypovolemic shock from blood loss and other injuries in the trauma patient.

Signs/Physical Exam

Perform a routine preanesthesia exam including a careful airway exam and assessment for cervical spine stability.
A detailed sensory and motor exam should be performed and documented in the acute post injury period as a baseline and to compare to the postoperative exam.

Treatment History

Phase 1–2: Fluid resuscitation, blood product administration, and use of experimental hypothermia therapy.
Phase 3–4: Prior anesthetic records, including intubation details, and prior tracheostomy history.

Medications

Phase 1–2: Vasopressors, vagolytics, and use and timing of corticosteroids (controversy exists regarding efficacy of glucocorticoids) (1).

Diagnostic Tests & Interpretation

Labs/Studies

Basic metabolic panel, complete blood count, coagulation studies
Type and Screen/Cross, depending on expected blood loss
EKG (acute higher level SCI can interrupt sympathetic fibers and cause unopposed parasympathetic activity; bradycardia is common. Other arrhythmias have also been reported).
Chest x-ray (pulmonary edema is possible with aggressive fluid administration).
Serial vital capacity measurements and arterial blood gases to monitor for respiratory decompensation in nonmechanically ventilated patient with possible SCI-induced respiratory dysfunction.

CONCOMITANT ORGAN DYSFUNCTION

Cardiovascular dysfunction with neurogenic shock. A relative bradycardia may be present instead of the expected compensatory tachycardia with hypotension (1). This is most common within the first couple weeks after injury; bradycardia is most prevalent on Day 4 after injury (4).
Respiratory dysfunction (restrictive pattern) depending on the level of SCI.
Other traumatic injuries, such as subdural hemorrhage or thoracic, abdominal, and orthopedic injuries.

Circumstances to delay/Conditions

Early emergent surgical decompression may be necessary. Unless the patient requires acute hemodynamic stabilization, emergency surgery should not be delayed.

PREOPERATIVE PREPARATION

Premedications

for recent trauma, patients are considered to have a full stomach. Drugs should be administered to decrease gastric fluid volume and increase gastric fluid pH (e.g., nonparticulate antacid, H2-receptor antagonist, and gastrokinetic agent).
If a fiberoptic intubation is planned, consider an antisialagogue to decrease secretions and improve visualization.
Determine if methylprednisolone has been administered or is being infused; NASCIS dosing (controversial) is 30 mg/kg bolus and 5.4 mg/kg/hour maintenance for up to 48 hours post injury (1).

INTRAOPERATIVE CARE

Choice of Anesthesia

General anesthesia for vertebral decompression. Avoid anesthetic techniques that interfere with the postoperative neurological exam.
for chronic SCI, consider regional or neuraxial techniques, as appropriate for the planned surgery.

Monitors

Standard ASA monitors
In the acute post injury phase, placement of arterial lines (continuous blood pressure monitoring) and central venous catheters (assess preload, help guide fluid management, and administer vasoactive drugs) is routine (1) [C].
Pulmonary artery catheterization may be considered depending on the degree of hemodynamic derangements.
Neuromonitoring (may include somatosensory and motor evoked potentials and electromyography) for spine surgery.
Decompress the stomach and bladder unless contraindicated since SCI can cause gastric paresis and/or dystonic bladder; organ distension may contribute to autonomic dysfunction.

Induction/Airway Management

Maintain cervical spine immobilization for an uncleared spine. There is no outcome data to support one intubation technique over another (5) [C].
- Awake fiberoptic intubation with topical anesthesia allows the head and neck position to remain in a neutral position, maintains protective airway reflexes, and allows for neurological exam postintubation.
- Direct laryngoscopy with manual in-line immobilization or other techniques can also be considered.
- Application of cricoid pressure, if clinically indicated, is permissible in cervical spine injury (5) [C].
Select a hemodynamically stable induction regimen (e.g., etomidate and ketamine).
Avoid succinylcholine for muscle relaxation after 48–72 hours of denervation states (risk of lethal hyperkalemia from up-regulation of muscle nicotinic acetylcholine receptors) (3) [C]. Many anesthesia providers avoid succinylcholine after even shorter durations (24 hours) of denervation states as a further precaution against hyperkalemia.

Maintenance

Balanced technique with intravenous and/or volatile agents. Neuromonitoring may require limiting volatile agents and avoiding neuromuscular blocking agents.
Acute post injury phase:
- Volume resuscitate to increase preload. Fluids may include crystalloids, colloid, and blood products. Optimal type of fluid therapy is unknown. However, hypotonic fluids are usually avoided since they can worsen cellular swelling.
- Administer vasopressors to restore vasomotor tone and inotropes to increase cardiac output. Choice of therapy depends on the hemodynamic condition of the patient; no specific algorithm exists to guide choice of therapy.
- Intraoperative blood loss may be considerable and utilization of blood cell salvage is helpful.

Extubation/Emergence

Prompt emergence is desired to facilitate a neurological exam.
Extubate when the patient is fully awake, following commands, and able to manage and protect their airway. Laryngeal edema may be present (especially after long spine surgery requiring large volume fluid resuscitation in the prone position); consider cuff-leak test prior to extubation.
Hypoxemia and endobronchial suctioning may worsen bradycardia from unopposed vagal stimulation (4).

Bed Acuity

Invasive hemodynamic monitoring and support in the intensive care unit is usually continued for 7 days post injury, based on studies in traumatic brain injury (1) [C].

Medications/Lab Studies/Consults

Multidisciplinary care is required including neurosurgery and/or orthopedic surgery, critical care, physiatry, and social service management.

Complications

Pulmonary dysfunction: Consider aggressive chest physiotherapy and, if prolonged intubation/mechanical ventilation is anticipated, consider tracheostomy.
Venous thromboembolism: Consider mechanical and/or anticoagulant prophylaxis.
Skin breakdown: Prevent unnecessary pressure points and monitor contact areas.
Stress ulceration: Initiate prophylaxis with H2-receptor antagonist or proton pump inhibitor.

Gupta R , Bathen ME , Smith JS , et al. Advances in the management of spinal cord injury. J Am Acad Orthop Surg. 2010;18:210–222.
Ditunno JF , Little JW , Tessler A , et al. Spinal shock revisited: A four-phase model. Spinal Cord. 2004;42:383–395.
Martyn JAJ , Richtsfeld M. Succinylcholine-induced hyperkalemia in acquired pathologic states. Anesthesiology. 2006;104:158–169.
Guly HR , Bouamra O , Lecky FE. The incidence of neurogenic shock in patients with isolated spinal cord injury in the emergency department. Resuscitation. 2008;76:57–62.
Crosby ET. Airway management in adults after cervical spine trauma. Anesthesiology. 2006;104:1293–318.

Fehlings MG , Rabin D , Sears W , et al. Current practice in the timing of surgical intervention in spinal cord injury. Spine. 2010;35:S166–173.
Veale P , Lamb J. Anaesthesia and acute spinal cord injury. BJA (CEPD Reviews). 2002;2:139–143.
Wuermser LA , Ho CH , Chiodo AE , et al. Spinal cord injury medicine. Acute care management of traumatic and nontraumatic injury. Arch Phys Med Rehabil. 2007;88:S55–61.

See Also (Topic, Algorithm, Electronic Media Element)

Neurogenic Shock
Autonomic Hyperreflexia/Dysreflexia
Somatosensory and Motor Evoked Potentials (Sseps and Meps)

ICD9

958.4 Traumatic shock

ICD10

T79.4XXA Traumatic shock, initial encounter

Spinal shock is a transient loss of spinal cord function that can occur after acute SCI. Neurogenic shock, with hypotension and bradycardia, often coexists with spinal shock.
Secondary SCI may be mitigated with supportive measures. Avoid hypotension and hypoxia and maintain elevated mean arterial pressure.

Laura B. Hemmer , MD

Antoun Koht , MD

section name header

Basics ⬇

Incidence

Morbidity

Diagnosis ⬆ ⬇

History

Signs/Physical Exam

Labs/Studies

Treatment ⬆ ⬇

Premedications

Choice of Anesthesia

Monitors

Induction/Airway Management

Maintenance

Extubation/Emergence

Follow-Up ⬆ ⬇

References ⬆ ⬇

Additional Reading ⬆ ⬇

Codes ⬆ ⬇

Clinical Pearls ⬆ ⬇

Author(s) ⬆

section name header

Basics ⬇

Incidence

Morbidity

Diagnosis ⬆ ⬇

History

Signs/Physical Exam

Labs/Studies

Treatment ⬆ ⬇

Premedications

Special Concerns for Informed Consent

Choice of Anesthesia

Monitors

Induction/Airway Management

Maintenance

Extubation/Emergence

Follow-Up ⬆ ⬇

References ⬆ ⬇

Additional Reading ⬆ ⬇

Codes ⬆ ⬇

Clinical Pearls ⬆ ⬇

Author(s) ⬆