Spinal Shock

Definition

Spinal shock occurs following an acute spinal cord injury and involves a reversible loss of all neurological function, including reflexes and rectal tone, below a particular level. It is defined as a state of transient physiologic (rather than anatomic) reflex depression of cord function below the level of injury, with associated loss of all sensorimotor functions. It is not a “shock” in the sense of a circulatory collapse, but a state of depressed spinal reflexes caudal to cord injury.

Spinal shock was first described by Whytt in 1750 as a loss of sensation accompanied by motor paralysis with initial loss but gradual recovery of reflexes, following a spinal cord injury (SCI)—most often a complete transection.

Reflexes generally return in a specific pattern after spinal shock, with cutaneous or polysynaptic reflexes returning before deep tendon reflexes. Ko et al. described a specific pattern of reflex return with the delayed plantar reflex (DPR) returning first, followed by the bulbocavernosus and cremasteric reflexes, and finally the ankle and knee jerk reflexes. The bulbocavernosus reflex usually returns 1–3 days after the injury. It is elicited by squeezing the penile glans or the clitoris (or tugging on the foley catheter) and feeling for an involuntary contraction of the anus.

The DPR is a pathological response elicited by an unusually strong stimulation of the sole of the foot and is characterized by a slow and protracted plantar flexion of the great toe and/or other toes and slow return to the neutral position. Presence of this reflex has a prognostic significance in spinal shock. The presence of a DPR immediately following injury has a poor prognostic correlation with recovery of ambulation.

Variant

Spinal shock is often confused with neurogenic shock. Neurogenic shock describes the hemodynamic changes resulting from a sudden loss of autonomic tone due to spinal cord injury. It is commonly seen when the level of the injury is above T6. Spinal shock, on the other hand, refers to loss of all sensation below the level of injury and is not circulatory in nature. Both may, however, coexist in a patient.

Neurogenic shock is a type of distributive shock, consisting of the hemodynamic triad of hypotension, bradycardia, and peripheral vasodilatation, attributed to severe central nervous system damage (head trauma, cervical cord trauma, or high thoracic cord injuries), resulting in loss of sympathetic stimulation to the blood vessels and unopposed vagal activity. Patients may be poikilothermic and may not be able to regulate their body temperature due to profound vasodilatation and heat loss. There is systemic hypotension due to a decrease in sympathetic fiber-mediated arterial and venous vascular resistance, along with venous pooling and loss of preload, with or without bradycardia. The bradycardia is often exacerbated by suctioning, defecation, turning, and hypoxia. The hypotension places patients at increased risk of secondary spinal cord ischemia due to impairment of autoregulation. Fluid resuscitation and vasopressors remain the mainstay of treatment. Norepinephrine is started initially but in refractory cases epinephrine and vasopressin infusions may be required. Bradycardia usually responds to atropine and glycopyrrolate but in severe cases dopamine infusion is required.

Important to note here is that shock associated with a spinal cord injury must always be considered hemorrhagic until proven otherwise. This differentiation is very necessary as the management to both forms of shock vary—while hypovolemic shock requires aggressive fluid resuscitation to treat hypotension and a thorough evaluation to exclude any ongoing blood loss, the choice of therapy in neurogenic shock is vasopressors to overcome low blood pressure, as the patients may be refractory to fluid resuscitation. Also, hemorrhagic shock is associated with tachycardia, but the loss of thoracic sympathetic innervation (T1–T5) may inhibit tachycardia and vasoconstriction as signs of hypovolemia, in patients where both conditions coexist. Moreover, neurogenic shock can persist for 1–6 weeks after the injury.