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CHAPTER 119: Spinal Injuries 1145

Medulla Baroreceptors
CN IX

CN X

DVPs
Cervical
HR (PNS)

HR (SNS)

Level of
injury

SPNs

Thoracic Arterioles

SPN

Lumbar

FIGURE 119-10. The sympathetic autonomic innervation of the cardiovascular system arises from the high thoracic (T1-T6) and cervical regions, below the parasympathetics that arise at the
brainstem level. (Reproduced with permission from Furlan JC1, Fehlings MG. Cardiovascular complications after acute spinal cord injury: Pathophysiology, diagnosis, and management. Neurosurg
Focus. 2008;25(5):E13.)
■ MANAGEMENT OF HEMODYNAMIC INSTABILITY norepinephrine, dopamine, or epinephrine are favored over pure vaso-

The management of hemodynamic instability or shock involves hemo- constrictors such as phenylephrine or vasopressin that may result in
dynamic support, rapid identification and control of bleeding, treatment greater degrees of relative bradycardia in more rostral and severe SCI
of significant anemia, and ventilatory support. After acute SCI, auto- associated with decreased sympathetic outflow.
regulation may be compromised and inadequate resuscitation may ■
aggravate systemic perfusion and oxygenation of the vulnerable spinal AUTONOMIC DYSREFLEXIA
cord leading to increased secondary ischemic injury. No bedside moni- Patients with acute SCI at T6 or higher levels may experience autonomic
tors of spinal perfusion exist. Uncontrolled studies suggest that fluid dysreflexia—sudden episodes of hypertension accompanied by auto-
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resuscitation and vasopressors to maintain the MAP at ≥85 mm Hg nomic hyperactivity (sweating, facial flushing, piloerection) or neuro-
during the 1st week after acute SCI may be beneficial, but randomized logical symptoms (headache, blurred vision) usually due to bladder or
controlled trials are needed to determine optimal goals. 5,44-46 bowel distension resulting in a stimulus causing massive sympathetic
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The most important considerations are maintaining adequate intra- outflow, unregulated by supraspinal input, below the level of SCI.
vascular volume and blood pressure. Level II to IV evidence supports Although more commonly seen weeks to months after acute SCI and
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the prevention and treatment of hypotension (systolic blood pressure persisting indefinitely, autonomic dysreflexia can occur during the
<90 mm Hg) with early appropriate fluid resuscitation and avoidance acute post-SCI phase. The treatment of acute autonomic dysreflexia
of volume overload to maintain tissue perfusion and resolve shock. To consists of positional therapy (place in sitting position if supine) and
5
optimize resuscitation, arterial line insertion for continuous systemic identification and relief of triggers such as bladder or bowel distention.
pressure monitoring is recommended. Volume resuscitation may be Antihypertensive agents are usually not necessary and may result in
accomplished with crystalloids or colloids, and if indicated, blood hypotension. If needed, agents with a short half-life are preferred.
output, which is not necessarily monitored; however, adequate CO can ■ SPINAL SHOCK
and blood products. There are no specific targets for absolute cardiac
be inferred by a combination of adequate urinary output, normal or The term “spinal shock” refers to the loss of sensation accompanied by
decreasing lactate, and physical signs of adequate perfusion. If fluid resus- motor paralysis and depression of spinal reflexes caudal to the level of acute
citation is unsuccessful, additional evaluation with echocardiography, SCI. Typical features include flaccidity, loss of voluntary movement, and
pulse pressure variability (PPV), or PAC may be utilized. reduced tendon reflexes. Resolution of spinal shock is not precisely defined,
Vasopressors should be added in patients with hypotension unre- but occurs when hyperactive spinal reflexes appear. Spinal shock may be
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sponsive to adequate (eg, 30 mL/kg body weight) volume resuscitation. divided into four phases: (1) areflexia/hyporeflexia (0-1 days), (2) initial
Vasoactive agents with inotropic and chronotropic properties such as reflex return (1-3 days), (3) early hyperreflexia (4 days to 1 month), and

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