Spinal Cord Injury
Primary Spinal Cord injury is any disruption of normal spinal cord anatomy and physiology. Secondary injury occurs when subsequent hypoxemia, hypoperfusion or inflammation causes further cell death in the areas surrounding the original injury, an area sometimes referred to as the injury 'penumbra'. It is loss of this additional tissue that worsens functional prognosis. This is why improved functional prognosis is seen in patients who receive early ICU care.
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Treatment goals should include:
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Avoid Hypotension... MAP goals of 85 mmHG x 7days*​
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Treatment of hypotension due to neurogenic shock following SCI should initially include volume resuscitation. Care should be taken to avoid fluid overload. Once normovolemia has been achieved, vasopressors may be added to maintain adequate perfusion goals
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If pressors are utilized, choose agents with both alpha and beta activity (e.g. norepinephrine)
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* The decision to use MAP goals of 85-90 mmHg for 7 days has to be weighed against the limitations of the data, and the risks for vasopressor use, prolonged immobilization, invasive monitoring, and prolonged consumption of limited critical care resources.
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Classification of Spinal Cord Injuries
The American Spinal Injury Association (ASIA) has created an International Standards for Neurological Classification of Spinal Cord Injury. This 'checklist' form allows a uniform grading system that can be used to communicate severity of injury amongst care teams and offers a prognostic framework to assist with treatment planning and patient discussions.
*Click on image to enlarge
What is the difference between "Spinal Shock" and "Neurogenic Shock"?
Neurogenic Shock = A state of severe vasodilation from loss of sympathetic tone to the distal vascular. The unapposed parasympathetic affect on the vast network of a patient's peripheral vascular conduits results in pooling of the patient's ~ 5 liters of blood in the periphery. This finding is more common if injury is above T6 cord level.
Overall physiologic effect of this occurence are:​
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Hypotension
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Bradycardia
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Loss of pre-load to the heart
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If sustained - sequela of distributive shock ensue
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end organ damage​
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lactic acidosis
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cardiovascular collapse
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Conversely:
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Spinal Shock = A physical exam finding that shows significant muscle flaccidity, loss of sensory and motor functions below the level of injury.
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Autonomic Dysreflexia
Autonomic dysreflexia (AD) can happen in complete or incomplete SCI, usually at or above T6 cord level. It occurs when there is a stimulus below the level of the cord injury such as bladder or bowel distension, pressure sores, or occult fractures. Anything that triggers painful stimuli, even though the patient cannot 'feel' it, can trigger the body to respond with a sympathetic response below the level of the injury. As blood pressure rises from this unregulated distal trigger, the areas above the injury respond with a compensatory parasympathetic response. These responses may or may not be associated with bradycardia.
in response to the trigger, the parasympathetic response in the higher, still innervated areas
aIt is a hypertensive crisis that is caused by unopposed sympathetic innervation. It can be trigged by bladder or bowel distension.
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Symptoms include:
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Acute hypertension
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Headache
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Diaphoresis
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Flushing
- Anxiety
- Nausea
- Nasal Congestion
- Blurred vision
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If untreated and severe, the hypertensive crises created by AD can lead to end-organ damage. Conditions precipitated by severe AD include:
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Myocardial infarction
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Stroke
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Seizures
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Pulmonary edema
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Treatment of acute AD consists of reducing the blood pressure by sitting the patient upright, followed by removal of tight-fitting garments, and correction of the inciting stimulus (most commonly fecal impaction or an obstructed indwelling urinary catheter). If hypertension persists despite nonpharmacologic interventions, administer a short-acting antihypertensive (e.g., nifedipine, captopril) with quick onset. Pharmacologic treatment of AD involves interrupting the sympathetic surge with such adjuncts as nitroglycerin cream and IV nifedipine. Prevention of AD is focused on avoiding potential precipitants.

Complications of Spinal Cord Injury in the Surgical ICU
The clinical implications of spinal cord injury are many. Loss of vascular tone and cardiac responsiveness to maldistribution of vascular volume early in a patient's course can cause end organ damage. The inability to cough and maintain pulmonary hygiene, sets a patient up for recurrent respiratory infections. Lack of mobility and loss of sensation increase the risk of tissue loss from pressure contact with beds / chairs. Autonomic dysregulation can create life / organ threatening adrenergic surges that require recognition and management to protect the patient.

