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Neurogenic Shock

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Neurogenic Shock NEUROGENIC SHOCK Introduction Neurogenic shock is a form of circulatory shock that may occur with severe injury to the upper spinal cord. It should not be confused with spinal shock, which refers to the initial flaccid muscle paralysis and loss of reflexes seen after spinal cord injury. Pathology Neurogenic shock results from severe spinal cord injury of the upper segments. This is usually at or above the level of T4, as the sympathetic cardiac nerves arise at the level of T1-4. Spinal cord lesions below this level do not result in neurogenic shock. The cause of the circulatory compromise is due to disruption of the descending sympathetic nervous supply of the spinal cord, hence a hallmark of the condition will be hypotension together with a bradycardia. Hypotension results from: ● Bradycardia, (or at least a failure of a tachycardic response to a fall in blood pressure). ● Reduced myocardial contractility ● Peripheral vasodilation. Note that isolated intracranial injuries to the CNS do not cause circulatory shock, and if this is present in such cases then other causes of shock need to be pursued. Clinical Features Patients with neurogenic shock usually have significant associated thoracic trauma and hypovolemic shock may co-exist with neurogenic shock. Hypovolemic shock is common, and immediately life-threatening, whilst neurogenic shock is uncommon, and rarely immediately life-threatening, in isolation. In the first instance any trauma patient who has hypotension must therefore be assumed to have hypovolemia until proven otherwise. The diagnosis of neurogenic shock must necessarily be one of exclusion. The classic description of neurogenic shock is hypotension without tachycardia or peripheral vasoconstriction. Typical clinical features of the condition include: 1. Hypotension: ● Hypotension is usually of a moderate degree only. 2. Bradycardia: ● Bradycardia is a characteristic feature, in contrast to all other types of circulatory shock. 3. Normal pulse pressure: ● A narrowed pulse pressure is not seen, (as it is for hypovolemic shock). 4. Peripheral perfusion: ● In pure cases of neurogenic shock, peripheral perfusion is not reduced. ● It may in fact be increased due to peripheral vasodilation, as may also be the case in septic or anaphylactic shock. This is in marked contrast to the far more common scenario of hypovolemic shock, where peripheral perfusion is significantly reduced. It is important to rule out other possible causes of bradycardia, before attributing it to neurogenic shock. Other important causes in this regard include: ● Drugs, in particular Beta-blockers. ● Intrinsic myocardial disease, such as complete heart block or other bradyarrhythmias. Investigations There is no investigation that can specifically diagnose neurogenic shock. The diagnosis will essentially be clinical and one of exclusion of the other more common causes of shock. Imaging investigations that demonstrate significant spinal cord injury at or above the level of T4 will raise suspicion that the condition exists, but this suspicion must always be assessed in the light of the overall clinical picture. Management Any hypotensive trauma patient must in the first instance be treated as for hypovolemic shock, as this may be rapidly fatal if not addressed. Patients with neurogenic shock usually have significant associated thoracic trauma and hypovolemic shock may co-exist with neurogenic shock. After ruling out other more common causes of shock, neurogenic shock is treated as follows: 1. Attention to any other immediate ABC issues. 2. Spinal immobilization, as required. 3. IV fluid resuscitation, and loading. ● Fluid administration alone may not be sufficient to restore blood pressure in neurogenic shock. 4. Vasopressors: ● Adrenaline or noradrenaline infusion may be required to restore blood pressure, when this fails to respond to fluid loading. Note that vasopressors are not a treatment for hypovolemic shock. 4. Atropine: ● This may be useful to treat bradycardia, contributing to the hypotension. 5. Establish monitoring: ● Continuous ECG monitoring ● Blood pressure, (preferably by arterial line). ● Pulse oximetry ● IDC, for urinary output ● Central venous line, for CVP measurements. 6. Avoid hypothermia References 1. ATLS Manual 8th ed 2008. Dr J. Hayes January 2009. .
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