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one of the problems with researching information on neurogenic shock is that various authors treat it in a wide variety of ways. commonly neurogenic shock is classified as a vasodilational or distributive shock because the cvs is intact and there is no actual loss of fluid - merely dilation of the vascular bed. it is classed this way because has features in common with anaphylactic shock and early septic shock. with all of these usually a combination threapy is used. you need some fluids to return volume but you also need pressors. however other authors disagree and define neurogenic shock in relation to the pathophysiology underlying it therefor they either group it with spinal shock or they differentiate it.
here is a nice outline on shock (with nursing diagnoses!) neurogenic is near the end of the page. as you see this author includes it as a distributive shock.
differentiate hypovolaemic from neurogenic shock in cervical and thoracic spinal cord injuries, neurogenic shock with bradycardia and hypotension are common.
in neurogenic shock, unlike hypovolaemic shock, the pulse rate is slow and of good amplitude and the skin is usually warm and dry except if the patient has been exposed to a cold environment (see 5). tachycardia and clammy skin are seen in hypovolaemia.
neurogenic and hypovolaemic shock may coexist.
when this happens, neurogenic shock exacerbates the effects of hypovolaemic shock by disabling the vasoconstrictive reflexes that ordinarily preserve blood flow to vital organs.
although many article lump neurogenic and spinal shock together this article goes further in differentiating spinal shock from neurogenic shock
spinal shock is a state of transient physiological (rather than anatomical) reflex depression of cord function below the level of injury with associated loss of all sensorimotor functions. an initial increase in blood pressure is noted due to the release of catecholamines, followed by hypotension. flaccid paralysis, including of the bowel and bladder, is observed, and sometimes sustained priapism develops. these symptoms tend to last several hours to days until the reflex arcs below the level of the injury begin to function again (eg, bulbocavernosus reflex, muscle stretch reflex [msr]). neurogenic shock
neurogenic shock is manifested by the triad of hypotension, bradycardia, and hypothermia. shock tends to occur more commonly in injuries above t6, secondary to the disruption of the sympathetic outflow from t1-l2 and to unopposed vagal tone, leading to decrease in vascular resistance with associated vascular dilatation. neurogenic shock needs to be differentiated from spinal and hypovolemic shock. hypovolemic shock tends to be associated with tachycardia.
Then there is neurocardiogenic shock to deal with also.The way to differentiate(msp) neurocardiogenic shock from a true MI is the ckmb and troponin.Mainly the ckmb...in a MI it will trend upward from the first initial draw to the next lab draw 6 hours later. In Neurocardiogenic shock the ckmb will always trend down from the first draw to the second ckmb lab draw 6 hours/so later....it will go down and down and down etc.
With a MI it will trend up before it goes down.
When my lab dummy goes into neurogenic shock on Friday I'm going to call the "doctor" (ICU nurse/teacher who will calmly make me look like a fool) and ask if she might want to prescribe...dopamine as a vasopressor and atropine for the bradycardia??? And monitor the basil temperature for poikilothermia?
We treat neurogenic shock with noradrenaline and dopamine probably just at a renal dose.Sometimes patients end up on huge doses of Norad' because if they have raised ICP you have to maintain cerebral perfusion which is equal to the Mean arterial BP MINUS the ICP. So if you have a low BP and a high ICP you don't get adequate cerebral perfusion.
Bradycardia usually occurs due to raised intracranial pressure and wouldn't usually be treated with atropine-need to reduce the ICP. Neurogenic shock and raised ICP don't always go hand in hand though.