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Management of Neurogenic Shock Outside
of the Hospital

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Meta Description: Pubrica provides sample work assistance for the
out-of-hospital practitioner for the Management of Neurogenic Shock
Outside Hospital methods.
Management of Neurogenic Shock Outside of the
Hospital
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critically injured patient outside of a
hospital will be examined in the
essay that follows
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Introduction
The following essay will examine the evidence for managing a critically
injured patient outside of a hospital. I'll specifically focus on managing
neurogenic shock outside of a hospital, looking at the pathophysiology,
current management, and analgesia and critically analyzing the data
supporting the current practice. I'll also consider potential future
management strategies for the out-of-hospital practitioner.
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Pathophysiology
A potentially fatal condition known as the shock is characterized by
poor tissue perfusion, which results in cellular hypoxia and insufficient
metabolic activity.(Adam Silverman and Vincent Wang, 2005). One of
the shock risks is that as the inadequate blood supply harms cells, they
release an inflammatory response that increases blood flow to the
area. However, because the circulating volume is already low, the
demand for blood supply can draw blood away from other parts of the
body, leading to organ failure. The body tries to become more alkaline
by hyperventilating because mitochondria undergo anaerobic
respiration at the cellular level, which produces lactic acid and leads to
acidosis. In response to hypotension, the body's arteries' baroreceptors
produce the vital hormones adrenaline and norepinephrine (Guyton,
Arthur, and Hall, John 2006). Epinephrine is largely responsible for
raising heart rate because when heartbeats are faster, more blood is
released after each contraction, which raises artery and blood
pressure.
The internal diameter of the arterioles and veins is reduced by
norepinephrine, which leaves less room for the circulating volume,
raising resistance and, consequently, blood pressure. The body can
also regulate the location of blood vessel constriction, which directs
blood flow away from peripheral areas and toward vital organs like the
heart, lungs, and brain while diverting blood away from less important
organs like the gastrointestinal tract and kidneys.

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Reduced blood supply to the kidneys results in less urine production,
which allows more water to stay in the bloodstream and raises blood
pressure (John P. Cunha, D.O., FACOEP 2017). It is known as a
compensated shock when the body can use these processes to keep
blood pressure and organ perfusion in a situation of decreased
circulation volume. Decompensated shock is when the body cannot
adjust for the loss of circulation volume, and the perfusion of important
organs is no longer maintained (Kris, Kaull, B.S., NREMT-P, CCEMT-P
et al. 2016). The topic of this essay, neurogenic shock, falls under the
category of "Distributive shock," which is distinguished from other types
of shock because it can happen even when the heart's output is within
normal limits. (r: 2013 Lalit K. Kanaparthi, MD). Neurogenic shock may
develop after a catastrophic lesion to the brain, brain stem, or other
part of the central nervous system.
Damage to the nervous system's autonomic pathways causes a lack of
sympathetic tone, which causes vasodilation and blood to pool in the
extremities. Unopposed vagal activity can also cause bradycardia
(Piepmeier, Lehmann, and Lane 1985). Priapism owing to the loss of
sympathetic tone and subsequent vasodilation, hypotension, warm
flushed skin, and other atypical presentations of neurogenic shock is
caused by the loss of two of the body's compensating mechanisms;
Bradycardia; depending on where in the spinal cord the lesion occurs,
respiratory discomfort may also be present; at C5, where intercostal
muscle control has been lost, diaphragmatic breathing develops.
Respiratory arrest will occur at C3 or above if the diaphragm is lost in
control.
Management
As the original trauma cannot be reversed by a paramedic on the
scene and any attempt to treat the trauma would delay transfer to a
large trauma centre and treatment by a specialist spinal team, the
management of neurogenic shock in the prehospital setting is
constrained. As a result, therapy aims to avoid or lessen the possibility
of subsequent harm brought on by the hypotension brought on by the
shock (Adam Fox, DPM, D.O., FACS 2014). The prehospital
practitioner should try to administer fluid resuscitation to prevent or
lessen the harm caused by hypotension. A wide-bore cannula (a 14 or
16-gauge) should be implanted, cleaned, and secured. Although
evidence supports colloid fluids, paramedics in London exclusively
carry crystalloid fluids.
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neurogenic shock may develop
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More than 5,000 patients were evaluated in a study that looked at the
mortality of ICU patients in 57 hospitals across France, Belgium, North
Africa, and Canada. The conclusion indicated a 90-day death rate of
30.7% in patients given colloids and 34.2% in those given crystalloids
(Annane D et al., 2013). The study used a large group size and many
ICUs from various countries to reduce anomalous errors, and a
randomizer was used to determine which type of fluid would be used,
further improving accuracy; however, the study focused on hemogenic
shock rather than neurogenic shock and was based in ICU so that the
results may differ in the prehospital arena and neurogenic shock. While
colloids had a marginally better 90 mortality rate, it is statistically too
close to draw any real conclusions; other factors need to be
considered, such as price versus efficacy; could the money spent on a
3.9% improvement in survival be spent better elsewhere to save more
lives? We might also infer that the study demonstrated the necessity for
more research on the difference in efficacy. Another research looked at
using Methylprednisolone, a corticosteroid, in acute, blunt spinal cord
injury, sending a questionnaire to "clinical directors of emergency
departments, spinal units, and neurosurgical units in the U.K." The
research received responses from 187 emergency departments
(Frampton and Eynon).
The results indicated that 128, or 68.4%, of the participants utilized
Methylprednisolone, although 69% did so only on the recommendation
of a professional team, and 31% gave steroids after confirmation of
acute, traumatic spinal damage. The study looked at 187 A&Es in the
U.K., and once again, the study did not focus on the prehospital arena,
so that the results may differ in paramedic practice; the study also
focused on the incidence of use of Methylprednisolone rather than the
efficacy in acute, blunt spinal injury. In conclusion, a more concentrated
double-masked trial on the effectiveness of Methylprednisolone should
be conducted. Another important step in treating acute spinal injury is
to prevent the original damage from deteriorating; current practice for
this is to use a rigid neck collar and a hard backboard to prevent
excess movement; Manual handling is important to consider as well, as
excess movement can worsen the spinal injury(Multidisciplinary
Association of Spinal Cord Injury Professionals. 2015).
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The 'log roll' is the best approach to moving a patient onto a spinal
board (Adam Fox, DPM, D.O., FACS 2014). In a retrospective study of
45,284 trauma patients, 4.3% received spinal immobilization, overall
mortality was 8.1%, and the ratio of spine immobilized patients death
was 2.06 (1.35-3.13) compared to non-immobilized patients (Haut et al.
2010). The study's shortcomings are mostly those of retrospective
studies; the data they obtained "does not report prehospital scene or
transport times or differentiate urban versus rural care." As a result, we
could not establish that the increased mortality in patients who received
spine immobilization was related to delays in transit to ultimate
treatment." As a result, their conclusion that the reason for the increase
in mortality is due to the extra time on-scene, and while it may account
for some increase in the death rate, it would be impossible to conclude
if it is solely reasonable for the increase or if it is due to other factors
such as the rise in intracranial pressure (ICP) due to placing the collar,
would be impossible to conclude. This work should be scrutinized, and
more research into why the death rate is greater should be conducted
utilizing technologies such as the intrascanner (Weigl et al. 2016). The
prehospital practitioner should constantly do repeated primary surveys
and handle issues as they arise, specifically emphasizing airway
management.
After treating the hypotension and ruling out other causes, such as
catastrophic haemorrhage, the patient should be transported to the
nearest major trauma centre, with a pre-alert in place, under 1B of the
major trauma decision tree (London Trauma Office n.d.) if they are
experiencing neurogenic shock, or 2F if they are experiencing
suspected spinal trauma. If the patient is conscious and in pain due to
the injury, analgesics should be administered for the patient's comfort.
Analgesia
Every prehospital practitioner should strive to improve patient comfort;
therefore, minimizing the patient's discomfort is critical. Assuming the
patient is aware and complains of pain, the WHO recommends a step-
by-step approach to utilize the most conservative, effective alleviation.
When the patient is not experiencing diminished levels of awareness,
non-opiate medications are considered the first line of therapy (Brown,
S. N. et al. 2017).
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However, in cases of lowered consciousness, Entonox should not be
administered; instead, intravenous drugs such as paracetamol infusion
or morphine sulphate would be administered; however, morphine has
the side effect of lowering blood pressure (Mahinda, Lovell, and Taylor
2004), so in an already shocked patient, further increasing the blood
pressure would be inappropriate.
Ketamine is utilized in analgesia as an adjuvant or in place of opiates,
with the added benefit of not eliciting the same deep hypotension as
morphine does (Wong and Jenkins 1975). They examined the
difference between morphine and ketamine dosages in a trial on
participants aged 18-55 with acute onset pain. The results revealed a
minimal difference in pain reduction between morphine and ketamine,
4.1 vs. 3.9. However, the study's tiny sample size of a single centre
and small sample size were limitations, but robust randomization and
unbiasing techniques were in place. This study suggests that ketamine
can give subjectively equivalent pain relief to morphine but without the
consequences on cardiovascular stability. Another research was
conducted to compare ketamine to morphine in prehospital trauma
treatment. The research included 308 patients from rural Vietnam. Both
medicines were shown to have a similar incidence of pain alleviation.
However, ketamine had a lower incidence of vomiting, 5% against 19%
for morphine, and ketamine was found to have a reduced risk of
breathing issues. The study was limited since it was conducted in rural
Vietnam, so comparisons with London paramedics may yield different
results; the sample size was appropriate but might be increased, and a
solid randomization mechanism was in place. You can conclude.
Conclusion
In conclusion, the present therapy of spinal cord injuries and
neurogenic shock in the U.K. is appropriate; however, more study on
the advantages of colloid fluids for resuscitation and the benefits vs
risks of spinal immobilization and stiff neck collars is required.
Ketamine, in this author's opinion, is a superior analgesic alternative in
the stunned patient and should be evaluated for usage in the
prehospital setting.
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Guly, H. R., O. Bouamra, and F. E. Lecky. "The incidence of
neurogenic shock in patients with isolated spinal cord injury in the
emergency department." Resuscitation 76.1 (2008): 57-62.
Meister, Rafael, et al. "Neurogenic shock." Revue Medicale Suisse
10.438 (2014): 1506-1510.
Dave, Sagar, and Julia J. Cho. "Neurogenic shock." (2017).
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