Original article
Presentation of neurogenic shock within
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1
Medical Teaching Centre,
Warwick Medical School,
University of Warwick, Coventry,
UK
2
Emergency Department,
University Hospital Coventry and Objective To improve understanding of how
Warwickshire, Coventry, UK
Correspondence to
Matthew Pritam Taylor,
Medical Teaching Centre,
Warwick Medical School,
University of Warwick, Gibbet
Hill, Coventry CV4 7AL, UK;
matthew.p.taylor@warwick.
ac.uk
Received 10 February 2016
Revised 20 July 2016
Accepted 15 September 2016
Published Online First
3 October 2016
To cite: Taylor MP, Wrenn P,
O'Donnell AD. Emerg Med J
2017;34:157–162.
the emergency department
Matthew Pritam Taylor,1 Paul Wrenn,2 Andrew David O’Donnell1
ABSTRACT
Background Injury to the spinal cord can result in loss
of sympathetic innervation causing a drop in BP and HR,
this condition is known as neurogenic shock. There is
debate among the literature on how and when
neurogenic shock presents and what values of HR and
BP should be used to define it. Previous studies do not
take into account multiple prehospital and emergency
department recordings.
neurogenic shock presents in humans, allowing better
identification and treatment.
Methods The Trauma Audit and Research Network
database for an adult major trauma centre was used to
isolate patients with a spinal cord injury. Qualifying
patients had all available BPs and HRs collated into a
database. Patients with neurogenic shock were isolated,
allowing data analysis.
Results Out of 3069 trauma patients, 33 met the
inclusion criteria, of which 15 experienced neurogenic
shock. 87% of the patients who had neurogenic shock
experienced it within 2 hours of injury. Neurogenic shock
below the T6 level was less common ( p=0.009);
however, there were still four cases in the cohort. More
patients with complete spinal cord injury had neurogenic
shock ( p=0.039).
Conclusions Neurogenic shock is variable and
unpredictable. It can present in the prehospital
environment and without warning in a patient with
previously normal vital signs. The medical team should
be aware of it in all patients with spinal cord injury
regardless of injury level.
BACKGROUND
An injury to the spinal cord can cause instantan-
eous and possibly permanent dysfunction below
the level of injury. If this involves part of the spinal
cord associated with the sympathetic nervous
system, a condition called neurogenic shock can
develop.
Shock is said to be a state of inadequate tissue
perfusion.1 Neurogenic shock occurs when the
spinal cord is injured and sympathetic innervation
to the heart along with vasomotor tone is lost, with
prevailing parasympathetic innervation by the
intact vagus nerve. This results in hypotension and
bradycardia, the classical signs of neurogenic shock.
This is in contrast to spinal shock, which is a condi-
tion that occurs within 24 hours following a spinal
cord injury (SCI) where a patient will have total
loss of reflexes, flaccid paralysis and complete loss
of sensation below the site of injury.2
Preganglionic sympathetic neurons originating in
the hypothalamus, pons and medulla are located in
the intermediolateral cell column of the spinal cord
Taylor MP, et al. Emerg Med J 2017;34:157–162. doi:10.1136/emermed-2016-205780
Key messages
What is already known on this subject?
▸ Animal studies show that neurogenic shock
does not always present immediately
postinjury.
▸ There are no agreed criteria used to define
neurogenic shock.
What this study adds?
▸ The presentation of neurogenic shock is highly
variable in both time and severity. Healthcare
professionals should be aware of the possibility
of neurogenic shock in the prehospital and
hospital environment.
▸ A more sensitive than specific screening criteria
could help physicians better identify neurogenic
shock, leading to more appropriate treatment
and better patient outcome.
between the first thoracic (T1) and second lumbar
(L2) vertebrae.3 4 Theoretically, any SCI within or
above this could cause sympathetic disruption.
Since sympathetic innervation of the heart only
occurs from T1 to T5,5 it is often said that neuro-
genic shock can only occur when the lesion is
above the mid-thoracic (T6) level.3 6
Animal studies in cats, dogs and rats demonstrate
inconsistency in the presentation of neurogenic
shock, with occurrence ranging from minutes to
hours post-transection.7 It has also been shown in
some animal studies that immediately following
transection of the spinal cord there is a tachycardia,
possibly due to massive release of catecholamines.4
In humans, the greatest level of bradycardia was
shown to occur around 4 days postinjury; however,
this study was conducted in a specialist spinal
injury unit and therefore did not take into account
the initial changes in BP either prehospital or in the
emergency department.8
Due to its complex nature, there are no rigid cri-
teria for defining neurogenic shock. This is partly
due to the evolving nature of a trauma patient’s BP
and HR and the possibility of other aetiologies of
shock occurring simultaneously. In previous
research, Guly and colleagues highlight how identi-
fying patients with neurogenic shock is especially
difficult in cases with a mixed picture shock, with
aspects such as pain, anxiety and haemorrhage
clouding any clear presentation.7 Because of these
issues, the BPs and HRs used in previous studies
are quite variable (table 1).
Identification of neurogenic shock is important.
Often treatment for neurogenic shock needs to take
157
 Original article
Table 1 A summary of the criteria used to define neurogenic
shock from a selection of papers
Paper sBP (mm Hg)
Bernhard et al9 <70
Grigorean et al10 <90
Guly et al7 <100
Lehmann et al8 <90
Levi et al11 <90
Ley et al12 ≤90
Moerman et al13 <80
Zipnick et al14 <100
The systolic BP (sBP) in mm Hg and HR in bpm were recorded if discussed in the
paper.
place before the definitive diagnosis of an SCI has been estab-
lished. The aim is to maintain perfusion to the body and com-
promised spinal cord, helping reduce secondary cord damage,
which can make a substantial difference to a patient’s morbid-
ity.15 16 Neurogenic shock also prevents the vasoconstriction
and increase in cardiac output required if the patient is also
hypovolaemic.
One characteristic of neurogenic shock is the partial resistance
to fluids, which could be misinterpreted as volume loss.17 This
could result in overhydration of the patient, causing pulmonary
or spinal cord oedema.17 Appropriate management involves
initial use of fluids followed by support of HR and BP by vaso-
pressors and sympathomimetics; the specific drugs are currently
debated in the literature.18 Identification of neurogenic shock
followed by appropriate treatment and maintenance of BP is
one of the few interventions linked with better neurological
outcome.16 18
To date most research into the effect of SCI on the cardiovas-
cular system has only been conducted in specialist spinal injury
units, leaving a gap in research investigating the time course of
neurogenic shock presenting to the emergency department. No
studies take into consideration all the prehospital BPs and HRs
recorded by the ambulance crew, and all the recordings taken in
the acute setting such as those recorded on the trauma sheet.
By looking at patient observations in the prehospital environ-
ment, in the emergency department and in the intensive treat-
ment unit (ITU), this research hopes to gain a better
understanding of how neurogenic shock presents in humans. In
turn, this will help physicians identify neurogenic shock more
effectively, leading to better patient outcomes.
METHODS
Because there is no agreed definition, before starting the study, a
BP and HR were required to help isolate patients presenting
with neurogenic shock. As the study included patient observa-
tions taken in an acute environment, selection criteria that were
encompassing enough to highlight all patients with neurogenic
shock were required. We, therefore, defined neurogenic shock as
a condition in those patients with an SCI, a systolic BP (sBP) of
≤100 mm Hg and a HR of ≤80/min. This HR is high enough
to encompass all neurogenic shock cases, while also excluding
pure haemorrhagic shock, which typically presents with an
increased HR.
Inclusion criteria
The study looked at patients presenting acutely to the adult
major trauma centre at University Hospital Coventry and
158
Warwickshire (UHCW, Coventry, UK), for a 3-year period start-
ing from 1 January 2012. Patients were selected using the
Trauma Audit and Research Network (TARN) database for the
HR (bpm) hospital. This database registers information regarding all
patients presenting with trauma, whose length of stay is ≥3
<60
days, who were admitted to a high-dependency area or who
–
died in the emergency department.19 The detailed inclusion cri-
<80
teria for TARN can be found on their website at http://www.
–
tarn.ac.uk.19
–
According to TARN, in this 3-year period, there were a total of
≤90
3069 trauma patients admitted to UHCW.20 An initial search was
<60
performed by the hospital TARN department to create a database
<80
of those patients with any ‘spinal injury’ (ICD-10 codes:
S120-133, S140-141, S220-2211, S230-233, S240-241,
S320-3201, S327-331, S340-341). A further search was com-
pleted of the injury summary of these patients, isolating those
with either neurological compromise or complete cord syndrome.
Out of these, any patient who fulfilled our criteria for neurogenic
shock on any sBP/HR combination recorded on the database was
selected. Additionally, all patients who were transferred to the
ITU were selected. Up until this point, patient identifiable data
were hidden behind a submission ID in the TARN database.
Ethical approval was gained from both The University of
Warwick (Ref: REGO-20150-1619) and UHCW (Ref: GF0010).
The selected patients’ submission IDs were used to request their
notes through the hospital TARN coordinator. Full clinical
notes were then examined, and the following data, where avail-
able, were anonymously recorded into a database created for
this purpose:
▸ Systolic and diastolic BPs and HRs with timestamps from:
– The ambulance clinical record sheet
– The emergency department trauma sheet
– The emergency department clinical observation sheet
– Ward observations from the VitalPAC system (The
Learning Clinic Limited)
– ITU observations from the QS Clinical Information
System (GE Healthcare)
▸ Time of incident and time of arrival at hospital
▸ Radiological level of the most superior SCI
▸ Neurological level of injury and completeness (derived from
the American Spinal Injury Association (ASIA) score)—for
full scoring criteria, see http://www.asia-spinalinjury.org.21
Exclusion criteria
The following criteria excluded patients from the study:
▸ Patients with interhospital transfer
▸ Patients currently undergoing treatment as an inpatient
▸ Patients whose full clinical notes could not be obtained from
clinical records
▸ If there was a greater than 2-hour delay from time of inci-
dent to presentation to emergency services
▸ The patient has a simple and stable spinal fracture not involv-
ing the spinal cord.
▸ The patient had a significant comorbidity at the time of the
injury, and this would include having a cardiac arrest.
▸ The patient already had spinal pathology.
▸ The patient’s most severe injury region, calculated by the
body region with the highest abbreviated injury scale score,
was coded as ‘head’. We found those with a severe head
injury difficult to assess.
Data analysis
For each patient accepted into the study, the number of episodes
of neurogenic shock was recorded. An episode of neurogenic
Taylor MP, et al. Emerg Med J 2017;34:157–162. doi:10.1136/emermed-2016-205780

shock was defined as a single sBP/HR combination of
≤100 mm Hg and ≤80/min, and additional qualifying readings
within 30 min were not counted as separate episodes. To highlight
the severity of neurogenic shock we also recorded any episode of
marked bradycardia (a single HR of ≤45/min), or persistent brady-
cardia, which we defined as an average HR of <60/min lasting for
≥6 hours.
Descriptive statistics was performed on the whole cohort of
patients accepted onto the study, as well as separately on those
patients who experienced at least one episode of neurogenic
shock. Error ranges are 1 SD unless stated.
The time from injury to the presentation of neurogenic shock
and the level at which the injury occurred was analysed. χ2 was
used to test for a significant ( p<0.05) difference in those
patients with an SCI above or below the T6 mid-thoracic level.
To test whether those with a complete SCI were more likely to
have neurogenic shock, the data were cross-tabulated and again
χ2 was used to produce a p value.
RESULTS
Of the 3069 patients analysed, 33 were included in the study, of
which 15 (45%) fulfilled our screening criteria for neurogenic
shock on at least one sBP/HR recording. The patients were
screened based on the inclusion and exclusion criteria documen-
ted in the methods section, and the results are shown in
Figure 1 Screening of patients using information from the TARN
database, and clinical notes. Our criteria for neurogenic shock were a
HR of ≤80/min and systolic BP of ≤100 mm Hg. ITU, intensive
treatment unit; TARN, Trauma Audit Research Network.
Taylor MP, et al. Emerg Med J 2017;34:157–162. doi:10.1136/emermed-2016-205780
Original article
figure 1. Online supplement 1 documents relevant case informa-
tion for each individual patient.
The first ambulance BP recording of patients was a mean
average of 34 min (±17 min, n=28) after the SCI occurred, and
five patients were excluded from this calculation as they had no
time recording on the first BP. The first BP recording in hospital
was a mean average of 92 min (±25 min, n=32) after the SCI
occurred, and one patient was excluded from this calculation
due to lack of time data on the recording. The first sBP and HR
recordings of those 15 patients who at some point experienced
neurogenic shock are shown in figure 2. Three patients pre-
sented with an sBP above 100 mm Hg, and five patients pre-
sented with a HR above 80/min.
The number of minutes from the time of injury until the first
presentation of neurogenic shock was analysed. For six out of
the 15 patients (40%), the first presentation was the same as the
first ambulance recording, and therefore onset was before the
recording. The earliest onset recorded was 13 min from injury,
and the latest onset was 263 min from injury. The frequency dis-
tribution of onset is shown in figure 3.
The distribution of the lowest, most severe sBP and HR
recordings for patients who had neurogenic shock is shown in
figure 4. The distribution of the level of injury for the patients
in the study is shown in figure 5.
All of the patients in the study were separated into two
groups, injury at/above or below the mid-thoracic (T6) level.
Analysis using χ2 showed significantly (p=0.009) more patients
with neurogenic shock in the group with an SCI at/above T6.
Out of the 33 patients accepted into the study, the complete-
ness of injury could be established in 29, with the remaining
four patients’ notes not containing the required information.
Analysis using χ2 showed significantly (p=0.039) more patients
with neurogenic shock in the group with a complete SCI.
Figure 2 A box plot showing the first recorded BP and first recorded
HRs of the 15 patients who had ≥1 episode of neurogenic shock. The
solid line at 100 mm Hg (systolic BP) and dashed line at 80 bpm (HR)
represent the maximum values for classification of neurogenic shock.
Circle points represent outliers (cases ≥1.5× the IQR).
159
 Original article
Figure 3 A histogram showing the
frequency distribution of the time until
first NS presentation. Dark cases are
those who presented at or before the
first ambulance recording, and light
cases are those who presented at
subsequent recordings. NS, neurogenic
shock; SCI, spinal cord injury.
Figure 4 A box plot showing the lowest recorded systolic BP (sBP)
and lowest recorded HRs of the 15 patients with neurogenic shock.
The solid line at 100 mm Hg (sBP) and dashed line at 80 bpm (HR)
represent our maximum values for classification of neurogenic shock.
Circle points represent outliers (cases ≥1.5× the IQR).
Severity of the neurogenic shock was assessed. Out of the 15
patients who had neurogenic shock, 13 experienced at least one
episode of persistent bradycardia. Of those 13, five experienced
at least one episode of marked bradycardia. There was no statis-
tical correlation between the patients who experienced marked
bradycardia and either the presenting HR ( p=0.86), sBP
( p=0.34), number of neurogenic shock episodes ( p=0.48) or
completeness of injury ( p=0.20).
The time to first presentation of neurogenic shock was com-
pared against the first sBP ( p=0.28), and the first HR ( p=0.25),
160
showing no statistically significant correlation. There was also
no correlation between the number of incidences of neurogenic
shock and the presenting sBP ( p=0.48) or HR ( p=0.52).
DISCUSSION
This study looked in detail at BPs and HRs of patients with SCI
from the recordings made by the ambulance crew to those made
on the ward or in the ITU. Due to the labour-intensive process
of obtaining the data from clinical notes, we narrowed our
cohort down using selection criteria (figure 1), allowing us to
concentrate our resources on those patients most likely to have
neurogenic shock. From the 3069 trauma patients over the
3-year period, only 15 showed the classical signs of neurogenic
shock. This was despite choosing a relatively high sBP and HR
for a selection tool.
By using prehospital recordings, it was possible to see how
neurogenic shock develops an average of 34 min (±17, n=28)
after the time of injury, versus the average 92 min (±25, n=32)
until the first readings in hospital.
Using patients who experienced neurogenic shock, and
looking at their first prehospital sBP and HR recording, we were
able to compare this to the criteria of ≤100 mm Hg and
≤80/min (figure 2). It appears that 80% of the patients had a BP
less than 100 mm Hg, and 66% had a HR of ≤80/min. No
patients presented with a marked bradycardia, with an average
presenting HR of 74/min (±21, n=15). This relatively high HR
at the time of presentation is in keeping with the research in
animal studies, which suggests that bradycardia does not
develop immediately.4
The time at which neurogenic shock begins is not clear in the
literature. Determining this point was somewhat difficult as
40% of the patients presented when the first ambulance reading
was recorded. The earliest of these presentations was just
13 min from the time of injury. The latest first appearance of
neurogenic shock was 263 min from the time of injury. In this
particular case the patient was hypotensive at the time of pres-
entation to the ambulance crew; however, their HR remained
high for over 4 hours until neurogenic shock occurred, at which
Taylor MP, et al. Emerg Med J 2017;34:157–162. doi:10.1136/emermed-2016-205780

Figure 5 The number of patients with each level of spinal cord injury. Those patients who experienced neurogenic shock are dark and those who
did not are light.
point the HR quickly dropped to 44/min. As shown by figure 3,
87% of patients presented within 2 hours of injury.
Using an sBP≤100 mm Hg and HR ≤80/min, it was likely
that patients who did not have neurogenic shock would be
accepted as having it. By recording the lowest sBP and HR for
each patient who met the screening criteria, it was possible to
assess how well this compared against other definitions used in
previous papers. Figure 4 shows the distribution of results, and
table 1 shows the various definitions. Most papers use an sBP of
≤90 mm Hg, which would encompass over 75% of the patients;
however, Bernhard et al9 used an sBP of ≤80 mm Hg, which
comes below the mean average lowest BP, and therefore selects
much fewer patients. The HRs used to definite neurogenic
shock range from <60/min (a typical bradycardia) to ≤90/
min.9 12 13 Using a HR of <60/min would exclude over half the
patients. This, along with the greater spread of data for HR,
demonstrates that it is a less sensitive marker for neurogenic
shock than BP.
It is often taught that because sympathetic innervation of the
heart only occurs from T1 to T5,5 neurogenic shock cannot
occur in lesions below the mid-thoracic (T6) level.3 6 Although
there were significantly fewer ( p=0.009) incidences of neuro-
genic shock below the mid-thoracic level, neurogenic shock did
still occur. This corroborates other researchers who report,
although uncommon, neurogenic shock in patients presenting
with isolated SCI in the lumbar region.2 7 Innervation of vessels
occurs throughout the length of the sympathetic cord (T1–L2),5
and it could be postulated that loss of vasomotor tone could
result in shock. Two-thirds of the cases were injuries to the cer-
vical vertebrae (figure 5).
Currently, there is no clear consensus concerning the link
between neurological completeness of an SCI and the presence
of BP abnormality.22 Using clinical notes it was possible to estab-
lish the completeness of injury in 29 patients. Patients with com-
plete injuries were significantly ( p=0.039) more likely to
experience neurogenic shock than those with incomplete injur-
ies. Very few patient notes contained information about the
autonomic completeness of injury. West et al suggest that often
the level of neurological completeness does not agree with the
level autonomic completeness, and it is the autonomic com-
pleteness that predicts cardiovascular abnormality in chronic
SCI.22 There is still no agreement on the best method to estab-
lish autonomic completeness of injury; however, there has been
development of the international standards to document
remaining autonomic functions after SCI (ISAFSCI).5 Perhaps
testing for autonomic completeness using ISAFSCI in the
Taylor MP, et al. Emerg Med J 2017;34:157–162. doi:10.1136/emermed-2016-205780
Original article
emergency department could help predict the risk of cardiovas-
cular abnormalities such as neurogenic shock.
Due to the small number of patients isolated with neurogenic
shock, it was difficult to find any meaningful way of predicting
its severity. Presentation can be highly variable between patients
and does not appear linked to the severity of either the SCI, or
the presenting observations.
There were some limitations to the study. Neurogenic shock is
rare, and, therefore, effectively isolating patients with this condi-
tion is somewhat difficult. Due to the small number of patients
isolated, the power of the conclusions drawn is limited. There
were certain limitations characteristic of dealing with emergency
cases. Often recordings were missing or incomplete, and there
were gaps in observations when transferring the patient. There
was also only space for two or three prehospital observations,
meaning that the resolution during this critical time was particu-
larly low.
CONCLUSION
This study highlights the variable and unpredictable nature of
how neurogenic shock can present. It is a condition which the
medical team should be aware of in all patients with SCI,
regardless of the level of injury. It can present in the prehospital
environment and without warning in a patient with previously
normal signs. Having a screening tool that is more sensitive
than specific, by using a higher sBP (≤100 mm Hg) and higher
HR (≤80/min), will allow physicians to identify patients experi-
encing neurogenic shock earlier. Ultimately, the diagnosis is
made on clinical grounds, taking into consideration the multiple
aetiologies of shock present in each individual case. From here
the physician should be aware of the effective treatment of
neurogenic shock and act accordingly in order to improve
patient outcome.
Acknowledgements The UHCW TARN team for providing support using the TARN
database.
Contributors MPT: planning, experimental design, execution, statistical analysis,
writing up, publication. PW: planning, experimental design, execution, statistical
analysis. ADO: statistical analysis, editorial work, literature search.
Competing interests None declared.
Ethics approval UHCW NHS Research, Development & Innovation.
Provenance and peer review Not commissioned; externally peer reviewed.
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