Resuscitation 66 (2005) 127–139

Review

Spinal cord injury (SCI)—Prehospital management夽,夽夽

Michael Bernhard a,∗ , André Gries a , Paul Kremer b , Bernd W. Böttiger a,∗
a Department of Anesthesiology, University of Heidelberg, Im Neuenheimer Feld 110, D-69120 Heidelberg, Germany
b Department of Neurosurgery, University of Heidelberg, Im Neuenheimer Feld 400, D-69120 Heidelberg, Germany

Received 8 April 2004; received in revised form 1 March 2005; accepted 1 March 2005

Abstract

Up to 20,000 patients annually suffer from spinal cord injury (SCI) and 20% of these die before being admitted to the hospital in the
United States as well as in the European Union. Prehospital management of SCI is of critical importance since 25% of SCI damage may
occur or be aggravated after the initial event. Prehospital management includes examination of the patient, spinal immobilisation, careful
airway management (intubation, if indicated, using manual in-line stabilisation), and cardiovascular support (maintenance of mean arterial
blood pressure above 90 mmHg) and blood glucose levels within the normal range. It is still not known whether additional specific therapy
is useful. Studies have not demonstrated convincingly that methylprednisolone (MPS) or other pharmacological agents really have clinically
significant and important benefits for patients suffering from SCI. Recently published statements from the United States also do not support
the therapeutic use of MPS in patients suffering from SCI in the prehospital setting any more. Moreover, at this stage, it is not known whether
therapeutic hypothermia or any further pharmacological intervention has beneficial effects or not. Therefore, networks for clinical studies in
SCI patients should be established, as a basic requirement for further improvement in outcome in such patients.
© 2005 Elsevier Ireland Ltd. All rights reserved.

Keywords: Spinal cord injury; Emergency treatment; Fluid therapy; Blood pressure; Drug therapy

Contents
1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128
1.1. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128
1.1.1. Incidence and prevalence of SCI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128
1.2. Causes of SCI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128
1.3. Location of SCI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128
1.4. Prehospital findings of SCI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128
1.5. SCI-associated injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129
2. Prehospital management of SCI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129
2.1. Primary evaluation and resuscitation of vital functions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129
2.2. Patient immobilisation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130
2.3. Oxygenation and airway management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130
2.3.1. Prehospital problems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130
2.3.2. Prehospital solutions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 130
2.4. Cardiovascular support . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131

夽 Presented in part at the Third International Interdisciplinary Congress “EuroNeuro 2002”, from 12–14 September 2002, in Munich, Germany
by B.W. Böttiger.
夽夽 A Spanish translated version of the Abstract and Keywords of this article appears as Appendix at 10.1016/j.resuscitation.2005.03.005.
∗ Corresponding authors. Tel.: +49 6221 56 6110; fax: +49 6221 56 5345.
E-mail address: michael.bernhard@med.uni-heidelberg.de (M. Bernhard).

0300-9572/$ – see front matter © 2005 Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.resuscitation.2005.03.005
128 M. Bernhard et al. / Resuscitation 66 (2005) 127–139

2.4.1. Effects of systemic hypotension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131

2.4.2. Fluid resuscitation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131
3. Pharmacological treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 134
3.1. NASCIS 1 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 134
3.1.1. NASCIS 1—clinical relevance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 134
3.2. NASCIS 2 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 134
3.2.1. NASCIS 2—clinical relevance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 134
3.3. NASCIS 3 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135
3.3.1. NASCIS 3—clinical relevance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135
3.4. Statement on the treatment with steroids in prehospital management of SCI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135
3.5. Steroids are harmful in traumatic brain injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 136
4. Transportation and type of trauma centre . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 136
5. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 136
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 137

1. Introduction

This paper presents an overview of current practice in the

prehospital management of acute spinal cord injury (SCI).
Epidemiology, examination, patient immobilisation, airway
management, cardiovascular support, and pharmacological
treatment are discussed.

1.1. Epidemiology

1.1.1. Incidence and prevalence of SCI

The annual incidence of SCI including prehospital fatali-
ties has been estimated at 43–77 per million inhabitants in the
United States which equates to about 20,000 patients every
year. About 20% of these patients die before they are admit-
ted to the hospital [1–3]. This incidence of SCI is associated
with a prevalence of about 200,000 patients in the United
States [1].
Of these SCI patients 50–70% are between 15 and 35 years
of age, while 4–14% are 15 years old or younger. The male-
to-female ratio is 4:1. In 1990, the estimated costs for therapy
of SCI in the United States were around US$ 4 billion per
year [1]. Therefore, SCI is a major cause of mortality and
morbidity in young individuals and as a result has a major
impact on society as a whole.
Fig. 1. Spine injury with fracture and dislocation of C5 . Rupture of front and
rear longitudinal ligament. Such injury is associated with a risk of spinal cord
1.2. Causes of SCI injury.

The most frequent causes of SCI in adults are motor vehi- 1.4. Prehospital findings of SCI
cle accidents (40%), falls (21%), acts of violence (15%), and
sports-related injuries (13%). In children SCIs are mostly due The following clinical symptoms associated with SCI are
to sports (24%) and water recreational activities (13%) [1,4]. useful in identifying patients who require specific prehospital
treatment: lumbar pain, head injury and altered mental status,
1.3. Location of SCI cervical pain, neurological deficit, thoracic pain, and spinal
tenderness (Table 1) [5].
In a retrospective chart view of 331 patients, Domeier et It is very important to know that pain from SCI is not
al. described the distribution of SCI as 29% cervical, 24% necessarily localized in the area of injury. In 18% of cervical,
thoracic, 37% lumbar, and 10% sacral, due to the varying in 63% of thoracic, and in 9% of lumbar injuries, the pain
stability of the spine (Figs. 1 and 2) [5]. is located elsewhere [5]. If there is pain in a site that can be
 M. Bernhard et al. / Resuscitation 66 (2005) 127–139
Fig. 2. Spinal cord injury: haematoma (H) with shift and compression of the
spinal cord (M; this figure is kindly provided by Dr. Bodo Kress, Department
of Neuroradiology, University of Heidelberg, Germany).
related to SCI, it is necessary to take special care because
the location of injury can be in another segment of the spine.
Moreover, if a spinal injury is identified, there can be further
injuries at other spine segments in up to 15% [6].
1.5. SCI-associated injuries
It is well known that SCI occurs in 5–10% of patients
suffering from severe traumatic brain injury (TBI); con-
versely, 25–50% of patients with SCI have an associated head
injury [7,8]. Moreover, SCI occurs in 10–30% of patients
with multiple trauma. The majority of trauma in Europe
is blunt. Abdominal and thoracic trauma are often associ-
ated with severe haemorrhage; SCI occurs in up to 30% of
these patients. Therefore, SCI should always be considered in
patients with multiple trauma, as well as in those with minor
trauma who report spinal pain and/or have sensory or motor
symptoms, and in those with an altered mental status [9,10].
Table 1
Prehospital clinical findings by cervical to lumbar spinal cord injury [5]
Lumbar pain 37%
Head injury 36%
Altered mental status 31%
Cervical pain 15%
Neurological deficit 15%
Back pain 13%
Thoracic pain 11%
Spinal tenderness 8%
129
Abdominal bleeding or traumatic brain injury in patients
suffering from multiple trauma cause higher mortality rates
than SCI. Therefore, it is necessary that in severely injured
patients, treatment priorities should be established based on
their injuries, vital signs, and the injury mechanisms, accord-
ing to established advanced trauma life support (ATLS)
principles. Therefore, prehospital treatment in patients with
multiple trauma should be always conducted in accordance
with the management of the principal life threatening injury,
but the subsequent management of SCI must be born in mind
all the time [11].
2. Prehospital management of SCI
The goal of prehospital management of SCI is to reduce
neurological deficit and to prevent any additional loss of
neurological function. Therefore, prehospital management
at the scene should include a rapid primary evaluation of
the patient, resuscitation of vital functions (airway, breath-
ing, circulation; the “ABCs”), a more detailed secondary
assessment, and finally definitive care (including transport
and admission to a trauma centre). Moreover, after arrival
at the scene, it is important to “read” the scene and to
appreciate the mechanism of injury in order to identify the
potential for SCI. Prehospital management in general and
the management of the airway and ventilation in particu-
lar should include immobilisation of the spine in suspicious
cases to reduce the risk of a secondary SCI. Cardiovascular
support and pharmacological treatment complete the initial
prehospital management of SCI. Ultimately, the level of the
trauma centre and the time to appropriate surgical treatment
may determine neurological outcome [12–15]. The improved
prognosis of patients suffering from SCI today is reflected
by the general changes in prehospital care, in particular
rapid triage to facilities with SCI expertise, and advances
in medical, surgical and rehabilitative care. From a scien-
tific point of view however, the specific factors determining
the improved outcome today have not been clearly identified
[8].
2.1. Primary evaluation and resuscitation of vital
functions
In the initial examination [16] of the patient, the airway,
breathing, and circulation (the “ABCs”) should be evaluated,
controlled and restored according to recommended guide-
lines [17].
Secondary examination: a more thorough evaluation
should be performed (“head to toe/whole-body check”). In
particular, this examination should focus on patients with a
potential SCI and complaints of pain in the neck or back, ten-
derness to palpation, signs of muscle weakness, paralysis or
altered sensation, signs of incontinence, priapism, increased
skin warmth or flushing, and other superficial signs of injury
[16]. Prehospital findings should be documented precisely.
130 M. Bernhard et al. / Resuscitation 66 (2005) 127–139
2.2. Patient immobilisation
Historically, it is estimated that up to 25% of SCI may be
aggravated after the initial insult, either during transport or
early in the course of treatment [18,19]. It should be men-
tioned that these data are more than 20-years old, and no data
are available from actual studies. Careful movement and the
use of appropriate extrication techniques are crucial in all
trauma patients with SCI or in mechanisms of injury with
the potential to cause spinal injury and SCI. Immobilisation
of the entire spine is a management priority and should be
undertaken in a systematic fashion. The patient should be
immobilised in a neutral spine position at the scene and dur-
ing transport by using a rigid cervical collar, sandbags on
either side of the head, and on a rigid backboard with straps
[8,18,19]. In Europe, the vacuum splint device in combination
with a rigid cervical collar is a common option for immobil-
isation [19]. However, although immobilisation devices are
generally effective in limiting motion of the cervical spine,
they may be associated with important morbidity (i.e., dis-
comfort, pressure sore, decubitus ulcer, and restriction of
respiration) [8,19]. Therefore, immobilisation devices should
be removed when any lesion of the spinal cord or spine is
excluded with certainty after in-hospital diagnostic tests have
been performed [19].
Systems of immobilisation such as the Kendrick extrica-
tion device (KED) in combination with a rigid cervical collar
are useful to provide almost complete immobilisation of the
head and torso. These systems are often used to immobilise
patients with suspected SCI during extrication after a motor
vehicle crash. The time to apply these devices may be long
and therefore, they should only be applied if there are no
life-threating injuries and the patient’s vital functions are sta-
ble. Moreover, these devices are inappropriate in situations
where rapid extrication is necessary (e.g., fire in car with an
entrapped patient) [11]. Here, the patient should be evacuated
using manual in-line stabilisation with all available rescue
manpower.
2.3. Oxygenation and airway management
2.3.1. Prehospital problems
Possible problems associated with SCI are acute respira-
tory failure and hypoxia caused by hypoventilation, aspira-
tion, or impaired diaphragmatic function as a consequence
of injuries to the upper cervical region (C3–5 ) [20]. When the
SCI spares the diaphragm but paralyses the intercostal and
abdominal muscles, there may be inadequate coughing, para-
doxical rib movement on spontaneous ventilation, decrease
in vital capacity (50%) and functional residual capacity (85%
of predicted values), and loss of active expiration [21]. Com-
plete injury above the C3 level leads to apnoic respiratory
arrest and death unless immediate ventilatory assistance is
provided [8]. This may indicate the need to intubate the tra-
chea urgently [20]. Other problems of airway management
in patients suffering from SCI may occur if there are asso-
ciated facial and thoracic injuries [9], i.e., pneumothorax or
aspiration from pharyngeal hamorrhage.
Tracheal intubation attempts in patients with an unsta-
ble spine – according to some case reports – may lead to
severe SCI and death [22,23]. To preserve the spine and spinal
cord integrity, to reduce any resulting neurological deficit and
to prevent any additional loss of neurological function, the
patient must be intubated with great care and benefits must
be balanced against risk.
The role of rapid sequence induction for intubation of
the trachea in the prehospital trauma setting by trained EMS
staff is crucial and may be used as an advanced airway man-
agement technique to improve the success of intubating the
trachea [24]. Intubation of the trachea in patients suffering
from SCI should be accompanied by rapid sequence induc-
tion in order to reduce coughing and spontaneous movements.
The use of succinylcholine in patients with SCI may cause
bradycardia leading to arrest secondary to hyperkalaemia, but
it is probably safe to use it during the first 48 h after SCI [25].
In a retrospective study of 140 patients suffering from
traumatic cervical spine fracture, the distribution of the frac-
ture site was as follows: 19% C1–2 , 21% C3–4 , and 60% C5–7
[26]. In human subjects without any cervical abnormality
[27], and in fresh human cadavers [28], the vast majority of
cervical movement from orotracheal intubation using direct
laryngoscopy occurs at the atlantooccipital and atlantoaxial
joints. The subaxial cervical segments (C2–5(7) ) are displaced
less frequently.
From studies on cadavers, it is known that the use of man-
ual in-line stabilisation (please see below) results in signifi-
cantly less anteriorposterior displacement during orotracheal
intubation than the use of a rigid cervical collar [29]. Fur-
thermore, it is more difficult to open the mouth with a rigid
cervical collar in place and cervical mobility is restricted,
which makes intubation more difficult with the risk of air-
way compromise, difficult intubation, and aspiration.
2.3.2. Prehospital solutions
Continuous pulse oximetry is used in patients with SCI
to detect hypoxia. Immediately after arrival at the scene and
always before intubation, the patient should receive oxygen
via a face mask (preoxygenation) and the neck should be
immobilised. Intubation of the trachea (or another method
of securing the airway) and controlled ventilation are indi-
cated if saturation (Sp O2 ) is persistently less than 90%, if
the respiratory rate is low, or if the Glasgow Coma Scale
(GCS) is less than 9. Intubation of the trachea should be per-
formed in accordance with the concept of rapid sequence
induction [24]. When intubation is urgent, the rigid cervi-
cal collar should be opened and manual in-line stabilisation
(MILS) applied to ensure mechanical stability of the spine
[8]. MILS means that a second person immobilises the cer-
vical spine in a neutral position using both hands on each
side of patient’s head in order to prevent any movement of
the neck [30]. After successful intubation the rigid cervi-
cal collar should be reapplied. MILS reduces cervical spine
 M. Bernhard et al. / Resuscitation 66 (2005) 127–139 131

movement during intubation of the trachea, but it does not

totally prevent movement [31,32].
Alternative airway devices such as the laryngeal mask,
the intubating laryngeal mask and the Combitube may exert
greater pressure on the cervical vertebrae than conventional
intubation techniques, these devices should only be used
when routine intubation is not possible [33]. An accepted
in-hospital standard in patients suffering from SCI is fibre-
optic tracheal intubation [25], but this technique is not often
used in the prehospital setting.

2.4. Cardiovascular support

Possible cardiovascular problems associated with SCI

are neurogenic and hypovolaemic shock. Neurogenic shock
may occur in SCI above T5 when the injury has caused a
sympathectomy below the level of injury. Neurogenic shock Fig. 3. Hypotension is a common phenomenon and may lead to secondary
is associated with hypotension secondary to arteriolar and brain damage in patients suffering from severe traumatic brain injury (TBI).
In a prospective study in patients suffering from severe TBI, early hypoten-
venous vasodilatation, hypotension secondary to loss of the
sion (systolic blood pressure (SBP) <90 mmHg; n = 248/717) during pre-
sympathetic outflow from the splanchnic vascular beds, and hospital care was associated with a doubling of mortality (55% vs. 27%;
bradycardia secondary to interruption of the sympathetic p < 0.05). Moreover, late hypotension (SBP <90 mmHg; n = 117/493) dur-
innervation of the heart [8,25]. These pathophysiological ing intensive care unit (ICU) stay was also associated with a 3.8-fold higher
changes cause pooling of blood in the extremities and mortality (66% vs. 17%; p < 0.05) and significantly worse neurological out-
come [36].
reduction of central venous return. Thus, neurogenic shock
may be associated with a systolic blood pressure (SBP) less
cause of cerebral ischemia secondary to severe traumatic
than 70 mmHg and with severe bradycardia below 60 beats
brain injury (TBI) [36]. In these patients, hypotension in
per minute.
the early stages (SBP less than 90 mmHg) was associated
Both multiple trauma and severe haemorrhage can be
with a doubling of mortality (55% versus 27%; p < 0.05).
associated with SCI in up to 30% of cases. Hypovolaemic
Moreover, hypotension occuring later during the intensive
shock may be associated with SBP of less than 90 mmHg
care unit (ICU) stay was associated with a 3.8-fold higher
and tachycardia. Other causes of hypotension associated with
mortality (66% versus 17%; p < 0.05) and significantly worse
tachycardia should be excluded (e.g., blood loss associated
neurological outcome (Fig. 3) [36]. These data demonstrate
with other injuries) [25]. It may be possible to distinguish
that when hypotension occurs, it may be associated with sec-
neurogenic from hypovolaemic shock but they are often com-
ondary brain damage in patients suffering from severe TBI.
bined in the prehospital situation [16].
Based on the extrapolation of these findings, hypotension
The major goal in SCI is to reestablish circulation to
should be avoided by adequate prehospital management.
the neural tissue. Therefore, during the management of neu-
rogenic shock, the patient should be in the Trendelenburg
2.4.2. Fluid resuscitation
position, with atropine and a catecholamine administered
2.4.2.1. Crystalloids and colloids. For fluid resuscitation in
intravenously, if indicated. To re-establish the circulation in
the prehospital setting crystalloids or colloids can be given
neural tissue during hypovolaemic shock the patient should
although which is to be preferred is still a matter of debate.
also be in the Trendelenburg position and receive intra-
Crystalloid solutions are isooncotic and offer varying
venous fluids. However, fluid resuscitation should be used
osmolarities (Table 2). Compared with crystalloids, colloids
with special care in this situation because it can lead to pul-
have the same osmolarity but a different oncotic pressure
monary oedema [25]. At least two 14G IV cannulae should
(Table 2). To varying degrees, colloids can cause anaphylaxis
be used. The desired mean arterial blood pressure (MAP) is
at least 90 mmHg; each episode of hypotension (SBP less Table 2
than 90 mmHg) should be avoided or corrected as quickly as Characteristics of crystalloid and colloid solutions [37]
possible [9,34]. To achieve the desired MAP, fluid resusci- Osmolarity (mOsmol/l) Oncotic pressure (mmHg)
tation plays an essential role in prehospital management of
Ringer’s lactate 273 0
SCI associated with hypovolaemia [35]. NaCl (0.9%) 309 0
NaCl (7.5%) 2567 0
2.4.1. Effects of systemic hypotension Plasma 295 21
Prospective controlled studies reflecting the effects of Dextran 70 (6%) 300 19
hypotension in SCI on neurological outcome are lacking. Dextran 40 (10%) 300 169
HES (6%) 310 31
Nevertheless, it is well known that hypotension is a frequent
132 M. Bernhard et al. / Resuscitation 66 (2005) 127–139

Table 3
Side effects of colloid solutions [38]
Blood coagulation Anaphylaxia
Dextran +++ ++
Gelatin + ++
HES (450/0.7) ++ +
HES (200/0.5; 130/0.4) + +
+++: high; ++: moderate; +: low.

and disturbances in blood coagulation. In particular, dextran

and HES (450) have clinically important effects on blood
coagulation (Table 3). Therefore, they may not be used in
a situation with SCI. Some clinicians prefer gelatin or HES
(200/0.5 or 300/0.4) in treating SCI patients (Table 3) [37,38].

2.4.2.2. Hypertonic–hyperosmotic solutions. The concept Fig. 4. Hypertonic–hyperosmotic solutions (HHS) may be administrated in
of “small-volume resuscitation” (SVR) uses hypertonic– prehospital management of patients suffering from multiple trauma or severe
traumatic brain injury (TBI) with systolic blood pressure (SBP) <100 mmHg:
hyperosmotic solutions and to provide the initial therapy for In a prospective, randomized, double-blind clinical trial, 166 trauma patients
severe hypovolaemia and shock associated with trauma [39]. with SBP < 100 mmHg were divided into two groups. One group (n = 83)
No clinical studies on SVR have been carried out in patients received 250 ml lactated Ringer’s solution as the initial volume loading,
with SCI. However, some data are available from patients while the second group (n = 83) was treated with 250 ml HHS (7.5% sodium
with multiple trauma, and severe TBI. In an earlier prospec- chloride/dextran 70), initially. In the entire cohort, patients with HHS treat-
ment showed a better survival to hospital discharge. In the subgroup with
tive, randomized, double-blinded clinical trial, 166 trauma patients suffering from TBI, differences in survival did not reach statistical
patients with SBP less than or equal to 100 mmHg were significance. However, HHS was associated with a tendency toward improv-
divided into two groups [40]. One group received 250 ml lac- ing survival in this subgroup [40].
tated Ringer’s solution as the initial volume loading, while
the second group was treated with 250 ml HHS (7.5% sodium
chloride/dextran 70). In the group with multiple trauma
(among them some with severe TBI), patients treated with
HHS showed a better survival at hospital discharge. In the
subgroup with severe TBI alone, the differences in survival
did not reach statistical significance. However, HHS also was
associated with a tendency toward improving survival in this
subgroup (Fig. 4) [40].
Another recently study by Cooper et al. [41] could
not show a significant benefit. In this prospective, dopple-
blinded, and controlled study, 229 patients suffering from
severe head injury (GCS < 9) and suffering from a SBP less
than or equal to 100 mmHg were randomly divided into two
groups: one group (n = 114) received an initial infusion with
250 ml of hypertonic 7.5% saline solution (without oncotic
combination), while the other group (n = 115) was treated
with 250 ml of lactated Ringer’s solution. Additionally, both
groups received conventional fluid management. Survival to
hospital discharge was similar in both groups (55% ver-
sus 50%; p = 0.32). After 6 months, the survival rate was Fig. 5. In a prospective, dopple-blinded, and controlled study, 229 patients
not significantly different between both groups (55% ver- suffering from severe head injury (GCS < 9) and a systolic blood pressure
less than or equal to 100 mmHg were randomly divided into two groups:
sus 47%; p = 0.23) (Fig. 5) [41]. It should be mentioned
one group (n = 114) received an initial infusion with 250 ml of hypertonic
however, that the difference of 8% between the groups was 7.5% saline solution (without oncotic combination), while the other group
perhaps remarkable. With more patients in such a trial, the (n = 115) was treated with 250 ml of lactated Ringer’s solution. Additionally,
difference could approach significance. Additionally, the data both groups received conventional fluid management. Survival to hospi-
from subgroup analysis presented by Cooper et al. [41] tal discharge was similar in both groups (55% vs. 50%; p = 0.32). After 6
months, the survival rate was not significant different between both groups
showed a non-significant lower median ICP (10 mmHg ver-
(55% vs. 47%; p = 0.23) [41]. Also in this recently published study, hyper-
sus 15 mmHg; p = 0.08) and a non-significant shorter dura- tonic saline solution was associated with a tendency toward improving
tion of CPP under 70 mmHg (9.5 h versus 17 h, p = 0.06) hospital discharge and survival after 6 months in patients suffering from
for patients treated with hypertonic saline solution in the neurotrauma.
 M. Bernhard et al. / Resuscitation 66 (2005) 127–139
intensive care unit, in comparison with patients treated with
Ringer’s solution. Lewis [42] discussed in his accompanying
editorial the expected effects of hypertonic solution. Because
there was a non-significant trend toward improving survival
to hospital discharge and survival at 6 month, Lewis sug-
gested that further studies with a larger sample size are
needed to determine the potential therapeutic effects of HHS
[42].
From the actually available data it is not absolutely clear
whether hypertonic or hypertonic–hyperosmotic solutions do
lead to a clinical benefit in the management of patients with
TBI. There are no further clinical data concerning HHS in
SCI available. We only have further data from experimental
studies. The positive effects of HHS in experimental SCI
include the attenuation of leukocyte adhesion, an increase in
spinal cord blood flow, and an improvement in neurological
function and survival [43–45]. From a scientific point of view,
it is still unknown whether HHS has a clinical benefit in the
management of patients with TBI or SCI.
Therefore, in cases where hypotension or multiple trauma
are combined with SCI, the use of HHS as SVR may be
justified and not harmful, and possibly indicated according
to these data, but controlled clinical trials in SCI patients are
still lacking.
2.4.2.3. Glucose. Fluid resuscitation in the prehospital set-
ting should not include glucose as an infusion, because there
are at least two problems associated with glucose. Firstly,
glucose metabolises rapidly, resulting in “free” water, which
supports oedema formation. Secondly, there is the risk of
hyperglycaemia with an increase in the anaerobic glycolysis
rate, which increases lactate and reduces pH. We know that
in different settings, including stroke, cardiac arrest, and oth-
ers, that elevated blood glucose levels are associated with a
negative effect on outcome [46,47]. Although clinical studies
about the effects of elevated blood glucose levels in SCI do
not exist, it can be speculated that they are probably the same
in SCI.
Clinical data do exist for the association of blood glucose
levels and outcome in patients with severe TBI and with a
GCS of 8 or below. In a prospective study in 267 patients
undergoing surgery to drain an intracranial hematoma and/or
to place a device for intracranial pressure monitoring, there
was a significant relationship between high blood glucose
levels and high intracranial pressure. To investigate neurolog-
ical outcome, the authors used the Glasgow Outcome Scale
(GOS, 1 = dead, 2 = vegetative state, 3 = severe disablility,
4 = moderate disability, 5 = good recovery). Post-operative
blood glucose levels higher than 200 mg/dl were associated
in 20% of cases with a GOS of 4 or 5 and in 80% with
a GOS of 1–3, while post-operative blood glucose levels
lower than 200 mg/dl were associated in 83% of cases with
a GOS of 4 or 5 and only in 17% with a GOS of 1–3 (Fig. 6)
[48].
No clinical data are available on treatment with insulin
in SCI patients, only for the use of insulin in critically ill
133
Fig. 6. Blood glucose levels higher than 200 mg/dl may lead to a worse neu-
rological outcome. In a prospective study in 267 patients undergoing surgery
to drain an intracranial haematoma and/or to place a device for intracra-
nial pressure monitoring, there was a significant relationship between high
blood glucose levels and high intracranial pressure. To investigate neurolog-
ical outcome, the authors used the Glasgow Outcome Scale (GOS, 1 = dead,
2 = vegetative state, 3 = severe disablility, 4 = moderate disability, 5 = good
recovery). Post-OP blood glucose levels higher than 200 mg/dl were associ-
ated in 20% of cases with a GOS of 4 or 5 and in 80% with a GOS of 1–3,
while post-OP blood glucose levels lower than 200 mg/dl were associated
in 83% of cases with a GOS of 4 or 5 and only in 17% with a GOS of 1–3
(p < 0.001) [48].
patients in the intensive care unit (ICU). A prospective, ran-
domised controlled study included 1548 patients admitted
to a surgical ICU who were being mechanically ventilated.
These patients were randomly assigned to receive either
intensive insulin therapy (blood glucose levels between 80
and 110 mg/dl) or conventional treatment if the blood glucose
levels exceeded 215 mg/dl with a maintenance of blood glu-
cose at a level between 180 and 200 mg/dl. Intensive insulin
therapy reduced mortality during the ICU stay from 8.0%
(conventional therapy; n = 783) to 4.6% (intensive insulin
therapy; n = 765) with p < 0.05 (Fig. 7) [49].
In a subgroup analysis including 63 patients with neu-
rological disease, cerebral trauma or brain surgery, intensive
insulin therapy was associated with a mortality rate of 18.2%,
compared to 23.3% in the conventional therapy group.
Therefore, the goal of treatment is probably – but this is
indirect evidence only and based on an extrapolation from
data obtained in other patient cohorts – to reach a blood glu-
cose level within normal range, which means i.v. glucose
administration is only necessary in cases of acute hypogly-
caemia. In the early management of patients with SCI, blood
glucose levels should be measured and if necessary, insulin
administered to produce blood glucose levels within the nor-
mal range as soon as possible. It should be mentioned that it
is uncommon to use insulin in the prehospital environment.
Therefore, in reality the glucose level should be measured
and treated as soon as possible in the course of in-hospital
management.
134 M. Bernhard et al. / Resuscitation 66 (2005) 127–139
Fig. 7. Intensive insulin therapy may improve outcome in critically ill
patients. A prospective, randomised, controlled study included 1548 patients
admitted to a surgical ICU who were being mechanically ventilated. These
patients were randomly assigned to receive either intensive insulin therapy
(blood glucose levels between 80 and 110 mg/dl) or conventional treatment,
if the blood glucose level exceeded 215 mg/dl with a maintenance of blood
glucose at a level between 180 and 200 mg/dl. Intensive insulin therapy
reduced mortality during the ICU stay from 8.0% (conventional therapy;
n = 783) to 4.6% (intensive insulin therapy; n = 765) with p < 0.05 [49].
3. Pharmacological treatment
Some experimental studies have suggested that treatment
with methylprednisolone (MPS) may be beneficial in SCI
[50,51]. Possible positive effects of MPS are cell membrane
stabilisation, inhibition of lipid peroxidation and a reduction
of oxygen free radicals, increased blood flow, and a reduction
of oedema and inflammation [9].
The most important clinical studies considered methyl-
prednisolone (MPS) naloxone, tirilazad mesylate, and GM-1
gangliosides. Indeed, the clinical use of MPS was investi-
gated in the United States in three National Acute SCI Studies
(NASCIS).
3.1. NASCIS 1
The first NASCIS trial was a multicentre study and
included 330 patients in a double-blind setting [52,53]. These
patients were randomised to receive either MPS 100 mg i.v.
bolus/day for 10 days or MPS 1000 mg i.v. bolus/day for
10 days. The results showed no difference in neurological
recovery at 6 weeks, 6 months, and 1 year after MPS admin-
istration. However, a significantly increased incidence of
wound infections was found in the group receiving the higher
dose of 1000 mg MPS as compared to the group receiving
100 mg MPS (9.3% versus 2.6%, relative risk 3.6; p = 0.01)
[52].
3.1.1. NASCIS 1—clinical relevance
The major problem of NASCIS 1 was related to the fact
that no results from placebo-treated groups were obtained.
Table 4
National Acute Spinal Cord Injury Study 2 [55]
Changes in functiona Placebo Methylprednisolone p
6 weeks (n = n.r.)
Motor n.r. n.r.
Pinprick 4.8 6.7 n.s.
Touch 3.9 6.1 n.s.
6 months (n = n.r.)
Motor n.r. n.r.
Pinprick 6.6 10.0 0.012
Touch 5.9 8.7 0.042
Results in all patients (n = 487). n.r. = not reported; n.s. = not significant.
a Change in function, scores for motor function ranged from 0 to 70, and
scores sensation of prinprick/touch ranged from 29 to 87.
Therefore, the results were inconclusive and it was still not
known whether MPS is useful in SCI [54].
3.2. NASCIS 2
Consequently, NASCIS 2 was performed in the 1980s
[55,56]. A multicentre, randomised, double-blind, placebo-
controlled trial of 487 patients evaluated the efficacy and
safety of MPS (30 mg i.v. bolus/kg + 5.4 mg/kg/h for 23 h
continuously, n = 162) and naloxone (5.4 mg i.v. bolus/kg +
4.0 mg/kg/h for 23 h continuously, n = 154) within 12 h after
SCI and placebo. Neurological function was assessed on
admission and based on an expanded motor score that ranged
from 0 to 70 and an expanded pinprick/touch sensitivity score
that ranged from 29 to 87. The study evaluated the changes
with regard to these scores.
Interestingly, no data on motor function were reported for
any patient (Table 4) [55]. Regarding reaction to pinprick and
touch, the patients in the MPS-treated group did not show a
significant increase as compared to the placebo group after 6
weeks. Nevertheless, the data did suggest a small but signifi-
cant increase in pinprick and touch function (p = 0.012) after
6 months (Table 4) [55]. However, the question remains as to
whether an improvement of 10.0 versus 6.6 on a scale from
29 to 87 really represents a clinically relevant improvement
[54,57]. The results from the 1-year follow-up did not show
any positive effect in either the MPS or the naloxone group.
Compared to placebo, the results in all patients were not as
positive as expected. Yet, a subgroup analysis in patients who
were treated within 8 h after SCI showed a small but sig-
nificant increase in motor function and prinprick and touch
sensitivity both after 6 weeks and after 6 months (Table 5)
[55]. The 1-year follow-up showed a small but significant
increase in motor function in MPS-treated patients (12.0 ver-
sus 17.2, p = 0.030; based on an expanded motor score that
ranged from 0 to 70) [56]. Naloxone used within 8 h after SCI
had no effect.
3.2.1. NASCIS 2—clinical relevance
After the NASCIS 2 trial, MPS treatment within 8 h of
SCI became a standard therapy in acute SCI in the United
States and in many other parts of the world, despite the fact
 M. Bernhard et al. / Resuscitation 66 (2005) 127–139 135

Table 5 Table 6
National Acute Spinal Cord Injury Study 2 [55] National Acute Spinal Cord Injury Study 3 [59]
Changes in functiona Placebo Methylprednisolone p Changes in functiona Methylprednisolone p
6 weeks (n = 196) 24 h 48 h
Motor 7.2 10.6 0.048
Pinprick 4.8 7.8 n.s. Intent-to-treat
Touch 2.5 6.3 0.034 6 weeks (motor) 9.0 (n = 151) 11.8 (n = 154) 0.09
6 months (motor) 13.4 (n = 142) 16.8 (n = 149) 0.07
6 months (n = 185)
Motor 11.2 16.0 0.033 Complied with protocol
Pinprick 6.6 11.4 0.016 6 weeks (motor) 8.8 (n = 144) 12.4 (n = 145) 0.04
Touch 4.3 8.9 0.030 6 months (motor) 13.2 (n = 136) 16.9 (n = 141) 0.06

Subgroup analysis. Patients treated within 8 h. n.s. = not significant. Results in all patients, treated with MPS.
a Change in function, scores for motor function ranged from 0 to 70.
a Change in function, scores for motor function ranged from 0 to 70, and

scores sensation of prinprick/touch ranged from 29 to 87.

an increase of 1◦ in motor function on the admission score.
that problems and major criticism were published about the Data for patients treated under 3 h after SCI did not show any
study [54,57,58]. Only minor benefits demonstrated in sub- effect.
group analyses were documented and a major criticism of
the subgroup analysis was that demographic data were lack- 3.3.1. NASCIS 3—clinical relevance
ing. It was not shown whether the minor positive effect was As for NASCIS 1 and 2, again, major problems and major
really balanced from baseline. In addition it was not stated criticisms of NASCIS 3 have been published [54,57,58]. The
whether the subgroup was defined in advance, which is a first problem was that the treatment arms appeared to be
major prerequisite for scientific quality of clinical studies in unbalanced. The numbers of patients with normal baseline for
any subgroup. Another problem was that no functional test motor function in the treatment arms of MPS administered
was performed, nor were group size calculations made in for 24 h and MPS administered for 48 h were significantly
advance. Apparently, there are major limitations and missing different (25% versus 14%; p = 0.007). Therefore, the major
data in the publication of this study. Moreover, MPS-treated results of the study should be interpreted with caution. More-
patients presented with clinically important side effects (e.g., over, again, most of the benefit is shown in subgroup analysis
wound infection: MPS 7.1% versus naloxone 3.3% versus only. In NASCIS 3, there are 36 potential subgroups. With 20
placebo 3.6%; p = 0.21). Clearly, therefore, this study could subgroups only and by chance alone, one subgroup reached
not be considered a basis for the general recommendation for statistical significance at p < 0.05. In addition, following the
using MPS in SCI patients [54]. administration of MPS for 48 h, an increase in side effects
was shown (e.g., severe pneumonia: 24 h MPS 2.6% ver-
3.3. NASCIS 3 sus 48 h tirilazad 0.6% versus 48 h MPS 5.8%; p = 0.02)
[54,57].
Following these unconvincing data, the NASCIS 3 study Therefore, even after NASCIS 3, it is still questionable
was performed in the 1990s [59,60]. This study evalu- from a scientific point of view whether treatment with MPS
ated the efficacy and safety of MPS (30 mg i.v. bolus/kg is beneficial in patients suffering from SCI or not.
initially + 5.4 mg/kg/h for 24 h continuously, n = 166) ver-
sus MPS (30 mg i.v. bolus/kg initially + 5.4 mg/kg/h for 3.4. Statement on the treatment with steroids in
48 h continuously, n = 167) versus tirilazad combined with prehospital management of SCI
MPS (initial 30 mg MPS i.v. bolus + 2.5 mg tirilazad i.v.
bolus/kg + 2.5 mg tirilazad i.v. bolus/kg every 6 h for 48 h, Based on the data presented above, some reviews refrained
n = 166) in a multicentre, randomized, double-blind trial in from use of MPS in the treatment of patients with SCI [61,62].
499 patients with SCI [59,60].
The analysis of all patients treated with MPS complying Table 7
with the protocol for 48 h showed a small but significant dif- National Acute Spinal Cord Injury Study 3 [59]
ference in motor function after 6 weeks compared to patients Changes in functiona Methylprednisolone p
treated with MPS for 24 h (8.8 versus 12.4, p = 0.04; based on 24 h 48 h
an expanded motor score that ranged from 0 to 70) (Table 6). Intent-to-treat
Interestingly, the results in the intent-to-treat analysis were 6 weeks (motor) 7.6 (n = 76) 12.5 (n = 84) 0.04
not significant (Table 6). Tirilazad showed the same effects 6 months (motor) 11.2 (n = 71) 17.6 (n = 80) 0.01
as MPS for 24 h (10.4 versus 12.4, p = 0.37). Complied with protocol
A subgroup analysis of patients treated within 3–8 h after 6 weeks (motor) 7.0 (n = 72) 13.4 (n = 80) 0.008
SCI showed small but significant changes in motor func- 6 months (motor) 10.8 (n = 68) 18.0 (n = 77) 0.008
tion for intent-to-treat and complied with protocol analyses Subgroup analysis. Patients treated within 3–8 h.
a Change in function, scores for motor function ranged from 0 to 70.
(Table 7). Patients treated within 3–8 h after SCI also showed
136 M. Bernhard et al. / Resuscitation 66 (2005) 127–139
Additionally, in a consensus conference, the American Asso-
ciation of Neurologic Surgeons and the Congress of Neuro-
logic Surgeons [63] stated with a review of the literature from
1966 to 2001 that “treatment with methylprednisolone for
either 24 or 48 h is recommended as an option in the treat-
ment of patients with acute spinal cord injuries that should
be undertaken only with the knowledge that the evidence
suggesting harmful side effects is more consistent than any
clinical benefit.” Moreover, in the recently published posi-
tion paper of the National Association of Emergency Medical
Services Physicians (NAEMSP) [64] in 2004, the NAEMSP
stated that the evidence on the use of high-dose steroids for
SCI remains inconclusive, the treatment with steroids should
not be considered the standard of care, and routine use of
steroids in EMS is not supported.
3.5. Steroids are harmful in traumatic brain injury
MPS has been used to treat neurotrauma for more than
three decades now. The corticosteroid randomization after
significant head injury (CRASH) trial was performed from
1999 to 2004 following the lack of sufficiently large trials
and was recently published in The Lancet [65]. This study
evaluated the efficacy and safety of MPS (initially 2000 mg
for 1 h i.v. + 400 mg/h for 48 h i.v., n = 4985) versus placebo
(n = 4979) in a large-scale multicentre, randomized trial in
patients suffering from head injury (GCS < 14) within 8 h of
injury. The intent-to-treat analysis showed a highly signifi-
cant increase in mortality within 2 weeks in the group treated
with MPS as compared to the group treated with placebo
(21.1%, n = 1052 versus 17.9%, n = 893; relative risk 1.18
with 95% confidence interval: 1.09–1.27; p = 0.0001). The
relative risk of death at 2 weeks due to MPS in prespe-
cific subgroup analyses was not different based on injury
severity (p = 0.22) [65]. The incidence of complications with
MPS as compared to placebo was as follows: seizure (8.7%
versus 7.6%), haematemesis or melaena requiring transfu-
sion (1.6% versus 1.3%), wound infection (3.2% versus
2.9%), and pneumonia (13.4% versus 12.4%), respectively
[65].
The authors of the CRASH trial stated that their results
could also have implications for use of corticosteroids in SCI
and that, because of the emphasis on the subgroup effects in
the NASCIS studies, the use of corticosteroids in SCI should
remain an area of debate [65].
When the results of the CRASH trial are extrapolated to
the annual incidence rate of severe head trauma worldwide, is
frightening to calculate how many patients might have been
harmed by treatment with corticosteroids. Therefore, Sauer-
land and Maegele [66] stated in their accompanying editorial
to the CRASH trial that “the key message of the CRASH,
however, is that applying treatments with unproven effective-
ness is like flying blindly. In future, we should avoid trusting
in underpowered clinical trails with surrogate rather than clin-
ical endpoints, and transferring evidence from one disease to
another.”
4. Transportation and type of trauma centre
The choice of vehicle depends on the patient and the local
setting. Both ground and helicopter transportation are pos-
sible. In order to make a decision about the type of trauma
centre, it is necessary to consider the status of the patient
(haemodynamically stable versus unstable). Stable patients
should be transported to the nearest level 1 centre, if it can be
reached within a given period. Sometimes a longer transporta-
tion time to a level 1 trauma centre is preferable. Unstable
patients should be transported to the nearest trauma centre in
order to achieve haemodynamic stabilisation, even if this is
not a level 1 trauma centre for SCI. Second-line transportation
to a level 1 injury centre for SCI should then be undertaken
after the patient has been stabilised haemodynamically [16].
Carvell and Grundy [14] compared the results of spinal
surgery in 420 consecutive patients with SCI in a spinal
treatment centre with other patients who underwent primary
surgery in another hospital and who were transported to the
spinal treatment centre secondarily. These authors stated that
“complications were more frequent in patients undergoing
spinal surgery before transfer to the centre. Furthermore, the
longer the delay in transfer, the higher the incidence of pres-
sure sores” [14].
Devivo et al. [15] compared patients admitted within 1 day
of injury who received all subsequent care within the system
with patients who received their acute care services elsewhere
and who were admitted to the system solely for rehabili-
tation. Both patient groups were comparable with respect
to age, neurological status and extent of spinal cord lesion,
pre-existing major medical conditions, associated injuries,
ventilator dependency and acute surgical procedure experi-
ence. Findings revealed a statistically significant reduction
in acute care and total length of stay and a highly signifi-
cant reduction in the incidence of pressure ulcers for patients
admitted within 1 day of injury. Moreover, for patients admit-
ted within 1 day of injury, mortality rates were lower than
reported previously for patients not admitted to an organised
SCI care system.
However, Jones and Bagnall [67] stated in their recently
published analyses for the Cochrane Database that “the cur-
rent evidence does not enable conclusions to be drawn about
the benefits or disadvantages of immediate referral versus
late referral to SICs. Well-designed, prospective experimen-
tal studies with appropriately matched controls are needed.”
Therefore, there is an ongoing discussion in this area.
5. Conclusions
There is no doubt that prehospital management of SCI is
very important, since 25% of SCI damage may occur or be
aggravated after the initial event. The prehospital manage-
ment of acute SCI includes examination of the patient, spinal
immobilisation, oxygenation, and careful airway manage-
ment as well as cardiovascular support (Table 8). Emergency
 M. Bernhard et al. / Resuscitation 66 (2005) 127–139 137

Table 8
Prehospital management of spinal cord injury (SCI)
Examination of the patient
Patient immobilisation
Airway management
Cardiovascular support
Fluid resuscitation
Blood glucose levels
Transportation and trauma centre
Primary survey: airways, breathing, and circulation (the “ABCs”). Secondary survey: more thorough evaluation
(“whole-body-check”)
Neutral supine position with rigid cervical collar, sandbags on either side of the head, and rigid backboard.
Alternative: vacuum splint device in combination with rigid cervical collar
Pulse oximetry, O2 administration via face mask, rigid cervical collar; intubation of the trachea, if saturation
persistently <90%, hypoventilation, Glasgow Coma Scale < 9; intubation of the trachea in patient under manual
in-line stabilisation
Neurogenic shock (SCI above Th5 ): systolic blood pressure <70 mmHg; bradycardia: Trendelenburg position; i.v.
administration of atropine, dopamine, arterenol. Hypovolemic shock (multiple trauma): systolic blood pressure
<100 mmHg; tachycardia: Trendelenburg position; fluid resuscitation. Maintenance of mean arterial blood pressure
>90 mmHg; avoid episodes of hypotension (systolic blood pressure below 90 mmHg)
Physiological NaCl or Ringer’s solution, colloids (prefer Gelatine or HES (200/0.5 or 300/0.4))
hypertonic–hyperosmotic solutions
Within normal range as soon as possible
Stable patient: nearest level 1 centre. Hemodynamically unstable patient: nearest trauma centre; second-line
transportation after hemodynamic stabilisation to a level 1 injury centre for SCI

treatment to reduce the risk of a secondary SCI includes
intubation of the trachea, if indicated (under manual in-line
stabilisation), and maintaining MAP above 90 mmHg and
blood glucose levels within the normal range (Table 8).
It is still not clear from a scientific point of view whether
additional specific therapy is useful or not. It has not been
demonstrated convincingly that early MPS treatment really
has clinically important benefits for a patient suffering from
SCI. Despite wider-spread use of MPS, important questions
concerning specific drug therapy have not been answered nor
have the available date shown convincingly whether treat-
ment with MPS really works. Therefore, a reevaluation of
NASCIS 2 and 3 primary data is indicated before definite
conclusions can be drawn [54].
In a consensus conference, the American Association of
Neurologic Surgeons and the Congress of Neurologic Sur-
geons stated that “the evidence of the treatment with MPS of
patients suffering from SCI suggesting harmful side effects
is more consistent than any suggestion of clinical beneftit”
[63]. Moreover, the National Association of Emergency Med-
ical Services Physicians (NAEMSP) do not support in their
actual position paper the routine use of MPS in the treatment
of patients with SCI [64]. After the results of the CRASH
trial it is clear from a scientific point of view that the treat-
ment with corticosteroids in head trauma is associated with
a significant increase in risk of death within 2 weeks [65].
Moreover, and at this stage, it is not known whether thera-
peutic hypothermia or any further pharmacological interven-
tion has beneficial effects. Therefore, networks for clinical
studies in SCI patients should be established, as a basic
requirement for further improvement in outcome in such
patients.
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