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com/esps/ World J Orthop 2015 January 18; 6(1): 17-23

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DOI: 10.5312/wjo.v6.i1.17 © 2015 Baishideng Publishing Group Inc. All rights reserved.

TOPIC HIGHLIGHT

Kemal NAS, Professor, Series Editor

Acute complications of spinal cord injuries

Ellen Merete Hagen

Ellen Merete Hagen, Spinal Cord Injury Centre of Western control and disturbance of sweating, vasodilatation
Denmark, Department of Neurology, Regional Hospital of Vi- and autonomic dysreflexia. Autonomic dysreflexia is
borg, 8800 Viborg, Denmark an abrupt, uncontrolled sympathetic response, elicited
Ellen Merete Hagen, Department of Clinical Medicine, Univer- by stimuli below the level of injury. The symptoms
sity of Bergen, 5020 Bergen, Norway may be mild like skin rash or slight headache, but can
Ellen Merete Hagen, Institute of Clinical Medicine, Aarhus
cause severe hypertension, cerebral haemorrhage
University, 8200 Aarhus, Denmark
Author contributions: Hagen EM solely contributed to this pa-
and death. All personnel caring for the patient should
per. be able to recognize the symptoms and be able to
Open-Access: This article is an open-access article which was intervene promptly. Disturbance of respiratory function
selected by an in-house editor and fully peer-reviewed by exter- are frequent in tetraplegia and a primary cause of
nal reviewers. It is distributed in accordance with the Creative both short and long-term morbidity and mortality is
Commons Attribution Non Commercial (CC BY-NC 4.0) license, pulmonary complications. Due to physical inactivity
which permits others to distribute, remix, adapt, build upon this and altered haemostasis, patients with SCI have a
work non-commercially, and license their derivative works on higher risk of venous thromboembolism and pressure
different terms, provided the original work is properly cited and ulcers. Spasticity and pain are frequent complications
the use is non-commercial. See: http://creativecommons.org/li-
which need to be addressed. The psychological stress
censes/by-nc/4.0/
associated with SCI may lead to anxiety and depression.
Correspondence to: Dr. Ellen Merete Hagen, Spinal Cord
Injury Centre of Western Denmark, Department of Neurology, Knowledge of possible complications during the acute
Regional Hospital of Viborg, Heibergs Alle 4, 8800 Viborg, phase is important because they may be life threatening
Denmark. [email protected] and/ or may lead to prolonged rehabilitation.
Telephone: +45-78-446177
Fax: +45-78-446159 Key words: Spinal cord injuries; Autonomic dysreflexia;
Received: October 24, 2013 Cardiovascular disease; Orthostatic hypotension;
Peer-review started: October 25, 2013 Bradycardia; Thromboembolism; Respiratory insufficiency
First decision: November 12, 2013
Revised: December 24, 2013 © The Author(s) 2015. Published by Baishideng Publishing
Accepted: May 28, 2014 Group Inc. All rights reserved.
Article in press: May 29, 2014
Published online: January 18, 2015 Core tip: The paper provides an overview of acute
complications of spinal cord injury. Frequent complications
in the acute phase of are bradyarrhythmias and
hypotension. Other complications are instability of
Abstract temperature (hypothermia and hyperthermia), pain,
The aim of this paper is to give an overview of acute spasticity and autonomic dysreflexia (AD). AD is associated
complications of spinal cord injury (SCI). Along with motor with an abrupt, uncontrolled sympathetic response,
and sensory deficits, instabilities of the cardiovascular, elicited by stimuli below the level of injury, and it can
cause severe hypertension, cerebral haemorrhage and
thermoregulatory and broncho-pulmonary system are
death. All personnel caring for the patient should be
common after a SCI. Disturbances of the urinary and
able to recognize the symptoms and intervene promptly.
gastrointestinal systems are typical as well as sexual
Knowledge of possible complications during the acute
dysfunction. Frequent complications of cervical and high
phase is important because they may be life-threatening
thoracic SCI are neurogenic shock, bradyarrhythmias,
and/or may lead to prolonged rehabilitation.
hypotension, ectopic beats, abnormal temperature

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 Hagen EM. Acute complications of SCI

Hagen EM. Acute complications of spinal cord injuries. World column) from the first thoracic (Th1) to the second lumbar
J Orthop 2015; 6(1): 17-23 Available from: URL: http://www. (L2) vertebrae. The consequences are abolished supraspinal
wjgnet.com/2218-5836/full/v6/i1/17.htm DOI: http://dx.doi. control of the sympathetic nervous system, and lack of
org/10.5312/wjo.v6.i1.17 inhibition of the parasympathetic nervous system resulting
in an increased sympathetic activity below the injury level.
Along with motor and sensory deficits, instabilities of the
cardiovascular, thermoregulatory and broncho-pulmonary
INTRODUCTION system are common after a SCI. Disturbances of the urinary
and gastrointestinal systems are typical as well as sexual
Traumatic spinal cord injury (SCI) may cause long- dysfunction[8,9]. Patients with injury below Th6 will have
lasting dysfunction in many organ systems, and together intact sympathetic and parasympathetic control of the heart
with permanent change of function, lead to a higher and lungs. Thus, the responses from the organ systems will
morbidity together with a lower quality of life[1,2]. The differ between patients with tetraplegia and patients with
management of acute SCI has changed significantly paraplegia[10].
during the past decades due to increased knowledge about
the pathophysiology of SCI together with new diagnostic
methods and treatment methods. The spinal cord is SURGERY
affected by both the immediate physical effects of trauma, After a traumatic SCI, the number of complications
and secondary pathologic processes. Especially ischemia during the acute phase hospitalization, depends on the
and oedema may worsen the injury during the first few timing of surgery, with less complications when surgery
hours after an injury. is performed soon after the injury[11]. It’s proposed that
Knowledge of possible complications during the acute patients with traumatic SCI should be operated within 24
phase is important because they may be life-threatening h following injury to reduce complications. If impossible
and/or may lead to prolonged rehabilitation. to operate within 24 h, efforts should be made to perform
surgery earlier than 72 h after a the injury[11].
DEFINITION
Traumatic spinal cord injury is defined as an acute injury ACUTE COMPLICATIONS
of the spinal cord which results in a varying degree of Neurogenic shock
paralysis and/or sensory disorder[3]. Injury to the cauda Neurogenic shock is due to severe hypotension and
equina is usually included in the definition, while other bradycardia in cervical injuries due to drop in blood
isolated injuries to nerve roots are excluded[4]. pressure in relation to an acute SCI[12,13]. Hypotension is
Based on pathophysiological changes the early acute defined as systolic blood pressure < 90 mmHg in supine
phase is defined to be 2-48 h after the injury, the subacute position, and is due to low intravascular volume (e.g., blood
phase from 2 d to 2 wk, and the intermediate phase from loss, dehydration)[8]. Because of an intact parasympathetic
2 wk to 6 mo[5]. Based on timing of surgery studies have influence via the vagal nerve and a loss of sympathetic
found that early decompression either < 24 h or < 72 tone due to disruption in supraspinal control, neurogenic
h resulted in statistically better outcomes compared to shock develops as a result of imbalance of the autonomic
delayed decompression[6]. However, the clinically acute control[12]. Depending on the severity of the SCI, prolonged
phase is usually defined as the first 4-5 wk after the injury. and severe hypotension, requiring vasopressive therapy may
last up to 5 wk after injury[12].
In the Trauma Audit and Research Network database,
ANATOMY the percentages of neurogenic shock was 19.3% in cervical
An acute traumatic SCI starts with an abrupt, injury to injuries[14]. In thoracic and lumbar injuries the reported
the spine leading to fractures or dislocations of vertebrae. incidence was 7.0% and 3.0%, respectively[14].
Displaced bone fragments and disc material causes the
immediate injury leading to irreversible damage of axons Cardiovascular disease
and broken neural cell membranes. Ruptured blood Injuries to the autonomic nervous system are the cause
vessels may cause bleeding in the spinal cord, and thereby of many of the cardiovascular complications following a
increase the damage during the subsequent hours. Several SCI. Cardiovascular dysfunction in patients with cervical
mechanisms contribute to the total injury of the spinal and high thoracic SCI may be life-threatening and may
cord tissue. exacerbate the neurological impairment due to the spinal
Goals in the management of SCI-patients include cord injury. Patients have higher morbidity and mortality
minimizing the primary neurological damage, and preventing as a result of the autonomic dysfunction[15-17]. A Canadian
secondary cord injury due to hypoperfusion, ischemia, and study found that SCI is associated with an increased odds
apoptotic, biochemical and inflammatory changes[7]. of heart disease (OR = 2.72) and stroke (OR = 3.72)
An acute injury above the sixth thoracic (Th6) compared to ablebody[18].
vertebra disturbs the descending pathways to neurons In the acute phase many irregularities of the cardiac
of the sympathetic trunk (in the intermediolateral cell rhythm may occur; sinus bradycardia and bradyarrhythmias

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 Hagen EM. Acute complications of SCI

(14%-77%)[19] including escape rhythm, supraventricular and amygdala[34]. Changes in sweat secretion often occur
ectopic beats (19%)[19], ventricular ectopic beats (18%-27%)[19,20], after SCI, and excessive sweating (hyperhidrosis), absence
orthostatic hypotension (33%-74%)[21,22], increased vasovagal of sweating (anhidrosis) and diminished sweating
reflex, vasodilatation and stasis[20]. Sidorov et al[23] found (hypohidrosis) may all occur.
that orthostatic hypotension persisted during the first Excessive sweating is a common problem in persons
month following SCI in 74% of cervical and 20% of upper with SCI[35,36]. In most individuals, episodic hyperhidrosis is
thoracic motor complete SCI patients. Following cervical usually associated with other autonomic dysfunctions such
injuries both sinus bradycardia and arterial hypotension as autonomic dysreflexia and orthostatic hypotension,
frequently arise[8,24-26]. Bradycardia is reported in 64% to 77% or with post-traumatic syringomyelia. Most common
of cervical SCI[20]. Studies have found a peak in incidence symptoms are minimal/abolished sweating under the level
four days post-injury, then a gradual decline in incidence[27]. of injury and profuse sweating over the level of injury.
Arterial hypotension is reported in 68% of patients with This is due to compensatory increase in sweat secretion
motor complete cervical SCI (ASIA A and B) who develop above the level of injury due to the loss of sympathetic
bradycardia. Of these will 35% require vasopressors, and stimulation below the level of injury, which results in
16% will have a cardiac arrest[28]. In the acute phase arterial reduced sweat production[37]. Sweating may also occur
hypotension in the acute phase can be misunderstood as exclusively below the level of injury. This type of sweat
loss of volume. This may lead to over hydration in the acute is reflex sweating, and is usually a symptom of a massive
phase. autonomic response that occurs particularly with cervical
Common autonomic disturbances after 4 to 5 wk post- and high thoracic injuries (above Th8-Th10).
injury are autonomic dysreflexia, orthostatic hypotension
(also in sitting position), reduced cardiovascular reflexes Respiratory complications and dysphagia
(which regulate blood pressure, blood volume and body Cervical injury has major effects on the pulmonary
temperature) and the absence of cardiac pain[20]. The system, and respiratory difficulties are one of the major
prevalence of autonomic dysreflexia in patients with SCI complications and a frequent cause of death, both in
with injury above Th6 is 48%-90%[28,29]. Krassioukov et al[30] the acute and chronic phase after injury[38]. Studies have
found an incidence of early AD of 5.2% in a population found that 67% of acute SCI patients experience severe
of acute SCI, the earliest episode of AD occurred on respiratory complications within the first days after the
the 4th post-injury day. Patients with cervical or thoracic injury; atelectasis (36.4%), pneumonia (31.4%), and
injuries above Th4 may have disrupted the sympathetic respiratory failure (22.6%)[39].
afferent fibres including cardiac pain fibres; their sensation In the acute phase 84% of patients with injuries
of ischemic cardiac pain may be changed (referred pain) above C4 and 60% of patients with injuries from C5 to
or absent[31]. C8, will experience respiratory problems[40], and 75%-80%
Secondary cardiac changes in patients with tetraplegia, of tetraplegia above C4 and 60% of tetraplegia caudal
are loss of muscle mass in the left ventricle (due to to C4 will need invasive mechanical ventilation[41]. Close
physiological adaptation to reduced myocardial load[32]) surveillance of respiration is important. In addition a
and pseudo infarction - a rise in Troponin with or without total of 65% of patients with injuries at levels from Th1
ECG changes[25,33]. to Th12 may have severe respiratory complications[42]. A
30%-50% reduction of vital capacity is described during
the first week post injury in patients with injuries at C5-C6.
TEMPERATURE REGULATION It is recommended that vital capacity and arterial blood
Abnormal temperature control is another well-known gases should be measured until the patient is stable[41-43].
clinical phenomenon after SCI, especially in patients with
cervical and high thoracic injuries. This is largely due to Thromboembolism
reduced sensory input to thermo-regulating centres and Individuals with SCI have a higher risk of coagulation
the loss of sympathetic control of temperature and sweat disorders and venous stasis due to physical inactivity,
regulation below the level of injury[34]. A number of altered haemostasis with reduced fibrinolytic activity
temperature regulation disorders following SCI have been and increased factor Ⅷ activity[44]. They are therefore
described. Some patients have poikilothermia-an inability predisposed to thromboembolism[45,46]. During the first
to maintain a constant core temperature irrespective of year post-injury, the incidences of deep vein thrombosis
the ambient temperature. Injuries above Th8 are often and pulmonary embolism are estimated to be 15% and
associated with fluctuating temperature, hypothermia and 5%, respectively[47]. The incidence is highest 2-3 wk after
hyperthermia[25]. the injury, followed by a small peak three months after
the injury[48]. During the chronic phase, the incidence of
clinically significant thromboembolism is less than 2%[44].
SWEAT SECRETION
The sweat glands are largely sympathetically innervated in Pressure ulcers
the upper part of the body from Th1-Th5, and in the lower Pressure ulcers are a common complication following SCI.
part of the body from Th6-L2. Supraspinal control of Good prevention requires identifying the individuals at
sweat excretion is located in regions of the hypothalamus risk for developing pressure ulcers[49]. Pressure ulcer is the

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 Hagen EM. Acute complications of SCI

most common long term complication in SCI. Meticulous Pain

surveillance in the acute phase and in the operating theatre In the acute phase the patients encounter a range of
to prevent pressure ulcers is vital[50]. sensory experiences following the trauma. Acute pain
commonly accompanies the injury and recedes as healing
Heterotopic ossification occurs. Chronic pain is a frequent, disabling complication
Heterotopic ossification (HO) is a frequent, irreversible of SCI. Up to 80% of patients with SCI are reported
complication after SCI[51], and involves para-articular to suffer from pain [64]. Patients with SCI may have
formation of mature lamellar bone in soft tissues [52]. nociceptive or neuropathic-type of pain or a combination
The incidence varies between 10% to 53% in different of the two[65].
studies[51,53]. The development of HO starts usually within In order to reduce the evolution of chronic pain, it is
the first 2-3 wk post injury below the level of injury[51,53]. important to minimize the primary neurological damage,
The most common joints affected are hip (70%-97%) and prevent secondary injury due to hypoperfusion,
and knee[51,53]. Substantial HO, the patients present with a ischemia, and apoptotic, biochemical and inflammatory
reduction in range of motion of the joint in 20%-30%[53], changes of the cord[66].
whereas ankylosis develops in only 3% to 8%[53].
MUSCULOSKELETAL AND METABOLIC
BLADDER COMPLICATIONS
SCI interrupts control of the bladder[54]. Immediately after
Musculoskeletal pain is common in chronic SCI[67]. The
SCI, the bladder and sphincter are frequently hypotonic.
muscles atrophy in response to reduced activity[61]. Studies
In the chronic phase the bladder dysfunction is classified
have found that all patients with complete SCI have some
as either an upper or lower motor neuron syndrome.
extent of deterioration of muscle, joints and ligaments[61].
Upper motor neuron syndrome (reflex bladder) involves
Therefore, the patients with SCI experience a period of
loss of cortical inhibition of sacral reflex arcs due to
“metabolic chaos”, i.e., an strong catabolic process, which is
disturbance of descending spinal tracts, leading to detrusor
generated by the loss of physical pressure on muscle, joints
hyperactivity often in combination with detrusor sphincter
and ligaments[61]. This results in bone demineralization
dyssynergia[55]. Inhibition of the stretch reflex by the pontine
leading to hypercalciuria, renal urolithiasis and bladder
storage centre is abolished. A minor amount of stretch will
stones, which may lead to renal failure[61].
give a contraction of the bladder wall, the external urethral
sphincter lacks voluntary control, resulting in recurrent,
spontaneous voiding. IMMUNOLOGICAL MEDIATED
Lower motor neuron syndrome is due to injury to
the sacral (S2-S4) part of the autonomic nervous system NEURO-INFLAMMATION
resulting in a diminished motor stimulation of the bladder Excessive activity of matrix metalloproteinases (MMP)
and reduced or absent contractility of the detrusor and in the cord immediately after the injury lead to break of
subsequently an enlarged bladder[56,57]. the blood-spinal cord barrier, entering of leukocytes into
the injured cord, and disintegration of cells[68]. Studies
have shown that MMP-9 and MMP-2 both are important
BOWEL in the regulation of inflammation and neuropathic pain
Between 27% and 62% of patients with SCI report having after peripheral nerve injury. They may also contribute to
problems with their bowel, the most frequent symptoms the SCI-induced pain[68]. By blocking the effects of MMP
are obstipation, distension and abdominal pain[58]. Other early using pharmacologic agents, an improvement in
symptoms are rectal bleeding, haemorrhoids, incontinence long-term neurological recovery may be possible, together
and autonomic dysreflexia[58]. Spinal shock leads to loss of with reduced glial scarring and neuropathic pain[68].
all activities, under the level of injury, including autonomic
function and reflexes. During the first four weeks, 4.7%
of patients experienced acute abdominal symptoms, SEXUALITY
while 4.2% reported acute gastro duodenal ulceration and Immediately after a SCI, most patients are focused on the
haemorrhage[58,59]. physical improvement. However, when they manage to
accept their injury, dealing with sexuality is an important
Spasticity step in the physical and psychological rehabilitation
Patients with an acute complete SCI present with spinal process[69].
shock associated with muscle paralysis, reduced muscle
tone and absent tendon reflexes under the level of
injury[60]. Spasticity is usually established after 2-6 mo post ANXIETY AND DEPRESSION
injury with exaggerated tendon reflexes, increased muscle Many patients with SCI experience psychological stress.
tone, and muscle spasms[61,62]. Up to 70% of patients with Patients with a good mental health are usually capable of
SCI develop spasticity[63]. coping with stress, but the patients response is affected

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 Hagen EM. Acute complications of SCI

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P- Reviewer: Gorgey AS, Kasai Y, Nas K, Panchal RR

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