AWARENESS OF

AUTONOMIC AND
METABOLIC
PROBLEMS IN
HIGH LEVEL SCI
FARIDA ARISANTI,dr., SpKFR.
 Autonomic dysfunctions are
common consequences of spinal
cord injury
 Spinal cord injury disrupts -the
descending spinal voluntary
sensory, motor and involuntary
autonomic pathways 
dysfunctions of the
cardiovascular system, motor
system, bladder, bowel and
Summary
sexual organs. Summary tagline or
sub-headline

Yukishita, et al: Autonomic dysfunction in spinal cord injury.

Juntendo Medical Journal 62 (5), 2016 page2
• Cardiovascular dysfunction in
patients with cervical and high
thoracic spinal cord injury 
may be life-threatening &may
exacerbate the neurological
impairment due to the spinal T5

cord injury
• Patients have higher morbidity
and mortality as a result of the
autonomic dysfunction.

Hagen, Rekan, Gronning, Faerestrand. Cardiovascular complications of

spinal cord injury. Tidsskr Nor Legeforen nr. 9, 2012; 132: 1115 – 20g
AUTONOMIC DYSFUNCTION FOLLOWING SCI
 Metabolic dysfunction following
spinal cord injury (SCI) is
characterized by a high prevalence
of lipid disorders, impaired glucose
tolerance, and insulin resistance
• Metabolic dysfunction is linked to
decreased muscle mass, increased
fat mass, and low anabolic
hormones
• 76% of individuals with SCI 
dyslipidemia, 50% paraplegia and
62% tetraplegia had impaired
glucose tolerance, decreased
anabolic hormone level with
abnormal lipid and metabolic
profiles

Kathleen C. Rankin, Laura C. O’Brien, Liron Segal,, M. Rehan Khan, and Ashraf S.
Gorgey. Liver Adiposity and Metabolic Profile in Individuals with Chronic Spinal Cord
Injury. Hindawi BioMed Research International. 2017
Volume 2017,
 • Cardiovascular disease (CVD) is a
leading cause of death in persons
with spinal cord injury (SCI) who
survive at least 1 year post injury
• Persons with SCI who are younger
than 45 years of age are 4 times
more likely to die of cardiac causes
than their age-matched
counterparts without SCI
 One of the significant risks of CVD
in persons with SCI is their
tendency to develop
cardiometabolic syndrome
 as a cluster of risk factors that
includes obesity, insulin resistance,
diabetes mellitus, dyslipidemia,
and subclinical atherosclerosis.

Schladen & Groah. State of the Science on Cardiometabolic Risk After Spinal Cord
Injury: Recap of the 2013 ASIA Pre-Conference on Cardiometabolic Disease. Top Spinal
Cord Inj Rehabil 2014;20(2):105–112
 Neurogenic shock, which often marked bradycardia, HR < 45bpm 
occurs simultaneously with common (71%) in individuals with
spinal shock is clinically severe cervical SCI duringthe acute
recognized by recovery period following injury
bradyarrhythmias, (Lehmann et al.,1987)
atrioventricular conduction
block and hypotension which
reflect ANS dysfunction
• significant hypotension (i.e.,
systolic BP (SBP) <90mmHg)
severe cervical lesions during
the initial period post-SCI, half
of whom required vasopressive
• persistent bradycardia < 60
bpm was reported to be
universal (100%)
• Neurogenic shock is mostoften
defined as a SBP of ≤100mmHg
and HR ≤ 80 bpm, although
other definitions have been
proposed (Mallek et al.,2012)
• Incidence : 25% in newly injured
individuals with cervicallesions,
longer Intensive Care Unit Neurogenic
and hospital stays (Mallek et al.,
2012) shock
• >> cervical and high thoracic
Could significantly affect clinical management
lesions  poorer outcomes of individuals with acute SCI  delay in the
(Piepmeier et al., 1985) timing of surgical intervention and surgical
decompression in patients with acute cervical
SCI (Tuli et al., 2007).
• The incidence of bradycardia
(HR 55 bpm) in complete
cervical lesions (69%)compared
to those with incomplete
cervical lesions (31%)
(Piepmeier et al., 1985).
• The need for cardiovascular
intervention was significantly
increased in those with C1-5
compared to those withC6-8
lesions (Bilello et al.,2003)
• 20% of individuals with
complete cervical lesions
required additional vasopressor
support
• Obvious picture of
flaccid paralysis and
areflexia  spinal
shock (disturbances
within the motor
and sensory nervous
systems) (Atkinson
and Atkinson, 1996;
Nacimiento and
Noth, 1999; Ditunno Spinal shock in humans usually last fr
et al., 2004)

F. Biering-Sørensen et al. / Autonomic Neuroscience: Basic and Clinical 209 (2018) 4–18
  usually lastfrom a few days to a
few weeks post-injury (4 to 6
weeks)  reflex activity below
the level of injury may be
detectable
 The end of spinal shock 
recovery of the
bulbocavernosus reflex (the first
few days injury)
Alternatively  recovery of deep
tendon reflexes within 2-weeks of
injury or recovery of bladder
F. Biering-Sørensen et al. / Autonomic Neuroscience: Basic and Clinical 209 (2018) 4–18
reflexes within 2 months of injury
 CARDIAC
DYSRHYTHMIAS

• In persons with injuries above

the sixth thoracic (T) vertebra,
reductions in sympathetic
cardiovascular control resultin
hypotension and bradycardia
• In the acute phase of SCI,
stimuli to the trachea, such as
suctioning, commonly induce
bradycardia
• In the first weeks after SCI
bradycardia may be life-threatening
with development of cardiac arrest
(Collins et al., 2006; Krassioukov et
al., 2007).
• Administration of atropine may be
required in the acute phase of SCI
• Chronic phase of SCI  higher
incidence of bradyarrhythmia in
persons with tetraplegia but rarely
in persons with paraplegia
Dysrhythmias, particularly atrial fibrillation,
may also occur during episodes of AD in
Krassioukov et.al. Assessment of autonomic dysfunction following spinal cord
individuals with high cord lesions and may
injury: Rationale
for additions to International Standards for Neurological Assessment. JRRD,
require immediate pharmacological
Volume 44, Number 1, 2007
intervention to restore the normal rhythm
F. Biering-Sørensen et al. / Autonomic Neuroscience: Basic and Clinical 209
(2018) 4–18
National Spinal Cord Injury Strategy Board on 18th May 2012 . THE INITIAL MANAGEMENT OF ADULTS WITH SPINAL CORD INJURIES
• AD is a constellation of signs
and/or symptoms following SCI
in response to noxious or non-
noxious stimuli below the
neurological level of injury (NLI),
usually seen in individuals
injured at or above the T6 spinal
cord level (Krassioukov et al.,
2012)
• AD is defined as an increase in SBP
N20mmHg above baseline, with or
without the following symptoms: Several life-
headache, flushing, piloerection, threatening
stuffy nose, sweating above the complications, (Ho
NLI, vasoconstriction below the and Krassioukov,
NLI, and dysrhythmias 2010;Dolinak and
(Krassioukov et al., 2012) Balraj, 2007)
F. Biering-Sørensen et al. / Autonomic Neuroscience: Basic and Clinical 209 (2018) 4–18
 ORTHOSTATIC
HYPOTENSION
 Decrease in systolic blood pressure of ≥20
mmHg or a decrease in diastolic blood
pressure of ≥10 mmHg when the subject
moves from an upright to supine posture
 Symptoms : dizziness, nausea, light-
headedness, or faintness
 Physical signs include pallor, diaphoresis, or
loss of consciousness
page 20
• Resting catecholamine
levels are lower in
individuals with cervical SCI
compared to paraplegia &
nondisabled no significant

Krassioukov et.al. Assessment of autonomic dysfunction following spinal cord injury:

Rationale for additions to International Standards for Neurological Assessment. JRRD,
Volume 44, Number 1, 2007
Yukishita, et al: Autonomic dysfunction in spinal cord injury.
Juntendo Medical Journal 62 (5), 2016
• Occurs in the acute phase
of SCI and can potentially
last a lifetime.
• Injuries above Th8 
fluctuating temperature,
hypothermia and
hyperthermia
 Poikilothermia, an inability
to maintain a constant core
temperature irrespective of
the ambient temperature
 Most people with complete
spinal cord injuries do not
sweat below the level of
the injury
 Many quadriplegics cannot
even sweat above the level
of the injury
  unable to lower their
body temperature in a hot
environment  stay in
temperature over 25℃
with high humidity  the
body core temperature symptoms : nausea, headache,nasal
begins to rise immediately congestion, tiredness, lowblood
 HYPERTHERMIA pressure and reduced concentration
TREATMENT
• to wrap a cold wet
towel around the neck
• avoid hot
environments and to
turn on an air
conditioner or an
electric fan
 Excessive sweating is acommon
problem in persons withSCI
Most common symptoms are
minimal/abolished sweating underthe
level of injury and profuse sweating
over the level of injury.

Sweating may also occur exclusively

below the level of injury reflex
sweating, and is usually a symptom of a
massive autonomic response that
• The sweat glands are largely occurs particularly with cervical and
sympathetically innervated in the upper
part of the body from Th1-Th5, and in the high thoracic injuries (above Th8-Th10)
lower part of the body from Th6-L2
• Supraspinal control of sweat excretion is
located in regions of the hypothalamus &
amygdala
Hagen EM. Acute complications of SCI. World J Orthop 2015 January 18;
6(1): 17-23
  Sugarman et al originated the term
quadriplegic fever for prolonged
periods of hyperthermia lasting up
to several months following acute
traumatic SCI
 tetraplegia and occasionally
those with high paraplegia.
 fever, often exceeding 40 °C
(101.5 °F), although only a mild
elevation in core temperature
may be present.
 This is a diagnosis of exclusion
because infection,
thromboembolic disease,
inflammation, and atelectasis

Savage et al. Neurogenic Fever after Acute Traumatic Spinal Cord Injury. Global Spine Journal Vol. 6 No. 6/2016
 METABOLIC PROBLEMS IN SCI

K. Wahman et al. Car diovas ular Disease Risk and the Need for Prevention after Paraplegia Determined by Conventional Multifactorial Risk Models: The Stockholm Spinal Cord Injury Study. J Rehabil Med 2011; 43: 237–242
EXERCISE!!!
Thank You
FARIDA ARISANTI

022-2034989

farida.arisanti@unpad.ac.id

www.ikfrbandung.com
page 31
 DEEP VEIN THROMBOSIS IN SCI

• Highest in 7 to 10 days afterthe

injury, during the early phases
of recovery and rehabilitation
• Blood flow diminishes with 50-
67% in inferior limbs following
SCI
• Leg swelling, vein dilation,
increased skin temperature,
pain, tenderness, and, rarely, a
bluish discolorationof the lower
leg
• Can be present withoutany
signs or symptoms
• Pharmacologic prophylactic
treatment : such as heparin,low
molecular weight heparin or
oral anticoagulants
• DVT intravenous heparin is
administrated for 7 to 10 days
an oral anticoagulant therapy NON-Pharmacologic
for 3 months Prophylaxis
Popa et.al. Journal of Medicine and Life Vol. 3, No. 3, July‐September 2010