SPINAL CORD INJURY

Dra. Rebeca Velázquez

R2 Neurología adultos
ANATOMY
Tracts and pathways:
Understanding the anatomy is vital

Sensory information
Early diagnosis /delayed diagnosis from organs Brain
peripheral receptors

Permanent disability Motor Internal &

information peripheral
from the brain effector organs
Somatotopically and segmentally
organize

Presentation
The descending motor pathways in the cord before
the anterior horns are called upper motor neurons.

Those of the anterior horns and somatic motor nerves

are called lower motor neurons.
 Somatic and afferent
(sensory)

Somatic motor neurons

(in lateral motor columns)
- upper and lower limbs

Somatic motor neurons

(in medial motor columns)
- Axial muscles of the Alpha & gamma
body motor neurons
and interneurons

CONTINUUM (MINNEAP MINN) 2021;27(1, SPINAL CORD DISORDERS): 12–29.

Spinal Cord Injury

Incidence
The annual incidence of Causes
SCI worldwide is between 1.- Collisions 38%
11.5 and 57.8 cases/million 2.- Falls 35%

persons

Bimodal age Gender

15-29 Years old M>F
>65 4:3

Dead Costs
Elevated because
Respiratory complications
aparaplegia ang tetraplegia

Amanda Sacino1 et. al. Critical Care Management of Acute Spinal Cord Injury. J Neuroanaesth Crit Care. 2019
Spinal Cord
Injury 1

Bifasic process
 Acute
Immediate inflamatory Secondary
damage process + insults**
astrogliosis
 PRIMARY INJURY
• Shearing
• Laceration
• Acute Disruption of
stretching • Demyelinated or
• Sudden dysmyelinated
• Axons
acceleration- axons
• Blood vessels • Substrate for
deceleration • Cell regeneration
Primary injury membranes
“Subpial rim”
mechanisms

2H
First minutes:
Elevated levels of cytokines, including TNF-α , (IL-1β), appear within minutes of the injury
Cytotoxic levels of glutamate ( astrocyte)
Bradley and Daroffs Neurology in
Clinical Practice. 8a Ed. Chapter 63
 Acute
Early acute phase Targeted for
neuroprotective
Subacute hpase therapies.
SECONDARY
INJURY

Intermediate

Chronic
stages
Bradley and Daroffs Neurology in
Clinical Practice. 8a Ed. Chapter 63
 Early acute pase → Ionic homeostasis is
desynchronized

Ca+ deregulation
Mitochondrial Low ATP
ysfrunction

Glutamate Energy-dependent
FAILURE
Glutamate transporters
Na+/K+/glutamate
Glutamate
pump Na+/K+/ATPase
Glutamate

12 H
Glutamate acts Free radical
NMDA-AMPA → reactions→
leading to an influx membrane
of Na+ and Ca2+. damage
Bradley and Daroffs Neurology in
Clinical Practice. 8a Ed. Chapter 63
The main mechanisms of primary injury to the spinal cord are
1.- Direct impact with persistent or transient compression
2.- Vertebral fracture and displacement
3.- Cord laceration or transection.

▪ Cervical injuries classification (bone,ligaments and intervertebral disks)

▪ Flexion injuries → can produce wedge fractures, vertebral subluxations,
and facet dislocation)
▪ Extension injuries → can cause fractures of the posterior column of the spine)

▪ Axial load injury → can result in burst fractures of C or T vertebrae.

▪ Penetrating injuries→ lacerations and transections

▪ All these are the direct consequences of mechanical forces:

Time of the injury y following hours
▪ Mostly not amenable to treatment 

CONTINUUM (MINNEAP MINN) 2018;24(2, SPINAL CORD DISORDERS): 551–566.

THERAPEUTIC

• The therapeutic focus in TSCI is the avoidance and correction of

secondary injuries.
• early hypoxia and hypoperfusion ()
• Animal models → elucidated mechanisms of secondary injury
• Reperfusion
• Acute inflammation
• Local swelling from intracellular and extracellular edema
• Impaired vasomotor function
• Blood–spinal cord barrier disruption,
• Microhemorrhages, microthrombosis
• Excitotoxicity, mitochondrial damage, etc.
CONTINUUM (MINNEAP MINN) 2018;24(2, SPINAL CORD DISORDERS): 551–566.
EVALUATION

1. Physical examination
2. Emergency spine imaging
3. Immediate neck immobilization

Avoid additional damage during transportation!

CONTINUUM (MINNEAP MINN) 2018;24(2, SPINAL CORD DISORDERS): 551–566.

CLINICAL ASSESMENT
RESPIRATORY PATTERN • CIRCULATION

• Lower C y upper T injuries • C and upper T injuries can

can precipitante V. failure cause refractory hypotension
• Quad breathing and bradycardia due to
neurogenic shock (loss of
sympathetic outflow with
• unopposed vagal activity)

• Severity of the neurologic impairment can initially be by spinal shock

• severe dysfunction that develops within the first hours and can last for days-weeks.
• Areflexic flaccid paralysis and anesthesia below the level of the lesion.

CONTINUUM (MINNEAP MINN) 2018;24(2, SPINAL CORD DISORDERS): 551–566.

CLINICAL ASSESMENT
NEUROLOGIC

• Determine the level of injury

• Motor: <3/5
• Sensation: light touch and
pincprick
• Each side of the body
• Sacral function (

• Severity of the neurologic impairment can lesion.

CONTINUUM (MINNEAP MINN) 2018;24(2, SPINAL CORD DISORDERS): 551–566.

• Thus, for prognostication purposes, it is
advisable to use the ASIA impairment
grade determined at the
• end of the initial hospitalization or
• at the beginning of the rehabilitation phase

CONTINUUM (MINNEAP MINN) 2018;24(2, SPINAL CORD DISORDERS): 551–566.

Spinal cord Injury Syndromes
-

Central Cord Syndrome

Anterior Cord Syndrome

Posterior column Syndrome
Brown-Séquard Syndrome
Cervicomedyllary Syndrome
Conus medullaris Syndrome
Cauda Equina Syndrome
Bradley and Daroffs Neurology in
Clinical Practice. 8a Ed. Chapter 63
Bradley and Daroffs Neurology in
Clinical Practice. 8a Ed. Chapter 63
Bradley and Daroffs Neurology in
Clinical Practice. 8a Ed. Chapter 63
Bradley and Daroffs Neurology in
Clinical Practice. 8a Ed. Chapter 63
Bradley and Daroffs Neurology in
Clinical Practice. 8a Ed. Chapter 63
Bradley and Daroffs Neurology in
Clinical Practice. 8a Ed. Chapter 63
 RADIOLOGICAL ASSESMENT
MRI • CT

• STIR sequences can detect • SCIWORA

ligamentous injury that could
explain persistent pain (risk for • Clinical signs and symptoms
subluxation). • Rx normal
• Ligamentous injury is best
appreciated within 48 hours of the
trauma. • Suggest MRI
• Finding may help to guide surgical
decision and have prognostic
implications.

CONTINUUM (MINNEAP MINN) 2018;24(2, SPINAL CORD DISORDERS): 551–566.

CONTINUUM (MINNEAP MINN) 2018;24(2, SPINAL CORD DISORDERS): 551–566.
 TREATMENT
▪ ABC
▪ Whether surgical decompression
• Avoid hypoperfusion by hypoTA.

Cervical inmovilization • Avoid succinilcholine (after 24h)

▪ Pain • potentially life-threatening
▪ pressure sores intracellular potassium efflux
▪ airway compromise
▪ risk of aspiration
▪ limitation of upper chest wall
expansion

Amanda Sacino1 et. al. Critical Care Management of Acute Spinal Cord Injury. J Neuroanaesth Crit Care. 2019
 SURGICAL INDICATIONS AND

GOALS
• Decompression of neural
elements with correction of
deformities of the spinal canal.
• Reduction of vertebral fractures
• Fixation and fusion to ensure long-
termspinal stability.

• Rapid closed reduction (spine

alignment)
• fracture and dislocation injuries
(until surgery)

Amanda Sacino1 et. al. Critical Care Management of Acute Spinal Cord Injury. J Neuroanaesth Crit Care. 2019
• Surgical Timing in Acute Spinal
Cord Injury Study (STASCIS) ANESTESIA
• 313 patients decompressive surgery
within 24 h (~14 h) were twice as likely to
have a two-grade improvement on the
ASIA Impairment Scale Avoid succinilcholine (after 24h)
• At 6 months vs surgery later (~48 h) • potentially life-threatening
intracellular potassium efflux
• Currently, there is insufficient evidence that
early surgery improves long-term outcomes

• <8?
• >12?

Amanda Sacino1 et. al. Critical Care Management of Acute Spinal Cord Injury. J Neuroanaesth Crit Care. 2019
 CRITICAL CARE

DURATION OF MV
• Prolongued
• Failure can occur acutely
• Liberation is posible
• From injury to the brain, brainstem, or cervical
spinal cordsecondary to • -Evolution of déficits
• If not immediate MVA→ 5 days • Pulmonary complications?
• Diaphragm c3 C5
• Accessory inspiratory muscles
• External intercostal (t1-T11) • Muscles flaccid → spastic = 
• Sternocleidomastoids & trapezii (CN XI) chest wall stability → )
• and scalenes (C3 through C8

• Active expiration
• Abdominal muscles (T7-L2)
Amanda Sacino1 et. al. Critical Care Management of Acute Spinal Cord Injury. J Neuroanaesth Crit Care. 2019
 CRITICAL CARE

Risk of neurogenic shock, unstable

arrhythmias, and autonomic
dysreflexia (AD) for weeks to
months after injury
• Aggressive treatment of hypotension→ better
outcomes
• Excessive intraoperative fluid resuscitation to meet
MAP→ pulmonary edema,
• precise clinical endpoints to guide therapy have
• There is no #Hb → transfused

Amanda Sacino1 et. al. Critical Care Early Management of Acute Spinal Cord Injury. J Neuroanaesth Crit Care. 2019
 SPINAL SHOCK NEUROGENIC SHOCK

• Autonomic manifestation of
• Affects all functions below the Spinal shock
injury (days –12 wk) • Bradicardia, hypotension and
vasodilation
• Reducen myocardial
contractility (los of
sympathetic)

• Preferred → N.E. or Epi.

Amanda Sacino1 et. al. Critical Care Early Management of Acute Spinal Cord Injury. Part II J Neuroanaesth Crit Care. 2019
• Supraspinal control of sympathetic output (T1-L2)
• Interruption of the positive chronotropic, inotropic, and
dromotropic effects → leaves parasympathetic activity
unopposed, resulting in circulatory collapse.

• norepinephrine >dopamine ( spinal cord perfusion P with 

increases in intrathecal pressure)

• Hypoperfusion→ perpetuates secondary injury.

• Class III evidence that MAP augmentation to 85 to 90 mm Hg for
the first 5 to 7 days →may improve clinical outcome

Amanda Sacino1 et. al. Critical Care Early Management of Acute Spinal Cord Injury. Part II J Neuroanaesth Crit Care. 201
 CRITICAL CARE
Monitoring electrolytes, hepatic enzymes,
coagulation parameters, and blood counts
manual evacuation of stool

proton-pump inhibitors
• Spinal shock SCI affects intrinsic Enteral nutrition (as soon as safely possible)
enteric nervous system control: Gastric ulceration prophylaxis
Nasogastric suctioning to reduce ileus.
• paralytic ileus Prokinetic agents
• gastroduodenal ulceration and
hemorrhage
Urinary retention is common and requires
• Pancreatitis bladder catheterization in the acute phase
• Cholecystitis
Amanda Sacino1 et. al. Critical Care Early Management of Acute Spinal Cord Injury. Part II J Neuroanaesth Crit Care. 2019
 STEROIDS
The National Acute Spinal Cord Injury Study
• corticosteroids to potentially (NASCIS) assessed the utility of
methylprednisolone (MP) therapy.
attenuate the inflammatory
cascade. Yes or not? Results suggested that when initiated within
3 hours MP therapy for 24 hours →
improved motor function.

Between 3 and 8 hours of injury, MP therapy

for 48 hours → greater improvement in
outcomes than the 24-hour duration.
For these reasons, in 2013, the AANS/CNS
released a level 1 (standard)
recommendation against using MP for acute
management of SCI.

Amanda Sacino1 et. al. Critical Care Early Management of Acute Spinal Cord Injury. Part II J Neuroanaesth Crit Care. 201
 NEUROPROTECTIVE AGENTS

Riluzole’s anti-glutaminergic actions are postulated to blunt

excitotoxicity at neuronal sites of injury

Minocycline has anti-inflammatory properties and has been shown to

reduce apoptosis and minimize lesion size in animal model.

Therapeutic hypothermia

Amanda Sacino1 et. al. Critical Care Early Management of Acute Spinal Cord Injury. Part II J Neuroanaesth Crit Care. 201
 INTRAOPERATORY
MONITORING
• Incomplete cord injury
• Level I evidence supports the use of SSEPand TcME
monitoring
• EMG → detect and prevent nerve root injury from
decompression

• Inhalational anesthetics cause a dose-related decrease in

amplitude and an increase in the latency of cortical SSEP

Amanda Sacino1 et. al. Critical Care Early Management of Acute Spinal Cord Injury. J Neuroanaesth Crit Care. 2019
THANK YOU
.