Case Report

Dr Atul Harnath Seth, Dr Ganaraj Bhaskar

Emergency Department
SKMCA
 39 years old male Asian brought by
ambulance
 Prehospital history of fall from height of
more than 3 meter on floor ( hard)around 4
hours back
 on initial assessment history of
unconsciousness / transient amnesia after
fall with complaint of weakness both lower
limbs and left upper limb.no compliant of
vomiting
 PRIMARY SURVEY- ABCDE
 Airway- Patent, neck pain/ tenderness +
Breathing- Bilateral air entry, No surgical emphysema, B/L
symmetrical, No flail segment,
Spo2-100%
Circulation- HR-84 bpm, BP 121/70 as per initial triage
 While assessing at resus room,
 BP systolic drop to 70 to 80 mm of Hg , HR -66 bpm ;
although Periphery warm
Pelvis stable
No Long bone fracture
No External bleeding
PRIMARY SURVEY- ABCDE
 E-FAST : ( Negative ), UB grossly distended , catheterization
done
Disability- GCS 15/15, Pupils B/L normal size, regular and
reacting, No lateralizing signs
 U/L -motor 3/5 in left UL , sensory loss below umbilicus
T10 level and motor 0/5 in L/L,
loss of sacral sparing & decreased sensation S3, S4

VBG- Ph- no acidosis, acceptable

Exposure- Norm thermic,

Secondary survey – abrasions left upper limb, neurological

examination as above
First impression

 Hypotension
 Weakness U/L , LL, ? Neurogenic bladder

NEUROGENIC SHOCK

AM I RIGHT OR WRONG

ATLS – hypotension with peripheral
neurological sign

I WAS WRONG
first need to check and rule out haemorrhagic
causes
In the first instance any trauma patient who has
hypotension must therefore be assumed to have
hypovolemia until proven otherwise. The diagnosis
of neurogenic shock must necessarily be one of
exclusion.
Management is different
 Patients with neurogenic shock usually have significant
associated thoracic/ abdominal trauma and hypovolemic shock
may co-exist with neurogenic shock.

 Hypovolemic shock is common, and immediately life-

threatening, whilst neurogenic shock is uncommon, and rarely
immediately life-threatening, in isolation
As neurological status may mask
underlying cause of hypotension
 RULE OUT
 BY EXAMINATION – FRACTURE OF LONG BONES
 Ix – FREE FLUID IN ABDOMEN
 CT Trauma
 Hemothorax/ pneumothorax
 Abdominal visceral injury
 Pelvic injury
 Management is different
 There is no investigation that can specifically
diagnose neurogenic shock.
 The diagnosis will essentially be clinical and one of
exclusion of the other more common causes of
shock.
 Imaging investigations that demonstrate significant
spinal cord injury at or above the level of T4 will
raise suspicion that the condition exists, but this
suspicion must always be assessed in the light of
the overall clinical picture.
CT Trauma- CT Cervical Spine
 C5/C6 anterior facet joint
dislocation seen as anterior and
superior translation of inferior
articular process of C5 resting
on the top of the C6 articular
process, resulting in complete
loss of articular apposition and
uncovering of C6 articular facet
… BILATERAL PERCHED FACET
JOINTS WITH ANTEROLITHESIS
( about 40 % )
·
Associated fractures seen in the
tip of the facets & upper
endplate of C6
·
Normal atlantooccipital ,
atlantoaxial articulation&
atlantodental distance
MRI Cervical Spine - T2W Sag image

 A. Hyperintense edema signal in B. Injury to C5-C6 disk

the cord at the level of injury
MRI findings
 OSSEOUS STRUCTURES: as mentioned in CT C6 upper endplate fracture. Fracture in the
tip of C5 /C6 facet plates (at the dislocation site)
  
 BRAINSTEM/SPINAL CORD: At C5& C6 level here is an area of increased cord signal
(cord traumatic edema / contusion) measuring about 35 mm in length. No frank
hemorrhagic spots within the cord
  
MRI findings
 PARASPINAL SOFT TISSUES:
 small epidural hematoma at the dislocation site
 Disruption of the ALL, PLL and ligamentous flavum, as well as the interspinous ligaments.
 Disco-ligamentous rupture with traumatic disc herniation
 Large amount of posterior interspinous & paraspinal muscles edema
 At C5/C6 levels bilateral nerve roots of increased signal ( traumatic ) with no salient
pseudo-meningocele
Disposition : Seen by neurosurgeon

 Quadriplegia, no movement in the legs, arms proximal function 2/5, sensation

level nipples
 MRI shows lesion on spinal cord C5-C6, hard collar plan for surgery with
decompression/repositioning and anterior and posterior fixation

 ICU for further management

discussion

 Neurogenic shock is a form of circulatory shock that may occur with severe injury to the upper spinal
cord. —a type of distributive shock; disruption of sympathetic fibers; occurs with high thoracic, cervical
spine, and profound brain injuries. Usually limited to SCI above T6 (just as autonomic hyperreflexia) .
 It should not be confused with spinal shock, which refers to the initial flaccid muscle paralysis which is
temporary, which will make incomplete spinal injury to appear as complete spinal cord injury
 The classic description of neurogenic shock is hypotension without tachycardia or peripheral
vasoconstriction.
 Typical clinical features of the condition include:
 1. Hypotension:
 2. Bradycardia: is a characteristic feature, in contrast to all other types of circulatory shock.
 3. Normal pulse pressure: A narrowed pulse pressure is not seen, (as it is for hypovolemic shock).
 4. Peripheral perfusion: In pure cases of neurogenic shock, peripheral perfusion is not reduced It may in
fact be increased due to peripheral vasodilation, as may also be the case in septic or anaphylactic shock.
This is in marked contrast to the far more common scenario of hypovolemic shock, where peripheral
perfusion is significantly reduced.
discussion

 Regarding pathology Neurogenic shock results from severe spinal cord injury of the
upper segments. This is usually at or above the level of T4, as the sympathetic cardiac
nerves arise at the level of T1-4. Spinal cord lesions below this level do not result in
neurogenic shock.
 The cause of the circulatory compromise is due to disruption of the descending
sympathetic nervous supply of the spinal cord, hence a hallmark of the condition will be
hypotension together with a bradycardia.
 Hypotension results from: ● Bradycardia, (or at least a failure of a tachycardic
response to a fall in blood pressure),● Reduced myocardial contractility
 Peripheral vasodilation.

 Note that isolated intracranial injuries to the CNS do not cause circulatory shock, and if
this is present in such cases then other causes of shock need to be pursued.
management
After ruling out other more common causes of shock, neurogenic shock is treated as
follows:
 1. Attention to any other immediate ABC issues.
 2. Spinal immobilization, as required.
 3. IV fluid resuscitation, and loading. ● Fluid administration alone may not be sufficient
to restore blood pressure in neurogenic shock.
 4. Vasopressors: ● Adrenaline or noradrenaline infusion may be required to restore
blood pressure, when this fails to respond to fluid loading. Note that vasopressors are
not a treatment for hypovolemic shock.
 5. Atropine: ● This may be useful to treat bradycardia, contributing to the hypotension.
 6. Establish monitoring: ●Continuous ECG monitoring , Blood pressure, (preferably by
arterial line), Pulse oximetry, IDC, for urinary output ,Central venous line, for CVP
measurements.
 7. Avoid hypothermia
reference

 ATLS MANNUAL 8TH OF 2008

 Tintinalli’s Emergency Medicine 9th Edition
 Morgan GE, Mikhail MS, Murray MJ, Clinical Anesthesiology, fourth ed., New
York, McGraw-Hill, 2006. Barash PG, Cullen BF, Stoelting RK, Clinical
Anesthesia, fifth ed., Philadelphia, Lippincott Williams & Wilkins, 2006.
 Cottrell JE, Smith DS, Anesthesia and Neurosurgery, fourth ed., St. Louis,
Mosby, 2001.
 Schreiber D, Spinal cord injuries,
http://www.emedicine.com/emerg/topic553.htm, last updated 2006
Traumatic Spinal cord
Injuries (TSCI)
Dr. Raj and Dr. Atul
 Causes of TSCI
 Motor vehicle accidents: (48 percent in Locals UAE)

 ●Falls: 16 percent (more then 50 percent in expats in UAE)

 ●Violence (especially gunshot wounds): 12 percent

 ●Sports accidents: 10 percent

 ●Other
Risk factors
 Cervical spondylosis

 Atlantoaxial instability

 Congenital conditions, eg, tethered cord

 Osteoporosis

 Spinal
arthropathies, including ankylosing spondylitis or
rheumatoid arthritis
ANATOMICAL
LOCALISATION 1
ANATOMICAL
LOCALISATION 2
Tracts at a glance 1
 Tracts at a glance 2
Tract Location Function

Transmits ipsilateral
Dorsal columns Posteromedial aspect of cord proprioception, vibration and light-
touch sensation

Transmits contralateral pain,

Spinothalamic tract Anterolateral aspect of cord crude-touch and temperature
sensation

Lateral corticospinal tract Posterolateral aspect of cord Controls ipsilateral motor power
Pathogenesis, mechanism of spinal cord injury

 Osseous disruption (fracture or displacement) is the most

common cause of spinal cord injury.
 Ligamentous injury, without osseous disruption, causing
spinal cord injury is common in children, resulting in spinal
cord injury without radiographic abnormality (SCIWORA)
 Forward flexion can lead to wedge or teardrop fractures,
which usually begin at or near the intervertebral disc .These
fractures are often encountered in motor vehicle accidents
involving passengers not wearing seat belts.
Axial loading, can cause burst fractures
Classification of injury

 Based on level.
 Severity of neurological deficit.
 Spinal cord syndromes
 Morphology.
Injury patterns

Cervical spine C1 to C7
Cervico-thoracic junction C7 to T1
Thoracic T1 to T10
Thoracolumbar T11 to L2
Lumbar L3 to L5
Sacral injuries
International Standards for Neurological
Classification of Spinal Cord Injury (ISNCSCI)
 ASIA Impairment Scale (AIS)

 Complete Injury: Absence of Sacral Sparing i.e. No

Sensory and Motor Function at S4-5
 Incomplete Injury: Presence of Sacral Sparing i.e.
Partial preservation of Sensory and/or Motor Function
at S4-5
 Sensory Incomplete: Sacral Sparing of Sensory Function
 Motor Incomplete: Sacral Sparing of Motor Function or
Sacral Sparing of Sensory and Motor Function more than
3 Levels below Injury
 Central cord syndrome
 Mechanism -Hyperextension injury of cervical spine in patient
with pre-existing cervical stenosis e.g. forward fall with facial
impact in elderly patient (can occur even without cervical spine
fracture/dislocation)
 Tracts affected – Corticospinal tract and spinothalamic tract
 Clinical Features
Bilateral motor loss
Varying degrees of sensory loss
Greater loss in upper limbs than lower limbs
Greater loss of motor function than sensory function
Anterior Cord syndrome
 Mechanism -Occlusion of anterior spinal artery
with infarction of anterior cord by direct anterior
cord compression, flexion injuries of the cervical
spine, or thrombosis of anterior spinal artery
 Tracts affected – Corticospinal, spinothalamic
and spinocerebellar tracts
 Clinical Features
Bilateral motor loss
Bilateral loss of crude touch/pain/temperature
sensation
Cerebellar dysfunction
Brown-Séquard syndrome
 Mechanism -Hemitransection e.g. penetrating trauma
or unilateral compression of the cord
 Tracts affected – all tracts of same side
 Clinical Features
Ipsilateral hemiparesis
Ipsilateral loss of proprioception/vibration/fine touch
sensation
Contralateral loss of crude touch/pain/temperature
sensation
 Posterior cord syndrome

 Mechanism -Penetrating trauma to the back or

hyperextension injury associated with vertebral arch
fractures

 Tracts affected – Dorsal column

 Clinical Features
Bilateral loss of proprioception/vibration/light-touch sensation
Complete cord transection
 Mechanism -Major trauma
 Tracts affected – All tracts

 Clinical Features
Death (C1 - C3)
Paralysis of voluntary/automatic breathing (above C6)
Quadriplegia (above T1)
Paraplegia (below C8)
Complete sensory loss below lesion