1. The document discusses various types of spinal cord injuries including complete injuries which involve a complete loss of motor and sensory function below the level of injury, and incomplete injuries which partially compromise spinal cord function with some sensation and muscle movement retained below the injury site.
2. It provides details on specific spinal cord syndromes like anterior cord syndrome, Brown-Séquard syndrome, and central cord syndrome which are characterized by variable patterns of motor and sensory loss.
3. The management of spinal cord injuries involves stabilizing the spine, treating shock, addressing airway and breathing issues, screening for associated injuries, and preventing complications like pressure sores through regular turning of immobilized patients.
3. Complete VS Incomplete injuries
Complete injuries :
A complete cord syndrome is characterized clinically as complete loss of
motor and sensory function below the level of the traumatic lesion.
In the days immediately following your spinal cord injury, the symptoms
of a complete and incomplete spinal cord injury are virtually
indistinguishable. Over time, though, small differences may begin to
emerge.
Those characteristics include:
-Loss of sensation below the site of the injury.
-Complete loss of motion below the site of the injury.
-Difficulty controlling bladder and bowels.
-If the injury is high enough in the spinal cord, difficulty breathing on
patients own.
4. Incomplete :
With an incomplete spinal cord injury, the spinal cord's functions
are only partially compromised.The effects of an incomplete
spinal cord injury, then, vary more widely.
Some characteristics of an incomplete spinal cord injury include:
-Retaining some sensation below the site of the injury.
-The feelings may come and go, and may be much weaker than
the sensations you used to experience.
-Being able to move some muscles below the site of the injury.
-The extent of movement may vary, and the patient may have
good control over some muscles, but no control over others.
-Pain below the injury; many incomplete spinal cord injury
survivors report issues with chronic pain.
5. Anterior cord syndrome involves a lesion causing variable loss of motor
function and pain and/or temperature sensation, with preservation of
proprioception
Brown-Séquard syndrome, which is often associated with a
hemisection lesion of the cord, involves a relatively greater ipsilateral
loss of proprioception and motor function, with contralateral loss of
pain and temperature sensation
Central cord syndrome usually involves a cervical lesion, with greater
motor weakness in the upper extremities than in the lower extremities,
with sacral sensory sparing.The pattern of motor weakness shows
greater distal involvement in the affected extremity than proximal
muscle weakness. Sensory loss is variable, and the patient is more likely
to lose pain and/or temperature sensation than proprioception and/or
vibration. Dysesthesias, especially those in the upper extremities (eg,
sensation of burning in the hands or arms), are common.
6.
7. Other cord syndromes
Conus medullaris syndrome is a sacral cord injury, with or without involvement
of the lumbar nerve roots.This syndrome is characterized by areflexia in the
bladder, bowel, and to a lesser degree, lower limbs, whereas the sacral
segments occasionally may show preserved reflexes (eg, bulbocavernosus and
micturition reflexes). Motor and sensory loss in the lower limbs is variable.
Cauda equina syndrome involves injury to the lumbosacral nerve roots in the
spinal canal and is characterized by an areflexic bowel and/or bladder, with
variable motor and sensory loss in the lower limbs. Because this syndrome is a
nerve root injury rather than a true spinal cord injury, the affected limbs are
areflexic. Cauda equina syndrome is usually caused by a central lumbar disk
herniation
A spinal cord concussion is characterized by a transient neurologic deficit localized to the
spinal cord that fully recovers without any apparent structural damage.
8. Neurogenic shock
Neurogenic shock refers to the hemodynamic
triad of hypotension, bradycardia, and peripheral
vasodilation resulting from severe autonomic
dysfunction and the interruption of sympathetic
nervous system control in acute spinal cord injury.
Hypothermia is also characteristic.
This condition does not usually occur with spinal cord
injury below the level ofT6 but is more common in
injuries aboveT6, secondary to the disruption of the
sympathetic outflow fromT1-L2 and to unopposed
vagal tone, leading to a decrease in vascular
resistance, with the associated vascular dilatation.
9. Spinal shock
spinal shock is defined as the complete loss of all
neurologic function, including reflexes and rectal tone,
below a specific level that is associated with
autonomic dysfunction.That is, spinal shock is a state
of transient physiologic (rather than anatomic) reflex
depression of cord function below the level of injury,
with associated loss of all sensorimotor functions.
An initial increase in blood pressure due to the release
of catecholamines, followed by hypotension, is noted.
Flaccid paralysis, including of the bowel and bladder, is
observed, and sometimes sustained priapism
develops.These symptoms tend to last several hours
to days until the reflex arcs below the level of the
injury begin to function again (eg, bulbocavernosus
reflex, muscle stretch reflex [MSR])
10. History and physical examination
As with all trauma patients, initial clinical evaluation of
a patient with suspected spinal cord injury (SCI) begins
with a primary survey.The primary survey focuses on
life-threatening conditions. Assessment of airway,
breathing, and circulation (ABCs) takes precedence.A
spinal cord injury must be considered concurrently.
Perform careful history taking, focusing on symptoms
related to the vertebral column (most commonly pain)
and any motor or sensory deficits.Ascertaining the
mechanism of injury is also important in identifying the
potential for spinal injury.
The axial skeleton should be examined to identify and
provide initial treatment of potentially unstable spinal
fractures from both a mechanical and a neurologic
basis.
11. Pulmonary evaluation
• The clinical assessment of pulmonary function in acute spinal cord
injury begins with careful history taking regarding respiratory
symptoms and a review of underlying cardiopulmonary comorbidity
such as chronic obstructive pulmonary disease (COPD) or heart failure
• Carefully evaluate respiratory rate, chest wall expansion, abdominal
wall movement, cough, and chest wall and/or pulmonary injuries.
Arterial blood gas (ABG) analysis and pulse oximetry are especially
useful, because the bedside diagnosis of hypoxia or carbon dioxide
retention may be difficult.
• The degree of respiratory dysfunction is ultimately
dependent on preexisting pulmonary comorbidity, the level
of the spinal cord injury, and any associated chest wall or
lung injury
12. • vital capacity is only 5-10% of normal, and cough is
absent
high lesions
(ie, C1 or C2)
• vital capacity is 20% of normal, and cough is weak
and ineffective
lesions at
C3 through C6
• vital capacity is 30-50% of normal, and cough is
weak
high thoracic cord
injuries
(ie,T2 throughT4)
• respiratory function improveslower cord injuries
• respiratory dysfunction is minimal; vital capacity is
essentially normal, and cough is strong.
injuries atT11,
13. Hemorrhage, hypotension, and
hemorrhagic and neurogenic shock
In all patients with spinal cord injury and
hypotension, a diligent search for sources of
hemorrhage must be made before hypotension is
attributed to neurogenic shock. In acute spinal
cord injury, shock may be neurogenic,
hemorrhagic, or both.
14. Neurogenic shock occurs only in the presence of acute spinal
cord injury aboveT6; hypotension and/or shock with acute
spinal cord injury at or belowT6 is caused by hemorrhage
Hypotension with a spinal fracture alone, without any
neurologic deficit or apparent spinal cord injury, is invariably
due to hemorrhage
The presence of vital sign confusion in acute spinal cord injury
and a high incidence of associated injuries requires a diligent
search for occult sources of hemorrhage
Patients with a spinal cord injury aboveT6 may not have the
classic physical findings associated with hemorrhage (eg,
tachycardia, peripheral vasoconstriction); this vital sign
confusion attributed to autonomic dysfunction is common in
spinal cord injury
Howtodifferentiate
16. Labs
Arterial blood gas (ABG) measurements may
be useful to evaluate adequacy of oxygenation
and ventilation
Lactate levels to monitor perfusion status can
be helpful in the presence of shock
Hemoglobin and/or hematocrit levels may be
measured initially and monitored serially to
detect or monitor sources of blood loss
Urinalysis can be performed to detect any
associated genitourinary injury
17. Imaging
Diagnostic imaging traditionally begins with the acquisition of
standard radiographs of the affected region of the spine.
Investigators have shown that computed tomography (CT) scanning
is exquisitely sensitive for the detection of spinal fractures and is cost
effective. In many centers, CT scanning has supplanted plain
radiographs.
A properly performed lateral radiograph of the cervical spine that
includes the C7-T1 junction can provide sufficient information to
allow the multiple trauma victim to proceed emergently to the
operating room if necessary without additional intervention other
than maintenance of full spinal immobilization and a hard cervical
collar.
Noncontiguous spinal fractures are defined as spinal fractures
separated by at least 1 normal vertebra. Noncontiguous fractures are
common and occur in 10-15% of patients with spinal cord injury.
Therefore, once a spinal fracture is identified, the entire axial
skeleton must be imaged, preferably by CT scanning, to assess for
noncontiguous fractures
18. Plain radiography
The standard 3 views of the cervical spine are recommended in patients with
suspected spinal cord injury (SCI): anteroposterior (AP), lateral, and odontoid
The cervical spine radiographs must include the C7-T1 junction to be considered
adequate. Subtle findings (eg, increased prevertebral soft tissue swelling or
widening of the C1-C2 preodontoid space) indicate potentially unstable
cervical spine injuries that could have serious consequences if they are not
detected.
Dynamic flexion/extension views are safe and effective for detecting
occult ligamentous injury of the cervical spine in the absence of fracture
Anteroposterior and lateral views of the thoracic and lumbar spine are
recommended for suspected injuries to the thoracolumbar spine.
19. Computed tomography scanning
Perform CT scanning in the following situations:
When plain radiography is inadequate or fails to visualize segments of the axial
skeleton
Convenience and speed: If a CT scan of the head is required, then it is usually
simpler and faster to obtain a CT of the cervical spine at the same time.
Similarly, CT images of the thoracic or lumbar spine might be easier and
faster to obtain than plain radiographs
To provide further evaluation when radiography depicts suspicious and/or
indeterminate abnormalities
When radiography depicts fracture or displacement, CT scanning provides better
visualization of the extent and displacement of the fracture
20.
21. MRI
Magnetic resonance imaging (MRI) is best for
suspected spinal cord lesions, ligamentous injuries,
or other soft-tissue injuries or pathology.This
imaging modality should be used to evaluate
nonosseous lesions, such as extradural spinal
hematoma; abscess or tumor; disk rupture; and
spinal cord hemorrhage, contusion, and/or edema.
Neurologic deterioration is usually caused by
secondary injury, resulting in edema and/or
hemorrhage. MRI is the best diagnostic image to
depict these changes.
24. Approach Considerations
Admit all patients with an acute spinal cord injury (SCI). Depending on the level of
neurologic deficit and associated injuries, the patient may require admission to the
intensive care unit (ICU), neurosurgical observation unit, or general ward.
The most common levels of injury on admission are C4, C5 (the most common), and
C6, whereas the level for paraplegia is the thoracolumbar junction (T12).The most
common type of injury on admission isAmerican Spinal InjuryAssociation (ASIA) level
A
Transfer
Depending on local policy, patients with acute spinal cord injury are best treated at a regional
spinal cord injury center.Therefore, once stabilized, early referral to a regional spinal cord injury
center is best.The center should be organized to provide ongoing definitive care.
Other reasons to transfer the patient include the lack of appropriate diagnostic imaging
(computed tomography [CT] scanning or magnetic resonance imaging [MRI]) and/or inadequate
spine consultant support (orthopedist or neurosurgeon).
Consultations
Consultation with a neurosurgeon and/or an orthopedist is required, depending on local
preferences. Because most patients with spinal cord injury have multiple associated injuries,
consultation with a general surgeon or a trauma specialist as well as other specialists may also
be required.
25. Prehospital management
Most prehospital care providers recognize the need to
stabilize and immobilize the spine on the basis of
mechanism of injury, pain in the vertebral column, or
neurologic symptoms. Patients are usually transported
to the emergency department (ED) with a cervical hard
collar on a hard backboard. Commercial devices are
available to secure the patient to the board.
The patient should be secured so that in the event of
emesis, the backboard may be rapidly rotated 90°
while the patient remains fully immobilized in a neutral
position. Spinal immobilization protocols should be
standard in all prehospital care systems.
26. Emergency department management
Most patients with spinal cord injuries (SCIs) have
associated injuries. In this setting, assessment and
treatment of airway, respiration, and circulation
(ABCs) takes precedence.
The patient is best treated initially in the supine
position. Occasionally, the patient may have been
transported prone by the prehospital care
providers. Logrolling the patient to the supine
position is safe to facilitate diagnostic evaluation
and treatment. Use analgesics appropriately and
aggressively to maintain the patient's comfort if he
or she has been lying on a hard backboard for an
extended period.
27.
28. Airway
The cervical spine
must be maintained
in neutral alignment
at all times.
Clearing of oral
secretions and/or
debris is essential to
maintain airway
patency and to
prevent aspiration
The modified jaw
thrust and insertion
of an oral airway may
be all that is required
to maintain an
airway in some cases
However, intubation may be required in
others. Failure to intubate emergently
when indicated because of concerns
regarding the instability of the patient's
cervical spine is a potential pitfall.
29. Hypotension, hemorrhage and shock
The most common sources of occult
hemorrhage are injuries to the chest, abdomen,
and retroperitoneum and fractures of the pelvis or
long-bones. Appropriate investigations, including
radiography or computed tomography (CT)
scanning, are required. In the unstable patient,
diagnostic peritoneal lavage or bedside FAST
(focused abdominal sonography for trauma)
ultrasonographic study may be required to detect
intra-abdominal hemorrhage.
30. Treatment of neurogenic shock
initial treatment of neurogenic shock focuses
on fluid resuscitation.
Judicious fluid replacement with isotonic
crystalloid solution to a maximum of 2 L is the
initial treatment of choice.
Overzealous crystalloid administration may cause
pulmonary edema, because these patients are at
risk for the acute respiratory distress syndrome
(ARDS).
31. Our goals are
1. A systolic blood pressure (BP) of 90-100 mm Hg should be achieved; systolic BPs
in this range are typical for patients with complete cord lesions.Compelling animal
and human studies recommend maintenance of systolic BP above 90 mm Hg and to
avoid any hypotensive episodes
2.The most important treatment consideration is to maintain adequate
oxygenation and perfusion of the injured spinal cord; supplemental oxygenation
and/or mechanical ventilation may be required
3. Heart rate should be 60-100 beats per minute (bpm) in normal sinus rhythm
4. Hemodynamically significant bradycardia may be treated with atropine
5. Urine output should be more than 30 mL/h; placement of a Foley catheter to
monitor urine output and to decompress the neurogenic bladder is essential
6. Rarely, inotropic support with dopamine or norepinephrine is required; this should
be reserved for patients who have decreased urinary output despite adequate fluid
resuscitation; usually, low doses of dopamine in the 2- to 5-mcg/kg/min range are
sufficient
7. Prevent hypothermia
32. Head injuries and neurologic
evaluation
Associated head injury occurs in about 25% of
patients with spinal cord injury. A careful neurologic
assessment for associated head injury is
compulsory.
The presence of amnesia, external signs of head
injury or basilar skull fracture, focal neurologic
deficits, associated alcohol intoxication or drug
abuse, and a history of loss of consciousness
mandates a thorough evaluation for intracranial
injury, starting with noncontrast head CT scanning.
GCS
33. Ileus
Ileus is common. Placement of a nasogastric (NG)
tube is essential. Aspiration pneumonitis is a serious
complication in the patient with a spinal cord injury
with compromised respiratory function (see
Antiemetics should be used aggressively.
Pressure sores
Prevent pressure sores. Denervated skin is particularly
prone to pressure necrosis.Turn the patient every 1-2
hours. Pad all extensor surfaces. Undress the patient
to remove belts and back pocket keys or wallets.
Remove the spine board as soon as possible
35. Steroid therapy
The National Acute Spinal Cord Injury Studies (NASCIS) II and III,
[42, 43] a Cochrane Database of Systematic Reviews article of all
randomized clinical trials, and other published reports, have verified
significant improvement in motor function and sensation in
patients with complete or incomplete spinal cord injuries (SCIs) who
were treated with high doses of methylprednisolone within 8 hours
of injury.
The current recommendation is to treat all patients with spinal
cord injury according to the local/regional protocol. If steroids
are recommended, they should be initiated within 8 hours of
injury with the following steroid protocol: methylprednisolone 30
mg/kg bolus over 15 minutes and an infusion of
methylprednisolone at 5.4 mg/kg/h for 23 hours beginning 45
minutes after the bolus.
36. Analgesics
Pregabalin (Lyrica):
Indicated for neuropathic pain associated with
spinal cord injury.The precise mechanism of action
is unknown but is a GABA analog which binds to a
subunit of voltage-gated calcium channels in CNS.
It does not affect sodium channels, opiate
receptors or cyclooxygenase enzyme activity. Its
interactions with descending noradrenergic and
serotonergic pathways originating from the
brainstem appear to reduce neuropathic pain
transmission from the spinal cord.
37. Treatment for pulmonary complications
Indications for intubation in spinal cord injury are:
- acute respiratory failure
- decreased level of consciousness (Glasgow score < 9)
- increased respiratory rate with hypoxia
-partial pressure of carbon dioxide (PCO2) greater than 50
mm Hg, and vital capacity less than 10 mL/kg
In the presence of autonomic disruption from cervical or
high thoracic spinal cord injury, intubation may cause
severe bradyarrhythmias from unopposed vagal
stimulation. Simple oral suctioning can also cause
significant bradycardia. Preoxygenation with 100% oxygen
may be preventive.Atropine may be required as an
adjunct.Topical lidocaine spray can minimize or prevent
this reaction.
38. Surgical intervention
Emergent decompression of the spinal cord is
suggested in the setting of acute spinal cord injury
with :
progressive neurologic deterioration
facet dislocation
bilateral locked facets.
spinal nerve impingement with progressive
radiculopathy
patients with extradural lesions such as epidural
hematomas or abscesses or in the setting of the
cauda equina syndrome.
39. Evidence
A prospective surgical trial, the Surgical Treatment for Acute Spinal Cord Injury
Study (STASCIS) conducted by the Spine Trauma Study Group, is ongoing.
Preliminary data from this study are showing that 24% of patients who receive
decompressive surgery within 24 hours of their injury experience a 2-grade or
better improvement on the ASIA scale, compared with 4% of those in the delayed-
treatment group. Furthermore, the study found that cardiopulmonary and urinary
tract complications were found to be 37% in the early surgery group compared
with the delayed group rate of 48.6%. The hope is that the final data from STASCIS
will better define the benefits and timing of early surgical decompression and
stabilization.
41. Neurologic deterioration :
The neurologic deficit of spinal cord injury (SCI) often increases during the hours to
days following acute injury, despite optimal treatment.
One of the first signs of neurologic deterioration is the extension of the sensory deficit
cephalad. Careful repeat neurologic examination may reveal that the sensory level has
risen 1 or 2 segments. Repeat neurologic examinations to check for progression are
essential.
Pressure sores :
Careful and frequent turning of the patient is required to prevent pressure sores.
Denervated skin is particularly prone to this complication. Remove belts and objects from
back pockets, such as keys and wallets.
Aspiration and pulmonary complications
Other complications :
Severe sepsis or pneumonia frequently follows treatment with high-dose
methylprednisolone that is frequently used in spinal cord injury
42. Prognosis
Patients with a complete spinal cord injury (SCI) have a less than
5% chance of recovery. If complete paralysis persists at 72 hours
after injury, recovery is essentially zero
In the early 1900s, the mortality rate 1 year after injury in patients
with complete lesions approached 100%. Much of the
improvement since then can be attributed to the introduction of
antibiotics to treat pneumonia and urinary tract infection (UTI).
The prognosis is much better for the incomplete cord syndromes
If some sensory function is preserved, the chance that the patient
will eventually be able walk is greater than 50%.
Ultimately, 90% of patients with spinal cord injury return to their
homes and regain independence.
Providing an accurate prognosis for the patient with an acute SCI
usually is not possible in the emergency department (ED) and is
best avoided.
43. Patient education
As part of inpatient therapy, patients with
spinal cord injury (SCI) should receive a
comprehensive program of physical and
occupational therapy.
44. Prevention
Many spinal cord injuries result from
incidents involving drunk driving, assaults,
and alcohol or drug abuse. Spinal cord injuries
from industrial hazards, such as equipment
failures or inadequate safety precautions, are
potentially preventable causes. Unfenced,
shallow, or empty swimming pools are known
hazards.
When comparing complete vs. incomplete spinal cord injuries, it is not always easy to discern which type you have. Particularly in the first weeks after an injury, swelling may interfere with function. When swelling goes down, an injury that appeared to be a complete spinal cord injury might turn out to be incomplete.
A complete spinal cord injury removes the brain's ability to send signals down the spinal cord below the site of the injury
Patients with a complete spinal cord injury (SCI) have a less than 5% chance of recovery. If complete paralysis persists at 72 hours after injury, recovery is essentially zero. In the early 1900s, the mortality rate 1 year after injury in patients with complete lesions approached 100%. Much of the improvement since then can be attributed to the introduction of antibiotics to treat pneumonia and urinary tract infection (UTI).
The prognosis is much better for the incomplete cord syndromes.
If some sensory function is preserved, the chance that the patient will eventually be able walk is greater than 50%.
Ultimately, 90% of patients with spinal cord injury return to their homes and regain independence.
Providing an accurate prognosis for the patient with an acute SCI usually is not possible in the emergency department (ED) and is best avoided.
occur when the spinal cord is compressed or injured, but the brain's ability to send signals below the site of the injury is not completely removed.
. The corticospinal tracts are descending motor pathways located anteriorly within the spinal cord Axons extend from the cerebral cortex in the brain as far as the corresponding segment, where they form synapses with motor neurons in the anterior (ventral) horn. They decussate (cross over) in the medulla before entering the spinal cord
The dorsal columns are ascending sensory tracts that transmit light touch, proprioception, and vibration information to the sensory cortex. They do not decussate until they reach the medulla
The lateral spinothalamic tracts transmit pain and temperature sensation. These tracts usually decussate within 3 segments of their origin as they ascend
The anterior spinothalamic tract transmits light touch
Autonomic function traverses within the anterior interomedial tract. Sympathetic nervous system fibers exit the spinal cord between C7 and L1, whereas parasympathetic system pathways exit between S2 and S4.
Injury to the corticospinal tract or dorsal columns, respectively, results in ipsilateral paralysis or loss of sensation of light touch, proprioception, and vibration. Unlike injuries of the other tracts, injury to the lateral spinothalamic tract causes contralateral loss of pain and temperature sensation. Because the anterior spinothalamic tract also transmits light touch information, injury to the dorsal columns may result in complete loss of vibration sensation and proprioception but only partial loss of light touch sensation. Anterior cord injury causes paralysis and incomplete loss of light touch sensation.
Autonomic function is transmitted in the anterior interomedial tract. The sympathetic nervous system fibers exit from the spinal cord between C7 and L1. The parasympathetic system nerves exit between S2 and S4. Therefore, progressively higher spinal cord lesions or injury causes increasing degrees of autonomic dysfunction.
Vascular supply
The blood supply of the spinal cord consists of 1 anterior and 2 posterior spinal arteries. The anterior spinal artery supplies the anterior two thirds of the cord. Ischemic injury to this vessel results in dysfunction of the corticospinal, lateral spinothalamic, and autonomic interomedial pathways. Anterior spinal artery syndrome involves paraplegia, loss of pain and temperature sensation, and autonomic dysfunction. The posterior spinal arteries primarily supply the dorsal columns. The anterior and posterior spinal arteries arise from the vertebral arteries in the neck and descend from the base of the skull. Various radicular arteries branch off the thoracic and abdominal aorta to provide collateral flow.
The primary watershed area of the spinal cord is the midthoracic region. Vascular injury may cause a cord lesion at a level several segments higher than the level of spinal injury. For example, a lower cervical spine fracture may result in disruption of the vertebral artery that ascends through the affected vertebra. The resulting vascular injury may cause an ischemic high cervical cord injury. At any given level of the spinal cord, the central part is a watershed area. Cervical hyperextension injuries may cause ischemic injury to the central part of the cord, causing a central cord syndrome.
Neurogenic shock needs to be differentiated from spinal and hypovolemic shock. Hypovolemic shock tends to be associated with tachycardia.
Shock associated with a spinal cord injury involving the lower thoracic cord must be considered hemorrhagic until proven otherwise.
After a suspected SCI, the goals are to establish the diagnosis and initiate treatment to prevent further neurologic injury from either mechanical instability secondary to injury from the deleterious effects of cardiovascular instability or respiratory insufficiency.
The posterior cervical spine and paraspinal tissues should be evaluated for pain, swelling, bruising, or possible malalignment.
Logrolling the patient to systematically examine each spinous process of the entire axial skeleton from the occiput to the sacrum can help identify and localize injury. The skeletal level of injury is the level of the greatest vertebral damage on radiograph.
Complete bilateral loss of sensation or motor function below a certain level indicates a complete spinal cord injury.
Any or all of the following determinants of pulmonary function may be impaired in the setting of spinal cord injury:
Loss of ventilatory muscle function from denervation and/or associated chest wall injury
Lung injury, such as pneumothorax, hemothorax, or pulmonary contusion
Decreased central ventilatory drive that is associated with head injury or exogenous effects of alcohol and drugs
A direct relationship exists between the level of cord injury and the degree of respiratory dysfunction, as follows:
Other findings of respiratory disfunction include the following:
Agitation, anxiety, or restlessness
Poor chest wall expansion
Decreased air entry
Rales, rhonchi
Pallor, cyanosis
Increased heart rate
Paradoxic movement of the chest wall
Increased accessory muscle use
Moist cough
Hemorrhagic shock may be difficult to diagnose, because the clinical findings may be affected by autonomic dysfunction. Disruption of autonomic pathways prevents tachycardia and peripheral vasoconstriction that normally characterizes hemorrhagic shock. This vital sign confusion may falsely reassure. In addition, occult internal injuries with associated hemorrhage may be missed
The following are clinical "pearls" useful in distinguishing hemorrhagic shock from neurogenic shock
Attributing hypotension to neurogenic shock in the setting of spinal cord injury (SCI) is a potentially devastating error. As noted under Clinical, before hypotension can be attributed to neurogenic shock, a diligent search for sources of hemorrhage must be completed. Shock may be hemorrhagic, neurogenic, or both in patients with acute spinal cord injury.
The presence of vital sign confusion in acute spinal cord injury coupled with the limitations of the physical examination can make the diagnosis of hemorrhage from associated injuries challenging.
Also consider other conditions in patients with suspected spinal cord injury, such as transverse myelitis, acute intervertebral disk herniation, and extradural spinal cord compression.
With regard to laboratory studies, the following may be helpful:
The negative predictive value of a normal The incidence of occult injury in the setting of normal findings on cervical spine radiography and CT scanning is low, so clinical judgment and the mechanism of injury should be used to guide the decision to order flexion/extension views.3-view cervical spine series and flexion/extension views exceeds 99%
Adequate spinal radiography supplemented by computed tomography (CT) scanning through areas that are difficult to visualize or are suspicious detects the vast majority of fractures with a reported negative predictive value between 99% and 100%. [
Computed tomography (CT) scanning is reserved for delineating bony abnormalities or fracture. Some studies have suggested that CT scanning with sagittal and coronal reformatting is more sensitive than plain radiography for the detection of spinal fractures.
Airway management in the setting of spinal cord injury, with or without a cervical spine injury, is complex and difficult
Hypotension may be hemorrhagic and/or neurogenic in acute spinal cord injury. Because of the vital sign confusion in acute spinal cord injury and the high incidence of associated injuries, a diligent search for occult sources of hemorrhage must be made
Once occult sources of hemorrhage have been excluded, initial treatment of neurogenic shock
The therapeutic goal for neurogenic shock is adequate perfusion with the following parameters
The goal of pharmacotherapy is to improve motor function and sensation in patients with spinal cord injuries (SCIs).
Various drugs are used for neuropathic pain
Try to remove the patient from the backboard as soon as possible. Some patients may require spinal immobilization in a halo vest or a Stryker frame. Many patients with acute spinal cord injury have stable vertebral fractures yet needlessly spend hours on a hard backboard
Patients with spinal cord injury are at high risk for aspiration. Nasogastric decompression of the stomach is mandatory.
Pulmonary complications in spinal cord injury are common. Such complications are directly correlated with mortality, and both are related to the level of neurologic injury. Pulmonary complications of spinal cord injury include the following:
Atelectasis secondary to decreased vital capacity and decreased functional residual capacity
Ventilation-perfusion (V/Q) mismatch due to sympathectomy and/or adrenergic blockade
Increased work of breathing because of decreased compliance
Decreased coughing, which increases the risk of retained secretions, atelectasis, and pneumonia
Muscle fatigue