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NEUROGENIC SHOCK
BY – TRIPARNA HALDER
ANATOMY AND PHYSIOLOGY:
NEUROGENIC SHOCK
 Introduction:
Neurogenic shock is a devastating
consequence of spinal cord injury (SCI). It
manifests as hypotension, bradyarrhythmia,
and temperature dysregulation due to
peripheral vasodilatation following an injury
to the spinal cord. This occurs due to the
sudden loss of sympathetic tone, with
preserved parasympathetic function, leading
to autonomic instability.
 Definition:
Neurogenic shock is a distributive type of
shock resulting in hypotension, and
bradycardia, caused by disruption of
autonomic nervous system pathways.
It is related to damage to the central
nervous system, such as spinal cord injury.
 Incidence: neurogenic shock is seen in (Higher
spine injury)
 19.3% of cervical spine injuries and
 7% of thoracic spine injuries.
 Etiology:
 Trauma (cervical or high thoracic spinal cord
injury)
Other causes: (very rare)
 Spinal anesthesia,
 Guillain-Barre syndrome,
 Autonomic nervous system toxins,
 Transverse myelitis,
 Other neuropathies.
PATHOPHYSIOLOGY:
Disruption of sympathetic nervous system
Heart rate
Parasympathetic
nervous system
response
Loss of sympathetic tone
Venous and arterial vasodilation
BP
Venous return
Stroke volume
Cardiac output
Cellular oxygen supply
Cellular hypoxia
Cell damage
Cell death
CLINICAL MANIFESTATION:
CLINICAL MANIFESTATION
 Sudden hypotension (due to sudden, massive vasodilation)
 Decrease in oxygen saturation (bronchoconstriction)
 Bradycardia (vagal response)
 Hemodynamic triad of neurogenic shock:
 hypotension,
 bradycardia,
 peripheral vasodilation
 Temperature dysregulation
 Warm, flushed skin (due to vasodilation)
 Priapism (due to vasodilation)
 Diaphragmatic breathing: The injury is below the 5th cervical vertebrae;
the patient will exhibit diaphragmatic breathing due to loss of nervous
control of the intercostal muscles.
 Respiratory arrest: The injury is above the 3rd cervical vertebrae, the
patient will go into respiratory arrest immediately following the injury,
due to loss of nervous control of the diaphragm.
CLINICAL MANIFESTATION
Spinal shock: temporary loss of sensation and motor function
Neurogenic shock: hemodynamic Instability caused by loss of sympathetic
tone and catecholamines
Spinal Shock Vs Neurogenic Shock
Spinal Shock Neurogenic Shock
Location Anywhere on spinal cord Above T6
Systemic Hypotension Possible Always
Onset Sudden to days Sudden
Resolution Long Short
AUTONOMIC DYSREFLEXIA
Autonomic dysregulation develops in SCI
at or above the sixth thoracic vertebral
level (T6). It is considered a medical
emergency and must be recognized
immediately.
 SNS below the level of injury responds to
stimuli. Vasoconstriction BP
 Systolic and diastolic blood pressure greater
than 20 mm Hg and 10 mm Hg, respectively.
 No opposition from PNS- through spinal cord
 Baroreceptor stimulate PNS HR
 Profuse sweating above the level of lesion -
especially in the face, neck, and shoulders
 Flushing of the skin above the level of the
lesion - especially in the face, neck, and
shoulders
 Goose bumps below the level of the lesion
DIAGNOSTIC EVALUATION:
 History collection (SCI)
 Hemodynamic monitoring, and clinical exam (location, extent etc.)
Although there are no clear guidelines, research suggests that the following
indicates neurogenic shock:
 Systolic BP below 90 mm Hg
 Heart Rate lower than 80 beats per minute
To examine the spinal cord for injury, may include the following:
 CT scan: identify the exact location and extent of injury.
 MRI scan: identify any abnormalities within the spine, such as herniated disks.
 Urinary catheter: to check spinal cord function. (May lose bladder control or
cannot empty the bladder as usual.)
Differential Diagnosis:
 Hypovolemic shock
 Obstructive shock
 Cardiogenic shock
 Septic shock
All these types of shocks are associated with tachycardia, whereas
neurogenic shock is associated with bradycardia.
MANAGEMENT
MEDICAL MANAGEMENT:
 C-spine immobilization: to prevent any further injury to the spinal cord. Eg:
Miami J or Philadelphia collar.
 IV fluids: treat low BP. (1st line treatment for hypovolemia.)
 Vasopressors: If hypotension persists despite euvolemia,
vasopressors and inotropes are the second lines.
Eg: epinephrine, norepinephrine, dopamine etc.
GOAL: MAP between 85 to 90 mmHg for the first 7 days to improve spinal cord
perfusion.
 Other medications:
Atropine and glycopyrrolate (to increase heart rate).
Isoproterenol (chronotropic agent).
Methylxanthines: theophylline and aminophylline (for refractory cases of
bradycardia).
 Steroids: methylprednisolone for SCI
 Heparin: heparin or LMWH to prevent thrombus formation.
MEDICAL MANAGEMENT:
To decompress the spine or treat a spinal injury,
either through traction or realignment.
 SURGICAL MANAGEMENT
Assessment :
ABCDE evolution
Physical assessment, including cranial nerve assessment
Assessment for other injuries
Examine for obstructions such as loose teeth,
foreign bodies
AIRWAY
Examine trachea for deviation, observe for signs of
circumoral cyanosis
Auscultate airway, listen for turbulence
With SCI, prevertebral swelling and hematoma may
occur, which can compromise airway.
NURSING MANAGEMENT:
ABCDE evolution
BREATHING
High cervical injuries – immediate intubation
Avoid flexion of neck
Monitor for high diaphragmatic/ abdominal breathing
CIRCULATION
Monitor BP, pulse, temperature, color, indications of cyanosis
Monitor Oxygen saturation
Use venous access to restore intravascular volume
Evaluate possible causes of hypotension. Hypotension with bradycardia –
SCI
DYSFUNCTION
/ DISABILITY
Assess GCS, neurological status
Assess reflexes to determine level of injury and integrity of spinal cord
Immobilize patient with rigid backboard and cervical spine collar until SCI is
ruled out
EXTERNAL
EXAMINATION
Note lacerations, fractures, edema and bruises
ABCDE evolution
 Risk for impaired breathing pattern related to
impairment of innervation of diaphragm (lesions at or
above C-5).
 Impaired physical mobility related to neuromuscular
impairment.
 Disturbed sensory perception related to destruction of
sensory tracts with altered sensory reception,
transmission, and integration.
 Risk for trauma related to temporary
weakness/instability of spinal column.
NURSING DIAGNOSIS
INTERVENTION
 Airway patency: Maintain patent airway:
keep head in neutral position,
elevate head of bed slightly if tolerated,
use airway adjuncts as indicated.
Monitor vital signs. (T P R BP)
HR & BP monitoring: Measure and monitor HR & BP before and after
activity in acute phases or until stable.
Oxygen: Administer oxygen by appropriate method (nasal prongs, mask,
intubation, ventilator.
 Thermoregulation:
o Peripheral temperature sensations cannot reach the
hypothalamus
o Ability to sweat or shiver to control temperature is impaired
below the level of injury
o Monitor temperature and adjust the environmental temperature
accordingly
o Provide blankets
INTERVENTION
INTERVENTION
 Lower extremity interventions: Applying anti-embolism stockings and elevating
the foot of the bed may help minimize pooling of the blood in the legs and
prevent thrombus formation.
 Exercise: Passive range of motion of the immobile extremities helps promote
circulation.
 Activities: Plan activities to provide uninterrupted rest periods and encourage
involvement within individual tolerance and ability.
 Reduce anxiety: Assist patient to recognize and compensate for alterations in
sensation.
CONCLUSION:
Neurogenic shock can occur after a spinal cord injury, and it can be fatal.
Injury or trauma to the spinal cord can cause nerve damage, which affects
body’s ability to regulate blood pressure and heart rate. This can impair
blood flow, resulting in a lack of oxygen and nutrients reaching vital organs.
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NUREGENIC SHOCK Nursing.pptx

  • 1. NEUROGENIC SHOCK BY – TRIPARNA HALDER
  • 3.
  • 4. NEUROGENIC SHOCK  Introduction: Neurogenic shock is a devastating consequence of spinal cord injury (SCI). It manifests as hypotension, bradyarrhythmia, and temperature dysregulation due to peripheral vasodilatation following an injury to the spinal cord. This occurs due to the sudden loss of sympathetic tone, with preserved parasympathetic function, leading to autonomic instability.
  • 5.  Definition: Neurogenic shock is a distributive type of shock resulting in hypotension, and bradycardia, caused by disruption of autonomic nervous system pathways. It is related to damage to the central nervous system, such as spinal cord injury.
  • 6.  Incidence: neurogenic shock is seen in (Higher spine injury)  19.3% of cervical spine injuries and  7% of thoracic spine injuries.  Etiology:  Trauma (cervical or high thoracic spinal cord injury) Other causes: (very rare)  Spinal anesthesia,  Guillain-Barre syndrome,  Autonomic nervous system toxins,  Transverse myelitis,  Other neuropathies.
  • 8. Disruption of sympathetic nervous system Heart rate Parasympathetic nervous system response Loss of sympathetic tone Venous and arterial vasodilation BP Venous return Stroke volume Cardiac output Cellular oxygen supply Cellular hypoxia Cell damage Cell death
  • 10. CLINICAL MANIFESTATION  Sudden hypotension (due to sudden, massive vasodilation)  Decrease in oxygen saturation (bronchoconstriction)  Bradycardia (vagal response)  Hemodynamic triad of neurogenic shock:  hypotension,  bradycardia,  peripheral vasodilation  Temperature dysregulation  Warm, flushed skin (due to vasodilation)  Priapism (due to vasodilation)
  • 11.
  • 12.  Diaphragmatic breathing: The injury is below the 5th cervical vertebrae; the patient will exhibit diaphragmatic breathing due to loss of nervous control of the intercostal muscles.  Respiratory arrest: The injury is above the 3rd cervical vertebrae, the patient will go into respiratory arrest immediately following the injury, due to loss of nervous control of the diaphragm. CLINICAL MANIFESTATION
  • 13. Spinal shock: temporary loss of sensation and motor function Neurogenic shock: hemodynamic Instability caused by loss of sympathetic tone and catecholamines Spinal Shock Vs Neurogenic Shock Spinal Shock Neurogenic Shock Location Anywhere on spinal cord Above T6 Systemic Hypotension Possible Always Onset Sudden to days Sudden Resolution Long Short
  • 14. AUTONOMIC DYSREFLEXIA Autonomic dysregulation develops in SCI at or above the sixth thoracic vertebral level (T6). It is considered a medical emergency and must be recognized immediately.
  • 15.  SNS below the level of injury responds to stimuli. Vasoconstriction BP  Systolic and diastolic blood pressure greater than 20 mm Hg and 10 mm Hg, respectively.  No opposition from PNS- through spinal cord  Baroreceptor stimulate PNS HR  Profuse sweating above the level of lesion - especially in the face, neck, and shoulders  Flushing of the skin above the level of the lesion - especially in the face, neck, and shoulders  Goose bumps below the level of the lesion
  • 16. DIAGNOSTIC EVALUATION:  History collection (SCI)  Hemodynamic monitoring, and clinical exam (location, extent etc.) Although there are no clear guidelines, research suggests that the following indicates neurogenic shock:  Systolic BP below 90 mm Hg  Heart Rate lower than 80 beats per minute To examine the spinal cord for injury, may include the following:  CT scan: identify the exact location and extent of injury.  MRI scan: identify any abnormalities within the spine, such as herniated disks.  Urinary catheter: to check spinal cord function. (May lose bladder control or cannot empty the bladder as usual.)
  • 17. Differential Diagnosis:  Hypovolemic shock  Obstructive shock  Cardiogenic shock  Septic shock All these types of shocks are associated with tachycardia, whereas neurogenic shock is associated with bradycardia.
  • 19. MEDICAL MANAGEMENT:  C-spine immobilization: to prevent any further injury to the spinal cord. Eg: Miami J or Philadelphia collar.  IV fluids: treat low BP. (1st line treatment for hypovolemia.)  Vasopressors: If hypotension persists despite euvolemia, vasopressors and inotropes are the second lines. Eg: epinephrine, norepinephrine, dopamine etc. GOAL: MAP between 85 to 90 mmHg for the first 7 days to improve spinal cord perfusion.
  • 20.  Other medications: Atropine and glycopyrrolate (to increase heart rate). Isoproterenol (chronotropic agent). Methylxanthines: theophylline and aminophylline (for refractory cases of bradycardia).  Steroids: methylprednisolone for SCI  Heparin: heparin or LMWH to prevent thrombus formation. MEDICAL MANAGEMENT:
  • 21. To decompress the spine or treat a spinal injury, either through traction or realignment.  SURGICAL MANAGEMENT
  • 22. Assessment : ABCDE evolution Physical assessment, including cranial nerve assessment Assessment for other injuries Examine for obstructions such as loose teeth, foreign bodies AIRWAY Examine trachea for deviation, observe for signs of circumoral cyanosis Auscultate airway, listen for turbulence With SCI, prevertebral swelling and hematoma may occur, which can compromise airway. NURSING MANAGEMENT: ABCDE evolution
  • 23. BREATHING High cervical injuries – immediate intubation Avoid flexion of neck Monitor for high diaphragmatic/ abdominal breathing CIRCULATION Monitor BP, pulse, temperature, color, indications of cyanosis Monitor Oxygen saturation Use venous access to restore intravascular volume Evaluate possible causes of hypotension. Hypotension with bradycardia – SCI DYSFUNCTION / DISABILITY Assess GCS, neurological status Assess reflexes to determine level of injury and integrity of spinal cord Immobilize patient with rigid backboard and cervical spine collar until SCI is ruled out EXTERNAL EXAMINATION Note lacerations, fractures, edema and bruises ABCDE evolution
  • 24.  Risk for impaired breathing pattern related to impairment of innervation of diaphragm (lesions at or above C-5).  Impaired physical mobility related to neuromuscular impairment.  Disturbed sensory perception related to destruction of sensory tracts with altered sensory reception, transmission, and integration.  Risk for trauma related to temporary weakness/instability of spinal column. NURSING DIAGNOSIS
  • 25. INTERVENTION  Airway patency: Maintain patent airway: keep head in neutral position, elevate head of bed slightly if tolerated, use airway adjuncts as indicated. Monitor vital signs. (T P R BP) HR & BP monitoring: Measure and monitor HR & BP before and after activity in acute phases or until stable. Oxygen: Administer oxygen by appropriate method (nasal prongs, mask, intubation, ventilator.
  • 26.  Thermoregulation: o Peripheral temperature sensations cannot reach the hypothalamus o Ability to sweat or shiver to control temperature is impaired below the level of injury o Monitor temperature and adjust the environmental temperature accordingly o Provide blankets INTERVENTION
  • 27. INTERVENTION  Lower extremity interventions: Applying anti-embolism stockings and elevating the foot of the bed may help minimize pooling of the blood in the legs and prevent thrombus formation.  Exercise: Passive range of motion of the immobile extremities helps promote circulation.  Activities: Plan activities to provide uninterrupted rest periods and encourage involvement within individual tolerance and ability.  Reduce anxiety: Assist patient to recognize and compensate for alterations in sensation.
  • 28. CONCLUSION: Neurogenic shock can occur after a spinal cord injury, and it can be fatal. Injury or trauma to the spinal cord can cause nerve damage, which affects body’s ability to regulate blood pressure and heart rate. This can impair blood flow, resulting in a lack of oxygen and nutrients reaching vital organs.

Notas do Editor

  1. Links: https://pixabay.com/photos/coronavirus-contact-no-thank-you-4904507/
  2. Links: https://pixabay.com/vectors/location-earth-map-world-pipeline-4496459/
  3. Links: https://pixabay.com/vectors/location-earth-map-world-pipeline-4496459/
  4. Links: https://pixabay.com/photos/nurse-stethoscope-medicine-2141808/
  5. Norepinephrine: acting on both alpha and beta receptor, (aiding both hypotension and bradycardia, thus the preferred agent.) Epinephrine (for refractory cases of hypotension, is rarely needed). Phenylephrine: alpha-1 agonist (peripheral vasoconstriction)