Neurogenic Shock


Article Author:
Sagar Dave


Article Editor:
Julia Cho


Editors In Chief:
Kranthi Sitammagari
Mayank Singhal


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
5/6/2019 1:45:57 AM

Introduction

Neurogenic shock is a devastating consequence of spinal cord injury (SCI), also known as vasogenic shock. Injury to the spinal cord results in sudden loss of sympathetic tone, which leads to the autonomic instability that is manifested in hypotension, bradyarrhythmia, and temperature dysregulation. Spinal cord injury is not to be confused with spinal shock, which is a reversible reduction in sensory and motor function following spinal cord injury. Neurogenic shock is associated with cervical and high thoracic spine injury. Early identification and aggressive management are vital in neurogenic shock to prevent secondary spinal injury. This chapter is a concise overview to further aid the care for these patients who develop Neurogenic shock. [1][2][3]

Etiology

Neurogenic shock is defined as the injury to the spinal cord with associated autonomic dysregulation. This dysregulation is due to a loss of sympathetic tone and unopposed parasympathetic response. Neurogenic shock is most commonly a consequence of traumatic spinal cord injuries. Review of trauma database showed the incidence of neurogenic shock in 19.3% of cervical spine injuries and 7% of thoracic spine injuries. Other causes of neurogenic shock that are far less common include spinal anesthesia, Guillain-Barre syndrome, autonomic nervous system toxins, transverse myelitis, and other neuropathies. Pediatric population reports the incidence of neurogenic shock in children with Trisomy 21, skeletal dysplasia, and tonsillopharyngitis. Neurogenic shock remains a diagnosis of exclusion in the traumatic patient—Advance Trauma Life Support states hemorrhagic shock is the more common cause of hypotension and once managed appropriately, neurogenic shock should be considered.[4]

Epidemiology

An estimated 8000 to 10,000 people experience traumatic spinal cord injury per year in the United States of America. A review of isolated spinal cord injury from the Trauma Audit and Research Network identified 490 isolated spinal cord injuries. Out of these isolated spinal cord injuries, 64 patients developed neurogenic shock, which is 14.2% of the isolated spinal cord injuries. However, a retrospective study at a high volume level 1 trauma center cited an incidence of the neurogenic shock of 8.8%. There are no defined universal hemodynamic parameters for neurogenic shock. However, most studies use the definition of systolic blood pressure less than 100 mmHg and heart rate less than 80 bpm. The epidemiology of neurogenic shock is difficult to assess as it is still unknown how hemorrhagic shock and other injuries impact the hemodynamic effects of spinal cord injury.

Pathophysiology

Neurogenic shock is the clinical state manifested from primary and secondary spinal cord injury. Hemodynamic changes are seen with an injury to the spinal cord above the level of T6. The descending sympathetic tracts are disrupted most commonly from associated fracture or dislocation of vertebrae in the cervical or upper thoracic spine. Primary spinal cord injury occurs within minutes of initial insult. Primary injury is direct damage to the axons and neural membranes in the intermediolateral nucleus, lateral grey mater, and anterior root that lead to disrupted sympathetic tone. Secondary spinal cord injury occurs hours to days after the initial insult. Secondary injury is a result of vascular insult, electrolyte shifts, and edema that lead to progressive central hemorrhagic necrosis of grey matter at the injury site. At a cellular level, there is excitotoxicity from NMDA accumulation, improper homeostasis of electrolytes, mitochondrial injury, and reperfusion injury which all lead to controlled and uncontrolled apoptosis. Neurogenic shock is a combination of both primary and secondary injury that lead to loss of sympathetic tone and thus unopposed parasympathetic response driven by the Vagus nerve. Consequently, patients suffer from instability in blood pressure, heart rate, and temperature regulation.

History and Physical

Neurogenic shock can be a difficult diagnosis to make and requires meticulous investigation. Neurogenic shock is most commonly associated with a blunt cervical spine injury. Identification of traumatic cord injury is vital to the investigation of neurogenic shock. Providers should ascertain mechanism of injury, the presence of midline spinal tenderness, a distracting injury that may take attention from a spinal area, loss of consciousness, neurologic deficits, or intoxication that may misconstrue exam, as these are associated with vertebral injury. Though neurogenic shock should be considered only after a hemorrhagic shock has been ruled out in a traumatic patient, the presence of vertebral fracture or dislocation raises the concern for neurogenic shock. Bradyarrhythmia, hypotension, flushed warm skin are the classic signs associated with neurogenic shock. The joint committee of the American Spinal Injury Association and the International Spinal Cord Society propose the definition of neurogenic shock to be general autonomic nervous system dysfunction that also includes symptoms such as orthostatic hypotension, autonomic dysreflexia, temperature dysregulation. A focal neurologic deficit is not necessary for the diagnosis of neurogenic shock.

Evaluation

Before advanced imaging, neurogenic shock was associated with spinal cord injury without radiologic abnormality (SCIWORA).With the advent of advanced imagining such as CT scan and Magnetic Resonance Imaging, spinal cord injury is more accurately identified. The diagnosis of neurogenic shock remains a combination of radiographic imaging, hemodynamic monitoring, and clinical exam.[3][5][6][7][8]

Treatment / Management

Initial management of neurogenic shock is focused on hemodynamic stabilization. Hypotension should be treated first to prevent secondary injury. The first-line treatment for hypotension is intravenous fluid resuscitation. This is to allow appropriate compensation for the vasogenic dilation that occurs. If hypotension persists despite euvolemia, vasopressors and inotropes are the second lines. No single agent is recommended. Phenylephrine is commonly used as it is a pure alpha-1 agonist that causes peripheral vasoconstriction to counteract the loss sympathetic tone. However, the lack of beta-activity leads to reflex bradycardia which augments the already unopposed vagal tone. Norepinephrine has both alpha and beta activity aiding both hypotension and bradycardia thus the preferred agent. Epinephrine has been cited for refractory cases of hypotension and is rarely needed. Recommend keeping the mean arterial pressure (MAP) at 85–90 mmHg for the first 7 days to improve spinal cord perfusion. Caution should be used when using vasopressors as there may be co-existing injuries exacerbated with vasoconstriction.[9][10][11][12]

Treatment for bradycardia is atropine and glycopyrrolate to oppose vagal tone especially before suctioning. Isoproterenol is considered for pure chronotropic effect. Methylxanthines such as theophylline and aminophylline have been cited for refractory cases of bradycardia.

Initial c-spine immobilization is important to prevent further spinal cord injury. Miami J or Philadelphia collar should be used. Methylprednisolone and corticosteroids showed promise in animal models. However, this has not been displayed in clinical trials, and steroids raise risk for complications such as infection and are not recommended by multiple societies. Ultimately, surgical intervention may be required for decompression of spinal injury and improvement of neurogenic shock. Symptoms of neurogenic shock have been reported to persist for as long as 4 to 5 weeks.

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Enhancing Healthcare Team Outcomes

The diagnosis and management of neurogenic shock is not easy, thus, the condition is best managed by a multidisciplinary team that includes the emergency department physician, neurologist, neurosurgeon, orthopedic surgeon, trauma specialist and the intensivist. These patients are usually monitored by neuro ICU nurses. While fluid resuscitation is the initial traetment, one should use vasopressors cautiously, since they may exacerbate any vasoconstriction. Most patients have other concomitant injuries that also require attention. Nurses should ensure that patients have DVT prophylaxis, pressure sore protection and a foley catheter. The outlook for these patients depends on the severity of the injury, presence of neurological deficits at time of presentation, age, concomitant other organ injury and a low GCS.[9][13]

 


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Neurogenic Shock - Questions

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A patient is involved in a motor vehicle collision and suffers multiorgan trauma. He is brought to the emergency department by emergency medical services and found to be hypotensive and bradycardic. He is disoriented and confused. He has a Glasgow coma scale score of 9. His abdomen is non-distended, legs warm, and pulses thready. His central venous pressure is 9 mmHg, heart rate 42 beats/min, and blood pressure 80/40 mmHg. What is the most likely cause of his shock state?



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A patient presents after falling 10 feet. Upon arrival, the vital signs are blood pressure 80/40 mmHg, heart rate 60 beats/min, respiratory rate 20, and oxygen saturation 96% on room air. Exam reveals diffuse spinal tenderness, and there is evidence of lower extremity weakness with sensory loss. What is the most likely diagnosis?



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Which of the following is not a correct association?



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A 17-year-old male is involved in a motor vehicle collision and suffers multi-organ trauma. He is hypotensive, bradycardic, and his abdomen is flat. He is disoriented and confused. He has a Glasgow coma scale of 9, his legs are warm, and pulses are thready. There is minimal movement of the legs to painful stimuli. What is the most appropriate treatment?



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Which of the following is not a feature of neurogenic shock?



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What type of shock occurs after a spinal cord injury?



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What is least likely in a patient with neurogenic shock?



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Which of the following are signs of neurogenic shock?



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Which of the following is not considered a cause of neurogenic shock?



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A 22-year-old male presents after a construction accident. Emergency medical services (EMS) reports there was a crane malfunction and patient was hit with a metal bar. Upon arrival, the patient has a Glasgow coma scale of 6, initial heart rate of 72 bpm, blood pressure of 84/48 mmHg, and oxygen saturation of 92%. The patient is intubated for airway protection with cervical stabilization. The rest of primary survey shows no abnormalities. The secondary survey shows diffuse abrasions over the torso, back, and extremities. There are no signs of abdominal ecchymosis or distention, bleeding wounds, extremity deformities, or pelvic instability. Extended Focused Assessment With Sonography for Trauma. (EFAST) is negative. The plan is for a CT scan if the patient can be hemodynamically stabilized. What initial treatment should be done?



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What is the difference between spinal shock and neurogenic shock?



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A nurse is caring for a patient after a fall from a second story balcony 36 hours ago. A spinal cord injury is present at the level of T6. Upon entering the room, the nurse notices the patient is flushed in appearance with warm, dry skin. The cardiac monitor reveals sinus bradycardia with a heart rate of 30 beats/min, blood pressure of 60/40 mmHg, pulse oximetry reading of 90% on room air, respiratory rate of 14, and temperature of 102.6 F (39.2 C). The patient is confused and lethargic, and decreased urine output is noted. How does the nurse proceed in providing care to this patient? Select all that apply.



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Neurogenic Shock - References

References

Kowalski A,Brandis D, Shock Resuscitation 2019 Jan;     [PubMed]
Kessler TM,Traini LR,Welk B,Schneider MP,Thavaseelan J,Curt A, Early neurological care of patients with spinal cord injury. World journal of urology. 2018 Oct;     [PubMed]
Stein DM,Knight WA 4th, Emergency Neurological Life Support: Traumatic Spine Injury. Neurocritical care. 2017 Sep;     [PubMed]
Taylor MP,Wrenn P,O'Donnell AD, Presentation of neurogenic shock within the emergency department. Emergency medicine journal : EMJ. 2017 Mar;     [PubMed]
Leng YX,Nie CY,Yao ZY,Zhu X, [Analysis of the risk factors for early death in acute severe traumatic cervical spinal cord injury]. Zhonghua wei zhong bing ji jiu yi xue. 2013 May;     [PubMed]
Tuli S,Tuli J,Coleman WP,Geisler FH,Krassioukov A, Hemodynamic parameters and timing of surgical decompression in acute cervical spinal cord injury. The journal of spinal cord medicine. 2007;     [PubMed]
Esteban Fuertes M,Salinas Casado J,Resel Estévez L,Sánchez Chapado M, [Postoperative vesicourethral neurogenic dysfunction: the conceptual and clinical aspects based on the analysis of a series of 152 patients]. Archivos espanoles de urologia. 1998 Nov;     [PubMed]
Watanabe T,Rivas DA,Chancellor MB, Urodynamics of spinal cord injury. The Urologic clinics of North America. 1996 Aug;     [PubMed]
Yue JK,Tsolinas R,Burke JF,Deng H,Upadhyayula PS,Robinson CK,Lee YM,Chan AK,Winkler EA,Dhall SS, Vasopressor support in managing acute spinal cord injury: a knowledge update. Journal of neurosurgical sciences. 2017 Mar 1;     [PubMed]
Liu N,Zhou M,Biering-Sørensen F,Krassioukov AV, Iatrogenic urological triggers of autonomic dysreflexia: a systematic review. Spinal cord. 2015 Jul;     [PubMed]
Furlan JC,Fehlings MG, Cardiovascular complications after acute spinal cord injury: pathophysiology, diagnosis, and management. Neurosurgical focus. 2008;     [PubMed]
Krassioukov AV,Karlsson AK,Wecht JM,Wuermser LA,Mathias CJ,Marino RJ, Assessment of autonomic dysfunction following spinal cord injury: rationale for additions to International Standards for Neurological Assessment. Journal of rehabilitation research and development. 2007;     [PubMed]
Gilson GJ,Miller AC,Clevenger FW,Curet LB, Acute spinal cord injury and neurogenic shock in pregnancy. Obstetrical     [PubMed]

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