spinal shock vs neurogenic shock (1).pptx

cme slide

1. SPINAL SHOCK AND NEUROGENIC SHOCK Nazimal Fikry

2. Spinal shock Spinal shock – phenomena surrounding physiologic or anatomic transaction of the spinal cord that results in temporary loss or depression of all or most spinal reflex activity (both cutaneous and deep tendon reflexes) below the level of the lesion. It may be accompanied by flaccid paralysis, autonomic dysfunction, loss of sympathetic outflow, resulting in incontinence, hypotension and bradycardia. Spinal shock may last from within 24 to 72 hours to several days or weeks

3. Reflexes generally return in a specific pattern with cutaneous reflexes returning prior to deep tendon reflexes. The reflexes commonly return in the following order; Firstly the return of abnormal plantar reflexes (Babinski’s sign) followed by the bulbocavernosus reflex (BCR), cremasteric reflex and finally the ankle and knee jerk reflexes. The bulbocavernosus reflex is commonly checked to mark the ending of the “spinal shock”.

4. HISTORY 1750-Whytt first described phenomenon. 1841- Hall introduced term spinal shock. 1890- Bastian defined it as complete severance of the spinal cord that results in total loss of motor and sensory function below the level of the lesion, as well as permanent extinction of tendon reflexes and muscular tone despite the reflex arc remaining intact. Sherrington- 1. Replaced Bastian's use of the term "permanent" with temporary extinction. 2. Polysynaptic reflexes are depressed for shorter duration than monosynaptic.

5. Causes of spinal shock Blunt force trauma , such as traffic collisions In patients older than 65, falls are the most common cause of SCIs. Penetrating trauma (eg, gunshot and stabbing injuries) Other primary etiologies include transection of the spinal cord, mechanical damage, abscess formation, and metastatic disease. Secondary SCIs are primarily due to ischemia from occlusion or disruption of the arterial blood supply to the spinal cord with resultant hypoperfusion and anoxic damage to the spinal cord

6. PATHOPHYSIOLOGIC CHARACTERISTICS OF SPINAL SHOCK Spinal shock may occur up to several hours after the onset of injury. More severe the physiologic or anatomic transection of the spinal cord, the more profound the state of spinal shock. Isolated spinal cord closest to the disruption is the most severely affected-loss of reflex function occurs. Spinal cord segment most distal to the transection may be depressed later.

7. Farther it is from the site of injury, more likely it will retain some reflex capabilities. Patients with high-level cervical spinal cord injuries are likely to retain distal sacral reflexes such as bulbocavernosus and anal wink despite loss of all other reflexes. ( It is a polysynaptic response mediated by S2-S4.) Lower the spinal cord injury, more likely that all distal reflexes will be absent. Reflex arcs at the level of spinal cord injury may remain permanently absent if portions or all of the arc components are permanently injured.

8. Proximal spinal cord may also undergoes changes, and these cephalad effects Transient loss of upper extremity reflexes with upper thoracic spinal cord lesions may be seen. Usually abates after a few hours or days. Transection of the spinal cord as low as the third lumbar segment affects the excitability of the forelimbs.

9. Causes of spinal shock primary insult by high-impact, direct trauma or fall. secondary injury ( eg , ischemia or infection) of the spinal cord Other  causes of SCI include myelopathies induced by autoimmune, infectious, neoplastic, vascular, and hereditary-degenerative diseases

10. Examination ABCDE Obtaining r elevant history ( eg , past medical history, mechanism of injury ) complete physical examination, including evaluation with the Glasgow Coma Scale (GCS) and American Spinal Injury Association (ASIA) Scale, and initiating spinal imaging studies . [ spine immobilization during evaluation and transportation to minimize secondary injury

11. Sign and symptom of Spina shock paralysis and absent reflexes impaired bowel and bladder control absent anal sphincter tone.

12. imaging Xray CT of the brain and cervical spine without contrast, as well as the chest, abdomen, and pelvis with and without contrast A spinal surgeon should be consulted if a fracture is identified on initial spine imaging in trauma patients MRI is indicated in patients with a negative CT scan suspected of having SCI due to increased sensitivity compared to CT imagin

13. management Hemodynamic Management hypotension - A mean arterial blood pressure of >85 to 90 mmHg for the first 5 to 7 days following an acute SCI is generally recommended, Judicious fluid management is recommended In adults, a dosage of norepinephrine 0.05 to 1 mcg/kg/min Bradycardia -  atropine administration Respiratory Management- mechanical ventilation  , Chest physiotherapy, including percussion, incentive spirometry, and deep suctioning, should be employed to decrease the risk of this complication

14. Surgical Decompression Supportive Therapy Venous thromboembolism (VTE) prophylaxis Bowel and bladder management Pressure ulcer prevention Nutrition management Pain management Physical therapy

15. CHARACTERISTIC OF SPINAL SHOCK Motor Effects – Paraplegia ,Quadriplegia Loss of tone -Muscles become flaccid Areflexia - All superficial and deep reflexes are lost Sensory Effects -All Sensations are lost below the level of transection Complete lesions above T1 will eliminate all sympathetic outflow. Lesions between T1 and T6 will preserve sympathetic tone in head and upper extremities but deny it to the adrenals and lower extremities. Lesions between T6 and the lumbar cord will preserve adrenal innervation but denervate the lower extremities.

16. PHASES OF SPINAL SHOCK PHASE POSSIBLE MECHANISM Phase 1 (0-1 days) Areflexia / hyporeflexia Loss of descending facilitation Phase 2(1-3 days) Initial reflex return Denervation supersensitivity Phase 3 (1-4 weeks) Initial hyper- reflexia Axon supported synapse growth Phase 4 (1-12 months) Final hyper- reflexia Soma supported synapse growth

17. Neurogenic shock Neurogenic shock ( form of distributive shock) is characterized by organ tissue hypoperfusion resulting from the disruption of normal sympathetic control over vascular tone. It refers to the hemodynamic triad of hypotension, bradycardia, and peripheral vasodilation resulting from severe autonomic dysfunction and interruption of the sympathetic nervous system in acute spinal cord injury. Loss of sympathetic outflow results in a vasoplegic hypotensive state commonly seen when the level of the injury is above T6 and associated bradycardia when the level of injury is above T1-T4.

18. Neurogenic shock is fatal if left untreated causing irreversible tissue damage from hypoperfusion and contributing to worsening of secondary injuries. Neurogenic shock generally last from 1 to 3 weeks however have been reported to persist for as long as 4 to 5 weeks.

19. The dysregulation arises due to the lack of sympathetic tone and an unopposed parasympathetic response. Other potential causes of neurogenic shock : spinal anesthesia Guillain-Barre syndrome toxins affecting the autonomic nervous system transverse myelitis various neuropathies involving the cervical and upper thoracic spinal cord .

20. The cervical spinal cord injury depicted in the figure has disrupted the descending vasomotor pathways and disconnected the spinal sympathetic preganglionic neurons from the supraspinal cardiovascular regulation centers, whereas the parasympathetic cardiac innervation carried by the vagal nerve remains intact. CN, cranial nerve; SNS, sympathetic nervous system; PNS, parasympathetic nervous system; SPN, sympathetic preganglionic neurons; DVP, descending vasomotor pathways.

21. examination Maintaining a high level of suspicion for neurogenic shock is crucial, especially when dealing with cases of spinal cord injury occurring above the T6 level. In such patients, healthcare practitioners should carefully assess the mechanism of injury, check for midline spinal tenderness or step-offs, consider distracting injuries that could divert attention from a spinal area, and evaluate for loss of consciousness, neurological deficits, or intoxication that might complicate the examination, as these factors can be associated with spinal trauma. Characteristic vital signs of neurogenic shock include hypotension accompanied by bradycardia . This differs from the presentation in patients with non-spinal cord injuries and experiencing hypovolemic shock, where hypotension is associated with tachycardia. Patients with neurogenic shock may exhibit  warm and pink skin , contrasting with cool and pallid skin often observed in patients with hypovolemic shock.  

22. Investigation and imaging After the initial assessment and stabilization, the focus shifts toward additional diagnostic procedures. High-quality computed tomography (CT) imaging of the spine is recommended to evaluate for fractures and alignment issues, particularly if suspicion of spinal cord injury persists. Once the patient's condition has been stabilized, magnetic resonance imaging (MRI) of the spine may be performed to help obtain a more detailed view of the ligamentous structures. MRI scans can also assess for any abnormal cord signal changes and the presence of compressive or herniated discs.  The diagnosis of neurogenic shock involves a combination of radiographic imaging, hemodynamic monitoring, and clinical examination.

23. management The primary objective in the initial management of neurogenic shock is centered on achieving hemodynamic stability The first-line treatment for hypotension involves intravenous fluid resuscitation The second-line treatment involves using vasopressors and inotropes in cases where hypotension continues even after euvolemia. Norepinephrine is preferred due to its dual α- and β-activity, effectively addressing hypotension and bradycardia. Maintaining a mean arterial pressure within the 85 to 90 mm Hg range for the initial 7 days is recommended to optimize spinal cord perfusion ( urine output >0.5 mL/kg/h ) . Atropine and glycopyrrolate are administered to counteract excessive vagal stimulation and alleviate bradycardia.  Be aware of vagal stimuli (e.g. suction, NG Tube insertion and intubation) whichmay exacerbate neurogenic shock

24. management Initial immobilization of the cervical spine surgical intervention may be necessary to alleviate ongoing neural compression and enhance the treatment of neurogenic shock . symptoms of neurogenic shock have been documented to persist for up to 4 to 5 weeks.

25. Spinal v/s neurogenic shock Spinal shock Neurogenic shock Definition Immediate temporary loss of total power, sensation and reflexes below the level of injury Sudden loss of the sympathetic nervous system signals BP Hypotension Hypotension Pulse Bradycardia Bradycardia Bulbocavernosus reflex Absent Variable Motor Flaccid paralysis Variable Time 48-72 hrs immediate after SCI Mechanism Peripheral neurons become temporarily unresponsive to brain stimuli Disruption of autonomic pathways  loss of sympathetic tone and vasodilation

26. THANK YOU

27. REFERENCES Spinal shock revisited: a four phase model International spinal cord society, march 2010 Spinal shock review, Mayo clinic proc 1996 Bradleys neurology in clinical practice, 6 th edition https://www.ncbi.nlm.nih.gov/books/NBK459361/ https://www.ncbi.nlm.nih.gov/books/NBK568799/#:~:text=Spinal%20shock%20refers%20to%20the,following%20a%20spinal%20cord%20trauma . TLSM manual