Overview
Definition:
Traumatic spinal cord injury (SCI) is damage to the spinal cord resulting from physical trauma, leading to temporary or permanent changes in its function
In adolescents and teens, SCI can cause significant autonomic dysfunction, particularly neurogenic shock, characterized by hypotension and bradycardia due to disruption of sympathetic nervous system outflow.
Epidemiology:
Traumatic SCI incidence in pediatric populations varies by age group, with adolescents (10-19 years) experiencing a higher incidence compared to younger children, often due to participation in high-risk activities
Motor vehicle accidents, sports injuries, and falls are common etiologies
Males are more frequently affected
Pediatric SCI represents a smaller proportion of overall SCI cases but carries unique physiological challenges.
Clinical Significance:
Adequate blood pressure support is critical in traumatic SCI to maintain spinal cord perfusion and prevent secondary injury
Hypotension, especially in the context of neurogenic shock, can worsen neurological outcomes by compromising oxygen delivery to the injured cord
Understanding the pathophysiology and management of blood pressure abnormalities is paramount for pediatric residents preparing for DNB and NEET SS examinations, as it directly impacts patient survival and long-term recovery.
Clinical Presentation
Symptoms:
Acute onset of weakness or paralysis below the level of injury
Sensory deficits including numbness or paresthesia
Loss of bowel or bladder control
Symptoms of autonomic dysreflexia (in chronic cases, but can manifest acutely)
Signs of hypovolemic shock (if associated with hemorrhage) or neurogenic shock (hypotension, bradycardia, warm extremities).
Signs:
Neurological deficits: motor weakness, sensory loss, altered reflexes
Vital sign abnormalities: hypotension (systolic BP < 50th percentile for age, or mean arterial pressure < 65 mmHg is often a target), bradycardia (heart rate < 60 bpm or lower depending on age), and normothermia or hypothermia
Presence of other trauma injuries.
Diagnostic Criteria:
Diagnosis is primarily clinical based on the history of trauma and neurological examination findings
Imaging (CT, MRI) confirms the presence and level of spinal injury and associated fractures
Hypotension in the setting of SCI, especially with bradycardia and absence of hypovolemia, strongly suggests neurogenic shock.
Diagnostic Approach
History Taking:
Detailed mechanism of injury is crucial
Age, pre-existing medical conditions, medications
Associated symptoms like headache, dizziness, or loss of consciousness
Last meal for potential intubation
Allergies.
Physical Examination:
Rapid primary survey (ABCDE approach)
Detailed neurological examination assessing motor strength, sensation, and reflexes in all extremities, including assessment of rectal tone if appropriate
Secondary survey for other injuries
Assessment for signs of shock (hypovolemic vs
neurogenic).
Investigations:
Complete Blood Count (CBC) to assess for anemia and platelet count
Coagulation profile (PT/INR, aPTT) if coagulopathy is suspected
Electrolytes, BUN, creatinine
Arterial Blood Gas (ABG) for acid-base status
Chest X-ray, CT scan of the entire spine (cervical, thoracic, lumbar) for bony and soft tissue injury
MRI of the spine for detailed assessment of the spinal cord itself, including edema or contusion
Echocardiogram may be useful to rule out cardiac contusion.
Differential Diagnosis:
Hypovolemic shock (due to hemorrhage from other injuries)
Septic shock
Anaphylactic shock
Spinal headache (post-dural puncture)
Spinal epidural hematoma or abscess (non-traumatic)
Spinal tumors.
Management
Initial Management:
Immediate stabilization: Airway, Breathing, Circulation
Spinal immobilization using a rigid cervical collar and backboard
Establish intravenous access and begin fluid resuscitation for hypotension, carefully monitoring for fluid overload
Administer oxygen therapy
Address other life-threatening injuries
Rapid transport to a trauma center with neurosurgical capabilities.
Medical Management:
Pharmacological support for hypotension: Vasopressors are key in neurogenic shock
Norepinephrine is the first-line agent
Dosing is weight-based and titrated to maintain MAP of at least 65 mmHg
Phenylephrine may be considered in specific situations
Atropine or glycopyrrolate for symptomatic bradycardia unresponsive to fluid challenge, if present
Avoidance of agents that can worsen hypotension (e.g., excessive beta-blockers)
Steroids (e.g., methylprednisolone) are generally NOT recommended for routine use in acute traumatic SCI due to lack of proven benefit and increased risk of complications, according to current guidelines.
Surgical Management:
Surgical intervention is indicated for spinal instability, spinal cord compression requiring decompression, or significant bony malalignment
The decision for surgery is based on imaging findings and neurological status, typically performed after initial stabilization and medical management
Early surgical decompression (<24 hours) may improve neurological outcomes in selected patients, particularly those with evidence of cord compression.
Supportive Care:
Continuous hemodynamic monitoring (arterial line preferred)
Neurological monitoring for changes
Mechanical ventilation if respiratory failure develops
Nasogastric tube insertion for gastric decompression and feeding
Strict attention to fluid balance and electrolyte management
Prevention of deep vein thrombosis (DVT) with prophylactic anticoagulation once bleeding is controlled and spinal stability is assessed
Bowel and bladder care
Pressure ulcer prevention.
Complications
Early Complications:
Neurogenic shock, spinal shock, respiratory failure, cardiovascular instability (arrhythmias, hypotension, hypertension), deep vein thrombosis (DVT), pulmonary embolism (PE), pressure ulcers, urinary tract infections (UTIs), autonomic dysreflexia (can occur acutely with bladder distension).
Late Complications:
Chronic pain syndromes, spasticity, neurogenic bladder and bowel dysfunction, pressure ulcers, respiratory compromise, psychological sequelae, autonomic dysreflexia, heterotopic ossification.
Prevention Strategies:
Rigorous spinal immobilization
Early and adequate blood pressure support to maintain spinal cord perfusion
Prompt surgical decompression when indicated
Prophylactic measures for DVT and PE
Meticulous skin care
Regular turning and repositioning
Early mobilization and physical therapy
Bowel and bladder management protocols
Education on recognizing and managing autonomic dysreflexia.
Prognosis
Factors Affecting Prognosis:
Severity of the initial neurological deficit (ASIA impairment scale score)
Level of the spinal cord injury
Presence and severity of associated injuries
Age of the patient
Timeliness and adequacy of initial management
Development of complications.
Outcomes:
Recovery is highly variable and depends on the extent of the initial injury
Significant neurological recovery, if it occurs, is typically seen within the first 6-12 months
Incomplete injuries have a better prognosis for recovery than complete injuries
Long-term functional outcomes require extensive rehabilitation and ongoing support.
Follow Up:
Regular follow-up with a multidisciplinary team including neurologists, physiatrists, urologists, and social workers
Periodic neurological assessments, management of spasticity, bladder and bowel function, and skin integrity
Rehabilitation should be a continuous process throughout the patient's life.
Key Points
Exam Focus:
Neurogenic shock in SCI is characterized by hypotension AND bradycardia
MAP goal in pediatric SCI is typically ≥ 65 mmHg
Norepinephrine is the first-line vasopressor
Steroids are generally NOT indicated for acute traumatic SCI
Early surgical decompression is debated but may be beneficial in selected cases.
Clinical Pearls:
Always consider spinal cord injury in any trauma victim with altered neurological status, especially with significant impact to the head or torso
Differentiate neurogenic shock from hypovolemic shock by assessing pulse rate and peripheral perfusion
Aggressive blood pressure support is crucial to optimize spinal cord perfusion
Monitor for autonomic dysreflexia even in the acute phase, especially with bladder distension.
Common Mistakes:
Failure to adequately support blood pressure, leading to spinal cord ischemia
Misinterpreting neurogenic shock as hypovolemic shock and administering excessive fluids, potentially leading to pulmonary edema
Delaying surgical decompression when indicated
Inappropriate use of corticosteroids.