week 13 SCI

Cards (152)

  • Spinal Cord Injury (SCI)

    Classification based on mechanism of injury, level of skeletal and neurological damage, and completeness of injury
  • Mechanisms of SCI
    • Flexion
    • Hyperextension
    • Flexion-rotation
    • Extension-rotation
    • Compression
  • Flexion-rotation injuries
    • Particularly unstable and often result in severe neurological deficits due to torn ligamentous structures
  • Skeletal level
    The vertebrae most extensively damaged
  • Neurological level
    The lowest segment of the spinal cord with normal sensory and motor function
  • Levels of SCI
    • Cervical
    • Thoracic
    • Lumbar
  • Complete SCI
    Total loss of sensory and motor function below the lesion
  • Incomplete SCI
    Mixed loss of function with varying degrees of sensory and motor loss depending on the level of the lesion and the specific nerve tracts damaged
  • American Spinal Injury Association Impairment Scale (ASIA)

    Assesses motor and sensory function to determine neurological level and completeness of injury, with grades ranging from A to E
  • Incomplete Cord Syndromes
    • Central cord
    • Anterior cord
    • Brown-Séquard
    • Posterior cord
    • Cauda equina
    • Conus medullaris
  • Central Cord Syndrome
    • Common in the cervical region due to hyperextension injuries, presents with motor weakness and sensory loss, often more pronounced in upper extremities than lower
  • Anterior Cord Syndrome

    • Caused by damage to the anterior spinal artery, usually from acute compression, results in motor paralysis and loss of pain and temperature sensation below the level of injury, while touch and motion senses remain intact
  • Brown-Séquard Syndrome

    • Result of damage to half of the spinal cord, typically from penetrating injuries, causes ipsilateral motor function loss and contralateral loss of pain and temperature sensation below the lesion
  • Posterior Cord Syndrome
    • Rare condition resulting from damage to the posterior spinal artery, presents with loss of proprioception but intact pain, temperature sensation, and motor function below the level of the lesion
  • Conus Medullaris Syndrome and Cauda Equina Syndrome
    • Result from damage to the lowest portion of the spinal cord (conus) and lumbar and sacral nerve roots (cauda equina), impairments include motor and sensory deficits, bladder, and bowel dysfunction
  • Manifestations of SCI typically result from trauma leading to cord compression, ischemia, edema, or transection, and vary based on the level and severity of the injury
  • Higher injuries, especially cervical, have more serious consequences due to proximity to vital structures like the brainstem
  • Sensory and motor functions are closely linked at all levels of the spinal cord
  • Immediate post-injury care focuses on maintaining airway patency, adequate ventilation, and circulating blood volume to prevent secondary spinal cord damage
  • Respiratory Complications in SCI
    • Cervical injuries above C4 result in total loss of respiratory muscle function, necessitating mechanical ventilation for survival
    • Injuries or fractures below C4 may spare diaphragmatic breathing if the phrenic nerve functions, but spinal cord edema and hemorrhage can still impair phrenic nerve function, leading to respiratory insufficiency
  • Hypoventilation and Impaired Coughing
    • Diaphragmatic respirations often lead to hypoventilation due to decreased vital capacity and tidal volume from intercostal muscle impairment
    • Paralysis of abdominal and intercostal muscles hinders effective coughing, increasing the risk of atelectasis and pneumonia
  • Artificial Airway and Infection Risk
    • Artificial airways, like endotracheal or tracheostomy tubes, provide direct access for pathogens, emphasizing the need for bronchial hygiene and chest physiotherapy to reduce infection risk
  • Neurogenic Pulmonary Edema
    • Occurs due to increased sympathetic nervous system activity post-injury, leading to pulmonary interstitial and alveolar fluid accumulation, fluid overload can also contribute
  • Cardiovascular Effects of SCI
    • SCI above T6 reduces sympathetic nervous system influence, leading to bradycardia and peripheral vasodilation causing hypotension, exacerbated by increased venous capacitance, resulting in relative hypovolemia
  • Cardiac monitoring is essential to track heart rate and blood pressure changes, bradycardia (<40 beats/min) may require medications like atropine, and peripheral vasodilation decreases venous return and cardiac output, necessitating IV fluids or vasopressor medications to maintain blood pressure and ensure adequate spinal cord perfusion
  • Urinary Complications in SCI
    • Urinary retention is common in acute SCIs and spinal shock, leading to bladder atony and overdistension, during spinal shock, an indwelling urinary catheter is necessary to drain the bladder
    • After the acute phase, the bladder may become hyperirritable due to loss of inhibition from the brain, resulting in reflex emptying, management involves removing the indwelling catheter promptly and initiating intermittent catheterization early to maintain bladder tone and reduce infection risk
  • Gastrointestinal Concerns in SCI
    • Above T5 level, hypomotility is a primary concern, leading to paralytic ileus and gastric distension, nasogastric tube suctioning may alleviate gastric distension, and metoclopramide can aid in gastric emptying
    • Excessive hydrochloric acid release in the stomach can lead to stress ulcers, histamine H2-receptor blockers and proton pump inhibitors are administered to prevent stress ulcers
    • Intra-abdominal bleeding can occur without subjective signs, persistent hypotension despite treatment and decreased hemoglobin and hematocrit levels may indicate bleeding, along with abdominal girth expansion
  • Neurogenic Bowel in SCI
    • Loss of neurological control leads to neurogenic bowel, in the early phase, the bowel is areflexic; as reflexes return, it becomes reflexic with enhanced sphincter tone, a regular bowel program coordinated with the gastrocolic reflex helps manage both types of neurogenic bowel to minimize incontinence
  • Lack of movement increases the risk of pressure injuries over bony prominences, potentially leading to severe infections, pressure injuries can develop rapidly and require careful monitoring and management
  • Thermoregulation Challenges
    • Poikilothermism, adjusting body temperature to room temperature, occurs due to interrupted sympathetic nervous system signaling, decreased ability to sweat or shiver below the lesion level affects temperature regulation, with higher cervical injuries posing greater challenges
  • Metabolic Needs

    • Nasogastric suctioning may cause metabolic alkalosis, while decreased tissue perfusion may lead to acidosis, electrolyte imbalances due to gastric suctioning necessitate monitoring until normal nutrition resumes, weight loss and nitrogen excretion increase, requiring higher nutritional intake, particularly protein, to prevent skin breakdown and muscle atrophy
  • Peripheral Vascular Conditions
    • Thromboembolism is common post-SCI, with peak incidence within the first 2 weeks, detection is challenging due to atypical symptoms, Doppler ultrasound and girth measurements aid in assessment, pulmonary embolism is a significant risk, necessitating vigilant monitoring and preventive measures
  • Initial goals of interprofessional care are to sustain life and prevent further cord damage, with emergency management outlined in Table 63.3
  • Interprofessional care in the acute phase involves assessing the degree of deficit, establishing the level and degree of injury, testing muscle groups, assessing motor and sensory function, and evaluating for history of unconsciousness, signs of concussion, increased intracranial pressure, musculoskeletal injuries, and internal trauma
  • Preventative measures include moving the patient in alignment to prevent further injury and closely monitoring respiratory, cardiac, urinary, and gastrointestinal functions
  • Nonoperative Stabilization

    • Nonoperative treatments focus on stabilization and realignment of the injured spinal segment through traction, with the goal of preventing secondary spinal cord damage caused by repeated contusion or compression
  • Surgical Therapy
    • Surgery is used to stabilize, realign, and decompress the spinal column, early surgical intervention has been shown to improve clinical and neurological outcomes and reduce healthcare costs, common procedures include decompression, realignment, and stabilization with instrumentation, performed either posteriorly or anteriorly depending on the level and location of the injury
  • Corticosteroid administration, traditionally used to improve outcomes, is no longer recommended due to lack of clinical benefit and increased risk of complications
  • Ongoing investigations explore measures to promote nerve regeneration and minimize scar tissue formation, including implantation of a polymer scaffold, injections of autologous incubated macrophages, and stem cell research
  • Vasopressor agents such as dopamine and norepinephrine are administered to maintain mean arterial pressure and improve spinal cord perfusion, and pharmacological agents are used to treat specific autonomic dysfunctions