Paed SCI Flashcards
Prophylactic Antiemetic and Doses
Ondansetron
4-8mg Oral/IV (A)
Paediatrics Small Child 2mg, Medium Child 4mg ORAL
Neurovascular Assessment
Colour
Temp
Sensation
Movement
Cap Refill
Pulse
Swelling
Ondans Indications
Undifferentiated nausea and vomiting
Prophylaxis where vomiting could be clinically detrimental (e.g. spinally immobilised,
penetrating eye trauma)
Ondans Contras
Apomorphine (see Significant Interactions)
Ondans Precautions
Pregnancy 1st trimester – consult with receiving hospital
Congenital Long QT syndrome – ondansetron causes QT prolongation (dose-dependent effect)
and increases the risk of Torsades de pointes in patients with a prolonged QT interval (QTC >
500 ms). Unlikely when administered at approved doses but avoid if patient has a history of
congenital Long QT syndrome.
1
Severe hepatic disease (e.g. cirrhosis) – limit total daily dose to a maximum of 8 mg (all routes
of administration)
Ondansetron ODT may contain aspartame which should be avoided in patients with
phenylketonuria. Ondansetron injection can be administered if appropriate
Ondans Side Effects
CNS: Headache, dizziness
CV: QT prolongation (rare)
GI: Constipation
Other: Visual disturbance, including transient loss of vision (rare, associated with rapid IV
administration)
Cervical Collar Indications
Indications as per SCI
- major trauma criteria after blunt trauma to head/trunk
- neurological deficits or changes
Cervical Collar Contras
- Surgical Airway
- Penetrating Neck Trauma
- Unable to achieve neutral position
Neurogenic Shock Pathophysiology
Neurogenic shock is the result of autonomic dysregulation following spinal cord injury, usually secondary to trauma. This dysregulation is due to a loss of sympathetic tone and an unopposed parasympathetic response.
Primary and Secondary Spinal Cord Injuries
Primary spinal cord injury occurs within minutes of the 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 results from vascular insult, electrolyte shifts, and edema that lead to progressive central hemorrhagic necrosis of grey matter at the injury site.