RT Book, Section A1 Bass, Candra Rowell A1 Kumar, Priya A. A2 Atchabahian, Arthur A2 Gupta, Ruchir SR Print(0) ID 57260719 T1 Chapter 32. Preexisting Spinal Cord Injury T2 The Anesthesia Guide YR 2013 FD 2013 PB The McGraw-Hill Companies PP New York, NY SN 978-0-07-176049-2 LK accessanesthesiology.mhmedical.com/content.aspx?aid=57260719 RD 2025/02/16 AB Spinal cord injury (SCI) is common (˜10,000–11,000 cases per year), occurring usually after traumaDegree of dysfunction is directly related to level of injury, especially severe if above T6Most common site of injury is lower cervical spine or upper lumbar region:Midthoracic injury less common due to rotational stabilization provided by the rib cage and intercostal musclesPathophysiology:Upregulation of acetylcholine receptors from immobilization causes resistance to nondepolarizing neuromuscular blockers and increased potassium release with depolarizing neuromuscular blockers (e.g., succinylcholine)Sympathetic hyperreflexia:Nociceptive afferent circuits rebranch below the lesion and anastomose with sympathetic efferents, especially between T5 and L2Hyperreflexia mostly if lesion above T6, but possible even around T12Higher risk with: Urological surgeryComplete cord sectionChronic painMaximal 1–6 months after injury, but can persist indefinitelySmall stimuli can evoke exaggerated, unopposed sympathetic response: Extreme HTN with reflex bradycardia and other dysrhythmiasHeadache, anxietySweatingFlushing or pallorPiloerectionComplications: Myocardial ischemiaCardiac arrestPulmonary edemaHemorrhagic CVAReduced lower limb blood flow, but increased arterial and venous pooling leads to increased risk of thromboembolic diseaseSpasticity: similar mechanism as hyperreflexiaNatural history of injury:Acute (<3 weeks from injury):Spinal shock: hypotension and bradycardiaLoss of thoracic sympathetic outflow, with vasodilatation and pooling of bloodRelative predominance of vagal stimulation to the heartRetention of urine/feces leading to diaphragm elevation, which may impair respirationHyperesthesia above the lesionReflexes and flaccid paralysis below the lesionIntermediate (3 days to 6 months): Hyperkalemic response to depolarizing NMBChronic (after 6 months):Return of muscle tonePositive Babinski signHyperreflexia syndrome