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Complications of Spinal Anesthesia | Neurologic & Cardiovascular Risks | Management Guidelines

Explore the potential complications of spinal anesthesia including neurologic risks such as paraplegia and cauda equina syndrome, cardiovascular issues like hypotension, and respiratory, infection, and other associated problems. Learn about risk factors, incidence rates, and management guidelines.

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Complications of Spinal Anesthesia | Neurologic & Cardiovascular Risks | Management Guidelines

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  1. بسم الله الرحمن الرحیم

  2. COMPLICATIONS of SPINAL Ans. • By: • Dr.roushanfekr/anesthesiologist

  3. COMPLICATIONS of neuraxial anesthesia: • 1--------NEUROLOGIC: • Paraplegia • CaudaEquina Syndrome • Epidural Hematoma • Nerve Injury • Post–Dural Puncture Headache • Transient Neurologic Symptoms • 2--------CARDIOVASCULAR: • Hypotension • Bradycardia • Cardiac Arrest • 3---------RESPIRATORY • 4-------INFECTION • 5-------BACKACHE • 6-------NAUSEA AND VOMITING • 7-------URINARY RETENTION • 8-------PRURITUS • 9-------SHIVERING

  4. NEUROLOGIC: • The physiologic effects of neuraxial blocks may be misinterpreted as complications • Serious neurologic complications→ are rare • The true incidence of most neurologic injury→ is unknown

  5. Paraplegia: • The frequency → 0.1 per 10,000 • the mechanism: • direct needle trauma to the spinal cord • the injection of a foreign substance into the CSF • Contamination by the descaling liquid used to cleanse the procedure • the chloroprocaine neurotoxicity • Adhesive arachnoiditis, caudaequina syndrome→ to be related to a combination of low pH and the antioxidant sodium bisulfite preservative • Profound hypotension or ischemia of the spinal cord • Anterior spinal artery syndrome→painless loss of motor and sensory function with sparing of proprioception→by the posterior column • The anterior cord→vulnerable to ischemic→ single and tenuous source of arterial blood supply (Adamkiewicz) • Ischemia caused →profound hypotension,mechanical obstruction, vasculopathy, or hemorrhage→irreversibleanterior cord damage

  6. CaudaEquina Syndrome • The rate → 0.1 per 10,000 • The lumbosacral roots →vulnerable to direct exposure of large doses of LA: • a single injection of highly concentrated LA (5% lidocaine) • prolonged exposure to a LA through a continuous catheter • spinal catheters smaller than 24 G(↓ headache) : 1- to pooling of LA around the lumbosacralnerve roots 2- slow injectate flow through the fine-bore catheter: exposing them to high concentrations of LA

  7. Epidural Hematoma: • the rates→ ˂ 0.06/10,000 after SA • after EA→ tenfold higher

  8. Epidural Hematoma: • risk factors including : • Difficult or traumatic needle or catheter insertion • coagulopathy • elderly age • female gender • commonly features: Radicularback pain,prolongedblockade longer and bladder or bowel dysfunction • should prompt MRI on an urgent basis

  9. Nerve Injury: • rate of radiculopathyorparesthesia orperipheral neuropathy→EA – CSE ˃SA • in adults for the purposes of perioperativeanesthesia or analgesia˃in the obstetric, pediatric, and chronic pain settings • difficult to determine because→ investigation, diagnosis, causation, outcomes are highly variable. • SA-EA (0.1 per 10,000) • CSEs (0.2 per 10,000), mostly in young, healthy patients.

  10. Post–Dural Puncture Headache: • A relatively common complication • to result from puncture of the duramembrane: • neuraxial anesthesia • after myelography • diagnostic lumbar puncture • First, the loss of CSF through the dura →traction on pain-sensitive intracranial structures • Alternatively, the loss of CSF → compensatorypainful intracerebralvasodilationto offset the reduction in intracranial pressure

  11. Post–Dural Puncture Headache: • The characteristic feature: a frontal or occipital headache that worsens with the upright or seated posture and is relieved by lying supine • Associated symptoms : nausea, vomiting, neck pain, dizziness, tinnitus, diplopia, hearing loss, cortical blindness, cranial nerve palsies, and even seizures. • In more than 90% of cases, the onset of characteristic symptoms →within 3days of the procedure, 66% start within the first 48h • Spontaneous resolution usually → within 7 days in the majority (72%) of cases, whereas 87% of cases resolve by 6 months

  12. Post–Dural Puncture Headache: • Factors That Can Increase the Incidence of Headache After Spinal Puncture • • Age: Younger, more frequent • • Sex: Females > males • • Needle size: Larger > smaller • • Needle bevel: Less when the needle bevel is placed in the long axis of the neuraxis – noncutting needle ˂cutting • • Pregnancy: More when pregnant • • Dural punctures: More with multiple punctures • Factors That Do Not Increase the Incidence of Headache After Spinal Puncture • • Insertion and use of catheters for continuous spinal anesthesia • • Timing of ambulation

  13. Post–Dural Puncture Headache: • Conservative management : • supine positioning • hydration • caffeine • and oral analgesics. • Sumatriptanhas also been used with varying effect but is not without side effects

  14. Post–Dural Puncture Headache: • Epidural blood patch →definitive therapy • its safety and efficacy →well-documented • a single epidural blood patch→˃90% initial improvement rate • persistent resolution →61% to 75% of cases

  15. Post–Dural Puncture Headache: • ideally performed 24 hours after dural puncture and after the development of classic symptoms • prophylactic epidural blood patching??? • the direction of spread was preferentially cephalad • A recent multinational, multicenter, randomized, blinded trial suggested that 20 mL of blood is a reasonable starting target volume→ blood will spread over a mean distance of nine spinal segments • A second patch may be performed 24 to 48 hours after the first in the case of ineffective or incomplete relief of symptoms

  16. Transient Neurologic Symptoms(transient radicular irritation): • after intrathecal administration of every LA (Traditionally ,lidocaine) →SA • is usually characterized: • bilateral or unilateral pain in the buttocks →legs or, less commonly, isolated buttock or leg pain. • Symptoms occur within 24 hours of the resolution of SA • not associated with any neurologic deficits or laboratory abnormalities • mild to severe pain and typically resolves spontaneously in 1 week or less • highest after intrathecallidocaineand mepivacaineand is far less frequent withbupivacaine • The type of needle → reduced by a double-orifice needle→single-orifice→ ↑injecting anesthetic caudally in the thecalsac • not commonly →with epidural procedures(occurred with lidocaine) • commonly→ the lithotomy position • NSAID → the first line of treatment,butpain severe →even require opioids.

  17. Hypotension: • in SA →hypotension (defined as SBP<90 mm Hg) • RISK FACTORS: • peak block height ≥T5 • age ≥ 40 years • basele SBP˂ 120 mm Hg • combined SA and GA • spinal puncture≥ L2-L3 interspace • the addition of phenylephrine to the LA • Hypotension (defined as a reduction MAP >30%) is associated with: chronic alcohol consumption,historyof hypertension, BMI, and the urgency of surgery. • TREATMENT: • prevention of hypotension caused by vasodilatation by a prophylactic (“preloading”) • infusion of colloid or crystalloid during the performance of the neuraxial block (“coloading”) • this is no longer recommended as a routine practice.

  18. Bradycardia: • blockade of the thoracic sympathetic fibers (preganglioniccardiac accelerator fibers at T1-T5) • reflexive slowing of the HR as vasodilation→ reduces the venous return to the RA → stretch receptors • exaggerated bradycardia(40 to 50) : • baselineHR˂60 • age ˂37 years • male gender • nonemergency status • β-adrenergic blockade • prolonged case duration • Severe bradycardia (<40) →a baseline ˂60 and male gender

  19. Cardiac Arrest: • The etiology→after SA is not understood • lack of vigilant monitoring and treatment • Hypoxemia • oversedation → severe bradycardia and asystole→suddenly ? during well-conducted SA • rare event • SA ˃epidural techniques • Most Recently → (0.04 per 10,000) during SA

  20. RESPIRATORY: • Neuraxialopioids →respiratory depression→dose dependent • 3% after the administration of 0.8 mg of intrathecalmorphine • Rostral spread of opioids→to the respiratory centers in the brainstem • With lipophilicopioid→an early phenomenon (the first 30 minutes) • respiratory depression has never been described more than 2 hours after intrathecalfentanyl or sufentanil • With intrathecal morphine, there is a risk of late respiratory depression →24 hours after injection→ Respiratory monitoring • Patients with especially sensitive → • Older patients • sleep apnea • Coadministration of systemic sedatives • →neuraxialopioids should be reduced

  21. INFECTION: • Bacterial meningitis and epidural abscess are rare, but potentially catastrophic • Sources of infection→ the equipment, the patient, or the practitioner • Staphylococcal infections(patient’s skin )are one of the most common → epidural • oral bacteri (Streptococcus viridans) are a common cause after SA→the clinician to wear a facemask • the presence of a concomitant systemic infection, diabetes, immunocompromisedstates and prolonged maintenance of an epidural (or spinal) catheter • ˂0.3 per 10,000 for SA→afterepidural techniques(Obstetric patients) ˃ SA˃ caudal block

  22. INFECTION: • Guidelines: • (1) aseptic techniques during RA • (2)RA in the febrile or infected patient or the immunocompromised patient • (3) infectious risk of chronic pain treatments • (4) chlorhexidine in an alcohol base is the most effective antiseptic → neurotoxicity? • Aseptic meningitis secondary to chemical contamination and detergents→no longer present in modern preservative-free preparations

  23. BACKACHE: • perhaps the most feared complication of neuraxial anesthesia • approximately 25% of all surgical patients • the incidence of which increases to 50% when surgery lasts 4 to 5 hours • neuraxialtechniques do not play a role in the development of back pain after delivery

  24. NAUSEA AND VOMITING: • multiple mechanisms → • direct exposure of the chemoreceptive trigger zone (opioids), • hypotension associated with generalized vasodilation • gastrointestinal hyperperistalsis secondary to parasympathetic activity • Factors associated with developing nausea or vomiting: • the addition of phenylephrineor epinephrine to the LA • peak block height ≥T5 • baseline HR˂ 60 • use of procaine • history of motion sickness • the development of hypotension during spinal anesthesia • morphineadded to intrathecal or epidural →the most frequent risk of nausea or vomiting, whereas fentanyl and sufentanil carry the least frequent risk • (dose dependent)Using less than 0.1 mg morphine reduces the risk, without compromising the analgesic effect

  25. URINARY RETENTION: • one third of patients after neuraxialanesthesia • blockade of the S2, S3,S4 → the detrusor muscle is weakened • Neuraxialopioids →suppressing detrusorcontractility and reducing the sensation of urge • Risk factor→ • male gender • Age • intrathecal morphine

  26. PRURITUS: • the most common side effect related to the intrathecalopioids, with rates between 30% and 100% • Pruritus actually occurs more commonly after intrathecal than after IV opioid →not dependent on the type or dose • The mechanism→ unclear but is likely related to the central opioid receptor activation rather than histamine release • because naloxone, naltrexoneor the partial agonist nalbuphine can be used for treatment • Ondansetron and propofol are also useful therapies

  27. SHIVERING: • The rate of shivering→55% • The intensity of shivering is likely related more to EA than spinal • profound motor block associated with SA compared with EA • can affect the thermosensitive basal sinuses • The addition of neuraxialopioids, specifically fentanyland meperidine, reduces of shivering • Recommended prevent strategies→ • prewarming (forced air warmer for at least 15minutes) • avoiding the administration of cold epidural and intravenous fluids

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