Regional Anasthesia

Caudal analgesia can be induced by injection of anesthetic through the sacral hiatus into the sacral epidural space of the vertebral canal well caudal to the termination of the dural sac.

The sacral hiatus represents the absence of a complete neural arch of the fifth sacral vertebra. The four anterior and posterior sacral foramina on either side of the midline join the intervertebral foramen and provide egress for the anterior and posterior primary rami of the sacral spinal nerves. The level to which the anesthesia blocks the spinal nerves is a function of the amount delivered.

·         Local anaesthetic drugs act by inhibiting sodium influx through sodium-specific ion channels in the neuronal cell membrane. When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is inhibited.

Local anaesthetics (LA) are weak bases. They are either aminoamides or aminoesters. Aminoamides are degraded by hepatic enzymes and aminoesters by the plasma cholinesterase. Local anaesthetic activity can be enhanced by altering the pH of a drug preparation to maximise the amount of drug in the unionized (unprotonated) form. It is well established that local acidosis such as caused by wound infection greatly reduces the action of local anesthetics. Sodium bicarbonate makes LA more hydrophobic thereby increasing its cellular penetration. This increases its potency. The use of adrenaline causes vasoconstriction and decreases the rate of removal of LA by the blood.

·         SAB-associated bradycardia:

Bradycardia may occur secondary to unopposed vagal tone from a high sympathectomy, blockade of the cardioaccelerator fibers (T1-T4), and the Bezold-Jarisch reflex (slowing of the heart rate secondary to a decrease in venous return). Patients with underlying increased vagal tone (children and adults with resting heart rates < 60) are at increased risk. Bradycardia may be treated with anticholinergic agents (atropine) or beta-adrenergic agonists, such as ephedrine.

·         SPINAL ANESTHESIA

1. Loss of afferent sensory and motor stimulation renders a patient sensitive to sedative medications secondary to deafferentation. For the same reason, neuraxial anesthesia decreases the minimum alveolar concentration of volatile anesthetics.
2. Vagal predominance suggests a patient may be at risk for cardiovascular collapse during neuraxial anesthesia.
3. Patients with sympathectomies from regional anesthesia will require aggressive resuscitation, perhaps with unfamiliarly large doses of pressors, to reestablish myocardial perfusion after cardiac arrest.
4. Suspect TNS in a patient who has received a lidocaine spinal anesthetic and has postanesthetic complaints of pain in buttocks and dorsal lower extremities. Notably, there are no objective neurologic findings with this syndrome.

·         EPIDURAL ANALGESIA AND ANESTHESIA

1. Epidural anesthesia is segmental; that is, it has an upper and lower level. The block is most intense near the site of catheter insertion and diminishes with distance.
2. Advantages include avoidance of airway manipulation, decreased stress response, less thrombogenesis, improved bowel motility, awake patient, less postoperative nausea and sedation, better postoperative pain control, and faster turnover.
3. Disadvantages include slow initiation and higher failure rate than general anesthesia.
4. Contraindications include coagulopathy, hemodynamic instability, spinal instrumentation, and patient refusal.
5. Complications include hypotension due to sympathetic blockade, intravascular injection of local anesthetic, subarachnoid injection of a large volume of local anesthetic ("total spinal"), postdural puncture headache, and epidural hematoma.