Neuraxial anesthesia can be used alone, in combination with general anesthesia, or for post-op pain control. It is also useful in the management of chronic pain.
 Advantages of these techniques — a potential reduction in post-operative morbidity, (and maybe mortality) o Decreased incidence of venous thrombosis or pulmonary embolism o Fewer cardiac complications in high risk patients by alleviating the stress response o Less bleeding and fewer transfusion requirements o Decreased incidence of vascular graft occlusion o Decreased incidence of pneumonia and respiratory depression after upper abdominal and thoracic surgery in patients with COPD o Possibly earlier return of GI function o In OB, neuraxial anesthesia allows the mother to stay awake for labor, vaginal delivery, or cesarean section, and is associated with less morbidity and mortality in cesarean sections than general anesthesia.
 Proposed mechanisms to achieve these benefits: o Amelioration of the hyper-coagulable state associated with surgery o Sympathectomy-induced increases in tissue blood flow o Improved oxygenation from decreased splinting o Enhanced peristalsis o Suppression of the neuro-endocrine stress response to surgery

 Anatomy o Spinal canal contains the spinal cord enclosed in the dura mater and bathed in CSF o The epidural space:
 Is bounded anteriorly by the posterior longitudinal ligament, laterally by the vertebral pedicles, and posteriorly by the ligamentum flavum.
 Communicates with the paravertebral space by way of the intervertebral foramina. o The spinal cord extends from the foramen magnum to L1 in adults, L3 in children. o Anterior (motor) and posterior (sensory) nerve roots from the spinal cord join and exit the spinal canal through the intervertebral foramena to form spinal nerves. The lower nerve roots form the cauda equina o The dural sac extends to S1. o Blood supply to the spinal cord: anterior two-thirds by the unpaired anterior spinal artery from the vertebral artery. Posterior one third by paired posterior spinal arteries from the inferior cerebellar arteries.
Additional flow comes from the intercostals and lumbar arteries.
 Mechanisms of action for neuraxial anesthesia o The principle site of action for neuraxial blockade is the nerve root.
Local anesthetic is injected into the CSF (spinal anesthesia) or into the epidural space (epidural and caudal anesthesia), where it then bathes the nerve root in the subarachnoid space or in the epidural space, respectively. o Direct injection of local anesthetic into the CSF for spinal anesthesia allows a relatively small dose and volume of local anesthetic to achieve a dense sensory and motor block. Achieving the same block with epidural or caudal administration of local anesthetic requires much higher volumes and quantities of drug.
o Other CNS effects: sedation, potentiation of sedative and hypnotic drugs, marked reduction of anesthetic requirements

 Autonomic Blockade o Sympathetic pre-ganglionic nerve fibers (small myelinated B fibers) exit the spinal cord with the spinal nerves from T1 to L2 and course up or down the sympathetic chain before synapsing with a postganglionic cell in a sympathetic ganglia.
o Parasympathetic pre-ganglionic fibers exit the brain and spinal cord with cranial and sacral nerves. Neuraxial anesthesia does not block the vagus or other cranial nerves. So the physiologic effects of neuraxial blockade results from decreased sympathetic tone and/or unopposed parasympathetic tone.
o Neuraxial blocks produce somatic blockade (interruption of transmission of painful stimuli, and abolition of skeletal muscle tone), with decreased sympathetic tone and/or unopposed parasympathetic tone.
 Cardiovascular o Cardiovascular effects, principally hypotension and bradycardia, are the most common and important physiologic changes associated with neuraxial anesthesia. o Blockade of sympathetic efferents is the mechanism by which these
CV effects are produced. o The higher the block, the greater the sympathectomy o Sympathectomy produces
 Venous pooling in capacitance vessels 
 Consequent decreased venous return to the heart 
 Decreased cardiac output
 Arteriolar vasodilation 
 Decreased peripheral vascular resistance 
 Decreased blood pressure

 Decrease in heart rate may occur
 Due to blockade of cardio-accelerator fibers at T1 –T4, leaving unopposed vagal tone to the heart which,
combined with profound hypotension, can progress to cardiac arrest.
 Pre-existing heartblock may be a risk factor for progression to higher grade block under neuraxial anesthesia. o The deleterious CV effects should be anticipated and preventative measures taken:
 IV volume loading
 Left uterine displacement in advanced pregnancy
 Head-down positioning
 Atropine for bradycardia
 Vasopressors for hypotension o Addition of epinephrine to epidural solutions will help counteract the cardiovascular effects of the anesthetic.
 Pulmonary o Pulmonary alterations with neuraxial anesthesia are usually minimal
(unless the block is very high) because the diaphragm is innervated by the phrenic nerve (C3-C5) with is rarely blocked. o Patients with severe chronic lung disease who rely on their accessory muscles of respiration may experience difficulty coughing and clearing secretions. Neuraxial anesthesia should be used with caution in such patients.
 Gastro-intestinal o Sympathetic blockade allows dominance of vagal tone and results in a small contracted gut with active peristalsis.
 Endocrine o Blocks surgical stress response o  Catecholamine release

It can be utilized for any most any surgical procedure below the neck, but it is most useful for surgery below the umbilicus.
 Patient refusal
 Bleeding diathesis
 Severe hypovolemia
 Elevated ICP
 Infection at the site of injection
 Severe aortic stenosis or LV outflow tract obstruction
Neuraxial blocks and concomitant anti-coagulants and anti-platelet drugs.
The concern with these drugs is the risk of spinal hematoma when the block is performed or when an epidural catheter is manipulated or removed.
 Oral anti-coagulants - Coumadin o Coumadin must be stopped 5-7 days prior to surgery, and a normalized PT and INR (<1.2) must be documented before neuraxial anesthesia can be initiated. o If the patient received one dose of coumadin for DVT prophylaxis less than 24 hours prior to the block, it is probably safe to proceed. If the patient received more than one dose, or if the dose was given more than 24 hours prior to the block, a normalized PT and INR must be documented. o Besides stopping Coumadin, oral administration of Vitamin K over several days will help normalize the INR. If the surgery cannot be delayed, IV administration of FFP should be used to provide coagulation factors.

 Anti-platelet drugs o Aspirin and NSAIDs do not appear to increase the risk of spinal hematoma.
o Others platelet inhibitors must be stopped long enough for their effects to wear off:
 Ticlopidine (Ticlid) — 14 days
 Clopidogrel (Plavix) — 7 days
 Abciximab (Rheopro) — 48 hours
 Eptifibatide (Integrilin)— 8 hours
 Unfractionated heparin o Minidose subq heparin is not a contraindication to neuraxial anesthesia.
o Blocks may be performed 1 hr or more before intraoperative heparin o Epidural catheters should be removed 1 hr. prior to, or 4 hrs. after subsequent heparin doses o Avoid neuraxial anesthesia in patients on theraputic doses of heparin and patients with increased PTT o If epidural catheter is already in place when the patient is heparinized, wait to remove the catheter until heparin is stopped and coags are checked.
 Lovenox o Avoid neuraxial anesthesia in patients already taking lovenox o If bloody needle or catheter placement occurs, delay lovenox 24 hrs o Remove epidural catheters 2 hrs. prior to initiation of lovenox. If already present, remove catheters 10 hrs after last dose of lovenox, and wait 2 hrs before any subsequent dosing.
 High block o Heralded by inability to talk, weak upper extremities
 Intubate to control ventilation and protect airway.
 Atropine for bradycardia
 Volume expansion and vasopressors for hypotension.

 Cardiac arrest during spinal anesthesia o Many cases were preceded by bradycardia. o Often occurred in young, healthy patients, i.e. patients with high vagal tone. o Prophylactic volume expansion is recommended, along with aggressive treatment of bradycardia with atropine, and vasopressors if necessary.
 Urinary retention o Blockade of S2-S4 foots decreases bladder tone and inhibits the voiding reflex. o Treatment: Foley catheterization until bladder function recovers.
 Failed block – not high enough, not long enough
 Intravascular injection during epidural or caudal blocks o High serum concentrations of local anesthetics affect the CNS
(seizures, unconsciousness) and the CV system (hypotension, rhythm and conduction abnormalities) o Minimize incidence by carefully aspirating before every injection, using a test dose, injecting local anesthetic in incremental doses, and observing for signs of intravascular injection.
 Subdural injection during epidural anesthesia o Produces a total spinal, except delayed 15-30 minutes o Requires intubation, mechanical ventilation, and CV support.
 Backache o Usually mild and self-limiting o Use Tylenol, Nsaids, and heating pad o 25-30% of patients receiving only general anesthesia have postoperative back ache. Many also have chronic back pain.

 Post-Dural Puncture Headache. (PDPH) o Headache usually starts 12-72 hrs after needling of the subarachnoid space. Is bifrontal or retrobulbar and occipital extending into the neck. Associated with photophobia and nausea o Headache is positional — increases when standing or sitting up, gone when lying flat o Cause is ongoing CSF loss o Incidence higher in young patients, female patients, and pregnant patients o Conservative therapy: recumbent position, analgesics, hydration, and caffeine to stimulate CSF production o If that fails, epidural blood patch to stop further CSF leakage. 90% effective. Carries same risks as epidural anesthesia, except higher risk of infection.
 Neurologic injury o Nerve roots or spinal cord may be injured o Most resolve spontaneously within 6 months, some don’t
 Spinal or epidural hematoma o Usually in anti-coagulated patients o Symptoms are sharp back and leg pain, progressing to numbness, weakness, and loss of sphincter control o If suspected, need immediate MRI and neurosurgical consultation.
Best results if decompressed within 8-12 hrs

Block height
 The height of a spinal block is determined by cephalad spread of local anesthetic in the CSF.
 Determining factors: o Baricity of the local anesthetic solution
 Hyperbaric solutions tend to drift downward due to gravity
 Hypobaric solutions tend to rise in CSF
 Isobaric solutions tend not to drift. o Patient position when the solution, whether hypobaric or hyperbaric, is injected or after it is injected o Spinal level of injection site o Lumbosacral CSF volume may play a part in determining block height, particularly in pregnant patients
Duration of block
 Spinal blocks recede gradually from the most cephalad dermatome to the most caudad.
 The principle determinant of block duration is the local anesthetic drug used: tetracaine > bupivacaine > lidocaine
 Increasing the local anesthetic dose prolongs the duration of the block
 Adding an adrenergic agonist (epinephrine or phenylepherine) to the local anesthetic solution may prolong the block. The mechanism is not clear – possibly by inducing local vasoconstriction, the rate of elimination of local anesthetic from the spinal cord and CSF is prolonged.

Block Height
 Injection site is the most important determinant of epidural block height.
Unlike spinal anesthesia, epidural anesthesia produces a segmental block that spreads both caudally and cranially from the site of injection.
 Local anesthetic dose
 Local anesthetic drug volume
 Effect of patient position during and after injection is controversial
 Age of patient – greater spread in older patients. The epidural space is less compliant, and epidural solutions cannot leak out intervertebral foramina as easily in elderly patients.
Duration of block
 As with spinal aesthesia, he principle determinant of block duration is the local anesthetic drug used: bupivacaine and ropivacaine > lidocaine and mepivacaine > chloroprocaine
 Dose of local anesthetic: increasing dose increases both duration and density of epidural block
 Addition of epinephrine to local anesthetic solution will prolong the block