Postoperative backache occurs after general anesthesia but is more common after spinal (11%) or epidural (30%) anesthesia.
Possible explanations for backache include needle trauma, local anesthetic irritation, and ligamentous strain secondary to muscle relaxation.
Postdural Puncture Headache
Headache is characteristically mild or absent when the patient is in the supine position, but head elevation results in fronto-occipital headache. Occasionally, cranial nerve symptoms (diplopia, tinnitus) and nausea and vomiting are present.
Headache is believed to result from the loss of CSF through the meningeal needle hole, resulting in decreased buoyant support for the brain.
In the upright position, the brain sags in the cranial vault, putting traction on pain-sensitive structures and possibly cranial nerves.
The incidence of PDPH decreases with increasing age and with the use of small-diameter spinal needles with noncutting tips.
Inserting cutting needles with the bevel aligned parallel to the long axis of the meninges results in a meningeal opening that is likely to be pulled closed by the longitudinal tension present on the dura mater.
Up to 50% of young patients develop PDPH after accidental meningeal puncture with a large epidural needle.
If age is considered, there does not seem to be a gender difference in the incidence of PDPH.
Remaining supine does not decrease the incidence of PDPH.
Use of fluid rather than air for determining loss of resistance during attempted location of the epidural space decreases the risk of developing PDPH in the event of an accidental meningeal puncture.
PDPH usually resolves spontaneously in a few days with conservative therapy (bed rest, analgesics, and caffeine).
Epidural blood patch (10–20 mL of autologous blood is aseptically injected into the epidural space near the interspace where the meningeal puncture occurred) produces relief in 85% to 95% of patients within 1 to 24 hours (it is presumed to form a clot over the meningeal hole).
The most common side effects of blood patch are backache and radicular pain.
Use of a prophylactic blood patch is effective in preventing PDPH in patients in whom the meninges are accidentally punctured during attempted epidural anesthesia.
Epidural administered fibrin glue (meningeal patch) is an effective alternative to a blood patch for treatment of PDPH.
Hearing loss (lasting 1–3 days) is common after spinal anesthesia, especially in female patients.
Systemic toxicity manifests as central nervous system (CNS) and cardiovascular toxicity during epidural anesthesia. (Drug doses are too low during spinal anesthesia.)
CNS toxicity may result from intravascular absorption from the epidural space but is more commonly caused by accidental IV injection of the local anesthetic solution.
Because plasma concentrations of local anesthetic required to produce cardiovascular toxicity are high, this complication likely results only from accidental IV injection of the local anesthetic solution.
An adequate test dose and incremental injection of the local anesthetic solution are the most important methods for preventing systemic toxicity during epidural anesthesia.
Total Spinal Anesthesia
Total spinal anesthesia occurs when the local anesthetic solution spreads high enough to block the entire spinal cord and occasionally the brain stem during either spinal or epidural anesthesia.
Profound hypotension and bradycardia may occur secondary to sympathetic nervous system blockade. Apnea may occur as a result of respiratory muscle dysfunction or depression of brain stem control centers.
Management includes administration of vasopressors, atropine, fluids, and oxygen plus controlled ventilation of the lungs. If the cardiovascular and ventilatory consequences are managed appropriately, total spinal block will resolve without sequelae.
Neurologic Injury
Neurologic injury occurs in approximately 0.03% to 0.1% of all spinal and epidural anesthesia. (Persistent paresthesias and limited motor weakness are the most common injuries.)
Hyperbaric 5% lidocaine has been implicated as a cause of cauda equina syndrome after subarachnoid injection through small-bore (high-resistance) catheters during continuous spinal anesthesia. (Injection through these high-resistance catheters produces little turbulence, and undiluted local anesthetic solution tends to pool around dependent cauda equina nerve roots.)
Transient neurologic symptoms (TNS) or transient radicular irritation (TRI) is defined as pain or dysesthesia in the buttocks or legs after spinal anesthesia (Table 34-11: Transient Neurologic Symptoms).
Use of a double-orifice pencil-point needle may reduce the risk of TNS compared with the use of a single-orifice needle.
Pain usually resolves spontaneously in 72 hours.
The mechanism responsible for TRI is unknown but it is not simply a milder form of cauda equina syndrome.
Spinal hematoma is a rare (estimated to occur in fewer than one in 150,000 patients) complication of spinal or epidural anesthesia manifesting as lower extremity numbness or weakness. Detection is difficult in patients receiving perioperative spinal local anesthetic solution pain control.
Early detection is critical because a delay of more than 8 hours in decompressing the spinal cord decreases the likelihood of neurologic recovery.
Coagulation defects are the principal risk factor for development of an epidural hematoma.
Patients receiving nonsteroidal anti-inflammatory drugs (NSAIDs) with antiplatelet effects or subcutaneous unfractionated heparin for deep thrombosis prophylaxis are not considered to be at increased risk for development of a spinal hematoma.
Patients taking antiplatelet drugs (thienopyridine derivatives such as ticlopidine and clopidogrel; glycoprotein IIb/IIIa antagonists such as abciximab) should generally not receive a neuraxial block.
Patients receiving fractionated low-molecular-weight heparin (LMWH; enoxaparin, dalteparin, tinzaparin) are considered to be at increased risk for development of a spinal hematoma. Patients receiving drugs preoperatively at thromboprophylactic doses should have the drug held for 10 to 12 hours before central neuraxial block.
For patients in whom LMWH is begun after surgery, single-shot neuraxial blocks are not contraindicated provided the first dose of heparin is not administered until 24 hours after surgery using twice-daily dosing regimens (or 6–8 hours if using once-daily dosing regimens).
If an indwelling central neuraxial catheter is in place, it should not be removed until 10 to 12 hours after the last dose of LMWH, and subsequent doses should not be administered until at least 2 hours after catheter removal.
Patients who are fully anticoagulated (prolonged prothrombin time and plasma thromboplastin time) at the time of block placement or removal of the epidural catheter are considered to be at increased risk for the development of a spinal hematoma.
The risk of spinal hematoma during removal of an epidural catheter is nearly as great as with placement of the catheter. The timing for removal of the epidural catheter and the degree of anticoagulation need to be coordinated.
Drugs or regimens not considered to increase the risk of neuraxial bleeding when used alone (minidose unfractionated heparin, NSAIDs) may increase the risk when combined.