What are the recognized complications of spinal anesthesia?

What are the recognized complications of spinal anesthesia?

The single most common complication of spinal anesthesia is probably hypotension. Postganglionic autonomic nerves, which are small, unmyelinated C fibers, are exquisitely sensitive to spinal blockade. The greater the extent of anesthesia, the greater the sympathectomy. Interruption of sympathetic stimuli to the capacitance vessels markedly increases peripheral venous pooling, resulting in decreased venous return to the heart. Consequently, cardiac output falls. The usual compensatory response to reduced cardiac output is an increase in heart rate. Sudden tachycardic responses are mediated through the cardiac accelerator nerves, which receives contributions from spinal nerves T₁–T₄. Blockade of the upper thoracic nerve roots not only prevents acute increases in heart but also allows for unopposed vagal influence, thereby slowing heart rate. Therefore, cardiac output is impaired by two mechanisms: peripheral venous pooling and bradycardia.

Before administration of spinal anesthesia, fluid loading with approximately 500 mL of a balanced salt solution helps to prevent the state of relative hypovolemia induced by venous dilatation. Most cases of spinal-induced hypotension respond favorably to altering the patient’s position into 10° of Trendelenburg, lithotomy, or left lateral uterine displacement. Intravenous volume infusion is frequently required to restore blood pressure toward its normal range. Hypotension unresponsive to fluid adminis-tration requires immediate treatment and usually responds to ephedrine, 5–10 mg, intravenously. Ephedrine works by stimulating both α- and β-receptors causing an increase in the heart rate, contractility, and peripheral resistance, which are frequently sufficient to correct hypotension. Hypotension, dysrhythmias, and myocardial ischemia are associated untoward effects. Ephedrine causes little or no alteration in uterine blood flow. Alternatively, a continuous infusion of phenylephrine may return vascular tone toward normal. The solution is frequently prepared by adding 10 mg of phenylephrine to 250 or 500 mL of 5% dextrose in water. Phenylephrine acts as an α-adrenergic agonist. Its side-effects include hypertension, bradycardia, and uterine vasoconstriction. It is not the first choice for treating hypotension in the pregnant patient. Bradycardia is effec-tively treated with atropine 0.4 mg intravenously, or ephedrine in small doses.

Ventilatory impairment frequently results from hypotension leading to impaired medullary blood flow and hypoxia of the respiratory center. Blockade of the phrenic nerve, composed of contributions from C₃–C₅, leading to impaired diaphragmatic movement, is highly unusual. Motor blockade of the intercostal and abdominal muscles may prevent effective coughing. Loss of the intercostal muscle’s proprioception frequently prevents the patient from appreciating chest expansion, thereby creating a sub-jective feeling of difficulty breathing.

Nausea and vomiting accompanying spinal anesthesia often result from parasympathetic imbalance, hypoten-sion, or hypoxemia. Treatment with atropine, vasopressors, or oxygen usually provides relief. Retching, apprehension, agitation, and shortness of breath may also be secondary to hypotension or hypoxemia. Treatment requires increasing the blood pressure, oxygen administration, and assisted or controlled ventilation.

Post-dural puncture headache (PDPH) remains the most commonly encountered postanesthetic side-effect of spinal anesthesia. The frequency of PDPH following dural puncture with a 17-gauge Tuohy needle has been reported to be as high as 75%. The incidence of PDPH is lower in the elderly and in those whose dura is punctured by a pencil-point or a fine needle. PDPH following the use of a 26-gauge needle may be as low as 2.5%. In an ambulatory setting, Kang et al. (1992) noted a PDPH rate of 9.6% and 1.5% associated with 26- and 27-gauge needles, respec-tively. Aligning the needle bevel parallel to the dural fibers seems to markedly reduce the incidence of PDPH. This approach tends to separate rather than cut the longitudinal dural fibers, resulting in a smaller, more readily repairable hole.

PDPH following subarachnoid block emanates from traction on the meninges and vascular structures, as CSF leaks through the dura. Symptomatic treatment requires mild analgesics, bed rest, and fluid administration. Injection of morphine into the subarachnoid space along with a local anesthetic does not decrease the incidence of PDPH. In patients with severe incapacitating headaches, or headaches of several days’ duration, an epidural blood patch is indicated. An epidural blood patch is performed by placing a needle in the epidural space at the suspected level of dural puncture. Fifteen to twenty milliliters of the patient’s own blood, drawn under sterile conditions, are injected through the newly placed epidural needle. This maneuver is highly successful, but risk of re-puncturing the dura exists. Slight elevations in temperature are occasionally seen for 1 or 2 days following this procedure. Low back pain and neck discomfort have also been reported following epidural blood patching. Caffeine, a cerebral vasoconstrictor, may also provide beneficial effects. Other causes of PDPH, such as septic or aseptic meningitis and arachnoiditis, are extremely rare. Urinary retention that is due to prolonged blockade has also been associated with spinal techniques.

Backache occurs frequently following spinal anesthesia but is usually short-lived and of only mild-to-moderate intensity. Its causes generally include lumbar ligamentum strain, paraspinous muscle spasm, and muscle hematoma formation. Severe back pain requires immediate neurologic investigation.

The incidence of major neurologic sequelae following spinal anesthesia approaches 0.5%. If exacerbations of pre-existing neurologic diseases are eliminated from this figure, the probability of encountering neurologic damage following spinal anesthesia diminishes even further. Transient radicular irritation (TRI) consists of pain, and/or dysesthesia in the legs or buttocks. This occurred more frequently with lidocaine, but has been seen with tetracaine and bupivacaine. Other factors that contribute to the incidence of TRI are the lithotomy position, ambu-latory patients, and obesity. TRI usually resolves within 72 hours but may take as long as 6 months.

Hematoma or abscess formation producing a cauda equina syndrome is potentially identifiable and reme-diable. Numerous cases of spontaneous subarachnoid and epidural hemorrhage exist in anticoagulated patients. Current American Society of Regional Anesthesia and Pain Medicine (ASRA) recommendations concerning the use of spinal or epidural anesthesia in patients on antiplatelet drugs are as follows. Nonsteroidal anti-inflammatory drugs and aspirin do not present an increased risk for intraspinal bleeding when used as a single agent. Use of spinal or epidural anesthesia is at the discretion of the anesthesiologist. However, there is the known risk of a hemorrhagic complication when these drugs are concur-rently given with other antiplatelet drugs such as heparin, low-molecular-weight heparin, warfarin, ticlopidine (Ticlid), or clopidogrel (Plavix). If spinal or epidural anesthesia is considered, there should be careful documentation of the lack of therapeutic effect (normal coagulation tests) of the second drug. Regarding the new antiplatelet drugs, ticlopidine and clopidogrel, which are drugs prescribed for prevention of myocardial infarction, stroke, and vaso-occlusive disorders, there are no current studies to establish the safety of performing regional anesthesia during their use.

There are also no data regarding their interaction with other anticoagulant drugs. Thus, ASRA guidelines recommend dis-continuing ticlopidine for 10–14 days and clopidogrel for 7 days prior to performing a spinal or epidural anesthetic.

Direct neurotoxicity of commonly used local anesthetic solutions is almost nonexistent. Chloroprocaine, however, represents a notable exception. Although apparently free of direct neurotoxicity in the epidural space, chloroprocaine possesses neurolytic properties in the subarachnoid space. Sodium bisulfite, a preservative, has been identified as the causative agent. Sodium bisulfite has been eliminated from many currently available preparations. At present, chloro-procaine is not recommended for use in the subarachnoid space. Cauda equina syndrome has been reported follow-ing administration of hyperbaric local anesthetics through subarachnoid catheters. Septic and aseptic meningitis has been attributed to contamination of drugs and needles with bacteria, detergents, and powder. Single-use, dispos-able equipment has almost eliminated this problem. Direct neural trauma may theoretically occur from needles or catheters but should be relegated to a practical improbabil-ity in most cases. Spinal cord ischemia has been associated with systemic hypotension and cross-clamping of the aorta. Pre-existing neurologic disease, improper patient posi-tioning, or pressure from retractors on the fetal head may also predispose the patient to neurologic defects following spinal anesthesia and are unrelated to the spinal anesthetic.

Failure of spinal anesthesia to provide adequate analge-sia remains another commonly encountered complication. Prospective studies have estimated the rate of failed spinals to be 4–16%. A study by Munhall et al. (1988) demon-strated that only 25% of spinal failures were due to factors such as inability to identify the subarachnoid space and lack of free-flowing CSF before, as well as after, injection of local anesthetic. Most inadequate spinal anesthetics were due to faulty selection of local anesthetic, dose, vasocon-strictor, baricity, position, interspace, or single-injection versus catheter technique. An example of such a judgment error is the selection of tetracaine 0.5% over bupivacaine 0.5% to block tourniquet pain.

Long-term follow-up studies of patients receiving large numbers of spinal anesthetics have shown spinal anesthe-sia to be a safe technique (e.g., Vandam and Dripps 1960).