Spinal anesthesia

Published on 07/02/2015 by admin

Filed under Anesthesiology

Last modified 22/04/2025

Print this page

This article have been viewed 1112 times

Spinal anesthesia

The use of spinal anesthesia gained popularity in the United States in the 1940s. However, due to reports of adverse neurologic effects, the number of spinal anesthetics administered declined until a large study demonstrated the relative rarity of such complications, leading to a resurgence in the use of spinal blocks.

When spinal anesthetics are used in appropriately selected patients, their advantages include a decreased incidence of thromboembolism, cardiac morbidity and death, and bleeding, the latter resulting in a decreased need for transfusion. In addition, the use of subarachnoid blocks decreases the incidence of lower extremity vascular graft occlusion and of postoperative pneumonia. The advantages of subarachnoid blocks are probably due to multiple factors, including a decreased hypercoagulable state, increased tissue blood flow (because of vasodilation below the level of the block), increased oxygenation (because of maintenance of normal ventilation), increased peristalsis (related to the need for lower doses of opioids), and decreased stress response (because of the blockade of afferent activity at the spinal cord level as opposed to blockade at the level of the reticular activating center/cortex).

The mechanism of action of spinal anesthesia is due to the effect of local anesthetic agents on the individual nerve roots, effects that depend on the size and myelin content of nerve fibers, concentration of the local anesthetic agent, and duration of contact between the nerve root and the local anesthetic agent. The loss of conductivity of impulses through the fibrils follows a fixed sequence—first, sympathetic and parasympathetic activity are lost, and then sensation in the C, B, and A fibers is lost. C—fibers quit firing first, progressing finally to loss of activity in the Aα fibers, which accounts for the loss of motor function lastly. Heavy myelinated fibers present in motor nerves are most resistant to the effects of local anesthetic agents; hence, loss of activity in these nerves is the last group of nerves to be blocked. Because of the increased sensitivity of autonomic nerve fibers, blockade of these nerves extends for two or more dermatomes above the level of skin anesthesia, and blockade of motor fibers is seen two or more levels below the level of skin anesthesia (Box 122-1, Table 122-1).

Table 122-1

Dose and Duration of Effect for Local Anesthetic Agents Commonly Administered Intrathecally

		Dose (mg)	Duration of Effect (min)
Drug	Preparation	Perineum	Lower Abdomen	Upper Abdomen	Plain	With Epinephrine
Bupivacaine	0.75% in 8.25% dextrose	4-10	12-14	12-18	90-120	100-150
Procaine	10% solution	75	125	200	45	60
Ropivacaine*	0.2-1% solution	8-12	12-16	16-18	90-120	90-120
Tetracaine	1% solution in 10% glucose	4-8	10-12	10-16	90-120	120-240

^*Intrathecal injection is an off-label use for ropivacaine.

Other factors affecting the level of blockade

The most important factors affecting the level of blockade are the baricity of the local anesthetic (density of a local anesthetic compared to the density of cerebrospinal fluid [∼ 1.0003]), patient positioning during and after placement, and local anesthetic dose. Hyperbaric solutions (often created by mixing the local anesthetic with 5% to 8% dextrose) are impacted by gravity and move to dependent portions of the intrathecal space, whereas hypobaric solutions (created by mixing the local anesthetic with distilled water) rise in the intrathecal space. Isobaric solutions remain at the site of the injection.

Spinal anesthetic agents

The most commonly used local anesthetic solutions are hyperbaric bupivacaine and hyperbaric tetracaine. Lidocaine has been used in the past but is rarely used in current practice because of its association with the development of transient neurologic symptoms and cauda equina syndrome. The quality and duration of blocks can be enhanced by adding a vasoconstrictor, such as epinephrine, or an opioid to the local anesthetic solution. Clonidine and neostigmine also have some analgesic properties when administered intrathecally.

Cardiovascular effects

The loss of sympathetic activity that accompanies a spinal anesthetic results in vasodilation below the level of blockade, decreasing systemic vascular resistance, and the associated venodilation decreases cardiac preload and, therefore, cardiac output. If the level of blockade is sufficiently cephalad, loss of activity occurs in the cardiac accelerator nerves, which is manifested by bradycardia. The net effect of these physiologic changes can manifest as a profound decrease in systemic blood pressure. The most effective approach to the sympathectomy is (1) to provide prophylaxis by administering a bolus of intravenous fluids to the patient before the intrathecal administration of the local anesthetic agent and (2) to have a vagolytic drug and a vasopressor readily available to administer intravenously to treat the bradycardia and hypotension. Risks for the development of bradycardia (<50 beats/min) following a spinal anesthetic include (1) a baseline heart rate below 60 beats/min, (2) the use of β-adrenergic receptor blocking agents prior to presentation for a spinal anesthetic, (3) prolonged PR interval on the electrocardiogram (4) sensory level above T6, (5) age younger than 50 years and (6) American Society of Anesthesiologists I physical status.

Pulmonary effects

Pulmonary effects seen with subarachnoid blocks are usually minimal because the diaphragm is innervated by motor fibers in the phrenic nerves that exit the spinal column at C3-C5. However, if spinal blockade is sufficiently high, in the midthoracic to upper thoracic region, vital capacity decreases because of loss of abdominal muscle activity, but tidal volume remains unchanged.

In patients with severe chronic lung disease, a high thoracic spinal anesthetic may lead to loss of accessory muscle function. Many patients with chronic lung disease depend on the accessory muscles for maintenance of ventilation.

As a general rule all patients should receive supplemental O₂ because acute airway closure, atelectasis, and hypoxia have been observed in patients with otherwise normal pulmonary function. The apnea seen with a high spinal block is more commonly due to hypoperfusion of the brainstem because of hypotension and not necessarily from the activity of the local anesthetic agents on the C3 to C5 nerve roots. When a high spinal block is identified, the patient should be placed in the Trendelenburg position to increase cardiac preload, cardiac output, and perfusion of the brainstem; if pulmonary ventilation remains compromised, tracheal intubation, assisted ventilation, or both may be necessary.

Gastrointestinal effects

The sympathectomy associated with a spinal anesthetic maintains peristalsis, leading to a small contracted gastrointestinal tract. Hepatic blood flow may be reduced secondary to the decreased mean arterial pressure.

Genitourinary effects

Spinal blockade has minimal effect on renal blood flow because renal blood flow is autoregulated. With spinal blockade at the lumbar or sacral level, autonomic control of bladder function can be lost, leading to urinary retention, which resolves when the blockade wears off.

Cerebral blood flow

Cerebral blood flow is maintained during spinal anesthesia. However, if mean arterial pressure is less than 60 mm Hg, cerebral blood flow can decrease, manifested by nausea and vomiting and, if sufficiently low, by apnea and hypoxia.

Contraindications to spinal anesthesia

Absolute contraindications include patient refusal, coagulation abnormalities, severe hypovolemia, increased intracranial pressure, infection, and severe stenotic aortic and mitral valvular heart disease (Box 122-2). Other relative and controversial contraindications are also listed in Box 122-2.

Related

Fausts Anesthesiology Review Expert Consult 4e