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Thoracic paravertebral block (TPVB) is the technique of injecting local anesthetic alongside the thoracic vertebra close to where the spinal nerves emerge from the intervertebral foramina. This produces ipsilateral somatic and sympathetic nerve blockade in multiple contiguous thoracic dermatomes (segmental thoracic anesthesia) both above and below the site of injection. It is effective in treating acute and chronic pain of unilateral origin from the chest and abdomen. Bilateral TPVB also has been described. Recently there has been an increase in interest in the use of ultrasound to assist or guide TPVB in real time. This chapter briefly describes the basic principles of TPVB, the sonoanatomy of the thoracic paravertebral space (TPVS), and the technique of ultrasound-guided (USG) TPVB.
The TPVS is a wedge-shaped space that lies on either side of the vertebral column ( Fig. 61.1 ). It is wider on the left than on the right, and the parietal pleura forms the anterolateral boundary. The base is formed by the vertebral body, intervertebral disc, and contents of the intervertebral foramen (see Fig. 61.1 ). The superior costotransverse ligament (SCTL) forms the posterior wall of the TPVS. This ligament extends from the lower border of the transverse process above to the upper border of the transverse process below ( Figs. 61.2 and 61.3 ), and the intertransverse ligament also is interposed between two transverse processes (see Figs. 61.2–61.4 ). The SCTL is continuous laterally with the internal intercostal membrane, which is the medial extension of the internal intercostal muscle medial to the angle of the rib (see Fig. 61.4 ). The apex of the TPVS is continuous with the intercostal space lateral to the tips of the transverse processes (see Fig. 61.4 ). Interposed between the parietal pleura anteriorly and the SCTL posteriorly is the fibroelastic endothoracic fascia (see Figs. 61.1 and 61.4 ), which is the deep fascia of the thorax that lines the internal aspect of the thoracic cage ( Fig. 61.5 ). In the paravertebral location, the endothoracic fascia is loosely applied to the ribs (see Fig. 61.5 ) and fuses medially with the periosteum at the midpoint of the vertebral body (see Fig. 61.1 ). There is an intervening layer of loose areolar connective tissue, “the subserous fascia,” between the parietal pleura and the endothoracic fascia (see Figs. 61.1 and 61.2 ). The endothoracic fascia thus divides the TPVS into two potential fascial compartments, the anterior extrapleural paravertebral compartment and the posterior subendothoracic paravertebral compartment (see Figs. 61.1 and 61.2 ). The TPVS contains fatty tissue that line the intercostal (spinal) nerve, the dorsal ramus, intercostal vessels, rami communicantes, and sympathetic chain (see Figs. 61.1 and 61.2 ). The spinal nerves in the TPVS are segmented into small bundles lying freely among the fat and devoid of a fascial sheath, which make them susceptible to local anesthetic blockade. The intercostal nerves and vessels are located behind the endothoracic fascia, while the sympathetic trunk is located anterior to it in the TPVS (see Fig. 61.5 ).
The TPVS is continuous with the epidural space medially via the intervertebral foramen, the intercostal space laterally, and the contralateral TPVS via the epidural and prevertebral space. The cranial extension of the TPVS is still not defined, but we have observed direct paravertebral spread of radio-opaque contrast medium from the thoracic to the cervical region, indicating that there is a direct continuity between the thoracic and cervical paravertebral regions. Ipsilateral Horner's syndrome after thoracic paravertebral injections also has been reported. The anatomic pathway for the spread of an injectate from the thoracic to the cervical paravertebral space is still not clear. The endothoracic fascia is continuous superiorly with the scalene or Sibson fascia and attached to the medial border of the first rib in front and the transverse process of the seventh cervical vertebra behind. Therefore, an injection posterior to the endothoracic fascia in the subendothoracic paravertebral compartment of the upper thoracic region is unlikely to spread cranially via the paravertebral space because of the attachment of the endothoracic fascia to the transverse process. However, we believe that an injection anterior to the endothoracic fascia in the extrapleural paravertebral compartment may spread to the cervical paravertebral region via the subserous layer of loose areolar connective tissue, which also provides the connective tissue investment for the mediastinal structures, and is continuous with the connective tissue investing the neurovascular structures in the root of the neck.
The caudal boundary of the TPVS is formed by the origin of the psoas major muscle, and spread through the TPVS to the lumbar region is thought to be unlikely. Ipsilateral lumbar spinal nerves are occasionally involved after a lower thoracic paravertebral injection. Saito and colleagues have demonstrated ipsilateral thoracolumbar spread of colored dye in cadavers. We also have reported ipsilateral thoracolumbar anesthesia and radiological spread of contrast below the diaphragm. These observations challenge the concept of lumbar nerve root sparing following TPVB. The exact mechanism for the ipsilateral thoracolumbar spread of local anesthetic or contrast medium is not clear, but it is suggested that it occurs via the subendothoracic fascial compartment to the retroperitoneal space where the ilioinguinal and iliohypogastric nerves are located.
A thoracic paravertebral injection may remain localized to the space injected or it may spread to the contiguous paravertebral spaces above and below, the intercostal space laterally, the epidural space medially or a combination of these to affect ipsilateral somatic and sympathetic nerves, including the posterior primary ramus in multiple contiguous thoracic dermatomes. The majority of the published data describing spread or distribution of anesthesia after TPVB have implemented the landmark based technique, and currently there is a paucity of data describing segmental spread of anesthesia in vivo after USG TPVB. Therefore caution must be exercised interpreting published data on the segmental spread of anesthesia after a TPVB, since it may not apply to the USG technique with a different direction of needle advancement (landmark based TPVB—anteroposterior directed needle—and USG TPVB—lateral to medial for the intercostal approach—see the following). There also are no published data describing the effects of volume or dose of local anesthetic on the segmental spread of anesthesia after USG TPVB.
Eason and Wyatt found that at least four intercostal spaces are covered by a single 15-mL injection of 0.375% bupivacaine. More recently, 15 mL of bupivacaine 0.5% injected into the TPVS has been shown to produce mean unilateral somatic block over 5 (range 1 to 9) dermatomes and sympathetic block over 8 (range 6 to 10) dermatomes. Similarly, 1.5 mg/kg of bupivacaine 0.5% produced sensory loss at the level of injection with a mean superior spread of 1.4 (range 0 to 4) dermatomes and a mean inferior spread of 2.8 (range 0 to 7) dermatomes. We also have observed a median ipsilateral loss of sensation to cold (ice) of 5 dermatomes (range 3 to 11 dermatomes) after a single paravertebral injection of 1.5 mg/kg (0.3 mL/kg) of 0.5% bupivacaine with epinephrine 1:200,000 in patients with multiple fractured ribs. The median distribution of sensory loss in our cohort of patients was 1.5 dermatomes (range, 1 to 3 dermatomes) above and 2.5 dermatomes (range, 0 to 9 dermatomes) below the level of injection. In children, 0.25 (SD 0.12) mL/kg of contrast medium injected into the TPVS produces radiological spread over 5.7 (SD 1.6) segments.
Cumulative evidence therefore suggests that a single-injection TPVB produces ipsilateral segmental thoracic anesthesia, but the dermatomal distribution of sensory blockade is unpredictable and variable. The reason for this variability is not clear, but anatomical and physical factors have been hypothesized. Factors such as age, gender, height, weight, injectate volume or the dose of bupivacaine, previous posterolateral thoracotomy, or the spread of a radio-opaque contrast medium does not appear to affect the distribution of sensory blockade after a single-injection TPVB. Paravertebral injections performed at 2-week intervals in the same patient also produces different degrees of sensory blockade. Thoracic paravertebral anesthesia does not appear to be gravity dependent, but there is a tendency for preferential caudal spread of somatic and sympathetic blockade.
Naja and colleagues recently studied the spread of a radiopaque contrast medium in the TPVS using chest radiographs after locating the TPVS using nerve stimulation. They defined the needle tip to be dorsal to the endothoracic fascia when the motor response was elicited at 2.5 mA and ventral to it (and presumably close to the spinal nerve) when the motor response was elicited at ≤0.5 mA. Naja and colleagues clearly demonstrated an association between an injection at two different locations within the TPVS or after identifying the TPVS using two different current thresholds and the pattern of spread of contrast. They concluded that an injection ventral to the endothoracic fascia, with a low nerve stimulating current (≤0.5 mA), more frequently results in a longitudinal and multisegmental spread of contrast, whereas an injection dorsal to the endothoracic fascia, with a high nerve-stimulating current (2.5 mA), results in a cloud-like and limited segmental spread of the contrast. The interpretation of the results of this study has been questioned, because with the methodology described, it is not possible to determine with certainty where the injections were made relative to the endothoracic fascia. While Naja and colleagues described the spinal nerves as ventral to the endothoracic fascia, published literature suggests that they are located dorsal to the endothoracic fascia and in the subendothoracic paravertebral compartment (see Figs. 61.1 and 61.5 ).
There is controversy about epidural spread and its contribution to the extension of TPVB. Radio-opaque contrast medium infused through an extrapleural paravertebral catheter placed intraoperatively under direct vision remains confined to the paravertebral space. In contrast, varying degrees of epidural spread has been shown to occur after 70% of percutaneous paravertebral injections. These injections are mostly unilateral, and the volume involved is considered too small to produce clinically significant epidural block. Cadaveric dissection also confirms that only a small proportion of the injectate enters the epidural space and remains confined to the side of injection. The vertebral attachment of the endothoracic fascia attenuates prevertebral spread and may influence epidural spread after an extrapleural paravertebral compartment injection. Clinically, sensory anesthesia is predominantly ipsilateral and greater after epidural spread than after only paravertebral spread. Therefore, current evidence suggests that ipsilateral epidural spread of discrete amounts of local anesthetic occurs after thoracic paravertebral injection and contributes to the extension of TPVB.
Bilateral symmetrical anesthesia is described and may be due to extensive epidural spread, inadvertent intrathecal injection into the dural sleeve, or inadvertent epidural injection via a catheter that was intended for the paravertebral space. Bilateral symmetrical anesthesia may also occur more commonly with the median injection technique or the use of large volumes of injectate (>25 mL). Segmental contralateral anesthesia adjacent to the site of injection has been shown to occur in 1.1% of paravertebral injections and may be due to either prevertebral or epidural spread to the contralateral TPVS. We also have observed mean segmental contralateral anesthesia of 2.5 (1.5) dermatomes in 20% of patients after a single-injection TPVB. More recently, we have reported contralateral anesthesia over 9 (7 to 11) dermatomes in 35% of patients after a multiple-injection TPVB that was used for surgical anesthesia during percutaneous radiofrequency ablation of liver tumors.
The exact mechanism for prevertebral spread is not clear, but we have proposed that it occurs through the “extrapleural compartment” of the TPVS via the subserous layer of connective tissue. It is also not known if there are differences in the incidence of contralateral anesthesia between a single-injection and a multiple-injection TPVB, but our experience (described previously) suggests that it may be more common after a multiple-injection technique. Bilateral sympathetic blockade may also occur in the absence of bilateral sensory blockade due to prevertebral spread to the contralateral sympathetic chain, which is more anteriorly placed in the TPVS and more susceptible to local anesthetic agents. This may be one explanation for bilateral Horner's syndrome reported after unilateral TPVB.
Ipsilateral lumbar spinal nerves also are occasionally involved after a lower thoracic paravertebral injection. This has also been our experience, and we have also observed ipsilateral radiological spread of contrast below the diaphragm. Saito and colleagues have shown in a group of volunteers that single-injection TPVB at T11 using 22 mL of local anesthetic produced mean loss of sensation to pin-prick of 6 (8 to 13) segment and extended from T5 to L5 segments. Saito and colleagues have also demonstrated ipsilateral thoracolumbar spread of colored dye in cadavers. These observations challenge the concept of lumbar nerve root sparing following TPVB.
There are several different techniques for TPVB, and it can be performed with the patient in the sitting, lateral decubitus (with the side to be blocked uppermost), or prone position. The two most commonly used techniques for TPVB involve eliciting “loss of resistance” or advancing the block needle by a fixed predetermined distance after the transverse process is located. At the appropriate dermatome and under strict aseptic precautions, a 22-G Tuohy needle (for a single-shot injection) or an 18 or 16-G Tuohy needle (if a catheter is to be inserted) is introduced 2.5 cm lateral to the highest point of the spinous process and advanced perpendicular to the skin in all planes until the transverse process is contacted. For safety, it is imperative to locate the transverse process before the needle is advanced any further to avoid deep needle insertion and possible inadvertent pleural puncture. Once the transverse process is located, the needle is withdrawn to the subcutaneous tissue and readvanced in a cephalad direction to pass through the space between the two transverse processes until loss of resistance is elicited as the needle traverses the SCTL, usually within 1.5 to 2 cm from the transverse process. Occasionally, a subtle pop may be felt. Unlike epidural space localization, the loss of resistance felt as the needle enters the TPVS is subjective and indefinite, and is usually a small change in resistance rather than a definite give. It is the author's experience that the loss of resistance is best appreciated if one uses a glass syringe filled with air. Luyet et al. have recently demonstrated the presence of a gap between the medial and lateral portions of the SCTL in cadavers, which they propose is a possible reason for not being able to elicit a loss of resistance in all cases.
Alternatively, for landmark based TPVB, the block needle may also be advance by a fixed predetermined distance (1 to 2 cm) once the needle is walked off the transverse process without eliciting loss of resistance. This variation has been used effectively with few complications such as pneumothorax. Other techniques that have been used to perform TPVB include “the medial approach,” “pressure measurement technique,” “paravertebral-peridural block,” “fluoroscopy guidance,” and “paravertebral catheter placement under direct vision at thoracotomy.”
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