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PubMed · 8311355

[Cervical epidural anesthesia].

Abstract

Cervical epidural anaesthesia (CEA) results in an effective sensory blockade of the superficial cervical (C1/C4) and brachial plexus (C5/T1-T2). It is used both intraoperatively and in the treatment of postoperative or chronic pain. The approach to the epidural space at the C7-T1 interspace is not technically difficult. Patients are placed in the sitting position, increasing the negative pressure in the epidural space, with the head flexed on the thorax, in order to open the lowest cervical interspace. A 18-gauge Tuohy needle is inserted by a midline approach into the C6-C7 or C7-T1 interspace. A catheter may be inserted and left in place for postoperative analgesia. Local anaesthetics are administered either alone, or in combination with opiates. The CEA blocks the cardiac sympathetic fibers and consequently decreases heart rate, cardiac output and contractility. The mean blood pressure is unchanged or decreased, depending on peripheral systemic vascular resistance changes. The baroreflex activity is also partly impaired. Sympathetic blockade also decreases myocardial ischaemia. The cardiovascular changes induced by CEA are also partly due to the systemic effect of the local anaesthetic. The respiratory effects are minimal and depend on the extent of the blockade and the concentration of the local anaesthetic. A moderate restrictive syndrome occurs. Since the phrenic nerves originate from C3 to C5, ventilation may be impaired by CEA. Extension of the block may also impair intercostal muscle function, with a risk of respiratory failure when a CEA is used in patients with compromised respiratory function. The potential specific complications, mainly cardiovascular and respiratory, are the exacerbation of the effects of CEA. Side effects such as bradycardia, hypotension and acute ventilatory failure in relation to respiratory muscle paralysis, may be observed. Close monitoring of haemodynamics, respiratory rate and level blockade is required. Cervical epidural anaesthesia may be used either alone, or in combination with general anaesthesia depending on the surgical procedure. This technique seems to be effective in carotid artery surgery since sensitive and reliable information on cerebral function may be obtained. It is also for shoulder and upper limb surgery as well as for pharyngolaryngeal surgery, providing efficient operative anaesthesia and postoperative analgesia. CEA is used for relief of chronic pain in the head and neck or cancer pain due to Pancoast-Tobias syndrome. It seems to be effective for treating pain in patients with unstable angina pectoris or acute myocardial infarction.

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BibTeXRIS

D Baylot, P Mahul, M L Navez, J Hajjar, J M Prades, C Auboyer. 1993. [Cervical epidural anesthesia].. https://doi.org/10.1016/s0750-7658(05)80996-7

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Effects of epidural anaesthesia on surgical stress-induced immunosuppression during upper abdominal surgery.

BACKGROUND: Previously, we have demonstrated that surgical stress rapidly induced transient hyporesponsiveness of blood cells to endotoxin and that monocyte mCD14 and HLA-DR expression decreased soon after the start of surgery under general anaesthesia. This study was designed to investigate the effects of epidural anaesthesia on surgical stress-induced immunosuppression in patients undergoing upper abdominal surgery. METHODS: After having obtained informed consent, patients were randomly allocated to receive general anaesthesia (Group G) or general anaesthesia with epidural anaesthesia (Group E). Perioperative changes in neutrophil phagocytic activity, neutrophil respiratory burst activity, monocyte mCD14 and HLA-DR expression, plasma IL-10 concentration, and the LPS-induced TNF-alpha production in whole blood were measured. RESULTS: Surgical stress rapidly depressed neutrophil phagocytic activity, monocyte mCD14 and HLA-DR expression, and LPS-induced TNF-alpha production ex vivo (P < 0.05 vs preoperation) in both Group G and Group E. In contrast, the plasma IL-10 concentration increased significantly 2 h after the start of surgery (P < 0.05) in both groups. There were no significant differences between the two groups. The neutrophil respiratory burst activity did not change during the operation in either group. CONCLUSION: This study showed that the innate immune system is suppressed from the early period of upper abdominal surgery. Subgroup analysis suggested that epidural anaesthesia to T4 dermatome as well as general anaesthesia may not protect patients from this immunosuppression. These results in part explain the impairment of host-defense mechanisms seen in the perioperative period.

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Local anesthetics.

Local anesthetics are used broadly to prevent or reverse acute pain and treat symptoms of chronic pain. This chapter, on the analgesic aspects of local anesthetics, reviews their broad actions that affect many different molecular targets and disrupt their functions in pain processing. Application of local anesthetics to peripheral nerve primarily results in the blockade of propagating action potentials, through their inhibition of voltage-gated sodium channels. Such inhibition results from drug binding at a site in the channel's inner pore, accessible from the cytoplasmic opening. Binding of drug molecules to these channels depends on their conformation, with the drugs generally having a higher affinity for the open and inactivated channel states that are induced by membrane depolarization. As a result, the effective potency of these drugs for blocking impulses increases during high-frequency repetitive firing and also under slow depolarization, such as occurs at a region of nerve injury, which is often the locus for generation of abnormal, pain-related ectopic impulses. At distal and central terminals the inhibition of voltage-gated calcium channels by local anesthetics will suppress neurogenic inflammation and the release of neurotransmitters. Actions on receptors that contribute to nociceptive transduction, such as TRPV1 and the bradykinin B2 receptor, provide an independent mode of analgesia. In the spinal cord, where local anesthetics are present during epidural or intrathecal anesthesia, inhibition of inotropic receptors, such as those for glutamate, by local anesthetics further interferes with neuronal transmission. Activation of spinal cord mitogen-activated protein (MAP) kinases, which are essential for the hyperalgesia following injury or incision and occur in both neurons and glia, is inhibited by spinal local anesthetics. Many G protein-coupled receptors are susceptible to local anesthetics, with particular sensitivity of those coupled via the Gq alpha-subunit. Local anesthetics are also infused intravenously to yield plasma concentrations far below those that block normal action potentials, yet that are frequently effective at reversing neuropathic pain. Thus, local anesthetics modify a variety of neuronal membrane channels and receptors, leading to what is probably a synergistic mixture of analgesic mechanisms to achieve effective clinical analgesia.

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