Sympathetic Blocks for Postoperative Pain Control After Surgery: Literature Review and Current Evidence

Aug 1, 2020, 16:40 PM by Deepak Thapa, MB, BS, DNB, MNAMS, PDCC

Current Zeal for Sympathetic Blocks

Sympathetic blocks have recently gained attention for the potential to supplement postoperative analgesia. The stellate ganglion block (SGB) is a well-studied block for the provision of analgesia following upper limb orthopedic surgeries.[1],[2],[3] SGB may prove beneficial at a time when motor and sensory assessment is requested by a surgeon in the immediate postoperative period.[1] It has been suggested that sympathetic blocks may also be beneficial as a strategy to limit the development of complex regional pain syndrome (CRPS) in the postoperative period.[4],[5]

The clinical features of CRPS are indistinguishable from those of acute pain in the early postoperative period, adding justification to the use of stellate ganglion block to address postoperative sympathetic stimulation.

Sympathetic blocks may also facilitate the prompt diagnosis of compartment syndrome (CS) via the provision of analgesia without significant motor or sensory blockade. Although dilute concentrations of local anesthetic (LA) used for peripheral nerve blockade and postoperative pain management may not hinder the diagnosis of CS, higher concentrations of LA may mask CS and delay diagnosis secondary to similarities in the clinical presentation of somatic nerve blockade and CS.[6] Although the benefits of sympathetic nerve blocks on the ability to detect CS are conceptually appealing, significantly more robust evidence is needed to confirm this hypothesis.

Guiding Principles

Pain caused by sympathetic stimulation tends to be considered more frequently in chronic pain. The rationale behind the use of SGB for postoperative pain management dates back to the 19th century. A correlation between the sympathetic nervous system (SNS) and acute pain was made in 1860 when Dr. Silas Weir Mitchell noticed sympathetic involvement following penetrating limb injuries in Civil War victims and defined those as causalgias.[7] In an editorial in 1992, Forrest described the involvement of the SNS throughout the nociceptive stages after tissue injury.[8] His description included four stages of events following initial cellular trauma until tissue healing. Stage 1 is the activation of chemical mediators of nociception; stage 2 describes primary hyperalgesia due to sensitization of peripheral nerve endings; stage 3 is marked by hyperalgesia in spinal nerves, efferent reflexes, and secondary hyperalgesia; and stage 4 is characterized by the resolution of sensitization. Intervention during these stages reduces postoperative pain. The SNS is implicated in mediation of both stage 1 (by augmenting release of chemical mediators) and stage 2 (by potentiating the effect of substance P and primary hyperalgesias). In 2000, Baron disclosed the existence of a “cross talk” mechanism between the SNS of pathologic nerves and sensitized afferent nociceptors and described how this relationship culminated in an enhancement of pain.[9]

Initial Realizations

These findings attracted further evaluation of sympathetic blockade for acute pain control. In human volunteers, under physiological conditions, an SGB placed prior to evoked acute pain appeared to be ineffective in reducing the acute pain due to absence of prior sensitization of nociceptive pathways by the pain.[10] In spite of the outcome, inhibiting transmission in the sympathetic nervous system seems to be beneficial as a mechanism to prevent progression from acute pain to CRPS.[7] This concept gained strength when sympathetic blocks prevented CRPS recurrence in the postoperative period in patients with a previous history of CRPS.[4] It has also been noticed that the clinical features of CRPS are indistinguishable from those of acute pain in the early postoperative period, and this adds justification to the use of SGB to address postoperative sympathetic stimulation.[5] It is interesting to note that SGB also has been effective in relieving severe, refractory postoperative pain following upper limb surgery in patients without a history of CRPS.[11] Therefore, inhibition of sympathetic activation prior to or during surgery may contribute to better analgesic control.[11]

Current Perception

A randomized, controlled trial investigating the effectiveness of preoperative SGB on postoperative pain demonstrated a nonsignificant reduction in postoperative opioid consumption in the SGB group versus saline in 30 patients following upper limb orthopedic surgeries. A limitation of this study is that it included only relatively healthy subjects which may limit its generalizability.[2] Dexmedetomidine also has been added as an adjuvant to LA for SGB and noted prolongation of SGB effect.[3] However, the clinical benefit remains uncertain.


In conclusion, the benefits of SGB for postoperative pain management need to be further investigated with robust clinical trials. There may be a role for sympatholysis in the prevention of CRPS following trauma and in the early detection of CS. However, current evidence has not been sufficient to support its widespread clinical implementation.


  1. McDonnell JG, Finnerty O, Laffey JG. Stellate ganglion blockade for analgesia following upper limb surgery. Anaesthesia. 2011;66(7):611–4.
  2. Kumar N, Thapa D, Gombar S, Ahuja V, Gupta R. Analgesic efficacy of pre-operative stellate ganglion block on postoperative pain relief: a randomised controlled trial. Anaesthesia. 2014;69(9):954–60.
  3. Thapa D, Dhiman D, Ahuja V, Gombar S, Gupta RK. Tramadol sparing effect of dexmedetomidine as an adjuvant with lignocaine in preoperative stellate ganglion block for postoperative pain relief following upper limb surgeries. Br J Pain. 2018;12(1):26-34.
  4. Reuben SS, Rosenthal EA, Steinberg RB. Surgery on the affected upper extremity of patients with a history of complex regional pain syndrome: a retrospective study of 100 patients. J Hand Surg. 2000;25(6):1147–51.
  5. Mar GJ, Barrington MJ, McGuirk BR. Acute compartment syndrome of the lower limb and the effect of postoperative analgesia on diagnosis. Br J Anaesth. 2009;102(1):3–11.
  6. Bantel C, Trapp S. The role of the autonomic nervous system in acute surgical pain processing – what do we know? Anaesthesia. 2011;66(7):541-4.
  7. Rho RH, Brewer RP, Lamer TJ, Wilson PR. Complex regional pain syndrome. Mayo Clin Proc. 2002;77(2):174-80.
  8. Forrest JB. Sympathetic mechanisms in postoperative pain. Can J Anaesth. 1992;39(6):523-7.
  9. Baron R. Peripheral neuropathic pain: from mechanisms to symptoms. Clin J Pain. 2000;16(2 Suppl):S12-20.
  10. Holthusen H, Stanton-Hicks M, Arndt JO. Sympathetic block does not reduce acute vascular pain in humans. Anesth Analg. 1998;86(3):588-90.
  11. Kakazu CZ, Julka I. Stellate ganglion blockade for acute postoperative upper extremity pain. Anesthesiology. 2005;102(6):1288–9.
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