A Realist Evaluation of a Rapid Response System for Mental State Deterioration in Acute Hospital Settings.

Herpes zoster (HZ) arises from reactivation of latent varicella‐zoster virus in cranial or dorsal root ganglia and often produces debilitating dermatomal pain []. Its most common chronic complication—postherpetic neuralgia (PHN) ‐ causes persistent neuropathic pain that impairs function and quality of life; reported PHN incidence after HZ ranges from ~5% to > 50% depending on definition and study design, and ~30% of patients may experience pain beyond 1 year [, ]. Mechanistically, PHN pain reflects a combination of deafferentation with loss of intraepidermal nerve fibers, “irritable” cutaneous nociceptors, hyperexcitable ectopic pacemaker sites within affected dorsal root ganglia and peripheral nerves, and secondary central sensitization in the spinal dorsal horn [, ]. Varicella–zoster virus induces neuropathic changes in DRG, including increased sodium current density and upregulation of Nav1.6/Nav1.7 channels that support ectopic discharges, and behavioral sensitization that is attenuated by gabapentin or sodium‐channel–blocking drugs []. Preventive and therapeutic strategies span antivirals, vaccination, corticosteroids, anticonvulsants, and antidepressants []. Gabapentin is widely used for PHN but has nonlinear pharmacokinetics, variable absorption, a short half‐life, and dose‐limiting adverse effects (e.g., dizziness and somnolence), challenges that are magnified in older adults with polypharmacy []. The erector spinae plane block (ESPB), first described in 2016, has quickly gained favor as a simple, versatile, ultrasound‐guided regional technique with a favorable safety profile across surgical, acute, and chronic pain indications []. By depositing local anesthetic deep to the erector spinae muscle at the transverse process, ESPB can spread to dorsal rami, ventral rami, and paravertebral spaces, potentially modulating both somatic afferents and segmental sympathetic fibers that may contribute to sympathetically maintained components of neuropathic pain through sympathetic–sensory coupling in the DRG []. For zoster‐related pain, ESPB has emerged as a minimally invasive option: case‐series and observational data suggested meaningful analgesia in refractory PHN [, , ], and in acute HZ, randomized data showed that ESPB with local anesthetic ± steroid improves pain and quality of life versus standard care []. Liposomal bupivacaine (LB; Exparel) provides extended release and is widely used perioperatively; however, its added value over conventional bupivacaine (CB) is context‐dependent. Some studies reported modest reductions in pain or opioid use (e.g., abdominal wall blocks and foot surgery) [, ], whereas broader syntheses across peripheral nerve blocks found trivial or no clinically meaningful superiority in pain, opioid consumption, or recovery endpoints [, ]. Given that PHN‐associated VZV strains increase Nav1.6/Nav1.7‐mediated sodium currents in sensory neurons‐molecular targets of amide local anesthetics‐prolonged perineural delivery of bupivacaine via a liposomal formulation may more effectively “silence” ectopic DRG firing and dampen early peripheral input during the critical early post‐block window, while entrenched central sensitization likely limits any durable benefit once drug levels wane [, ]. In PHN specifically, a randomized double‐blind trial demonstrated that ESPB with 0.25% CB reduced pain during the first week and lowered pregabalin/acetaminophen use through weeks 3–12 versus sham, supporting ESPB with bupivacaine as an effective strategy []. Although ESPB‐LB has seen growing clinical use (e.g., lower 0–48 h pain AUC but unchanged opioid in a matched cesarean cohort; favorable postoperative analgesia in a spinal cord stimulator series) [, ], rigorous comparative data in PHN are lacking.