Intraoperative Hypertension Following Tourniquet Inflation in a Rheumatoid Arthritis PatientClinical ContextA 62-year-old female with rheumatoid arthritis (RA), weighing 65 kg and off disease-modifying medications for one year, underwent the following procedures for avascular necrosis of the talus with ankle subluxation, subtalar involvement, and cavus deformity:
- Tibiotalocalcaneal nailing
- Tibialis posterior release
- Peroneus longus to brevis tendon transfer
- First metatarsal closing wedge osteotomy
The total surgical duration was 3 hours, with a tourniquet applied for 75 minutes.
Intraoperative Anesthesia SummaryInduction was achieved with fentanyl 200 micrograms, propofol 150 mg, and atracurium 40 mg. Maintenance was likely with sevoflurane at MAC 1.2, and the BIS remained between 40 and 48 throughout the procedure. Neuromuscular blockade was maintained with an atracurium infusion of 10 mg/hr.
Adjuncts included dexamethasone 8 mg, dexmedetomidine 30 micrograms, magnesium sulfate 1 g, paracetamol 1 g, and diclofenac 100 mg (suppository). At the end of the case, morphine 5 mg intramuscularly was administered, and neuromuscular reversal was given more than 25 minutes after the last atracurium dose.
The tourniquet was inflated to 300 mmHg, with a baseline blood pressure of 110/70 mmHg. During tourniquet time, blood pressure rose to greater than 180/100 mmHg and returned to baseline immediately after deflation.
Pathophysiologic InsightsTourniquet-Induced HypertensionTourniquet-induced hypertension (TIH) is a well-recognised phenomenon, attributed to central sensitisation driven by ischemic nociceptive input from the tourniqueted limb. Even with adequate anesthetic depth, nociceptive afferents below the cuff continue to discharge, activating the spinal cord and sympathetic outflow.
C-fibres release glutamate, substance P, and CGRP at the dorsal horn, leading to NMDA receptor upregulation and a “wind-up” phenomenon. Activation of spinoreticular and spinothalamic tracts amplifies sympathetic activity, increasing systemic vascular resistance and blood pressure.
On a molecular level, glutamate activates NMDA receptors, increasing intracellular calcium. This in turn activates protein kinase C and nitric oxide synthase, propagating central sensitisation. In this patient, dexmedetomidine and magnesium, both modulators of NMDA-mediated pathways, were administered and likely attenuated but did not abolish the hypertensive response.
A key clinical clue is that hypertensive surges resolve rapidly upon tourniquet deflation, as observed here.
Management strategies include NMDA antagonists such as ketamine, alpha-2 agonists such as dexmedetomidine, magnesium sulfate, regional nerve blocks to interrupt afferent transmission, and minimising tourniquet time and pressure.
References
Estebe JP, Davies JM, Richebe P. The pneumatic tourniquet: mechanical, ischemia-reperfusion and systemic effects. Eur J Anaesthesiol. 2011;28(6):404–11.
Rivat C, Richebé P, et al. Pain and anesthesia-induced plasticity of sensory and nociceptive pathways. Prog Brain Res. 2009;175:275–91.
Opioid Insufficiency and Inadequate AnalgesiaIn patients with chronic pain syndromes such as rheumatoid arthritis or longstanding deformities, persistent nociceptive input can drive sympathetic surges even under general anesthesia. In this case, after the initial induction bolus, no continuous opioid infusion such as remifentanil was used. Although the BIS reflected adequate unconsciousness, nociception proceeded unchecked.
At the dorsal horn, glutamate and substance P from C and Aδ fibres activated neurons, but without sustained mu-opioid receptor activation, ascending signals were insufficiently suppressed. This mismatch...