Chronic Pain After Lung Resection: Risk Factors, Neuropathic Pain, and Quality of Life.

CONTEXT: Chronic postsurgical pain (CPSP) can occur frequently after thoracic surgery. OBJECTIVES: This retrospective study aimed to determine CPSP prevalence, risk factors, neuropathic pain (NP) occurrence, and its impact on quality of life. METHODS: About 200 patients who underwent lung resection via minithoracotomy or thoracoscopy between January 2017 and December 2017 were assessed 4-12 months postoperatively via phone interview for chronic pain by a 0-10 Numeric Rating Scale, for NP using the Douleur Neuropathique 4 test, and for quality of life using a Short Form-36 (SF-36) Health Survey (Italian version). RESULTS: CPSP incidence was 35% (n = 70 of 200; 95% CI 41-28) of which 31.5% (n = 22 of 70; 95% CI 41-21) was with NP. Only 10% of patients with CPSP reported severe chronic pain. According to univariate analysis, CPSP was associated to moderate and severe acute postoperative pain (P < 0.001), open surgery (P = 0.001), and female gender (P = 0.044). According to multivariable analysis, independent risk factors for CPSP development included moderate-to-severe acute postoperative pain occurrence (odds ratio 32.61; 95% CI 13.37-79.54; P < 0.001) and open surgery (odds ratio 6.78; 95% CI, 2.18-21.03; P = 0.001). NP incidence was higher in female patients (16% in women and 6% in men, respectively; P = 0.040). A significant decrease in all SF-36 Health Survey domain scores was recorded for patients with CPSP and NP (P < 0.001). CONCLUSION: More than one of three patients who underwent lung resection could develop CPSP, frequently showing neuropathic component. Female gender reported a higher CPSP and NP incidence. Moderate-to-severe acute postoperative pain occurrence and open surgery seem to be independent risk factors for CPSP. Chronic pain and NP have a negative impact on quality of life, decreasing the SF-36 scores of all domains.

Low-dose buprenorphine infusion to prevent postoperative hyperalgesia in patients undergoing major lung surgery and remifentanil infusion: a double-blind, randomized, active-controlled trial.

BACKGROUND: Postoperative secondary hyperalgesia arises from central sensitization due to pain pathways facilitation and/or acute opioid exposure. The latter is also known as opioid-induced hyperalgesia (OIH). Remifentanil, a potent µ-opioid agonist, reportedly induces postoperative hyperalgesia and increases postoperative pain scores and opioid consumption. The pathophysiology underlying secondary hyperalgesia involves N-methyl-D-aspartate (NMDA)-mediated pain pathways. In this study, we investigated whether perioperatively infusing low-dose buprenorphine, an opioid with anti-NMDA activity, in patients receiving remifentanil infusion prevents postoperative secondary hyperalgesia. METHODS: Sixty-four patients, undergoing remifentanil infusion during general anaesthesia and major lung surgery, were randomly assigned to receive either buprenorphine i.v. infusion (25 µg h-1 for 24 h) or morphine (equianalgesic dose) perioperatively. The presence and extent of punctuate hyperalgesia were assessed one day postoperatively. Secondary outcome variables included postoperative pain scores, opioid consumption and postoperative neuropathic pain assessed one and three months postoperatively. RESULTS: A distinct area of hyperalgesia or allodynia around the surgical incision was found in more patients in the control group than in the treated group. Mean time from extubation to first morphine rescue dose was twice as long in the buprenorphine-treated group than in the morphine-treated group: 18 vs 9 min (P=0.002). At 30 min postoperatively, patients receiving morphine had a higher hazard ratio for the first analgesic rescue dose than those treated with buprenorphine (P=0.009). At three months, no differences between groups were noted. CONCLUSIONS: Low-dose buprenorphine infusion prevents the development of secondary hyperalgesia around the surgical incision but shows no long-term efficacy at three months follow-up.

Propofol sedation reduces diaphragm activity in spontaneously breathing patients: ultrasound assessment.

BACKGROUND: The diaphragm is the most important respiratory muscle in humans, and the close relationship between inspired volume and diaphragmatic movement in normal subjects has led to investigations into diaphragmatic activity using ultrasound, during spontaneous breathing and sedative drug infusion. METHODS: A total of 36 consecutive patients undergoing diagnostic procedures under deep propofol sedation were studied. Ultrasound measurements included the following: diaphragmatic thickening end-inspiration (TEI) and end-expiration (TEE). Diaphragmatic thickening fraction (DTF) was calculated from [(TEI - TEE) / TEE] at various time points (at T0 basal; at T1 during propofol infusion; at T2 awakening). Oxygen was administered at 4 L/min, and oxygen saturation (SpO2), end tidal CO2 (EtCO2) and respiratory rate (RR) were recorded. RESULTS: TEI, and TEE decreased by 26.7% and 17.4%, respectively, during propofol infusion (T0 versus T1) (P<0.001), and rapidly recovered at T2 (22.7% and 15.8%). At procedure end (T0 versus T2), TEI maintained a significant reduction (10%, P<0.001), whereas TEE recovered completely. DTF decreased by 56.7% at T1 (P<0.001) but increased by 76.9% (P=0.001) at T2. Recovery after awakening (T0 versus T2) did not reach the baseline value, with a 23.4% difference (P<0.001). SpO2 remained above 96% and EtCO2 below 43 mmHg with no desaturation episodes observed. CONCLUSIONS: Our study showed that deep propofol sedation affects muscle activity in healthy patients. While diaphragmatic strength decreased during sedation, there was no clinically relevant effect on SpO2. The study also confirmed that ultrasound is suitable for measuring diaphragm activity during a normal clinical procedure.

Effects of passive leg raising on microvascular venous compartment in critically ill patients.

BACKGROUND: Even though fluid loading is thought to improve organ perfusion, the way in which it does so remains unclear. We assessed how the microvascular bed in skeletal muscle reacts to passive leg raising in patients with and without sepsis or septic shock. METHODS: We studied 40 critically ill patients (group A) and 30 healthy controls (group B). The forearm microvascular bed was assessed using near-infrared spectroscopy before and after passive leg raising. We measured stressed and unstressed volumes, inside pressures, blood flow, microvascular compliance and tone. RESULTS: In group A, passive leg raising induced a microvascular bed increase from 4.9 (3.2-6.5) mL/100 mL tissue to 5.7 (3.9-8.1) mL/100 mL tissue (P=0.005), leaving inside pressures unchanged, whereas in group B neither volumes nor pressures changed. Patients without sepsis showed an increase in the stressed volume from 0.22 (0.10-0.28) mL/100 mL tissue to 0.34 (0.23-0.66) mL/100 mL tissue (P=0.039) and a decrease in compliance (P=0.004), whereas, in septic shock, the unstressed volume increased from 4.20 (3.01-5.82) mL/100 mL tissue to 5.32 (4.01-11.50) mL/100 mL tissue (P=0.036). In critically ill patients near-infrared spectroscopy showed no difference in microvascular variables between responders and non-responders to passive leg raising, but responders showed a cardiovascular response shorter than healthy subjects. CONCLUSIONS: Our study provides evidence that macrocirculatory parameters are unreliable to derive measurements of stressed and unstressed volumes. Our results indicate that in septic shock, the enlargement of the unstressed volume associated with passive leg raising induces loss of fluids to the interstitium, thus leaving organ perfusion unchanged or worse.