Do Patients Accurately Recall Pain Levels Following Sacroiliac Joint Steroid Injection? A Cohort Study of Recall Bias in Patient-reported Outcomes.

BACKGROUND: Sacroiliac joint (SIJ) injections are crucial in the diagnostic toolkit for evaluating SIJ pathology. Recall bias is an important component in patient-reported outcomes that has not been well studied in SIJ injection. OBJECTIVE: The purpose of this study was to characterize the accuracy, direction, and magnitude of pain level recall bias following SIJ steroid injection and study the factors that affect patient recollection. STUDY DESIGN: Prospective cohort study. SETTING: Level 1 academic medical center. METHODS: Using standardized questionnaires, baseline Numeric Rating Scale (NRS-11) scores were recorded for patients undergoing SIJ steroid injections at preinjection, at 4 hours postinjection, and at 24 hours postinjection. At a minimum of 2 weeks postinjection, patients were asked to recall their preinjection, 4-hour, and 24-hour postinjection NRS-11 scores. Actual and recalled NRS-11 scores were compared using paired t tests for each time interval. Multivariable linear regression was used to identify factors that correlated with consistent recall. RESULTS: Sixty patients with a mean age of 66 years (65% women) were included. Compared to their preinjection pain score, patients showed considerable improvement at both 4 hours (mean difference [MD] = 3.28; 95% CI, 2.68 - 3.89), and 24 hours (MD = 3.23; 95% CI, 2.44 - 4.03) postinjection. Patient recollection of preinjection symptoms was more severe than actual (MD = 0.65; 95% CI, 0.31 - 0.99). Patient recollection of symptoms was also more severe than actual at 4 hours (MD = 0.50; 95% CI .04 - 1.04) as well as at 24 hours postinjection (MD = 0.80; 95% CI, 0.16 - 1.44). The magnitude of recall bias was mild and did not exceed the minimal clinically important difference. There was a moderate correlation between actual and recalled pain levels when comparing preinjection with the 4-hour postinjection NRS-11 score (correlation coefficient [r] =0.64; P < 0.001) and moderate correlation when comparing preinjection with the 24-hour postinjection NRS-11 score (r = 0.62; P < 0.001). Linear regression models showed that at preinjection, patients with a lower body mass index and the presence of coexisting psychiatric diagnoses were better at recalling their pain (P < 0.05). Patients with a higher body mass index also experienced less pain relief when comparing preinjection with the 4-hour postinjection NRS-11 score (P < 0.05). LIMITATIONS: Recall pain scores were obtained via telephone surveys, which can lead to interview bias. One patient died, and 3 were lost to follow-up. We did not control for patient use of adjunctive pain relief modalities, which may modulate the overall response to injection. SIJ injections can also be diagnostic, so some patients may not have shared the same indication for injection or pain-generating diagnosis. CONCLUSIONS: Patients had favorable pain level responses to their SIJ steroid injection for both actual and recall surveys. Although patients demonstrated poor recall of absolute pain scores at preinjection, 4-hour postinjection, and 24-hour postinjection, they demonstrated robust recall of their net pain score improvement at both 4- and 24-hours postinjection. These findings suggest that there is utility in using patient recollection to describe the magnitude of pain relief following treatment for sacroiliac joint dysfunction.

Learning curve associated with minimally invasive surgery for hallux valgus: A systematic review.

BACKGROUND: The purpose of this systematic review is to examine the learning curve associated with minimally invasive surgery (MIS) for the treatment of hallux valgus (HV). METHODS: A systematic review was performed using PubMed, ScienceDirect, Web of Science, CINAHL and MEDLINE databases from database inception to February 16th, 2023. Inclusion criteria was articles with level of evidence I-III, any outcomes associated with learning curve, minimally invasive surgery, and diagnosis of hallux valgus' in adult patients. RESULTS: Six articles out of 165 articles meet inclusion criteria. For all six articles, 368 total patients (422 total feet) were included in the study with an average age of 55.69 years. Three studies reported the number of surgeries needed to reach the plateau phase of the learning curve of MIS for HV, with a frequency weighted mean of 35.5 surgeries (range 27 - 40). In the selected articles, significant results were found for increased operating room (OR) time and fluoroscopy shots in the learning phase. There was no significant increase in complications in the learning phase. There was no significant decrease in patient outcomes, or the quality of correction performed during the learning phase. CONCLUSION: An average of 35.5 surgeries (range 27 - 40) are needed to reach the plateau phase for MIS for HV. The learning phase of the learning curve of MIS for HV has a significant increase in OR time and fluoroscopy usage. However, the learning phase of the learning curve of MIS for HV is not associated with decreased outcomes or higher complication rates based on the small sample size in this study. LEVEL OF EVIDENCE: Level III, Systematic Review.

Compartment Syndrome After Tibial Intramedullary Nail Removal and Intramedullary Debridement: A Case Report.

CASE: A 45-year-old man who sustained an open tibial shaft fracture treated with intramedullary (IM) nailing 9 years earlier presented with persistent pain and concern for occult infection. He underwent tibial nail removal and debridement with reamer-irrigator-aspirator. Postoperative course was complicated by acute compartment syndrome. CONCLUSION: This is a unique case of postoperative compartment syndrome after IM debridement and tibial hardware removal. A high index of suspicion should be prioritized in patients who complain of severe or unexpected pain to mitigate delays in diagnosis and aid in early treatment.

Culturing explants for Cutibacterium at revision shoulder arthroplasty: an analysis of explant and tissue samples at corresponding anatomic sites.

BACKGROUND: Culturing of deep tissues obtained at revision arthroplasty for Cutibacterium is a key component of diagnosing a periprosthetic infection. The value of culturing explanted components has not been well described. This study sought to answer the following questions: (1) How does the culture positivity of explant cultures compare with that of deep tissue cultures? (2) How often are explant cultures positive when tissue cultures are not, and vice versa? (3) How does the bacterial density in explant cultures compare with that in tissue cultures? METHODS: A total of 106 anatomic arthroplasties revised over a 7-year period were included. Explant (humeral head, humeral stem, and glenoid) and tissue (collar membrane, humeral canal tissue, and periglenoid tissue) specimens were sent for semiquantitative Cutibacterium culture. We compared culture positivity and bacterial density when cultures of an explant and tissue adjacent to the implant were both available. RESULTS: Explants had positive cultures at a higher rate than adjacent tissue specimens for most anatomic sites. Of the shoulders that had Cutibacterium growth, a higher proportion of explants were culture positive when tissue samples were negative (23%-43%) than vice versa (0%-21%). The Cutibacterium density was higher in explants than in tissues. Considering only the results of tissue samples, 16% of the shoulders met our threshold for infection treatment (≥2 positive cultures); however, with the inclusion of the results for explant cultures, additional 14% of cases-a total of 30%-met the criteria for infection treatment. CONCLUSIONS: In this group of patients, culturing explants in addition to tissue cultures increased the sensitivity for detecting Cutibacterium in revision shoulder arthroplasty.

Microglial depletion abolishes ischemic preconditioning in white matter.

Ischemic preconditioning (IPC) is a phenomenon whereby a brief, non-injurious ischemic exposure enhances tolerance to a subsequent ischemic challenge. The mechanism of IPC has mainly been studied in rodent stroke models where gray matter (GM) constitutes about 85% of the cerebrum. In humans, white matter (WM) is 50% of cerebral volume and is a critical component of stroke damage. We developed a novel CNS WM IPC model using the mouse optic nerve (MON) and identified the involved immune signaling pathways. Here we tested the hypothesis that microglia are necessary for WM IPC. Microglia were depleted by treatment with the colony stimulating factor 1 receptor (CSF1R) inhibitor PLX5622. MONs were exposed to transient ischemia in vivo, acutely isolated 72 h later, and subjected to oxygen-glucose deprivation (OGD) to simulate a severe ischemic injury (i.e., stroke). Functional and structural axonal recovery was assessed by recording compound action potentials (CAPs) and by microscopy using quantitative stereology. Microglia depletion eliminated IPC-mediated protection. In control mice, CAP recovery was improved in preconditioned MONs compared with non-preconditioned MONs, however, in PLX5622-treated mice, we observed no difference in CAP recovery between preconditioned and non-preconditioned MONs. Microgliadepletion also abolished IPC protective effects on axonal integrity and survival of mature (APC+ ) oligodendrocytes after OGD. IPC-mediated protection was independent of retinal injury suggesting it results from mechanistic processes intrinsic to ischemia-exposed WM. We conclude that preconditioned microglia are critical for IPC in WM. The "preconditioned microglia" phenotype might protect against other CNS pathologies and is a neurotherapeutic horizon worth exploring.

Ischemic Preconditioning in White Matter: Magnitude and Mechanism.

Ischemic preconditioning (IPC) is a robust neuroprotective phenomenon whereby brief ischemic exposure confers tolerance to a subsequent ischemic challenge. IPC has not been studied selectively in CNS white matter (WM), although stroke frequently involves WM. We determined whether IPC is present in WM and, if so, its mechanism. We delivered a brief in vivo preconditioning ischemic insult (unilateral common carotid artery ligation) to 12- to 14-week-old mice and determined WM ischemic vulnerability [oxygen-glucose deprivation (OGD)] 72 h later, using acutely isolated optic nerves (CNS WM tracts) from the preconditioned (ipsilateral) and control (contralateral) hemispheres. Functional and structural recovery was assessed by quantitative measurement of compound action potentials (CAPs) and immunofluorescent microscopy. Preconditioned mouse optic nerves (MONs) showed better functional recovery after OGD than the non-preconditioned MONs (31 ± 3 vs 17 ± 3% normalized CAP area, p < 0.01). Preconditioned MONs also showed improved axon integrity and reduced oligodendrocyte injury compared with non-preconditioned MONs. Toll-like receptor-4 (TLR4) and type 1 interferon receptor (IFNAR1), key receptors in innate immune response, are implicated in gray matter preconditioning. Strikingly, IPC-mediated WM protection was abolished in both TLR4(-/-) and IFNAR1(-/-) mice. In addition, IPC-mediated protection in WM was also abolished in IFNAR1(fl/fl) LysM(cre), but not in IFNAR1(fl/fl) control, mice. These findings demonstrated for the first time that IPC was robust in WM, the phenomenon being intrinsic to WM itself. Furthermore, WM IPC was dependent on innate immune cell signaling pathways. Finally, these data demonstrated that microglial-specific expression of IFNAR1 plays an indispensable role in WM IPC. SIGNIFICANCE STATEMENT: Ischemic preconditioning (IPC) has been studied predominantly in gray matter, but stroke in humans frequently involves white matter (WM) as well. Here we describe a novel, combined in vivo/ex vivo mouse model to determine whether IPC occurs in WM. It does. Using genetically altered mice, we identified two innate immune cell receptors, Toll-like receptor 4 and type 1 interferon receptor (IFNAR1), that are required for IPC-mediated protection in WM. Furthermore, using microglia-targeted IFNAR1 knockdown, we demonstrate that interferon signaling specifically in microglia is essential for this protection. The discovery of IPC as an intrinsic capability of WM is novel and important. This is also the first in vivo demonstration that cell-type-specific expression of an individual gene plays an indispensable role in IPC-mediated protection.