One-year Patient-reported Outcomes After Arthroscopic Rotator Cuff Repair Do Not Correlate With Mild to Moderate Psychological Distress

Background

Patients with shoulder and rotator cuff pathology who exhibit greater levels of psychological distress report inferior preoperative self-assessments of pain and function. In several other areas of orthopaedics, higher levels of distress correlate with a higher likelihood of persistent pain and disability after recovery from surgery. To our knowledge, the relationship between psychological distress and outcomes after arthroscopic rotator cuff repair has not been similarly investigated.

Questions/purposes

(1) Are higher levels of preoperative psychological distress associated with differences in outcome scores (visual analog scale [VAS] for pain, Simple Shoulder Test, and American Shoulder and Elbow Surgeons score) 1 year after arthroscopic rotator cuff repair? (2) Are higher levels of preoperative psychological distress associated with less improvement in outcome scores (VAS for pain, Simple Shoulder Test, and American Shoulder and Elbow Surgeons score) 1 year after arthroscopic rotator cuff repair? (3) Does the prevalence of psychological distress in a population with full-thickness rotator cuff tears change when assessed preoperatively and 1 year after arthroscopic rotator cuff repair?

Methods

Eighty-five patients with full-thickness rotator cuff tears were prospectively enrolled; 70 patients (82%) were assessed at 1-year followup. During the study period, the three participating surgeons performed 269 rotator cuff repairs; in large part, the low overall rate of enrollment was related to two surgeons enrolling only two patients total in the initial 14 months of the study. Psychological distress was quantified using the Distress Risk Assessment Method questionnaire, and patients completed self-assessments including the VAS for pain, the Simple Shoulder Test, and the American Shoulder and Elbow Surgeons score preoperatively and 1 year after arthroscopic rotator cuff repair. Fifty of 85 patients (59%) had normal levels of distress, 26 of 85 (31%) had moderate levels of distress, and nine of 85 (11%) had severe levels of distress. Statistical models were used to assess the effect of psychological distress on patient self-assessment of shoulder pain and function at 1 year after surgery.

Results

With the numbers available, distressed patients were not different from nondistressed patients in terms of postoperative VAS for pain (1.9 [95% confidence interval {CI}, 1.0–2.8] versus 1.0 [95% CI, 0.5–1.4], p = 0.10), Simple Shoulder Test (9 [95% CI, 8.1–10.4] versus 11 [95% CI, 10.0–11.0], p = 0.06), or American Shoulder and Elbow Surgeons scores (80 [95% CI, 72–88] versus 88 [95% CI, 84–92], p = 0.08) 1 year after arthroscopic rotator cuff repair. With the numbers available, distressed patients also were not different from nondistressed patients in terms of the amount of improvement in scores between preoperative assessment and 1-year followup on the VAS for pain (3 [95% CI, 2.2–4.1] versus 2 [95% CI, 1.4–2.9], p = 0.10), Simple Shoulder Test (5.2 [95% CI, 3.7–6.6] versus 5.0 [95% CI, 4.2–5.8], p = 0.86), or American Shoulder and Elbow Surgeons scale (38 [95% CI, 29–47] versus 30 [95% CI, 25–36], p = 0.16). The prevalence of psychological distress in our patient population was lower at 1 year after surgery 14 of 70 (20%) versus 35 of 85 (41%) preoperatively (odds ratio, 0.36; 95% CI, 0.17–0.74; p = 0.005).

Conclusions

Mild to moderate levels of distress did not diminish patient-reported outcomes to a clinically important degree in this small series of patients with rotator cuff tears. This contrasts with reports from other areas of orthopaedic surgery and may be related to a more self-limited course of symptoms in patients with rotator cuff disease or possibly to a beneficial effect of rotator cuff repair on sleep quality or other unrecognized determinants of psychosocial status.

Level of Evidence

Level I, prognostic study.     

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Strontium fructose 1, 6‐diphosphate alleviate cyclophosphamide‐induced oligozoospermia by improving antioxidant and inhibiting testicular apoptosis via FAS/FASL pathway

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Unloading, neural lesions, and hormonal disorders after acute motor‐complete spinal cord injury (SCI) cause one of the most severe forms of bone loss, a condition that has been refractory to available interventions tested to date. Thus, these features related to acute SCI provide a unique opportunity to study complex bone problems, potential efficacious interventions, and mechanisms of action that are associated with these dramatic pathological changes. This study was designed to explore the therapeutic potential of sclerostin antibody (Scl‐Ab) in a rat model of bone loss after motor‐complete SCI, and to investigate mechanisms underlying bone loss and Scl‐Ab action. SCI rats were administered Scl‐Ab (25 mg/kg/week) or vehicle beginning 7 days after injury then weekly for 7 weeks. SCI resulted in significant decreases in bone mineral density (–25%) and trabecular bone volume (–67%) at the distal femur; Scl‐Ab completely prevented these deteriorations of bone in SCI rats, concurrent with markedly increased bone formation. Scanning electron microscopy revealed that SCI reduced numbers of osteocytes and dendrites concomitant with a morphology change from a spindle to round shape; Scl‐Ab corrected these abnormalities in osteocytes. In ex vivo cultures of bone marrow cells, Scl‐Ab inhibited osteoclastogenesis, and promoted osteoblastogenesis accompanied by increases in mRNA levels of LRP5, osteoprotegerin (OPG), and the OPG/RANKL ratio, and a decrease in DKK1 mRNA. Our findings provide the first evidence that robust bone loss after acute motor‐complete SCI can be blocked by Scl‐Ab, at least in part, through the preservation of osteocyte morphology and structure and related bone remodeling. Our findings support the inhibition of sclerostin as a promising approach to mitigate the striking bone loss that ensues after acute motor‐complete SCI, and perhaps other conditions associated with disuse osteoporosis as a consequence of neurological disorders. © 2015 American Society for Bone and Mineral Research     

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