Risk factors for revision surgery in operative treatment of traumatic injuries of the olecranon and prepatellar bursa.

INTRODUCTION: Traumatic lacerations of the prepatellar (PB) and olecranon bursa (OB) are common injuries. The aim of this study was to gain descriptive data and to identify risk factors associated with complications that made revision surgery after primary bursectomy necessary. MATERIAL AND METHODS: In this retrospective monocentric study at a level I trauma center, all patients with traumatic lacerations of the PB or OB who were treated with primary surgical bursectomy from 2015 to 2020 were analyzed. RESULTS: 150 consecutive patients were included. In 44% of cases, the PB was affected (n = 66), in 56% the OB (n = 84). The reoperation rate after surgical bursectomy was 10.7% (n = 16). The main cause of reoperation was wound infection (50%; n = 8). The most common pathogen of postoperative infections was Staphylococcus aureus (87.5%). Several comorbidities have been identified as risk factors for reoperation after primary surgical bursectomy, such as heart diseases, arterial hypertension, the use of antihypertensives and anticoagulation. In contrast, surgical expertise, use of drains, postoperative immobilization, and postoperative antibiotics had no statistically significant effect. A significantly higher postoperative infection rate (17.6%) was observed in patients who were operated more than 48 h after initial trauma. CONCLUSIONS: Given the limited recommendations for therapy of these common injuries, further investigations should focus on standardized therapeutic options for lacerations of the PB or OB. Delayed surgical interventions after trauma were associated with higher complication rates. Therefore, urgent surgery within 48 h after trauma may help to prevent revisions. LEVEL OF EVIDENCE: Level of evidence IV.

[Challenges of primary hip arthroplasty with high hip dislocation]. / Herausforderungen der primären Hüftendoprothetik bei hoher Hüftluxation.

BACKGROUND: Endoprosthetic care of high hip dislocation is a surgical challenge. The hip anatomy is greatly altered in these patients, including a rather flat and small acetabulum with impaired bone quality and a relevant chance of a bony defect of the acetabular roof. Additionally, the front coverage and in some cases even the dorsal coverage of the hip are missing. The proximal femur is characterized with an increased antetorsion, a coxa valga position and an enlarged greater trochanter. The medullary cavity is narrowed, the offset is reduced, and the absolut leg length can be enlarged. Further anatomic variations can have been caused by previous surgeries. AIM OF THE TREATMENT: The goal of the endoprosthetic care is the re-creation of a hip with an anatomic center of rotation, an anatomic offset and equal leg length. TREATMENT: This can be achieved by a medial shift of the acetabular cup. An acetabular osteotomy including central cancellous bone graft or a bony graft to reinforce the acetabular roof might be necessary. In cases in which an anatomic acetabular cup placement is not possible, a more cranial placement can be done. Further strategies that are essential in several cases are shortening or re-orientation osteotomies of the femur, reaming of the medullary cavity and correct implant selection. Additionally, thorough soft tissue management is of main importance. Generally, the surgery should be well prepared preoperatively.

Reversibility of preglomerular active vasoconstriction in the first weeks after complete unilateral ureteral obstruction by inhibition of prostaglandin synthesis.

In previous studies our group has shown that unilateral complete ureteral ligation is followed by flow reduction, which clearly precedes renal atrophy and contributes to hydronephrotic renal cortical damage by ischemia. Long-term followup studies in dogs have demonstrated that increased hydronephrotic vascular resistance could be eliminated by infusion of 2-benzyl-2-imidazole, an inhibitor of thromboxane A2 synthesis. This was shown after 1 and 4 weeks of complete renal obstruction, and there was no such effect on the vascular resistance of the contralateral, unobstructed kidney. Flow reduction and vascular resistance were not influenced by the same inhibition of prostaglandin synthesis after 8 weeks of ureteral occlusion, although renal perfusion still responded to a nonspecific vasodilator, such as dopamine. Thus, active preglomerular vasoconstriction, influenced by imidazole, is present only when renal atrophy develops. Irreversible parenchymal loss, judged by renal cortical thickness, begins after 1 to 2 weeks and is complete 6 to 8 weeks after ureteral ligation. Once renal atrophy is established (that is, after 8 weeks of ureteral occlusion), flow reduction represents loss of renal parenchyma, and not active vasoconstriction. The specificity of the possible thromboxane A2 reaction in flow reduction is shown by its absence in the kidney that has been obstructed for 5 to 8 hours when postglomerular vasoconstriction is the cause of flow reduction (indicated by high renal pelvic pressure and intrarenal pressure). If we accept that imidazole selectively inhibits thromboxane A2 synthesis, we reach 2 conclusions that are clinically relevant: 1) thromboxane A2-mediated active vasoconstriction is 1 factor in the pathophysiology of hydronephrotic atrophy, and 2) the presence of thromboxane A2-mediated active vasoconstriction indicates when hydronephrotic atrophy develops and (more importantly) when it is still reversible, with respect to renal function. These findings can be used as a physiologic basis of a clinical test to predict reversibility of hydronephrotic damage.