A Single Institution 30-Year Review of Abnormal First Rib Resection for Thoracic Outlet Syndrome.

OBJECTIVES: Congenital abnormalities of the first rib (ABNFR) are a rare cause of thoracic outlet syndrome (TOS). The range of abnormalities have not been clearly documented in the literature. Surgical decompression in these patients presents with increased complexity secondary to anomalous anatomy. Our goal is to review an institutional experience of first rib resection (FRR) performed for ABNFRs, to present a novel classification system, and to analyze outcomes according to clinical presentation. METHODS: A prospectively collected database was used to identify individuals with ABNFRs who underwent FRR for TOS between 1990-2021. These individuals were identified both by preoperative imaging and intraoperative descriptions of the first rib after resection. Demographic, clinical, perioperative and pathological data were reviewed. ABNFRs were classified into 3 categories according to anatomical criteria: (I) Hypoplastic, (II) Fused, and (III) Hyperplastic. Outcomes were rated using the standardized Quick Disability of Arm Shoulder and Hand Scores (QDS), Somatic Pain Scores (SPS) and Derkash Scores (DkS). RESULTS: Among the 2200 cases of TOS, there were 19 patients (0.8%) with ABNFR who underwent FRR. Average age at surgery was 30.5 (range 11-74), including 13 men and 6 women. Presentations included 9 arterial (ATOS), 6 neurogenic (NTOS), and 4 venous (VTOS) cases. There were 6 class I, 6 class II, and 7 class III ABNFRs. Among 6 NTOS patients there were 4 abnormal nerve conduction tests and 5 positive anterior scalene muscle blocks. Among the 9 patients with ATOS, thrombolysis was attempted in 5 patients, and of these, 3 ultimately required surgical thrombectomy. Of 4 VTOS cases, 2 were managed with thrombolysis, and 2 with anticoagulation alone. The approach for FRR was transaxillary in all patients. Secondary procedures included 1 pectoralis minor tenotomy, 1 scalenectomy, and 1 contralateral rib resection. No major neurological or vascular complications occurred. There was 1 patient who required surgical evacuation of a hematoma. Intraoperative chest tube placement was required in 5 patients secondary to pleural entry during dissection. There was an overall improvement in symptoms over an average follow-up of 7.4 months. QDS reduced from 49.7 pre-op to 22.1 (P < 0.05). SPS improved from 3.4 pre-op to 1.8. DkS scores were good to excellent in 79% of patients. Residual symptoms were noted in 7, and ATOS accounted for 5 (70%) of these. All patients were able to return to work. CONCLUSIONS: Despite increased complexity, ABNFRs may be safely resected via transaxillary approach with low incidence of complications, very good symptom relief, and excellent outcomes. Congenital ABNFRs may by classified into 3 categories (hypoplastic, fused, and hyperplastic) with a variety of presentations, including ATOS, NTOS, and VTOS. Classification of ABNFRs allows concise description of abnormal anatomy which facilitates comparison between series and provides direction for surgical management to ultimately optimize patient outcomes.

The natural history of type 2 endoleaks after endovascular aneurysm repair justifies conservative management.

Objective Management of type 2 endoleaks after endovascular aneurysm repair has been controversial. Some advocate for conservative management, while others believe that intervention is indicated. This study investigated the natural history of type 2 endoleaks in order to derive direction in management. Methods Patients who had endovascular aneurysm repair at the Veterans Affairs Long Beach were retrospectively identified and computerized tomographic angiography was independently reviewed by a radiologist and a vascular surgeon. Type 2 endoleaks were analyzed for the following outcomes: rupture, duration of endoleak, spontaneous resolution, changes in the size of the aneurysm sac, and reintervention rates. Results Of the 160 patients who had completed required follow-up to date (mean 3 years) after endovascular aneurysm repair, 39 (24.4%) patients were identified as having a type 2 endoleak on computerized tomographic angiography imaging. 6 (15.4%) of these 39 patients required repair due to aneurysm sac growth >1 cm. 2 (5.13%) were repaired with an open procedure and 4 (10.3%) with an endovascular approach. Of these 6 aneurysm leaks requiring repair, 4 (66.7%) had a simultaneous endoleak (types 1 or 3) in addition to the identified type 2 endoleak. Spontaneous resolution of type 2 endoleaks occurred in 16 (41.0%) patients. 4 patients (10.3%) had delayed type 2 endoleaks that presented 4, 9, 12, and 23 months after their 30 day post op computed tomography was normal. None of the 4 patients with delayed type 2 endoleaks required reintervention and none had aneurysm sac growth greater than 5 mm. Conclusions Overall, we found that 85% of patients who had type 2 endoleaks did not require intervention after a mean follow-up time of 3 years. The association of a type 1 or 3 endoleak with a type 2 endoleak was more likely to require correction due to aneurysm expansion >1 cm, thus type 2 endoleaks associated with another type of endoleak require more aggressive management.

High resolution x-ray: a reliable approach for quantifying osteoporosis in a rodent model.

Osteoporosis is the most common metabolic disease of bone, resulting in significant worldwide morbidity. Currently, there are insufficient imaging modalities available to evaluate osteoporotic bones in small animal models. Here, we demonstrate the feasibility of using high resolution X-ray imaging as a comparable measure of bone degeneration to dual-energy X-ray absorptiometry (DXA) in an osteoporosis rodent model. At week 0, animals underwent either an ovariectomy (OVX) or sham procedure (SHAM). DXA analysis was performed weekly to confirm and compare the bone degenerative changes induced by OVX. A comparison using high resolution X-ray imaging (Faxitron(®)) was then performed postmortem due to need of soft tissue removal. Two regions of interest (ROIs) were utilized: the distal third of the femur and the lumbar spine (L4/L5). It was observed that SHAM animals maintained a relatively constant bone mineral density (BMD), in comparison to OVX animals, whereby a significant decrease in BMD was appreciated. Post mortem X-ray scans were performed and converted to 8-bit color and quantified. A high level of agreement with DXA quantifications was observed with X-ray quantifications, and a significant correlation between the radiopacity, visualized by color distributions, and the DXA BMD values between animal groups was evident. Our study demonstrates the applicability of high resolution X-ray imaging both qualitatively and quantitatively as a reliable approach for quantifying osteoporosis in rodent osteoporotic models. With DXA being a highly user dependent modality, our technique is a unique secondary methodology to verify DXA findings and minimize inter-observer variability.

Interleukin-22: implications for liver ischemia-reperfusion injury.

BACKGROUND: Ischemia-reperfusion injury (IRI) is common in general surgery and organ transplantation, and in the case of liver, it triggers proinflammatory innate immune cascade and hepatic necrosis, leading to increased incidence of early and late organ rejection. Interleukin (IL)-22, an inducible cytokine of T-cell origin and a member of the IL-10 superfamily, acts on target tissues through IL-22 receptor (IL-22R1). METHODS: Partial hepatic warm ischemia was induced in C57Bl/6 wild-type (WT) and type 1 interferon receptor-deficient (KO) mice for 90 min followed by 6 to 24 hr of reperfusion. WT mice were treated at 30 min before the ischemia insult with recombinant IL-22 or anti-IL-22 neutralizing antibody; phosphate-buffered saline and IgG served as respective controls. RESULTS: IL-22 was detected at 24 hr but not 6 hr of liver IRI. The expression of IL-22R1 was increased by 6 hr of reperfusion in WT but not type 1 interferon receptor KO mice that were protected from IRI. Treatment of WT mice with recombinant IL-22 decreased serum aspartate aminotransferase levels, ameliorated cardinal histological features of IR damage (Suzuki's score) and diminished leukocyte sequestration, along with the expression of IL-22R1 and pro-inflammatory cytokines. IL-22 antibody did not appreciably affect IRI but increased IL-22R1 transcription in the liver. Administration of IL-22 protein exerted hepatoprotection by STAT3 activation. CONCLUSIONS: This is the first report investigating immune modulation by T-cell-derived IL-22 in liver injury caused by warm ischemia and reperfusion. Treatment with IL-22 protein may represent a novel therapeutic strategy to prevent liver IRI in transplant recipients.