Complications in total shoulder and reverse total shoulder arthroplasty by body mass index.

INTRODUCTION: The purpose of this study was to identify the effects of body mass index (BMI) on long-term outcomes (revision rate, 1-year mortality rate, 3-year surgical site infection rate, and 90-day inpatient all-cause readmission rate) after total shoulder arthroplasty (TSA) and reverse TSA (RTSA). METHODS: A large shoulder arthroplasty registry was used to review outcomes after TSA and RTSA. The registry monitors patient's revision, mortality, infection, and readmission rates. The exposure of interest was the patient's BMI at the time of the surgery, which was stratified by 5 kg/m2 increments. RESULTS: Selected for this study were 4630 patients who underwent TSA and RTSA between 2007 and 2013, of which 3483 (75.2%) were TSA and 1147 (24.8%) were RTSA. The overall combined (TSA and RTSA) revision rate was 1.7%. After adjusting for confounders in the overall models (TSA and RTSA combined), higher BMI was not associated with higher risk of aseptic revision, 1-year mortality, or 3-year deep infection. In TSA-specific models, every 5 kg/m2 increase in BMI was marginally associated with a 16% increase in the likelihood of 90-day readmission. This association was not observed in the RTSA model. In RTSA-specific models, every 5 kg/m2 increase in BMI was marginally associated with higher risk of 3-year deep infection. This association was not observed in the TSA model. CONCLUSION: Shoulder arthroplasty in obese patients is not associated with higher risk of aseptic revision. The BMI has different effects on TSA and RSA. The surgeon should anticipate increased risk of readmission after TSA and infection after RSA.

Computed Tomography Assessment of Peroneal Tendon Displacement and Posteromedial Structure Entrapment in Pilon Fractures.

OBJECTIVES: To determine the proportion of (1) peroneal tendon displacement (PTD) and posteromedial structure entrapment (PMSE) cases in a sample of pilon fractures, (2) missed diagnoses of PTD and PMSE on computed tomography (CT) by radiologists and attending orthopaedic trauma surgeons, and PTD and PMSE cases by (3) OTA/AO classification, and (4) fibular fracture. DESIGN: Retrospective cohort review. SETTING: Regional level 1 Trauma Center. PATIENTS/PARTICIPANTS: Two hundred patients treated between July 2008 and November 2014. INTERVENTION: Axial and reconstructed CT images were used in bone and soft tissue windows to identify PTD and PMSE. MAIN OUTCOME MEASUREMENTS: Medical charts were reviewed to identify OTA/AO fracture classification, the presence of concomitant fibular fracture, whether radiologist CT interpretation noted PTD or PMSE, and whether attending orthopaedic trauma surgeons' operative notes mentioned recognition of and management of PTD or PMSE. RESULTS: From the retrospective review of CT, PTD was identified in 11.0% and PMSE in 19.0% of all pilon fractures. Of the 22 patients with PTD, 59.1% sustained a concomitant fibular fracture and 90.9% sustained a 43-C fracture. Patients with PTD sustained more 43-C fractures (90.9% vs. 62.9%) but significantly fewer fibular fractures (59.1% vs. 80.3%; P = 0.023) than patients without PTD. Of the 38 patients with PMSE, 81.6% sustained a fibular fracture and 86.8% sustained a 43-C fracture. PMSE was more common in patients with 43-C fractures (86.8% vs. 61.1%). The final preoperative radiologist CT interpretation commented on PTD and PMSE in 50.0% of cases. CONCLUSIONS: Higher energy pilon fractures (43-C) are associated with higher incidence of PMSE and PTD. Concomitant fibula fracture may play a protective role in PTD in the setting of pilon fractures. Both attending radiologists and attending orthopaedic trauma surgeons frequently fail to recognize the diagnoses of PTD and PMSE. LEVEL OF EVIDENCE: Prognostic level III. See Instructions for Authors for a complete description of levels of evidence.

Analysis of responses to the Rho-kinase inhibitor Y-27632 in the pulmonary and systemic vascular bed of the rat.

Responses to the Rho kinase inhibitor Y-27632 were investigated in the anesthetized rat. Under baseline conditions intravenous injections of Y-27632 decreased pulmonary and systemic arterial pressures and increased cardiac output. The decreases in pulmonary arterial pressures were enhanced when baseline tone was increased with U-46619, and under elevated tone conditions Y-27632 produced similar percent decreases in pulmonary and systemic arterial pressures. Injections of Y-27632 prevented and reversed the hypoxic pulmonary vasoconstrictor response. The increase in pulmonary arterial pressure in response to ventilation with a 10% O(2)-90% N(2) gas mixture was not well maintained during the period of hypoxic exposure. Treatment with the nitric oxide (NO) synthase (NOS) inhibitor nitro-l-arginine methyl ester (l-NAME) increased pulmonary arterial pressure and prevented the decline or fade in the hypoxic pulmonary vasoconstrictor response. The hypoxic pulmonary vasoconstrictor response was reversed by Y-27632 in control and in l-NAME-treated animals. The Rho kinase inhibitor attenuated increases in pulmonary arterial pressures in response to intravenous injections of serotonin, angiotensin II, and Bay K 8644. Y-27632, sodium nitrite, and BAY 41-8543, a guanylate cyclase stimulator, decreased pulmonary and systemic arterial pressures and vascular resistances in monocrotaline-treated rats. These data suggest that Rho kinase is involved in the regulation of baseline tone and in the mediation of pulmonary vasoconstrictor responses. The present data suggest that the hypoxic pulmonary vasoconstrictor response is modulated by the release of NO that mediates the nonsustained component of the response in the anesthetized rat. These data suggest that Rho kinase and NOS play important roles in the regulation of vasoconstrictor tone in physiological and pathophysiological states and that monocrotaline-induced pulmonary hypertension can be reversed by agents that inhibit Rho kinase, generate NO, or stimulate soluble guanylate cyclase.

Cardiovascular effects of peroxynitrite.

1. Peroxynitrite (PN) is formed in biological systems from the reaction of nitric oxide (*NO) with superoxide (O2(-)*) and both exist as free radicals. By itself, PN is not a free radical, but it can generate nitrogen dioxide (*NO2) and carbonate radical (CO3(-)*) upon reaction with CO2. 2. The reaction of CO2 constitutes a major pathway for the disposition of PN produced in vivo and this is based on the rapid reaction of PN anion with CO2 and the availability of CO2 in both intra- and extracellular fluids. The free radicals *NO2 and CO3(-)*, in combination with *NO, generated from nitric oxide synthase, can bring about oxidation of critical biological targets resulting in tissue injury. However, the reactions of *NO2, CO3(-)* and *NO with carbohydrates, protein and non-protein thiols, phenols, indoles and uric acid could result in the formation of a number of nitration and nitrosation products in the vasculature. These products serve as long-acting *NO donors and, therefore, contribute to vasorelaxant properties, protective effects on the heart, inhibition of leucocyte-endothelial cell interactions and reduction of reperfusion injury. 3. Herein, we review the chemistry of PN, the observations that the effects of PN could be mediated by formation of an *NO donor-like substance and review the physiological and beneficial effects of PN.

Angiotensin-(1-7) potentiates responses to bradykinin but does not change responses to angiotensin I.

Angiotensin-(1-7) (Ang-(1-7)), a bioactive peptide in the renin-angiotensin system, has counterregulatory actions to angiotensin II (Ang II). However, the mechanism by which Ang-(1-7) enhances vasodepressor responses to bradykinin (BK) is not well understood. In the present study, the effects of Ang-(1-7) on responses to BK, BK analogs, angiotensin I (Ang I), and Ang II were investigated in the anesthetized rat. The infusion of Ang-(1-7) (55 pmol/min i.v.) enhanced decreases in systemic arterial pressure in response to i.v. injections of BK and the BK analogs [Hyp3, Tyr(Me)8]-bradykinin (HT-BK) and [Phe8psi (CH2-NH) Arg9]-bradykinin (PA-BK) without altering pressor responses to Ang I or II, or depressor responses to acetylcholine and sodium nitroprusside. The angiotensin-converting enzyme (ACE) inhibitor enalaprilat enhanced responses to BK and the BK analog HT-BK without altering responses to PA-BK and inhibited responses to Ang I. The potentiating effects of Ang-(1-7) and enalaprilat on responses to BK were not attenuated by the Ang-(1-7) receptor antagonist A-779. Ang-(1-7)- and ACE inhibitor-potentiated responses to BK were attenuated by the BK B2 receptor antagonist Hoe 140. The cyclooxygenase inhibitor sodium meclofenamate had no significant effect on responses to BK or Ang-(1-7)-potentiated BK responses. These results suggest that Ang-(1-7) potentiates responses to BK by a selective B2 receptor mechanism that is independent of an effect on Ang-(1-7) receptors, ACE, or cyclooxygenase product formation. These data suggest that ACE inhibitor-potentiated responses to BK are not mediated by an A-779-sensitive mechanism and are consistent with the hypothesis that enalaprilat-induced BK potentiation is due to decreased BK inactivation.

Sternal nourishment in various conditions of vascularization.

BACKGROUND: Early changes in sternal perfusion were studied after midline sternotomy and different methods of mammary artery (MA) harvesting. METHODS: Our observations were made in the swine model after midline sternotomy. In group 1 (6 animals), after unilateral skeletonized MA harvesting, (99m)Tc particles were injected intravenously. In group 2 (7 animals), after unilateral mammary artery and vein harvesting (semiskeletonized technique), (99m)Tc particles were injected intravenously. In group 3 (5 animals), after skeletonized bilateral MA harvesting, 99mTc particles were injected into the intercostal musculature lateral to the sternal border. In groups 1 to 3, sternal samples were analyzed using gamma counting. In group 4 (6 animals), unilateral skeletonized MA harvesting was performed. In group 5 (5 animals), the MA was harvested unilaterally using the semiskeletonized technique. In groups 4 and 5, sternal blood flow was assessed using thermography. Data were collected in all groups for 5 hours postoperatively. RESULTS: Both radioactive and thermographic flow measurements showed a statistically significant decrease in sternal blood flow on the side of harvested mammary vessels, regardless of harvesting technique. Radioactivity of the devascularized hemisterni on the side of intramuscular particle injection was substantially higher than in the contralateral half, confirming the role of diffusion in sternal nourishment. The distal sternal segments were least perfused by the MA. CONCLUSIONS: There is an acute reduction of sternal perfusion during the early postoperative period, even if collaterals are preserved by skeletonized MA harvesting. Diffusion plays an important role in sternal nourishment, particularly of the xiphoid, and even more so after MA harvesting.