A Systematic Approach to Intraoperative Venous Congestion in the Deep Inferior Epigastric Artery Perforator (DIEAP) Flap.

The deep Inferior epigastric artery perforator (DIEAP) flap is currently the gold standard for autologous breast reconstruction. This flap is susceptible to venous congestion, which can result in partial or complete flap loss. Apart from external causes, venous congestion may be caused by the flap's vascular architecture, either due to a dominance of the superficial venous system or due to impaired communication between the superficial and deep venous systems. This inefficient vascular architecture can be detected during surgery, and the venous outflow drainage can be improved through several techniques. We present two case reports of intraoperative venous congestion. In the first case, we performed an intra-flap rerouting, through a venous anastomosis between the superficial and the deep venous systems. In the second case, an extra-flap rerouting was executed, through a venous anastomosis between the superficial venous system and a recipient vein. We present the current institutional approach to DIEAP flap breast reconstruction, incorporating surgical insights for addressing intraoperative venous congestion.

Peptides Derived from a Plant Protease Inhibitor of the Coagulation Contact System Decrease Arterial Thrombus Formation in a Murine Model, without Impairing Hemostatic Parameters.

Several plant protein inhibitors with anticoagulant properties have been studied and characterized, including the Delonix regia trypsin inhibitor (DrTI). This protein inhibits serine proteases (trypsin) and enzymes directly involved in coagulation, such as plasma kallikrein, factor XIIa, and factor XIa. In this study, we evaluated the effects of two new synthetic peptides derived from the primary sequence of DrTI in coagulation and thrombosis models to understand the mechanisms involved in the pathophysiology of thrombus formation as well as in the development of new antithrombotic therapies. Both peptides acted on in vitro hemostasis-related parameters, showing promising results, prolonging the Partially Activated Thromboplastin Time (aPTT) and inhibited platelet aggregation induced by adenosine diphosphate (ADP) and arachidonic acid. In murine models, for arterial thrombosis induced by photochemical injury, and platelet-endothelial interactions monitored by intravital microscopy, both peptides at doses of 0.5 mg/kg significantly extended the time of artery occlusion and modified the platelet adhesion and aggregation pattern with no changes in bleeding time, demonstrating the high biotechnological potential of both molecules.

A snake venom-analog peptide that inhibits SARS-CoV-2 and papain-like protease displays antithrombotic activity in mice arterial thrombosis model, without interfering with bleeding time.

BACKGROUND: (p-BthTX-I)2 K, a dimeric analog peptide derived from the C-terminal region of phospholipase A2-like bothropstoxin-I (p-BthTX-I), is resistant to plasma proteolysis and inhibits severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) strains with weak cytotoxic effects. Complications of SARS-CoV-2 infection include vascular problems and increased risk of thrombosis; therefore, studies to identify new drugs for treating SARS-CoV-2 infections that also inhibit thrombosis and minimize the risk of bleeding are required. OBJECTIVES: To determine whether (p-BthTX-I)2 K affects the hemostatic system. METHODS: Platelet aggregation was induced by collagen, arachidonic acid, and adenosine diphosphate (ADP) in the Chronolog Lumi-aggregometer. The coagulation activity was evaluated by determining activated partial thromboplastin clotting time (aPTT) and prothrombin time (PT) with (p-BthTX-I)2 K (5.0-434.5 µg) or 0.9% NaCl. Arterial thrombosis was induced with a 540 nm laser and 3.5-20 mg kg- 1 Rose Bengal in the carotid artery of male C57BL/6J mice using (p-BthTX-I)2 K. Bleeding time was determined in mouse tails immersed in saline at 37 °C after (p-BthTX-I)2 K (4.0 mg/kg and 8.0 mg/kg) or saline administration. RESULTS: (p-BthTX-I)2 K prolonged the aPTT and PT by blocking kallikrein and FXa-like activities. Moreover, (p-BthTX-I)2 K inhibited ADP-, collagen-, and arachidonic acid-induced platelet aggregation in a dose-dependent manner. Further, low concentrations of (p-BthTX-I)2 K extended the time to artery occlusion by the formed thrombus. However, (p-BthTX-I)2 K did not prolong the bleeding time in the mouse model of arterial thrombosis. CONCLUSION: These results demonstrate the antithrombotic activity of the peptide (p-BthTX-I)2 K possibly by kallikrein inhibition, suggesting its strong biotechnological potential.

Anionic Ultrasmall Gold Nanoparticles Bind to Coagulation Factors and Disturb Normal Hemostatic Balance.

Ultrasmall gold nanoparticles (usNPs) and nanoclusters are an emerging class of nanomaterials exhibiting distinctive physicochemical properties and in vivo behaviors. Although understanding the interactions of usNPs with blood components is of fundamental importance to advance their clinical translation, currently, little is known about the way that usNPs interact with the hemostatic system. This study describes the effects of a model anionic p-mercaptobenzoic acid-coated usNP on the coagulation cascade, with particular emphasis on the contact pathway. It is found that in a purified system, the anionic usNPs bind to and activate factor XII (FXII). The formed usNP-FXII complexes are short-lived (residence time of ∼10 s) and characterized by an affinity constant of ∼200 nM. In human plasma, the anionic usNPs activate the contact pathway and promote coagulation. The usNPs also exhibit anticoagulant activity in plasma by interfering with the thrombin-mediated cleavage of fibrinogen. Taken together, these findings establish that anionic usNPs can disturb the normal hemostatic balance, which in turn may hinder their clinical translation. Finally, it is shown that usNPs can be designed to be nearly inert in plasma by surface coating with the natural peptide glutathione.

Chronic sclerosing sialadenitis (Küttner's tumour) of the submandibular gland: a neoplastic mimic.

A 74-year-old man was referred for a plastic surgery consultation for two previous acute episodes of right submandibular sialadenitis. Physical examination revealed a lump in the right submandibular region, painful on palpation. The initial impression on clinical examination was of sialolithiasis. The sonography demonstrated a structural heterogeneity of the submandibular gland with a hypoechogenic and vascularised nodular formation (1.5×1.2 cm), suggestive of a mixed tumour of the right maxillary gland, requiring histological evaluation. He underwent a right submandibulectomy and an IgG4-positive chronic sclerosing sialadenitis was diagnosed. The patient's condition evolved favourably, resulting in a full recovery. The clinical features and differential diagnosis of this entity are debated in light of relevant literature.