Browsing by Author "Patel, Shivani S."

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    Corrigendum: Iatrogenic air embolism: pathoanatomy, thromboinflammation, endotheliopathy, and therapies
    (Frontiers Media, 2024-02-06) Marsh, Phillip L.; Moore, Ernest E.; Moore, Hunter B.; Bunch, Connor M.; Aboukhaled, Michael; Condon, Shaun M., II; Al-Fadhl, Mahmoud D.; Thomas, Samuel J.; Larson, John R.; Bower, Charles W.; Miller, Craig B.; Pearson, Michelle L.; Twilling, Christopher L.; Reser, David W.; Kim, George S.; Troyer, Brittany M.; Yeager, Doyle; Thomas, Scott G.; Srikureja, Daniel P.; Patel, Shivani S.; Añón, Sofía L.; Thomas, Anthony V.; Miller, Joseph B.; Van Ryn, David E.; Pamulapati, Saagar V.; Zimmerman, Devin; Wells, Byars; Martin, Peter L.; Seder, Christopher W.; Aversa, John G.; Greene, Ryan B.; March, Robert J.; Kwaan, Hau C.; Fulkerson, Daniel H.; Vande Lune, Stefani A.; Mollnes, Tom E.; Nielsen, Erik W.; Storm, Benjamin S.; Walsh, Mark M.; Medicine, School of Medicine
    [This corrects the article DOI: 10.3389/fimmu.2023.1230049.].
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    COVID-associated non-vasculitic thrombotic retiform purpura of the face and extremities: A case report
    (Wiley, 2022-12-27) Bunch, Connor M.; Zackariya, Nuha; Thomas, Anthony V.; Langford, Jack H.; Aboukhaled, Michael; Thomas, Samuel J.; Ansari, Aida; Patel, Shivani S.; Buckner, Hallie; Miller, Joseph B.; Annis, Christy L.; Quate-Operacz, Margaret A.; Schmitz, Leslie A.; Pulvirenti, Joseph J.; Konopinski, Jonathan C.; Kelley, Kathleen M.; Hassna, Samer; Nelligan, Luke G.; Walsh, Mark M.; Medicine, School of Medicine
    SARS-CoV-2 infection can manifest many rashes. However, thrombotic retiform purpura rarely occurs during COVID-19 illness. Aggressive anti-COVID-19 therapy with a high-dose steroid regimen led to rapid recovery. This immunothrombotic phenomenon likely represents a poor type 1 interferon response and complement activation on the endothelial surface in response to acute infection.
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    SHock-INduced Endotheliopathy (SHINE): A mechanistic justification for viscoelastography-guided resuscitation of traumatic and non-traumatic shock
    (Frontiers Media, 2023-02-27) Bunch, Connor M.; Chang, Eric; Moore, Ernest E.; Moore, Hunter B.; Kwaan, Hau C.; Miller, Joseph B.; Al-Fadhl, Mahmoud D.; Thomas, Anthony V.; Zackariya, Nuha; Patel, Shivani S.; Zackariya, Sufyan; Haidar, Saadeddine; Patel, Bhavesh; McCurdy, Michael T.; Thomas, Scott G.; Zimmer, Donald; Fulkerson, Daniel; Kim, Paul Y.; Walsh, Matthew R.; Hake, Daniel; Kedar, Archana; Aboukhaled, Michael; Walsh, Mark M.; Graduate Medical Education, School of Medicine
    Irrespective of the reason for hypoperfusion, hypocoagulable and/or hyperfibrinolytic hemostatic aberrancies afflict up to one-quarter of critically ill patients in shock. Intensivists and traumatologists have embraced the concept of SHock-INduced Endotheliopathy (SHINE) as a foundational derangement in progressive shock wherein sympatho-adrenal activation may cause systemic endothelial injury. The pro-thrombotic endothelium lends to micro-thrombosis, enacting a cycle of worsening perfusion and increasing catecholamines, endothelial injury, de-endothelialization, and multiple organ failure. The hypocoagulable/hyperfibrinolytic hemostatic phenotype is thought to be driven by endothelial release of anti-thrombogenic mediators to the bloodstream and perivascular sympathetic nerve release of tissue plasminogen activator directly into the microvasculature. In the shock state, this hemostatic phenotype may be a counterbalancing, yet maladaptive, attempt to restore blood flow against a systemically pro-thrombotic endothelium and increased blood viscosity. We therefore review endothelial physiology with emphasis on glycocalyx function, unique biomarkers, and coagulofibrinolytic mediators, setting the stage for understanding the pathophysiology and hemostatic phenotypes of SHINE in various etiologies of shock. We propose that the hyperfibrinolytic phenotype is exemplified in progressive shock whether related to trauma-induced coagulopathy, sepsis-induced coagulopathy, or post-cardiac arrest syndrome-associated coagulopathy. Regardless of the initial insult, SHINE appears to be a catecholamine-driven entity which early in the disease course may manifest as hyper- or hypocoagulopathic and hyper- or hypofibrinolytic hemostatic imbalance. Moreover, these hemostatic derangements may rapidly evolve along the thrombohemorrhagic spectrum depending on the etiology, timing, and methods of resuscitation. Given the intricate hemochemical makeup and changes during these shock states, macroscopic whole blood tests of coagulative kinetics and clot strength serve as clinically useful and simple means for hemostasis phenotyping. We suggest that viscoelastic hemostatic assays such as thromboelastography (TEG) and rotational thromboelastometry (ROTEM) are currently the most applicable clinical tools for assaying global hemostatic function—including fibrinolysis—to enable dynamic resuscitation with blood products and hemostatic adjuncts for those patients with thrombotic and/or hemorrhagic complications in shock states.
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    Type B Lactic Acidosis in a Patient with Mantle Cell Lymphoma
    (Hindawi, 2023-08-16) Nzenwa, Ikemsinachi C.; Berquist, Margaret; Brenner, Toby J.; Ansari, Aida; Al-Fadhl, Hamid D.; Aboukhaled, Michael; Patel, Shivani S.; Peck, Ethan E.; Al-Fadhl, Mahmoud D.; Thomas, Anthony V.; Zackariya, Nuha; Walsh, Mark M.; Bufill, Jose A.; Medicine, School of Medicine
    Type B lactic acidosis is an uncommon medical emergency in which acid production overwhelms hepatic clearance. This specific etiology of lactic acidosis occurs without organ hypoperfusion and has been most commonly described in patients with hematologic malignancies but also in patients with solid tumors. The mechanism by which cancer cells switch their glucose metabolism toward increasingly anaerobic glycolytic phenotypes has been described as the "Warburg effect." Without treating the underlying malignancy, the prognosis for patients diagnosed with malignancy-related type B lactic acidosis is extremely poor. Here, we present a case of a 66-year-old male who was diagnosed with type B lactic acidosis secondary to mantle cell lymphoma. Bicarbonate drip was started to correct the lactic acidosis. The patient was also immediately treated with rituximab chemotherapy combined with rasburicase to avoid the hyperuricemia associated with tumor lysis syndrome. He responded to the early treatment and was discharged with normal renal function. Type B lactic acidosis secondary to hematologic malignancy is important to recognize. In order to successfully treat this syndrome, early diagnosis and simultaneous treatment of the imbalance of lactic acid levels and the underlying malignancy are necessary.
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    Viscoelastic Hemostatic Assays: A Primer on Legacy and New Generation Devices
    (MDPI, 2022-02-07) Volod, Oksana; Bunch, Connor M.; Zackariya, Nuha; Moore, Ernest E.; Moore, Hunter B.; Kwaan, Hau C.; Neal, Matthew D.; Al-Fadhl, Mahmoud D.; Patel, Shivani S.; Wiarda, Grant; Al-Fadhl, Hamid D.; McCoy, Max L.; Thomas, Anthony V.; Thomas, Scott G.; Gillespie, Laura; Khan, Rashid Z.; Zamlut, Mahmud; Kamphues, Peter; Fries, Dietmar; Walsh, Mark M.; Medicine, School of Medicine
    Viscoelastic hemostatic assay (VHAs) are whole blood point-of-care tests that have become an essential method for assaying hemostatic competence in liver transplantation, cardiac surgery, and most recently, trauma surgery involving hemorrhagic shock. It has taken more than three-quarters of a century of research and clinical application for this technology to become mainstream in these three clinical areas. Within the last decade, the cup and pin legacy devices, such as thromboelastography (TEG® 5000) and rotational thromboelastometry (ROTEM® delta), have been supplanted not only by cartridge systems (TEG® 6S and ROTEM® sigma), but also by more portable point-of-care bedside testing iterations of these legacy devices (e.g., Sonoclot®, Quantra®, and ClotPro®). Here, the legacy and new generation VHAs are compared on the basis of their unique hemostatic parameters that define contributions of coagulation factors, fibrinogen/fibrin, platelets, and clot lysis as related to the lifespan of a clot. In conclusion, we offer a brief discussion on the meteoric adoption of VHAs across the medical and surgical specialties to address COVID-19-associated coagulopathy.