Your browser doesn't support javascript.
loading
Symmetrical peripheral gangrene in critical illness.
Warkentin, Theodore E; Ning, Shuoyan.
Afiliación
  • Warkentin TE; Department of Medicine, Michael G. DeGroote School of Medicine, McMaster University, Hamilton, Ontario, Canada; Department of Pathology and Molecular Medicine, Michael G. DeGroote School of Medicine, McMaster University, Hamilton, Ontario, Canada; McMaster Centre for Transfusion Research, Canada; Hamilton Regional Laboratory Medicine Program, Hamilton, Ontario, Canada; Service of Clinical Hematology, Hamilton General Hospital, Hamilton Health Sciences, Hamilton, Ontario, Canada. Electronic addre
  • Ning S; Department of Medicine, Michael G. DeGroote School of Medicine, McMaster University, Hamilton, Ontario, Canada; Department of Pathology and Molecular Medicine, Michael G. DeGroote School of Medicine, McMaster University, Hamilton, Ontario, Canada; McMaster Centre for Transfusion Research, Canada; Hamilton Regional Laboratory Medicine Program, Hamilton, Ontario, Canada; St. Joseph's Healthcare, Hamilton, Ontario, Canada.
Transfus Apher Sci ; 60(2): 103094, 2021 Apr.
Article en En | MEDLINE | ID: mdl-33627309
ABSTRACT
Symmetrical peripheral gangrene (SPG) is a disabling complication that affects a small proportion of patients who survive critical illness. Its pathogenesis reflects profoundly disturbed procoagulant-anticoagulant balance in susceptible tissue beds secondary to circulatory shock (cardiogenic, septic). There is a characteristic SPG triad (a) shock (hypotension, lactic acidemia, normoblastemia, multiple organ dysfunction), (b) disseminated intravascular coagulation (DIC), and (c) natural anticoagulant depletion (protein C, antithrombin). In recent years, risk factors for natural anticoagulant depletion have been identified, most notably acute ischemic hepatitis ("shock liver"), which is seen in at least 90% of patients who develop SPG. Moreover, there is a characteristic time interval (2-5 days, median 3 days) between the onset of shock/shock liver and the beginning of ischemic injury secondary to peripheral microthrombosis ("limb ischemia with pulses"), reflecting the time required to develop severe depletion in hepatically-synthesized natural anticoagulants. Other risk factors for natural anticoagulant depletion include chronic liver disease (e.g., cirrhosis) and, possibly, transfusion of colloids (albumin, high-dose immunoglobulin) lacking coagulation factors. A causal role for vasopressor therapy is unproven and is unlikely; this is because critically ill patients who develop SPG do so usually after at least 36-48 hours of vasopressor therapy, implicating a time-dependent pathophysiological mechanism. The most plausible explanation is a progressive time-dependent decline in key natural anticoagulant factors, reflecting ongoing DIC ("consumption"), proximate liver disease whether acute or chronic ("impaired production"), and colloid administration ("hemodilution"). Given these evolving concepts of pathogenesis, a rationale approach to prevention/treatment of SPG can be developed.
Asunto(s)
Palabras clave

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Gangrena Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Humans Idioma: En Revista: Transfus Apher Sci Asunto de la revista: HEMATOLOGIA Año: 2021 Tipo del documento: Article

Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Gangrena Tipo de estudio: Prognostic_studies / Risk_factors_studies Límite: Humans Idioma: En Revista: Transfus Apher Sci Asunto de la revista: HEMATOLOGIA Año: 2021 Tipo del documento: Article