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  • Book
    Edoardo Picetti, [and 4 others], editors.
    Summary: This book provides the basis needed for a dialogue between intensivists and emergency surgeons regarding the management and monitoring of acute care surgery (ACS) patients who require Intensive Care Unit (ICU) admission. It puts forward a practical approach to the treatment of common emergencies in daily clinical practice, and shares essential information on the treatment and monitoring of hemodynamic, respiratory, metabolic and neurological problems related to acute surgical patients requiring ICU admission. Furthermore, it includes two chapters regarding diagnostic and interventional radiology (fundamentals in daily emergency clinical practice), and addresses important issues such as ethics, mass casualty care, and care in low-resource settings. As such, the book not only offers a valuable guide for all practicing surgeons and intensivists, but is also relevant for residents and fellows who are newcomers to ACS.

    Contents:
    Intro; Foreword; Preface; Contents;
    1: Admission/Discharge Criterion for Acute Care Surgery Patients in the ICU: A General Review of ICU Admission and Discharge Indications; 1.1 Introduction; 1.2 Admission to the ICU; 1.3 Rapid Response Teams as an Aid to ICU Triage; 1.4 Frailty; 1.5 Futility vs Appropriate Care; 1.6 Advanced Directives; 1.7 ICU Economics; 1.8 Scoring Systems; 1.9 Organization of the ICU; 1.10 Communication Best Practices; 1.11 Engaging Family; 1.12 Criterion for ICU Discharge; 1.13 Summary; References
    2: Acute Respiratory Failure and Acute Respiratory Distress Syndrome in ACS Patient: What Are the Indications for Acute Intervention?2.1 Introduction; 2.2 Can You Clarify Some of the Terminology I See About Respiratory Failure and ARDS?; 2.3 How Do I Recognize Respiratory Failure and What Qualifies It as ARDS?; 2.4 How Frequently Will I See Respiratory Failure, and How Bad Can It Be for My Patient?; 2.5 What is Different About the Pathophysiology of ARDS that Makes Management Different? 2.6 Is My Patient at Risk for Respiratory Failure and What Can I Do to Mitigate It as Much as Possible?2.7 My Patient Has Developed Respiratory Failure, Now What Can I Do?; 2.7.1 Neurologic; 2.7.2 Cardiovascular; 2.7.3 Respiratory; 2.7.4 Fluids, Electrolytes, Nutrition, Gastrointestinal (FENGI); 2.7.5 Renal; 2.7.6 Hematologic; 2.7.7 Endocrine; 2.7.8 Infectious Disease; 2.7.9 Musculoskeletal; 2.8 Conclusion; References;
    3: Nuts and Bolts of Ventilator Management: When Is Invasive or Noninvasive Mechanical Ventilation Appropriate for Your Patient?; 3.1 Introduction 3.2 Modes of Ventilatory Support3.2.1 Invasive Mechanical Ventilation; 3.2.2 Noninvasive Mechanical Ventilation; 3.2.3 High-Flow Nasal Cannula; 3.2.4 Continuous Positive Airway Pressure; 3.2.5 Bi-level Positive Airway Pressure; 3.3 Choice of Approach; 3.4 Conclusion; References;
    4: Principles of Weaning from Ventilatory Support: When and Why to Wean and When to Consider a Tracheostomy; 4.1 Introduction; 4.2 Weaning: Definition and Relevance; 4.3 Classification of the Difficult-to-Wean Patients; 4.4 The Weaning Process; 4.5 Assessing the Readiness to Wean 4.6 Assessing Readiness for Extubation Attempt4.7 Does Post-Extubation Noninvasive Positive-Pressure Ventilation Prevent Reintubation?; 4.8 The Role of Tracheostomy in Difficult-to-Wean Patients; 4.9 Tracheostomy: Definition and Relevance; 4.10 Indications, Contraindications, Complications, and Mortality After Discharge; 4.11 Early vs. Late Tracheostomy; 4.12 Percutaneous Versus Surgical; 4.13 Ultrasound; References;
    5: Circulatory Failure and Support in the ACS Patient: What Are the Optimal Methods of Providing Circulatory Monitoring and Support?; 5.1 Introduction
    Digital Access Springer 2019
  • Article
    Robinson CV, Upton AC.
    J Natl Cancer Inst. 1978 May;60(5):995-1007.
    The theory of competing risks, extended by the addition of several newly defined estimators, was applied to the analysis of mortality data for acutely X-irradiated, male RF mice, in which the cause of each death was assigned to one of four categories: myeloid leukemia (M), thymic lymphoma (T), lymphosarcoma and reticulum cell sarcoma (L), and all remaining causes (R), Doses from 0 to 450 rads were delivered within two age ranges: A) 5-6 weeks and B) 9-10 weeks, to give 11 treatment groups totaling 2,073 mice. The data were analyzed in terms of: 1) the nonparametric, Kaplan-Meier (K-M) adjusted survival function; 2) its logarithmic transform, the cumulative force of mortality (cumFM) function; 3) a disease model called "early terminating," applied to causes M and T; and 4) a "late-terminating" model, applied to causes L and R. For any given cause and group, two estimators were used, which measured, respectively: a) the relative lateness of the corrected (or adjusted) time course and b) the relative corrected incidence. For causes M and T, these were: a) the mean age of the force of mortality distribution (MAF), or corrected mean latent period; and b) the final cumFM. For causes L and R, the estimators were: a) the adjusted mean age at death (adjMAD), given an upper limit (as %) of adjusted mortality (adjMAD, 50% for L; adjMAD, 100%--the K-M estimator--for R) and b) the cumFM at a cutoff time of 640 days. For causes M and T, the MAF values showed highly significant decreases of the latent periods with dose, through 300 rads. The final cumFM data showed a marked increase of corrected incidence with dose, for both M and T. In addition, the data for cause M were consistent with a three-parameter, leukemogenic cell model that incorporated two opposing radiation effects: leukemogenic cell potentiation and cell killing. For cause R, the adjMAD, 100% data showed a general decrease with dose and considerable scatter. For cause L, the adjMAD, 50% values showed: for treatment A, a gradual decrease with dose through 300 rads; for treatment B, a highly significant drop for 150 rads, with little change for higher doses. The cumFM, 640-day values for both L and R showed a general increase of corrected incidence with dose. The mortality curves for all causes combined showed the expected life shortening, i.e., decreases of the mean age at death with dose, in the 0- to 300-rad range. In addition, the standard deviations of the mortality curves were significantly less for animals irradiated at age range B than at age range A, for each of the doses--150, 300, and 450 rads.
    Digital Access Access Options