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  • Book
    David A. Edwards, Padma Gulur, Christopher M. Sobey, editors.
    Summary: This practical guide provides the perspectives needed to treat acute and chronic pain in the hospital. Authored by experts of diverse specialty backgrounds, chapters bring the available evidence together with modern strategies for caring for patients with complex pain. Basic considerations and multimodal and multidisciplinary approaches with the greatest impact on minimizing suffering and burden of care are covered in detail. The material in this text will assist the learner, the teacher, and the life-long learning practitioner by providing basic considerations for treating acute and chronic pain in the hospital. This book may also serve as a quick reference, review manual or teaching tool by teachers on rounds.

    Contents:
    Preface
    Introduction to the Chronic Pain Patient
    Definitions
    Acute Pain
    Chronic Pain
    Opioid-induced Hyperalgesia
    History
    Physical Examination
    The SCRIPT History Template
    Patient Reported Outcomes
    Clinical and Experimental Tools for Measuring Pain
    Case 1: High Dose Opioids & Multiple Pain Medications
    Case 2: Buprenorphine
    Case 3: Methadone
    Case 4: Abdominal Pain
    Case 5: Unknown Pain Source
    Case 6: Sickle Cell Disease
    Case 7: A Cancer Pain Crisis
    Case 8: Spasticity & Pain
    Case 9: Renal & Hepatic Disease
    Case 11: Angry Patient
    Case 12: Intrathecal Pain Pump
    Case 13: Spinal Cord Stimulation
    Case 14: Opioid Use Disorder
    Case 15: Comorbid Psychological Condition
    Case 16: Poor Prognosis in a Palliative Care Patient
    Case 17: Management of a Pain/Dyspnea in an Actively Dying Patient
    Opioids
    Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)
    Acetaminophen
    Local Anesthetics
    NMDA Antagonists
    Alpha-2 Agonists
    Gabapentin & Pregabalin
    Tricyclic Antidepressants & Serotonin-Norepinephrine Reuptake Inhibitors
    Steroids
    Cannabinoids
    Peripheral Regional Anesthesia Blocks
    Neuraxial Blocks
    Vertebroplasty & Kyphoplasty
    Surgical Interventions for Pain
    Opioid and Non-Opioid Therapies in Palliative Care
    Crisis Management and Refractory Pain
    Transition to Outpatient Care & Readmissions
    Opioid Tapering for Acute on Chronic Non-Cancer Pain. .
    Digital Access Springer 2022
  • Article
    Hyman AL, Mathe AA, Leslie CA, Matthews CC, Bennett JT, Spannhake EW, Kadowitz PJ.
    J Pharmacol Exp Ther. 1978 Nov;207(2):388-401.
    The effects of bolus injections of arachidonic acid and prostaglandins (PG) E2 and F2a on the pulmonary vascular bed were compared under resting conditions and after alteration in the physiologic state of the lung. Studies were carried out in the vascularly isolated lung lobe of the intact, anesthetized dog under conditions of controlled blood flow. Arachidonic acid, PGE2 and PGF2a increased pulmonary vascular resistance by constricting intrapulmonary veins and arteries in a dose-related manner, as did an analog of the endoperoxide, PGH2, whereas PGI2 dilated the pulmonary vascular bed. The response to arachidonate was associated with a 2- to 3-fold increase in levels of PGE- and PGF-like substances in pulmonary venous blood and was blocked by indomethacin. The effects of arachidonic acid, but not the PGs, were greatly enhanced during perfusion with either dextran or saline and the enhanced response in saline was associated with a 15 to 20-fold increase in levels of PG-like substances in the pulmonary effluent. Responses to arachidonate were not dependent upon the presence of formed elements in blood but were related to perfusate protein concentration. Alveolar hypoxia decreased responses to the precursor while those to PGE2 and PGF2a were enhanced. Responses to the PGs, but not those to arachidonate, were affected by changes in blood pH. Sublethal doses of Escherichic coli endotoxin increased the response to arachidonic acid, but not those to PGE2 and PGF2a. Results of the present study indicate that the effects of bolus injection of arachidonic acid on the pulmonary vascular bed are due mainly to formation of constrictor metabolites which may overshadow the actions of any dilator (PGI2) formed and suggest that metabolism of the precursor is altered by changes in physiologic state.
    Digital Access Access Options