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  • Book
    Michael E. Edmonds, Bauer E. Sumpio, editors.
    Contents:
    Intro; Preface; Contents; Contributors; Abbreviations;
    Chapter 1: Assessment, Classification, Staging and Intervention; 1.1 Assessment of the Diabetic Foot; 1.1.1 History; 1.1.2 Examination; 1.1.2.1 Skin Breakdown; 1.1.2.2 Infection; 1.1.2.3 Necrosis; 1.1.2.4 Ischaemia; 1.1.2.5 Grading Regarding Wound, Ischaemia and foot Infection in WIfI; 1.1.2.6 Neuropathy; Motor Neuropathy; Autonomic Neuropathy; Sensory Neuropathy; 1.1.2.7 Deformity; 1.1.2.8 Callus; 1.1.2.9 Oedema; Unilateral Oedema; Bilateral Oedema; 1.2 Classification of the Diabetic Foot; 1.2.1 The Neuropathic Foot 1.2.2 The Ischaemic Foot1.2.3 Neuroischaemic Foot; 1.2.4 Critically Ischaemic Foot; 1.2.5 Acutely Ischaemic Foot; 1.3 Staging of the Diabetic Foot; 1.3.1 Stage 1; 1.3.2 Stage 2; 1.3.3 Stage 3; 1.3.4 Stage 4; 1.3.5 Stage 5; 1.3.6 Stage 6; 1.4 Intervention; 1.5 Conclusion; References; Part I: Neuropathic Foot;
    Chapter 2: Introduction to the Neuropathic Foot: Limb Salvage Pathway and Algorithm; 2.1 Introduction; 2.2 Management of Neuropathic Ulceration; 2.2.1 Step 1. Wound Control: Debridement and Standard Wound Care; 2.2.2 Step 2. Mechanical Control: Off loading 2.2.3 Step 3. Advanced Wound Therapy with Evidence-Based Adjunctive Therapies2.2.4 Step 4. Soft Tissue Coverage; 2.3 Conclusion; References;
    Chapter 3: Diabetic Neuropathy; 3.1 Introduction; 3.2 Definitions of Diabetic Neuropathy; 3.3 Type of Nerve Fibres; 3.4 Classification of Diabetic Neuropathy; 3.5 Epidemiology; 3.6 Risk Factors for Diabetic Neuropathy; 3.7 Pathogenesis of DN; 3.8 Clinical Features; 3.8.1 Typical DN: Diabetic Sensorimotor Peripheral Neuropathy (DSPN); 3.8.2 Atypical DN; 3.8.2.1 Diabetic Painful Peripheral Neuropathy (DPPN); 3.8.2.2 Focal or Multifocal Neuropathies 3.8.2.3 Diabetic Autonomic Neuropathy (DAN)3.9 Diagnosis; 3.10 Differential Diagnosis; 3.11 Management of Diabetic Neuropathy; 3.11.1 Glycaemic Control; 3.11.2 Management of Neuropathic Pain; 3.11.3 Management of Autonomic Neuropathy; 3.11.4 Control of Cardiovascular Risk Factors; 3.11.5 Disease Modifying Treatments; 3.11.6 Diabetic Foot Risk Assessment; 3.12 Conclusions; References;
    Chapter 4: Neuropathic Diabetic Foot Ulceration; 4.1 Introduction; 4.2 Diabetic Foot Ulceration; 4.3 Epidemiology and Risk Factors for Neuropathic DFU; 4.3.1 Presence of Neuropathy in DFU 4.3.2 Risk Factors for Development of Neuropathic DFU4.3.3 Risk Factors for Delayed Healing in Neuropathic DFU; 4.3.4 Risk Factors for Recurrence of Neuropathic DFU; 4.3.5 Risk Factors for Amputation in Neuropathic DFU; 4.4 Pathway to Ulceration if Neuropathic DFU; 4.5 Clinical Features; 4.6 Investigations and Assessments; 4.6.1 Confirmation of Neuropathy; 4.6.2 Identification of Infection; 4.6.3 Imaging; 4.6.4 Laboratory Blood Panel; 4.6.5 Assessment of Foot Deformities and Abnormal Pressure; 4.6.6 Assessment of Comorbidities; 4.7 Management of Neuropathic DFU; 4.7.1 Wound Control
    Digital Access Springer 2019
  • Article
    Greenleaf JE.
    Experientia Suppl. 1978;32:33-44.
    The evidence for threshold concentrations of Na+ and Ca++ that alter body temperature when introduced into (a) the hypothalamus and cerebral ventricles, and (b) intravenously and by oral ingestion is examined. For hypothamic and ventricular perfusion the threshold for any increase in core temperature (Tc) at rest with excess Na+ is about 10 mM, while there is a linear relationship between the level of excess Ca++ and the decrease in Tc, with a correlation co-efficient of 0.85. With intravenous and oral ingestion the resting threshold plasma concentration for an excess Na+ effect is about 5 mEq/1 per 0.1 degrees C rise in Tc, and the excess Ca++ level is about 1 mEq/1 per 0.1 degrees C decrease in Tc. With exercise, there is a dose-dependent attenuation of the rise in core temperature that is also about 0.1 degrees C per mM excess Ca++.
    Digital Access Access Options