Relevant bibliographies by topics / Oedema / Books

Books on the topic 'Oedema'

To see the other types of publications on this topic, follow the link: Oedema.
Author: Grafiati
Published: 4 June 2021
Last updated: 4 March 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 books for your research on the topic 'Oedema.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse books on a wide variety of disciplines and organise your bibliography correctly.

1

Tiwary, Satyendra K., ed. Approach to Lower Limb Oedema. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-6206-5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

McCreesh, Brendan Michael. Early detection and monitoring of diabetic macular oedema. [S.l: The Author], 2003.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Ubolsakka, Chulee. Cardiovascular responses to external compression and peripheral oedema during rest and exercise in man: A role for a muscle mechanoreflex? Birmingham: University of Birmingham, 2001.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Gábor, M. Experimentally-induced paw oedemas in mice. Budapest: Akadémiai Kiadó, 2007.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Verdonk, H. P. M., ed. Oedeem en oedeemtherapie. Houten: Bohn Stafleu van Loghum, 2011. http://dx.doi.org/10.1007/978-90-313-8442-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Evans, A. Ernest. Acenion Gwynfyd: Canllawiau Cynnal oedfa. (Aberystwyth): (Cyngor Llyfrau Cymraeg), 1987.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Casley-Smith, J. R. High-protein oedemas and the benzo-pyrones: The causes, effects, incidence and treatment of high-protein oedemas, including lymphoedema, and how these are improved by the benzo-pyrones, including the coumarins and the flavonoids. Sydney: Lippincott, 1986.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

1931-, Roberts Brynley F., ed. Cynnal oedfa: Cyfrol o wasanaethau crefyddol, gweddïau ac emynau. Caernarfon: Gwasg Pantycelyn, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Kyŏngyŏng ŭn sallimsari oeda: Kyŏngyŏng susang. Sŏul Tʻŭkpyŏlsi: Ilsinsa, 1986.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Gyda'r ifanc: Deunydd cynnal oedfa i blant a phobl ifainc. Abertawe: T^y John Penry, 1985.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
11

Michael, Düsing, and Christliches Jugenddorfwerk Deutschlands Chemnitz, eds. Wir waren zum Tode bestimmt: Lódz, Theresienstadt, Auschwitz, Freiberg, Oederan, Mauthausen ; jüdische Zwangsarbeiterinnen erinnern sich. Leipzig: Forum, 2002.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
12

Timperley, Jonathan, and Sandeep Hothi. Peripheral oedema. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0014.

Full text
Abstract:
Peripheral oedema is a palpable swelling caused by increased interstitial fluid in soft tissues, and can be due to local or systemic disease. Fluid distribution between capillaries and the interstitium is governed by Starling forces. The lymphatic system returns excess fluid and protein from the extracellular, interstitial space to the bloodstream. Thus, interstitial oedema may arise from factors that increase capillary pressure or permeability, factors that reduce plasma colloid osmotic pressure, factors that impede lymphatic drainage, or a combination of these causes. This topic addresses the diagnosis of peripheral oedema.
APA, Harvard, Vancouver, ISO, and other styles
13

(Editor), G. Mchedlishvili, and et al (Editor), eds. Brain Oedema. Akademiai Kiado, 1988.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
14

Tiwary, Satyendra K. Approach to Lower Limb Oedema. Springer Singapore Pte. Limited, 2022.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
15

Krzesinski, Jean-Marie, and Eric P. Cohen. Approach to the patient with oedema. Edited by Robert Unwin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0030_update_001.

Full text
Abstract:
Generalized oedema reflects retention of salt and water that can be triggered by disease of several organs, but notably kidneys, heart and liver. Management is based on salt restriction and the use of diuretics. Diuretics have greatly improved its management, but in severe cases, ultrafiltration or dialysis may be needed for its treatment. In congestive heart failure, the nephrotic syndrome, or primary sodium retention, one proceeds rapidly, using mainly loop diuretics. Weight loss of 1 kg/day is a typical goal. Fluid removal in patients with cirrhosis and ascites, but without peripheral oedema, must proceed more slowly, often only 0.5 kg/day or less. For other causes of generalized oedema, loop diuretics are usually preferred, and higher split doses may be required. Patients with resistant oedema from any cause may require high-dose loop diuretics frequently in combination with a diuretic acting at a more distal site in the nephron, typically a thiazide diuretic but also sometimes potassium sparing drugs. A high-salt diet and use of non-steroidal anti-inflammatory drugs should be ruled out.
APA, Harvard, Vancouver, ISO, and other styles
16

Turner, Neil, and Premil Rajakrishna. Pathophysiology of oedema in nephrotic syndrome. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0053.

Full text
Abstract:
The mechanism by which loss of serum proteins into the urine causes expansion of extracellular fluid volume and oedema has become clearer. A key initiating abnormality is avid sodium retention by the kidney, leading to increased whole-body sodium and increased extracellular fluid volume. This appears to be driven primarily by overactivation of the amiloride-sensitive epithelial sodium channel (ENaC) in the collecting duct, activated proteolytically through abnormal filtration of plasminogen, and its activation to plasmin in the nephron. Conventional explanations for nephrotic oedema focused on low colloid osmotic pressure as a consequence of loss of serum proteins, leading to egress of extracellular fluid from the intravascular compartment. It was hypothesized that this led to underfilling of the circulation and a drive to sodium retention. While low osmotic pressure may play a part in the clinical picture of nephrotic syndrome, a variety of observations suggest that underfilling is not a common feature except in the most severe nephrotic syndrome. Furthermore the gradient in colloid osmotic pressure between serum and interstitium tends to be preserved in nephrotic syndrome. The distribution of excess extracellular fluid is markedly different in patients with nephrotic syndrome from that seen in patients who have reduced glomerular filtration rate as the cause of sodium retention. This is not fully understood but hypotheses centre on capillary permeability and colloid osmotic pressure effects.
APA, Harvard, Vancouver, ISO, and other styles
17

Whittle, Ian. Raised intracranial pressure, cerebral oedema, and hydrocephalus. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198569381.003.0604.

Full text
Abstract:
The brain is protected by the cranial skeleton. Within the intracranial compartment are also cerebrospinal fluid, CSF, and the blood contained within the brain vessels. These intracranial components are in dynamic equilibrium due to the pulsations of the heart and the respiratory regulated return of venous blood from the brain. Normally the mean arterial blood pressure, systemic venous pressure, and brain volume are regulated to maintain physiological values for intracranial pressure, ICP. There are a range of very common disorders such as stroke, and much less common, such as idiopathic intracranial hypertension, that are associated with major disturbances of intracranial pressure dynamics. In some of these the contribution to pathophysiology is relatively minor whereas in others it may be substantial and be a major contributory factor to morbidity or even death.Intracranial pressure can be disordered because of brain oedema, disturbances in CSF flow, mass lesions, and vascular engorgement of the brain. Each of these may have variable causes and there may be interactions between mechanisms. In this chapter the normal regulation of intracranial pressure is outlined and some common disease states in clinical neurological practice that are characterized by either primary or secondary problems in intracranial pressure dynamics described.
APA, Harvard, Vancouver, ISO, and other styles
18

Tanaka, Sébastien, and Jacques Duranteau. Management of acute non-cardiogenic pulmonary oedema. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0165.

Full text
Abstract:
Severe capillary leak is an important factor in the pathogenesis of organ dysfunction following inflammatory syndromes such as sepsis-induced acute lung injury and acute respiratory distress syndrome (ARDS). Various interventions, such as a conservative fluid strategy, albumin, and diuretics are designed to maintain an adequate intravascular colloid osmotic pressure, reduce capillary leak and reduce extravascular water. Of these, only a conservative, rather than liberal fluid strategy is currently recommended. Preclinical studies in ARDS and sepsis suggest that preventing microvascular leak may represent a viable therapeutic approach to prevent or ameliorate organ dysfunction. The challenge is to now go further with carefully designed clinical trials.
APA, Harvard, Vancouver, ISO, and other styles
19

Jonge, Jan-Willem De. Diuretic Drug Cessation in General Practice: Withdrawing Diuretic Drugs Prescribed for Ankle Oedema. Thesis Pub, 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
20

McAuley, Danny F., and Thelma Rose Craig. Measurement of extravascular lung water in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0140.

Full text
Abstract:
The accumulation of fluid in the interstitium and alveolar space is known as extravascular lung water (EVLW). EVLW is associated with increased morbidity and mortality in critically ill patients and is elevated in patients with cardiogenic pulmonary oedema, acute lung injury (ALI), and the acute respiratory distress syndrome (ARDS). Pulmonary oedema is a consequence of increased pulmonary capillary hydrostatic pressure and/or an increased capillary permeability. The quantity of pulmonary oedema fluid is dependent on the balance of fluid formation and clearance, and this contributes to the overall dynamic net lung fluid balance. Measurement of EVLW is therefore an indirect surrogate measurement of the alveolar epithelial and endothelial damage in ALI/ARDS. The single indicator transpulmonary thermodilution technique is an available bedside technique to measure EVLW.
APA, Harvard, Vancouver, ISO, and other styles
21

Oedema; a Study of the Physiology and the Pathology of Water Absorption by the Living Organism. Creative Media Partners, LLC, 2022.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
22

Oedema; a Study of the Physiology and the Pathology of Water Absorption by the Living Organism. Franklin Classics, 2018.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
23

Fischer, Martin. Oedema; a Study of the Physiology and the Pathology of Water Absorption by the Living Organism. Creative Media Partners, LLC, 2018.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
24

Oedema; a Study of the Physiology and the Pathology of Water Absorption by the Living Organism. Creative Media Partners, LLC, 2022.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
25

Oedema; a Study of the Physiology and the Pathology of Water Absorption by the Living Organism. Franklin Classics, 2018.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
26

Coppola, Silvia, and Franco Valenza. Inhalation injury in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0107.

Full text
Abstract:
Inhalation injury represents one of the most serious associated injuries complicating the care of thermally-injured patient. It can result in severe respiratory failure and acute respiratory distress syndrome (ARDS) by three mechanisms—thermal or chemical injury, and impairment of systemic oxygen supply. Thermal injury can cause erythema, ulceration, and progressive, life-threatening oedema, particularly of the upper airways. Chemical injury is due to irritants or cytotoxic compounds, and depends on the material burned, the temperature of the fire, and the amount of oxygen present in the fire environment. It is responsible for irritation, ulceration, and oedema of the mucosal surface, and the initiation of a lung inflammatory reaction when small particles reach the alveoli. Moreover, the increased vascular permeability, and the reduced surfactant production carry a significant risk in the development of pneumonia and ARDS. Bronchospasm and upper airway oedema can occur rapidly, while lower airway oedema can be asymptomatic for up to 24 hours. Lung imaging techniques may not reveal injured areas for the first 24–48 hours. Fibre optic bronchoscopy is considered to be the most direct diagnostic method for the definitive diagnosis of inhalation injury. The patient management includes airways assessment, adequate fluid resuscitation, and mechanical ventilation when required. All victims of smoke inhalation should be always evaluated for cyanide and carbon monoxide poisoning.
APA, Harvard, Vancouver, ISO, and other styles
27

Keeley, Vaughan. Lymphoedema. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0113.

Full text
Abstract:
Lymphoedema is a chronic oedema developing as a result of failure of the lymphatic system to drain fluid and other substances, such as proteins, from the tissues. It typically affects the limbs but can involve any part of the body. The management of all types of lymphoedema is largely palliative in nature in that there are no surgical or other treatments which offer a cure for the problem in the vast majority of cases. This chapter focuses on oedema associated with advanced cancer and other diseases, encountered towards the end of life with some reference to cancer treatment-related lymphoedema, as this may also be present in people with advanced disease.
APA, Harvard, Vancouver, ISO, and other styles
28

Harrois, Anatole, and Jacques Duranteau. Pathophysiology of severe capillary leak. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0164.

Full text
Abstract:
Severe capillary leak plays an important role in the pathogenesis of several inflammatory syndromes, including sepsis, acute lung injury, and shock syndromes. Microvascular leak is caused by an increase in endothelial permeability. This is due to a range of inflammatory mediators that destabilize endothelial junctions, thereby causing tissue oedema with potential harmful effects on tissue oxygenation and organ function. Tissue oedema can impair tissue oxygenation by increasing the distance required for the diffusion of oxygen to cells, and by decreasing microvascular perfusion due to an increase in interstitial pressure. Better understanding of the pathogenesis of microvascular permeability may lead to new therapies targeting the microvascular barrier in sepsis and the acute respiratory distress syndrome.
APA, Harvard, Vancouver, ISO, and other styles
29

Ware, Lorraine B. Pathophysiology of acute respiratory distress syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0108.

Full text
Abstract:
The acute respiratory distress syndrome (ARDS) is a syndrome of acute respiratory failure characterized by the acute onset of non-cardiogenic pulmonary oedema due to increased lung endothelial and alveolar epithelial permeability. Common predisposing clinical conditions include sepsis, pneumonia, severe traumatic injury, and aspiration of gastric contents. Environmental factors, such as alcohol abuse and cigarette smoke exposure may increase the risk of developing ARDS in those at risk. Pathologically, ARDS is characterized by diffuse alveolar damage with neutrophilic alveolitis, haemorrhage, hyaline membrane formation, and pulmonary oedema. A variety of cellular and molecular mechanisms contribute to the pathophysiology of ARDS, including exuberant inflammation, neutrophil recruitment and activation, oxidant injury, endothelial activation and injury, lung epithelial injury and/or necrosis, and activation of coagulation in the airspace. Mechanical ventilation can exacerbate lung inflammation and injury, particularly if delivered with high tidal volumes and/or pressures. Resolution of ARDS is complex and requires coordinated activation of multiple resolution pathways that include alveolar epithelial repair, clearance of pulmonary oedema through active ion transport, apoptosis, and clearance of intra-alveolar neutrophils, resolution of inflammation and fibrinolysis of fibrin-rich hyaline membranes. In some patients, activation of profibrotic pathways leads to significant lung fibrosis with resultant prolonged respiratory failure and failure of resolution.
APA, Harvard, Vancouver, ISO, and other styles
30

Farmer, Brenna M., and Neal Flomenbaum. Management of salicylate poisoning. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0317.

Full text
Abstract:
Salicylates are weak acids that work as neurotoxins. The goal of management is to keep salicylates out of the brain and enhance elimination. Acute salicylate toxicity manifests as tinnitus, nausea, vomiting, and hyperventilation in a patient who takes a single large ingestion. Chronic salicylate toxicity is associated with long-term use, has a more insidious onset, and symptoms tend to be less severe, resulting in delayed diagnosis. It is more commonly seen in elderly patients. Therapeutic interventions for toxicity include gastrointestinal decontamination, serum and urine alkalinization, and haemodialysis. Mechanical ventilation may lead to clinical deterioration and death in a salicylate-poisoned patient due to worsening acidosis from respiratory failure. This results in severe acidosis, cerebral oedema, pulmonary oedema, and cardiac arrest.
APA, Harvard, Vancouver, ISO, and other styles
31

Wiffen, Philip, Marc Mitchell, Melanie Snelling, and Nicola Stoner. Therapy-related issues: cardiovascular system. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199603640.003.0017.

Full text
Abstract:
Angina 338Tolerance to nitrate therapy 341Heart failure 342Drug interventions for severe heart failure 348Acute cardiogenic pulmonary oedema 350Treatment of hypertension 352Understanding anticoagulation 356Clinical use of anticoagulants 358Warfarin dosing 362Counselling patients treated with warfarin 364Reversing the effects of warfarin (or other vitamin K antagonists) ...
APA, Harvard, Vancouver, ISO, and other styles
32

Keshav, Satish, and Alexandra Kent. Pancreatic disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0201.

Full text
Abstract:
Acute pancreatitis is an acute inflammatory process of the pancreas and is potentially reversible. It is characterized by oedema and necrosis of peripancreatic fat and may progress to necrosis of glandular and surrounding tissue. Activation of pancreatic enzymes leads to pancreatic autodigestion and systemic effects.
APA, Harvard, Vancouver, ISO, and other styles
33

Foster, Helen, and Paul A. Brogan, eds. Rashes in paediatric rheumatology. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199592630.003.0010.

Full text
Abstract:
Systemic JIA 448Palmar psoriasis in a patient with psoriatic JIA 448Nail pits and psoriasis in a patient with psoriatic JIA 449Psoriatic JIA (elbows) 449Psoriatic JIA (hands) 450HSP with bilateral ankle swelling 450Juvenile dermatomyositis with periorbital oedema 451Severe juvenile dermatomyositis with anterior chest wall vasculitis—‘shawl sign’ ...
APA, Harvard, Vancouver, ISO, and other styles
34

Mee, Sarah, and Zoe Clift. Hand Therapy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757689.003.0002.

Full text
Abstract:
Rehabilitation is a multidisciplinary, patient-centred, evidence-based process to promote healing, restore function, and promote independence. The physical and psychological and social consequences of the hand condition or injury have to be considered. Mobilization can be active or passive, supplemented by accessory movements and proprioceptive rehabilitation. Splinting may be static, serial static, static progressive, dynamic. Many materials are available. Oedema may be acute or chronic; it is treated with elevation, active movement, retrograde massage, compression, kinesiotaping, cold therapy, and contrast bathing. Scars may be mature or immature; keloid or hypertrophic. Management is generally empiric: massage, silicone, pressure therapy, steroid injections, and surgery all have roles. Hypersensitivity (allodynia, causalgia, dysaesthesia, hyperpathia, etc.) is treated with desensitization, graded textures, percussion, and mirror visual feedback. Stiffness is managed especially by prevention; movement, splinting, and surgery have a role. Pain is treated with medication, oedema control, acupuncture, TENS, education, psychological measures. Complex Regional Pain Syndrome has sensory, vasomotor, sudomotor, and trophic elements. Treatment includes medication, hand therapy, and occasionally surgery.
APA, Harvard, Vancouver, ISO, and other styles
35

Martin, Daniel S., and Michael P. W. Grocott. Pathophysiology and management of altitude-related disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0350.

Full text
Abstract:
Acute high-altitude related illnesses include acute mountain sickness (AMS), high altitude pulmonary oedema (HAPO) and high altitude cerebral oedema (HACO). AMS is characterized by headache, lack of appetite, poor sleep, lethargy, and fatigue. AMS is a common, generally benign, self-limiting condition if managed with rest, no ascent, and symptomatic treatment. Descent is indicated in severe cases. HACO and HAPO are rare, but serious conditions that should be considered life-threatening medical emergencies. HACO is characterized by the presence of neurological signs (including confusion) at altitude, commonly in the presence of headache. HAPO is characterized by breathlessness and signs of respiratory distress at altitude, particularly accompanying exercise. Management of HACO and HAPO involves urgent descent, supplemental oxygen (cylinder, concentrator, or portable hyperbaric chamber) if available, and specific treatment with dexamethasone (HACO) or nifedipine (HAPO). Slow controlled ascent (adequate acclimatization) is the best prophylaxis against the acute high-altitude-related illnesses. Acetazolamide is an effective prophylaxis against AMS.
APA, Harvard, Vancouver, ISO, and other styles
36

Jolly, Elaine, Andrew Fry, and Afzal Chaudhry, eds. Allergy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0002.

Full text
Abstract:
Chapter 2 covers the basic science and clinical topics relating to allergy which trainees are required to learn as part of their basic training and demonstrate in the MRCP. It covers basic science, atopy, food, drug, latex, and venom allergy, urticaria and angio-oedema, anaphylaxis, approach to the immunosuppressed individual, immunodeficiency, immunology investigations, and immunological therapies.
APA, Harvard, Vancouver, ISO, and other styles
37

Waldmann, Carl, Neil Soni, and Andrew Rhodes. Obstetric emergencies. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199229581.003.0031.

Full text
Abstract:
Pre-eclampsia 518Eclampsia 520HELLP syndrome 522Postpartum haemorrhage 524Amniotic fluid embolism 526Pre-eclampsia is a common complication of pregnancy, UK incidence is 3–5%, with a complex hereditary, immunological and environmental aetiology.Abnormal placentation is characterized by impaired myometrial spiral artery relaxation, failure of trophoblastic invasion of these arterial walls and blockage of some vessels with fibrin, platelets and lipid-laden macrophages. There is a 30–40%, reduction in placental perfusion by the uterine arcuate arteries as seen by Doppler studies at 18–24 weeks gestation. Ultimately the shrunken, calcified, and microembolized placenta typical of the disease is seen. The placental lesion is responsible for fetal growth retardation and increased risks of premature labour, abruption and fetal demise. Maternal systemic features of this condition are characterized by widespread endothelial damage, affecting the peripheral, renal, hepatic, cerebral, and pulmonary vasculatures. These manifest clinically as hypertension, proteinuria and peripheral oedema, and in severe cases as eclamptic convulsions, cerebral haemorrhage (the most common cause of death due to pre-eclampsia in the UK), pulmonary oedema, hepatic infarcts and haemorrhage, coagulopathy and renal dysfunction....
APA, Harvard, Vancouver, ISO, and other styles
38

Foster, Brogan, and Paul A. Brogan. Rashes in paediatric rheumatology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198738756.003.0010.

Full text
Abstract:
This chapter provides colour plate images of important cutaneous manifestations of autoimmune and autoinflammatory diseases of the young. Images provided are: the evanescent rash of systemic JIA; palmar psoriasis, nail pitting, and typical rash associated with psoriatic JIA; HSP; JDM (periorbital oedema, shawl sign, Gottron’s papules); periungual erythema associated with mixed connective tissue disease; livedo reticularis and cutaneous necrosis associated with medium vessel vasculitis; EBV driven haemophagocytic lymphohistiocytosis; erythema nodosum; Kawasaki disease; and C1q deficiency.
APA, Harvard, Vancouver, ISO, and other styles
39

Jolly, Elaine, Andrew Fry, and Afzal Chaudhry, eds. Acute medical emergencies and practical procedures. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0001.

Full text
Abstract:
Chapter 1 covers the basic science and clinical topics relating to acute medical emergencies and practical procedures which trainees are required to learn as part of their basic training and demonstrate in the MRCP. It covers cardiorespiratory arrest, shock, acute coronary syndromes, tachycardia, bradycardia, hypertensive emergencies, pulmonary oedema, acute asthma, massive pulmonary embolism, acute upper gastrointestinal haemorrhage, acute kidney injury, coma, traumatic brain injury, status epilepticus, adrenal crisis, thyroid emergencies, acute poisoning, and burns.
APA, Harvard, Vancouver, ISO, and other styles
40

Mee, Sarah, and Zoe Clift. Assessment. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757689.003.0001.

Full text
Abstract:
Meticulous assessment—both subjective and objective—is an essential part of managing hand conditions. Objective measures include range of motion, power grip, pinch grip, oedema, and dexterity testing. Subjective measures include a clinical history, sensibility, and sensation testing, pain scales, and Patient Related Outcome Measures (PROMS), global (e.g. EQ5D, VAS pain), region specific (e.g. Michigan Hand Questionnaire, Disabilities of the Hand, Arm, Shoulder, QuickDASH, Patient Related Wrist and Hand Evaluation), and condition specific (e.g. Boston Carpal Tunnel Questionnaire).
APA, Harvard, Vancouver, ISO, and other styles
41

Rahimi, Kazem. Acute heart failure. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0091.

Full text
Abstract:
Heart failure is a clinical syndrome characterized by an inadequate cardiac output for the needs of the body in the absence of low filling pressures, and reflects abnormal cardiac structure or function. Although various definitions for acute heart failure (AHF) exist, here AHF is defined as new-onset heart failure or an acute exacerbation of chronic heart failure, requiring urgent therapy. Patients with AHF typically have clinical features of organ hypoperfusion, with or without pulmonary and peripheral oedema.
APA, Harvard, Vancouver, ISO, and other styles
42

Mebazaa, Alexandre, and Mervyn Singer. Pathophysiology and causes of cardiac failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0151.

Full text
Abstract:
Organ congestion upstream of the dysfunctional left and/or right ventricle, with preserved stroke volume, is the most frequkeywordent feature of myocardial failure.Clinical manifestations do not necessarily correlate with the degree of left ventricular systolic dysfunction (i.e. left ventricular ejection fraction).Systolic and/or diastolic dysfunction may be present, with systolic dysfunction usually predominating.Pulmonary oedema is related to left ventricular diastolic dysfunction. Compensatory mechanisms (within the heart and/or periphery) may prove paradoxically disadvantageous on ventricular stroke work and stroke volume.
APA, Harvard, Vancouver, ISO, and other styles
43

Hatfield, Anthea. Fluid balance. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199666041.003.0023.

Full text
Abstract:
This chapter will tell you how surgery affects fluid balance and how the body controls fluids. Fluid compartments in the body and the nature of fluids are described. Disorders of fluid balance, the use of fluids to restore blood volume, and extra cellular fluid volume are all discussed. Management of fluid deficit, fluid overload, and pulmonary oedema and how to correct electrolyte balance are all clearly set out. Recommendations for fluids after different types of surgery and fluids for patients with renal and cardiac failure are given.
APA, Harvard, Vancouver, ISO, and other styles
44

Ostermann, Marlies, and Ruth Y. Y. Wan. Diuretics in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0058.

Full text
Abstract:
Fluid overload and chronic hypertension are the most common indications for diuretics. The diuretic response varies between different types and depends on underlying renal function. In patients with congestive heart failure, diuretics appear to reduce the risk of death and worsening heart failure compared with placebo, but their use in acute decompensated heart failure is questionable. Diuretics are also widely used in chronic kidney disease to prevent or control fluid overload, and treat hypertension. In acute kidney injury, there is no evidence that they improve renal function, speed up recovery, or change mortality. In patients with chronic liver disease and large volume ascites, paracentesis is more effective and associated with fewer adverse events than diuretic therapy, but maintenance treatment with diuretics is indicated to prevent recurrence of ascites. Mannitol has a role in liver patients with cerebral oedema and normal renal function. The use of diuretics in rhabdomyolysis is controversial and restricted to patients who are not fluid deplete. In conditions associated with resistant oedema (chronic kidney disease, congestive heart failure, chronic liver disease), combinations of diuretics with different modes of action may be necessary. Diuresis is easier to achieve with a continuous furosemide infusion compared with intermittent boluses, but there is no evidence of better outcomes. The role of combination therapy with albumin in patients with fluid overload and severe hypoalbuminaemia is uncertain with conflicting data.
APA, Harvard, Vancouver, ISO, and other styles
45

Hedenstierna, Göran, and Hans Ulrich Rothen. Physiology of positive-pressure ventilation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0088.

Full text
Abstract:
During positive pressure ventilation the lung volume is reduced because of loss of respiratory muscle tone. This promotes airway closure that occurs in dependent lung regions. Gas absorption behind the closed airway results sooner or later in atelectasis depending on the inspired oxygen concentration. The elevated airway and alveolar pressures squeeze blood flow down the lung so that a ventilation/perfusion mismatch ensues with more ventilation going to the upper lung regions and more perfusion going to the lower, dependent lung. Positive pressure ventilation may impede the return of venous blood to the thorax and right heart. This raises venous pressure, causing an increase in systemic capillary pressure with increased capillary leakage and possible oedema formation in peripheral organs. Steps that can be taken to counter the negative effects of mechanical ventilation include an increase in lung volume by recruitment of collapsed lung and an appropriate positive end-expiratory pressure, to keep aerated lung open and to prevent cyclic airway closure. Maintaining normo- or hypervolaemia to make the pulmonary circulation less vulnerable to increased airway and alveolar pressures, and preserving or mimicking spontaneous breaths, in addition to the mechanical breaths, since they may improve matching of ventilation and blood flow, may increase venous return and decrease systemic organ oedema formation (however, risk of respiratory muscle fatigue, and even overexpansion of lung if uncontrolled).
APA, Harvard, Vancouver, ISO, and other styles
46

Lancellotti, Patrizio, and Bernard Cosyns. Critically Ill Patients. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713623.003.0012.

Full text
Abstract:
Echocardiography is one of the most powerful diagnostic and monitoring tools available to the modern emergency/critical care practitioners. It can provide important information throughout the whole patient pathway. This chapter details the role of lung ultrasound and 2D echocardiography and colour Doppler for a variety of critical acute care conditions. These include acute cardiogenic pulmonary oedema, acute dyspnoea, and acute lung injury. More general information on how to perform a lung ultrasound, specific problems in ventilated patients and echocardiographic examination in cardiorespiratory arrest and focused echocardiography protocols are also discussed.
APA, Harvard, Vancouver, ISO, and other styles
47

Bunker, Professor Christopher, and Dr Arani Chandrakumar. Dermatological diseases and emergencies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199565979.003.00017.

Full text
Abstract:
Chapter 17 covers dermatological diseases and emergencies including a general introduction to the subject, followed by information on erythroderma, drug eruptions, angio-oedema, Kawasaki disease, staphylococcal toxic shock syndrome, Streptococcal toxic shock syndrome (streptococcal TSS), staphylococcal scalded skin syndrome, necrotizing fasciitis, psoriasis, eczema and dermatitis, cutaneous vasculitis, immunobullous disorders, pyoderma gangrenosum, scarring alopecia, herpes simplex viruses 1 and 2, varicella zoster virus infection, bacterial infections affecting the skin, fungal infections affecting the skin, ectoparasitic disease, HIV infection and the skin, malignant melanoma, non-melanoma skin cancer, and cutaneous T cell lymphoma.
APA, Harvard, Vancouver, ISO, and other styles
48

Bowker, Lesley K., James D. Price, Ku Shah, and Sarah C. Smith. Cardiovascular. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198738381.003.0010.

Full text
Abstract:
This chapter provides information on the ageing cardiovascular system, chest pain, stable angina, acute coronary syndromes, myocardial infarction, hypertension, treatment of hypertension, presentation of arrhythmias, management of arrhythmias, atrial fibrillation, rate/rhythm control in atrial fibrillation, stroke prevention in atrial fibrillation, bradycardia and conduction disorders, common arrhythmias and conduction abnormalities, heart failure assessment, acute heart failure, chronic heart failure, dilemmas in heart failure, heart failure with preserved left ventricular function, valvular heart disease, peripheral oedema, preventing venous thromboembolism in an older person, peripheral vascular disease, gangrene in peripheral vascular disease, and vascular secondary prevention.
APA, Harvard, Vancouver, ISO, and other styles
49

Ellison, David H., and Arohan R. Subramanya. Clinical use of diuretics. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0033.

Full text
Abstract:
Diuretics are widely employed to treat extracellular fluid volume expansion caused by heart failure, cirrhosis of the liver, nephrotic syndrome, and chronic kidney disease. Major classes of diuretic inhibit sodium reabsorption along the proximal tubule, the loop of Henle, the distal convoluted tubule, and the connecting and collecting tubules. Loop diuretics have the highest ceiling of action and often form the cornerstones of diuretic treatment of oedema. Members of this class are short-acting drugs, with different bioavailabilities, the specifics of which contribute importantly to a rational and effective approach to their use. They are not filtered substantially because they are all protein bound. They enter tubules by secretion along the proximal tubule, thereby gaining access to the Na-K-2Cl cotransporter of the thick ascending limb. Their dose–response curves are sigmoidal and altered by several disease processes. Chronic administration can elicit adaptive processes along the nephron that limit their efficacy. Distal convoluted tubule diuretics, such as the thiazides, inhibit NaCl absorption along the distal convoluted tubule. While used predominantly to treat hypertension, they are also useful to treat oedema, especially when combined with loop diuretics. Drugs acting along the connecting tubule and collecting duct either inhibit Na+ channels directly or block mineralocorticoid receptors. These drugs are effective in states of very high aldosterone secretion, and can also be used to reduce the hypokalaemia caused by other classes of diuretics. An evidence-based approach to treating the oedematous patient is described.
APA, Harvard, Vancouver, ISO, and other styles
50

Jolly, Elaine, Andrew Fry, and Afzal Chaudhry, eds. Dermatology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0006.

Full text
Abstract:
Chapter 6 covers the basic science and clinical topics relating to dermatology which trainees are required to learn as part of their basic training and demonstrate in the MRCP. It covers eczema/dermatitis, psoriasis, blistering skin disorders, bacterial and viral infections of the skin, fungal infections and infestations, erythema multiforme, Stevens-Johnson syndrome/toxic epidermal necrolysis, erythema nodosum, drug eruptions, benign skin tumours, malignant skin tumours, the skin and systemic disease, cutaneous lupus erythematosus, systemic sclerosis (scleroderma), vasculitis, structure and function of the skin, hair, and nails, nail disorders, alopecia, hirsutism and hypertrichosis, acne vulgaris, rosacea, hidradenitis suppurativa, disorders of pigmentation, urticaria and angio-oedema, and photosensitivity.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the bibliographies on the topic 'Oedema' for other source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography