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Статті в журналах з теми "Muscle oedema"
1
Ray, Aritra Kumar, Poulami Karmakar, Atanu Chandra, Sudip Kumar Ghosh, and Partha Sarathi Karmakar. "Generalised oedema as a presenting manifestation of inflammatory myopathy." BMJ Case Reports 15, no. 3 (March 2022): e248036. http://dx.doi.org/10.1136/bcr-2021-248036.
Повний текст джерелаАнотація:
Polymyositis is an immune-mediated inflammatory myopathy usually presenting with weakness of proximal muscles in a symmetric pattern. Generalised subcutaneous oedema as presenting feature of inflammatory myopathy, especially polymyositis, has rarely been reported. We report here a case of a young woman who was admitted to our facility with generalised severe subcutaneous oedema. During hospital stay, she gradually developed significant proximal muscle weakness with bulbar symptoms. The initial presentation of the patient masqueraded with other causes of anasarca. However, detailed clinical features, laboratory evaluation, electromyography and muscle biopsy clinched the diagnosis of polymyositis. She was treated with systemic corticosteroids and azathioprine. The patient responded well to treatment and the swelling gradually subsided.
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Gazulla, José, Esteban Mayayo-Sinués, Isabel Benavente, Pedro J. Modrego, and José Berciano. "Ataxia of Charlevoix-Saguenay: MR and Clinical Results in Lower-Limb Musculature." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 41, no. 1 (January 2014): 37–41. http://dx.doi.org/10.1017/s0317167100016231.
Повний текст джерелаАнотація:
Objective:Peripheral neuropathy is a cardinal manifestation of the autosomal recessive spastic ataxia of Charlevoix- Saguenay (ARSACS), although its type of neuromuscular involvement has not been definitely established, and magnetic resonance imaging (MRI) plays an important role in the assessment of muscle and nerve diseases. The objective of this work has been to define the patterns of muscle weakness and of abnormal muscular MRI in ARSACS.Patients and Methods:Five patients with a molecular diagnosis of ARSACS, aged 39 to 59 years, whose electrophysiological findings were consistent with an axonal neuropathy of distal distribution superimposed on a developmental defect of myelinization, underwent neurological and MRI lower-limb examinations. Conventional FSE T1-weighted and STIR sequences were performed, looking for fatty infiltration and oedema in the musculature of the thighs, legs and feet, together with their distribution along the longitudinal axis of the muscle bellies.Results:On clinical examination, paralysis was apparent in foot muscles; moderate weakness, in leg musculature; and normal strength, in thigh muscles. MRI demonstrated massive fat deposition in the foot muscles and medial gastrocnemii in every case, distal fat infiltration and oedema in every leg muscle group, and preservation of thigh muscles, albeit with diffuse minimal non-specific fat infiltration. An inverse correlation between strength and degree of fat infiltration in lower-limb muscles became apparent.Conclusion:The preponderance of weakness and MRI abnormalities in distal muscle groups was concordant with the presence of a length-dependent axonopathy, as described in ARSACS.
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Glenn-Cox, Sophie, Robert William Foley, John D. Pauling, and Jonathan C. L. Rodrigues. "Fulminant immune-mediated necrotising myopathy (IMNM) mimicking myocardial infarction with non-obstructive coronary arteries (MINOCA)." BMJ Case Reports 13, no. 11 (November 2020): e236603. http://dx.doi.org/10.1136/bcr-2020-236603.
Повний текст джерелаАнотація:
A 74-year-old man, with inflammatory arthritis, recently commenced on adalimumab, presented with a 4-week history of left-sided chest pain, malaise and shortness of breath. Admission ECG showed age-indeterminate left bundle branch block. Troponin T was 4444 ng/L (normal range <15 ng/L) and acute coronary syndrome treatment was commenced. Catheter angiogram revealed mild-burden non-obstructive coronary disease. Cardiac magnetic resonance (CMR) was performed to refine the differential diagnosis and demonstrated no myocardial oedema or late gadolinium enhancement. Extracardiac review highlighted oedema and enhancement of the left shoulder girdle muscles consistent with acute myositis. Creatine kinase was subsequently measured and significantly elevated at 7386 IU/L (normal range 30–200 IU/L in men). Electrophoresis clarified that this was of predominantly skeletal muscle origin. Myositis protocol MRI revealed florid skeletal muscle oedema. The MR findings, together with positive anti-Scl-70 antibodies, suggested fulminant immune-mediated necrotising myopathy presenting as a rare mimic of myocardial infarction with non-obstructive coronary arteries, diagnosed by careful extracardiac CMR review.
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Sahan, N. T. "PECULIARITIES OF MORPHOFUNCTIONAL CHANGES OF MASTICATORY MUSCLES IN IODINE-DEFICIENT CONDITIONS." Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 20, no. 3 (November 12, 2020): 200–204. http://dx.doi.org/10.31718/2077-1096.20.3.200.
Повний текст джерелаАнотація:
The problem of iodine deficiency is becoming increasingly important in Ukraine. According to the United Nations Children’s Fund (UNICEF), each and all regions of Ukraine suffer from “hidden hunger”. The World Health Assembly has stated that the elimination of iodine deficiency will be as much a triumph for health care system as the eradication of smallpox and poliomyelitis. The goal of this study was to establish the peculiarities of structural organization of the masticatory muscles of rats in experimentally induced iodine deficiency. The research material involved masticatory muscle of 36 white outbred male rats, which were divided into groups: group І – intact animals; group ІІ – kept in iodine deficiency condition; group III – exposed to iodine deficiency with the addition of goitriferous food. All manipulations with test animals were performed in agreement with the regulations on the protection of vertebrate animals. The methods used in the study included: biochemical, histological, histochemical, submicroscopic, morphometric and statistical research methods. It has been established that under the conditions of iodine deficiency the lumen of arterial vessels in masticatory muscles becomes narrowed, the vascular vessels become thickened due to membrane oedema. The number of hemocapillaries per unit area of muscle fibre goes down in all the studied muscles. The number of muscle fibres with intermediate succinate dehydrogenase activity decreases with the simultaneous increase in muscle fibres with low succinate dehydrogenase activity. Furthermore, the oedematous changes are the most prominent in muscle fibres with low succinate dehydrogenase activity. In conditions of iodine deficiency with the addition of goitriferous products, we can observe the progression of luminal narrowing of the artery and wall thickening in masticatory muscles where oedematous-dystrophic changes are considerably marked. There is a tendency in the growth in haemocapillaries number per 1 μm2. Histostructurally, the loss of cross striation is quite noticeable. The cross-section diameter increases, especially in muscle fibres with low succinate dehydrogenase activity and muscle fibres with high succinate dehydrogenase activity in the masticatory muscle proper of immature animals. Ultrastructurally, the oedematous-dystrophic changes of myofibrils and mitochondria were revealed. Thus, under the conditions of iodine deficient diet the lumen of arterial vessels narrows in the masticatory muscles, their wall thickens due to oedema of the membranes, which progresses in iodine deficient diet with the addition of goitriferous products. The number of hemocapillaries per unit area of muscle fibre decreases in both study groups. Changes in vascular bed lead to the redistribution of the number of muscle fibres and their significant oedema.
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Cosgrove, Jeremy, Saira Alli, Hawraman Ramadan, and Helen L. Ford. "Myocarditis and diffuse skeletal muscle oedema: new features of neuromyelitis optica spectrum disorder? A case report." Multiple Sclerosis Journal 20, no. 1 (July 11, 2013): 120–22. http://dx.doi.org/10.1177/1352458513495939.
Повний текст джерелаАнотація:
We present a case report of newly diagnosed neuromyelitis optica spectrum disorder (NMOSD) with associated myocarditis and diffuse oedema of the pelvic and anterior compartment thigh muscles on magnetic resonance imaging. Aquaporin 4 antibodies are expressed in skeletal myofibres but involvement of skeletal muscle is rarely reported in NMOSD and myocarditis has not previously been described in this context. This case highlights the need for further research into the involvement of cardiac and skeletal muscle in NMOSD.
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Deane, M. N., M. A. Gregory, and M. Mars. "Histological and morphometric changes in untraumatised rabbit skeletal muscle treated with deep transverse friction." South African Journal of Physiotherapy 58, no. 1 (February 28, 2002): 28–33. http://dx.doi.org/10.4102/sajp.v58i1.484.
Повний текст джерелаАнотація:
Deep transverse friction (DTF) is used in clinical practice and by its nature it may cause muscle injury. This study investigates the morphologic and morphometric changes in untraumatised rabbit skeletal muscle treated with DTF.Method: 16 New Zealand white rabbits were studied. The right vastus lateralis muscle was used as a control and the left vastus lateralis was treated with DTF. Muscle biopsies were taken 10 min, 24 h and 48 h after 1 treatment, 48 h after 2 treatments and 48 h and 6 days after 3 treatments. Treatments were 48 h apart. Biopsies were prepared for light microscopy and tissue morphometry.Results: After 1 DTF treatment, intracellular and extracellular oedema was noted. Contraction bands seen throughout the fibres suggested severe mechanical trauma to the muscle. 48 hours after 1, 2, and 3 treatments, the muscle appeared to be recovering with reduced oedema, and the contraction banding was limited to small focal areas throughout each fibre. Six days after the last treatment, the myofibers, although normal in diameter, showed small focal areas of super contraction and large internalised inclusion bodies composed of a pool of myofilaments or whorls of membranous material. Morphometry showed oedema to be maximal immediately after treatment.Conclusion: DTF causes a severe but reversible injury to untraumatized myofibers. Its possible mode of action in treatment of injured muscle requires further investigation.
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Pinal-Fernandez, Iago, Maria Casal-Dominguez, John A. Carrino, Arash H. Lahouti, Pari Basharat, Jemima Albayda, Julie J. Paik, et al. "Thigh muscle MRI in immune-mediated necrotising myopathy: extensive oedema, early muscle damage and role of anti-SRP autoantibodies as a marker of severity." Annals of the Rheumatic Diseases 76, no. 4 (September 20, 2016): 681–87. http://dx.doi.org/10.1136/annrheumdis-2016-210198.
Повний текст джерелаАнотація:
ObjectivesThe aims of this study were to define the pattern of muscle involvement in patients with immune-mediated necrotising myopathy (IMNM) relative to those with other inflammatory myopathies and to compare patients with IMNM with different autoantibodies.MethodsAll Johns Hopkins Myositis Longitudinal Cohort subjects with a thigh MRI (tMRI) who fulfilled criteria for IMNM, dermatomyositis (DM), polymyositis (PM), inclusion body myositis (IBM) or clinically amyopathic DM (CADM) were included in the study. Muscles were assessed for intramuscular and fascial oedema, atrophy and fatty replacement. Disease subgroups were compared using univariate and multivariate analyses. Patients with IMNM with anti-signal recognition particle (SRP) autoantibodies were compared with those with IMNM with anti-HMG-CoA reductase (HMGCR) autoantibodies.ResultsThe study included 666 subjects (101 IMNM, 176 PM, 219 DM, 17 CADM and 153 IBM). Compared with DM or PM, IMNM was characterised by a higher proportion of thigh muscles with oedema, atrophy and fatty replacement (p<0.01). Patients with IMNM with anti-SRP had more atrophy (19%, p=0.003) and fatty replacement (18%, p=0.04) than those with anti-HMGCR. In IMNM, muscle abnormalities were especially common in the lateral rotator and gluteal groups. Fascial involvement was most widespread in DM. Fatty replacement of muscle tissue began early during the course of disease in IMNM and the other groups. An optimal combination of tMRI features had only a 55% positive predictive value for diagnosing IMNM.ConclusionsCompared with patients with DM or PM, IMNM is characterised by more widespread muscle involvement. Anti-SRP-positive patients have more severe muscle involvement than anti-HMGCR-positive patients.
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Khiabani, Anvar, Rostad, Stranden, and Kroese. "Verteilung des Ödems von Patienten mit chronischer kritischer Ischämie: Eine computertomographische Studie." Vasa 28, no. 4 (November 1, 1999): 265–70. http://dx.doi.org/10.1024/0301-1526.28.4.265.
Повний текст джерелаАнотація:
Background: A substantial number of patients with chronic critical limb ischaemia (CLI) have considerable oedema at the distal leg and foot of non deep venous thrombosis origin. The primary aim of the pre-sent study was to quantify the distribution of oedema in the different tissues of the leg and foot by applying computed tomography and planimetry. The interstitial fluid hydrostatic pressure (Pif) in the subcutaneous tissue was measured to evaluate the effect of oedema on local tissue pressure. Patients and methods: Six men and 12 women with unilateral CLI and peripheral pitting oedema were included. Cross sectional areas (CSA) of subcutaneous tissue, muscle and bone were measured by computer tomography combined with planimetry to assess the distribution of oedema within the soft tissues. Pif was measured by “wick-in-needle” technique. Results: The median total CSA of soft tissue, subcutaneous and muscle tissues at the foot level were respectively 17%, 34% and 9% greater in the limbs with CLI compared to the contralateral limb (p < 0.001). At ankle level these differences were 13%, 30% and 4%, respectively (p < 0.001). At the level of the calf these differences were not significant. Mean Pif in the limbs with CLI was 0.3 mmHg, significantly higher than in limbs without CLI (–1.8 mmHg), (p < 0.003). Conclusion: The study verified oedema of considerable magnitude at the ankle and foot. The great part of the oedema was located within the subcutaneous tissue, which was associated with a relatively moderate, but significant increase in Pif confirming the high compliance of the subcutaneous tissue. The combination of the excessive fluid and increased Pif in the interstitial tissue might aggravate the microcirculation. The aetiology of oedema formation is probably multifactorial.
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Aginor, Spanoulis, Yalatia Papastergiou, Panagiota Mitropoulou, and Georgina Burke. "WED 242 A challenging case of periorbital swelling." Journal of Neurology, Neurosurgery & Psychiatry 89, no. 10 (September 13, 2018): A35.2—A35. http://dx.doi.org/10.1136/jnnp-2018-abn.122.
Повний текст джерелаАнотація:
A 54 year old lady was referred with a eighteen month history of slowly progressive, asymmetric, periorbital and facial oedema. She was thought to have inflammatory orbital pseudotumour.During this time, she had also developed a dry mouth, joint pains and enlarged salivary glands. A salivary gland ultrasound scan was suggestive of Sjogren’s disease although antinuclear antibody and rheumatoid factor were negative. She had recently been prescribed omeprazole for mild dysphagia and hoarse voice from vocal cord oedema.Past medical history included Hashimoto thyroiditis for which she was taking levothyroxine.Clinical examination revealed peri-orbital and facial oedema causing proptosis of the right globe and complete lid closure. Visual acuity, eye movements and visual fields of the left eye were normal. Her voice was hoarse and she had mouth ulcers. She had a widespread erythematous rash that was thought to be a drug reaction to omeprazole.Apart from mild lymphopenia and mildly deranged liver function, blood tests, including inflammatory markers and thyroid function, were unremarkable.MRI of the brain and orbits revealed diffuse oedema of facial structures, including the orbital muscles. A CT body scan was unremarkable.A temporalis muscle biopsy confirmed a high grade NK/T cell lymphoma.
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Braithwaite, B. D., P. V. Petrik, W. S. Moore, H. Gelabert, D. N. Pollen, J. J. Earnshaw, and W. J. Quinones-Baldrich. "Aspirin increases tissue oedema after skeletal muscle ischaemia and reperfusion." European Journal of Vascular and Endovascular Surgery 12, no. 1 (July 1996): 76–80. http://dx.doi.org/10.1016/s1078-5884(96)80279-6.
Повний текст джерелаДисертації з теми "Muscle oedema"
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Ubolsakka, Chulee. "Cardiovascular responses to external compression and peripheral oedema during rest and exercise in man : a role for a muscle mechanoreflex?" Thesis, University of Birmingham, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368382.
Повний текст джерела
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Coulange, Mathieu. "Conséquences neuromusculaires et cardiorespiratoires de l'immersion." Aix-Marseille 2, 2007. http://www.theses.fr/2007AIX20699.
Повний текст джерелаАнотація:
Les données de la littérature sur le retentissement de l’immersion sur la performance physique sont nombreuses mais les protocoles sont multiples et les résultats discordants. L’objectif de ce travail est d’analyser la réponse physiologique neuromusculaire et cardiorespiratoire à une immersion dans des conditions expérimentales les plus proches de la réalité (c’est à dire : immersion totale, prolongée, à différentes températures, au repos et au cours d’une nage avec palmes). Ce travail a également pour but d’évaluer un éventuel impact physiopathologique lié à ces contraintes environnementales. La première partie étudie la force maximale contractile volontaire, la tolérance à l’effort isométrique sous maximal mené jusqu’à épuisement et l’activité électromyographique au niveau de deux muscles de métabolisme différent, au sec puis lors d’une immersion à neutralité thermique ou en eau froide. Bien qu’il n’y ait pas de baisse de performance maximale à neutralité thermique, l’immersion majore la réponse adaptative électromyographique à l’effort physique probablement en agissant sur la commande motrice par la stimulation des afférences inhibitrices du groupe III-IV. En effet, l’augmentation de la température cutanée et l’élévation de la pression interstitielle intramusculaire constatées lors d’une immersion à neutralité thermique (35°C) pourraient provoquer l’activation de ces afférences. Dans l’eau froide, même si la réponse adaptative est insuffisante au maintien des performances, elle est maximale et serait plutôt liée à une augmentation des concentrations plasmatiques d’acide lactique et de potassium. Cependant, ces observations se limitent à des immersions statiques sans évaluation cardiorespiratoire. La deuxième partie analyse la réponse cardiorespiratoire à une épreuve d’effort maximale lors d’un exercice de palmage. L’originalité de ce protocole est de comparer les variables mesurées lors du palmage à celles obtenues lors d’un effort équivalent sur bicyclette en ambiance sèche. Les résultats montrent au cours du palmage des performances similaires voire supérieures et une augmentation de la consommation en oxygène maximale malgré la réduction de la réponse cardiaque chronotrope et du régime ventilatoire. Cette augmentation de la consommation en oxygène maximale peut résulter de l’accroissement du débit cardiaque par l’augmentation du volume d’éjection systolique et/ou de l’augmentation de l’extraction de l’oxygène au niveau tissulaire par une meilleure perfusion. L’absence de seuil ventilatoire ou son déplacement vers des valeurs plus élevées chez tous les sujets au cours du palmage sont en faveur d’une augmentation du métabolisme aérobie musculaire. La dernière étude analyse 18 cas d’oedèmes pulmonaires survenus chez des sujets sains en plongée en scaphandre autonome. Le lien commun est l’apparition de signes respiratoires lors de la remontée après une plongée profonde de plus de 30 minutes nécessitant des efforts physiques importants et/ou accompagnées d’une sensation désagréable de froid. Ceci suggère que l’exercice en immersion puisse entraîner des contraintes mécaniques, inflammatoires et pressionnelles suffisantes pour altérer la membrane alvéolocapillaire et provoquer un oedème pulmonaire. Les résultats de ces travaux démontrent la présence d’ajustements physiologiques permettant le maintien des performances lors d’un exercice en immersion. Cependant, des études complémentaires restent indispensables pour mieux définir les limites de ces adaptations afin de prévenir une réponse pathologique.
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O’Riordan, Shane F. "The Influence of Sports Compression Garments on Blood Flow and Post-Exercise Muscle Recovery." Thesis, 2021. https://vuir.vu.edu.au/42973/.
Повний текст джерелаАнотація:
Sports compression garments (SCG) are commonly used in athletic applications to improve recovery from exercise. Although the underlying mechanisms are not yet fully understood, they may be closely associated with alterations in blood flow, consistent with that reported in therapeutic medicine. As such, SCG have been implicated in increasing venous and muscle blood flow, and subsequently reducing symptoms of exercise-induced muscle damage (EIMD). However, research investigating the effects of SCG on blood flow, particularly during the post-exercise period, is limited.
Chapter 2 systematically reviewed and analysed the effects of SCG on peripheral measures of blood flow (i.e., venous and muscle blood flow) at rest, during, immediately post, and in recovery from a physiological challenge. From the 19 studies included in this meta-analysis, SCG appear to enhance venous and arterial measures of peripheral blood flow during and in the recovery of a physiological challenge. Also, this chapter highlighted that further research should aim to address the limitations of current compression research by reporting the pressure of the SCG, the blinding of participants, and assessing changes in blood flow during recovery.
The first experimental study of this thesis (Chapter 3) aimed to comprehensively investigate the effects of three different SCG types (socks, shorts, and tights) on resting markers of venous return, muscle blood flow and muscle oxygenation. Although sports compression tights were the most effective garment, all SCG types positively affected lower- limb blood flow. Thus, SCG may be a practical strategy for augmenting blood flow in the lower limbs at rest.
The next study of this thesis (Chapter 4) aimed to investigate the effects of SCG on blood flow post-eccentric resistance exercise, and the influence on aspects of muscle recovery. This study also aimed to determine if the placebo effect is responsible for the improved exercise recovery associated with SCG use post-exercise. This was achieved by incorporating a placebo intervention that participants were informed was as effective as SCG for recovery and matching belief between the SCG and placebo conditions. Compression tights used post-exercise appear to increase blood flow and enhance psychological and performance indices of exercise recovery compared to both placebo and control conditions. These findings highlight that the benefits of SCG are likely not due to a placebo effect.
The final study of this thesis (Chapter 5) investigated the effects of SCG on skeletal muscle microvascular blood flow by using contrast-enhanced ultrasound (CEU), a novel technique in compression research. In addition, macrovascular blood flow (i.e., femoral artery), muscle oxygenation, and exercise performance were measured before, during, and following repeated-sprint exercise (RSE). Compression tights attenuated muscle microvascular blood flow following exercise, but a divergent increase in femoral artery blood flow was also observed. However, despite these compression-induced alterations in macro and microvascular blood flow, there was no difference in exercise performance with SCG.
Based on this thesis's findings, SCG appear to benefit macrovascular blood flow, with a divergent effect on microvascular blood flow. Also, compression-induced increases in blood flow for up to 4 h post-resistance exercise coincided with improved muscle recovery.
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Chatauret, Nicolas. "Études du métabolisme cérébral et musculaire lors d'une insuffisance hépatique aiguë : implications pour de nouvelles stratégies thérapeutiques." Thèse, 2005. http://hdl.handle.net/1866/15328.
Повний текст джерелаКниги з теми "Muscle oedema"
1
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.
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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.
Повний текст джерелаАнотація:
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).
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Grau, Josep M., and Esteban Poch. Pathophysiology and management of rhabdomyolysis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0355.
Повний текст джерелаАнотація:
Rhabdomyolysis is a potentially life-threatening syndrome characterized by the breakdown of skeletal muscle. It is associated with myalgia, muscle tenderness, swelling, and/or stiffness, accompanied by weakness and raised levels of creatine kinase (CK), myoglobin, phosphate and potassium, sometimes with acute kidney injury (AKI). There are multiple causes of this syndrome, traumatisms and myotoxic effect of drugs being the most frequent in developed countries. The pathophysiology involves direct trauma, as well as energy (ATP) depletion with disruption of sarcolemma integrity and muscle destruction. The sequestration of plasma water leads to hypovolaemic shock, while the release of muscle content, mainly myoglobin and potassium lead to the most severe complications of this syndrome, acute kidney injury/hyperkalaemia. The kidney injury is driven both by renal ischaemia due to vasoconstriction and to the toxic effects of myoglobin. The local oedema produced by the release of muscle content remains trapped within the fascia and can lead to compartment syndrome. Volume repletion with saline is essential to avoid hypovolaemic shock and acute kidney injury (AKI). With respect to compartment syndrome, close monitoring of clinical signs and compartment pressures is essential, since it can evolve to a surgical emergency. The prognosis of rhabdomyolysis is determined by age, baseline conditions and, most importantly, whether or not severe AKI develops.
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Cantu, Robert V., and Robert C. Cantu. Injuries to the head and cervical spine. Edited by Neil Armstrong and Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0046.
Повний текст джерелаАнотація:
Traumatic brain and cervical spine injuries in young athletes encompass a wide spectrum, with some injuries occurring in otherwise ‘safe’ sports, and others in high-risk sports where head and cervical spine injuries are the norm. Athletic brain injuries include concussion, intracranial haemorrhage, malignant brain oedema syndrome, and axonal shear. In the cervical spine, injuries include muscle strains, contusions, fractures, or ligamentous disruptions with nerve root or spinal cord injury. Knowledge of these injuries and their signs and symptoms is important for the physician covering a sporting contest or practice. Additionally, preparedness for potential head or cervical spine injury must be addressed by health professionals providing sporting event coverage. This chapter reviews how traumatic brain and cervical spine injuries typically occur in young athletes. It also discusses what the initial treatment of these injuries should entail, along with a discussion of return to play considerations.
Частини книг з теми "Muscle oedema"
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Clark, Andrew L., and John G. F. Cleland. "Acute cardiac failure: definitions, investigation, and management." In Oxford Textbook of Medicine, 2728. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.16512.
Повний текст джерелаАнотація:
Presentations of acute heart failure fall into three overlapping categories: (1) acute breathlessness and pulmonary oedema, (2) chronic fluid retention and peripheral oedema (anasarca), and (3) cardiogenic shock. Examination features include tachycardia, hypotension, a raised venous pressure, basal crackles, and peripheral oedema. Auscultation may reveal a third heart sound or features of precipitating valvular heart disease. Initial management focuses on confirming the diagnosis and identification of the immediate precipitant (e.g. arrhythmias, myocardial infarction, decompensating valvular heart disease). Initial investigations include a 12-lead electrocardiogram (ECG), chest radiograph, full blood count, biochemical screen, troponin and thyroid function. Brain natriuretic peptide (BNP) is useful in confirming the diagnosis where clinical features are present and a normal BNP is helpful in excluding the diagnosis. All patients should undergo echocardiographic assessment early in the course of a hospital admission to assess left ventricular function and to look for underlying valvular heart disease. In patients with acute pulmonary oedema investigation and management should proceed simultaneously. Intravenous loop diuretics and nitrates are commonly used therapies and may be combined with ventilatory support with oxygen and continuous positive airways ventilation. Mechanical support may be appropriate as a bridge to definitive therapy in potentially reversible causes. Inotropes are often used but without convincing evidence that they improve outcome. In patients with features are of peripheral oedema and low cardiac output, fluid retention (usually >5 litres) is the predominant feature. Management is principally with bed rest, loop diuretics (usually by intravenous infusion), and, where appropriate, aldosterone antagonists. Thiazide diuretics can be added in resistant cases. Prophylactic low molecular weight heparin should be prescribed. Careful monitoring of fluid balance with daily weights and daily electrolytes is essential. Angiotensin converting enzyme (ACE) inhibitors and subsequently β-blockade can be introduced once a satisfactory diuresis has been achieved. Management of cardiogenic shock is usually determined by the cause. Fluid status should be assessed and an adequate left ventricular filling pressure ensured by the administration of intravenous fluids where required (particularly in the case of right ventricular infarction). Revascularization is the mainstay of therapy in acute myocardial infarction. Circulatory support with intra-aortic balloon counter-pulsation (IABP), inotropic agents, ventricular assist devices (VADs), and extracorporeal membrane oxygenation should be considered for reversible causes (e.g. ventricular septal rupture, papillary muscle rupture, acute myocarditis and postpartum cardiomyopathy). Hospital admission with acute heart failure caries a poor prognosis with an average in-hospital mortality of 10–15% rising to up to 60% at 30 days in cases of cardiogenic shock.
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Fielding, Richard E., and Ken Farrington. "Clinical presentation of renal disease." In Oxford Textbook of Medicine, edited by John D. Firth, 4764–80. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0475.
Повний текст джерелаАнотація:
Renal disease may present in many ways, including (1) the screening of asymptomatic individuals; (2) with symptoms and signs resulting from renal dysfunction; and (3) with symptoms and signs of an underlying disease, often systemic, which has resulted in renal dysfunction. History and clinical signs—in many cases these are nonspecific or not apparent, and detection of renal disease relies on a combination of clinical suspicion and simple investigations, including urinalysis and estimation of renal function. Asymptomatic renal disease—this is common and most often detected as chronic depression of eGFR (known as chronic kidney disease, CKD), proteinuria, or haematuria, either as isolated features or in combination. Symptomatic renal disease—may present in many ways, including (1) with features of severe chronic depression of glomerular filtration rate—‘uraemia’, manifesting with some or all of anorexia, nausea, vomiting, fatigue, weakness, pruritus, breathlessness, bleeding tendency, apathy and loss of mental concentration, and muscle twitching and cramps; (2) acute kidney injury (AKI); (3) with urinary symptoms—frequency, polyuria, nocturia, oliguria, anuria, and visible (macroscopic) haematuria; and (4) loin pain. Specific renal syndromes—these include (1) nephrotic syndrome—comprising oedema, proteinuria, and hypoalbuminaemia—caused by primary or secondary glomerular disease; and (2) rapidly progressive glomerulonephritis with AKI. Other conditions—renal disease may be associated with and present in the context of many underlying conditions, including (1) diabetes mellitus; (2) renovascular disease; (3) myeloma and other malignancies; (4) infectious diseases, either as a nonspecific manifestation of the sepsis syndrome or as a specific complication of the particular infection; (5) systemic inflammatory diseases; (6) drug-induced renal disease; and (7) pregnancy.
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Hart, Andrew. "Pathophysiology." In Oxford Textbook of Plastic and Reconstructive Surgery, 293–94. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780199682874.003.0044.
Повний текст джерелаАнотація:
Compression neuropathy is the commonest form of peripheral nerve injury and refers to the symptoms and clinicopathological findings that arise when a peripheral nerve is subjected to acute or chronic external compression or impingement of sufficient magnitude to impair its microcirculation. As aerobic glycolysis fails, membrane potential regulation is impaired, and action potential transmission fails. The differential susceptibility of the various fibre types, which subserve different functions, results in a typical progression of symptoms from impaired fine touch and proprioception, through paraesthesia, to poorly localized pain. If compression persists, then secondary intraneural and vascular anatomical changes establish a downward spiral of worsening intraneural oedema and fibrosis, axonotmesis, and denervation atrophy of target muscles. The condition becomes refractory to decompression. The impact on the patient depends upon the severity of neuropathy, and the nerve affected. A small number of anatomical sites particularly predispose to compression (e.g. the carpal tunnel), resulting in the common clinical syndromes.