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1
Thomas, Michael, and K. L. Mittal, eds. Atmospheric Pressure Plasma Treatment of Polymers. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118747308.
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service), SpringerLink (Online, ed. Low Pressure Plasmas and Microstructuring Technology. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2009.
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3
Kogoma, Masuhiro. Generation and application of atmospheric pressure plasmas. Hauppauge, N.Y: Nova Science Publishers, 2011.
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4
Wells, Nikita. Soviet research on the transport of intense relativistic electron beams through low-pressure air. [Santa Monica, Calif.]: Rand Corp., 1986.
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5
Franz, Gerhard. Low Pressure Plasmas and Microstructuring Technology. Springer, 2010.
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7
Thomas, Michael, and K. L. Mittal. Atmospheric Pressure Plasma Treatment of Polymers: Relevance to Adhesion. Wiley & Sons, Incorporated, John, 2013.
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Thomas, Michael, and K. L. Mittal. Atmospheric Pressure Plasma Treatment of Polymers: Relevance to Adhesion. Wiley & Sons, Incorporated, John, 2013.
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9
Thomas, Michael, and K. L. Mittal. Atmospheric Pressure Plasma Treatment of Polymers: Relevance to Adhesion. Wiley-Interscience, 2013.
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10
Non-Equilibrium Air Plasmas at Atmospheric Pressure (Series in Plasma Physics) (Plasma Physics). Taylor & Francis, 2004.
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11
Metcalf, Myers Roger, and United States. National Aeronautics and Space Administration., eds. Mechanisms of anode power deposition in a low pressure free burning arc. [Washington, DC]: National Aeronautics and Space Administration, 1994.
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12
Metcalf, Myers Roger, and United States. National Aeronautics and Space Administration., eds. Mechanisms of anode power deposition in a low pressure free burning arc. [Washington, DC]: National Aeronautics and Space Administration, 1994.
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13
United States. Environmental Protection Agency. Office of Municipal Pollution Control. Office of Water. and Metcalf & Eddy., eds. Heat treatment/low pressure oxidation systems: Design and operational considerations. Washington, D.C: Office of Municipal Pollution Control, Office of Water, U.S. Environmental Protection Agency, 1985.
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14
United States. Environmental Protection Agency. Office of Municipal Pollution Control. Office of Water. and Metcalf & Eddy., eds. Heat treatment/low pressure oxidation systems: Design and operational considerations. Washington, D.C: Office of Municipal Pollution Control, Office of Water, U.S. Environmental Protection Agency, 1985.
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15
United States. Environmental Protection Agency. Office of Municipal Pollution Control. Office of Water and Metcalf & Eddy, eds. Heat treatment/low pressure oxidation systems: Design and operational considerations. Washington, D.C: Office of Municipal Pollution Control, Office of Water, U.S. Environmental Protection Agency, 1985.
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16
Langer, Thomas, and Pietro Caironi. Pathophysiology and therapeutic strategy of respiratory alkalosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0114.
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Respiratory alkalosis is a condition characterized by low partial pressure of carbon dioxide and an associated elevation in arterial pH caused by an imbalance between CO2 production and removal, in favour of the latter. Conditions that cause increased alveolar ventilation, without having a reduction in pH as input stimulus, will cause hypocapnia associated with a variable degree of alkalosis. The major effect of hypocapnia is the increase in pH (alkalosis) and the consequent shift of electrolytes that occurs in relation to it. As a general law, in plasma, anions will increase, while cations will decrease. The acute reduction in ionized calcium, due to the change in extracellular pH, may cause neuromuscular symptoms ranging from paraesthesias, to tetany and seizures. The effect on urine is an increase in urinary strong ion difference/urinary anion gap and a consequent increase in urinary pH. Finally, acute hypocapnic alkalosis causes a constriction of cerebral arteries that can lead to a reduction of cerebral blood flow. The clinical approach to respiratory alkalosis is usually directed toward the diagnosis and treatment of the underlying clinical disorder.
17
H, Becker Kurt, ed. Non-equilibrium air plasmas at atmospheric pressure. Bristol: Institute of Physics, 2005.
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18
A, Kothari, and Risk Reduction Engineering Laboratory (U.S.), eds. Separation of hazardous organics by low pressure membranes: Treatment of soil-wash rinse-water leachates. Cincinnati, Ohio: Risk Reduction Engineering Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, 1992.
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19
Separation of hazardous organics by low pressure membranes: Treatment of soil-wash rinse-water leachates. Cincinnati, Ohio: Risk Reduction Engineering Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, 1992.
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20
Low cost pressure infiltration casting of reinforced superalloy components: Contract no.: NAS 3-27541. [Washington, DC: National Aeronautics and Space Administration, 1997.
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21
Fagard, Robert, Giuseppe Mancia, and Renata Cifkova. Blood pressure. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0014.
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Prevention of hypertension can help prevent cardiovascular disease and renal complications. Obesity, a high sodium and low potassium intake, physical inactivity, and high alcohol consumption all contribute to the development of hypertension, and randomized controlled trials have shown that appropriate lifestyle modifications are able to reduce blood pressure and/or prevent the development of hypertension. The major complications of hypertension are stroke, coronary heart disease, heart failure, peripheral artery disease, and chronic kidney disease. Multiple randomized controlled trials and their meta-analyses have shown that treatment with antihypertensive drugs reduces the incidence of fatal and non-fatal cardiovascular events. In addition, meta-analyses have shown that there are no clinically relevant differences in the effects of the five major drug classes on outcome, so all of them are considered suitable for the initiation and maintenance of antihypertensive therapy. Nevertheless, the therapeutic approach in the elderly, women, and patients with diabetes, cerebrovascular, cardiac, or renal disease deserves special attention.
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Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghant. Disorders of plasma calcium. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0175.
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The extracellular calcium ion concentration is tightly regulated through the actions of parathyroid hormone (PTH) and vitamin D (1,25-dihydroxyvitamin D) on bone, kidney, and intestines. Abnormalities in these homeostatic mechanisms may lead to increased or decreased serum calcium concentrations, resulting in hypercalcaemia or hypocalcaemia, respectively. Hypercalcaemic disorders may be further divided into those associated with a high/high-normal serum PTH level, and those associated with a low serum PTH concentration. Hypocalcaemia occurs when abnormalities in the physiological regulation of PTH and vitamin D results in calcium levels lower than the desired normal range. Failure of release of calcium from bone, and increased binding of calcium in the circulation, are other factors causing hypocalcaemia. This chapter discusses hypercalcaemia and hypocalcaemia, exploring definitions of the diseases, their etiologies, typical and uncommon symptoms, demographics, natural history, complications, diagnostic approaches, other diagnoses that should be considered, prognosis, and treatment.
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Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. An 80-Year-Old Myasthenia Gravis Patient with Worsening Weakness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0031.
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In myasthenia gravis, weakness and respiratory insufficiency can occur quickly. It is important for the treating physician to recognize this and institute treatment rapidly. Increasing weakness of the neck may herald impending respiratory insufficiency. The single breath count is an easy way ti assess ventilatory function. Because of bulbar weakness and increasing secretions usually bi-level positive pressure airway pressure is used with extreme caution. Intubation with effective management if the airway is preferred. Differentiation of myasthenic crisis from cholinergic crisis is explained; although cholinergic crisis is relatively uncommon. Treatment modalities can include intravenous immunoglobulin, plasma exchange, and corticosteroids. Corticosteroids should be used with caution since they may exacerbate myasthenic symptoms. Treatment with a steroid sparing agent is discussed. A table is presented which lists signs and symptoms that can suggest the need for intubation.
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Egan, Brian N. Hyponatremia/Hypernatremia. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0037.
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lSodium is the most abundant cation in the extracellular fluid and is important for regulation of plasma water concentrations and cell volume. Sodium cannot readily cross the blood-brain barrier, and changes in plasma sodium levels by altering free water movement can expand or shrink brain cells. Changes in brain cell volume can cause brain cell dysfunction and apoptosis. Correction of both high and low sodium levels must be done gradually, as rapid correction of dysnatremias can also damage brain cells. In this chapter we review the physiology of sodium regulation, and discuss the clinical implications of these disorders as well as present a treatment plan for safe correction.
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Murphy, Elaine. Tyrosinemia Type II. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0014.
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Tyrosinemia type II is a rare oculocutaneous disorder that in some individuals is also associated with developmental delay or other neurological problems. Bilateral keratitis and painful hyperkeratotic lesions of the palms and soles are the typical presenting lesions. Diagnosis is suggested by the clinical picture, elevated plasma tyrosine levels, and specific urinary metabolites. It is an autosomal recessive condition caused by mutations in the tyrosine aminotransferase (TAT) gene. Treatment is aimed at reducing plasma tyrosine levels and consists of a low-protein diet with age-appropriate amino acid (phenylalanine-free and tyrosine-free), vitamin, and mineral supplements. Significant maternal hypertyrosinemia is associated with a poor fetal outcome.
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Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson, and Nathaniel M. Robbins. A 30-Year-Old Male Requiring Management of Progressive Weakness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0006.
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Management of Guillain-Barré syndrome involves several factors. Pulmonary function tests are important to monitor. Telemetry and blood pressure must be monitored because of the significant risk of autonomic dysfunction. Intravenous immunoglobulin is the immunotherapy of choice for this disease, as it is less complicated to administer than plasma exchange. Supportive management issues to address include deep vein thrombosis prophylaxis, bowel/bladder care as ileus and urinary retention may be develop secondary to dysautonomia, physical/occupational/speech therapy consults, nutrition, and pain control. Gabapentin can also be helpful for GBS-related pain. This chapter discusses an approach to treatment that includes the role of respiratory and autonomic monitoring as well as immunotherapy considerations.
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O’Neal, M. Angela. Ringing in the Ears and Pain in the Head. Edited by Angela O’Neal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190609917.003.0015.
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The case illustrates the classic clinical features of a low-pressure headache. The pathophysiology results from the loss of cerebrospinal fluid (CSF). This causes sagging of the brain, stretching of the bridging veins, and venodilatation. The clinical history is of a headache that is worse in the upright position and remits when the patient is supine. Due to the connection of the perilymphatic fluid and CSF, postural tinnitus is a frequent symptom. Risk factors for low-pressure headache include those that are patient-specific: female sex, low body mass index, prior history of a low-pressure headache, and an underlying headache disorder. Operator-specific factors that decrease the risk of a postdural puncture headache (PDPH) include greater operator experience and the use of a smaller-gauge, non-cutting lumbar puncture needle. The best treatment for low-pressure headache is a blood patch with resolution in over 90% of low-pressure headaches.
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Dionisi-Vici, Carlo, Diego Martinelli, Enrico Bertini, and Claude Bachmann. HHH Syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0020.
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Hyperornithinemia-hyperammonemia-homocitrullinuria (HHH) syndrome is an autosomal recessive disorder of the urea cycle characterized by impaired transport of ornithine across the inner mitochondrial membrane. As seen in other urea cycle defects, in the acute phase the disease is characterized by intermittent episodes of hyperammonemia accompanied by vomiting, lethargy, and coma, with or without signs of acute liver failure. The disease course is characterized by a pyramidal tract dysfunction associated with myoclonic seizures and cerebellar symptoms. Most patients reaching adulthood manifest variable degrees of cognitive impairment and abnormal behavior. Long-term treatment consists of a low-protein diet supplemented with citrulline, arginine, or ornithine. Protein restriction may be combined with sodium benzoate. If plasma creatine levels are low, creatine supplementation should be instituted. Acute treatment is similar to other urea cycle defects.
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Wiklund, Olov, and Jan Borén. Pathogenesis of atherosclerosis: lipid metabolism. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0011.
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Lipids are carried in plasma as microparticles, lipoproteins, composed of a core of hydrophobic lipids and a surface of amphipathic lipids. In addition, the particles carry proteins (i.e. apolipoproteins). The proteins have key functions in the metabolism as receptor ligands, enzymes or activators. Lipoproteins are classified based on density into: chylomicrons, VLDL, IDL, LDL, and HDL. Retention of apoB-containing lipoproteins (LDL, IDL, and VLDL) in the arterial intima is the initiating event in the development of atherosclerosis. Retention is mediated by binding of apoB to structural proteoglycans in the intima. Increased plasma concentration of apoB-containing lipoproteins is the main risk factor for atherosclerotic cardiovascular disease (CVD) and the causative role of LDL has been demonstrated in several studies. Lp(a) is a subclass of LDL and elevated Lp(a) is an independent risk-factor, primarily genetically mediated. Genetic data support that high Lp(a) causes atherosclerosis. Elevated triglycerides in plasma are associated with increased risk for CVD. Whether triglycerides directly induce atherogenesis is still unclear, but current data strongly support that remnant particles from triglyceride-rich lipoproteins are causal. HDL are lipoproteins that have been considered to be important for reversed cholesterol transport. Low HDL is a strong risk-factor for CVD. However, the causative role of HDL is debated and intervention studies to raise HDL have not been successful. Reduction of LDL is the main target for prevention and treatment, using drugs that inhibit the enzyme HMG-CoA reductase, i.e. statins. Other drugs for LDL reduction and to modify other lipoproteins may further reduce risk, and new therapeutic targets are explored.
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Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0073_update_001.
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Cyclophosphamide and plasma exchange are the standard of care in rapidly progressive glomerulonephritis or lung haemorrhage caused by antiglomerular basement membrane (anti-GBM) disease, and it is unusual to encounter patients at earlier stages. Steroids are universally used in addition. There is some evidence that plasma exchange may not be a critical part of treatment at an earlier stage. There is no more than anecdotal evidence for other therapies. Slower-onset therapies such as antibodies to B cells are rarely appropriate. If untreated, patients with severe anti-GBM disease will not recover renal function and are at risk of pulmonary haemorrhage. Evidence for the pathogenicity of circulating anti-GBM antibodies provides rationale for removal of circulating antibodies as rapidly as possible, whilst simultaneously inhibiting their synthesis. This was behind the introduction of the combination of plasma exchange with immunosuppressive therapy in mid 1970s, which revolutionized outcomes. Plasmapheresis aims to remove circulating pathogenic antibodies against GBM and possibly other mediators; cyclophosphamide prevents further synthesis of autoantibodies; and steroids act as anti-inflammatory agents to attenuate the glomerular inflammatory response initiated by anti-GBM antibodies. It is clear from experimental models and occasional observations in man that the anti-cell mediated effects of current therapies are important too. Outcomes vary, but in general patient survival is now good, while renal survival remains poor, in many series less than 50% at 1 year. Treatment is toxic and after an early peak in deaths due to pulmonary haemorrhage, secondary infections are the next threat. It may therefore be best not to immunosuppress patients with a very poor renal prognosis who appear to be at low risk of pulmonary haemorrhage. Treatment can usually be curtailed after 3 months without recurrence. ANCA and anti-GBM antibodies occur together in some patients. This is typically an older group which often has features of vasculitis, and the anti-GBM response may often be secondary. Longer treatment as for small vessel vasculitis is usually indicated.
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de Koning, Tom J. Serine Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0023.
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Serine deficiency is a rare cause of intractable seizures and severe psychomotor retardation in infants and young children. However, in recent years it has become clear that serine deficiency in adolescents and adults can give rise to milder forms of seizure disorders and mild mental retardation or to a phenotype with severe progressive polyneuropathy. Serine deficiency can be diagnosed on the basis of low values of serine in plasma and CSF using routine amino acid analysis. However, with the introduction of next generation sequencing in clinical diagnostics the majority of patients are diagnosed through molecular testing of the three genes of the synthesis pathway. L-serine therapy is highly effective in the treatment of seizures and improvement of wellbeing and daily activities. Early diagnosis and timely treatment are important to prevent irreversible damage to the central or peripheral nervous system.
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Wijdicks, Eelco F. M., and Sarah L. Clark. Antihypertensives and Antiarrhythmics. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190684747.003.0013.
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Acute brain injury can precipitate a hypertensive response, which for the most part is the result of stress-induced, increased sympathetic activity. Acute stroke with hypertension may not be a response but more often a prior, untreated hypertension or a patient with no access to medication. This hypertensive response may wane quickly, and aggressive treatment of these temporary surges in blood pressure could have unwanted consequences. Important characteristics of most antihypertensive drugs used in the neurosciences intensive care unit are cost, having a rapid onset with a short duration of action, and having a low incidence of adverse side effects. Many of the antiarrhythmic drugs also have antihypertensive effects, so these drug classes are best combined in one chapter. This chapter discusses blood pressure targets, the most appropriate antihypertensive medications to use for acute management, and clinically relevant cardiac arrhythmias and their treatment.
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Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne, and Gareth Morris-Stiff. Bone and soft tissue malignancies. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199689842.003.0025.
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Haematological malignancies examines the epidemiology, genetics, clinical presentation and classification of these diseases, and presents current treatment approaches for each. First are the acute leukaemias, and the management of acute lymphoblastic leukaemia (ALL) and acute myeloid leukaemia (AML). Chronic myeloid leukaemia, its genetics and sensitivity to tyrosine kinase inhibitors, is described. Myelodysplastic syndromes and their management, are followed by chronic lymphoid leukaemias, a large heterogeneous group of diseases, and their treatment. Hodgkin lymphoma, its pathology and presentation, staging and role of PET scanning, is described along with current treatment with chemotherapy and limited radiotherapy. Non-Hodgkin lymphoma is another heterogeneous group of diseases, divided into low-grade and high-grade pathology, and varying in their genetics, presentation, and management. Rituximab is a key component of chemotherapy regimens against B-cell lymphoma. Myeloma and other plasma cell dyscrasias are described, and treatment options reviewed. Myeloma remains incurable, but with appropriate management consistent with prolonged good quality life. Treatment includes chemotherapy, bisphosphonate therapy, analgesics and radiotherapy, Throughout this chapter is emphasised the importance of clinical trials in driving the rapid improvements in treatment of these diseases.
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Buchaklian, Adam H., and David P. Dimmock. Citrin Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0018.
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Citrin deficiency is an inborn error of metabolism that appears to affect both the urea cycle and energy generation. Worldwide, citrin deficiency is likely one of the commonest inborn errors of metabolism, 60,000–80,000 individuals are estimated to have citrin deficiency in China alone. Children typically present with an abnormal newborn screen or neonatal intrahepatic cholestasis with citrin deficiency (NICCD). Adults typically present clinically with neuropsychiatric symptoms, hepatic dysfunction and hyperammonemia. As plasma amino acids typically show an elevated citrulline at the time of crisis, this presentation is known as citrullinemia type II (CTLN2). Without therapy, cases may progress to liver failure. Individuals may also suffer recurrent pancreatitis. In contrast to other urea cycle defects, the treatment for citrin deficiency requires a high protein, low carbohydrate diet. Acute hyperammonemia responds to arginine therapy. Sodium pyruvate has been reported to provide benefit. In addition many cases will require restriction of galactose. Liver transplant fully corrects the CTLN2 phenotype.
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Mebazaa, Alexandre, and Mervyn Singer. Therapeutic strategy in cardiac failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0152.
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The fundamental therapeutic principles of heart failure management are for acute heart failure with mainly signs of pulmonary congestion, normal or high blood pressure, and no signs of low cardiac output to reduce pulmonary congestion without affecting blood pressure. Management principles of cardiogenic shock management comprise improvement of forward flow with restoration/maintenance of adequate organ perfusion. Appropriate management requires sound appreciation of the underlying pathophysiology, awareness of the actions and potential side-effects of each therapeutic intervention, and a level of monitoring and investigation sophisticated enough to assess disease severity, and the effectiveness (or otherwise) of any treatment being given. Where possible, consideration of previous comorbidity factors and chronic symptomatology should guide how aggressive intervention should be. However, these must be based on documented fact, rather than hearsay or supposition. The patient should always be given the benefit of the doubt.
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Candido, Kenneth D., Teresa M. Kusper, Bora Dinc, and Nebojsa Nick Knezevic. Epidural Blood Patch. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190271787.003.0036.
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Post-dural-puncture headache (PDPH) is a consequence of neuraxial anesthesia, diagnostic lumbar puncture, intrathecal drug delivery systems, or any other technique involving dural trespass. The spinal headache results from a dural puncture that leads to cerebrospinal fluid (CSF) leakage from the subarachnoid space to the epidural space, culminating in intracranial hypotension and development of a low-pressure headache. A key element of PDPH is an increase in pain severity upon a change in position from supine to upright, which corresponds to a gravity-induced influence on CSF pressure dynamics. Age, sex, and design of the needle used correlate with the risk of headache. Sometimes, the headache resolves spontaneously. At other times, conservative treatment or aggressive measures are required to terminate the pain. An autologous epidural blood patch is an established way preventing or treating PDPH. A careful history must be obtained to identify other causes of headache before the blood patch is attempted.
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Gattinon, Luciano, and Eleonora Carlesso. Acute respiratory failure and acute respiratory distress syndrome. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0064.
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Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.
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Gattinon, Luciano, and Eleonora Carlesso. Acute respiratory failure and acute respiratory distress syndrome. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0064_update_001.
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Respiratory failure (RF) is defined as the acute or chronic impairment of respiratory system function to maintain normal oxygen and CO2 values when breathing room air. ‘Oxygenation failure’ occurs when O2 partial pressure (PaO2) value is lower than the normal predicted values for age and altitude and may be due to ventilation/perfusion mismatch or low oxygen concentration in the inspired air. In contrast, ‘ventilatory failure’ primarily involves CO2 elimination, with arterial CO2 partial pressure (PaCO2) higher than 45 mmHg. The most common causes are exacerbation of chronic obstructive pulmonary disease (COPD), asthma, and neuromuscular fatigue, leading to dyspnoea, tachypnoea, tachycardia, use of accessory muscles of respiration, and altered consciousness. History and arterial blood gas analysis is the easiest way to assess the nature of acute RF and treatment should solve the baseline pathology. In severe cases mechanical ventilation is necessary as a ‘buying time’ therapy. The acute hypoxemic RF arising from widespread diffuse injury to the alveolar-capillary membrane is termed Acute Respiratory Distress Syndrome (ARDS), which is the clinical and radiographic manifestation of acute pulmonary inflammatory states.
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Castle, David J., Peter F. Buckley, and Fiona P. Gaughran. The metabolic syndrome in schizophrenia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198811688.003.0003.
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The metabolic syndrome (MS) is a constellation of risk factors including increased waist circumference, high blood pressure, and elevated fasting glucose and triglycerides in conjunction with low levels of high-density lipoprotein. MS is associated with an elevated risk of adverse cardiovascular and other events. The general population rate of MS is increasing, but people with schizophrenia have markedly elevated rates compared to people without a mental illness. Reasons for this excess are complex, but certain antipsychotic agents can exacerbate risk and due care needs to be taken in prescribing such medications, with awareness of longitudinal risk. Treatment needs to be provided following established guidelines, to address aspects of MS should they occur.
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Yarlagadda, Vamsi V., and Ravi R. Thiagarajan. Cardiac Disease in Pediatric Intensive Care. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199918027.003.0007.
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This chapter on cardiac disease in pediatric intensive care provides essential information on cardiovascular physiology, how to assess cardiovascular and hemodynamic status, and principles of treatment of congenital and acquired cardiac disease in children. The review of physiology includes definitions of preload, afterload, oxygen content, cardiac output, vascular resistance, blood pressure, and cardiopulmonary interactions. Formulas to calculate key parameters are provided. The authors also summarize the presentation and care of most common cyanotic and acyanotic congenital heart defects, including treatment of low cardiac output syndrome, clinical sequelae of cardiopulmonary bypass, and the key aspects of treating pre- and postoperative patients with single-ventricle lesions (e.g., hypoplastic left heart syndrome). All three stages of single-ventricle palliation are discussed, with management summaries of children undergoing the Norwood, bidirectional Glenn, and Fontan operations. Finally, the chapter includes a discussion of the clinical presentation and management of viral myocarditis and cardiomyopathy.
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Banerjee, Amitava, and Kaleab Asrress. Screening for cardiovascular disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0351.
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Screening involves testing asymptomatic individuals who have risk factors, or individuals who are in the early stages of a disease, in order to decide whether further investigation, clinical intervention, or treatment is warranted. Therefore, screening is classically a primary prevention strategy which aims to capture disease early in its course, but it can also involve secondary prevention in individuals with established disease. In the words of Geoffrey Rose, screening is a ‘population’ strategy. Examples of screening programmes are blood pressure monitoring in primary care to screen for hypertension, and ultrasound examination to screen for abdominal aortic aneurysm. The effectiveness and feasibility of screening are influenced by several factors. First, the diagnostic accuracy of the screening test in question is crucial. For example, exercise ECG testing, although widely used, is not recommended in investigation of chest pain in current National Institute for Health and Care Excellence guidelines, due to its low sensitivity and specificity in the detection of coronary artery disease. Moreover, exercise ECG testing has even lower diagnostic accuracy in asymptomatic patients with coronary artery disease. Second, physical and financial resources influence the decision to screen. For example, the cost and the effectiveness of CT coronary angiography and other new imaging modalities to assess coronary vasculature must be weighed against the cost of existing investigations (e.g. coronary angiography) and the need for new equipment and staff training and recruitment. Finally, the safety of the investigation is an important factor, and patient preferences and physician preferences should be taken into consideration. However, while non-invasive screening examinations are preferable from the point of view of patients and clinicians, sometimes invasive screening tests may be required at a later stage in order to give a definitive diagnosis (e.g. pressure wire studies to measure fractional flow reserve in a coronary artery). The WHO’s principles of screening, first formulated in 1968, are still very relevant today. Decision analysis has led to ‘pathways’ which guide investigation and treatment within screening programmes. There is increasing recognition that there are shared risk factors and shared preventive and treatment strategies for vascular disease, regardless of arterial territory. The concept of ‘vascular medicine’ has gained credence, leading to opportunistic screening in other vascular territories if an individual presents with disease in one territory. For example, post-myocardial infarction patients have higher incidence of cerebrovascular and peripheral arterial disease, so carotid duplex scanning and measurement of the ankle–brachial pressure index may be valid screening approaches for arterial disease in other territories.
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Schiller, Adalbert, Adrian Covic, and Liviu Segall. Chronic tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0086_update_001.
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Chronic tubulointerstitial nephropathies (CTINs) are a group of renal diseases, characterized by variable interstitial inflammation and fibrosis and tubular atrophy, and a slow course towards end-stage renal disease (ESRD). The causes of CTIN are numerous, including nephrotoxic drugs and chemicals, infections, autoimmune diseases, obstructive uropathies, and metabolic disorders. Taken together, CTIN are responsible for less than 10% of all ESRD cases requiring renal replacement therapy. The clinical manifestations of CTIN typically comprise low-grade proteinuria, leucocyturia, and variably reduced glomerular filtration rate (GFR), whereas the blood pressure is usually normal or moderately increased. Tubular abnormalities are common, including type 2 (proximal) renal tubular acidosis, Fanconi syndrome, nephrogenic diabetes insipidus, and type 1 (distal) renal tubular acidosis, with hypokalaemia and nephrolithiasis. Radiology exams reveal shrunken kidneys, sometimes with irregular outlines. A renal biopsy is often required for the diagnosis of CTIN and its aetiology. The treatment of CTIN mainly involves discontinuation of exposure to nephrotoxins and specific therapy of renal infections, urinary tract obstruction, or underlying systemic diseases. Agents like ACE inhibitors and pirfenidone, which might reduce interstitial inflammation and fibrosis, are still under clinical evaluation.
43
Paech, Michael J., and Patchareya Nivatpumin. Postdural puncture headache. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0027.
Full textAbstract:
Postdural puncture headache (PDPH) may follow either deliberate or unintentional (accidental) penetration of the interdigitating meninges, the dura and arachnoid mater. It is one of the most common and clinically important complications of regional anaesthesia and analgesia in the obstetric population. The headache develops as a consequence of cerebrospinal fluid loss, low intracranial pressure and cerebrovascular changes in the upright position and can prove debilitating. The diagnosis is clinical, making thorough assessment and regular review all the more important, to revise treatment plans, exclude rare serious pathology such as subdural haematoma, and avoid misdiagnosis. This chapter reviews the pathophysiology, incidence, risk factors (needle, technical and patient related), features, natural history, diagnosis, and management of PDPH. High level evidence supports prevention by using small gauge, non-cutting spinal needles, but other preventative strategies against either unintentional dural puncture or PDPH are poorly supported. The absent or poor efficacy of measures such as bed rest, hydration, cerebral vasoconstrictor therapy, epidural or intrathecal saline injection, intrathecal catheter placement or prophylactic epidural blood patch, is noted. Validation of better evidence supporting epidural morphine or intravenous cosyntropin is required. Symptomatic treatment of PDPH is also unreliable. Very limited evidence that requires substantiation supports a modest benefit from caffeine, gabapentinoids or intravenous hydrocortisone. The intervention of epidural blood patch is highly likely to relieve post-spinal PDPH, but only completely resolves epidural needle-induced PDPH in 30–50% of cases. Much detail about EBP remains undetermined, but delayed intervention and injection of approximately 20 mL of autologous blood appear appropriate.
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Gevaert, Sofie A., Eric Hoste, and John A. Kellum. Acute kidney injury. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0068.
Full textAbstract:
Acute kidney injury is a serious condition, occurring in up to two-thirds of intensive care unit patients, and 8.8-55% of patients with acute cardiac conditions. Renal replacement therapy is used in about 5-10% of intensive care unit patients. The term cardiorenal syndrome refers to combined heart and kidney failure; three types of acute cardiorenal syndrome have been described: acute cardiorenal syndrome or cardiorenal syndrome type 1, acute renocardiac syndrome or cardiorenal syndrome type 3, and acute cardiorenal syndrome type 5 (cardiac and renal injury secondary to a third entity such as sepsis). Acute kidney injury replaced the previously used term ‘acute renal failure’ and comprises the entire spectrum of the disease, from small changes in function to the requirement of renal replacement therapy. Not only failure, but also minor and less severe decreases, in kidney function are of clinical significance both in the short and long-term. The most recent definition for acute kidney injury is proposed by the Kidney Disease: Improving Global Outcomes clinical practice guidelines workgroup. This definition is a modification of the RIFLE and AKIN definitions and staging criteria, and it stages patients according to changes in the urine output and serum creatinine (see Tables 68.1 and 68.2). Acute kidney injury is a heterogeneous syndrome with different and multiple aetiologies, often with several insults occurring in the same individual. The underlying processes include nephrotoxicity, and neurohormonal, haemodynamic, autoimmune, and inflammatory abnormalities. The most frequent cause for acute kidney injury in intensive cardiac care patients are low cardiac output with an impaired kidney perfusion (cardiogenic shock) and/or a marked increase in venous pressure (acute decompensated heart failure). Predictors for acute kidney injury in these patients include: baseline renal dysfunction, diabetes, anaemia, and hypertension, as well as the administration of high doses of diuretics. In the intensive cardiac care unit, attention must be paid to the prevention of acute kidney injury: monitoring of high-risk patients, prompt resuscitation, maintenance of an adequate mean arterial pressure, cardiac output, and intravascular volume (avoidance of both fluid overload and hypovolaemia), as well as the avoidance or protection against nephrotoxic agents. The treatment of acute kidney injury focuses on the treatment of the underlying aetiology, supportive care, and avoiding further injury from nephrotoxic agents. More specific therapies have not yet demonstrated efficacy. Renal replacement therapy is indicated in life-threatening changes in fluid, electrolyte, and acid-base balance, but there are also arguments for more early initiation.
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Gevaert, Sofie A., Eric Hoste, and John A. Kellum. Acute kidney injury. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0068_update_001.
Full textAbstract:
Acute kidney injury is a serious condition, occurring in up to two-thirds of intensive care unit patients, and 8.8-55% of patients with acute cardiac conditions. Renal replacement therapy is used in about 5-10% of intensive care unit patients. The term cardiorenal syndrome refers to combined heart and kidney failure; three types of acute cardiorenal syndrome have been described: acute cardiorenal syndrome or cardiorenal syndrome type 1, acute renocardiac syndrome or cardiorenal syndrome type 3, and acute cardiorenal syndrome type 5 (cardiac and renal injury secondary to a third entity such as sepsis). Acute kidney injury replaced the previously used term ‘acute renal failure’ and comprises the entire spectrum of the disease, from small changes in function to the requirement of renal replacement therapy. Not only failure, but also minor and less severe decreases, in kidney function are of clinical significance both in the short and long-term. The most recent definition for acute kidney injury is proposed by the Kidney Disease: Improving Global Outcomes clinical practice guidelines workgroup. This definition is a modification of the RIFLE and AKIN definitions and staging criteria, and it stages patients according to changes in the urine output and serum creatinine (see Tables 68.1 and 68.2). Acute kidney injury is a heterogeneous syndrome with different and multiple aetiologies, often with several insults occurring in the same individual. The underlying processes include nephrotoxicity, and neurohormonal, haemodynamic, autoimmune, and inflammatory abnormalities. The most frequent cause for acute kidney injury in intensive cardiac care patients are low cardiac output with an impaired kidney perfusion (cardiogenic shock) and/or a marked increase in venous pressure (acute decompensated heart failure). Predictors for acute kidney injury in these patients include: baseline renal dysfunction, diabetes, anaemia, and hypertension, as well as the administration of high doses of diuretics. In the intensive cardiac care unit, attention must be paid to the prevention of acute kidney injury: monitoring of high-risk patients, prompt resuscitation, maintenance of an adequate mean arterial pressure, cardiac output, and intravascular volume (avoidance of both fluid overload and hypovolaemia), as well as the avoidance or protection against nephrotoxic agents. The treatment of acute kidney injury focuses on the treatment of the underlying aetiology, supportive care, and avoiding further injury from nephrotoxic agents. More specific therapies have not yet demonstrated efficacy. Renal replacement therapy is indicated in life-threatening changes in fluid, electrolyte, and acid-base balance, but there are also arguments for more early initiation.