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1
G, Rock, ed. Apheresis: Proceedings of the 2nd International Congress of the World Apheresis Association, held in Ottawa, Ontario, Canada, May 18-20, 1988. New York, NY: Wiley-Liss, 1990.
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2
Patrias, Karen. Therapeutic plasmapheresis in neurological disorders: January 1980 through April 1986 : 371 citations. Bethesda, Md: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 1986.
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3
Adam, Sheila, Sue Osborne, and John Welch. Haematological problems. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199696260.003.0012.
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This chapter discusses specific haematological disorders that require the patient to be admitted to the critical care unit. It describes the normal physiology of blood cells, clotting mechanisms, and fibrinolysis, and the management of related conditions such as thrombocytopenia, leukaemia, and clotting disorders such as disseminated intravascular coagulation. It also includes the management of the critical care patient with haematological malignancy. Specific therapies such as plasma exchange and anticoagulation therapy are discussed in detail and the monitoring of coagulation tests is explained. The chapter also describes the administration of blood and blood products, together with their associated hazards, and the effects of massive transfusions of blood.
4
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.
5
V, Prowse Christopher, ed. Plasma and recombinant blood products in medical therapy. Chichester: Wiley, 1992.
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6
Treib, Johannes. Volume Therapy. Edited by Johannes Treib. SPRINGER-VERLAG, 2000.
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7
Treib, Johannes. Volume Therapy. Springer, 2012.
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8
Valverde, Jose Luis. Blood, Plasma and Plasma Proteins: A Unique Contribution to Modern Healthcare. IOS Press, 2006.
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9
Fabrizi, Fabrizio, and Patrice Cacoub. The patient with cryoglobulinaemia. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0151.
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AbstractCryoglobulinaemia is characterized by the presence in the blood of proteins showing the that precipitate when serum is cooled. Clinically recognised cryoprecipitates are predominantly immunoglobulin-containing. In Type 1 cryoglobulinaemia, the precipitate is formed from a monoclonal paraprotein, usually IgG. In Type 2, a monoclonal IgM binds IgG to form a mixed precipitate. Type 3 cryoglobulins do not contain a monoclonal element.Type 1 cryoglobulins are a rare cause of renal disease, but cause a membranoproliferative glomerulonephritis (MPGN) with nephrotic syndrome and haematuria and usually with severe cutaneous involvement.Type 2 is most typically associated with renal disease, again characterized by MPGN and haematuria, with variable cutaneous signs and vasculitis in other organs. Many cases are associated with Hepatitis C virus (HCV) infection – but not all.Therapeutic approaches include optimal antiviral regimen, immunosuppressive therapy (corticosteroids, rituximab, and cytotoxic agents), and plasma exchange. Treatment of HCV-related mixed cryoglobulinaemia vasculitis should be adjusted according to the clinico-biological presentation.
10
Summers, Stephanie H., Dennis M. Smith, and Viktor A. Agranenko. Transfusion Therapy: Guidelines for Practice. Amer Assn of Blood Banks, 1990.
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11
Stephanie, Summers, Smith Dennis M, and Agranenko V. A, eds. Transfusion therapy: Guidelines for practice. Arlington, Va: American Association of Blood Banks, 1990.
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12
Telford, Richard. Blood products and fluid therapy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198719410.003.0039.
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This chapter discusses the anaesthetic uses of blood products and other fluids. It begins with a discussion of blood products (red cells, platelets, fresh frozen plasma, and so on). It goes on to describe blood conservation techniques such as cell salvage. Massive transfusion is discussed with its protocol. The problems posed by Jehovah’s Witnesses who refuse blood products are explored. The chapter concludes with a discussion of fluid and electrolyte therapy.
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Telford, Richard. Blood products and fluid therapy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198719410.003.0039_update_001.
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This chapter discusses the anaesthetic uses of blood products and other fluids. It begins with a discussion of blood products (red cells, platelets, fresh frozen plasma, and so on). It goes on to describe blood conservation techniques such as cell salvage. Massive transfusion is discussed with its protocol. The problems posed by Jehovah’s Witnesses who refuse blood products are explored. The chapter concludes with a discussion of fluid and electrolyte therapy.
14
Qu, Lirong, and Darrell J. Triulzi. Blood product therapy in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0267.
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Transfusions are among the most common medical procedures in the intensive care unit. Several randomized controlled trials (RCT) indicate that restrictive red cell transfusion practice using a haemoglobin of <7g/dL is safe in critically-ill patients. Although similar RCT are not available for plasma or platelet transfusion guidelines, a large body of observational studies suggest that plasma transfusion for an invasive procedure has not been shown to be of benefit in patients with INR <2.0. Similarly, in thrombocytopenic patients, the target platelet count for bleeding or for an invasive procedure is 50,000/µl. Viral transmission risk has become exceedingly low. Other risks such as transfusion-associated circulatory overload and, to a lesser extent, transfusion-related acute lung injury, are much more common. Storage of red cells does not seem to be associated with adverse clinical outcomes. Alternatives using haemostatic agents, salvaged blood, and adherence to evidence-based transfusion guidelines probably reduce the need for transfusion in critically-ill patients.
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El Kenz, Hanane, and Philippe Van der Linden. The physiology of blood in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0011.
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Following the discovery of the ABO blood groups by Landsteiner in 1901, Albert Hustin described the first transfusion of a whole blood unit in 1914. The modern transfusion era really begins in 1916 with the discovery of sodium citrate as an anticoagulant by the same physician, allowing blood conservation in dedicated packs. Since that time, many advances have been made especially over the past two decades in the storage, the conservation, and the laboratory testing of blood components and in transfusion medicine practice. Transfusion of whole blood has been replaced by blood component therapy, which consists of the administration of packed red blood cells, fresh frozen plasma, or platelets. Although blood transfusion is safer than ever, the risk of complications will never reach zero. The risk of infectious transfusion-transmitted diseases has been markedly reduced by the implementation of extensive infectious disease testing, donor selection, and pathogen-inactivation procedures. In countries with a high human development index, the leading causes of allogeneic blood transfusion-related deaths actually resulted from immunological and septic complications. The first section of this chapter describes the structure, function, and immunological aspects of the different blood components that are routinely transfused today. The second section details the composition of the different blood components, their indications, the pre-transfusion compatibility tests, and the main adverse effects associated with their transfusion.
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Noris, Marina, and Tim Goodship. The patient with haemolytic uraemic syndrome/thrombotic thrombocytopenic purpura. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0174.
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The patient who presents with microangiopathic haemolytic anaemia, thrombocytopenia, and evidence of acute kidney injury presents a diagnostic and management challenge. Haemolytic uraemic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) are two of the conditions that frequently present with this triad. They are characterized by low platelet count with normal or near-normal coagulation tests, anaemia, and signs of intravascular red cell fragmentation on blood films, and high LDH levels.HUS associated with shiga-like toxins produced usually by E.coli (typically O157 strains) may occur in outbreaks or sporadically, with geographical variations in incidence. It is predominantly a disease of young children in which painful blood diarrhoea in a minority of infected patients is succeeded by microangiopathy and acute kidney injury. Management is supportive and recovery is usual, although permanent renal damage may lead to later deterioration. Older patients may be affected and tend to have worse outcomes. Neuraminidase-producing Streptococcus pneumoniae infections (usually pneumonia) very rarely cause a similar HUS.Atypical HUS occurs sporadically and is increasingly associated with defects in the regulation of the complement pathway, either genetic or autoimmune-caused. It may respond to plasma exchange for fresh frozen plasma. Recurrences are common, including after transplantation.TTP is associated with more neurological disease and less renal involvement, but HUS and TTP overlap substantially in their manifestations. The underlying problem is in von Willebrand factor (vWF) cleavage. The plasma metalloprotease ADAMTS13 is responsible for cleaving vWF multimers, a process that is important to prevent thrombosis in the microvasculature. Autoantibodies or rarely genetic deficiency may impair this process. Plasma exchange may remove antibodies and replenish the protease.
17
Wijdicks, Eelco F. M., and Sarah L. Clark. Immunosuppression and Immunotherapy. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190684747.003.0010.
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Immune modulation in the neurosciences intensive care unit mostly involves high-dose corticosteroids, plasma exchange, and immunoglobulin. Corticosteroids are frequently used in patients with neurologic complications of cancer. Neurosurgeons typically use corticosteroids after performing a craniectomy to reduce cerebral edema. Corticosteroids are the established initial treatment modality of choice for patients with acute metastatic epidural spinal cord compression. Therapeutic apheresis or immunoglobulin is generally used as supportive therapy in patients with Guillain-Barré syndrome, myasthenia crisis, and autoimmune encephalitis. Immune modulation has been considered essential in autoimmune encephalitis despite lack of controlled clinical trials. In these now better characterized disorders, a combination of corticosteroids, intravenous immune globulin (IVIG), plasma exchange, rituximab, or cyclophosphamide are used. The use of acute immunotherapy and precautionary measures are discussed in this chapter.
18
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.
19
Fabrizi, Fabrizio. Hepatitis C. Edited by Vivekanand Jha. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0186.
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Hepatitis C virus (HCV) is associated with a large spectrum of histopathological lesions in both native and transplanted kidneys. The exact frequency of kidney damage in HCV-infected patients remains unknown, but the most frequent associated renal lesion is membranoproliferative glomerulonephritis (MPGN) with deposition of immunoglobulin and complement (MPGN type 1), usually in the context of type II mixed cryoglobulinaemia associated with a monoclonal IgM which binds IgG.Various approaches have been tried for the treatment of HCV-related glomerulonephritis, including immunosuppressive therapy (corticosteroids and cytotoxic agents), plasma exchange, and antiviral agents. Use of antiviral drugs for treatment of HCV-associated glomerulonephritis has shown encouraging results. Immunosuppressive therapy is recommended for cryoglobulinaemic kidney disease. Two distinct approaches should be considered for the treatment of HCV-associated cryoglobulinaemic glomerulonephritis according to the level of proteinuria and kidney failure. Preliminary evidence on rituximab therapy for HCV-related cryoglobulinaemic glomerulonephritis exists but several questions related to its use remain unclear.
20
Meyrier, Alain, and Patrick Niaudet. Primary focal segmental glomerulosclerosis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0057_update_001.
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Primary focal segmental glomerulosclerosis (FSGS) causes nephrotic syndrome and by definition is not caused by any of the known causes of podocyte toxicity or focal segmental sclerosis such as viral infections or toxins. A number of genetic causes of FSGS are commonly diagnosed in early childhood. Other causes of segmental scarring need to be distinguished. Genotypes in APOL1 of African origin are associated with higher incidence of FSGS and poorer responses to treatment. Cellular and collapsing FSGS are variants of FSGS in which there is overt acute podocytopathy and they have a relatively poor prognosis. A glomerular tip lesion is thought to have a slightly better prognosis than other types. Some cases of primary FSGS respond to high-dose corticosteroids, sometimes only after prolonged therapy. Response to steroids is a good prognostic sign, and without a response, progressive loss of renal function is likely. A circulating factor is implicated by the observation that proteinuria can recur in a donor kidney within hours of transplant. Plasma exchange appears to remove this factor but it is not conclusively identified.
21
Waldek, Stephen. Fabry disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0337.
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Fabry disease is a rare X-linked lysosomal storage disorder in which deficiency of alpha-galactosidase A leads to accumulation of substrate, mostly globotriaosylceramide, which causes a progressive, multiorgan disease affecting predominantly the kidneys, skin, heart, and nervous system. Painful peripheral (‘acral’) neuropathy is characteristic.Key clinical signs are angiokeratoma found by close examination of skin; characteristic eye lesions may be seen; lipid deposits may be seen in urine. Renal biopsy appearances are characteristic and this is commonly where the diagnosis is first made. Increasingly, cardiologists are suspecting the condition in adults with echocardiographic appearances of left ventricular hypertrophy. Diagnosis in men is usually made by measurement of alpha-galactosidase in either white cells or plasma (or using blood spots). Unfortunately, many female patients can have normal enzyme levels so that genetic testing is the only way to confirm a diagnosis. Non-selective screening strategies (e.g. males on renal replacement therapy with uncertain renal diagnoses) have had low yields.
22
Harper, Lorraine, and David Jayne. The patient with vasculitis. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0160.
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The goals of treatment in renal vasculitis are to stop vasculitic activity and recover renal function. Subsequent strategies are required to prevent vasculitis returning and to address longer-term co-morbidities caused by tissue damage, drug toxicity, and increased cardiovascular and malignancy risk.Cyclophosphamide and high-dose glucocorticoids remain the standard induction therapy with alternative immunosuppressives, such as azathioprine, to prevent relapse. Plasma exchange improves renal recovery in severe presentations. Refractory disease resulting from a failure of induction or remission maintenance therapy requires alternative agents and rituximab has been particularly effective. Replacement of cyclophosphamide by rituximab for remission induction is supported by recent evidence. Methotrexate is effective in non-renal vasculitis but difficult to use in patients with renal impairment. Mycophenolate mofetil seems to be effective but there is less long-term evidence.Drug toxicity contributes to co-morbidity and mortality and has led to newer regimens with reduced cyclophosphamide exposure. Glucocorticoid toxicity remains a major problem with controversy over the rapidity with which glucocorticoids can be reduced or withdrawn.Disease relapse occurs in about 50% of patients. Early detection is less likely to lead to an adverse affect on outcomes. Rates of cardiovascular disease and malignancy are higher than in control populations but strategies to reduce their risk, apart from cyclophosphamide-sparing regimens, have not been developed. Thromboembolic events occur in 10% and may be linked to the recently identified autoantibodies to plasminogen and tissue plasminogen activator.Renal impairment at diagnosis is a strong predictor of patient survival and renal outcome. Other predictors include patient age, antineutrophil cytoplasmic antibody subtype, disease extent and response to therapy. Chronic kidney disease can stabilize for many years but the risks of end-stage renal disease are increased by acute kidney injury at presentation or renal relapse. Renal transplantation is successful with similar outcomes to other causes of end-stage renal disease.
23
Kuypers, Dirk R. J., and Maarten Naesens. Immunosuppression. Edited by Jeremy R. Chapman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0281_update_001.
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Combination immunosuppressive therapy produces excellent short-term results after kidney transplantation. Long-term graft survival has improved, but less dramatically. Death with a functioning graft remains the primary cause of graft loss. Dosing of current immunosuppressive therapy balances between careful clinical interpretation of time-driven immunological risk assessments and drug-related toxicity on the one hand, and the use of simple surrogate drug exposure indicators like blood/plasma concentrations on the other. The combined use of calcineurin-inhibitors (CNIs) with mycophenolic acids and corticosteroids has been fine-tuned over the last decade, based on empirically derived observations as well as on the results of large multicentre randomized clinical studies. Corticosteroid withdrawal and avoidance are feasible, at least in patients with a low immunological risk, but CNI-free protocols have had few long-term successes. Some minimization strategies have increased risk of developing acute rejection or (donor-specific) anti-HLA antibodies, with deleterious effects on the graft. Mammalian target of rapamycin inhibitors (mTORi) have shown limited benefit in early CNI replacement regimens and their long-term use as primary drug is hampered by intolerance. In the setting of particular malignant disease occurring after transplantation, such as squamous cell carcinoma of the skin and Kaposi’s sarcoma, mTORi seem promising. Induction agents (anti-interleukin 2 receptor monoclonal antibodies, antithymocyte globulins) effectively diminish the risk of early immunological graft loss in recipients with moderate to high immunological risk but at the price of more infectious or malignant complications. While personalized transplantation medicine is only in its early stages of development, attempts are made to quantitatively measure the clinical degree of immunosuppression, to tailor immunosuppressive therapy more specifically to the patient’s individual profile, and to monitor graft status by use of invasive (e.g. surveillance renal biopsies) and non-invasive biomarkers. These scientific endeavours are a necessity to further optimize the current immunosuppressive therapy which will remain for some time to come.
24
Bellani, Giacomo, and Antonio Pesenti. Treating respiratory failure with extracorporeal support in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0105.
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During extracorporeal support or extracorporeal membrane oxygenation (ECMO) blood is diverted from the patient to an artificial lung for gas exchange, then returned into the patient’s circulation once arterialized. While a low-blood-flow bypass can remove comparatively high amounts of CO2, oxygenation is limited by venous haemoglobin saturation and requires high flows. Several technical improvements led to a profound change in the safety and applicability of ECMO in recent years, even permitting the transfer of patients undergoing ECMO. ECMO has been proposed as salvage therapy for the most severe acute respiratory distress syndrome patients—warranting viable levels of oxygenation. In 2009, the ‘CESAR’ trial provided formal evidence in favour of ECMO application in adults with ARDS. An important indication for the early use of ECMO in ARDS came from the outbreaks of H1N1 influenza, when several countries set up networks aimed at coordinating the application of ECMO. Recent reports suggest the use of ECMO in less severe patients with the purpose of removing CO2, decreasing the need for ventilation and ventilator-induced lung injury,
25
Jayne, David. Treatment of ANCA-associated vasculitis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0132.
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The goals of treatment in anti-neutrophil cytoplasm antibody (ANCA) vasculitis are to stop vasculitic activity, to prevent vasculitis returning, and to address longer-term comorbidities caused by tissue damage, drug toxicity, and increased cardiovascular and malignancy risk. Cyclophosphamide and high-dose glucocorticoids remain the standard induction therapy with alternative immunosuppressives, such as methotrexate or azathioprine, to prevent relapse. Refractory disease resulting from a failure of induction or remission maintenance therapy requires alternative agents and rituximab has been particularly effective. Replacement of cyclophosphamide by rituximab for remission induction is supported by recent evidence. Additional therapy with intravenous methylprednisolone and plasma exchange is employed in severe presentations with failing vital organ function. Drug toxicity contributes to comorbidity and mortality and has led to newer regimens with reduced cyclophosphamide exposure. Glucocorticoid toxicity remains a major problem, with controversy over the rapidity with which glucocorticoids can be reduced or withdrawn. Disease relapse occurs in 50% and requires early detection at a stage when it will not adversely affect outcomes. Rates of cardiovascular disease and malignancy are higher than in control populations but strategies to reduce their risk, apart from cyclophosphamide-sparing regimens, have not been developed. Thromboembolic events occur in 10% and may be linked to the recently identified autoantibodies to plasminogen and tissue plasminogen activator. Outcomes of vasculitis depend heavily on the level of tissue damage at diagnosis, especially renal dysfunction, but are also influenced by patient age, ANCA subtype, disease extent, and response to therapy. Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)is treated along similar principles to granulomatosis with polyangiitis (GPA) and microscopic polyangiitis but the persistence of steroid-dependent asthma in over one-third and differences in pathogenesis has suggested alternative treatment approaches. Chronic morbidity results from tissue damage and is especially common in the upper and lower respiratory tract and kidneys. Tracheobronchial disease is a severe late complication of GPA, while deafness, nasal obstruction, and chronic sinusitis are sequelae of nasal and ear vasculitis. Chronic infection of damaged epithelial surfaces acts as a drive for vasculitic activity and adequate infection control is necessary for stable remission. Chronic kidney disease can stabilize for many years but the risks of endstage renal disease (ESRD) are increased by acute kidney injury at presentation or renal relapse. Renal transplantation is successful, with similar outcomes to other causes of ESRD.
26
Pollock, Rob. Total hip replacement: modes of failure. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.007010.
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♦ Total hip replacements (THRs) may fail in various ways. They may become infected, they may be subject to aseptic loosening, they may dislocate, or a periprosthetic fracture may occur. The patient with a failed THR must be thoroughly assessed before treatment is contemplated♦ Infection may be acute or chronic. Assessment involves clinical assessment, plain radiographs, blood tests (C-reactive protein and erythrocyte sedimentation rate), hip aspiration, and, sometimes, nuclear medicine. The acutely infected hip may be treated with one-stage revision. This involves thorough lavage, debridement, and exchange of all modular components as well as long-term antibiotic therapy. The gold standard of treatment for a chronically infected THR is a two-stage revision. Success rates of 80–90% can be expected♦ Aseptic loosening typically occurs at the cement bone interface in hips where a metal-on-polyethylene bearing couple has been used. Bone resorption takes place as a result of an inflammatory response to small wear particles. After infection has been excluded the treatment of choice is a single-stage revision♦ Dislocation may be the result of patient factors, implant factors, or poor surgical technique. It is imperative for the clinician to minimize the risk by selecting patients carefully, using the correct combination of implants and performing surgery accurately♦ The management of periprosthetic fractures depends on how well the implants are fixed and quality of bone stock. Treatment ranges from simple fixation of the fracture through to revision augmented with strut allograft.