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1
Dorinsky, Paul M. The Sepsis syndrome. Philadelphia: W.B. Saunders, 1996.
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2
Barra, Pedro Miguel Craveiro. RNA turnover and energy metabolism of children with systemic inflammatory response syndrome and sepsis. London: University of Surrey Roehampton, 2001.
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3
K, Choi Augustine M., Hrsg. Acute respiratory distress syndrome. 2. Aufl. New York: Informa Healthcare USA, 2009.
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4
Cavaillon, Jean-Marc, und Christophe Adrie. Sepsis and non-infectious systemic inflammation: From biology to critical care. Weinheim: Wiley-VCH, 2009.
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5
Moaveni, Daria M. Systemic Inflammatory Response Syndrome and Sepsis in the Pregnant Patient. Herausgegeben von Matthew D. McEvoy und Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0047.
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The chapter “Systemic Inflammatory Response Syndrome and Sepsis in the Pregnant Patient” reviews diagnostic criteria for sepsis in pregnant women, as well as the etiology, risk factors, workup, and treatment of this preventable and treatable cause of maternal morbidity and mortality. It also briefly reviews the history and epidemiology of sepsis. It compares the original diagnostic criteria for systemic inflammatory response syndrome established in 1992, the sepsis diagnostic criteria from the Surviving Sepsis Campaign, and the Sepsis in Obstetrics Score. It discusses the initial workup and resuscitation, fluid management, vasopressor choice and dosing, and antimicrobial treatment for pregnant women with sepsis. It also reviews the obstetric implications of septic parturients.
6
Choi, Augustine M. K. Acute Respiratory Distress Syndrome. Taylor & Francis Group, 2016.
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7
Acute respiratory distress syndrome. 2. Aufl. New York: Informa Healthcare USA, 2010.
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8
Choi, Augustine M. K. Acute Respiratory Distress Syndrome. Taylor & Francis Group, 2016.
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9
(Editor), Arthur E. Baue, Eugen Faist (Editor) und Donald Fry (Editor), Hrsg. Multiple Organ Failure: Pathophysiology, Prevention, and Therapy. Springer, 2000.
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10
Yurdakul, Sebahattin, Emire Seyahi und Hasan Yazici. Behçet’s syndrome. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0135.
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Behçet's syndrome is a systemic inflammatory panvasculitis (affecting all sizes of vessels) of unknown aetiology. It is in vogue to include it among the systemic autoinflammatory conditions. Behçet's syndrome is more frequent along the ancient 'Silk Route' across Asia than it is in Western countries. The usual onset is the second or third decade, equally affecting either gender. However, young patients and male patients have more severe disease. Almost all patients have recurrent oral ulceration. Scar-forming genital ulcers, a variety of skin lesions including acneiform, erythema nodosum-like lesions, arthritis, potentially blinding panuveitis, thrombophlebitis, gastrointestinal disease, central nervous system (CNS) involvement, and life-threatening bleeding pulmonary artery aneurysms are seen. The pathergy phenomenon is a heightened tissue inflammatory response. The strongest genetic association is with HLA B51. There are immunological aberrations but not prominent enough to call it an autoimmune disease. Similarly, Behçet's syndrome does not fit easily into the broad concept of autoinflammatory diseases. The histopathology is also non-specific and the diagnosis is mainly clinical. Differentiation from Crohn's disease is very difficult. In more than one-half of the patients the disease burns out in time, thus only symptomatic therapy is indicated in some patients. However, eye involvement, pulmonary vascular disease, thrombophilic complications, CNS involvement, and gastrointestinal disease need prompt recognition and treatment. Brief courses of glucocorticosteroids along with immunosuppressives including the newer biologicals, interferon, and colchicine are commonly used. However, controlled clinical trials are not available for some of these medications especially when thrombophilia, CNS, and gastrointestinal disease are present.
11
Bittner, Edward A., und Shawn P. Fagan. The host response to trauma and burns in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0304.
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Following severe traumatic injury, patients enter a state of immune dysregulation consisting of both exaggerated inflammation and immune suppression. Traditionally, the host response has been viewed as an early systemic inflammatory response syndrome (SIRS) followed temporally by a compensatory anti-inflammatory or immune-suppressive response syndrome (CARS). While this paradigm has been widely accepted across both medical and scientific fields, recent advances have challenged this concept. The Glue grant investigators recently characterized both the initial inflammatory response to injury and the dynamic evolving recovery process. They found: (1) severe injury produces a rapid (< 12 hours) genomic reprioritization in which 80% of the leukocyte transcriptome is altered; (2) similarities in gene expression patterns between different injuries reveal an apparently fundamental response to severe inflammatory stress, which is far more common than different; (3) alterations in the expression of classical inflammatory and anti-inflammatory as well as adaptive immunity genes occur simultaneously, not sequentially after severe injury; (4) the temporal nature of the current SIRS/CARS paradigm is not supported at the level of the leukocyte transcriptome. Complications are not associated with genomic evidence of a ‘second hit’ and differ only in the magnitude and duration of this genomic reprioritization. Furthermore, the delayed clinical recovery with organ injury is not associated with dramatic qualitative differences in the leukocyte transcriptome. Finally, poor correlation between human and rodent inflammatory genomic responses will alter how the host response is studied in the future.
12
(Editor), John C. Marshall, und Jonathan Cohen (Editor), Hrsg. Immune Response in the Criticaly Ill (Update in Intensive Care and Emergency Medicine). Springer-Verlag Telos, 1999.
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13
Cavaillon, Jean-Marc, und Christophe Adrie. Sepsis and Non-Infectious Systemic Inflammation: From Biology to Critical Care. Wiley & Sons, Incorporated, John, 2009.
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14
Cooke, Graham. Sepsis. Herausgegeben von Patrick Davey und David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0309.
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Sepsis is a clinical syndrome defined by the presence of both infection and a systemic inflammatory response with or without organ damage. The pathogenesis of sepsis is complex and may differ according to the infecting microbe, the site of primary infection, and the host’s immunological and physiological status prior to infection. The term ‘systemic inflammatory response syndrome’ refers to the clinical manifestations of a dysregulated host immune response, while ‘bacteraemia’, in contrast, refers to the presence of viable organisms that can be cultured from blood.
15
Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson und Nathaniel M. Robbins. A 63-Year-Old Male with Severe Flaccid Weakness Post Motor Vehicle Accident. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0009.
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Neuromuscular disorders are important causes of newly acquired weakness in the intensive care unit. Although evaluation usually begins with physical examination findings, these can be compromised in the intensive care unit environment. Therefore, electrodiagnostic study becomes even more important as a tool in localizing weakness to nerve, muscle or neuromuscular junction. Critical illness neuropathy and myopathy occurs in the setting of sepsis and multiple organ failure where sepsis is accompanied by the systemic inflammatory response syndrome. Additional, intensive care unit-specific risk factors exist, predominantly relating to administration of high-dose steroids, nondepolarizing neuromuscular blocking agents, and sedating agents such as propofol. There is no specific treatment except for optimizing medical management of the underlying disorder, including prevention and management of sepsis, systemic inflammatory response syndrome, and organ damage, as well as avoidance of exacerbating medications.
16
Adam, Sheila, Sue Osborne und John Welch. Sepsis and multiple organ dysfunction. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199696260.003.0010.
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Sepsis—a dysregulated systemic inflammatory response to infection—occurs at some point in most critical illnesses, and is the most common cause of multiple organ dysfunction syndrome (MODS). Patients with MODS always present great challenges to the critical care team and are often at high risk of death. This chapter discusses the latest thinking about the infective causes and complex evolution of sepsis, with details of how each of the main body systems can be affected (e.g. in the form of acute respiratory distress syndrome) and how different organ functions can be assessed and dysfunction recognized. The priorities, principles, and practicalities of holistic care and management of patients with sepsis and MODS, including adjunct therapies and blood purification, is also described.
17
Shaefi, Shahzad, und Aaron Mittel. Disruption of Diffusion. Herausgegeben von Matthew D. McEvoy und Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0019.
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Acute respiratory distress syndrome (ARDS), transfusion-related acute lung injury (TRALI), and transfusion-associated circulatory overload (TACO) are common conditions in critically ill patients that lead to pulmonary edema and hypoxemia. The nonhydrostatic edema characteristic of ARDS and TRALI is caused by an intense inflammatory response leading to increased microvascular permeability and alveolar injury. TACO is an acute hydrostatic edema temporally associated with events that precipitate lung injury. Lung-protective ventilation is the mainstay of therapy for ARDS and TRALI; optimizing gas exchange is the goal for all three. Prompt recognition is an important skill for perioperative practitioners.
18
Waldmann, Carl, Neil Soni und Andrew Rhodes. Infection and inflammation. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199229581.003.0027.
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Pathophysiology of sepsis and multi-organ failure 462Infection control—general principles 464HIV 466Severe falciparum malaria 468Vasculitides in the ICU 470Source control 472Selective decontamination of the digestive tract (SDD) 474Markers of infection 476Adrenal insufficiency and sepsis 478Infectious agents entering the body lead to local inflammation, pus and abscess formation, and affect the whole body through systemic inflammation. Systemic inflammation is recognized by the presence of fever, abnormal WCC, and increased heart and respiratory rate, and is known as systemic inflammatory response syndrome (SIRS). If SIRS is due to infection (as distinct from other causes such as pancreatitis, burns or major trauma) it is defined as sepsis....
19
Patel, Sameer, und Julia Wendon. Pathophysiology and causes of acute hepatic failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0194.
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Acute liver failure (ALF) is a rare, life-threatening clinical syndrome, resulting in loss of hepatic metabolic and immunological function, in a person with no prior history of liver disease. Mortality can still exceed 50%. ALF is characterized by hepatic encephalopathy (HE) and coagulopathy, occurring within days or weeks. Establishing aetiology is essential for treatment, prognostication, and liver transplantation consideration. Viral hepatitis and drug-induced liver failure are the two commonest causes worldwide. Aetiology and time of onset of encephalopathy determines prognosis. Disease progression can rapidly result in multi-organ failure. Ammonia has been postulated in the development of HE, cerebral oedema and intracranial hypertension. Coagulopathy can be highly variable, with some patients prothrombotic, or exhibiting balanced coagulation disorders. Systemic inflammatory response syndrome (SIRS) and associated infection are frequently observed. Significant haemodynamic changes are common while renal failure is an independent risk factor for mortality. Respiratory failure is less common. Deranged homeostasis results in severe hypoglycaemia, and metabolic disturbance.
20
Nicholson, Grainne, und George M. Hall. Neuroendocrine physiology in anaesthetic practice. Herausgegeben von Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0008.
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This chapter describes the hormonal, metabolic, and inflammatory response to surgery—commonly known as the surgical stress response. The changes in protein, carbohydrate, and fat metabolism to provide fuel for oxidation are outlined as well as changes in salt and water metabolism. Psychological sequelae of fatigue and malaise are also common in patients undergoing surgery. Attenuating the metabolic and endocrine changes associated with surgery may reduce postoperative morbidity and expedite recovery; the choice of anaesthetic drugs and techniques (regional vs general anaesthesia) and the increasing use of laparoscopic surgery have all been used to try to achieve this objective. The most common metabolic disease which anaesthetists have to manage is diabetes mellitus (DM) and its pathophysiology and medical management, as well as that of the related metabolic syndrome are discussed. Adrenal tumours are rare but usually require surgical excision. Phaeochromocytomas present unique anaesthetic challenges, but pre-, intra-, and postoperatively in terms of fluid management and blood pressure control. Conn’s syndrome (primary hyperaldosteronism) can also result in hypertension and electrolyte disturbances. Cushing’s disease (glucocorticoid excess) presents with the clinical effects of steroid excess and many patients have concomitant DM. Finally, perioperative steroid supplementation for patients already taking steroids and undergoing surgery is discussed.
21
Keh, Didier. Steroids in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0054.
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The benefit of prolonged application of moderate-dose corticosteroids in systemic inflammatory diseases remains controversial. In critical illness, the endogenous cortisol effect may become insufficient due to adrenal dysfunction and corticosteroid resistance to counterbalance an exaggerated and protracted inflammatory response, which has been termed ‘critical illness-related corticosteroid insufficiency’ (CIRCI). There is evidence that moderate-dose hydrocortisone (200–300 mg/day) significantly fastens shock reversal in patients with septic shock, but may improve survival probably only in patients with high risk of death. Thus, therapy should be considered only in refractory shock with poor response to fluid administration and vasopressor therapy. The indication should be based on clinical judgement and not on cortisol measurement. The application prolonged of moderate-dose methylprednisolone (1 mg/kg/day) was found to be most effective in early acute respiratory distress syndrome, and associated with improved lung function, reduction of mechanical ventilation, and faster discharge from the ICU, but a survival benefit was found only in pooled data, including cohort studies. A continuous infusion and weaning of corticosteroids may be preferable to bolus applications and abrupt withdrawal to avoid side effects such as rebound of inflammation and shock, glucose variability, or respiratory failure. There is currently no evidence that prolonged application of moderate-dose corticosteroids increase the risk of secondary infections or muscle weakness, but infection surveillance should be implemented and combination with muscle relaxants be avoided.
22
Rider, Lisa G., und Frederick W. Miller. Outcome assessment in the idiopathic inflammatory myopathies. Herausgegeben von Hector Chinoy und Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0016.
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Due to their rarity, heterogeneity, and multispecialty nature, the myositis syndromes have limited data-driven consensus on appropriate outcome measures. Recently, two international, multispecialty consortia developed new tools and consensus on core set measures of myositis disease activity and damage, as well as response criteria that are now recommended for use as clinical trial endpoints but will also be useful in clinical practice. Magnetic resonance imaging, muscle ultrasound, selected laboratory tests, and immunological biomarkers—including cytokines, chemokines, lymphocyte flow cytometry, and endothelial activation markers—can all be helpful adjuncts to serum muscle enzyme levels in assessing disease activity and damage, but these have not yet been fully validated. Definitions of clinically inactive disease, complete clinical response, and remission have also been proposed but require further validation. These advances should enhance the development of therapies by standardizing our ability to demonstrate their efficacy in treating the idiopathic inflammatory myopathies.
23
Smith, Rebecca. Smallpox. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199976805.003.0063.
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Symptoms of the smallpox virus include fever and a progressive papular rash that becomes vesicular and then pustular. A systemic inflammatory response syndrome (SIRS) leads to septic shock and death in 30% of cases. The definitive diagnosis can be confirmed via blood samples, lesion contents, or scrapings from crusts analyzed using electron microscopy, viral antigen immunohistochemistry, or polymerase chain reaction. The suspicion of a single smallpox case should lead to immediate notification of local public health authorities and the hospital epidemiologist. Because the disease does not exist in nature, smallpox should be considered the result of a bioterrorist attack until proven otherwise. An epidemiologic investigation is essential for determining the perimeter of the initial release so that tracking and quarantine of those exposed can be completed. Patients are extremely contagious and must be placed on contact, droplet, and airborne precautions in a negative pressure room.
24
Dalbeth, Nicola. Basic calcium phosphate crystal deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0053.
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Basic calcium phosphate (BCP) crystals deposit within periarticular and articular sites, leading to a variety of clinical presentations. The most well-recognized clinical syndromes associated with BCP crystal deposition are calcific tendinitis and BCP crystal-associated destructive arthritis such as Milwaukee shoulder syndrome. There is emerging evidence that BCP crystals also play a role in osteoarthritis pathogenesis. Within the joint, tissue responses to BCP crystals include induction of pro-catabolic and inflammatory pathways. Clinical management of BCP crystal-associated arthropathies is limited by the lack of reliable and feasible methods to detect crystals, and the current unavailability of systemic therapies that promote BCP crystal dissolution.
25
Ramdass, Ranjit. Neurophysiology in the assessment of inflammatory myopathies. Herausgegeben von Hector Chinoy und Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0015.
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Clinical neurophysiology (electrodiagnosis) includes the assessment of peripheral nerves by electrical stimulation (nerve conduction studies, NCS) and needle examination of muscles (electromyography, EMG). Electrodiagnostic assessment is a functional extension of clinical examination into the laboratory. It plays an important role in the investigation of a patient suspected of having myositis, providing valuable information regarding peripheral nerve, neuromuscular junction and muscle functions, to better characterize clinical syndromes. NCS can establish the presence and quantify the severity of a primary or co-existing peripheral neuropathy, while EMG examination can help discriminate between primary myogenic and primary neurogenic disorders. EMG is potentially more sensitive than clinical examination, as abnormalities can be detected in muscles apparently unaffected on clinical examination. Additionally, a number of muscles can be sampled to help target an optimal muscle biopsy site. Neurophysiology can also assist in monitoring treatment responses and detecting emerging problems, such steroid myopathy or drug-induced neuropathy.
26
O’Brien, Alastair. Pathophysiology, diagnosis, and assessment of acute or chronic hepatic failure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0199.
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Cirrhosis is an increasing problem and prognosis following intensive care unit admission is poor. Acute on chronic liver failure (ACLF) is a separate entity to cirrhosis with organ failure at the core of this syndrome. Infection and the associated systemic inflammatory responses are the most important precipitants of ACLF. Clinical assessment should follow the standard airway breathing circulation disability exposure approach to the critically-ill patient.
27
Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0022.
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Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
28
Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_002.
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Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
29
Straub, Rainer H. Neuroendocrine system. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199642489.003.0022_update_003.
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Endocrine abnormalities are very common in patients with chronic autoimmune rheumatic diseases (CARDs) due to the systemic involvement of the central nervous system and endocrine glands. In recent years, the response of the endocrine (and also neuronal) system to peripheral inflammation has been linked to overall energy regulation of the diseased body and bioenergetics of immune cells. In CARDs, hormonal and neuronal pathways are outstandingly important in partitioning energy-rich fuels from muscle, brain, and fat tissue to the activated immune system. Neuroendocrine regulation of fuel allocation has been positively selected as an adaptive programme for transient serious, albeit non-life-threatening, inflammatory episodes. In CARDs, mistakenly, the adaptive programmes are used again but for a much longer time leading to systemic disease sequelae with endocrine (and also neuronal) abnormalities. The major endocrine alterations are depicted in the following list: mild activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system, inadequate secretion of ACTH and cortisol relative to inflammation, loss of androgens, inhibition of the hypothalamic-pituitary-gonadal axis and fertility problems, high serum levels of oestrogens relative to androgens, fat deposits adjacent to inflamed tissue, increase of serum prolactin, and hyperinsulinaemia (and the metabolic syndrome). Neuroendocrine abnormalities are demonstrated using this framework that can explain many CARD-related endocrine disturbances. This chapter gives an overview on pathophysiology of neuroendocrine alterations in the context of energy regulation.
30
Kamat, Deepak M., Henry M. Adam und Rebecca A. Baum, Hrsg. Quick Reference Guide to Pediatric Care. 2. Aufl. American Academy of Pediatrics, 2017. http://dx.doi.org/10.1542/9781610021128.
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Significantly revised and updated, the second edition of this popular quick reference guide provides information and advice on 190 areas of current pediatric care, everything from abdominal pain and ADHD, to headache and herpes infections, to weight loss and wheezing. This indispensable resource delivers practical, action-orientated, clinical solutions for healthcare professionals to use during or between patient encounters. Authoritative content is presented in a concise outline format that helps speed and simplify decision-making. Regardless of the patient presentation you're confronted with, you'll have quick access to the help you need to Efficiently evaluate signs and symptoms. Order the right screening/diagnostic tests. Implement approved therapeutic strategies. Prescribe safe and effective medications. Recommend proven prevention measures. Confidently respond to parent questions. 35 new chapters including Adjustment disorder Anxiety Ataxia Coagulation disorders Cyanosis Dental problems Depression Drug interactions and adverse effects Fetal alcohol spectrum disorder Fragile X syndrome Hemangiomas Hypocalcemia, hypercalcemia, and hypercalcuria Inattention Inflammatory bowel disease Klinefelter syndrome Learning difficulty Learning disorders Metabolic disorders beyond the newborn period Munchausen syndrome by proxy: medical child abuse Neural tube defects Oppositional defiant disorder Pancreatitis Papulosquamous disease Pierre Robin syndrome Prader-Willi syndrome Screening for genetic-metabolic diseases Self-harm Sexual abuse of children Sleep disturbances Speech and language concerns Substance use Symptoms of emotional disturbances in young children (birth to 5) Temper tantrums and breath-holding spells Turner syndrome and Noonan syndrome Vitamin D inadequacy
31
Whitworth, Caroline, und Stewart Fleming. Malignant hypertension. Herausgegeben von Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0216.
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Malignant hypertension (MH) is recognized clinically by elevated blood pressure together with retinal haemorrhages or exudates with or without papilloedema (grades III or IV hypertensive retinopathy); and may constitute a hypertensive emergency or crisis when complicated by evidence of end-organ damage including microangiopathic haemolysis, encephalopathy, left ventricular failure, and renal failure. Though reversible, it remains a significant cause of end-stage renal failure, and of cardiovascular and cerebrovascular morbidity and mortality in developing countries.MH can complicate pre-existing hypertension arising from diverse aetiologies, but most commonly develops from essential hypertension. The absolute level of blood pressure appears not to be critical to the development of MH, but the rate of rise of blood pressure may well be relevant in the pathogenesis. The pathogenesis of this transformation remains unclear.The pathological hallmark of MH is the presence of fibrinoid necrosis (medial vascular smooth muscle cell necrosis and fibrin deposition within the intima) involving the resistance arterioles in many organs. Fibrinoid necrosis is not specific to MH and this appearance is seen in other conditions causing a thrombotic microangiopathy such as haemolytic uraemic syndrome, scleroderma renal crisis, antiphospholipid syndrome, and acute vascular rejection post transplant. MH can both cause a thrombotic microangiopathy (TMA) but can also complicate underlying conditions associated with TMA.The pathophysiological factors that interact to generate and sustain this condition remain poorly understood. Risk factors include Afro-Caribbean race, smoking history, younger age of onset of hypertension, previous pregnancy, and untreated hypertension associated with non-compliance or cessation of antihypertensive therapy.Evidence from clinical studies and animal models point to a central role for the intrarenal renin–angiotensin system (RAS) in MH; there is good evidence for renal vasoconstriction and activation of the renal paracrine RAS potentiating MH once established; however, there may also be a role in the predisposition of MH suggested by presence of increased risk conferred by an ACE gene polymorphism in humans and polymorphisms for both ACE and AT1 receptor in an animal model of spontaneous MH. Other vasoactive mediators such as the endothelin and the inflammatory response may be important contributing to and increasing endothelial damage. There have been no randomized controlled trials to define the best treatment approach, but progressive lowering of pressures over days is considered safest unless made more urgent by critical clinical state. It seems logical to introduce ACE inhibition cautiously and early, but in view of the risk of rapid pressure lowering some recommend delay.
32
Shaibani, Aziz. Distal Leg Weakness. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199898152.003.0016.
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Plantar flexion and/or extension weakness is usually neuromuscular in nature. Rarely, focal foot dystonia, ankle arthritis, and spasticity lead to diagnostic confusion. Painful sequential foot drop is a common feature of vasculitis. Preserved EDB bulk in the face of foot drop is a feature of myopathy. Progressive painless weakness of the foot flexion and extension with normal sensation and brisk deep tendon reflexes are typically seen in ALS. In patients with chronic bilateral foot drop, examination of the scapulae is essential to rule out scapuloperoneal syndrome and FSHD. In inflammatory neuropathies, distal leg weakness is the last to respond to therapy and some residual deficit is common.
33
Shaibani, Aziz. Distal Leg Weakness. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190661304.003.0016.
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Plantar flexion and extension weakness are usually neuromuscular in nature. Rarely, focal foot dystonia, ankle arthritis, and spasticity lead to diagnostic confusion. Painful, sequential foot drop is a common feature of vasculitis. Preserved extensor digitorum brevis (EDB) bulk in the face of foot drop is a feature of myopathy. Progressive, painless weakness of the foot flexion and extension with normal sensation and brisk deep tendon reflexes (DTRs) are typically seen in amyotrophic lateral sclerosis (ALS). In patients with chronic, bilateral foot drop, examination of the scapulae is essential to rule out scapuloperoneal syndrome and facioscapulohumeral muscular dystrophy (FSHD). In inflammatory neuropathies, distal leg weakness is the last to respond to therapy, and some residual deficit is common.
34
Amato, Marcelo, und Andreas Wolfgang Reske. Ventilator trauma in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0101.
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Ventilator trauma refers to complications of mechanical ventilation, which have an impact on morbidity and mortality. Two major forms of ventilator trauma may be distinguished—an acute form related to rupture of airspaces causing air-leak syndrome and a subacute form causing protracted inflammatory responses. A key feature of mechanically-ventilated lungs is the presence of non-aerated and unstable regions due to atelectasis, oedema, or consolidation. Because of mechanical interdependence, pressures acting in non-uniformly expanded lungs at the boundaries between non-aerated and aerated lung may be a multiple of the apparent transpulmonary pressure. The resulting effects have been reported to precipitate or contribute to ventilator-induced lung injury (VILI). The engineering terms stress and strain were recently proposed for better definition of risk-constellations for VILI. Because the aerated lung volume is positively correlated to compliance, driving-pressure can aid in identifying disproportionate combinations of tidal volumes and compliance.
35
Froio, Sara, und Franco Valenza. Aspiration of gastric contents in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0106.
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This chapter focuses on the pathophysiology, clinical features, management and prevention of aspiration pneumonitis, aspiration pneumonia, and airway obstruction. Aspiration is defined as the inhalation of oropharyngeal or gastric contents into the larynx and lower respiratory tract. Pulmonary syndromes caused by aspiration are different, depending on the amount and nature of the aspirated material, the frequency of aspiration and the host’s response. This results in a chemical burn of tracheobronchial tree and pulmonary parenchyma. The caustic effects of the low pH of the aspirate cause an intense inflammatory reaction. As a consequence, severe hypoxaemia and infiltrates on chest radiograph occur. If colonized oropharyngeal material enters the lungs, aspiration pneumonia develops and antibiotics are needed. Even if not toxic per se, large volumes of fluids may cause suffocation by mechanical obstruction. Prevention of aspiration is of vital importance and the patient at risk must be identified. The major therapeutic approach is to correct hypoxia, support pulmonary function, and prevent pneumonia development.
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Lloyd, Sheelagh, und Eric R. Morgan. Toxocarosis. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0071.
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Toxocara canis and the syndromes of visceral and ocular larva migrans (VLM, OLM), covert toxocarosis, and neurological toxocarosis are described. Other potential agents, particularly Toxocara cati and Baylisascaris procyonis , are described. The transmission dynamics of toxocarosis to humans have never been fully elucidated, but the potential roles of pet and stray dogs, foxes, cats, and the influence of their population densities, and age demographies, are discussed in relation to contamination of the environment with eggs. Routes of infection with eggs by geophagia, poor hygiene outdoors and with dogs, and fly-borne contamination of food, and meat-borne ingestion of larvae are described. The development of prolonged in vitro culture and analyses of T. canis larval excretions/secretions (TES) and surface antigens helped explain the importance of the rapid production and shedding of TES in the prolonged course of infection and pathogenesis of disease. TES also have greatly improved serodiagnosis. However, we still have insufficient understanding of differences in the aetiology of the larvae or differences in immune responses among individuals to account for development of VLM, covert toxocarosis, or OLM in different individuals. Our understanding of the immunopathological response of the host to TES has emphasized the need for anti-inflammatory therapy in treatment; unfortunately, less information is available on the true efficacy of the anthelmintics available. The complexity of the T. canis life cycle in dogs is described and therapeutic regimens to prevent excretion of eggs by pet dogs are given. This, plus adequate control or exclusion of stray or wild canids from a property could prevent most cases of VLM. Control of infection from free-ranging stray dogs, cats and foxes, will be difficult and more data are needed to clarify the importance of these and of fly-borne and meat-borne transfer of infection to humans for control.
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Voll, Reinhard E., und Barbara M. Bröker. Innate vs acquired immunity. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0048.
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The innate and the adaptive immune system efficiently cooperate to protect us from infections. The ancient innate immune system, dating back to the first multicellular organisms, utilizes phagocytic cells, soluble antimicrobial peptides, and the complement system for an immediate line of defence against pathogens. Using a limited number of germline-encoded pattern recognition receptors including the Toll-like, RIG-1-like, and NOD-like receptors, the innate immune system recognizes so-called pathogen-associated molecular patterns (PAMPs). PAMPs are specific for groups of related microorganisms and represent highly conserved, mostly non-protein molecules essential for the pathogens' life cycles. Hence, escape mutants strongly reduce the pathogen's fitness. An important task of the innate immune system is to distinguish between harmless antigens and potentially dangerous pathogens. Ideally, innate immune cells should activate the adaptive immune cells only in the case of invading pathogens. The evolutionarily rather new adaptive immune system, which can be found in jawed fish and higher vertebrates, needs several days to mount an efficient response upon its first encounter with a certain pathogen. As soon as antigen-specific lymphocyte clones have been expanded, they powerfully fight the pathogen. Importantly, memory lymphocytes can often protect us from reinfections. During the development of T and B lymphocytes, many millions of different receptors are generated by somatic recombination and hypermutation of gene segments making up the antigen receptors. This process carries the inherent risk of autoimmunity, causing most inflammatory rheumatic diseases. In contrast, inadequate activation of the innate immune system, especially activation of the inflammasomes, may cause autoinflammatory syndromes.
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Septic Shock: Methods and Protocols (Methods in Molecular Medicine). Humana Press, 2000.
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