Mark Corson

By Z. Pedar. University of Texas at Brownsville. 2018.

Diagnostic and prognostic stratification in the emergency department using urinary biomarkers of nephron damage a multicenter prospective cohort study cheap 75mg triamterene mastercard. Plasma neutrophil gelatinase-associated lipocalin for the prediction of acute kidney injury in acute heart failure purchase 75 mg triamterene with visa. Additive value of blood neutrophil gelatinase- associated lipocalin to clinical judgement in acute kidney injury diagnosis and mortality prediction in patients hospitalized from the emergency department discount triamterene 75 mg with visa. Evaluation of 32 urine biomarkers to predict the progres- sion of acute kidney injury after cardiac surgery. Urinary biomarkers in the clinical prognosis and early detection of acute kidney injury. Postoperative biomarkers predict acute kidney injury and poor outcomes after adult cardiac surgery. Plasma neutrophil gelatinase-associated lipocalin is an early marker of acute kidney injury in adult critically ill patients: a prospective study. Cystatin C in prediction of acute kidney injury: a systemic review and meta-analysis. Serum and urine cystatin C are poor biomarkers for acute kidney injury and renal replacement therapy. Rapid detection of acute kidney injury by plasma cystatin C in the intensive care unit. Biomarker strategies to predict need for renal replacement therapy in acute kidney injury. Urine neutrophil gelatinase-associated lipocalin moderately predicts acute kidney injury in critically ill adults. Plasma and urine neutrophil gelatinase-associated lipocalin in septic versus non-septic acute kidney injury in critical illness. Neutrophil gelatinase-associated lipocalin in adult septic patients with and without acute kidney injury. Serum neutrophil gelatinase-associated lipocalin at inception of renal replacement therapy predicts survival in critically ill patients with acute kidney injury. Serum cystatin concentration as a marker of acute renal dysfunction in critically ill patients. Discovery and validation of cell cycle arrest biomarkers in human acute kidney injury. Urinary and serum biomarkers for the diagnosis of acute kidney injury: an in-depth review of the literature. Validation of cell-cycle arrest biomarkers for acute kidney injury using clinical adjudication. Plasma and urine neutrophil gelatinase associated lipocalin in the diagnosis of new onset acute kidney injury in critically ill patients. Urinary N-acetyl-beta-(D)-glucosaminidase activity and kidney injury molecule-1 level are associated with adverse outcomes in acute renal failure. Urinary biomarkers and renal recovery in critically ill patients with renal support. Test characteristics of urinary biomarkers depend on quantitation method in acute kidney injury. Deceased donor neutrophil gelatinase-associated lipocalin and delayed graft function after kidney trans- plantation: a prospective study. Plasma neutrophil gelatinase-associated lipocalin in kidney transplantation and early renal function prediction. Novel biomarkers for the prediction of acute kidney injury in patients undergoing liver transplantation. Promise of new translational safety biomarkers in drug development and challenges to regulatory qualification. Diagnostic value of urinary Kidney Injury Molecule 1 for acute kidney injury: a meta-analysis. In this line, renal imaging plays a key role both in identifying the causal mechanism of the syndrome and, more recently, in evaluating renal hemodynamics. While excessive fluid loading may be associated with important side effects and a positive fluid balance with a poor clinical outcome, development of tools to better estimate renal perfusion in response to treatment appears of paramount importance. In this chapter, we describe different renal imaging tools used to assess the cause of kidney failure and clinical value to image the kidney. Legrand (*) Department of Anesthesiology and Critical Care, Hôpital Européen Georges Pompidou Assistance Publique- Hopitaux de Paris, 20 Rue Leblanc , Paris 75015 , France e-mail: matthieu. Darmon Medical Intensive Care Unit, Hôpital Saint Louis, 1 Avenue Claude Vellefaux , Paris 75010 , France e-mail: michael. Using the brightness mode (B-mode), a grey-scale image is produced when the high-frequency sound waves are generated and then received by the ultrasonogra- phy transducer, in which returning echoes are represented as bright dots. The two basic things provided by B mode ultrasonography of the kidney include kidney size and echogenicity. Therefore, brighter renal parenchyma will therefore be brighter than normal liver or spleen. The longitudinal length of the kidney is mostly used to determine kidney size due to reproducibility and easy measurement. The size of the kidney can provide evidence for underlying chronic disease or for some causes of renal failure. This enlargement includes thickness of the renal parenchyma (including the cortex and the medulla which is about 1. However, because of presence of fat tissue, the caliceal system appears hypoechogenic. In the same line, because the medullary pyramids contain urine in parallel tubules, they appear hypoechogenic compared to the cor- tex. In pathology, although echogenicity is not specific, results of renal echography can provide useful information.

Therefore buy triamterene 75 mg line, the focus in such cases should be on treating the underlying condition rather than the “periodontal disease discount 75mg triamterene with amex. This disease is a good example of a condition that is probably best treated with the combined expertise of a dentist or periodontist and a nutritionally minded physician purchase 75 mg triamterene with visa. Although oral hygiene is of great importance in treating and preventing periodontal disease, it is not sufficient in many cases. The patient’s immune system and other defense mechanisms must be normalized if development and progression of the disease are to be controlled. The rate of periodontal disease is approximately 15% at age 10, 38% at age 20, 46% at age 35, and 54% at age 50. As a group, men have a higher prevalence and severity of periodontal disease than women. The occurrence of periodontal disease is inversely related to increasing levels of education and income; rural dwellers have a higher level of severity and prevalence than city dwellers. In periodontal disease, this means understanding the normal protective factors in the gums and supporting structures (periodontium). Many experts agree that the presence of bacteria is not sufficient to cause disease; a person’s immune status and other defense mechanisms must be involved. The Environment of the Gingival Sulcus The gingival sulcus is the V-shaped crevice that surrounds each tooth. The anatomy of the gingival sulcus is ideal for growth of bacteria, as it is resistant to the cleansing action of saliva. Furthermore, the gingival fluid (the fluid found in the sulcus) provides a rich nutrient source for microorganisms. The clinical determination of the depth of the gingival sulcus is an important part of the diagnosis. Individuals who have periodontal disease should see their dentist no less than once every six months for proper evaluation and cleaning. Bacterial Factors Bacterial plaque has long been considered the causative agent in most forms of periodontal disease. As they defend the body against microbes, neutrophils release numerous free radicals (which break down collagen), inflammatory compounds, and a compound that stimulates alveolar bone destruction. The complement system plays a critical role in the resistance to infection, but it also plays a big role in the tissue injury of periodontal disease, because complement activation increases gingival permeability, allowing bacteria and bacterial by- products to penetrate gum tissue. IgE and Mast Cell Function Mast cells are white blood cells that reside in tissues. They contain histamine and other inflammatory compounds in packets known as granules. The release of the contents of these packets (in response to allergy antibodies, complement activation, trauma, endotoxins, and free radicals) is a major factor in periodontal disease. If the restoration is a silver amalgam filling, there may be even more involvement because over time the mercury in those fillings is released into the body, where it decreases the activity of antioxidant enzymes, including glutathione peroxidase, superoxide dismutase, and catalase. The health of this collagen matrix affects its ability to resist inflammatory mediators, bacteria and their by-products, and destructive enzymes. Because periodontal collagen is constantly being renewed, it is extremely vulnerable when the necessary cofactors for collagen synthesis (protein, zinc, copper, vitamins C, B6, and A, etc. Miscellaneous Factors Numerous local factors favor the progression of periodontal disease. These include food residue, unreplaced missing teeth, malocclusion, tongue thrusting, bruxism (grinding of the teeth), toothbrush trauma, mouth breathing, and tobacco smoking. Tobacco smoking is associated with increased susceptibility to severe periodontal disease and tooth loss. Furthermore, smoking greatly reduces vitamin C levels, thereby intensifying its damaging effects. Subclinical vitamin C deficiency plays a significant role in periodontal disease through these effects and through its role in delaying wound healing. Decreased vitamin C levels are also associated with increased susceptibility of the oral tissues to endotoxins and bacterial by-products, as well as impaired function of white blood cells (particularly neutrophils). Sugar Sugar is known to significantly increase plaque accumulation while decreasing white blood cell function. Vitamin C and glucose are known to compete for intracellular transport sites, with this intracellular transport being largely insulin-dependent. Deficiency of vitamin A is associated with abnormal cell structures in the periodontium, inflammatory infiltration and degeneration, periodontal pocket formation, plaque formation, increased susceptibility to infection, and abnormal alveolar bone formation. This is clearly a factor in the increasing prevalence of periodontal disease with age, although the geriatric population as a whole is at higher risk for developing numerous nutrient deficiencies. The functions of zinc in the gingiva and periodontium include stabilization of membranes, antioxidant activity, collagen synthesis, inhibition of plaque growth, inhibition of mast-cell degranulation, and numerous immune-enhancing activities. Plaque growth can be inhibited by the use twice per day of a mouthwash that contains 5% zinc. Vitamin E and Selenium These two nutrients function synergistically in antioxidant mechanisms and seem to potentiate each other’s effect. Vitamin E alone has been demonstrated to be of considerable value in treating patients with severe periodontal disease. The antioxidant effects of vitamin E are particularly needed if amalgam fillings are present. Mercury depletes the tissues of the antioxidant enzymes superoxide dismutase, glutathione peroxidase, and catalase. Higher levels allow it to better compete with mercury for inclusion in the enzymes.

Charron C buy triamterene 75mg overnight delivery, Prat G discount triamterene 75mg without a prescription, Caille V et al (2007) Validation of a skills assessment scoring system for transesophageal echocardiographic monitoring of hemodynamics purchase 75 mg triamterene. Giacomin E, Palmerini E, Ballo P et al (2008) Acute effects of caffeine and cigarette smoking on ventricular long-axis function in healthy subjects. Oki T, Tabata T, Mishiro Y et al (1999) Pulsed tissue Doppler imaging of left ven- tricular systolic and diastolic wall motion velocities to evaluate differences between long and short axes in healthy subjects. Yock P, Popp R (1984) Noninvasive estimation of right ventricular systolic pres- sure by Doppler ultrasound in patients with tricuspid regurgitation. Vieillard-Baron A, Prin S, Chergui K et al (2002) Echo-Doppler demonstration of acute cor pulmonale at the bedside in the medical intensive care unit. Vieillard-Baron A, Chergui K, Augarde R et al (2003) Cyclic changes in arterial pulse during respiratory support revisited by Doppler echocardiography. Jardin F, Vieillard-Baron A (2003) Right ventricular function and positive pressure ventilation in clinical practice: from haemodynamic subsets to respirator settings. Schmitt J, Vieillard-Baron A, Augarde R et al (2001) Positive end-expiratory pres- sure titration in acute respiratory distress syndrome: impact on right ventricular outÀow impedance evaluated by pulmonary artery Doppler Àow velocity measure- ments. Poelaert J, Visser C, Everaert J et al (1993) Acute hemodynamic changes of inverse ratio ventilation in adult respiratory distress syndrome. Barbier C, Loubieres Y, Schmit C et al (2004) Respiratory changes in inferior vena cava diameter are helpful in predicting Àuid responsiveness in ventilated septic pa- tients. Vieillard-Baron A, Augarde R, Prin S et al (2001) InÀuence of superior vena caval zone condition on cyclic changes in right ventricular outÀow during respiratory support. Beaulieu Y (2007) Speci¿c skill set and goals of focused echocardiography for criti- cal care clinicians. Such deaths are often caused by sudden cardiac arrest, and the estimated number of out-of-hospital cardiac arrest cases is 300,000 per year in the United States, where median rate of survival to hospital discharge is 7. Favourable outcome of patients admitted to the hospital ranges between 11% and 48% [2, 3], indicating a large number of patients die after successful resuscitation during hospital stay or develop permanent severe brain damage. The only therapy that has been shown to improve survival and neurological outcome after sudden cardiac arrest is induction of mild therapeutic hypothermia for 12-24 h [4, 5]. Mild hypothermia is an exciting and powerful therapy but is still confronted with un- deruse in clinical practice [6, 7]. Fortunately, a growing amount of evidence documents its mechanisms of action, safety and effectiveness. However, the full potential of mild hypothermia after cardiac arrest has yet to be explored. Metabolism is reduced by 5–8% [8, 9] per degree Celsius reduction of core tempera- ture. Metabolism reduction at mild hypothermia alone, however, would not account for its marked protective effect [9]. Cellular depolarisation releases excitatory amino acids such as glutamate, which in turn further promotes Ca++ inÀux. Several steps of this cascade have been shown to be attenuated by hypothermia [10–12]. Glutamate and dopamine release after global ischaemia is inhibited [13], and mild hypothermia induces brain-derived neurotrophic factor, which in turn further reduces glutamate release [14, 15]. Several studies have shown that hypothermia attenuates oxidative stress [16–18] and lipid peroxidation [19]. The inÀammatory response to an ischaemic insult contributes to delayed tissue injury. Hypothermia functions as an immunomodulator by inhibiting neutrophil in¿ltration [20] and function [21], reducing lipid peroxidation and leukotriene production [10, 22]. Induc- tion of programmed cell death after ischaemia is inÀuenced by pro- and antiapoptotic factors. Inhibition of apoptosis can be explained partly by mechanisms described above because calcium overload and glutamate release contribute to induction of apoptosis. Translocation of cytochrome C from the mi- tochondrium into the cytosol – an early step in the initiation of apoptosis [23] – and subse- quent caspase activation are attenuated [24, 25]. Another bene¿cial mechanism of hypothermia is the reduction of brain oedema after ischaemia [22]. This led to several randomised trials of therapeutic hypothermia after cardiac arrest. In the hypothermia group (n = 43), 21 (49%) survived to favourable neurological recovery compared with nine (26%) of 34 in the normothermia group (p = 0. In the hypothermia group (n = 16), two (13%) survived to favourable neurological recovery compared with 0 (0%) of 14 in the normothermia group. A meta-analysis performed on these three trials included individual data of 384 patients and showed a number needed to treat of six for favourable neurological outcome at hospi- tal discharge and neurologically intact survival at 6 months. Arrich [33] published the largest and most compelling observational study from the European Resuscitation Council Hypothermia After Cardiac Arrest Reg- istry that followed 587 patients, of whom 462 were treated with therapeutic hypothermia irrespective of the presenting rhythm. This study demonstrates a bene¿t in terms of neu- rological outcome (unfavourable outcome 55% in the hypothermia group and 68% in the normothermia group; p = 0. Neurologi- cal outcome was signi¿cantly improved in the cooling group (55% favourable outcome vs 16%; p = 0. This proved to be safe and feasible and was achieved without delaying door-to- balloon time [35]. Possible side effects must be kept in mind to prevent or counteract them in a timely manner but should not prevent the use of hypothermia when indicated. The European multicentre trial did not report a signi¿cant difference in complication rate, but there was a trend towards more infections and sepsis in the hypothermia group [4].

We generally tell people taking Coumadin to avoid these products at higher dosages (more than the equivalent of one clove of garlic per day or more than 240 mg per day of ginkgo extract) but not to worry if they are just on the typical support dose buy triamterene 75mg line. Iron cheap triamterene 75 mg on-line, magnesium order 75 mg triamterene overnight delivery, and zinc may bind with Coumadin, potentially decreasing its absorption and activity. Take Coumadin at least two hours before or after any product that contains iron, magnesium, or zinc. Nutritional Supplements Magnesium The level of magnesium in the blood correlates with the ability of the heart muscle to manufacture enough energy to beat properly. Not surprisingly, many disorders of heart rhythm are related to an insufficient level of magnesium in the heart muscle. Magnesium was first shown to be of value in the treatment of cardiac arrhythmias in 1935. More than 75 years later, there are now many clinical studies that show magnesium supplementation to be of benefit in treating many types of arrhythmias, including atrial fibrillation, ventricular premature contractions, ventricular tachycardia, and severe ventricular arrhythmias. Given the importance of these two electrolytes for proper nerve and muscle firing, it is little wonder that low levels of these substances can produce arrhythmias. According to the results from one double-blind, placebo-controlled study, magnesium supplementation may offer significant benefit in the treatment of new-onset atrial fibrillation. Because of the benefits noted in several studies of patients with atrial fibrillation who were taking magnesium, researchers decided to conduct a study to determine if magnesium and digoxin were better than digoxin alone in controlling ventricular response. Eighteen people with atrial fibrillation of less than seven days’ duration received either digoxin plus a placebo or digoxin plus magnesium, both intravenously. Those who received magnesium were given 20% of a magnesium solution during the initial 15 minutes, with the rest infused over the next six hours. The benefit of magnesium was obvious within the first 15 minutes, as heart rate decreased immediately from an average of 130 to 120 beats per minute. After 24 hours, the group that received the magnesium had an average heart rate of roughly 80, while the group that received only digoxin had an average heart rate of 105. In the magnesium group, 6 of 10 patients (60%) converted to normal rhythm, whereas just 3 of 8 in the digoxin-only group (37. The recommended intake for oral magnesium in arrhythmia appears to be approximately 6 to 10 mg/kg per day. Be sure to use a form that is easily absorbed, such as citrate, as other forms can cause diarrhea at these dosages. Coenzyme Q10 (CoQ10) Coenzyme Q10 plays a critical role in the cellular production of energy. As the heart is among the most metabolically active tissues in the body, a CoQ10 deficiency can lead to serious problems there. A good analogy is that the role of CoQ10 is similar to the role of a spark plug in a car engine. Just as the car cannot function without that initial spark, the human body cannot function without CoQ10. Because of its safety and possible benefit, CoQ10 supplementation is indicated in any condition affecting the heart. Botanical Medicines Hawthorn Hawthorn (Crataegus species) preparations have a long history of use in minor arrhythmias. The benefits in congestive heart failure have been repeatedly demonstrated in double-blind studies (see the chapter “Congestive Heart Failure”). Follow the general guidelines on diet and lifestyle in the chapter “Heart and Cardiovascular Health. Estimates have indicated that 50% of those over 50 years of age have symptomatic hemorrhoidal disease, and up to one-third of the total U. Although most individuals may begin to develop hemorrhoids in their 20s, hemorrhoidal symptoms usually do not become evident until the 30s. Causes The causes of hemorrhoids are similar to the causes of varicose veins (see the chapter “Varicose Veins”): genetic weakness of the veins and/or excessive pressure on the veins. Because the venous system that supplies the rectal area contains no valves, factors that increase venous congestion in the region can lead to hemorrhoid formation. These factors include increased intra-abdominal pressure (caused by defecation, pregnancy, coughing, sneezing, vomiting, physical exertion, or portal hypertension due to cirrhosis); an increase in straining during defecation due to a low-fiber diet; diarrhea; and standing or sitting for prolonged periods of time. Classification of Hemorrhoids Hemorrhoids are typically classified according to location and degree of severity. External hemorrhoids occur below the anorectal line—the point in the 3-cm-long anal canal where the skin lining changes to mucous membrane. They may be full of either blood clots (thrombotic hemorrhoids) or connective tissue (cutaneous hemorrhoids). A thrombotic hemorrhoid is produced when a hemorrhoidal vessel has ruptured and formed a blood clot (thrombus), while a cutaneous hemorrhoid consists of fibrous connective tissue covered by anal skin. Cutaneous hemorrhoids can be located at any point on the circumference of the anus. Typically, they are caused by the resolution of a thrombotic hemorrhoid: that is, the thrombus becomes organized and replaced by connective tissue. Occasionally, an internal hemorrhoid enlarges to such a degree that it prolapses and descends below the anal sphincter. The following types of mixed hemorrhoids can occur: • Without prolapse: Bleeding may be present, but there is no pain. Diagnostic Considerations The symptoms most often associated with hemorrhoids include itching, burning, pain, inflammation, irritation, swelling, bleeding, and seepage. Itching is caused when there is mucous discharge from prolapsing internal hemorrhoids; tissue trauma resulting from excessive use of harsh toilet paper; Candida albicans; parasitic infections; and food allergies. However, as there are no sensory nerve endings above the anorectal line, uncomplicated internal hemorrhoids rarely cause pain.