Mary Catherine Beach, M.D., M.P.H.

• Professor of Medicine

https://www.hopkinsmedicine.org/profiles/results/directory/profile/0011907/mary-catherine-beach

The use of extended-release niacin with laropip rant (a prostaglandin antagonist) in high-risk patients tak ing a statin also did not reduce the risk of cardiovascular events man health urban athlon on fincar 5 mg buy free shipping. An increase in adverse events was also seen when niacin plus laropiprant was added to statins prostate revive reviews order 5 mg fincar fast delivery. Safety and efficacy of statin treatment alone and in combination with fibrates in patients with dyslipidemia: a meta-analysis prostate discomfort buy 5 mg fincar with visa. Effect of ezetimibe on major atherosclerotic disease events and all-cause mortality prostate cancer bracelet 5 mg fincar buy free shipping. Comparative tolerability and harms of individual statins: a study level network meta-analysis of 246 prostate cancer questionnaire order fincar with american express,955 partici pants from 1 3 5 randomized, controlled trials. The patho physiology is not certain, since pancreatitis never develops in some patients with very high triglyceride levels. Most patients with congenital abnormalities in triglyceride metabolism present in childhood; hypertriglyceridemia induced pancreatitis first presenting in adults is more com monly due to an acquired problem in lipid metabolism. Although there are no clear triglyceride levels that pre dict pancreatitis, most clinicians treat fasting levels above 500 mg/dL (5 mmol/L). The risk of pancreatitis may be more related to the triglyceride level following consump tion of a fatty meal. Because postprandial increases in tri glyceride are inevitable if fat-containing foods are eaten, fasting triglyceride levels in persons prone to pancreatitis should be kept well below that level. In patients with fasting triglycerides greater than or equal to 500 mg/dL (5 mmol! Evaluation and treatment of hypertriglyceride mia: an Endocrine Society clinical practice guideline. For example, dimin ished energy intake may result from poor dentition or various gastrointestinal disorders. Clin ical Findings Clinical manifestations of protein-energy malnutrition range from mild growth retardation and weight loss to a number of distinct clinical syndromes. Progressive wasting that begins with weight loss and proceeds to more severe cachexia typically develops in most patients with marasmus-like secondary protein-energy malnutrition. In the most severe form of this disorder, most body fat stores disappear and muscle mass decreases, most noticeably in the temporalis and interosseous muscles. Laboratory studies may be unremarkable-serum albumin, for example, may be normal or slightly decreased, rarely decreasing to less than 2. In contrast, owing to its rapidity of onset, kwashiorkor-like secondary protein energy malnutrition may develop in patients with normal subcutaneous fat and muscle mass or, if the patient is obese, even in patients with excess fat and muscle. The serum protein level, however, typically declines and the serum albumin is often less than 2. As with primary protein-energy malnutrition, combinations of the maras mus-like and kwashiorkor-like syndromes can occur simul taneously, typically in patients with progressive chronic disease in whom a superimposed acute illness develops. General Considerations Protein-energy malnutrition occurs as a result of a relative or absolute deficiency of energy and protein. It may be primary, due to inadequate food intake, or secondary, as a result of other illness. For most developing nations, pri mary protein-energy malnutrition remains among the most significant health problems. Kwashiorkor, caused by a deficiency of protein in the presence of adequate energy, is typically seen in weaning infants at the birth of a sibling in areas where foods containing protein are insufficient. Maras mus, caused by combined protein and energy deficiency, is seen where adequate quantities of food are simply not available. In industrialized societies, protein-energy malnutri tion is most often secondary to other diseases. Kwashior kor-like secondary protein-energy malnutrition occurs primarily in association with hypermetabolic acute ill nesses such as trauma, burns, and sepsis. These two syndromes are estimated to be present in at least 20% of hospitalized patients. A substantially greater number of patients have risk factors that could result in them. In both syndromes, protein-energy malnutrition is caused either by decreased intake of energy and protein or. Treatment the treatment of severe protein-energy malnutrition is a slow process requiring great care. Of particular concern are depletion of potassium, magnesium, and calcium and acid-base abnor malities. The second phase of treatment is directed at reple tion of protein, energy, and micronutrients. Either the enteral or parenteral route can be used, although the former is preferable. Patients with less severe pro tein-calorie undernutrition can be given calories and pro tein simultaneously with the correction of fluid and electrolyte abnormalities. Patients who are re-fed too rapidly may develop a num ber of untoward clinical sequelae. During refeeding, circu lating potassium, magnesium, phosphorus, and glucose move intracellularly and can result in low serum levels of each. The administration of water and sodium with carbo hydrate refeeding can result in heart failure in persons with depressed cardiac function. Enteral refeeding can lead to malabsorption and diarrhea due to abnormalities in the gastrointestinal tract. Changes in renal sodium reabsorp tion and poor skin and blood vessel integrity result in the development of dependent edema without other signs of heart disease. Treatment includes reassurance, elevation of the dependent area, and modest sodium restriction. Diuretics are usually ineffective, may aggravate electrolyte deficiencies, and should not be used. The prevention and early detection of protein-energy malnutrition in hospitalized patients require awareness of its risk factors and early symptoms and signs. Patients at risk require formal assessment of nutritional status and close observation of dietary intake, body weight, and nutri tional requirements during the hospital stay. Consensus statement of the Academy of Nutrition and Dietetics/ American Society for Parenteral and Enteral Nutrition: characteristics recommended for the identification and documentation of adult malnutrition (undernutrition). General Considerations Obesity is one of the most common disorders in medical practice and among the most frustrating and difficult to manage. Little progress has been made in prevention or treatment, yet maj or changes have occurred in our under standing of its causes and its implications for health. It is calculated by dividing measured body weight in kilo grams by the height in meters squared. Upper body obesity (excess fat around the waist and flank) is a greater health hazard than lower body obe sity (fat in the thighs and buttocks). Obese patients with increased abdominal circumference (greater than 1 02 em in men and 88 em in women) or with high waist-hip ratios (greater than 1. Furthermore, visceral fat within the abdominal cav ity is more hazardous to health than subcutaneous fat around the abdomen. Malnutrition, fatigue, frailty, vulnerability, sarcopenia and cachexia: overlap of clinical features. Malnutrition among cognitively intact, non critically ill older adults in the emergency department. Treatment Using conventional dietary techniques, only 20% of patients will lose 20 lb and maintain the loss for over 2 years; only 5% maintain a 40-lb loss. Continued close provider-patient contact appears to be more important for success of treatment than the specific features of any given treatment regimen. Careful patient selection improves suc cess rates and decreases frustration of both patients and therapists. Specific attempts to identify motivated patients-eg, requesting a 3 -day diet record-are often useful. Most successful programs employ a multidisciplinary approach to weight loss, with hypocaloric diets, behavior modification to change eating behavior, aerobic exercise, and social support. Dietary instructions for most patients incorporate the same principles that apply to healthy people who are not obese. These instructions emphasize intake of a wide vari ety of predominantly "unprocessed" foods, with special attention to limiting foods that provide large amounts of calories without other nutrients, ie, fat, sucrose, and alco hol. There is no physiologic advantage to diets that restrict carbohydrates, advocate relatively larger amounts of pro tein or fats, or recommend ingestion of foods one at a time. Diets that are restricted in carbohydrates (such as the Atkins and South B each diets), however, can be effective in achieving a lower total calorie intake. Several studies have demonstrated that low-carbohydrate diets can be used safely and effectively for weight loss without adverse effects on lipids or other metabolic parameters. Meal replacement diets can also be used effectively and safely to achieve weight loss. Although formal behavior modifica tion programs are available to which patients can be referred, the clinician caring for obese patients can teach a number of useful behavioral techniques. Patients can be taught to plan menus and exercise sessions and to record their actual behavior. Record keep ing not only aids in behavioral change, but also helps the provider to make specific suggestions for problem solving. Patients can be taught to recognize "eating cues" (emo tional, situational, etc) and how to avoid or control them. Regular self-monitoring of weight is also associated with improved long-term weight maintenance. Exercise offers a number of advantages to patients try ing to lose weight and keep it off. Aerobic exercise directly increases the daily energy expenditure and is particularly useful for long-term weight maintenance. Etiology Obesity has been considered to be the direct result of a sedentary lifestyle plus chronic ingestion of excess calories. One gene codes for a protein expressed by adipose tissue-leptin-and another for the leptin receptor in the brain. Only a small percentage of human obesity is thought to be due to single gene mutations. Most human obesity undoubtedly develops from the interactions of multiple genes, environmental factors, and behavior. The rapid increase in obesity in the last several decades clearly points to major roles for environmental and behavioral fac tors in its development. Medical Eva l uation of the Obese Patient Historical information should be obtained about age at onset, recent weight changes, family history of obesity, occupational history, eating and exercise behavior, ciga rette and alcohol use, previous weight loss experience, and psychosocial factors including assessment for depression and eating disorders. Particular attention should be directed at use oflaxatives, diuretics, hormones, nutritional supplements, and over-the-counter medications. Less than 1 % of obese patients have an identifiable secondary, nonpsychiatric, cause of obesity. Hypothyroid ism and Cushing syndrome are important examples that can usually be diagnosed by physical examination in patients with unexplained recent weight gain. All obese patients should be assessed for medical con sequences of their obesity by screening for the metabolic syndrome. Continued close contact with clinicians and involvement of the family and peer group are useful techniques for reinforcing behavioral change and preventing social isolation. Very-low-calorie diets (typically 800- 1 000 kcal/day) result in rapid weight loss and marked initial improvement in obesity-related metabolic compli cations. Long-term weight maintenance following meal replacement programs is less predictable and requires concurrent behavior modification, long-term use of low calorie diets, careful self-monitoring, and regular exercise. Side effects such as fatigue, orthostatic hypotension, cold intolerance, and fluid and electrolyte disorders are observed in proportion to the degree of calorie reduction and require regular supervision by a clinician. Other less common complications include gout, gallbladder disease, and cardiac arrhythmias. Although weight loss is more rapidly achieved with very-low-calorie diets as compared with traditional diets, long-term outcomes are equivalent. Medications for the treatment of obesity are available both over the counter and by prescription. Considerable controversy exists as to the appropriate use of medications for obesity. However, few data suggest that medications can improve long-term outcomes associated with obesity. Cat echolaminergic medications (eg, phentermine, diethylpro pion, benzphetamine, and phendimetrazine) are approved for short-term use only and have limited utility. Orlistat (1 20 mg orally up to three times daily with each fat-con taining meal) is available by prescription for longer-term treatment of obesity. Rather than in the central ner vous system, orlistat works in the gastrointestinal tract to inhibit intestinal lipase, reducing fat absorption. Not unex pectedly, it may cause diarrhea, gas, and cramping and perhaps reduced absorption of fat-soluble vitamins. In randomized trials with up to 2 years of follow-up, orlistat resulted in 2-4 kg greater weight loss than placebo. A ben eficial impact on long-term obesity-related clinical out comes has not been established. Lorcaserin, a selective serotonin recep tor agonist given in a dose of 10 mg orally twice daily, is associated with modest weight loss, about 3% of initial weight more than placebo. Post-marketing sur veillance is focused on concerns about increased breast tumors in animal studies, valvular heart disease in patients receiving earlier drugs of this class, and psychiatric side effects. Since the medications increase heart rate, a large clinical trial to assess cardiovascular risk is being conducted. The combi nation is also associated with increased birth defects and should not be used during pregnancy. Concerns include an increased risk of suicidal thoughts and behav iors, other neuropsychiatric events, seizures, and elevation of blood pressure and heart rate. Other side effects include nausea and vomiting, diarrhea and constipation, headache, and dry mouth.

Syndromes

• Angiodysplasia of the colon
• Get drugs that suppress the immune system, such as corticosteroids or rituximab
• Abdominal pain
• Death
• Alcohol
• Low blood sugar

In several studies prostate hypertrophy order 5 mg fincar, the rate of colorectal cancer within 3 years of a screening colonoscopy was 0 androgen hormone 1 fincar 5 mg buy on line. This may be attributable to adenomatous and serrated polyps and early cancers that were overlooked during colonoscopy mens health juice recipes order fincar 5 mg visa. Studies of back-to hack colonoscopies confirm that endoscopists overlook 6- 1 2% of polyps greater than 1 em in size and up to 25% of smaller adenomas mens health living purchase cheap fincar on line. Polyps that are small mens health 012013 chomikuj discount fincar 5 mg line, flat, or located behind folds are easily missed, especially if the bowel prep a ration is poor. Population-based case-control and cohort studies suggest that colonoscopy is associated with greater reduction in colorectal cancer incidence and mortality in the distal colon than the proximal colon. This may be attrib utable to incomplete examination of the proximal colon, and differences between the proximal and distal colon that include worse bowel preparation, suboptimal colonoscopic technique, and a higher prevalence of serrated polyps and flat adenomas. The latter are more common than previously recognized, are more likely to contain advanced pathology, and are more difficult to identify than raised (sessile or pedunculated) polyps. To optimize diagnostic accuracy as well as patient safety and comfort, colonoscopy should be performed after optimal bowel preparation by a well trained endoscopist who spends sufficient time (at least 7 minutes) carefully examining the colon (especially the proximal colon) while withdrawing the endoscope. Nonetheless, this examination is performed rapidly and requires no sedation or intravenous contrast. Several large studies have compared the accuracy of virtual colonoscopy with colonoscopy for colorectal screening. Using current imaging software with multidetector helical scanners, the sensitivity is greater than 95% for the detection of cancer and greater than 84-92% for the detection of polyps 1 0 mm or larger. The sensitivity for polyps 6-9 mm in size ranges from 57% to 84%; for polyps 5 mm or less, the sensitivity is extremely poor. If no polyps are found, the interval for repeat screening examination is uncertain; however, 5 years may be reasonable. All patients with pol yps 10 mm or larger should be referred for colonoscopy with polypectomy because of the high prevalence (30%) of advanced pathology (cancer, high-grade dysplasia, or vil lous features) within these polyps. The optimal manage ment of patients with polyps less than 1 0 mm in size is controversial. In a prospective comparative trial conducted in persons at average risk for colorectal cancer undergoing colonoscopy, the sensitivity for colorectal can cer for "Cologuard" was 92. Flexible sigmoidoscopy-Use of a 60-cm flexible sig moidoscope permits visualization of the rectosigmoid and descending colon. Adenomatous polyps are identified in 1 0-20% and colorectal cancers in 1 % of patients. The chief disadvantage of screening with flexible sig moidoscopy is that is does not examine the proximal colon. The prevalence of proximal versus distal neoplasia is higher in people over age 65 years of age, African Americans, and women. In men, approximately 50% of advanced neoplasms (cancer, adenomas 1 em or larger, polyps with villous histology, or high-grade dysplasia) are located in the proximal colon, compared with 60-70% in women. The finding at sigmoidoscopy of an adenomatous polyp in the distal colon increases the likelihood at least twofold that an advanced neoplasm is present in the proximal colon. Therefore, patients found on screening sigmoidos copy to have an adenomatous polyp of any size should subsequently undergo colonoscopy to evaluate the proxi mal colon. In addition to detecting early cancers, colo noscopy allows removal of adenomatous polyps by biopsy or polypectomy, which is believed to reduce the risk of subsequent cancer. Over the past decade, there has been a dramatic increase in screening colonoscopy and a similar decrease in screening sigmoidoscopy due to poor reim bursement and the perceived inferiority of sigmoidoscopy compared with colonoscopy. The incidence of serious complications after colonoscopy (perforation, bleeding, cardiopulmonary events) is 0. In asymptomatic individuals between 50 and 75 years of age undergoing screening colonoscopy, the prevalence of advanced neoplasia is 4- 1 1 % and of cancer is 0. At the present time, there is no consensus on the management of patients with polyps smaller than 6 mm; however, some radiologists choose not even to report these findings. Barium enema-Double-contrast barium enema was previously used as a screening technique because it was widely available, relatively inexpensive, and safe. Patients with suspected colorectal cancer or adenomatous polyps of any size should be referred for colonoscopy. Virtually all patients with proven colorectal cancer should be referred to a surgeon for resection. Patients with clinical stage T3 or node-positive rectal tumors (or both) also should be referred to medical and radiation oncologists preoperatively for neoadjuvant therapy. When to Ad mit Patients with complications of colorectal cancer (obstruction, acute bleeding) requiring urgent evalua tion and intervention. Fecal immunochemical test program perfor mance over 4 rounds of annual screening: a retrospective cohort study. Colorectal cancer in the elderly and the influence of lead time bias: better survival does not equate with improved life expectancy. Accuracy of fecal immunochemical tests for colorectal cancer: systematic review and meta -analysis. Cancer screening in the United States, 20 1 6: a review of current American Cancer Society guidelines and current issues in cancer screening. Estimating the magnitude of colorectal cancers prevented during the era of screening: 1 976 to 2009. Tumors arising from the mucosa of the anal canal are relatively rare, comprising only 1 -2% of all cancers of the anus and large intestine. Anal cancer is increased among people practicing receptive anal inter course and those with a history of anorectal warts. These tumors tend to become annular, invade the sphincter, and spread upward via the lymphatics into the perirectal mes enteric lymphatic nodes. Small (less than 3 em) superficial lesions of the perianal skin may be treated with wide local excision. Adenocarcinoma of the anal canal is treated in similar fash ion to rectal cancer (see above), commonly by abdomino perineal resection with neoadjuvant chemoradiotherapy and adjuvant chemotherapy. Squamous cancer of the anal canal and large perianal tumors invading the sphincter or rectum are treated with combined-modality therapy that includes external radiation with simultaneous chemother apy (5-fluorouracil plus mitomycin). Radical surgery (abdominoperineal resection) is reserved for patients who fail chemotherapy and radiation therapy. Metastatic disease is generally treated with 5-fluorouracil in combination with cisplatin. Optimal management of squamous cell carcinoma of the anal canal: where are we now Human papillomavirus and genital warts: a review of the evidence for the 20 1 5 Centers for Disease Control and Prevention Sexually Transmitted Diseases Treatment Guide lines. Anal cancer incidence in the United States, 1 977-20 1 1: distinct patterns by histology and behavior. General Considerations Prostatic cancer is the most common noncutaneous cancer detected in American men and the second leading cause of cancer-related death in men. However, the clini cal incidence of the disease does not match the prevalence noted at autopsy, where more than 40% of men over 50 years of age are found to have prostatic carcinoma. Most such occult cancers are small and contained within the prostate gland; few are associated with regional or distant disease. Whereas 30% of men aged 60-69 years will have the disease at autopsy, its incidence increases to 67% in men aged 80-89 years. Although the global prevalence of pros tatic cancer at autopsy is relatively consistent, the clinical incidence varies considerably (high in North America and European countries, intermediate in South America, and low in the Far East). A 50-year-old American man has a lifetime risk of 40% for latent cancer, 16% for developing clinically apparent cancer, and a 2. African American race, family history of prostatic cancer, and history of high dietary fat intake are risk factors for prostate cancer. Obstructive voiding symptoms are most often due to benign prostatic hyperplasia, which occurs in the same age group. Nevertheless, large or locally extensive prostatic cancers can cause obstructive voiding symptoms. Because the axial skeleton is the most com mon site of metastases, patients may present with back pain or pathologic fractures. The serum level is typically low and cor relates with the volume of (benign and malignant) prostate tissue. Miscellaneous laboratory testing-Patients with uri nary retention or with ureteral obstruction due to loco regionally advanced prostate cancers may present with elevations in blood urea nitrogen or serum creatinine. Patients with bony metastases may have elevations in serum alkaline phosphatase or calcium. Laboratory and clinical evidence of disseminated intravascular coagulation can occur in patients with advanced prostate cancers. Prostate biopsy-Transrectal ultrasound-guided biopsy is the standard method for detection of prostate cancer. The use of a spring-loaded, 1 8-gauge biopsy needle has allowed transrectal biopsy to be performed with minimal patient discomfort and morbidity. Local anesthesia is rou tinely used and increases the tolerability of the procedure. Extended-pattern biopsies, including a total of at least ten biopsies, are associated with improved cancer detection and risk stratification of patients with newly diagnosed disease. Patients with abnormalities of the seminal vesicles can have these structures specifically biopsied to identify local tumor invasion. Imaging Transrectal ultrasonography has primarily been used for the staging of prostate carcinomas, where tumors typically appear as hypoechoic areas. In addition, transrectal ultra sound-guided, rather than digitally-guided, biopsy of the prostate is a more accurate way to evaluate suspicious lesions. Use of imaging should be tailored to the likelihood of advanced disease in newly diagnosed cases. Conventional radionudide (99-technetium) bone scans are superior to conventional plain skeletal radio graphs in detecting bony metastases. Most prostate cancer metastases are multiple and most commonly localized to the axial skeleton. Because of the high frequency of abnor mal scans in patients in this age group resulting from degenerative joint disease, plain films are often necessary in evaluating patients with indeterminate findings on bone scan. Intravenous urography and cystoscopy are not rou tinely needed to evaluate patients with prostate cancer. Despite application of modern, sophisticated tech niques, understaging of prostate cancer occurs in at least 20% of patients. Screening fo r Prostate Cancer Whether screening for prostate cancer results in a decrease in its mortality rates is controversial. Two large, randomized trials question the benefit of screening men for prostate cancer. Although screening resulted in a 12% increase in pros tate cancer detection, the cancer-specific mortality rate was similar in the screening and control arms (3. Most arise in the peripheral zone of the prostate, though a small percentage arise in the central (5- 1 0%) and transition zones (20%) of the gland. Pathologists utilize the Gleason grading system whereby a "primary" grade is applied to the architectural pattern of malignant glands occupying the largest area of the specimen and a "secondary" grade is assigned to the next largest area of cancer. Grading is based on architectural rather than histologic criteria, and five "grades" are possible. Adding the score of the primary and secondary grades gives a Gleason score from 2 to 10. Morbidity is limited, and the survival of patients with localized cancers (T l, T2, and selected T3) approaches 65% at 10 years. As with surgery, the likelihood of local failure correlates with technique and cancer characteristics. The likelihood of a positive prostate biopsy more than 1 8 months after radia tion varies between 20% and 60%. Patients with local recurrence are at an increased risk of cancer progression and cancer death compared with those who have negative biopsies. Ambiguous target definitions, inadequate radia tion doses, and understaging of the cancer may be respon sible for the failure noted in some series. Three-dimensional conformal radiation delivers a higher dose because of improved targeting and appears to be associated with greater efficacy as well as lower likelihood of adverse side effects compared with previous techniques. Brachyther apy-the implantation of permanent or temporary radio active sources (palladium, iodine, or iridium) into the prostate can be used as monotherapy in those with low grade or low-volume malignancies or combined with external beam radiation in patients with higher-grade or higher-volume disease. Cryosurgery In cryosurgery, liquid nitrogen is circulated through small hollow-core needles inserted into the prostate under ultra sound guidance. Local ized Disease Although selected patients may be candidates for active surveillance based on age or health and evidence of small volume or well-differentiated cancers, most men with an anticipated life expectancy in excess of 10 years should be considered for treatment. Newly introduced genomic tests may provide novel information to help guide treatment decisions. Both radiation therapy and radical prostatec tomy result in acceptable levels of local control. A large, prospective, randomized trial compared active surveillance with radical prostatectomy in 695 men with clinically local ized and well-differentiated to moderately differentiated cancers. Radical prostatectomy significantly reduced dis ease-specific mortality, overall mortality, and risks of metastasis and local progression. Active Surveilla nce the optimal treatment for patients with clinically localized prostate cancers remains controversial. A beneficial impact of treating localized prostate cancer has not been conclu sively demonstrated with respect to survival. Patients need to be advised of all treatment options, including active surveillance, with the specific benefits, risks, and limita tions. The goal of active surveillance is to avoid treatment in men who never experience disease progression while recognizing and effectively treating men with evidence of progression. Currently, treatment decisions are made based on stage and cancer grade (Gleason score) as well as the age and health of the patient.

With heat syncope prostate cancer blood in urine fincar 5 mg buy without a prescription, there is usually a history of pro longed vigorous physical activity or prolonged standing in a hot humid environment followed by a sudden collapse prostate cancer hormone injections purchase 5 mg fincar mastercard. The skin is cool and moist prostate oncology yakima fincar 5 mg purchase visa, the pulse is weak prostate cancer xmas cards buy fincar with american express, and the sys tolic blood pressure is low mens health week purchase fincar once a day. Presenting symptoms include all find ings seen in heat exhaustion with additional neurologic symptoms such as dizziness, weakness, emotional lability, confusion, delirium, blurred vision, convulsions, collapse, and unconsciousness. Exertional heat stroke may present with sudden collapse and loss of conscious ness followed by irrational behavior. Providers should be vigilant in monitoring for kidney injury, liver failure, metabolic derangements, respi ratory compromise, coagulopathy, and ischemia. There is a spectrum of preventable heat-related illnesses related to environmental exposure, ranging from mild forms, such as heat cramps, to severe forms, such as heat stroke. Risk factors related to exertion include longer dura tion of exertion, hot environment, insufficient acclimatiza tion, and dehydration. Additional risk factors include skin disorders or other medical conditions that inhibit sweat production or evaporation, obesity, prolonged seizures, hypotension, reduced cutaneous blood flow (ie, vasocon strictors, beta-adrenergic blocking agents, dehydration), reduced cardiac output, the use of drugs that increase metabolism or muscle activity or impair sweating, and withdrawal syndromes. Medications that impair sweating include anticholinergics, antihistamines, phenothiazines, tricyclic antidepressants, monoamine oxidase inhibitors, and diuretics. Reduced cutaneous blood flow results from use of vasoconstrictors and beta-adrenergic blocking agents and dehydration results from use of alcohol. Illicit drugs, including stimulants, some hallucinogens and anti psychotic agents, can cause increased muscle activity and thus generate increased body heat. Classic (nonexertional) heat-related illness may occur in any individual in a hot relaxing environment (ie, hot bath, steam room, sunbathing, or sauna). It may also occur when a high-risk individual is in extreme heat environ mental conditions (heat, humidity) even if that individual is not physically active. Heat cramping results from dilutional hyponatremia as sweat losses are replaced with water alone. Heat exhaus tion results from prolonged strenuous activity in a hot environment without adequate water or salt intake. It is characterized by dehydration, sodium depletion, or iso tonic fluid loss with accompanying cardiovascular changes. Heat syncope or sudden collapse may result in uncon sciousness from volume depletion and cutaneous vasodila tion with consequent systemic and cerebral hypotension. Exercise-associated postural hypotension is usually the cause of heat syncope: it may occur during or immediately following exercise. Classic (nonexertional) heat stroke occurs in patients with impaired thermoregula tory mechanisms or in extreme environmental conditions. Exertional heat stroke occurs in healthy persons undergo ing strenuous exertion in a hot or humid environment. Persons at greatest risk are those who are at the extremes of age, chronically debilitated, and taking medications that interfere with heat-dissipating mechanisms (ie, anticholin ergics, antihistamines, phenothiazines). Heat Cra m ps the patient must be moved to a shaded, cool environment and given oral rehydration solution to replace both electro lytes and water. The patient may have to rest for at least 2 days with continued dietary supplementation before returning to work or resuming strenuous activity in the heat. Heat Exhaustion Treatment consists of moving patient to a shaded, cool environment, providing adequate fluid and electrolyte replacement, and active cooling (ie, fans, cool packs) if necessary. Physiologic saline or isotonic glucose solution should be administered intravenously when oral adminis tration is not appropriate. Heat Syncope Treatment consists of rest and recumbency in a shaded, cool place, and fluid and electrolyte replacement by mouth (or intravenously if necessary). Clin ical Findings For all types of heat related illnesses, skin temperature may not reflect core temperature; thus, it is important to use an internal rectal, foley, or esophageal thermometer when diagnosing and treating disorders due to heat. Circulatory failure in heat-related illness is mostly due to shock from relative or absolute hypovolemia. Oral or intravenous fluid administration must be provided to ensure adequate uri nary output. Clinicians must also assess for and treat concurrent conditions (infection; trauma; and drug effects). Choice of cooling method depends on which can be insti tuted the fastest with the least compromise to the overall care of the patient. Evaporative cooling is preferred for nonexer tional heat stroke and conductive-based cooling for exer tional heat stroke. Evaporative cooling is a noninvasive, effective, quick and easy way to reduce temperature. This method is done by placing the undressed patient in lateral recumbent position or supported in a hands-and-knees posi tion to expose maximum skin surface to the air. Large fans circulate the room air while the entire undressed body is sprayed with lukewarm water (20°C). Conductive-based cooling involves cool fluid infusion, gastric or bladder lavage, ice packs, and immersion into ice water or cool water. When immersion in ice water or cold water is available in the field, it is the pre ferred method of cooling for exertional heat stroke. Ice packs are most effective when covering the whole body, as opposed to the traditional method of just the axilla and groin. Research suggests that brain cooling may lessen cerebrovascular injury from heat stroke. Shivering must be avoided because it inhibits the effec tiveness of cooling by increasing internal heat production. Medications can be used to suppress shivering including magnesium, quick-acting opioid analgesics, benzodiaze pines, and quick-acting anesthetic agents. Those who are physically active in a hot environment should increase fluid consumption before, during, and after physical activities. Water consumption alone may lead to electrolyte imbalance, particularly hypo natremia. It is not recommended to have salt tablets avail able for use because of the risk of hypertonic hypernatremia. Close monitoring of fluid and electrolyte intake and early intervention are recommended in situations necessitating exertion or activity in hot environments. Prog nosis Mortality is high from heat stroke; multiorgan dysfunction is the usual cause of heat stroke-related death. When to Refer Potential consultants include surgeons for susptcwn of compartment syndrome, nephrologist for kidney injury, and transplant surgeon for fulminant liver failure. When to Ad m it All patients with suspected heat stroke must be admitted to the hospital with intensive care capability for close monitoring. A case of severe heatstroke and review of pathophysiology, clinical presentation, and treatment. Prevention Public education is necessary to improve prevention and early recognition of heat-related disorders. Individuals should take steps to reduce personal risk factors and to gradually acclimatize to the hot environment. Coaches, athletic trainers, athletes, and parents of young athletes must be educated about heat-related illness, spe cifically about prevention, risks, signs and symptoms, and treatment. Coma, loss of reflexes, rigor mortis, asystole, or ventricular fibrillation may falsely lead the clinician to assume that patient is dead despite reversible hypothermia. This may be primary (from exposure to prolonged ambient extremely low temperature) or secondary (due to thermo regulatory dysfunction). Hypothermia should be considered in any patient with prolonged exposure to an ambient cold environment, espe cially in any patients with prior cold weather injury as well as risk factors listed in Cold & Heat section. Treatment Rewarming is the initial, imperative treatment for all hypo thermic patients. Resuscitation begins with rapid assessment and support of airway, breathing and circulation, simultane ously with the initiation of rewarming, and prevention of further heat loss. All cold, wet clothing must be removed and replaced with warm, dry clothing and blankets. Mild or stage I hypothermia can be treated by passive external rewarming (ie, removing wet clothing and provid ing dry clothes) and active external rewarming (ie, a warm environment, warm blankets, and warm beverages). In con trast to those with more severe hypothermia, it is safe and recommended for the uninjured patient with mild hypo thermia to become physically active to generate heat. Examples include warm bedding, heated blankets, heat packs, and immersion into a 40°C bath. Warm bath immersion limits the ability to moni tor the patient or treat other coexisting conditions. Patients with mild hypothermia and previous good health usually respond well to passive and active external warming. This requires close monitoring of vital signs, pulse oximetry and cardiac rhythm during rewarming. Warm intravenous fluids (38-42°C) are considered mini mally invasive and effective. As hypothermia becomes more severe there are increased complications of both hypothermia itself and rewarming. Complications of rewarming occur as colder peripheral blood returns to central circulation. This may result in core temperature afterdrop, rewarming lactic acidosis from shunting lactate into the circulation, rewarming shock from peripheral vasodilation and hypovolemia, ventricular fibrillation, and other cardiac arrhythmias. Afterdrop can be lessened by active external rewarming of the trunk but not the extremities and by avoiding any muscle move ment by the patient. Extreme caution must be taken when handling the hypothermic patient to avoid triggering poten tially fatal arrhythmias in a phenomenon known as rescue collapse. Laboratory stud ies should assess acid-base status, electrolyte derangements (particularly potassium and glucose), coagulopathy, kidney failure, rhabdomyolysis and liver or pancreas dysfunction. Inaccurate laboratory values will occur if the blood sample is warmed to 37°C for the testing. All patients should be evaluated for associated conditions (ie, hypoglycemia, trauma, infection, overdose, and peripheral cold injury). Shivering stops; bradycardia, dilated pupils, slowed reflexes, cold diuresis, and confusion and lethargy ensue. The European Resuscitation Council recommends withholding epinephrine until warmed to 30°C, and decreasing the frequency from 30°C to 35°C. The American Heart Association permits dosage as usual in conjunction with rewarming. L) or evidence of death from a traumatic cause such as decapitation or asphyxiation in an avalanche. Any hypothermic patient with return of spontaneous circulation must be monitored very closely because of the high likelihood of subsequent multiorgan system failure. Those most at risk are people with underlying diseases or medica tions that decrease tissue perfusion and those with envi ronmental exposure to a prolonged cold environment. Caution must be taken to avoid cramped positions; con strictive clothing; prolonged dependency of the feet; use of tobacco, alcohol, and sedative medications; and exposure to wet muddy ground and windy conditions. Chilblains or erythema pernio are inflammatory skin changes caused by exposure to cold without actual freezing of the tissues. These skin lesions may be red or purple papular lesions, which are painful or pruritic, with burning or paresthesias. With continued exposure, ulcerative or hemorrhagic lesions may appear and progress to scarring, fibrosis, and atrophy. Treatment consists of elevating and passively externally rewarming the affected part. Caution must be taken to avoid rubbing or massaging injured tissues and to avoid applying ice or heat. The area must be protected from trauma, secondary infection, and further cold exposure. When to Ad mit Hypothermia patients must undergo close monitoring for potential complications. Wilderness Medical Society practice guidelines for the out -of-hospital evaluation and treatment of accidental hypothermia: 20 14 update. Prehyper emic stage is marked by early symptoms of cold and anesthesia of the affected area. Posthyperemic stage occurs with ongoing cold exposure; the affected part becomes pale or cyanotic with diminished pulsations due to vasospasm. This may result in blistering, swelling, redness, ecchymoses, hemorrhage, necrosis, peripheral nerve injury, or gangrene. Treatment consists of air drying, protecting the extrem ities from trauma and secondary infection, and gradual rewarming by exposure to air at room temperature (not ice or heat). Caution must be taken to avoid massaging or moistening the skin and to avoid further cold injury and water immersion. Clin ical Findings Cold-induced injuries to the extremities range from mild to severe. Cold exposure of the extremities produces immediate localized vasoconstriction followed by general ized vasoconstriction. Tissue damage may result from ischemia and intravascular thromboses, endothelial dam age, or by actual freezing. Freezing (frostbite) may occur when the temperature drops or in the presence of wind, water, immobility, malnutrition, or vascular disease. Intra arterial thrombolytic administration within 24 hours of exposure has resulted in improved tissue perfusion and has reduced amputation. There is insufficient evidence to rec ommend hyperbaric oxygen, heparin, or sympathectomy. Follow-Up Care Patient education must include ongoing care of the cold injury and prevention of future hypothermia and cold injury. Gentle, progressive physical therapy to promote circulation should be instituted as tolerated. Debridement and amputation should be considered only after it is estab lished that the tissues are necrotic.

In the survivor of a transplant associated outbreak prostate order 5 mg fincar with mastercard, ribavirin (which is effective against other arenaviruses) was used successfully along with decreasing immunosuppression prostate cancer john hopkins fincar 5 mg order with mastercard. Congenital infection is more severe with about 30% mortality rate among infected infants mens health february 2013 cheap fincar 5 mg fast delivery, and more than 90% of survivors suffering long term neurologic abnormalities hormone androgen deprivation therapy for prostate cancer order fincar 5 mg with amex. Lymphocytic choriomen ingitis in solid organ transplant recipients is associated with a poor prognosis; of reported cases carlson prostate 5 mg fincar buy overnight delivery, the mortality rate is more than 80%. Sym ptoms and Signs the incubation period is 8-13 days to the appearance of systemic manifestations and 15-21 days to the appearance of meningeal symptoms. Symptoms are biphasic, with a prodromal illness characterized by fever, chills, headache, myalgia, cough, and vomiting, occasionally with lymph adenopathy and maculopapular rash. After 3-5 days the fever subsides only to return after 2-4 days alongside the meningeal phase, characterized by headache, nausea and vomiting, lethargy, and variably present meningeal signs. Transverse myelitis, deafness, Guillain-Barre syndrome, and transient and permanent hydrocephalus are reported. Lymphocytic choriomeningitis virus is a well-known, albeit underrecog nized, cause of congenital infection frequently complicated with obstructive hydrocephalus and chorioretinitis. In fetuses and newborns with ventriculomegaly or other abnormal neuroimaging findings, screening for congenital lymphocytic choriomeningitis may be considered; mothers are asymptomatic half the time. Occasionally, a syndrome resembling the viral hemorrhagic fevers is described in transplant recipients of infected organs and in patients with lymphoma. Laboratory Findings Leukocytosis or leukopenia and thrombocytopenia may be initially present. During the meningeal phase, cerebrospi nal fluid analysis frequently shows lymphocytic pleocytosis (total count is often 500-3000/mcL) alongside a slight increase in protein, while a low to normal glucose is seen in at least 25%. The virus may be recovered from the blood and cerebrospinal fluid by mouse inoculation. Prevention Pregnant women should be advised of the dangers to their unborn children inherent in exposure to rodents. General Considerations the transmissible spongiform encephalopathies are a group of fatal neurodegenerative diseases affecting humans and animals. These agents show slow replicative capacity and long latent intervals in the host. They induce the conformational change of a normal brain protein (prion protein; PrP [C]) into an abnormal isoform (PrP [Sc]) that accumulates and causes neuronal vacuolation (spon giosis), reactive proliferation of astrocytes and microglia and, in some cases, the deposition of beta-amyloid oligo meric plaques. Hereditary disorders are caused by germ line mutations in the PrP [C] gene causing familial. Differential Diag nosis the influenza-like prodrome and latent period may dis tinguish this from other aseptic meningitides, and bacte rial and granulomatous meningitis. A history of exposure to mice or other potential vectors is an important diagnos tic clue. The degree of organ involvement is often extensive, and the clinical symptoms are unique, mainly characterized by prominent psychiatric and sensory symptoms. The assay is available through academic specialty prion clinics in the United Kingdom. The differentiation and definitive diagnosis of these neurodegenerative diseases are estab lished by neuropathologic confirmation. Kuru, once prevalent in central New Guinea, is now rare, a decline in prevalence that started after the abandon ment of cannibalism in the late 1 950s (a protective allele of the PrP gene is now identified at codon 127). The overall annual incidence of prion disease world wide is approximately 1 -2 in 1 million persons per year. Differential Diag nosis Autoimmune encephalitis can have a similar clinical pic ture. Clinical features of these three forms of disease usually involve mental deterioration (dementia, behavioral changes, loss of cortical function) progressive over several months, as well as myoclonus, extrapyramidal (hypokinesia) and cerebellar manifesta tions (ataxia, dysarthria). Finally, coma ensues, usually associated with an akinetic state and less commonly decer ebrate/decorticate posturing. Flupirtine (an analgesic drug) is sometimes useful in slowing the associated cognitive decline but does not affect survival. Studies are in progress to identify vaccines, but no promis ing candidates exist to date. Reference centers are available at Case Western Reserve University in the United States and the University College London Hospitals in the United Kingdom. Association of cerebrospinal fluid prion protein levels and the distinction b etween Alzheimer disease and Creutzfeldt-Jacob disease. Variant Creutzfeldt-Jakob disease with extremely low lymphoreticular deposition of prion protein. Neuronal antibodies in patients with suspected or confirmed sporadic Creutzfeldt-Jakob disease. Symptoms include altered mental status, aphasia, ataxia, hemiparesis or hemi plegia and visual field disturbances. These findings may not be distinguishable from immune reconstitution inflammatory syndrome. Increased uptake of methionine with concomitant decreased uptake of fluorodeoxyglucose in positron emission tomog raphy may be helpful for diagnosis. This polyomavirus usually causes its primary infec tion during childhood with about 80% of adults typically being seropositive. The virus remains latent in the kidneys, lymphoid tissues, epithelial cells, peripheral blood leuko cytes, bone marrow, and possibly brain until reactivation occurs and symptoms become evident. It is also reported among those with lymphopro liferative and myeloproliferative disorders; granulomatous, inflammatory, and rheumatic diseases (systemic lupus ery thematosus and rheumatoid arthritis in particular); as well as in those who have undergone solid and hematopoietic cell transplantation; and occasionally in those who have other medical states, including cirrhosis and kidney disease. Immune restoration can induce worsening of the clinical picture in a small number of cases. Opportunistic infections, such as Pneumocystis jirovecii pneumonia and cryptococcal meningitis, are common. A chronic inflammation of the spinal cord leads to progressive motor weakness and symmetric spastic paraparesis, nociceptive low back pain, and para plegia with hyperreflexia. Bladder and sexual disorders (eg, dyspareunia, erectile dysfunction), sensory disturbances, and constipation are also common. It is endemic to many regions in the world including southern Japan, the Caribbean, much of sub-Saharan Africa, South America, Eastern Europe, and Oceania. The Caribbean basin and southwestern Japan show the highest prevalence of infection (4-3 7%). Over 85% of cases found in the United States are located in the West or South west. The virus is transmitted horizontally (sex), vertically (intrauterine, peripartum, and breast feeding), and paren terally (injection drug use and blood transfusion). A pri mary cutaneous tumor is also described and shows a worse prognosis compared with the smoldering type. Human T lymphotropic virus type- 1 -associated myelopathy manifesting shortly after living-donor renal transplantation. Clinical outcomes of a novel therapeutic vaccine with Tax peptide-pulsed dendritic cells for adult T cell leukae mia/lymphoma in a pilot study. Five species of Ebolavirus have been identified, and each species has an associated virus: l. While the zoonotic reservoir is unknown, evidence from Marbug suggests fruit bats as a possible vector. After a zoonotic transmission to a human occurs, Ebola can continue to be transmitted among humans who directly contact infected body fluids (droplet and contact precau tions advised). There is no evidence supporting airborne transmission; however, the virus aerosolizes, meaning that certain settings such as health care facilities carry addi tiona! Ebola has a 2-2 1 day incuba tion period, and over 95% of cases present with symptoms during the first 14 days. Even at symptom onset, the risk of transmission is extremely low but increases over time. The first Ebola outbreak occurred in 1 976 as a simulta neous epidemic in Congo and Sudan. The first cases were identified along the Ebola River, in Congo but near the Sudanese border, resulting in naming of the disease. Subse quent outbreaks had been confined to Congo, Uganda, and Sudan until March 2014 when the first Ebola case in West Africa was identified in Gueckedou, Guinea, near the bor ders of Sierra Leone and Liberia. There were 8 8 1 cases with 5 3 1 deaths in these three countries among health care workers. Several factors led to the unprecedented magnitude of the 2014-20 1 5 Ebola epidemic. Another compounding factor was the size of the epidemic at the time it was uncovered, with the epidemic already having reached Conakry, the capital of Guinea, and having progressed into Sierra Leone and Libe ria. Aside from the earlier Kikwik outbreak in Congo, which occurred in an isolated, quarantined city, this epi demic has been recognized as the first truly urbanized outbreak, making traditional public health measure such as contact tracing more difficult. Travel and contact history are crucial when considering the differential diagnosis in areas where Ebola is not endemic. If such histories are present, patients need to be asked if they had unprotected expo sures to persons with Ebola. Along with fevers, patients tend to experience malaise, fatigue, myalgia, and arthral gia. Nausea and vomiting continue to worsen until the patient can no longer tolerate oral intake, and diarrhea becomes large volume (5 or more liters per day). This stage of the illness may continue for a week during which time neurologic symptoms gain prominence. Encephalitis is commonly observed and includes the symptoms of confu sion, slowed cognition, agitation, and occasional seizures. Shock develops in most patients, but hemorrhagic manifes tations develop in only 1 -5% of patients. Blood samples obtained within the first 3 days of illness should be repeated if the results are negative and clinical symptoms and signs persist. After about 10 days, IgM antibodies begin to develop and, after approximately 2 weeks, an IgG antibody response develops. The nature of this illness and its significant fluid loss tend to cause electrolyte abnormalities and accel erate acute kidney injury. For many patients in highly affected countries, non-Ebola diagnostic testing is inaccessible. In the presence of oral rehydra tion salts, mortality rates are approximately 70%. Several studies have shown that intravenous fluids can reduce the mortality rates to less than 50%. In these studies, the amount of intravenous fluid replacement was relatively less than what would be used in countries with developed health systems. Most were healthcare workers who were evacuated to biocontainment units in the United States and received intensive care and experimental thera pies. Aside from Ebola treatment and experimental thera pies, patients typically receive empiric antimalarial agents and broad-spectrum antibiotics. Empiric therapies are important at presentation because the risk associated with non-Ebola diagnostics prevents studies from being con ducted until results are obtained. Differential Diag nosis the differential diagnosis varies with the stage of illness. As gastroin testinal symptoms develop, health providers should also consider viral hepatitis, toxins, leptospirosis, and rickettsial diseases. Prog nosis the prognosis depends greatly on patient, exposure, and clinical characteristics. In the 2014-20 1 5 epidemic, a small but significant percent age of pregnant women survived. Flaviviruses, such as the pathogens causing dengue and yellow fever (both with occasional hemor rhagic complications), and Filoviridae, causing Ebola and Marburg, are discussed in separate sections. Lassa fever (an Old World arenavirus) is rodent associ ated and transmission usually occurs through aerosolized particles (from rodents or infected individuals). Transmis sion through direct contact with infected biologic fluids or tissues is also documented and food-borne transmission, while considered, is not definitively proven. Similar modes of transmission are assumed for Junin virus and other members of the New World Arenaviridae (Machupo virus, Sabia virus, Guanarito virus, Whitewater Arroyo virus). The bunyaviruses include the Crimean-Congo hemor rhagic fever (transmitted by infected animal exposure or tick bite), the Rift Valley fever (transmitted by exposure to infected animal products or bite of an infected mosquito or flea), and the hantaviruses (associated with rodent expo sure and discussed separately below). The geographic dis tribution of Crimean-Congo hemorrhagic fever, like that of its tick vector, is widespread with cases reported in Asia, the Middle East, and Eastern Europe. Rift Valley cases have also been confirmed outside the African continent, in Saudi Arabia and Yemen. Its differential diagnosis includes anaplasmo sis, hemorrhagic fever with renal syndrome, or leptospiro sis. There is no evidence for the transmission of viral hemor rhagic fever through air travel. Prevention Disinfection, hygiene, and sanitation are the cornerstones to infection prevention and control measures. For example, the screening procotol from the Ministry of Health and Sanitation in Sierra Leone includes: - Any person suffering from a fever (or history of fever) and having had contact with suspected, prob able, or confirmed Ebola case; or - Any person with a fever (or history of fever) and at least three of the following symptoms: headaches, vomiting, anorexia/loss of appetite, diarrhea, lethargy, stomach pain, aching muscles or joints, difficulty swallowing, breathing difficulties, or hiccups; or - Any person with inexplicable bleeding. Nomenclature- and database-compatible names for the two Ebola virus variants that emerged in Guinea and the Democratic Republic of the Congo in 2014. Clinical features and viral kinetics in a rapidly cured patient with Ebola virus disease: a case report. Symptoms and Signs the incubation period can be as short as 2 days for the Rift Valley fever or as long as 2 1 days for Lassa fever. The clini cal symptoms in the early phase of a viral hemorrhagic fever are very similar, irrespective of the causative virus, and resemble a flu-like illness or gastroenteritis. Certain arenaviruses (the Lassa pathogen, Junin virus in its viscerotropic phase, Machupo virus) and bunyavi ruses (the Congo-Crimean hemorrhagic fever and Rift Valley fever pathogens) respond to oral ribavirin if it is started promptly.

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