{"title":"Diseases of the Pancreas","authors":"S. Sheth, G. Ketwaroo, Steven Freedman","doi":"10.2310/fm.1115","DOIUrl":"https://doi.org/10.2310/fm.1115","url":null,"abstract":"<jats:p />","PeriodicalId":10989,"journal":{"name":"DeckerMed Family Medicine","volume":"28 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87005786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In peritoneal dialysis (PD), the peritoneum serves as a biological dialyzing membrane. The endothelium of the vast capillary network perfusing the peritoneum functions as a semipermeable membrane and allows bidirectional solute and water transfer between the intravascular space and dialysate fluid dwelling in the peritoneal cavity. PD is a renal replacement strategy for patients presenting with end-stage renal disease. It can also be offered for ultrafiltration in patients with diuretic-resistant fluid overload even in those without advanced renal failure. PD can also be used for patients with acute kidney injury, although in the developed world this occurs rarely compared to the use of extracorporeal therapies. This review contains 9 videos, 8 figures, 4 tables, and 73 references. Keywords: peritoneal dialysis, peritoneal cavity, catheter, dialysis fluid, ultrafiltration, tunnel infection, osmotic pressure, renal failure
{"title":"Peritoneal Dialysis","authors":"K. François, J. Bargman","doi":"10.2310/fm.12057","DOIUrl":"https://doi.org/10.2310/fm.12057","url":null,"abstract":"In peritoneal dialysis (PD), the peritoneum serves as a biological dialyzing membrane. The endothelium of the vast capillary network perfusing the peritoneum functions as a semipermeable membrane and allows bidirectional solute and water transfer between the intravascular space and dialysate fluid dwelling in the peritoneal cavity. PD is a renal replacement strategy for patients presenting with end-stage renal disease. It can also be offered for ultrafiltration in patients with diuretic-resistant fluid overload even in those without advanced renal failure. PD can also be used for patients with acute kidney injury, although in the developed world this occurs rarely compared to the use of extracorporeal therapies.\u0000This review contains 9 videos, 8 figures, 4 tables, and 73 references. \u0000Keywords: peritoneal dialysis, peritoneal cavity, catheter, dialysis fluid, ultrafiltration, tunnel infection, osmotic pressure, renal failure","PeriodicalId":10989,"journal":{"name":"DeckerMed Family Medicine","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89809790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cushing syndrome is a condition with protean manifestations that are caused by chronic exposure to excess glucocorticoids. Treatment with supraphysiologic doses of glucocorticoids is the most common cause. Pathologic hypercortisolism may result from autonomous adrenal production or as a result of the action of excessive adrenocorticotropic hormone (ACTH) production by a tumor, which stimulates adrenal cortisol production. Primary adrenal forms include unilateral adenoma or carcinoma or, rarely, bilateral hyperplasia and/or nodules. This chapter covers the epidemiology, etiology, pathophysiology, and diagnosis of Cushing syndrome. Clinical manifestations, physical examination findings, and laboratory tests, including tests of the blood and other body fluids, imaging studies, and biopsy, are discussed. The differential diagnosis, treatment options, complications, and prognosis are described. Tables outline clinical features and causes of Cushing syndrome, abnormalities associated with primary adrenal causes of Cushing syndrome, diagnostic accuracy of screening tests, endogenous hypercortisolism without Cushing syndrome, and medical therapy for Cushing syndrome. Figures illustrate the causes of Cushing syndrome and a comparison of the hypothalamic-pituitary-adrenal axis in patients with ACTH-dependent Cushing syndrome and those with pseudo–Cushing syndrome. Algorithms show the evaluation of possible Cushing syndrome and evaluation of the causes of Cushing syndrome. Second-line treatments for Cushing syndrome when surgery fails or is not possible are also detailed. This chapter contains 5 figures, 7 tables, 50 references.
{"title":"Cushing Syndrome","authors":"L. Nieman","doi":"10.2310/fm.1394","DOIUrl":"https://doi.org/10.2310/fm.1394","url":null,"abstract":"Cushing syndrome is a condition with protean manifestations that are caused by chronic exposure to excess glucocorticoids. Treatment with supraphysiologic doses of glucocorticoids is the most common cause. Pathologic hypercortisolism may result from autonomous adrenal production or as a result of the action of excessive adrenocorticotropic hormone (ACTH) production by a tumor, which stimulates adrenal cortisol production. Primary adrenal forms include unilateral adenoma or carcinoma or, rarely, bilateral hyperplasia and/or nodules. This chapter covers the epidemiology, etiology, pathophysiology, and diagnosis of Cushing syndrome. Clinical manifestations, physical examination findings, and laboratory tests, including tests of the blood and other body fluids, imaging studies, and biopsy, are discussed. The differential diagnosis, treatment options, complications, and prognosis are described. Tables outline clinical features and causes of Cushing syndrome, abnormalities associated with primary adrenal causes of Cushing syndrome, diagnostic accuracy of screening tests, endogenous hypercortisolism without Cushing syndrome, and medical therapy for Cushing syndrome. Figures illustrate the causes of Cushing syndrome and a comparison of the hypothalamic-pituitary-adrenal axis in patients with ACTH-dependent Cushing syndrome and those with pseudo–Cushing syndrome. Algorithms show the evaluation of possible Cushing syndrome and evaluation of the causes of Cushing syndrome. Second-line treatments for Cushing syndrome when surgery fails or is not possible are also detailed.\u0000This chapter contains 5 figures, 7 tables, 50 references.","PeriodicalId":10989,"journal":{"name":"DeckerMed Family Medicine","volume":"18 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78602085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune illness characterized by autoantibodies directed at nuclear antigens that cause clinical and laboratory abnormalities, such as rash, arthritis, leukopenia and thrombocytopenia, alopecia, fever, nephritis, and neurologic disease. Most or all of the symptoms of acute lupus are attributable to immunologic attack on the affected organs. Many complications of long-term disease are attributable to both the disease and its treatment. Intense sun exposure, drug reactions, and infections are circumstances that induce flare; the aim of treatment is to induce remission. This chapter is divided into sections dealing with SLE’s definitions; epidemiology; pathogenesis; disease classification, diagnosis, and differential diagnosis; and treatment. This review contains 10 figures, 12 tables, and 97 references. Key Words: Systemic lupus erythematosus, Dermatomyositis, Sjögren syndrome, rheumatoid arthritis, systemic sclerosis, Discoid lupus erythematosus, truncal psoriasiform, annular polycyclic rash
{"title":"Systemic Lupus Erythematosus","authors":"K. Kirou, M. Lockshin","doi":"10.2310/fm.1049","DOIUrl":"https://doi.org/10.2310/fm.1049","url":null,"abstract":"Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune illness characterized by autoantibodies directed at nuclear antigens that cause clinical and laboratory abnormalities, such as rash, arthritis, leukopenia and thrombocytopenia, alopecia, fever, nephritis, and neurologic disease. Most or all of the symptoms of acute lupus are attributable to immunologic attack on the affected organs. Many complications of long-term disease are attributable to both the disease and its treatment. Intense sun exposure, drug reactions, and infections are circumstances that induce flare; the aim of treatment is to induce remission. This chapter is divided into sections dealing with SLE’s definitions; epidemiology; pathogenesis; disease classification, diagnosis, and differential diagnosis; and treatment.\u0000\u0000This review contains 10 figures, 12 tables, and 97 references.\u0000Key Words: Systemic lupus erythematosus, Dermatomyositis, Sjögren syndrome, rheumatoid arthritis, systemic sclerosis, Discoid lupus erythematosus, truncal psoriasiform, annular polycyclic rash","PeriodicalId":10989,"journal":{"name":"DeckerMed Family Medicine","volume":"59 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77898643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The normal and abnormal development of the organs lying within the fetal thorax is discussed. The abnormalities reviewed include more common findings of pulmonary hypoplasia, congenital diaphragmatic hernia, congenital pulmonary airway malformation, bronchopulmonary sequestration, as well as the rarer conditions of congenital fetal hydrothorax, congenital high airway obstruction syndrome, bronchogenic cysts, neurenteric cysts, and lung agenesis. With each abnormality, the clinical implications for the fetus, best methods for prenatal diagnosis, as well as possible additional anomalies, syndromes, and aneuploidies are described. In utero and postnatal treatments are also reviewed. This review contains 10 figures, and 37 references. Key Words: Pulmonary hypoplasia, lung-head ratio, congenital diaphragmatic hernia, congenital pulmonary airway malformation, congenital fetal hydrothorax, bronchopulmonary sequestration, congenital high airway obstruction syndrome, bronchogenic cyst, neurenteric cyst, lung agenesis
{"title":"Abnormalities of the Fetal Chest","authors":"K. Davidson","doi":"10.2310/fm.19087","DOIUrl":"https://doi.org/10.2310/fm.19087","url":null,"abstract":"The normal and abnormal development of the organs lying within the fetal thorax is discussed. The abnormalities reviewed include more common findings of pulmonary hypoplasia, congenital diaphragmatic hernia, congenital pulmonary airway malformation, bronchopulmonary sequestration, as well as the rarer conditions of congenital fetal hydrothorax, congenital high airway obstruction syndrome, bronchogenic cysts, neurenteric cysts, and lung agenesis. With each abnormality, the clinical implications for the fetus, best methods for prenatal diagnosis, as well as possible additional anomalies, syndromes, and aneuploidies are described. In utero and postnatal treatments are also reviewed. This review contains 10 figures, and 37 references. Key Words: Pulmonary hypoplasia, lung-head ratio, congenital diaphragmatic hernia, congenital pulmonary airway malformation, congenital fetal hydrothorax, bronchopulmonary sequestration, congenital high airway obstruction syndrome, bronchogenic cyst, neurenteric cyst, lung agenesis","PeriodicalId":10989,"journal":{"name":"DeckerMed Family Medicine","volume":"55 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72655704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pulmonary edema is characterized by the movement of excess fluid into the alveoli of the lungs. Although the alterations of cardiovascular and pulmonary physiology in pregnancy may predispose patients to pulmonary edema, it is never normal and constitutes severe maternal morbidity. The etiologies of pulmonary edema are diverse, ranging from disease processes independent of pregnancy to pathophysiology unique to the gravid state. The causes of pulmonary edema can be broadly classified as either cardiogenic or noncardiogenic, which constitutes the first important branch point in the diagnosis and management of the disease. The treatment of pulmonary edema in pregnancy parallels that in the nonpregnant population with an emphasis on maintaining the physiologic alterations of pregnancy through supportive care, including mechanical ventilation if needed. In all cases of pulmonary edema, the decision to proceed with delivery to improve the maternal status should be considered within the context of the etiology and anticipated disease course, the gestational age, and the goals of care. This review contains 3 figures, 4 tables, and 60 references. Key Words: Pulmonary edema, respiratory alkalosis, acute respiratory distress syndrome (ARDS), cardiogenic pulmonary edema, transfusion-related acute lung injury (TRALI), transfusion-associated circulatory overload (TACO), mechanical ventilation, extra corporeal membrane oxygenation (ECMO).
{"title":"Pulmonary Edema in Pregnancy","authors":"S. Easter, N. Smith","doi":"10.2310/fm.19037","DOIUrl":"https://doi.org/10.2310/fm.19037","url":null,"abstract":"Pulmonary edema is characterized by the movement of excess fluid into the alveoli of the lungs. Although the alterations of cardiovascular and pulmonary physiology in pregnancy may predispose patients to pulmonary edema, it is never normal and constitutes severe maternal morbidity. The etiologies of pulmonary edema are diverse, ranging from disease processes independent of pregnancy to pathophysiology unique to the gravid state. The causes of pulmonary edema can be broadly classified as either cardiogenic or noncardiogenic, which constitutes the first important branch point in the diagnosis and management of the disease. The treatment of pulmonary edema in pregnancy parallels that in the nonpregnant population with an emphasis on maintaining the physiologic alterations of pregnancy through supportive care, including mechanical ventilation if needed. In all cases of pulmonary edema, the decision to proceed with delivery to improve the maternal status should be considered within the context of the etiology and anticipated disease course, the gestational age, and the goals of care.\u0000This review contains 3 figures, 4 tables, and 60 references.\u0000Key Words: Pulmonary edema, respiratory alkalosis, acute respiratory distress syndrome (ARDS), cardiogenic pulmonary edema, transfusion-related acute lung injury (TRALI), transfusion-associated circulatory overload (TACO), mechanical ventilation, extra corporeal membrane oxygenation (ECMO).","PeriodicalId":10989,"journal":{"name":"DeckerMed Family Medicine","volume":"39 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79261097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Approach to the Patient with a Pelvic Mass","authors":"C. Runowicz, Mary I. Fatehi, J. T. Chambers","doi":"10.2310/fm.1253","DOIUrl":"https://doi.org/10.2310/fm.1253","url":null,"abstract":"<jats:p />","PeriodicalId":10989,"journal":{"name":"DeckerMed Family Medicine","volume":"50 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84471520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pulmonary embolism (PE) is a frequently encountered clinical condition with both short- and long-term adverse consequences. An integrated approach to diagnosis is important to maximize early diagnosis but also to minimize the unnecessary utilization of diagnostic imaging. Comprehensive risk stratification with clinical features and assessment of right ventricular strain by diagnostic imaging and cardiac biomarker results are essential to guide initial management decisions. There is a growing treatment arsenal for acute PE, including increased anticoagulation and advanced therapeutic options such as catheter-based therapy. Despite such advances, mortality remains high, particularly among those who present critically ill with PE, and long-term physical and psychological effects can persist in many patients for years after the initial diagnosis. This review contains 7 figures, 6 tables, and 69 references. Key Words: anticoagulation, catheter-directed therapy, chronic thromboembolic pulmonary hypertension pulmonary embolism, computed tomography, echocardiography, fibrinolysis, risk stratification, venous thromboembolism
{"title":"Acute Pulmonary Embolism","authors":"B. Carroll, Eric A. Secemsky","doi":"10.2310/fm.1632","DOIUrl":"https://doi.org/10.2310/fm.1632","url":null,"abstract":"Pulmonary embolism (PE) is a frequently encountered clinical condition with both short- and long-term adverse consequences. An integrated approach to diagnosis is important to maximize early diagnosis but also to minimize the unnecessary utilization of diagnostic imaging. Comprehensive risk stratification with clinical features and assessment of right ventricular strain by diagnostic imaging and cardiac biomarker results are essential to guide initial management decisions. There is a growing treatment arsenal for acute PE, including increased anticoagulation and advanced therapeutic options such as catheter-based therapy. Despite such advances, mortality remains high, particularly among those who present critically ill with PE, and long-term physical and psychological effects can persist in many patients for years after the initial diagnosis.\u0000This review contains 7 figures, 6 tables, and 69 references.\u0000Key Words: anticoagulation, catheter-directed therapy, chronic thromboembolic pulmonary hypertension pulmonary embolism, computed tomography, echocardiography, fibrinolysis, risk stratification, venous thromboembolism","PeriodicalId":10989,"journal":{"name":"DeckerMed Family Medicine","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90753049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Acute renal failure (ARF) has been defined as a syndrome in which an abrupt decrease in renal function produces retention of nitrogenous waste products. Translating this abstract description into a clinically useful, accurate, and widely accepted definition has been challenging, in large part because of the focus on serum creatinine concentration, which is easily obtained but has the inherent limitation of poor detection of rapid or subtle, but clinically important, changes in the glomerular filtration rate (GFR). In recent years, therefore, the term acute kidney injury (AKI) has replaced ARF because AKI denotes the entire clinical spectrum from mild increases in serum creatinine to overt renal failure. AKI is defined by the Risk-Injury-Failure-Loss-ESRD (RIFLE) criteria, based on serum creatinine concentration and urine flow rate. The Acute Kidney Injury Network (AKIN) subsequently modified the definition further and divided AKI into three stages. This chapter includes discussions of the etiology and diagnosis of AKI in hospitalized patients and community-acquired AKI. The specific causes, management, and complications of AKI are also discussed. Figures illustrate the pathophysiologic classification of AKI and the effect of hyperkalemia on cardiac conduction—electrocardiogram (ECG) changes. A worksheet for following patients with AKI is provided. This review contains 3 figures, 20 tables, and 46 references. Keywords:Acute kidney injury, dialysis, contrast, rhabdomyolysis, nephropathy, urinalysis, multiple myeloma, ethylene glycol, sepsis, hepatorenal syndrome
{"title":"Acute Kidney Injury - Part I","authors":"P. Sanders, A. Agarwal","doi":"10.2310/fm.1164","DOIUrl":"https://doi.org/10.2310/fm.1164","url":null,"abstract":"Acute renal failure (ARF) has been defined as a syndrome in which an abrupt decrease in renal function produces retention of nitrogenous waste products. Translating this abstract description into a clinically useful, accurate, and widely accepted definition has been challenging, in large part because of the focus on serum creatinine concentration, which is easily obtained but has the inherent limitation of poor detection of rapid or subtle, but clinically important, changes in the glomerular filtration rate (GFR). In recent years, therefore, the term acute kidney injury (AKI) has replaced ARF because AKI denotes the entire clinical spectrum from mild increases in serum creatinine to overt renal failure. AKI is defined by the Risk-Injury-Failure-Loss-ESRD (RIFLE) criteria, based on serum creatinine concentration and urine flow rate. The Acute Kidney Injury Network (AKIN) subsequently modified the definition further and divided AKI into three stages. This chapter includes discussions of the etiology and diagnosis of AKI in hospitalized patients and community-acquired AKI. The specific causes, management, and complications of AKI are also discussed. Figures illustrate the pathophysiologic classification of AKI and the effect of hyperkalemia on cardiac conduction—electrocardiogram (ECG) changes. A worksheet for following patients with AKI is provided. \u0000This review contains 3 figures, 20 tables, and 46 references.\u0000Keywords:Acute kidney injury, dialysis, contrast, rhabdomyolysis, nephropathy, urinalysis, multiple myeloma, ethylene glycol, sepsis, hepatorenal syndrome","PeriodicalId":10989,"journal":{"name":"DeckerMed Family Medicine","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77612411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Syncope is a common presenting complaint in the emergency department, accounting for approximately 1 to 3% of presentations and up to 6% of admissions. Syncope is properly defined as a brief loss of consciousness and postural tone followed by spontaneous and complete recovery. Often syncope must be distinguished from other etiologies of transient loss of consciousness, such as seizures and hypoglycemia. Comprehension of the pathogenesis, clinical presentation, and prognosis of the varied causes of syncope is essential if emergency physicians are to succeed in identifying patients at risk for adverse events while also reducing unnecessary syncope admissions. This review covers the pathophysiology, stabilization and assessment, diagnosis and treatment, and disposition and outcomes of syncope. Figures show heart block, prolonged QTc and torsades de pointes, Wolff-Parkinson-White syndrome, hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia, and Brugada syndrome. This review contains 6 figures, 15 tables, and 58 references. Keywords: Syncope, near-syncope, pre-syncope, arrhythmia, dysrhythmia, sudden cardiac death, vasovagal, passing out, neurocardiogenic
{"title":"Syncope","authors":"A. Baker","doi":"10.2310/fm.4075","DOIUrl":"https://doi.org/10.2310/fm.4075","url":null,"abstract":"Syncope is a common presenting complaint in the emergency department, accounting for approximately 1 to 3% of presentations and up to 6% of admissions. Syncope is properly defined as a brief loss of consciousness and postural tone followed by spontaneous and complete recovery. Often syncope must be distinguished from other etiologies of transient loss of consciousness, such as seizures and hypoglycemia. Comprehension of the pathogenesis, clinical presentation, and prognosis of the varied causes of syncope is essential if emergency physicians are to succeed in identifying patients at risk for adverse events while also reducing unnecessary syncope admissions. This review covers the pathophysiology, stabilization and assessment, diagnosis and treatment, and disposition and outcomes of syncope. Figures show heart block, prolonged QTc and torsades de pointes, Wolff-Parkinson-White syndrome, hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia, and Brugada syndrome. \u0000This review contains 6 figures, 15 tables, and 58 references.\u0000Keywords: Syncope, near-syncope, pre-syncope, arrhythmia, dysrhythmia, sudden cardiac death, vasovagal, passing out, neurocardiogenic\u0000\u0000 ","PeriodicalId":10989,"journal":{"name":"DeckerMed Family Medicine","volume":"140 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86740027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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