Pneumococci, or Streptococcus pneumoniae, are gram-positive, lancet-shaped diplococci but may also grow in short chains. The polysaccharide polymer that forms the outer capsule of S pneumoniae is chemically and antigenically unique and is crucial to virulence. There are at least 90 distinct serotypes. The capsule allows the bacteria to resist phagocytosis by leukocytes unless the organisms have been opsonized by antibody or serum complement components. Certain pneumococcal serotypes, such as the heavily encapsulated type 3 pneumococcus, are particularly virulent. In fact, only 23 serotypes account for 80% of bacteremic pneumococcal infections in the United States; capsular polysaccharides from these 23 serotypes are incorporated into the polyvalent polysaccharide pneumococcal vaccine (PPSV23), which has been available since 1983. This review covers the epidemiology and pathogenesis of pneumococcal infections, clinical pneumococcal infections, and prevention of pneumococcal infections. Adverse outcomes in pneumococcal pneumonia, antibiotic treatment for penicillin-resistant S pneumoniae, and Centers for Disease Control and Prevention child and adolescent immunization schedules are discussed. This review contains 1 figure, 6 tables, and 41 references. Key words: bacterial pneumonia, PCV13, penicillin-resistant Streptococcus pneumoniae, pneumococcal pneumonia, pneumococcus, PPSV23, pneumonia vaccine, Streptococcus pneumoniae
{"title":"Infections Due to Streptococcus pneumoniae","authors":"D. Stevens, Sarah E. Hobdey","doi":"10.2310/im.1391","DOIUrl":"https://doi.org/10.2310/im.1391","url":null,"abstract":"Pneumococci, or Streptococcus pneumoniae, are gram-positive, lancet-shaped diplococci but may also grow in short chains. The polysaccharide polymer that forms the outer capsule of S pneumoniae is chemically and antigenically unique and is crucial to virulence. There are at least 90 distinct serotypes. The capsule allows the bacteria to resist phagocytosis by leukocytes unless the organisms have been opsonized by antibody or serum complement components. Certain pneumococcal serotypes, such as the heavily encapsulated type 3 pneumococcus, are particularly virulent. In fact, only 23 serotypes account for 80% of bacteremic pneumococcal infections in the United States; capsular polysaccharides from these 23 serotypes are incorporated into the polyvalent polysaccharide pneumococcal vaccine (PPSV23), which has been available since 1983. This review covers the epidemiology and pathogenesis of pneumococcal infections, clinical pneumococcal infections, and prevention of pneumococcal infections. Adverse outcomes in pneumococcal pneumonia, antibiotic treatment for penicillin-resistant S pneumoniae, and Centers for Disease Control and Prevention child and adolescent immunization schedules are discussed.\u0000This review contains 1 figure, 6 tables, and 41 references. \u0000Key words: bacterial pneumonia, PCV13, penicillin-resistant Streptococcus pneumoniae, pneumococcal pneumonia, pneumococcus, PPSV23, pneumonia vaccine, Streptococcus pneumoniae","PeriodicalId":11220,"journal":{"name":"DeckerMed Medicine","volume":"18 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81331180","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}
Thyroid disorders are the most common endocrine conditions encountered in clinical practice and can range from clinically obvious to clinically silent. This review provides the definition and epidemiology of the conditions of hypothyroidism and hyperthyroidism. Hypothyroidism can be congenital or acquired, and its pathogenesis, diagnosis, and management are presented. The three most common disorders of thyrotoxicosis (diffuse toxic goiter [Graves disease], toxic nodular goiter, and iatrogenic thyrotoxicosis in thyroid hormone–treated patients are addressed, as well as the many diseases in each of these categories. This review also discusses thyroiditis, goiter, thyroid nodules, and thyroid cancer. Tables list the causes of elevated serum thyroid-stimulating hormone (TSH) levels, the etiologic classification of thyrotoxicosis, characteristic features of thyroiditis, and causes of elevated serum total thyroxine levels. Figures show the prevalence of abnormalities in thyroid function tests in different populations, certain forms of hyperthyroidism that result from pathophysiologic activation of the TSH receptor, and inflammation of thyroid tissue in acute thyroiditis. This review contains 3 figures, 12 tables, and 61 references. Key Words: Hypothyroidism, Thyrotoxicosis, Thyrotropin, celiac disease, vitiligo, pernicious anemia, Sjögren syndrome, Graves disease, Munchausen syndrome
{"title":"Hypothyroidism and Thyrotoxicosis","authors":"P. Ladenson","doi":"10.2310/im.1229","DOIUrl":"https://doi.org/10.2310/im.1229","url":null,"abstract":"Thyroid disorders are the most common endocrine conditions encountered in clinical practice and can range from clinically obvious to clinically silent. This review provides the definition and epidemiology of the conditions of hypothyroidism and hyperthyroidism. Hypothyroidism can be congenital or acquired, and its pathogenesis, diagnosis, and management are presented. The three most common disorders of thyrotoxicosis (diffuse toxic goiter [Graves disease], toxic nodular goiter, and iatrogenic thyrotoxicosis in thyroid hormone–treated patients are addressed, as well as the many diseases in each of these categories. This review also discusses thyroiditis, goiter, thyroid nodules, and thyroid cancer. Tables list the causes of elevated serum thyroid-stimulating hormone (TSH) levels, the etiologic classification of thyrotoxicosis, characteristic features of thyroiditis, and causes of elevated serum total thyroxine levels. Figures show the prevalence of abnormalities in thyroid function tests in different populations, certain forms of hyperthyroidism that result from pathophysiologic activation of the TSH receptor, and inflammation of thyroid tissue in acute thyroiditis.\u0000 \u0000This review contains 3 figures, 12 tables, and 61 references.\u0000Key Words: Hypothyroidism, Thyrotoxicosis, Thyrotropin, celiac disease, vitiligo, pernicious anemia, Sjögren syndrome, Graves disease, Munchausen syndrome","PeriodicalId":11220,"journal":{"name":"DeckerMed Medicine","volume":"58 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74296054","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}
Thrombosis is common in clinical practice. Venous thromboembolism in particular raises questions of a possible underlying hereditary or acquired thrombophilic state. Despite considerable data describing the impact of various thrombophilic states on risks of initial and recurrent thromboembolic events, thrombophilia testing is not standardized. An understanding of the utility and pitfalls of clinical thrombophilia testing is necessary to employ this testing properly. When utilized appropriately, thrombophilia testing can be vital in informing an individual patient’s thrombosis risk and pursuing optimal anticoagulant management. Hereditary thrombophilia testing involves investigation for factor V Leiden, the prothrombin G202010A gene mutation, and deficiencies of the natural anticoagulants protein C, protein S, and antithrombin. Assessment for acquired thrombophilias is perhaps even more important, recognizing the possibility for myeloproliferative neoplasms, antiphospholipid antibody syndrome, occult malignancy and other important acquired thrombotic predispositions. Timing of thrombophilia testing in relation to anticoagulation, acute thrombosis, and use of hormonal agents or pregnancy is critical to ensure accurate diagnosis. This review describes each of the most important hereditary and acquired thrombophilias, explains their relationship to venous and arterial thrombosis, delineates evidence-based indications for thrombophilia testing, identifies potential testing pitfalls, and synthesizes the key points in outlining algorithms for thrombophilia testing in clinical practice. This review contains 4 figures, 4 tables, and 48 references. Key words: thrombophilia, venous thromboembolism, pulmonary embolus, deep vein thrombosis, factor V Leiden, prothrombin gene mutation, protein C deficiency, protein S deficiency, antiphospholipid antibody syndrome, hypercoagulability of malignancy
{"title":"Heritable and Acquired Thrombophilias in Clinical Practice","authors":"H. Al‐Samkari, Nathan T Connell","doi":"10.2310/im.1649","DOIUrl":"https://doi.org/10.2310/im.1649","url":null,"abstract":"Thrombosis is common in clinical practice. Venous thromboembolism in particular raises questions of a possible underlying hereditary or acquired thrombophilic state. Despite considerable data describing the impact of various thrombophilic states on risks of initial and recurrent thromboembolic events, thrombophilia testing is not standardized. An understanding of the utility and pitfalls of clinical thrombophilia testing is necessary to employ this testing properly. When utilized appropriately, thrombophilia testing can be vital in informing an individual patient’s thrombosis risk and pursuing optimal anticoagulant management. Hereditary thrombophilia testing involves investigation for factor V Leiden, the prothrombin G202010A gene mutation, and deficiencies of the natural anticoagulants protein C, protein S, and antithrombin. Assessment for acquired thrombophilias is perhaps even more important, recognizing the possibility for myeloproliferative neoplasms, antiphospholipid antibody syndrome, occult malignancy and other important acquired thrombotic predispositions. Timing of thrombophilia testing in relation to anticoagulation, acute thrombosis, and use of hormonal agents or pregnancy is critical to ensure accurate diagnosis. This review describes each of the most important hereditary and acquired thrombophilias, explains their relationship to venous and arterial thrombosis, delineates evidence-based indications for thrombophilia testing, identifies potential testing pitfalls, and synthesizes the key points in outlining algorithms for thrombophilia testing in clinical practice.\u0000This review contains 4 figures, 4 tables, and 48 references.\u0000Key words: thrombophilia, venous thromboembolism, pulmonary embolus, deep vein thrombosis, factor V Leiden, prothrombin gene mutation, protein C deficiency, protein S deficiency, antiphospholipid antibody syndrome, hypercoagulability of malignancy","PeriodicalId":11220,"journal":{"name":"DeckerMed Medicine","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80130797","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/im.12057","DOIUrl":"https://doi.org/10.2310/im.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":11220,"journal":{"name":"DeckerMed Medicine","volume":"105 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76347394","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 arterial hypertension (PAH) is a rare spectrum of closely related diseases with myriad genetic, infectious, toxic, and immunologic triggers characterized by pathologic pulmonary vascular remodeling. While the natural history of PAH is marked by progressive dyspnea, hypoxia, right ventricular failure, and death, modern insights into disease pathogenesis, combined with breakthroughs in therapeutics, has greatly improved morbidity and time to disease worsening over the past two decades. Traditionally thought of as a disease of imbalance between vasodilators, such as nitric oxide and prostacyclin, and vasoconstrictors such as endothelin-1, more recent investigations have revealed important roles for perturbations in cellular metabolism, fibroblast activity, extracellular matrix maintenance, and apoptosis which contribute to pulmonary artery smooth muscle cell proliferation. Careful history and physical exam, along with echocardiography and right heart catheterization, remain essential for accurate workup and diagnosis. Cardiopulmonary exercise testing, cardiac magnetic resonance, and genetic testing have important ancillary roles. The number of approved pulmonary vasodilator therapies for PAH continues to expand, with evidence demonstrating the survival benefits of up-front combination therapy. Future prospects of next generation therapies that address the molecular origins of disease combined with comprehensive molecular profiling may usher in a new era of precision medicine for PAH. This review contains 7 figures, 5 tables, and 57 references. Keywords: pulmonary hypertension, vascular biology, therapeutics, hemodynamics, epidemiology, exercise physiology, genetic basis of disease, connective tissue disease, cardiac magnetic resonance imagining
{"title":"Pulmonary Arterial Hypertension: Advancing Insights into a Historically Neglected Disease","authors":"M. Genuardi, S. Y. Chan","doi":"10.2310/im.1647","DOIUrl":"https://doi.org/10.2310/im.1647","url":null,"abstract":"Pulmonary arterial hypertension (PAH) is a rare spectrum of closely related diseases with myriad genetic, infectious, toxic, and immunologic triggers characterized by pathologic pulmonary vascular remodeling. While the natural history of PAH is marked by progressive dyspnea, hypoxia, right ventricular failure, and death, modern insights into disease pathogenesis, combined with breakthroughs in therapeutics, has greatly improved morbidity and time to disease worsening over the past two decades. Traditionally thought of as a disease of imbalance between vasodilators, such as nitric oxide and prostacyclin, and vasoconstrictors such as endothelin-1, more recent investigations have revealed important roles for perturbations in cellular metabolism, fibroblast activity, extracellular matrix maintenance, and apoptosis which contribute to pulmonary artery smooth muscle cell proliferation. Careful history and physical exam, along with echocardiography and right heart catheterization, remain essential for accurate workup and diagnosis. Cardiopulmonary exercise testing, cardiac magnetic resonance, and genetic testing have important ancillary roles. The number of approved pulmonary vasodilator therapies for PAH continues to expand, with evidence demonstrating the survival benefits of up-front combination therapy. Future prospects of next generation therapies that address the molecular origins of disease combined with comprehensive molecular profiling may usher in a new era of precision medicine for PAH.\u0000This review contains 7 figures, 5 tables, and 57 references.\u0000Keywords: pulmonary hypertension, vascular biology, therapeutics, hemodynamics, epidemiology, exercise physiology, genetic basis of disease, connective tissue disease, cardiac magnetic resonance imagining","PeriodicalId":11220,"journal":{"name":"DeckerMed Medicine","volume":"119 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86186609","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}
Hypernatremia is an electrolyte disorder most prevalent in the elderly and the critically ill, with over 60% of cases developing over the course of an inpatient stay. Characterized by elevated serum sodium concentrations, this disorder is manifested either by pure-water loss without replacement, or excessive sodium intake without appropriate water balance. Left untreated it may lead to seizures and coma. General treatment in the case of severe hypernatremia is infusion of isotonic saline followed by pure-water after the patient is stabilized. Further treatment of the underlying cause may involve diuretics, thiazides, and a variety of other medications in conjunction with dietary and lifestyle modifications. This review offers an overview of various disorders of water balance: diabetes insipidus, nephrotic syndrome, cirrhosis, idiopathic edema, and volume depletion, as well as their clinical presentations, lab tests, and management. This review contains 1 figure, 1 table, and 25 references. Key words: Hypernatremia, Edematous States , Diabetes insipidus, Volume Depletion, Cirrhosis, Diuretics
{"title":"Disorders of Water and Sodium Balance: Hypernatremia","authors":"D. M. Carmona Matos, Herbert Chen","doi":"10.2310/surg.2410","DOIUrl":"https://doi.org/10.2310/surg.2410","url":null,"abstract":"Hypernatremia is an electrolyte disorder most prevalent in the elderly and the critically ill, with over 60% of cases developing over the course of an inpatient stay. Characterized by elevated serum sodium concentrations, this disorder is manifested either by pure-water loss without replacement, or excessive sodium intake without appropriate water balance. Left untreated it may lead to seizures and coma. General treatment in the case of severe hypernatremia is infusion of isotonic saline followed by pure-water after the patient is stabilized. Further treatment of the underlying cause may involve diuretics, thiazides, and a variety of other medications in conjunction with dietary and lifestyle modifications. This review offers an overview of various disorders of water balance: diabetes insipidus, nephrotic syndrome, cirrhosis, idiopathic edema, and volume depletion, as well as their clinical presentations, lab tests, and management.\u0000This review contains 1 figure, 1 table, and 25 references.\u0000Key words: Hypernatremia, Edematous States , Diabetes insipidus, Volume Depletion, Cirrhosis, Diuretics","PeriodicalId":11220,"journal":{"name":"DeckerMed Medicine","volume":"75 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76491157","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}
Normal neurologic function requires a constantly balanced environment of electrolytes. Normal hepatic and renal function is critical in maintaining this balance while removing toxins, maintaining a physiologic pH and regulating the excretion of electrolytes. Nutritional intake provides essential nutrients but deficiencies can lead to characteristic syndromes such as Wernicke's encephalopathy and pellagra and exposure to neurotoxic substances such as heavy metals can lead to encephalopathy. Thyroid and adrenal dysfunction are common endocrine causes of encephalopathy and symptoms can often improve rapidly with treatment. A subset of idiopathic encephalopathy is increasingly being recognized as having an autoimmune basis, often presenting as a paraneoplastic process, and having a constellation of symptoms which can aide in the diagnosis. Timely recognition and treatment of the autoantibodies which target neural structures, with immunosuppressive therapy, can improve outcome in these patients. This review contains 4 figures, 3 tables, and 42 references. Key words: osmotic demyelination syndrome,hepatic encephalopathy, renal failure, triphasic waves, dialysis disequilibrium syndrome, Wernicke encephalopathy, Korsakoff syndrome, myxedema coma, Hashimoto encephalopathy
{"title":"Metabolic Encephalopathy - Part II","authors":"R. Gill, Matthew A. McCoyd, S. Ruland, J. Biller","doi":"10.2310/im.1393","DOIUrl":"https://doi.org/10.2310/im.1393","url":null,"abstract":"Normal neurologic function requires a constantly balanced environment of electrolytes. Normal hepatic and renal function is critical in maintaining this balance while removing toxins, maintaining a physiologic pH and regulating the excretion of electrolytes. Nutritional intake provides essential nutrients but deficiencies can lead to characteristic syndromes such as Wernicke's encephalopathy and pellagra and exposure to neurotoxic substances such as heavy metals can lead to encephalopathy. Thyroid and adrenal dysfunction are common endocrine causes of encephalopathy and symptoms can often improve rapidly with treatment. A subset of idiopathic encephalopathy is increasingly being recognized as having an autoimmune basis, often presenting as a paraneoplastic process, and having a constellation of symptoms which can aide in the diagnosis. Timely recognition and treatment of the autoantibodies which target neural structures, with immunosuppressive therapy, can improve outcome in these patients. \u0000This review contains 4 figures, 3 tables, and 42 references.\u0000Key words: osmotic demyelination syndrome,hepatic encephalopathy, renal failure, triphasic waves, dialysis disequilibrium syndrome, Wernicke encephalopathy, Korsakoff syndrome, myxedema coma, Hashimoto encephalopathy","PeriodicalId":11220,"journal":{"name":"DeckerMed Medicine","volume":"10 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80026475","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}
Encephalopathy can range from the acute confusional state to frank coma, and is broadly defined as a constellation of symptoms and signs reflecting diffuse cerebral dysfunction. The potential causes of encephalopathy are vast requiring a thorough initial assessment and systematic diagnostic approach. Obtaining a comprehensive history may be challenging and ancillary sources of information are often helpful in narrowing the differential diagnosis. The general examination may provide hints as to the cause of encephalopathy and the neurologic examination can guide both acute management and focus the diagnostic investigations on specific etiologies which fit the clinical presentation. The systemic manifestations of infection and toxic exposures are common causes of encephalopathy. In sepsis, not only is brain perfusion compromised, multi system dysfunction is common and additional factors related to the specific infection such as hypoxia in pneumonia or secondary CNS involvement can complicate management. An understanding of the common physical examination findings of toxic exposures can aid in the diagnosis and rapid treatment of reversible toxic encephalopathies such as narcotics, benzodiazepines or environmental toxins. Cardiopulmonary dysfunction can lead to hypoxic-ischemic encephalopathy and advances in critical care, and particularly targeted temperature management following cardiac arrest, have improved the neurologic outcome in these patients. This review contains 2 figures, 3 tables, and 25 references. Key words: encephalopathy, delirium, ascending reticular activating system, acute confusional state, subclinical seizures, Glasgow Coma Scale, Full Outline of Unresponsiveness (FOUR) Score , hypoxic-ischemic encephalopathy, neuroleptic malignant syndrome, serum neuron-specific enolase
{"title":"Metabolic Encephalopathy - Part I","authors":"R. Gill, Matthew A. McCoyd, S. Ruland, J. Biller","doi":"10.2310/im.1392","DOIUrl":"https://doi.org/10.2310/im.1392","url":null,"abstract":"Encephalopathy can range from the acute confusional state to frank coma, and is broadly defined as a constellation of symptoms and signs reflecting diffuse cerebral dysfunction. The potential causes of encephalopathy are vast requiring a thorough initial assessment and systematic diagnostic approach. Obtaining a comprehensive history may be challenging and ancillary sources of information are often helpful in narrowing the differential diagnosis. The general examination may provide hints as to the cause of encephalopathy and the neurologic examination can guide both acute management and focus the diagnostic investigations on specific etiologies which fit the clinical presentation. The systemic manifestations of infection and toxic exposures are common causes of encephalopathy. In sepsis, not only is brain perfusion compromised, multi system dysfunction is common and additional factors related to the specific infection such as hypoxia in pneumonia or secondary CNS involvement can complicate management. An understanding of the common physical examination findings of toxic exposures can aid in the diagnosis and rapid treatment of reversible toxic encephalopathies such as narcotics, benzodiazepines or environmental toxins. Cardiopulmonary dysfunction can lead to hypoxic-ischemic encephalopathy and advances in critical care, and particularly targeted temperature management following cardiac arrest, have improved the neurologic outcome in these patients. \u0000This review contains 2 figures, 3 tables, and 25 references.\u0000Key words: encephalopathy, delirium, ascending reticular activating system, acute confusional state, subclinical seizures, Glasgow Coma Scale, Full Outline of Unresponsiveness (FOUR) Score , hypoxic-ischemic encephalopathy, neuroleptic malignant syndrome, serum neuron-specific enolase","PeriodicalId":11220,"journal":{"name":"DeckerMed Medicine","volume":"70 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74126221","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}
Ectopic pregnancy, the implantation of an embryo outside the endometrial cavity, is the leading cause of morbidity and mortality in the first trimester. The embryo may be implanted in the fallopian tubes, ovaries, abdomen, or cervix, with the fallopian tubes being the site of implantation in 95% of cases. If left untreated, ectopic pregnancy can result in rupture of the fallopian tube, which can lead to hemorrhagic shock and death. The signs and symptoms of ectopic pregnancy and diagnosis and treatment are detailed in the chapter. Spontaneous abortion, defined as a natural termination of a pregnancy before 20 weeks’ gestation, occurs in almost 30% of known pregnancies and an estimated 50% of all conceptions. Causes include genetic, environmental, endocrine, and immunologic factors; anatomic abnormalities; antiphospholipid syndrome; and polycystic ovary syndrome. This review contains 6 figures, 7 tables, and 42 references. Keywords: Ectopic pregnancy, miscarriage, spontaneous abortion, early pregnancy loss, vaginal spotting
{"title":"Ectopic Pregnancy and Spontaneous Abortion","authors":"E. Levens, A. DeCherney","doi":"10.2310/im.1219","DOIUrl":"https://doi.org/10.2310/im.1219","url":null,"abstract":"Ectopic pregnancy, the implantation of an embryo outside the endometrial cavity, is the leading cause of morbidity and mortality in the first trimester. The embryo may be implanted in the fallopian tubes, ovaries, abdomen, or cervix, with the fallopian tubes being the site of implantation in 95% of cases. If left untreated, ectopic pregnancy can result in rupture of the fallopian tube, which can lead to hemorrhagic shock and death. The signs and symptoms of ectopic pregnancy and diagnosis and treatment are detailed in the chapter. Spontaneous abortion, defined as a natural termination of a pregnancy before 20 weeks’ gestation, occurs in almost 30% of known pregnancies and an estimated 50% of all conceptions. Causes include genetic, environmental, endocrine, and immunologic factors; anatomic abnormalities; antiphospholipid syndrome; and polycystic ovary syndrome. \u0000This review contains 6 figures, 7 tables, and 42 references.\u0000Keywords: Ectopic pregnancy, miscarriage, spontaneous abortion, early pregnancy loss, vaginal spotting","PeriodicalId":11220,"journal":{"name":"DeckerMed Medicine","volume":"84 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83419612","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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