Managing Hyponatremia in Patients with Syndrome of Inappropriate Antidiuretic Hormone Secretion
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Edema II, Clinical Significance
EDEMA II CLINICAL SIGNIFICANCE F. A. LeFEVRE, M.D., R. H. McDONALD, M.D., AND A. C. CORCORAN, M.D. It is the purpose of this paper to outline the clinical syndromes in which edema significantly appears, to discuss their differentiation, and to comment on the changes to which edema itself may give rise. The frequency with which edema occurs indicates the variety of its origins. Its physiologic bases have been reviewed in a former paper.1 Conditions in which edema commonly appears are summarized in Table 1. Although clinical edema usually involves more than one physiologic mechanism, it is not difficult to determine the predominant disturbance. Table 2 illustrates the physiologic mechanisms of clinical edema. Physiologically, edema is an excessive accumulation of interstitial fluid. Clinically, it may be latent or manifest, and, by its nature, localized or generalizing. These terms, with the exception of generalizing, have been defined, and may be accepted. By generalizing edema is meant a condi- tion in which edema is at first local in its appearance, but in which, as the process extends, edema will become general, causing anasarca. The degree of edema in any area is limited by tissue tension and the sites of its first appearance and later spread are partly determined by gravity. CARDIAC EDEMA Generalizing edema is an early manifestation of cardiac failure. It is usually considered to be evidence of inadequacy of the right ventricu- lar musculature (back pressure theory). Peripheral edema may be accompanied by pulmonary edema in cases where there is simultaneous left ventricular failure. Actually, the genesis of cardiac edema may depend more on sodium retention2,3'4 due to "forward cardiac failure" and renal constriction than on venous back pressure alone. -
1 Fluid and Elect. Disorders of Serum Sodium Concentration
DISORDERS OF SERUM SODIUM CONCENTRATION Bruce M. Tune, M.D. Stanford, California Regulation of Sodium and Water Excretion Sodium: glomerular filtration, aldosterone, atrial natriuretic factors, in response to the following stimuli. 1. Reabsorption: hypovolemia, decreased cardiac output, decreased renal blood flow. 2. Excretion: hypervolemia (Also caused by adrenal insufficiency, renal tubular disease, and diuretic drugs.) Water: antidiuretic honnone (serum osmolality, effective vascular volume), renal solute excretion. 1. Antidiuresis: hyperosmolality, hypovolemia, decreased cardiac output. 2. Diuresis: hypoosmolality, hypervolemia ~ natriuresis. Physiologic changes in renal salt and water excretion are more likely to favor conservation of normal vascular volume than nonnal osmolality, and may therefore lead to abnormalities of serum sodium concentration. Most commonly, 1. Hypovolemia -7 salt and water retention. 2. Hypervolemia -7 salt and water excretion. • HYFERNATREMIA Clinical Senini:: Sodium excess: salt-poisoning, hypertonic saline enemas Primary water deficit: chronic dehydration (as in diabetes insipidus) Mechanism: Dehydration ~ renal sodium retention, even during hypernatremia Rapid correction of hypernatremia can cause brain swelling - Management: Slow correction -- without rapid administration of free water (except in nephrogenic or untreated central diabetes insipidus) HYPONA1REMIAS Isosmolar A. Factitious: hyperlipidemia (lriglyceride-plus-plasma water volume). B. Other solutes: hyperglycemia, radiocontrast agents,. mannitol. -
Evaluation and Treatment of Alkalosis in Children
Review Article 51 Evaluation and Treatment of Alkalosis in Children Matjaž Kopač1 1 Division of Pediatrics, Department of Nephrology, University Address for correspondence Matjaž Kopač, MD, DSc, Division of Medical Centre Ljubljana, Ljubljana, Slovenia Pediatrics, Department of Nephrology, University Medical Centre Ljubljana, Bohoričeva 20, 1000 Ljubljana, Slovenia J Pediatr Intensive Care 2019;8:51–56. (e-mail: [email protected]). Abstract Alkalosisisadisorderofacid–base balance defined by elevated pH of the arterial blood. Metabolic alkalosis is characterized by primary elevation of the serum bicarbonate. Due to several mechanisms, it is often associated with hypochloremia and hypokalemia and can only persist in the presence of factors causing and maintaining alkalosis. Keywords Respiratory alkalosis is a consequence of dysfunction of respiratory system’s control ► alkalosis center. There are no pathognomonic symptoms. History is important in the evaluation ► children of alkalosis and usually reveals the cause. It is important to evaluate volemia during ► chloride physical examination. Treatment must be causal and prognosis depends on a cause. Introduction hydrogen ion concentration and an alkalosis is a pathologic Alkalosis is a disorder of acid–base balance defined by process that causes a decrease in the hydrogen ion concentra- elevated pH of the arterial blood. According to the origin, it tion. Therefore, acidemia and alkalemia indicate the pH can be metabolic or respiratory. Metabolic alkalosis is char- abnormality while acidosis and alkalosis indicate the patho- acterized by primary elevation of the serum bicarbonate that logic process that is taking place.3 can result from several mechanisms. It is the most common Regulation of hydrogen ion balance is basically similar to form of acid–base balance disorders. -
Palliative Care in Advanced Liver Disease (Marsano 2018)
Palliative Care in Advanced Liver Disease Luis Marsano, MD 2018 Mortality in Cirrhosis • Stable Cirrhosis: – Prognosis determined by MELD-Na score – Provides 90 day mortality. – http://www.mdcalc.com/meldna-meld-na-score-for-liver-cirrhosis/ • Acute on Chronic Liver Failure (ACLF) – Mortality Provided by CLIF-C ACLF Calculator – Provides mortality at 1, 3, 6 and 12 months. – http://www.clifresearch.com/ToolsCalculators.aspx • Acute Decompensation (without ACLF): – Mortality Provided by CLIF-C Acute decompensation Calculator – Provides mortality at 1, 3, 6 and 12 months. – http://www.clifresearch.com/ToolsCalculators.aspx • Survival of Ambulatory Patients with HCC (MESIAH) – Provides survival at 1, 3, 6, 12, 24 and 36 months. – https://www.mayoclinic.org/medical-professionals/model-end-stage-liver- disease/model-estimate-survival-ambulatory-hepatocellular-carcinoma-patients- mesiah Acute Decompensation Type and Mortality Organ Failure in Acute-on-Chronic Liver Failure Organ Failure Mortality Impact Frequency of Organ Failure 48% have >/= 2 Organ Failures The MESIAH Score Model of Estimated Survival In Ambulatory patients with HCC Complications of Cirrhosis Affecting Palliative Care • Ascites and Hepatic Hydrothorax. • Hyponatremia. • Hepatorenal syndrome. • Hepatic Encephalopathy. • Malnutrition/ Anorexia. • GI bleeding: Varices, Portal gastropathy & Gastric Antral Vascular Ectasia • Pruritus • Hepatopulmonary Syndrome. Difficult Decisions with Shifting Balance • Is patient a liver transplant candidate? • Effect of illness in: – patient’s survival – patient’s Quality of Life • patient’s relation to family • family’s Quality of Life • Effect of therapy in: – patient’s survival – patient’s Quality of Life • patient’s relation to family • family’s Quality of life Ascites and Palliation • PATHOGENESIS • CONSEQUENCES • Hepatic sinusoidal HTN • Abdominal distention with early stimulates hepatic satiety. -
Real Facts About Fluid Overload
Real Facts About Fluid Overload Venkat K. Iyer, MD, MBA Assistant Professor, Mayo School of Medicine Medical Director, Quality and Process Improvement, Mayo Clinic Dialysis System ©2017 MFMER | slide-1 Disclosure • None Objectives Discuss the meaning of fluid overload and its negative physiological effects on the body of a person who has kidney failure. Two major functions of dialysis Uremic solute removal Excess ECF volume removal Main Process Diffusion Ultrafiltration How is adequacy Clearance of surrogate BP control, Dry weight measured? solute - urea Quantification of spKt/V, Std Kt/V, URR No objective measure to quantify adequacy adequacy of fluid removal. Trial & Error method to achieve DW Debate Small versus middle What is the best method to molecular clearance quantify ECF volume removal. (diffusive versus Clinical versus Non-clinical Convective clearance) methods What is dry weight? • Lowest tolerated post-dialysis weight achieved via a gradual reduction in post dialysis weight at which there are minimal signs or symptoms of hypovolemia or hypervolemia Dry Weight ECF volume LBM Initiation of HD High Low Adequate Maintenance HD Euvolemic Improves Acute illness Increases Decreases Negative Effects of Fluid Overload (“Volutrauma”) Acute Fluid Overload Chronic Fluid Overload • Dyspnea • Hypertension • CHF • LVH • Hospitalization • CHF • Decreased vascular compliance • Increased cardiovascular mortality • Organ dysfunction • Gut edema: malabsorption • Tissue edema: poor wound healing • Renal edema: renal BF, reduced GFR • Pulmonary edema Cost of Hospitalization for Volume Overload % of Fluid Overload admission % of 41,699 episodes 25,291 pts of 176,790 100 86 14.3 80 60 40 85.7 20 9 5 0 Inpatient ED Observation FO admission Others care Average cost per episode $6,372 Total cost $266 million • Arneson et al. -
Anasarca As the Presenting Symptom of Juvenile Dermatomyositis: a Case Series Emily E
Schildt and De Ranieri Pediatric Rheumatology (2021) 19:120 https://doi.org/10.1186/s12969-021-00604-3 CASE REPORT Open Access Anasarca as the presenting symptom of juvenile dermatomyositis: a case series Emily E. Schildt and Deirdre De Ranieri* Abstract Background: Juvenile Dermatomyositis (JDM) is an autoimmune disease that typically presents with classic skin rashes and proximal muscle weakness. Anasarca is a rare manifestation of this disease and is associated with a more severe and refractory course, requiring increased immunosuppression. Early recognition of this atypical presentation of JDM may lead to earlier treatment and better outcomes. Case presentation: We present two female patients, ages 11 years old and 4 years old, who presented to the ED with anasarca and were subsequently diagnosed with JDM. Both patients required ICU-level care and significant immunosuppression, including prolonged courses of IV methylprednisolone, IVIG, and Rituximab. Conclusions: Anasarca is a rare presentation of Juvenile Dermatomyositis, but it is important for clinicians to recognize this manifestation of the disease. Early recognition and treatment will lead to better outcomes in these children and hopefully decrease the need for prolonged hospitalization and ICU level care. Keywords: Juvenile dermatomyositis, Anasarca, Generalized edema, Vascular permeability, Muscle enzymes, Myositis, Immunosuppression Background We describe two patients with a final diagnosis of Ju- Juvenile dermatomyositis (JDM) is the most common venile Dermatomyositis who presented with anasarca, chronic inflammatory myopathy of childhood. It is an both of whom required ICU-level care. Anasarca is a autoimmune disease that primarily affects the muscles rare presentation of this disease but can be life- and skin but can also affect the blood vessels, manifest- threatening, and expedient identification and treatment ing as localized edema. -
Outcome of Acute Kidney Injury: How to Make a Difference?
Jamme et al. Ann. Intensive Care (2021) 11:60 https://doi.org/10.1186/s13613-021-00849-x REVIEW Open Access Outcome of acute kidney injury: how to make a diference? Matthieu Jamme1,2,3* , Matthieu Legrand4 and Guillaume Geri2,3,5 Abstract Background: Acute kidney injury (AKI) is one of the most frequent organ failure encountered among intensive care unit patients. In addition to the well-known immediate complications (hydroelectrolytic disorders, hypervolemia, drug overdose), the occurrence of long-term complications and/or chronic comorbidities related to AKI has long been underestimated. The aim of this manuscript is to briefy review the short- and long-term consequences of AKI and discuss strategies likely to improve outcome of AKI. Main body: We reviewed the literature, focusing on the consequences of AKI in all its aspects and the management of AKI. We addressed the importance of clinical management for improving outcomes AKI. Finally, we have also pro- posed candidate future strategies and management perspectives. Conclusion: AKI must be considered as a systemic disease. Due to its short- and long-term impact, measures to prevent AKI and limit the consequences of AKI are expected to improve global outcomes of patients sufering from critical illnesses. Keywords: Acute kidney injury, Long-term outcome, Chronic kidney disease, Intensive care Introduction Why physicians should worry about AKI? Acute kidney injury (AKI) is one of the most frequent Occurrence of AKI represents a sharp prognostic turn organ failure encountered in intensive care units (ICU). for patients by afecting both short- and long-term Since his frst defnition by Homer W. -
2015 Diagnostic Criteria for TAFRO (Thrombocytopenia-Anasarca-Fever-Renal Insufficiency-Organomegaly) Syndrome
2015 diagnostic criteria for TAFRO (Thrombocytopenia-anasarca-fever-renal insufficiency-organomegaly) syndrome Masaki Y. et al. Int J Hematol, 2016, 103:686-692 This research was originally published in International Journal of Hematology, Masaki Y, et al., Proposed diagnostic criteria, disease severity classification and treatment strategy for TAFRO syndrome. 2015 version. Int J Hematol. 2016, 103:686-92 © 2016 by The Japanese Society of Hematology. Reproduced with permission. http://link.springer.com/article/10.1007%2Fs12185-016-1979-1. A. Major categories (1) Anasarca, including pleural effusion, ascites and general edema (2) Thrombocytopenia; defined as a pre-treatment platelet count ≤100,000/μl (3) Systemic inflammation, defined as fever of unknown etiology above 37.5 °C and/or serum C-reactive protein concentration ≥2 mg/dl B. Minor categories (1) Castleman’s disease-like features on lymph node biopsy (2) Reticulin myelofibrosis and/or increased number of megakaryocytes in bone marrow (3) Mild organomegaly, including hepatomegaly, splenomegaly and lymphadenopathy (4) Progressive renal insufficiency C. Diseases to be excluded (1) Malignancies, including lymphoma, myeloma, mesothelioma, etc. (2) Autoimmune disorders, including systemic lupus erythematosus (SLE), ANCA-associated vasculitis, etc. (3) Infectious disorders, including acid fast bacterial infection, rickettsial disease, lyme disease, severe fever with thrombocytopenia syndrome (SFTS), etc. (4) POEMS syndrome (5) IgG4-related disease (6) Hepatic cirrhosis (7) Thrombotic thrombocytopenic -
4 Edema in Childhood
Kidney International, Vol. 51, Suppl. 59 (1997). pp. S-100-S-104 (1) Red Hypo Ne] Liv Edema in childhood Ma Pre Sev SATOSHI HISANO, SEUNGHOON HAHN, NANCY B. KUEMMERLE, JAMES CM. CHAN, (2) Incr. and NATALE G. DESANTO Cardi He: h Pediatric Nephrology Division, Virginia Commonwealth University's Medical College of Virginia, Richmond, Virginia, USA, and Divisione di Nefrologia Art dell' Adulto e del Bambino, Seconda Universita'degli Studi di Napoli, Naples, Italy Renal Act ACt Idiops Fan Edema in childhood. There are two types of edema: localized edema sympathetic nervous system (SNS) activity; and (3) antidiuretic Nor and generalized edema. The causes ofgeneralized edema in childhoodare hormone (ADH) release [4-6]. These forces and perhaps as yet diverse. Formation of generalizededema involves retention of sodium and Prej unidentified factors give rise to the consequential water and water in the kidney. The treatment of generalized edema depends on the (3) Incre primary etiology. Supportive nutritional and medicaltherapies are needed sodium retention, which promotes the development of edema, Allerg to prevent further edema. These and related features of edema in The sodium and water retention leads to further decreased Vascu childhood are discussed in this review. den plasma oncotic pressure, setting up a vicious cycle perpetuating dise the edema formation. The movement of water from intracellular space to interstitial space by itself also contributes to the devel opment of edema formation [1, 3]. Edema can be defined as the presence of excess fluid in the In contrast, the mechanism of "overfilling edema" is expanded interstitial space of the body. Edema is divided into two types, extracellular volume that results from primary renal sodium localized edema and generalized edema. -
Restrictive Fluid and Fluid Removal Approach in Diabetic Ketoacidosis with Septic AKI: a Case Report
Case report Crit Care Shock (2021) 24:125-129 Restrictive fluid and fluid removal approach in diabetic ketoacidosis with septic AKI: A case report Elvia AS1, Mayang Indah Lestari2, Yohannes WH George3 Abstract to the intensive care unit. Aggressive fluid re- Diabetic ketoacidosis is a life-threatening com- suscitation carries potential adverse effects such plication that requires a rapid restoration of as hyperchloremic metabolic acidosis, intersti- intravascular volume usually with aggressive tial multi-organ edema, and increased incidence administration of intravenous fluid with 0.9% of acute kidney injury. The first day of ICU sodium chloride as recommended by the Ameri- treatment, positive cumulative fluid balance can Diabetes Association. We report a 50-year- occurred and fluid removal was indicated. Fluid old obese female patient with a history of diabe- removal using diuretic or ultrafiltration is a tes mellitus (DM) since 20 years ago and rou- part of the treatment of organ congestion and tinely using insulin. She experienced dyspnea fluid overload after the initial phase of shock and presumably was caused by diabetic ketoac- resuscitation to achieve negative fluid balance. idosis. The patient was given fluid resuscitation This case showed that restricted fluid and fluid with normal saline, but the dyspnea did not re- removal improve the patient outcome, especially solve and the work of breathing increased fur- in diabetic ketoacidosis and septic AKI patients. ther, so the patient was intubated and admitted . Key words: Diabetic ketoacidosis, septic AKI, restricted fluid, fluid removal, negative cumulative balance. Introduction (1) Recent guidelines from American Diabetes As- Diabetic ketoacidosis (DKA) is a life-threatening sociation (ADA) recommend fluid resuscitation complication that can occur in patients with diabe- using normal saline 15-20 ml/kg/hour (1-1.5 liter) tes mellitus. -
Mechanisms and Management of Nephrotic Edema
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Kidney International, Vol. 45 (1994),pp.266—281 NEPHROLOGY FORUM Mechanisms and management of nephrotic edema Principal discussant: MICHAEL H. HUMPHREYS University of California San Francisco, San Francisco, California showed a normal heart size and regular rhythm; heart sounds were distant through a thickened chest wall, but no murmurs or gallops were Editors heard, The abdomen was nontender without evidence of hepatic or JORDAN J. COHEN splenic enlargement. The stool was guaiac positive. The extremities JOHN T. HARR1NGTON showed no clubbing, but massive anasarca was present, with pitting edema of all extremities as well as the abdominal and thoracic wall. The NICOLAOS B. MADIAS penis and scrotum were edematous, and paraphimosis was evident, Neurologic examination was normal except for a slowed relaxation Managing Editor phase of the deep-tendon reflexes. CHERYL J. ZUSMAN Laboratory values on admission were: hematocrit, 29.5; white blood cell count, 16,700/mm3 with a left shift; and a platelet count of 212 x 103/mm'. The serum sodium concentration was 145 mEq/liter; potas- sium, 4.3 mEq/liter; chloride, 121 mEq/liter; total CO2. 16 mmol/liter; State University of New York at Stony Brook BUN, 65 mg/dl; and serum creatinine, 5.5 mgldl. The serum albumin and concentration was 0.6 g/dl; calcium, 6.9 mg/dl; phosphorus, 5.4 mg/dl; and magnesium, 1.8 mg/dl. The erythrocyte sedimentation rate was 139 Tufts University School of Medicine mm/hr, and the serum cholesterol was 554 mg/dl. -
Neurologic Complications of Electrolyte Disturbances and Acid–Base Balance
Handbook of Clinical Neurology, Vol. 119 (3rd series) Neurologic Aspects of Systemic Disease Part I Jose Biller and Jose M. Ferro, Editors © 2014 Elsevier B.V. All rights reserved Chapter 23 Neurologic complications of electrolyte disturbances and acid–base balance ALBERTO J. ESPAY* James J. and Joan A. Gardner Center for Parkinson’s Disease and Movement Disorders, Department of Neurology, UC Neuroscience Institute, University of Cincinnati, Cincinnati, OH, USA INTRODUCTION hyperglycemia or mannitol intake, when plasma osmolal- ity is high (hypertonic) due to the presence of either of The complex interplay between respiratory and renal these osmotically active substances (Weisberg, 1989; function is at the center of the electrolytic and acid-based Lippi and Aloe, 2010). True or hypotonic hyponatremia environment in which the central and peripheral nervous is always due to a relative excess of water compared to systems function. Neurological manifestations are sodium, and can occur in the setting of hypovolemia, accompaniments of all electrolytic and acid–base distur- euvolemia, and hypervolemia (Table 23.2), invariably bances once certain thresholds are reached (Riggs, reflecting an abnormal relationship between water and 2002). This chapter reviews the major changes resulting sodium, whereby the former is retained at a rate faster alterations in the plasma concentration of sodium, from than the latter (Milionis et al., 2002). Homeostatic mech- potassium, calcium, magnesium, and phosphorus as well anisms protecting against changes in volume and sodium as from acidemia and alkalemia (Table 23.1). concentration include sympathetic activity, the renin– angiotensin–aldosterone system, which cause resorption HYPONATREMIA of sodium by the kidneys, and the hypothalamic arginine vasopressin, also known as antidiuretic hormone (ADH), History and terminology which prompts resorption of water (Eiskjaer et al., 1991).