dehydration_ background, pathophysiology, epidemiology

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 Dehydration  Author: Lenn ox H Huang, MD; Chie f Editor: Timothy E Cor den, MD more... Updated: Sep 25, 2014 Background Dehydrat ion describes a state of negative fluid balance that may be caused by numerous disease entities. Diarrheal illnesses are the most common etiologies. Worldwide, dehydration secondary to diarrheal illness is the leading cause of infant and child mortality. Pathophysiology The negative fluid balance that causes dehydration results from decreased intake, increased output (renal, GI, or insensible losses), or fluid shift ( ascites , effusions, and capillary leak states such as burns and sepsis). The decrease in total body water causes reductions in both the intracellular and extracellular fluid volumes. Clinical manifestations of dehydration are most closely related to intravascular volume depletion. As dehydration progresses, hypovolemic shock ultimately ensues, resulting in end organ failure and death. Young children are more susceptible to dehydration due to larger body water content, renal immaturity, and inability to meet their own needs independently. Older children show signs of dehydration sooner than infants due to lower levels of extracellular fluid (ECF). Dehydration can be categorized according to osmolarity and severity. Serum sodium is a good surrogate marker of osmolarity assuming the patient has a normal serum glucose. Dehydration may be isonatremic (130-150 mEq/L), hyponatremic (< 130 mEq/L), or hypernatremic (>150 mEq/L). Isonatremic dehydration is the most common (80%). Hypernatremic and hyponatremic dehydration each comprise 5-10% of cases. Variations in serum sodium reflect the composition of the fluids lost and have different pathophysiologic effects, as follows: Isonatremic (isotonic) dehydration occurs when the lost fluid is similar in sodium concentration to the blood. Sodium and water losses are of the same relative magnitude in both the intrav ascular and extravascular fluid compartments. Hyponatremic (hypotonic) dehydration occurs when the lost fluid contains more sodium than the blood (loss of hypertonic fluid). Relatively more sodium than water is lost. Because the serum sodium is low, intravascular water shifts to the extravascula r space, exaggerating intravascular volume depletion for a given amount of total body water loss. [1, 2] Hypernatremic (hypertonic) dehydration occurs when the lost fluid contains less sodium than the blood (loss of hypotonic fluid). Relatively less sodium than water is lost. Because the serum sodium is high, extravascular water shifts to the intravascular space, minimizing intravascular volume depletion for a given amount of total body water loss. [2, 3, 4] Neurologic complications can occur in hyponatremic and hypernatremic states. Severe hyponatremia may lead to intractable seizures, whereas rapid correction of chronic hyponatremia (>2 mEq/L/h) has been associated with central pontine myelinolysis. During hypernatremic dehydration, water is osmotically pulled from cells into the extracellular space. To compensate, cells can generate osmotically active particles (idiogenic osmoles) that pull water back into the cell and maintain cellular fluid volume. During rapid rehydration of hypernatremia, the increased osmotic activity of these cells can result in a large influx of water, causing cellular swelling and rupture; cerebral edema is the most devastating consequence. Slow rehydration over 48 hours generally minimizes this risk. Epidemiology Frequency United States Diarrheal illnesses in children causes 3 million physician visits, 220,000 hospitalizations (10% of all children who require hospitalization), and 400 deaths per year. On average, North American children younger than 5 years have 2 episodes of gastroenteritis per year. International Diarrheal illnesses with subsequent dehydration account for nearly 4 million deaths per year in infants and children. The overwhelming majority of these deaths occur in developing nations. Mortality/Morbidity The prognosis is excellent if the child is promptly and effectively treated. However, the child with severe dehydration and hypovolemic shock can have significant morbidity and mortality if treatment is delayed. Mortalit y and morbidity generally depend on the severity of dehydration and the promptness of oral or intravenous rehydration. If treatment is rapidly and appropriately obtained, morbidity and mortality are low. Routine use of hypotonic parenteral fluids in hospitalized children has been associated with hyponatremia and subsequent neurologic complications and death. Monitoring the efficacy and complications of parenteral rehydration with accurate fluid balances and serum electrolytes is crucial. Complications may include irreversible shock, sagittal or other venous sinus thrombosis, intractable seizures, and renal failure.  Ag e Children younger than 5 years are at the highest risk. Dehydration: Background, Pathophysiology , Epidemiology  http://emedicine.medscape.com/article/906999-overview 1 of 4 10/07/2015 14:47

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  • DehydrationAuthor: Lennox H Huang, MD; Chief Editor: Timothy E Corden, MD more...

    Updated: Sep 25, 2014

    BackgroundDehydration describes a state of negative fluid balance that may be caused by numerous disease entities. Diarrhealillnesses are the most common etiologies. Worldwide, dehydration secondary to diarrheal illness is the leading causeof infant and child mortality.

    Pathophysiology

    The negative fluid balance that causes dehydration results from decreased intake, increased output (renal, GI, orinsensible losses), or fluid shift (ascites, effusions, and capillary leak states such as burns and sepsis). The decreasein total body water causes reductions in both the intracellular and extracellular fluid volumes. Clinical manifestationsof dehydration are most closely related to intravascular volume depletion. As dehydration progresses, hypovolemicshock ultimately ensues, resulting in end organ failure and death.

    Young children are more susceptible to dehydration due to larger body water content, renal immaturity, and inabilityto meet their own needs independently. Older children show signs of dehydration sooner than infants due to lowerlevels of extracellular fluid (ECF).

    Dehydration can be categorized according to osmolarity and severity. Serum sodium is a good surrogate marker ofosmolarity assuming the patient has a normal serum glucose. Dehydration may be isonatremic (130-150 mEq/L),hyponatremic (< 130 mEq/L), or hypernatremic (>150 mEq/L). Isonatremic dehydration is the most common (80%).Hypernatremic and hyponatremic dehydration each comprise 5-10% of cases. Variations in serum sodium reflect thecomposition of the fluids lost and have different pathophysiologic effects, as follows:

    Isonatremic (isotonic) dehydration occurs when the lost fluid is similar in sodium concentration to the blood.Sodium and water losses are of the same relative magnitude in both the intravascular and extravascular fluidcompartments.Hyponatremic (hypotonic) dehydration occurs when the lost fluid contains more sodium than the blood (lossof hypertonic fluid). Relatively more sodium than water is lost. Because the serum sodium is low, intravascularwater shifts to the extravascular space, exaggerating intravascular volume depletion for a given amount oftotal body water loss. [1, 2]Hypernatremic (hypertonic) dehydration occurs when the lost fluid contains less sodium than the blood (lossof hypotonic fluid). Relatively less sodium than water is lost. Because the serum sodium is high, extravascularwater shifts to the intravascular space, minimizing intravascular volume depletion for a given amount of totalbody water loss. [2, 3, 4]

    Neurologic complications can occur in hyponatremic and hypernatremic states. Severe hyponatremia may lead tointractable seizures, whereas rapid correction of chronic hyponatremia (>2 mEq/L/h) has been associated withcentral pontine myelinolysis. During hypernatremic dehydration, water is osmotically pulled from cells into theextracellular space. To compensate, cells can generate osmotically active particles (idiogenic osmoles) that pullwater back into the cell and maintain cellular fluid volume. During rapid rehydration of hypernatremia, the increasedosmotic activity of these cells can result in a large influx of water, causing cellular swelling and rupture; cerebraledema is the most devastating consequence. Slow rehydration over 48 hours generally minimizes this risk.

    Epidemiology

    Frequency

    United States

    Diarrheal illnesses in children causes 3 million physician visits, 220,000 hospitalizations (10% of all children whorequire hospitalization), and 400 deaths per year. On average, North American children younger than 5 years have 2episodes of gastroenteritis per year.

    International

    Diarrheal illnesses with subsequent dehydration account for nearly 4 million deaths per year in infants and children.The overwhelming majority of these deaths occur in developing nations.

    Mortality/Morbidity

    The prognosis is excellent if the child is promptly and effectively treated. However, the child with severe dehydrationand hypovolemic shock can have significant morbidity and mortality if treatment is delayed.

    Mortality and morbidity generally depend on the severity of dehydration and the promptness of oral or intravenousrehydration. If treatment is rapidly and appropriately obtained, morbidity and mortality are low.

    Routine use of hypotonic parenteral fluids in hospitalized children has been associated with hyponatremia andsubsequent neurologic complications and death. Monitoring the efficacy and complications of parenteral rehydrationwith accurate fluid balances and serum electrolytes is crucial.

    Complications may include irreversible shock, sagittal or other venous sinus thrombosis, intractable seizures, andrenal failure.

    Age

    Children younger than 5 years are at the highest risk.

    Dehydration: Background, Pathophysiology, Epidemiology http://emedicine.medscape.com/article/906999-overview

    1 of 4 10/07/2015 14:47

  • Contributor Information and DisclosuresAuthorLennox H Huang, MD FAAP, Associate Professor and Chair, Department of Pediatrics, McMaster UniversitySchool of Medicine; Chief of Pediatrics, McMaster Children's Hospital

    Lennox H Huang, MD is a member of the following medical societies: American Academy of Pediatrics, AmericanAssociation for Physician Leadership, Canadian Medical Association, Ontario Medical Association, Society ofCritical Care Medicine

    Disclosure: Nothing to disclose.

    Coauthor(s)Dan L Ellsbury, MD Consulting Staff, Pediatrix Medical Group of Iowa; Consulting Staff, Department ofPediatrics, Neonatology Intensive Care Unit, Mercy Medical Center of Des Moines

    Dan L Ellsbury, MD is a member of the following medical societies: American Academy of Pediatrics

    Disclosure: Nothing to disclose.

    Caroline S George, MD Associate Professor, Consulting Staff, Department of Pediatrics, Division of Critical CareMedicine, University of Minnesota Medical School

    Caroline S George, MD is a member of the following medical societies: American Academy of Pediatrics, Societyof Critical Care Medicine

    Disclosure: Nothing to disclose.

    Krishnapriya R Anchala, MD, MS FAAP, Assistant Professor, Department of Pediatrics, Division of PediatricEmergency Medicine, McMaster University

    Krishnapriya R Anchala, MD, MS is a member of the following medical societies: American Academy ofPediatrics, Canadian Medical Association, Ontario Medical Association

    Disclosure: Nothing to disclose.

    Specialty Editor BoardMary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College ofPharmacy; Editor-in-Chief, Medscape Drug Reference

    Disclosure: Nothing to disclose.

    Barry J Evans, MD Assistant Professor of Pediatrics, Temple University Medical School; Director of PediatricCritical Care and Pulmonology, Associate Chair for Pediatric Education, Temple University Children's MedicalCenter

    Barry J Evans, MD is a member of the following medical societies: American Academy of Pediatrics, AmericanCollege of Chest Physicians, American Thoracic Society, Society of Critical Care Medicine

    Disclosure: Nothing to disclose.

    Chief EditorTimothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center,Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

    Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi BetaKappa, Society of Critical Care Medicine, Wisconsin Medical Society

    Disclosure: Nothing to disclose.

    Additional ContributorsG Patricia Cantwell, MD FCCM, Professor of Clinical Pediatrics, Chief, Division of Pediatric Critical CareMedicine, University of Miami, Leonard M Miller School of Medicine; Medical Director, Palliative Care Team,Director, Pediatric Critical Care Transport, Holtz Children's Hospital, Jackson Memorial Medical Center; MedicalManager, FEMA, Urban Search and Rescue, South Florida, Task Force 2; Pediatric Medical Director, Tilli Kids Pediatric Initiative, Division of Hospice Care Southeast Florida, Inc

    G Patricia Cantwell, MD is a member of the following medical societies: American Academy of Hospice andPalliative Medicine, American Academy of Pediatrics, American Heart Association, American Trauma Society,National Association of EMS Physicians, Society of Critical Care Medicine, Wilderness Medical Society

    Disclosure: Nothing to disclose.

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