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Smith CR, Chua P, Papaioannou C, Warrier R, Nolan GJG, Hsiao YFF, Duke T. Fluid and electrolyte pathophysiology in common febrile illness in children and the implications for clinical management. Arch Dis Child 2024; 109:794-800. [PMID: 39097402 DOI: 10.1136/archdischild-2024-327407] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/15/2024] [Accepted: 07/22/2024] [Indexed: 08/05/2024]
Abstract
Achieving fluid homeostasis and the management of fluid and electrolyte complications are constants in the treatment of seriously ill children worldwide. Consensus on the most appropriate fluid strategy for unwell children has been difficult to achieve and has evolved over the last two decades, most notably in high-income countries where adverse events relating to poor fluid management were identified more readily, and official robust inquiries were possible. However, this has not been the situation in many low-income settings where fluids that are prohibited from use in high-income countries may be all that are available, local guidelines and processes to recognise adverse events are not developed, and there has been limited training on safe fluid management for front-line healthcare workers. This narrative review outlines the fluid and electrolyte pathophysiology of common febrile illnesses in children, describes the evolution of this field and concludes with implications and principles of a fluid management strategy for seriously ill children. This review was prepared as a physiological background paper to support evidence presented to the WHO Guideline Development Group for Fluid Guidelines in Children, Geneva, March 2024.
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Affiliation(s)
- Clare Ruth Smith
- Paediatric Intensive Care Unit, The Royal Children's Hospital Melbourne, Melbourne, Victoria, Australia
| | - Poh Chua
- Library, The Royal Children's Hospital Melbourne, Melbourne, Victoria, Australia
| | - Catherine Papaioannou
- Paediatric Intensive Care Unit, The Royal Children's Hospital Melbourne, Melbourne, Victoria, Australia
| | - Ranjana Warrier
- Paediatric Intensive Care Unit, The Royal Children's Hospital Melbourne, Melbourne, Victoria, Australia
| | - Gregory J G Nolan
- Paediatric Intensive Care Unit, The Royal Children's Hospital Melbourne, Melbourne, Victoria, Australia
| | | | - Trevor Duke
- Paediatric Intensive Care Unit, The Royal Children's Hospital Melbourne, Melbourne, Victoria, Australia
- Department of Paediatrics, University of Melbourne, Parkville, Victoria, Australia
- Child health, School of Medicine and Health Sciences, University of Papua New Guinea, Port Moresby, Papua New Guinea
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Büyükkaragöz B, Bakkaloğlu SA. Serum osmolality and hyperosmolar states. Pediatr Nephrol 2023; 38:1013-1025. [PMID: 35779183 DOI: 10.1007/s00467-022-05668-1] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/15/2022] [Revised: 05/26/2022] [Accepted: 06/14/2022] [Indexed: 11/26/2022]
Abstract
Serum osmolality is the sum of the osmolalities of every single dissolved particle in the blood such as sodium and associated anions, potassium, glucose, and urea. Under normal conditions, serum sodium concentration is the major determinant of serum osmolality. Effective blood osmolality, so-called blood tonicity, is created by the endogenous (e.g., sodium and glucose) and exogenous (e.g., mannitol) solutes that are capable of creating an osmotic gradient across the membranes. In case of change in effective blood osmolality, water shifts from the compartment with low osmolality into the compartment with high osmolarity in order to restore serum osmolality. The difference between measured osmolality and calculated osmolarity forms the osmolal gap. An increase in serum osmolal gap can stem from the presence of solutes that are not included in the osmolarity calculation, such as hypertonic treatments or toxic alcoholic ingestions. In clinical practice, determination of serum osmolality and osmolal gap is important in the diagnosis of disorders related to sodium, glucose and water balance, kidney diseases, and small molecule poisonings. As blood hypertonicity exerts its main effects on the brain cells, neurologic symptoms varying from mild neurologic signs and symptoms to life-threatening outcomes such as convulsions or even death may occur. Therefore, hypertonic states should be promptly diagnosed and cautiously managed. In this review, the causes and treatment strategies of hyperosmolar conditions including hypernatremia, diabetic ketoacidosis, hyperglycemic hyperosmolar syndrome, hypertonic treatments, or intoxications are discussed in detail to increase awareness of this important topic with significant clinical consequences.
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Affiliation(s)
- Bahar Büyükkaragöz
- Department of Pediatric Nephrology, Gazi University, 06560, Besevler, Ankara, Turkey.
| | - Sevcan A Bakkaloğlu
- Department of Pediatric Nephrology, Gazi University, 06560, Besevler, Ankara, Turkey
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Boutin A, Carceller A, Desjardins MP, Sanchez M, Gravel J. Association Between Dehydration and Fever During the First Week of Life. Clin Pediatr (Phila) 2017; 56:1328-1335. [PMID: 28198193 DOI: 10.1177/0009922816687323] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 10/20/2022]
Abstract
BACKGROUND Trying to differentiate serious bacterial infection (SBI) from a self-limiting illness in febrile infants seen in the pediatric emergency department (PED) is a significant challenge. The aim of the study was to determine the prevalence of dehydration and its relationship to SBI in febrile full-term newborns under 1 week of age seen in a PED. METHODS A retrospective observational study was carried out on all children younger than 8 days of age with fever who presented to a single, tertiary care, PED from January 2009 to April 2014. Dehydration was defined as plasma sodium >150 mmol/L or >10% loss of birth weight. SBI was defined by the presence of a positive culture in the blood, urine, cerebrospinal fluid; osteoarticular infection; bacterial enteritis; or pneumonia. The primary analysis was the proportion of children with dehydration. A secondary analysis compared proportion of infection according to hydration status. RESULTS Of the 895 children under 8 days of age who visited the PED, 69 consulted for fever. Seven patients were excluded because they were transferred from another hospital. Sixty-two eligible patients were included in the final analysis. Of these, 17 (27%) were dehydrated according to our definition. Only 2 patients had an SBI while 2 others had a final diagnosis of viral myocarditis and encephalitis, respectively. None of the 4 children with serious infection fulfilled our definition of dehydration, and all had a plasma sodium level lower than 145 mmol/L. CONCLUSIONS Dehydration is frequently associated with fever in infants younger than 8 days of age seen in a PED. Early identification of dehydration may be useful in limiting the aggressive intervention in some of these infants.
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Affiliation(s)
- Ariane Boutin
- 1 CHU Sainte-Justine, Montreal, Quebec, Canada.,2 Montreal University, Montreal, Quebec, Canada
| | - Ana Carceller
- 1 CHU Sainte-Justine, Montreal, Quebec, Canada.,2 Montreal University, Montreal, Quebec, Canada
| | - Marie Pier Desjardins
- 1 CHU Sainte-Justine, Montreal, Quebec, Canada.,2 Montreal University, Montreal, Quebec, Canada
| | - Marisol Sanchez
- 1 CHU Sainte-Justine, Montreal, Quebec, Canada.,2 Montreal University, Montreal, Quebec, Canada
| | - Jocelyn Gravel
- 1 CHU Sainte-Justine, Montreal, Quebec, Canada.,2 Montreal University, Montreal, Quebec, Canada
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Rondon-Berrios H, Argyropoulos C, Ing TS, Raj DS, Malhotra D, Agaba EI, Rohrscheib M, Khitan ZJ, Murata GH, Shapiro JI, Tzamaloukas AH. Hypertonicity: Clinical entities, manifestations and treatment. World J Nephrol 2017; 6:1-13. [PMID: 28101446 PMCID: PMC5215203 DOI: 10.5527/wjn.v6.i1.1] [Citation(s) in RCA: 18] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/13/2016] [Revised: 08/17/2016] [Accepted: 11/02/2016] [Indexed: 02/06/2023] Open
Abstract
Hypertonicity causes severe clinical manifestations and is associated with mortality and severe short-term and long-term neurological sequelae. The main clinical syndromes of hypertonicity are hypernatremia and hyperglycemia. Hypernatremia results from relative excess of body sodium over body water. Loss of water in excess of intake, gain of sodium salts in excess of losses or a combination of the two are the main mechanisms of hypernatremia. Hypernatremia can be hypervolemic, euvolemic or hypovolemic. The management of hypernatremia addresses both a quantitative replacement of water and, if present, sodium deficit, and correction of the underlying pathophysiologic process that led to hypernatremia. Hypertonicity in hyperglycemia has two components, solute gain secondary to glucose accumulation in the extracellular compartment and water loss through hyperglycemic osmotic diuresis in excess of the losses of sodium and potassium. Differentiating between these two components of hypertonicity has major therapeutic implications because the first component will be reversed simply by normalization of serum glucose concentration while the second component will require hypotonic fluid replacement. An estimate of the magnitude of the relative water deficit secondary to osmotic diuresis is obtained by the corrected sodium concentration, which represents a calculated value of the serum sodium concentration that would result from reduction of the serum glucose concentration to a normal level.
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Congenital nephrogenic diabetes insipidus: the current state of affairs. Pediatr Nephrol 2012; 27:2183-204. [PMID: 22427315 DOI: 10.1007/s00467-012-2118-8] [Citation(s) in RCA: 80] [Impact Index Per Article: 6.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/23/2011] [Revised: 01/14/2012] [Accepted: 01/17/2012] [Indexed: 01/02/2023]
Abstract
The anti-diuretic hormone arginine vasopressin (AVP) is released from the pituitary upon hypovolemia or hypernatremia, and regulates water reabsorption in the renal collecting duct principal cells. Binding of AVP to the arginine vasopressin receptor type 2 (AVPR2) in the basolateral membrane leads to translocation of aquaporin 2 (AQP2) water channels to the apical membrane of the collecting duct principal cells, inducing water permeability of the membrane. This results in water reabsorption from the pro-urine into the medullary interstitium following an osmotic gradient. Congenital nephrogenic diabetes insipidus (NDI) is a disorder associated with mutations in either the AVPR2 or AQP2 gene, causing the inability of patients to concentrate their pro-urine, which leads to a high risk of dehydration. This review focuses on the current knowledge regarding the cell biological aspects of congenital X-linked, autosomal-recessive and autosomal-dominant NDI while specifically addressing the latest developments in the field. Based on deepened mechanistic understanding, new therapeutic strategies are currently being explored, which we also discuss here.
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Gill MC, O’Shaughnessy K. Insensible water loss from the Hilite 2400LT oxygenator: an in vitro study. Perfusion 2012; 28:70-5. [DOI: 10.1177/0267659112464097] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/17/2022]
Abstract
Background: Neonatal extracorporeal membrane oxygenation (ECMO) patients are particularly vulnerable to the effects of uncompensated insensible water loss resulting in hypernatraemia. There exists a long-standing relationship between hypernatraemia and varying degrees of cerebral dysfunction. The aim of this study is to explore the degree to which free water loss occurs across a commonly used ECMO oxygenator, the polymethylpentene (PMP) membrane Hilite® 2400LT (Medos, Medizintechnik AG, Stolberg, Germany). The secondary aim is to assess to what extent the addition of heat and/or humidity ameliorates this water loss. Methods: An ECMO circuit consisting of a centrifugal pump and a Hilite® 2400LT oxygenator was primed with crystalloid and albumin. Each experimental trial was carried out in triplicate, with gas flow rates of 1, 3 and 4.8 L/min being investigated. Fluid loss was assessed at six time points over a 24-hour period. Results: Water loss increased significantly from 1 to 3 L/min gas flow (p=0.05) and from 3 to 4.8 L/min gas flow (p=0.025). The mean water loss differences between the differing gas flow trials per L/min gas flow were non-significant (72.4 ±3.9 ml/24hrs). The effect of heating the gas to 37°C did not significantly alter water loss, whereas heat and humidity reduced water loss significantly (p=0.009). Conclusions: Insensible water loss from a Hilite® 2400LT oxygenator is approximately 72 ml/day per L/min gas flow over 24 hrs. Heating and humidifying the gas reduces the fluid loss significantly to approximately 8 ml/L/min gas flow over 24 hrs (p=0.009).
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Affiliation(s)
- MC Gill
- Perfusion Department, Heart Centre for Children, Sydney, Australia
| | - K O’Shaughnessy
- Perfusion Department, Heart Centre for Children, Sydney, Australia
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Liamis G, Milionis HJ, Elisaf M. A review of drug-induced hypernatraemia. NDT Plus 2009; 2:339-46. [PMID: 25949338 PMCID: PMC4421386 DOI: 10.1093/ndtplus/sfp085] [Citation(s) in RCA: 13] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/08/2009] [Accepted: 06/23/2009] [Indexed: 01/07/2023] Open
Abstract
Drug-induced electrolyte abnormalities have been increasingly reported and may be associated with considerable morbidity and/or mortality. In clinical practice, hypernatraemia (serum sodium higher than 145 mmol/L) is usually of multifactorial aetiology and drug therapy not infrequently is disregarded as a contributing factor for increased serum sodium concentration. Strategies to prevent this adverse drug effect involve careful consideration of risk factors and clinical and laboratory evaluation in the course of treatment. Herein, we review evidence-based information via PubMed and EMBASE and the relevant literature implicating pharmacologic treatment as an established cause of hypernatraemia and discuss its incidence and the underlying pathophysiologic mechanisms.
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Affiliation(s)
- George Liamis
- Department of Internal Medicine, School of Medicine , University of Ioannina , Ioannina , Greece
| | - Haralampos J Milionis
- Department of Internal Medicine, School of Medicine , University of Ioannina , Ioannina , Greece
| | - Moses Elisaf
- Department of Internal Medicine, School of Medicine , University of Ioannina , Ioannina , Greece
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Lejarraga H, Caletti MG, Caino S, Jiménez A. Long-term growth of children with nephrogenic diabetes insipidus. Pediatr Nephrol 2008; 23:2007-12. [PMID: 18584216 DOI: 10.1007/s00467-008-0844-8] [Citation(s) in RCA: 15] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/07/2007] [Revised: 03/17/2008] [Accepted: 03/19/2008] [Indexed: 10/21/2022]
Abstract
Primary nephrogenic diabetes insipidus (NDI) is a genetic, chronic disease characterised by lack of distal renal tubule to antidiuretic hormone. The condition produces polyuria, polydipsia, and consequently, reduced caloric intake and growth failure. There is very scarce information on physical growth of affected children. The objective of the paper is to describe long-term growth of 14 patients from 11 families, studied retrospectively and followed for 3-16 years (median 11.6 years). Diagnosis was made on the basis of clinical and laboratory data and concentration test under pitressin. Patients were treated with indomethacin, thiazides, and amiloride. Weight and standing height was measured periodically at the Laboratory of Anthropometry, following standardised techniques. Information was obtained from clinical notes. The majority of children grew below the third centile of local standards, and many showed improvement of weight, height, and body mass index (BMI) over time. Mean height, weight, and BMI gain during follow-up was 1.72, 1.06, and 1.46 standard deviations (SDs), respectively. Three children who did not adhere to treatment showed growth delay. Height gain during the first 2 years of follow-up was inversely associated with height deficit at diagnosis. Further studies on growth at adolescence and in different mutations are recommended.
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Affiliation(s)
- Horacio Lejarraga
- Department of Growth and Development, Hospital Garrahan, Buenos Aires, Argentina.
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Al-Kandari SR, Pandey T, Badawi MH. Intracranial calcification in central diabetes insipidus. Pediatr Radiol 2008; 38:101-3. [PMID: 17955235 DOI: 10.1007/s00247-007-0608-9] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/14/2007] [Revised: 07/21/2007] [Accepted: 07/23/2007] [Indexed: 11/28/2022]
Abstract
Intracranial calcification is a known but extremely rare complication of diabetes insipidus. To date, only 16 patients have been reported and all had the peripheral (nephrogenic) type of diabetes insipidus. We report a child with intracranial calcification complicating central diabetes insipidus. We also report a child with nephrogenic diabetes insipidus, and compare the patterns of intracranial calcification.
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Affiliation(s)
- Salwa Ramadan Al-Kandari
- Department of Clinical Radiology, Al Razi Hospital, Gamal Abdel Nasser Street, Kuwait 4234, Kuwait
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12
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Bindu PS, Kovoor JME. Nephrogenic diabetes insipidus: a rare cause of intracranial calcification in children. J Child Neurol 2007; 22:1305-7. [PMID: 18006962 DOI: 10.1177/0883073807307087] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/17/2022]
Abstract
Causes of intracranial calcification in children are numerous. This article describes an unusual cause of intracranial calcification and white matter changes in a child, namely, nephrogenic diabetes insipidus. A 4-year-old boy presented with history of polyuria, polydipsia, failure to thrive, and developmental delay. On examination, he had mild dysmorphic features and spastic paraparesis. Evaluation showed findings suggestive of nephrogenic diabetes insipidus. Computed tomography and magnetic resonance imaging revealed calcification and signal changes in the frontal and parietal subcortical white matter and gray white junction in the parietal and occipital lobes. The involvement of the white matter, in addition to the calcification in this disease, is stressed because it may predict the neurologic outcome.
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Affiliation(s)
- Parayil S Bindu
- Departments of Neurology National Institute of Mental Health and Neurosciences, Bangalore, India.
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Escobar GJ, Liljestrand P, Hudes ES, Ferriero DM, Wu YW, Jeremy RJ, Newman TB. Five-year neurodevelopmental outcome of neonatal dehydration. J Pediatr 2007; 151:127-33, 133.e1. [PMID: 17643761 PMCID: PMC2233705 DOI: 10.1016/j.jpeds.2007.03.009] [Citation(s) in RCA: 16] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/10/2006] [Revised: 02/08/2007] [Accepted: 03/02/2007] [Indexed: 10/23/2022]
Abstract
OBJECTIVE To determine the long-term outcome of neonatal dehydration. STUDY DESIGN We identified 182 newborns who were rehospitalized with dehydration (weight loss > or =12% of birth weight and/or serum sodium > or =150 mEq/L) and 419 randomly selected controls from a cohort of 106,627 term and near-term infants with birth weight > or =2000 g born between 1995 and 1998 in northern California Kaiser Permanente hospitals. Outcomes data were obtained from electronic records, interviews, questionnaire responses, and neurodevelopmental evaluations performed in a masked fashion. RESULTS Follow-up data to age at least 2 years were available for 173 of 182 children with a history of dehydration (95%) and 372 of 419 controls (89%) and included formal evaluation at a mean age (+/-standard deviation) of 5.1 +/- 0.12 years for 106 children (58%) and 168 children (40%), respectively. None of the cases developed shock, gangrene, or respiratory failure. Neither crude nor adjusted scores on cognitive tests differed significantly between groups. There was no significant difference between groups in the proportion of children with abnormal neurologic examinations or neurologic diagnoses. Frequencies of parental concerns and reported behavior problems also were not significantly different in the 2 groups. CONCLUSIONS Neonatal dehydration in this managed care setting was not associated with adverse neurodevelopmental outcomes in infants born at or near term.
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Affiliation(s)
- Gabriel J. Escobar
- Kaiser Permanente Medical Care Program, Division of Research, Perinatal Research Unit, 2000 Broadway, 2 floor, Oakland, California 94612, 510-891-3502, 510-891-3408 (fax),
- Kaiser Permanente Medical Center, Department of Inpatient Pediatrics, 1425 S. Main St., Walnut Creek, California 94596
| | - Petra Liljestrand
- Kaiser Permanente Medical Care Program, Division of Research, Perinatal Research Unit, 2000 Broadway, 2 floor, Oakland, California 94612, 510-891-3502, 510-891-3408 (fax),
- University of California, San Francisco, Department of Epidemiology and Biostatistics, UCSF Box 0560, San Francisco, California 94143
| | - Esther S. Hudes
- University of California, San Francisco, Department of Epidemiology and Biostatistics, UCSF Box 0560, San Francisco, California 94143
| | - Donna M. Ferriero
- University of California San Francisco, Department of Neurology, Box 0663, 521 Parnassus Ave. C215, San Francisco, CA 94143-0663
- University of California San Francisco, Department of Pediatrics, Box 0105, 505 Parnassus Ave, San Francisco, CA 94143
| | - Yvonne W. Wu
- University of California San Francisco, Department of Neurology, Box 0663, 521 Parnassus Ave. C215, San Francisco, CA 94143-0663
- University of California San Francisco, Department of Pediatrics, Box 0105, 505 Parnassus Ave, San Francisco, CA 94143
| | - Rita J. Jeremy
- University of California San Francisco, Department of Pediatrics, Box 0105, 505 Parnassus Ave, San Francisco, CA 94143
| | - Thomas B. Newman
- Kaiser Permanente Medical Care Program, Division of Research, Perinatal Research Unit, 2000 Broadway, 2 floor, Oakland, California 94612, 510-891-3502, 510-891-3408 (fax),
- University of California, San Francisco, Department of Epidemiology and Biostatistics, UCSF Box 0560, San Francisco, California 94143
- University of California San Francisco, Department of Pediatrics, Box 0105, 505 Parnassus Ave, San Francisco, CA 94143
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Abstract
Disorders of water imbalance manifest as hyponatremia and hypernatremia. To diagnose these disorders, emergency physicians must maintain a high index of suspicion, especially in the high-risk patient, because clinical presentations may be nonspecific. With severe water imbalance, inappropriate fluid resuscitation in the emergency department may have devastating neurological consequences. The rate of serum sodium concentration correction should be monitored closely to avoid osmotic demyelination syndrome in hyponatremic patients and cerebral edema in hypernatremic patients.
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Affiliation(s)
- Michelle Lin
- San Francisco General Hospital Emergency Services, University of California San Francisco, 1001 Potrero Avenue, Suite 1E21, San Francisco, CA 94110, USA.
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16
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Gomez-Daspet J, Elko L, Grebenev D, Vesely DL. Survival with serum sodium level of 180 mEq/L: permanent disorientation to place and time. Am J Med Sci 2002; 324:321-5. [PMID: 12495299 DOI: 10.1097/00000441-200212000-00006] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/26/2022]
Abstract
A 41-year-old woman who had undergone transfrontal craniotomy for a pituitary tumor 4 months before presentation was admitted with confusion and orientation only to self. She had a fever of 40 degrees C. Serum sodium and chloride levels on admission were 180 and 139 mEq/L, respectively. Measured serum osmolality was 380 mOsmol/L with a urine osmolality of 360 mOsmol/L. Magnetic resonance imaging revealed a 1.5-cm mass in the sella turcica, which was nonfunctioning on endocrine evaluation. The "bright spot" of a normal posterior pituitary was absent. Central diabetes insipidus was confirmed by a 300% increase in urine osmolality with desmopressin. The patient survived her severe hypernatremia, which has 70% mortality with a serum sodium level of 160 mEq/L or above. However, she developed permanent (6 months) disorientation to time and place even when hypernatremia was corrected, which has not been described previously.
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Affiliation(s)
- Joaquin Gomez-Daspet
- Department of Internal Medicine, University of South Florida for Health Sciences, James A. Haley Veterans Medical Center, 13000 Bruce B. Downs Blvd, Tampa, FLorida 33612, USA
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Manganaro R, Mamì C, Marrone T, Marseglia L, Gemelli M. Incidence of dehydration and hypernatremia in exclusively breast-fed infants. J Pediatr 2001; 139:673-5. [PMID: 11713445 DOI: 10.1067/mpd.2001.118880] [Citation(s) in RCA: 93] [Impact Index Per Article: 3.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/22/2022]
Abstract
OBJECTIVES To verify in exclusively breast-fed, term infants the incidence of hypernatremic dehydration and identify possible maternal and/or infant factors that interfere with successful breast-feeding. STUDY DESIGN We prospectively included all healthy breast-fed neonates referred to our Neonatology Unit between October 1999 and March 2000. All neonates with a weight loss > or = 10% of birth weight had a breast-feeding test and a determination of serum sodium, urea, and base excess. Student t test and chi-square test were used for statistical analysis of the data. RESULTS Of 686 neonates, 53 (7.7%) had a weight loss > or = 10% of the birth weight, and 19 also had hypernatremia. These 53 neonates had a significantly higher incidence of caesarean delivery and lower maternal education than neonates with a weight loss < 10%. CONCLUSION Our prospective study demonstrates that a weight loss > or = 10% during the first days of life is frequent. Daily weight evaluation, careful breast-feeding assessment, and early routine postpartum follow-up are effective methods to prevent hypernatremic dehydration and promote breast-feeding.
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Affiliation(s)
- R Manganaro
- Neonatology Unit of the University of Messina, 98100 Messina, Italy
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Spandorfer PR, Alessandrini E. Sugar and spice and everything nice. Pediatr Ann 2001; 30:603-6. [PMID: 11641852 DOI: 10.3928/0090-4481-20011001-09] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/20/2022]
Affiliation(s)
- P R Spandorfer
- Division of Emergency Medicine, Department of Pediatrics, Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
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19
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Abstract
As part of a population based regional review of all neonatal readmissions, the incidence of dehydration with hypernatraemia in exclusively breast fed infants was estimated. All readmissions to hospital in the first month of life during 1998 from a population of 32 015 live births were reviewed. Eight of 907 readmissions met the case definition, giving an incidence of at least 2.5 per 10 000 live births. Serum sodium at readmission varied from 150 to 175 mmol/l. One infant had convulsions. The sole explanation for hypernatraemia was unsuccessful breast feeding in all cases. The eight cases are compared with the 65 cases published in the literature since 1979. Presentation, incidence, risk factors, pathophysiology, treatment, and prevention are discussed.
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Affiliation(s)
- S Oddie
- Neonatal Unit, Royal Victoria Infirmary, Newcastle-upon-Tyne NE1 4LP, UK.
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20
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Abstract
Breast milk is acknowledged as the best source of nutrition for neonates. We present the case of a full-term newborn who was fed solely breast milk and developed severe dehydration and hypernatremia. The patient developed cerebral edema, transverse sinus thrombosis, and died. The literature on the uncommon entity of breast-feeding hypernatremia and dehydration is reviewed, and management strategies are presented.
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Affiliation(s)
- R H van Amerongen
- Department of Emergency Medicine, New York Methodist Hospital, Brooklyn 11215, USA.
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Abstract
Although the risk factors for stroke in children are numerous and differ greatly from the causes of stroke in adults, a thorough diagnostic evaluation can identify one or more risk factors in most patients. Cardiac disorders and hemoglobinopathy are the most common causes of ischemic infarction, whereas various congenital anomalies of the blood vessels or defects in coagulation or platelet function are often found in children with intraparenchymal hemorrhage. More than one risk factor is commonly identified, especially in children with dural venous thrombosis. Identification of the underlying risk factors for cerebrovascular disorders in children is important because many of the risk factors can be treated, reducing the risk of subsequent strokes.
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Affiliation(s)
- E S Roach
- Department of Neurology, University of Texas, Southwestern Medical School, Dallas 75235, USA
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Abstract
A 7-month-old infant presented to the emergency department with diarrhea, vomiting, and decreased activity. The infant was febrile, tachycardic, tachypneic, lethargic, and had a prolonged capillary refill. Initial serum sodium was 197 mmol/L. Ultimately, the infant was diagnosed with central diabetes insipidus complicated by severe dehydration secondary to rotavirus infection. A brief review of infant hypernatremia and its evaluation and treatment in the emergency department follows.
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Affiliation(s)
- T G Price
- Department of Emergency Medicine, University of Louisville, School of Medicine, Louisville, KY 40292, USA
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23
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Abstract
OBJECTIVES Past studies have revealed that hypernatremia occurs primarily in infants with diarrheal dehydration. With improved infant feeding practices and the advent of pediatric critical care medicine, the pattern of hypernatremia in children has likely changed. The purpose of this study was to evaluate the current pattern of hypernatremia in hospitalized children. METHODS Medical records were reviewed for 68 patients admitted to a large urban children's hospital during a 3-year period, all with a serum sodium greater than 150 mEq/L. The etiologies, predisposing factors, and morbidity and mortality associated with hypernatremia were evaluated. RESULTS The average patient age was 3.9 years (range, 1 day to 19. 7 years), and the peak serum sodium concentration was 159 mEq/L (range, 151-184 mEq/L). Hypernatremia was hospital acquired in 60% of children. The majority of children (71%) were admitted for reasons other than hypernatremia. In 76% of the patients, inadequate fluid intake was the main cause of hypernatremia. Gastroenteritis contributed to the hypernatremia in only 20% (14 out of 68) of children. Eleven of these were infants <1 year of age with hypernatremia on admission. Eighty-eight percent of patients (60 out of 68) suffered from neurologic impairment, critical illness, chronic disease, or prematurity before developing hypernatremia. The overall mortality was 16%. Patients in whom hypernatremia was not corrected had a significantly higher mortality than those in whom hypernatremia was corrected (4 out of 8 [50%] vs 7 out of 60 [12%]). Peak serum sodium was no different for survivors than nonsurvivors. No deaths were attributable to cerebral edema caused by correction of hypernatremia. Neurologic complications related to hypernatremia occurred in 15% of patients. CONCLUSIONS Hypernatremia occurs in children of all ages, with the vast majority having significant underlying medical problems. Hypernatremia caused by gastroenteritis in infants has become much less common than previously reported. Hypernatremia is primarily a hospital-acquired disease, produced by the failure to administer sufficient free water to patients unable to care for themselves. Failure to correct hypernatremia may result in a high mortality rate.
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Affiliation(s)
- M L Moritz
- Department of Pediatrics, Texas Children's Hospital, Baylor College of Medicine, Houston, Texas, USA.
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24
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Kirchlechner V, Koller DY, Seidl R, Waldhauser F. Treatment of nephrogenic diabetes insipidus with hydrochlorothiazide and amiloride. Arch Dis Child 1999; 80:548-52. [PMID: 10332005 PMCID: PMC1717946 DOI: 10.1136/adc.80.6.548] [Citation(s) in RCA: 58] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/16/2022]
Abstract
Nephrogenic diabetes insipidus (NDI) is characterised by the inability of the kidney to concentrate urine in response to arginine vasopressin. The consequences are severe polyuria and polydipsia, often associated with hypertonic dehydration. Intracerebral calcification, seizures, psychosomatic retardation, hydronephrosis, and hydroureters are its sequelae. In this study, four children with NDI were treated with 3 mg/kg/day hydrochlorothiazide and 0.3 mg/kg/day amiloride orally three times a day for up to five years. While undergoing treatment, none of the patients had signs of dehydration or electrolyte imbalance, all showed normal body growth, and there was no evidence of cerebral calcification or seizures. All but one had normal psychomotor development and normal sonography of the urinary tract. However, normal fluid balance was not attainable (fluid intake, 3.8-7.7 l/m2/day; urine output, 2.2-7.4 l/m2/day). The treatment was well tolerated and no side effects could be detected. Prolonged treatment with hydrochlorothiazide/amiloride appears to be more effective and better tolerated than just hydrochlorothiazide. Its efficacy appears to be similar to that of hydrochlorothiazide/indomethacin but without their severe side effects.
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Affiliation(s)
- V Kirchlechner
- Department of Pediatrics, University of Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria
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25
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Abstract
Disorders of serum sodium are both the most common and probably most the poorly understood electrolyte disorders in clinical medicine. In the past few years increased knowledge about the non-osmotic release of vasopressin and the cloning of vasopressin receptors and of vasopressin-regulated water channels (AQP2) has enhanced our understanding of these disorders. Also controversies surrounding the treatment of hyponatraemic patients have led to well-accepted therapeutic guidelines.
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Affiliation(s)
- S Kumar
- Department of Medicine, University of Colorado School of Medicine, Denver 80262, USA
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26
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Zaki M, Ismail EA, Nadi HM, Nour el Din A. Recurrent dehydration in a young girl. Postgrad Med J 1997; 73:367-9. [PMID: 9246346 PMCID: PMC2431327 DOI: 10.1136/pgmj.73.860.367] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/04/2023]
Affiliation(s)
- M Zaki
- Department of Paediatrics, Farwania Hospital, Kuwait
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27
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Abstract
OBJECTIVE To determine the aetiology, symptoms and outcome of extreme sodium derangement in a paediatric inpatient population. METHODOLOGY A retrospective study of children with extreme disturbance of their plasma sodium (> or = 165 mmol/L or < or = 115 mmol/L) admitted to a tertiary referral centre during a 72-month period. RESULTS Twenty-seven cases of hypernatraemia and 21 of hyponatraemia were reviewed. Sodium disturbance developed after hospital admission in 27/57 cases (57%). Gastroenteritis was the most common cause of hypernatraemia (8/27; 30%), four of 27 (15%) had iatrogenic hypernatraemia. Water overload accounted for 8/21 (38%) cases of hyponatraemia. Neurologic symptoms occurred in 19/24 (79%) with hypernatraemia and in 11/19 (58%) with hyponatraemia. Ten (37%) with hypernatraemia and four (19%) with hyponatraemia died. A deterioration in functional status was seen in two patients with hypernatraemia. There was no apparent deterioration in the survivors with hyponatraemia. CONCLUSION Extreme sodium disturbance often develops after admission to hospital and is caused by a variety of diseases and interventions. Neurologic symptoms are common and the mortality rate is high. The outcome in survivors is survivors is most likely to be dependent on the underlying disease process.
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Affiliation(s)
- K Dunn
- Intensive Care Unit, Royal Children's Hospital, Parkville, Victoria, Australia
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28
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Ayus JC, Armstrong DL, Arieff AI. Effects of hypernatraemia in the central nervous system and its therapy in rats and rabbits. J Physiol 1996; 492 ( Pt 1):243-55. [PMID: 8730599 PMCID: PMC1158877 DOI: 10.1113/jphysiol.1996.sp021305] [Citation(s) in RCA: 56] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/01/2023] Open
Abstract
1. We studied the effects of acute (1 or 4 h) and chronic (1 week) hypernatraemia (plasma [Na+], 170-190 mM) on brain histology, and brain water and solute contents in rats and rabbits. 2. In rabbits with acute hypernatraemia, there was significant loss of intracellular brain water, with increases in brain [Na+ + K+], amino acid concentration, and undetermined solute (idiogenic osmole). After 1 week of recovery, brain intracellular water content had returned to normal. 3. In hypernatraemic rats there was myelinolysis of brain white matter, with karyorrhexis and necrosis of neurons. 4. Hypernatraemic rabbits were treated with 77 mM NaCl (i.v.) to normalize plasma [Na+] over 4-24 h intervals. Therapy of either acute or chronic hypernatraemia resulted in significant brain oedema because brain osmolality failed to decrease at the same rate as plasma osmolality. 5. It is concluded that: (a) untreated hypernatraemia results in brain lesions demonstrating myelinolysis and cellular necrosis; (b) normalization of hypernatraemia over 4-24 h results in cerebral oedema, due primarily to failure of brain amino acids and idiogenic osmoles to dissipate as plasma [Na+] is decreased to normal.
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Affiliation(s)
- J C Ayus
- Department of Medicine, Baylor College of Medicine, Houston, TX 77024, USA
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29
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Hoekstra JA, van Lieburg AF, Monnens LA, Hulstijn-Dirkmaat GM, Knoers VV. Cognitive and psychosocial functioning of patients with congenital nephrogenic diabetes insipidus. AMERICAN JOURNAL OF MEDICAL GENETICS 1996; 61:81-8. [PMID: 8741926 DOI: 10.1002/(sici)1096-8628(19960102)61:1<81::aid-ajmg17>3.0.co;2-s] [Citation(s) in RCA: 55] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 02/01/2023]
Abstract
Mental retardation (MR) is generally considered one of the main complications of congenital nephrogenic diabetes insipidus (NDI). However, psychometric studies of NDI patients are scarce and outdated. In the present study, 17 male NDI patients underwent psychological evaluation. Total intelligence quotient of 14 patients was within (n = 13) or above (n = 1) the normal range, 1 patient had an intelligence score between -1 and -2 standard deviations (S.D.) and 2 young patients had a general cognitive index more than 2 S.D. below the norm. Attention deficit hyperactivity disorder criteria were met by 8 out of 17 patients and scores on short-term memory were low in 7 out of 10. No relation between test performances and age at diagnosis or hypernatremia could be found, with the exception of a negative correlation between age at start of therapy and verbal IQ in one age group. Although several explanations for an association between MR and NDI can be postulated, it seems that the current prevalence of MR among patients with this disease is considerably lower than suggested in literature.
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Affiliation(s)
- J A Hoekstra
- Department of Medical Psychology, University Hospital Nijmegen, Netherlands
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30
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Bagga A, Kumar A, Bajaj G, Gupta A, Srivastava RN. Intracranial calcification in nephrogenic diabetes insipidus. Clin Pediatr (Phila) 1996; 35:34-6. [PMID: 8825849 DOI: 10.1177/000992289603500107] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/02/2023]
Affiliation(s)
- A Bagga
- Department of Pediatrics and Radiodiagnosis, All India Institute of Medical Sciences, New Delhi
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31
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Affiliation(s)
- K H Molteni
- Department of Pediatrics, Medical College of Wisconsin, Milwaukee 53226-0509
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32
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Tohyama J, Inagaki M, Koeda T, Ohno K, Takeshita K. Intracranial calcification in siblings with nephrogenic diabetes insipidus: CT and MRI. Neuroradiology 1993; 35:553-5. [PMID: 8232891 DOI: 10.1007/bf00588723] [Citation(s) in RCA: 12] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/29/2023]
Abstract
Computed tomography and magnetic resonance imaging (MRI) were used to examine three male siblings with nephrogenic diabetes insipidus (NDI). The two elder brothers had varying degrees of unusual intracranial calcification; the eldest also showed involvement of the cerebral white matter on MRI. The severity of intracranial calcification was related to the time before initiation of treatment and inversely to mental ability. Brain damage and mental retardation in NDI may be caused by a delay in initiating treatment; early detection and treatment are important to prevent brain damage.
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Affiliation(s)
- J Tohyama
- Division of Child Neurology, Faculty of Medicine, Tottori University, Yonago, Japan
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33
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Nozue T, Uemasu F, Endoh H, Sako A, Takagi Y, Kobayashi A. Intracranial calcifications associated with nephrogenic diabetes insipidus. Pediatr Nephrol 1993; 7:74-6. [PMID: 8439485 DOI: 10.1007/bf00861577] [Citation(s) in RCA: 14] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/30/2023]
Abstract
A 6-year-old boy with nephrogenic diabetes insipidus (NDI) and intracranial calcification is reported. The calcifications were symmetrical and located in the basal ganglia and in the subcortical regions of the frontal, temporal, parietal and occipital lobes. Episodes of hyperosmolality during infancy are considered to be one of the causes of intracranial calcification in NDI. However, other unknown factors may be involved, because up to now there have been no reports of intracranial calcification in patients with central diabetes insipidus.
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Affiliation(s)
- T Nozue
- Department of Paediatrics, Showa University, Toyosu Hospital, Tokyo, Japan
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34
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Knoers N, Monnens LA. Nephrogenic diabetes insipidus: clinical symptoms, pathogenesis, genetics and treatment. Pediatr Nephrol 1992; 6:476-82. [PMID: 1457333 DOI: 10.1007/bf00874020] [Citation(s) in RCA: 55] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/27/2022]
Abstract
This review summarizes various aspects of the inherited kidney disorder nephrogenic diabetes insipidus (NDI). The clinical manifestations of the disease are presented. The important role of the genetic localization of the NDI gene to the X-chromosome long arm, in region Xq28, for carrier detection and early (prenatal) diagnosis of the disorder is emphasized. Following an overview of the cellular physiology involved in the antidiuretic action of vasopressin, possible mechanisms in the pathogenesis of NDI are discussed. We hypothesize that NDI is most probably due to the absence or abnormality of the renal V2 receptor. This assumption is strengthened by recent findings in receptor studies, which indicate a general V2 receptor defect in NDI, and in experiments with somatic cell hybrid cell lines, which are consistent with a co-localization of the genes for NDI and for the V2 receptor in the Xq28 region. Finally, the efficacy of the combination amiloride-hydrochlorothiazide, compared with the indomethacin-hydrochlorothiazide regimen, in the treatment of NDI is presented and the advantages of the former combination are discussed.
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Affiliation(s)
- N Knoers
- Department of Human Genetics, University of Nijmegen, The Netherlands
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35
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Kovacs L, Robertson GL. Disorders of water balance--hyponatraemia and hypernatraemia. BAILLIERE'S CLINICAL ENDOCRINOLOGY AND METABOLISM 1992; 6:107-27. [PMID: 1739390 DOI: 10.1016/s0950-351x(05)80334-9] [Citation(s) in RCA: 23] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/28/2022]
Abstract
Plasma sodium concentration depends on water balance, and is normally maintained in a narrow range by an integrated system involving the precise regulation of water intake via thirst mechanism and control of water output via vasopressin secretion. Anything that interferes with the full expression of either osmoregulatory function exposes the patient to the hazards of abnormal decreases or increases in plasma sodium level. Hyponatraemia is almost always due to a defect in water excretion. Increased intake may contribute to the problem but is rarely, if ever, a sufficient cause. Hypernatraemia is almost always due to deficient water intake; excessive water losses may contribute to the problem, but they are never a sufficient cause. The most dangerous and usually the most blatant clinical effects of the disturbed water balance are those involving the central nervous system. Complex adaptive mechanisms have been developed to mitigate the impact of both hypo- and hypernatraemia on brain cells. However, the same protective changes render the brain more susceptible to severe neuropathology that may arise from inappropriate treatment of these disorders.
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36
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Abstract
Hypernatremia results when the water content of body fluids is deficient compared with sodium content. Hypernatremia can be the result of pure sodium excess but is usually associated with dehydration, secondary to excess losses of water or hypotonic fluids. Hypernatremic dehydration is less common than hyponatremic or isonatremic dehydration, but is associated with the highest morbidity and mortality rate, primarily related to CNS dysfunction. Except when hypernatremia has developed rapidly, the serum sodium concentration should be corrected slowly with frequent monitoring of serum electrolytes. Even then CNS damage can result, either as a consequence of the hypernatremia itself or of rapid lowering of the serum sodium concentration.
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Affiliation(s)
- S B Conley
- Division of Pediatric Nephrology, University of Texas Medical School, Houston
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37
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Votey SR, Peters AL, Hoffman JR. Disorders of Water Metabolism: Hyponatremia and Hypernatremia. Emerg Med Clin North Am 1989. [DOI: 10.1016/s0733-8627(20)30315-1] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/16/2023]
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38
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Abstract
A 2 1/2-month-old patient is reported with computed tomographic evidence of bilateral choroid plexus hemorrhage associated with hypernatremic dehydration. Choroid plexus hemorrhage may have caused increased cerebrospinal fluid protein observed in hypernatremic dehydration, as well as intraventricular hemorrhage.
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Affiliation(s)
- P D Larsen
- Department of Neurology, Scott and White Memorial Hospital, Temple, Texas 76508
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39
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Murtaza A, Zulfiqar I, Khan SR, Lindblad BS, Aperia A. Regulation of serum sodium in dehydrated and orally rehydrated infants. Influence of age and of purging rates. ACTA PAEDIATRICA SCANDINAVICA 1987; 76:424-30. [PMID: 3604661 DOI: 10.1111/j.1651-2227.1987.tb10493.x] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/06/2023]
Abstract
We have examined the control of serum sodium concentration (S-Na) in 60 male infants with acute diarrheal disease, moderate dehydration, but without the presence of fever, vomiting or other conditions. The infants were studied on admission and during oral rehydration therapy (ORT). We examined the effect of rapid reduction of the purging rate on the control of S-Na by adding pulverized rice and pulses (dal moong) to the rehydration solution. On admission S-Na was significantly inversely related to age. This correlation could not only be attributed to difference in stool sodium losses. Changes in S-Na and urinary K/Na ratio during oral rehydration therapy (ORT), were analyzed separately in infants below and above 4 month of age. During the first six hours of ORT, there was an increase in S-Na in all groups. During the following 18 hours, S-Na tended to normalize around 138 mmol/l. Normalization occurred faster if purging rate was reduced. In all groups urinary K/Na ratio (index of aldosterone production and, inversely, of sodium balance), was high at admission and fell during ORT. In the youngest infants (below 4 month of age) the fall was significantly more pronounced if the purging was reduced. We conclude that it is important to consider age when prescribing ORT. The capacity to correct disturbances in S-Na becomes more efficient during maintenance stage of ORT. Correction of S-Na and sodium balance is enhanced by rapid reduction of abnormal intestinal losses.
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40
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41
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Hogan GR, Pickering LK, Dodge PR, Shepard JB, Master S. Incidence of seizures that follow rehydration of hypernatremic rabbits with intravenous glucose or fructose solutions. Exp Neurol 1985; 87:249-59. [PMID: 3967710 DOI: 10.1016/0014-4886(85)90215-8] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/08/2023]
Abstract
Hypernatremic dehydration was induced in rabbits during a 3- to 5-day period resulting in mean plasma sodium concentrations of 187 meq/liter. The animals were then rehydrated during a 4-h period by intravenous administration of a 2.5% glucose or fructose solution. The water content of four regions of brain sample showed a significant (P less than 0.05) increase in brain water content above normal in the rehydrated groups. Brain water content was significantly (P less than 0.01) greater in those animals with seizures compared with those without seizures, suggesting the importance of water intoxication in the pathogenesis of seizure activity. Changes in muscle Na, K, Cl, and water content were not similar to those of brain, indicating that muscle content of these substances was not an accurate reflection of the brain content specific time. The incidence of seizures was significantly (P less than 0.05) greater when glucose solution was used for rehydration (49%) compared with the use of fructose solution (25%). The mechanism(s) by which fructose resulted in a lower incidence of seizures is not known. The frequency of seizure activity was directly proportional to the rate of administration of intravenous solutions utilized to correct hypernatremia. In addition, the specific carbohydrate of the solution appeared to play an important role in the pathophysiology of the development of seizures.
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42
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Arieff AI. Central nervous system manifestations of disordered sodium metabolism. CLINICS IN ENDOCRINOLOGY AND METABOLISM 1984; 13:269-94. [PMID: 6488574 DOI: 10.1016/s0300-595x(84)80022-5] [Citation(s) in RCA: 66] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/20/2023]
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43
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Abstract
Of 1045 children admitted with gastroenteritis over a 12-month period and studied retrospectively, serum sodium level was tested in 802. Sixty patients (7.5%) had hypernatremic dehydration (HD). The peak incidence of HD, the highest serum sodium levels, and the worst outcome were all encountered in infants under the age of 3 months. An association with pre-admission high solute feeding was less obvious. Pre-admission volume intake could not be evaluated. There was no association of HD with the etiological pathogen or climatic conditions. The weight-for-age was below the fifth percentile in 21 patients (35%). One patient (1.7%) died, another (1.7%) developed peripheral gangrene, and four (6.7%) were left with significant neurologic complications. All of these patients were under the age of 4 months. In this subtropical country, the most important risk factor for the development of hypernatremia in the course of gastroenteritis is the young age. Environmental risk factors do not seem to play a significant role.
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44
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Puczynski MS, Cunningham DG, Mortimer JC. Sodium intoxication caused by use of baking soda as a home remedy. CANADIAN MEDICAL ASSOCIATION JOURNAL 1983; 128:821-2. [PMID: 6299494 PMCID: PMC1875065] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [MESH Headings] [Subscribe] [Scholar Register] [Indexed: 01/19/2023]
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45
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Aperia A, Broberger O, Zetterström R. Implications of limitation of renal function for the nutrition of low birthweight infants. ACTA PAEDIATRICA SCANDINAVICA. SUPPLEMENT 1982; 296:49-52. [PMID: 6961742 DOI: 10.1111/j.1651-2227.1982.tb09595.x] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/22/2023]
Abstract
Renal function is immature in low-birth-weight infants. The glomerular filtration rate is low during the entire first month of life. It is 20-50% of that observed in older children and adults. This limits the excretory capacity of the kidney and might set an upper limit for the protein intake. The capacity to reabsorb bicarbonate is not fully developed. This predisposes the low-birth-weight infant to metabolic acidosis. The capacities to excrete sodium when in positive sodium balance and to retain sodium when in negative sodium balance are limited. If the daily sodium balance is not well monitored, conditions of negative sodium balance with hyponatremia as well as of positive sodium balance with hypernatremia might occur.
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46
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Jaffe KM, Kraemer MJ, Robison MC. Hypernatremia in breast-fed newborns. West J Med 1981; 135:54-5. [PMID: 7257379 PMCID: PMC1272923] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [MESH Headings] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/24/2023]
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47
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Abstract
Ninety infants with severe hypernatraemic dehydration (plasma sodium greater than 150 mmol/l) were studied. Most had had a convulsion before admission. They were allocated to two treatment groups. Both groups received intravenous plasma followed by slow intravenous rehydration and correction of acidosis. In addition, one group received intramuscular phenobarbitone, the other group received dexamethasone 0.3 mg by intramuscular injection every 6 hours for 48 hours. Fewer infants receiving dexamethasone had convulsions during treatment (18% compared with 52%), and fewer (18%) of them died than in the group who did not receive dexamethasone (40%). Dexamethasone may have a role in the management of hypernatraemic dehydration in infants.
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48
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Thurston JH, Hauhart RE, Dirgo JA. Taurine: a role in osmotic regulation of mammalian brain and possible clinical significance. Life Sci 1980; 26:1561-8. [PMID: 7382728 DOI: 10.1016/0024-3205(80)90358-6] [Citation(s) in RCA: 149] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/25/2023]
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49
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Mason JK, Harkness RA, Elton RA, Bartholomew S. Cot deaths in Edinburgh: infant feeding and socioeconomic factors. J Epidemiol Community Health 1980; 34:35-41. [PMID: 7189206 PMCID: PMC1052037 DOI: 10.1136/jech.34.1.35] [Citation(s) in RCA: 21] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/23/2023]
Abstract
One hundred and twenty-six consecutive cases of sudden infant death syndrome (SIDS) in the Edinburgh area have been studied with particular reference to the interrelationship of feeding, associated biochemical changes, and social status. There was an excess of cases born to parents in Social Classes IV and V: the effect was maximal in children who dies beyond 12 weeks of age. A low-grade uraemia was discovered in approximately one-fifth of the cases; analysis showed this to be related most strongly to bottle-feeding. Feeding habits were found to be associated with social class and this accounted for the relationship between bottle-feeding and the youth of mothers and also for an apparent relationship between uraemia in the infant and social class of the mother. Mothers of SIDS children were younger than expected and SIDS was found to be electrolyte imbalance is common in SIDS cases, nor did the findings support the suggestion that cross-infection due to overcrowding is an important aetiological factor. The significant factors of young motherhood, low social status, bottle-feeding, and mild uraemia in the babies are interrelated and seem to focus attention on unwitting 'mothering problems'. It is, however, not easy to see how this, or any other hypothesis, can account for all cases of SIDS.
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50
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Weitzman RE, Kleeman CR. The clinical physiology of water metabolism. Part III: The water depletion (hyperosmolar) and water excess (hyposmolar) syndromes. West J Med 1980; 132:16-38. [PMID: 6246683 PMCID: PMC1271937] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/19/2023]
Abstract
Hyperosmolality occurs when there are defects in the two major homeostatic mechanisms required for water balance-thirst and arginine vasopressin (AVP) release. In this situation hypotonic fluids are lost in substantial quantities causing depletion of both intracellular and extracellular fluid compartments. Patients with essential hypernatremia have defective osmotically stimulated AVP release and thirst but may have intact mechanisms for AVP release following hypovolemia. Hyperosmolality can also be seen in circumstances in which impermeable solutes are present in excessive quantities in extracellular fluid. Under these conditions there is cellular dehydration and the serum sodium may actually be reduced by water drawn out of cells along an osmotic gradient. Hyposmolality and hyponatremia may be seen in a variety of clinical conditions. Salt depletion, states in which edema occurs and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) may all produce severe dilution of body fluids resulting in serious neurologic disturbances. The differential diagnosis of these states is greatly facilitated by careful clinical assessment of extracellular fluid volume and by determination of urine sodium concentration. Treatment of the hyposmolar syndromes is contingent on the pathophysiology of the underlying disorder; hyponatremia due to salt depletion is treated with infusions of isotonic saline whereas mild hyponatremia in cirrhosis and ascites is best treated with water restriction. Severe symptomatic hyponatremia due to SIADH is treated with hypertonic saline therapy, sometimes in association with intravenous administration of furosemide. Less severe, chronic cases may be treated with dichlormethyltetracycline which blocks the action of AVP on the collecting duct.
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