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Hyponatremia
Selected AbstractsHyponatremia and Heart Failure,Treatment ConsiderationsCONGESTIVE HEART FAILURE, Issue 1 2006Domenic A. Sica MD Hyponatremia as it occurs in the heart failure patient is a multifactorial process. The presence of hyponatremia in the heart failure patient correlates with both the severity of the disease and its ultimate outcome. The therapeutic approach to the treatment of hyponatremia in heart failure has traditionally relied on attempts to improve cardiac function while at the same time limiting fluid intake. In more select circumstances, hypertonic saline, loop diuretics, and/or lithium or demeclocycline have been used. The latter two compounds act by retarding the antidiuretic effect of vasopressin but carry with their use the risk of serious renal and/or cardiovascular side effects. Alternatively, agents that selectively block the type 2 vasopressin receptor increase free water excretion without any of the adverse consequences of other therapies. Conivaptan, lixivaptan, and tolvaptan are three such aquaretic drugs. Vasopressin receptor antagonists will redefine the treatment of heart failure-related hyponatremia and may possibly evolve as adjunct therapies to loop diuretics in diuretic-resistant patients. [source] Carbamazepine-Related Hyponatremia Following Cardiopulmonary BypassJOURNAL OF CARDIAC SURGERY, Issue 2 2003Theodore Velissaris A.F.R.C.S. Following an initially uncomplicated recovery, he developed symptomatic hyponatremia. The symptoms and biochemical abnormality improved after gradual discontinuation of carbamazepine. We discuss the association between carbamazepine and hyponatremia and the causes of hyponatremia after cardiopulmonary bypass. Surgeons should consider stopping carbamazepine before operations with cardiopulmonary bypass. (J Card Surg 2003;18:155-157) [source] Well Tolerated Spironolactone-Related HyponatremiaJOURNAL OF CLINICAL HYPERTENSION, Issue 4 2008Joel Handler MD First page of article [source] Oxytocin infusion: acute hyponatraemia, seizures and comaACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 6 2009D. BERGUM Hyponatremia is not uncommon, serious cases can cause dangerous complications as seizures, brain damage and even death. We present a case of a young mother with post partum hemorrhage and some of the serious complications. [source] Pathological Role of Aquaporin-2 in Impaired Water Excretion and HyponatremiaJOURNAL OF NEUROENDOCRINOLOGY, Issue 4 2004S. Ishikawa Abstract In the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), inappropriately elevated secretion of vasopressin can result in a reduction of antidiuretic efficacy: a phenomenon known as ,vasopressin escape'. We compared experimental SIADH with 1-deamino-8- d -arginine vasopressin (dDAVP)-excess rats, where both groups received continuous subcutaneous administration of dDAVP by osmotic minipump but the SIADH rats also received a liquid diet that induced hyponatraemia. The SIADH rats, but not the dDAVP excess rats, showed a marked attenuation of urinary concentrating ability. Vasopressin V2 receptor binding capacity and mRNA expression were similar between the two groups, but the SIADH rats showed a diminished up-regulation of aquaporin-2 (AQP-2) mRNA and protein expression. These findings indicate the presence of tonicity-response regions in the AQP-2 promoter gene, and that either hypervolemia or hypotonicity may attenuate the postreceptor signalling of vasopressin in renal collecting duct cells in SIADH rats. [source] Current issues for nurse practitioners: HyponatremiaJOURNAL OF THE AMERICAN ACADEMY OF NURSE PRACTITIONERS, Issue 11 2007Ruth Haskal NP-C (Adult Nurse Practitioner) Abstract Purpose: To review the assessment, diagnosis, and management of hyponatremia (serum sodium <135 mEq/L), the most common electrolyte disturbance as a result of dysregulation of water balance in hospitalized or institutionalized patients. Data sources: Comprehensive search using keywords AVP receptor antagonists, hyponatremia, SIADH, conivaptan, tolvaptan, lixivaptan, nurse practitioner, and others was carried out using the National Library of Medicine (PubMed) Web site from which full-text articles were obtained. Meeting abstracts were obtained from scientific sessions including the American Society of Nephrology Renal Week 2004 and the Endocrine Society,s 87th Annual Meeting (2005). The Vaprisol (conivaptan hydrochloride injection) package insert was referenced and obtained from FDA.gov. Conclusions: A diagnosis of hyponatremia requires thorough investigation for underlying causes and prompt treatment to prevent poor patient outcomes. In clinical trials, a new class of drugs called the arginine vasopressin (AVP) receptor antagonists or aquaretics has been shown to be safe and effective for the treatment of hyponatremia. Among this class of agents, intravenous conivaptan hydrochloride, indicated for the treatment of euvolemic hyponatremia in hospitalized patients, is the first drug in class approved for use. Implications for practice: Elderly patients, and those with certain conditions such as heart failure, tuberculosis, cirrhosis, and head injury, may be at increased risk for hyponatremia. In hospitalized patients following surgery and the use of certain medications, hyponatremia is a common condition. A thorough understanding of the physiology of water balance and the risk factors associated with hyponatremia is essential for prompt and effective intervention. Awareness of the limitations of conventional therapies and the availability of new treatment options for hyponatremia allows clinicians to optimize patient care. [source] Desmopressin treatment in nocturia; an analysis of risk factors for hyponatremiaNEUROUROLOGY AND URODYNAMICS, Issue 2 2006A. Rembratt Abstract Aims To explore the incidence, severity, time course, and risk factors of clinically significant hyponatremia in desmopressin treatment for nocturia. Methods Data from three multi-center phase III trials were pooled. Hyponatremia was categorised as borderline (134,130 mmol/L) or significant (<130 mmol/L). Risk factors were explored with logistic regression and subgroup analysis performed to explore threshold values for contra-indication. Results In total 632 patients (344 men, 288 women) were analyzed. During dose-titration, serum sodium concentration below normal range was recorded in 95 patients (15%) and 31 patients (4.9%) experienced significant hyponatremia. The risk increased with age, lower serum sodium concentration at baseline, higher basal 24-hr urine volume per bodyweight and weight gain at time of minimum serum sodium concentration. Age was the best single predictor. Elderly patients (,65 years of age) with a baseline serum sodium concentration below normal range were at high risk (75%). Limiting treatment in elderly with normal basal serum sodium concentration to those below 79 years and with a 24-hr urine output below 28 ml/kg would reduce the risk from 8.1% to 3.0% at the cost of 34% fulfilling the contra-indication. Conclusions The majority of nocturia patients tolerate desmopressin treatment without clinically significant hyponatremia. However, the risk increases with increasing age and decreasing baseline serum sodium concentration. Treatment of nocturia in elderly patients with desmopressin should only be undertaken together with careful monitoring of the serum sodium concentration. Patients with a baseline serum sodium concentration below normal range should not be treated. © 2005 Wiley-Liss, Inc. [source] Concomitant-Acquired Long QT and Brugada Syndromes Associated with Indapamide-Induced Hypokalemia and HyponatremiaPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2008NGAI-SHING MOK M.B.B.S. Electrolyte disturbances are known to cause acquired Long QT syndrome (LQTS) and Brugada syndrome. While a reduction in INa due to SCN5A mutation is implicated as the underlying mechanism in Brugada syndrome, hyponatremia, which can give rise to a reduced INa, has never been reported in literature as a cause or precipitating factor in this syndrome. We detailed a case in which concomitant-acquired LQTS and Brugada syndrome were associated with severe hypokalemia and hyponatremia following indapamide use for treatment of hypertension and highlighted the potential role of hyponatremia in the pathogenesis of the acquired form of Brugada syndrome. [source] Intraoperative hyponatremia during craniofacial surgeryPEDIATRIC ANESTHESIA, Issue 4 2009K. RANDO MD Summary Background:, Hyponatremia is an important cause of morbidity in some groups of hospitalized children. Our aim is to describe the incidence and severity of intraoperative hyponatremia in children undergoing craniofacial surgery, and determine the associated risk factors. Methods:, A descriptive retrospective study of children who underwent primary craniofacial surgery between March 1994 and February 2008 was performed. All administered fluids contained a minimum sodium concentration of 140 mmol·l,1. Hyponatremia was classified as follows: severe ,125 mmol·l,1; moderate 126,130 mmol·l,1; and, mild 131,134 mmol·l,1. Results:, Hundred and seven cases are reported. Severe, moderate and mild intraoperative hyponatremia occurred in 14 (13%), 21 (19%) and 23 (22%) children respectively. Mannitol was given to 31 (29%) children, but was not associated with the development of hyponatremia. Neither the type nor duration of surgery, type of fluid replacement nor hourly urinary output, was associated with development of hyponatremia. Most episodes of significant intraoperative hyponatremia (44%) were detected between the 2nd and the 4th hour of surgery. There were no identified neurological sequelae (e.g. coma, neurological deficit) attributable to the hyponatremia. Conclusion:, Despite strict avoidance of low sodium solutions (<140 mmol·l,1), hyponatremia occurs frequently in children undergoing craniofacial surgery in our practice; and is unrelated to the administration of mannitol. Although the mechanisms are yet to be determined, anesthesiologists should be aware of this issue and be prepared to monitor and treat this potentially serious complication. [source] Effects of polydipsia,hyponatremia on seizures in patients with epilepsyPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 3 2007MITSUTOSHI OKAZAKI md Abstract Aggravation of seizures due to hyponatremia was investigated in five patients with epilepsy and polydipsia,hyponatremia. They experienced marked increases in the frequency of their complex partial seizures with a decrease in the serum sodium level to 118,127 mEq/L. In all cases, the serum sodium level returned to normal through restriction of fluids, and the clinical seizures improved. All patients had shown intellectual impairment and/or psychotic episodes, and all had been given antipsychotics. Hyponatremia caused by polydipsia appears to be a risk factor for aggravation of habitual seizures in patients with epilepsy. [source] Hyponatremia in Heart Failure: Revisiting Pathophysiology and Therapeutic StrategiesCLINICAL CARDIOLOGY, Issue 6 2010Amir Kazory MD Hyponatremia is frequently encountered in patients with heart failure (HF), and its association with adverse outcomes is well-established in this population. While hyponatremia is an independent marker for severity of HF, it is not certain whether it has a causal impact on the progression of the disease. There are no universally accepted consensus guidelines regarding therapeutic strategies for HF-associated hyponatremia and volume overload; current societal guidelines do not address management of this complication. Whereas thiazide diuretics are known to induce or worsen hyponatremia in this setting through a number of mechanisms, loop diuretics can be considered a readily available first-line pharmacologic therapy. Consistent with pathophysiology of the disease and mechanisms of action of loop diuretics, available clinical evidence supports such an approach provided that patients can be closely monitored. Use of vasopressin receptor antagonists is an emerging therapeutic strategy in this setting, and the efficacy of these agents has so far been shown in a number of clinical studies. These agents can be reserved for patients with HF in whom initial appropriate loop diuretic therapy fails to improve serum sodium levels. Copyright © 2010 Wiley Periodicals, Inc. [source] Hyponatremia and Vasopressin Antagonism in Congestive Heart FailureCLINICAL CARDIOLOGY, Issue 11 2007Siva Kumar M.D Abstract In a national heart failure registry, hyponatremia (serum sodium < 130 mEq/L) was initially reported in 5% of patients and considered a risk factor for increased morbidity and mortality. In a chronic heart failure study, serum sodium level on admission predicted an increased length of stay for cardiovascular causes and increased mortality within 60 days of discharge. Hyponatremia in patients with congestive heart failure (CHF) is associated with a higher mortality rate. Also, by monitoring and increasing serum sodium levels during hospitalization for CHF, patient outcomes may improve. This review describes the pathophysiology of hyponatremia in relation to CHF, including the mechanism of action of vasopressin receptors in the kidney, and assesses the preclinical and clinical trials of vasopressin receptor antagonists,agents recently developed to treat hyponatremia. In hospitalized patients with CHF, hyponatremia plays a major role in poor outcomes. Vasopressin receptor antagonists have been shown to be safe and effective in clinical trials in patients with hyponatremia. Copyright © 2007 Wiley Periodicals, Inc. [source] Hyponatremia and Heart Failure,Treatment ConsiderationsCONGESTIVE HEART FAILURE, Issue 1 2006Domenic A. Sica MD Hyponatremia as it occurs in the heart failure patient is a multifactorial process. The presence of hyponatremia in the heart failure patient correlates with both the severity of the disease and its ultimate outcome. The therapeutic approach to the treatment of hyponatremia in heart failure has traditionally relied on attempts to improve cardiac function while at the same time limiting fluid intake. In more select circumstances, hypertonic saline, loop diuretics, and/or lithium or demeclocycline have been used. The latter two compounds act by retarding the antidiuretic effect of vasopressin but carry with their use the risk of serious renal and/or cardiovascular side effects. Alternatively, agents that selectively block the type 2 vasopressin receptor increase free water excretion without any of the adverse consequences of other therapies. Conivaptan, lixivaptan, and tolvaptan are three such aquaretic drugs. Vasopressin receptor antagonists will redefine the treatment of heart failure-related hyponatremia and may possibly evolve as adjunct therapies to loop diuretics in diuretic-resistant patients. [source] Review article: Hypertonic saline use in the emergency departmentEMERGENCY MEDICINE AUSTRALASIA, Issue 4 2008Colin J Banks Abstract Hypertonic saline (HS) is being increasingly used for the management of a variety of conditions, most notably raised intracranial pressure. This article reviews the available evidence on HS solutions as they relate to emergency medicine, and develops a set of recommendations for its use. To conclude, HS is recommended as an alternative to mannitol for treating raised intracranial pressure in traumatic brain injury. HS is also recommended for treating severe and symptomatic hyponatremia, and is worth considering for both recalcitrant tricyclic antidepressant toxicity and for cerebral oedema complicating paediatric diabetic ketoacidosis. HS is not recommended for hypovolaemic resuscitation. [source] Alterations in electrolyte equilibrium in patients with acute leukemiaEUROPEAN JOURNAL OF HAEMATOLOGY, Issue 6 2005Theodosios D. Filippatos Abstract:,Background and aim:,A wide array of disturbances in electrolyte equilibrium is commonly seen in patients with acute leukemia (AL). These abnormalities present a potential hazard in these patients, as that of enhancing the cardiotoxic effects of certain chemotherapeutic regimens. The literature dealing with AL-related electrolyte abnormalities and their interactions in leukemic patients was reviewed. Data synthesis:,Sources included MEDLINE and EMBASE. The search strategy was based on the combination of ,acute leukemia', ,electrolyte abnormalities', ,acid-base disorders', ,potassium', ,sodium', ,magnesium', ,calcium', and ,phosphorus'. References of retrieved articles were also screened. A decrease in serum potassium, mainly owing to lysozyme-induced tubular damage, appears to be one of the most frequent and potentially hazardous abnormalities. Other clinically significant metabolic perturbations include hyponatremia and hypercalcemia. Conclusion:,A broad spectrum of electrolyte abnormalities is encountered in the clinical setting of AL, which are related to the disease process per se and/or to the therapeutic interventions. Clinicians should be vigilant for early detection and appropriate management of these disorders before the initiation of chemotherapy regimens as well as during treatment. [source] Ammonia impairs neutrophil phagocytic function in liver disease,HEPATOLOGY, Issue 4 2008Debbie L. Shawcross Hyperammonemia is a feature of liver failure, which is associated with increased risk of infection. The aims of the present study were to determine in vitro, in rats fed an ammoniagenic diet and in patients with cirrhosis, whether induction of hyperammonemia results in neutrophil dysfunction. As hyperammonemia produces cell swelling, we explored the role of the osmoregulating, p38 mitogen-activated protein kinase (p38MAPK) pathway in mediating this neutrophil dysfunction. Neutrophils were isolated from blood of healthy volunteers and incubated with either 75 ,M ammonia or phosphate-buffered saline. Both groups were studied under hyponatremic conditions and/or with the addition of p38MAPK modulators. Neutrophil phagocytosis was measured in naive rats and rats fed an ammoniagenic diet and in patients with stable cirrhosis given placebo (n = 8) or an amino acid solution inducing hyperammonemia (n = 8). Cell volume and phagocytosis was analyzed by fluorescent-activated cell sorting using fluorescein isothiocyanate,labeled E. coli. p38MAPK phosphorylation was measured by western blotting. In healthy neutrophils incubated with ammonia and in rats fed an ammoniagenic diet, neutrophils showed evidence of swelling, impaired phagocytosis, and increased spontaneous oxidative burst compared to controls. Phagocytosis was significantly impaired in patients with induced hyperammonemia compared to placebo. The effects of hyperammonemia and hyponatremia were synergistic. The p38MAPK intracellular signaling pathways were activated in healthy neutrophils exposed to ammonia in association with increased burst activity. Neutrophil phagocytic dysfunction was abrogated by the addition of a p38MAPK agonist. Conclusion: Ammonia produces neutrophil swelling and impairs neutrophil phagocytosis. The p38MAPK intracellular signaling pathway has been shown to be important in mediating the ammonia-induced neutrophil dysfunction. (HEPATOLOGY 2008.) [source] Treatment for cirrhosis-associated hyponatremia?HEPATOLOGY, Issue 4 2007Vaptans, aquaresis No abstract is available for this article. [source] Aquaporin-1 and aquaporin-2 urinary excretion in cirrhosis: Relationship with ascites and hepatorenal syndrome,HEPATOLOGY, Issue 6 2006Christina Esteva-Font Several experimental models of cirrhosis have shown dysregulation of renal aquaporins in different phases of liver disease. We investigated the urinary excretion of both aquaporin-1 and aquaporin-2 in patients with cirrhosis at different stages of the disease. Twenty-four-hour urine was collected from 11 healthy volunteers, 13 patients with compensated cirrhosis (without ascites), and 20 patients with decompensated cirrhosis (11 with ascites without renal failure and 9 with hepatorenal syndrome). Aquaporin-1 and aquaporin-2 excretion was analyzed by immunoblotting. Urinary aquaporin-2 excretion was reduced in patients with cirrhosis compared to healthy subjects. A progressive decrease in urinary aquaporin-2 excretion was observed as the severity of cirrhosis increased, from compensated cirrhosis to cirrhosis with ascites and hepatorenal syndrome. Patients with hyponatremia had lower urinary aquaporin-2 excretion than patients without hyponatremia. Vasopressin plasma level did not correlate with aquaporin-2 excretion. There were no differences between healthy subjects and patients with cirrhosis with or without ascites in urinary excretion of aquaporin-1, but urinary aquaporin-1 excretion of those with hepatorenal syndrome was extremely low. In conclusion, patients with cirrhosis appear to exhibit a decreased abundance of renal aquaporin-2 and therefore lower water permeability in the collecting tubules. This may represent an adaptive renal response to sodium retention, with expansion of extracellular fluid volume and dilutional hyponatremia observed in those who have cirrhosis with ascites. Finally, aquaporin-1 does not appear to play a role in the progressive dysregulation of extracellular fluid volume in cirrhosis. (HEPATOLOGY 2006;44:1555,1563.) [source] Cytochrome P450 2D6 genotype does not predict SSRI (fluoxetine or paroxetine) induced hyponatraemiaHUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 4 2002Catherine A. M. Stedman Abstract Aims The aims of this study were to determine if patients with SSRI-related hyponatraemia were (1) genetically poor metabolizers of CYP2D6, and/or (2) had excessive plasma concentrations of the SSRI antidepressant. Methods Plasma DNA from 20 people with hyponatraemia attributable to fluoxetine or paroxetine was analysed for the CYP2D6 alleles *1,*16. Trough plasma concentrations of fluoxetine and norfluoxetine, or paroxetine were assayed in nine people who remained on the antidepressant. Results Genotype results were compared with those published in a large population study. The poor metabolizer PM/PM genotype was present in one subject only, or 5% of the study population, compared with 7.2% of a general population. The 95% Cl of this result was 0,21%, suggesting that it is most unlikely that hyponatremia is related to the PM/PM genotype. The intermediate IM/PM genotype was present in 5% compared with 19.7% of a general population. All differences were not statistically significant. Antidepressant concentrations of fluoxetine (n,=,5, all EM) and paroxetine (n,=,1,IM/PM and n,=,3,EM) were all within the lower half of the reference range. Conclusions These results do not support the hypothesis that SSRI-related hyponatraemia is linked to genetically poor metabolizers, or excessive drug concentrations. Copyright © 2002 John Wiley & Sons, Ltd. [source] A case of fatal caffeine poisoningACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 4 2010T. RUDOLPH Caffeine is a natural alkaloid methylxanthine that is found in various plants such as coffee or tea. Symptoms of a severe overdose may present with hypokalemia, hyponatremia, ventricular arrhythmias, hypertension followed by hypotension, respiratory failure, seizures, rhabdomyolysis, ventricular fibrillation and finally circulatory collapse. A 21-year-old woman called for the ambulance herself soon after the ingestion of about 10,000 mg of caffeine. At the arrival of the ambulance, the patient went into cardiac arrest almost immediately. After a total resuscitation period of 34 min including seven counter-shocks and 2 mg epinephrine, the patient was stable enough to be transferred to the hospital. The patient soon went into VF again and received two more counter-shocks and 1 mg epinephrine and finally an intravenous bolus dose of 300 mg amiodarone. The initial arterial blood gas showed pH at 6.47, lactate at 33 mmol/l and potassium level at 2.3 mmol/l. Unfortunately, no blood samples for caffeine analysis were taken. Three days after hospital admission, the patient developed myoclonus, which did not respond to medical treatment. Excessive intake of caffeine may produce arrhythmias and pronounced hypokalemia and ensuing ventricular fibrillation. In case of counter-shock-resistant VF, it can be necessary to give an early loading dose of amiodarone. Furthermore, it may be beneficial to replace the potassium as early as possible. Epinephrine and buffer solutions used during resuscitation may further decrease blood potassium levels and should be administrated cautiously. Epinephrine can be replaced by other vasopressor drugs, such as vasopressin without effects on ,-receptors. [source] Carbamazepine-Related Hyponatremia Following Cardiopulmonary BypassJOURNAL OF CARDIAC SURGERY, Issue 2 2003Theodore Velissaris A.F.R.C.S. Following an initially uncomplicated recovery, he developed symptomatic hyponatremia. The symptoms and biochemical abnormality improved after gradual discontinuation of carbamazepine. We discuss the association between carbamazepine and hyponatremia and the causes of hyponatremia after cardiopulmonary bypass. Surgeons should consider stopping carbamazepine before operations with cardiopulmonary bypass. (J Card Surg 2003;18:155-157) [source] Use of sodium concentration and anion gap to improve correlation between serum chloride and bicarbonate concentrationsJOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 4 2006Mark Feldman Abstract Although most acid-base disorders cause opposite and equal changes in serum chloride and bicarbonate concentrations, this inverse relationship can be distorted by changes in the anion gap and/or water balance. Therefore, we examined the relationship between chloride and bicarbonate before and after adjusting for anion gap and serum sodium concentration. Patients with abnormal electrolytes were grouped by chloride and bicarbonate concentrations (low, normal, and high). Then, chloride and anion gap-adjusted bicarbonate were adjusted for water excess (or deficit), manifesting as hyponatremia (or hypernatremia), after which patients were reclassified. Classification by chloride and bicarbonate changed in 82% of the 135 patients after adjustment for anion gap and sodium. Serum chloride and bicarbonate were each low (concordant) in 23 patients, while 18 had discordant chlorides and bicarbonates (9 low/high, 9 high/low). After adjustments, chloride and bicarbonate were discordant in 40 patients (31 low/high, 9 high/low) and concordant in none. The correlation between serum chloride and bicarbonate improved from ,0.459 to ,0.998 after adjustments for sodium and anion gap. A very close inverse relationship between serum chloride and bicarbonate concentrations is commonly distorted by concomitant water disturbances and anion gap acidoses in internal medicine patients admitted with electrolyte disorders. J. Clin. Lab. Anal. 20:154,159, 2006. © 2006 Wiley-Liss, Inc. [source] Diagnostic approach and management of inpatient hyponatremia,JOURNAL OF HOSPITAL MEDICINE, Issue S3 2010Biff F. Palmer MD First page of article [source] Managing hyponatremia in cirrhosis,JOURNAL OF HOSPITAL MEDICINE, Issue S3 2010Elizabeth Ross MD Abstract The development of hyponatremia represents an ominous event in the progression of cirrhosis to end-stage liver disease. It usually develops in those with refractory ascites and is a manifestation of the non-osmotic release of arginine vasopressin (AVP). In the hospitalized cirrhotic patient, hyponatremia is associated with increased disease severity and mortality. In this article, we review the pathophysiology of hyponatremia, its clinical implications, evaluation, and treatment. Journal of Hospital Medicine 2010;5:S8,S17. © 2010 Society of Hospital Medicine. [source] Managing hyponatremia in patients with syndrome of inappropriate antidiuretic hormone secretion,JOURNAL OF HOSPITAL MEDICINE, Issue S3 2010Joseph G. Verbalis MD This review will address the management of hyponatremia caused by the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in hospitalized patients. To do so requires an understanding of the pathogenesis and diagnosis of SIADH, as well as currently available treatment options. The review will be structured as responses to a series of questions, followed by a presentation of an algorithm for determining the most appropriate treatments for individual patients with SIADH based on their presenting symptoms. Journal of Hospital Medicine 2010;5:S18,S26. © 2010 Society of Hospital Medicine. [source] Hospitalized patients with acute decompensated heart failure: Recognition, risk stratification, and treatment reviewJOURNAL OF HOSPITAL MEDICINE, Issue S6 2008Alpesh Amin MD Abstract Acute decompensated heart failure (ADHF) has emerged as a major healthcare problem. It causes approximately 3% of all hospitalizations in the United States, with the direct medical cost of these hospitalizations estimated at $18.8 billion per year. Early recognition, risk stratification, and evidence-based treatment are crucial in reducing the morbidity, mortality, and costs associated with this disorder. Classic signs and symptoms of ADHF, such as rales, dyspnea, and peripheral edema, may be absent at hospital presentation and, even when present, are not specific to this disorder. As a result, serum B,type natriuretic peptide level is now used to rapidly and accurately detect ADHF. Multivariate analyses have identified renal dysfunction, hypotension, advanced age, hyponatremia, and comorbidities as significant and independent mortality risk factors. Based on these factors, mortality risk can be stratified from very low to very high using published algorithms that have been validated in independent populations. Evidence-based guidelines for the treatment of ADHF are available from both the European Society of Cardiology and the Heart Failure Society of America. In general, an intravenous loop diuretic, either alone or in combination with a vasodilator, is recommended as initial therapy in patients with volume overload, depending on the patient's clinical status. Use of inotropic agents should be limited to the small subset of patients with low-output syndrome and significant hypotension. In any event, frequent monitoring of clinical response is essential, with subsequent therapy determined by this response. Finally, focused patient education during hospitalization may help reduce readmissions for ADHF. Journal of Hospital Medicine 2008;3(Suppl 6):S16,S24. © 2008 Society of Hospital Medicine. [source] Current issues for nurse practitioners: HyponatremiaJOURNAL OF THE AMERICAN ACADEMY OF NURSE PRACTITIONERS, Issue 11 2007Ruth Haskal NP-C (Adult Nurse Practitioner) Abstract Purpose: To review the assessment, diagnosis, and management of hyponatremia (serum sodium <135 mEq/L), the most common electrolyte disturbance as a result of dysregulation of water balance in hospitalized or institutionalized patients. Data sources: Comprehensive search using keywords AVP receptor antagonists, hyponatremia, SIADH, conivaptan, tolvaptan, lixivaptan, nurse practitioner, and others was carried out using the National Library of Medicine (PubMed) Web site from which full-text articles were obtained. Meeting abstracts were obtained from scientific sessions including the American Society of Nephrology Renal Week 2004 and the Endocrine Society,s 87th Annual Meeting (2005). The Vaprisol (conivaptan hydrochloride injection) package insert was referenced and obtained from FDA.gov. Conclusions: A diagnosis of hyponatremia requires thorough investigation for underlying causes and prompt treatment to prevent poor patient outcomes. In clinical trials, a new class of drugs called the arginine vasopressin (AVP) receptor antagonists or aquaretics has been shown to be safe and effective for the treatment of hyponatremia. Among this class of agents, intravenous conivaptan hydrochloride, indicated for the treatment of euvolemic hyponatremia in hospitalized patients, is the first drug in class approved for use. Implications for practice: Elderly patients, and those with certain conditions such as heart failure, tuberculosis, cirrhosis, and head injury, may be at increased risk for hyponatremia. In hospitalized patients following surgery and the use of certain medications, hyponatremia is a common condition. A thorough understanding of the physiology of water balance and the risk factors associated with hyponatremia is essential for prompt and effective intervention. Awareness of the limitations of conventional therapies and the availability of new treatment options for hyponatremia allows clinicians to optimize patient care. [source] Predictors of the recurrence of hepatic encephalopathy in lactulose-treated patientsALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 9 2010J. S. BAJAJ Aliment Pharmacol Ther,31, 1012,1017 Summary Background, Lactulose is considered first-line therapy for hepatic encephalopathy. However, the effect of adherence with lactulose on recurrence of hepatic encephalopathy outside clinical trials remains unclear. Aim, To determine the association of lactulose use with recurrence of hepatic encephalopathy episodes. Methods, Patients with cirrhosis who were initiated on lactulose after an index hepatic encephalopathy episode in a liver-transplant centre were retrospectively reviewed. Recurrence of hepatic encephalopathy, precipitating factors and adherence on lactulose were investigated using chart review and electronic pharmacy records. Patients with/without hepatic encephalopathy recurrence were compared, and predictors of recurrence were analysed. Results, A total of 137 patients with cirrhosis (age 55 ± 6years, MELD 17 ± 7) who were initiated on lactulose after the index hepatic encephalopathy episode were included. Of these, 103 patients developed recurrent hepatic encephalopathy 9 ± 1 months after their index episode; 39 (38%) of these were not adherent on lactulose, 56 (54%) were adherent and 8 (8%) had lactulose-associated dehydration leading to recurrence. Recurrent hepatic encephalopathy precipitants in lactulose-adherent patients were sepsis (19%), GI bleeding (15%), hyponatremia (4%) and TIPS (7%). Overall, all patients who did not suffer recurrence were adherent on lactulose. In contrast, the adherence rate for those who recurred was only 64% (P = 0.00001). On multivariate regression, lactulose non-adherence (OR 3.26) and MELD score (OR 1.14) were the factors that predicted recurrence. Conclusion, Lactulose non-adherence and lactulose-associated dehydration were associated with nearly half of recurrent hepatic encephalopathy episodes. [source] Retrospective Study: Surgical intervention in the management of severe acute pancreatitis in cats: 8 cases (2003,2007)JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 4 2010Tolina T. Son DVM Abstract Objective , To evaluate clinical characteristics and outcomes of cats undergoing surgical intervention in the course of treatment for severe acute pancreatitis. Design , Retrospective observational study from 2003 to 2007 with a median follow-up period of 2.2 years (range 11 d,5.4 y) postoperatively. Setting , Private referral veterinary center. Animals , Eight cats. Interventions , None. Measurements and Main Results , Quantitative data included preoperative physical and clinicopathologic values. Qualitative parameters included preoperative ultrasonographic interpretation, perioperative and intraoperative feeding tube placement, presence of free abdominal fluid, intraoperative closed suction abdominal drain placement, postoperative complications, microbiological culture, and histopathology. Common presenting clinical signs included lethargy, anorexia, and vomiting. Leukocytosis and hyponatremia were present in 5 of 8 cats. Hypokalemia, increased total bilirubin, and hyperglycemia were present in 6 of 8 cats. Elevated alanine aminotransferase and aspartate transferase were present in all cats. Surgery for extrahepatic biliary obstruction was performed in 6 cats, pancreatic abscess in 3 cats, and pancreatic necrosis in 1 cat. Six of the 8 cats survived. Five of the 6 cats that underwent surgery for extrahepatic biliary obstruction and 1 cat that underwent pancreatic necrosectomy survived. All 5 of the cats with extrahepatic biliary obstruction secondary to pancreatitis survived. The 2 nonsurvivors included a cat with a pancreatic abscess and a cat with severe pancreatitis and extrahepatic biliary obstruction secondary to a mass at the gastroduodenal junction. Postoperative complications included progression of diabetes mellitus, septic peritonitis, local gastrostomy tube stoma inflammation, local gastrostomy tube stoma infection, and mild dermal suture reaction. Conclusion , Cats with severe acute pancreatitis and concomitant extrahepatic biliary obstruction, pancreatic necrosis, or pancreatic abscesses may benefit from surgical intervention. Cats with extrahepatic biliary obstruction secondary to severe acute pancreatitis may have a good prognosis. [source] Use of a point-of-care urine drug test in a dog to assist in diagnosing barbiturate toxicosis secondary to ingestion of a euthanized carcassJOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 3 2009DACVA, DACVECC, Vicki L. Campbell DVM Abstract Objective , To describe a case of barbiturate toxicosis in a dog secondary to ingestion of a previously buried euthanized goat carcass and to discuss the utility of urine drug testing in diagnosing barbiturate toxicosis. Case Summary , A 6-year-old neutered male Border Collie was presented to a university veterinary teaching hospital for evaluation of ataxia and acute collapse. Past pertinent history included Addison's disease that had been managed for 1 year. A companion dog was seen 12 hours earlier chewing on the partially decomposed head of a goat that had been euthanized 47 days previously and buried on the owner's property. The dog was laterally recumbent, unresponsive to stimuli, and hypothermic on physical examination. Initial blood work revealed hyponatremia and hyperkalemia, with a Na/K ratio of 18.5. The dog was volume resuscitated and received an injection of dexamethasone sodium phosphate due to a suspected Addisonian crisis. Despite this treatment, the dog remained laterally recumbent and unresponsive to stimuli. A urine drug screen was performed and was positive for barbiturates. A diagnosis of barbiturate toxicosis secondary to ingestion of a euthanized goat carcass was made. The dog was treated supportively over 12 hours with IV fluids and activated charcoal. The dog was able to walk 11 hours after presentation and was subsequently discharged from the hospital. New or Unique Information Provided , Urine drug testing is a fast, easy, and point-of-care test that may be useful in dogs to assist in the diagnosis of barbiturate intoxication. Proper disposal of euthanized animals is necessary to prevent toxicosis and possible death of companion animals and wildlife. [source] | ||||||||||||||||||||||||||||||||||