Proper Hydration During Ultra-endurance Activities.

The health and performance of ultra-endurance athletes is dependent on avoidance of performance limiting hypohydration while also avoiding the potentially fatal consequences of exercise-associated hyponatremia due to overhydration. In this work, key factors related to maintaining proper hydration during ultra-endurance activities are discussed. In general, proper hydration need not be complicated and has been well demonstrated to be achieved by simply drinking to thirst and consuming a typical race diet during ultra-endurance events without need for supplemental sodium. As body mass is lost from oxidation of stored fuel, and water supporting the intravascular volume is generated from endogenous fuel oxidation and released with glycogen oxidation, the commonly promoted hydration guidelines of avoiding body mass losses of >2% can result in overhydration during ultra-endurance activities. Thus, some body mass loss should occur during prolonged exercise, and appropriate hydration can be maintained by drinking to the dictates of thirst.

Considerations for ultra-endurance activities: part 2 - hydration.

It is not unusual for those participating in ultra-endurance (> 4 hr) events to develop varying degrees of either hypohydration or hyperhydration. Yet, it is important for ultra-endurance athletes to avoid the performance limiting and potentially fatal consequences of these conditions. During short periods of exercise (< 1 hr), trivial effects on the relationship between body mass change and hydration status result from body mass loss due to oxidation of endogenous fuel stores, and water supporting the intravascular volume being generated from endogenous fuel oxidation and released with glycogen oxidation. However, these effects have meaningful implications during prolonged exercise. In fact, body mass loses well over 2% may be required during some ultra-endurance activities to avoid hyperhydration. Therefore, the typical hydration guidelines to avoid more than 2% body mass loss do not apply in ultra-endurance activities and can potentially result in hyperhydration. Fortunately, achieving the balance of proper hydration during ultra-endurance activities need not be complicated and has been well demonstrated to generally be achieved by simply drinking to thirst and avoiding excessive sodium supplementation with intention of replacing all sodium losses during the exercise.

[Can water be poisonous?]. / Kann man sich mit Wasser intoxikieren? - Fall 5 / 2015.

HISTORY AND ADMISSION FINDINGS: Two female patients aged over 80 years developed central nervous symptoms after drinking large amounts of water (more than 3 l per day). INVESTIGATIONS: Both had a hypoosmolar hyponatremia that was induced by concomitant treatment with hydrochlorothiazid (HCT) in the one case and in the other case relied on a distal tubular damage due to reflux nephropathy. DIAGNOSIS, TREATMENT AND COURSE: Hyponatremia was corrected after withdrawal of HCT and fluid restriction and central nervous symptoms disappeared rapidly. CONCLUSIONS: Distal tubular urinary dilution can be disturbed by HCT and parenchymal renal disease and can result in symptomatic hyponatremia after drinking large amounts of water.

Dialysate Sodium: Choosing the Optimal Hemodialysis Bath.

Fluid overload in patients undergoing hemodialysis contributes to cardiovascular morbidity and is a major cause of hospitalizations. It is often addressed by reinforcing the importance of a low-salt diet with patients and challenging estimated dry weights. More recently, interest has shifted toward the dialysate sodium prescription as a strategy to improve fluid overload and its adverse sequelae. The availability of high-flux high-efficiency dialysis in conjunction with the need to ensure its tolerability for patients has resulted in an increase in dialysate sodium prescriptions from 120 to ≥140 mEq/L. However, we are now tackling the unforeseen consequences associated with high dialysate sodium prescriptions. High dialysate sodium concentration is associated with high interdialytic weight gain, a commonly used surrogate for hypervolemia contributing to hypertension. The association between mortality and high dialysate sodium concentration remains controversial with conflicting data. It is clear that fluid management in the diverse end-stage renal disease population is extremely complex and more clinical trials are needed. In the meantime, while patients require treatments and clinical decisions need to be made, this review article attempts to summarize the current evidence for individualized dialysate sodium prescriptions based on patients' volume status, comorbid conditions, plasma sodium level, and hemodynamic response to dialysis therapy.

[Hyperhydration and dialysis in acute kidney failure]. / Überwässerung und Dialyse beim akuten Nierenversagen.

Despite the advances in critical care medicine, the hospital mortality in patients with acute kidney injury (AKI) requiring dialysis remains high. Depending on the underlying disease the in-house mortality is reported to be up to 80%. Several observational studies demonstrated an association between mortality and fluid overload. A primary mechanism of interest is that fluid overload causes tissue edema and subsequent reduction of perfusion, oxygenation and nutrient delivery. This results in further renal damage. In addition, fluid overload-related dilution within the extracellular space causes artificially low serum creatinine, which masks AKI diagnosis. As a consequence, renal protective management strategies are deferred, which further aggravates kidney injury. This aggravation of renal damage subsequently increases the mortality. This review discusses the role of fluid overload for outcomes in critically ill patients as described in the current literature and assesses criteria for the initiation of renal replacement therapy in this critically ill population.

Fatal water intoxication and cardiac arrest in runners during marathons: prevention and treatment based on validated clinical paradigms.

Cerebral edema due to exercise-associated hyponatremia and cardiac arrest due to atherosclerotic heart disease cause rare marathon-related fatalities in young female and middle-aged male runners, respectively. Studies in asymptomatic middle-aged male physician-runners during races identified inflammation due to skeletal muscle injury after glycogen depletion as the shared underlying cause. Nonosmotic secretion of arginine vasopressin as a neuroendocrine stress response to rhabdomyolysis mediates hyponatremia as a variant of the syndrome of inappropriate antidiuretic hormone secretion. Fatal hyponatremic encephalopathy in young female runners was curtailed using emergent infusion of intravenous hypertonic (3%) saline to reverse cerebral edema on the basis of this paradigm. This treatment was arrived at through a consensus process within the medical community. An increasing frequency of cardiac arrest and sudden death has been identified in middle-aged male runners in 2 studies since the year 2000. Same-aged asymptomatic male physician-runners showed post-race elevations in interleukin-6 and C-reactive protein, biomarkers that predict acute cardiac events in healthy persons. Hypercoagulability with in vivo platelet activation and release of cardiac troponin and N-terminal pro-brain natriuretic peptide were also observed post-race in these same subjects. High short-term risk for atherothrombosis during races as shown by stratification of biomarkers in asymptomatic men may render nonobstructive coronary atherosclerotic plaques vulnerable to rupture. Pre-race aspirin use in this high-risk subgroup is prudent according to conclusive evidence for preventing first acute myocardial infarctions in same-aged healthy male physicians. On the basis of validated clinical paradigms, taking a low-dose aspirin before a marathon and drinking to thirst during the race may avert preventable deaths in susceptible runners.

Strategies for removing fluids during hemodialysis.

Dry weight has most frequently been defined by the patient becoming symptomatic when fluid removal is attempted Hypervolemia and fluid removal require ongoing evaluation and the use of a number of strategies. This article reviews strategies for removing fluid during hemodialysis, hemodynamics of fluid removal, and interventions associated with the strategies for fluid removal.

A pinch of salt.

Pregnant women in labour are generally encouraged by their carers to continue taking plenty of oral fluids. This is sometimes supplemented by intravenous fluids either due to a clinical necessity or in preparation for a caesarean section. It is important that there is clear documentation of the amount of fluids received by pregnant women in the perinatal period as excessive maternal fluid has been associated with low serum sodium in neonates. This often goes under-recognised; therefore it is important to consider this in a neonate presenting with hyponatraemia in the first day of life. Presented here is a case of neonatal hyponatraemia secondary to excessive fluid taken in the perinatal period.

Hyper-alkalinization without hyper-hydration for the prevention of high-dose methotrexate acute nephrotoxicity in patients with osteosarcoma.

PURPOSE: To evaluate the reliability and renal safety of an original schedule of high-dose methotrexate (HDMTX) administration with hyper-alkalinization, and without hyper-hydration. METHODS: Patients with osteosarcoma received HDMTX (8-12 g/m(2)) as a 4-h infusion. Hypertonic 8.4% sodium bicarbonate was infused prior to HDMTX, then once daily for 3 days. Methotrexate serum concentrations were measured at hour 4 (Cmax), hour 24, hour 48, and hour 72. Urinary pH was measured on each miction. Serum creatinine was assessed on days 1, 3, and 8. RESULTS: Twenty-six patients (median age: 18 years, range: 15-25) received a total of 344 cycles of HDMTX, including 16 patients treated in an outpatient basis. Urinary pH remained constantly higher than 7.5 in all patients. Grade 1 creatininemia toxicity was observed in 31 cycles (9%), and grade 2 creatinine toxicity was observed in one patient. No episode of acute severe nephrotoxicity was observed. No significant worsening was observed in serum creatinine and calculated creatinine clearance from baseline to the end of therapy (P = 0.74). The main extra-renal toxicity was alkalinization-related hypokalemia from H48. No re-hospitalization was required. CONCLUSION: Hyper-alkalinization appears an efficient and reliable method to prevent the acute renal toxicity of HDMTX and allows its safe administration in the outpatient setting.

Exercise-associated hyponatremia: overzealous fluid consumption.

Exercise-associated hyponatremia is hyponatremia occurring during or up to 24 hours after prolonged exertion. In its more severe form, it manifests as cerebral and pulmonary edema. There have now been multiple reports of its occurring in a wilderness setting. It can now be considered the most important medical problem of endurance exercise. The Second International Exercise-Associated Hyponatremia Consensus Conference gives an up-to-date account of the nature and management of this disease. This article reviews key information from this conference and its statement. There is clear evidence that the primary cause of exercise-associated hyponatremia is fluid consumption in excess of that required to replace insensible losses. This is usually further complicated by the presence of inappropriate arginine vasopressin secretion, which decreases the ability to renally excrete the excess fluid consumed. Women, those of low body weight, and those taking nonsteroidal anti-inflammatory drugs are particularly at risk. When able to be biochemically diagnosed, severe exercise-associated hyponatremia is treated with hypertonic saline. In a wilderness setting, the key preventative intervention is moderate fluid consumption based on perceived need ("ad libitum") and not on a rigid rule. (Editor's Note: This paper was written at my request in an effort to increase awareness of this important clinical entity among members of the wilderness community, many of whom are involved in activities that place them at risk of its development. I thank the authors for their diligent efforts.)

[Water intoxication in two girls with anorexia nervosa]. / Waterintoxicatie bij twee meisjes met anorexia nervosa.

Two girls, 16 and 18 years old, with anorexia nervosa developed generalized convulsion as a result of drinking excessive amounts of water. The neurological symptoms disappeared, but the girls held on to their excessive drinking habits, despite psychoeducation. Although fluid restriction is known to be a major problem for anorexia nervosa patients within the context of extreme fasting, one should realize that these patients can also run the risk of water intoxication following excessive water intake. Therefore all patients should be questioned explicitly about their daily fluid intake. In the case of polydipsia, the patient's blood should be tested and serum electrolytes should be measured. Patients should be given psychoeducation in order to make them more aware of the possible dangers of excessive water intake.

A potentially aborted neuroleptic malignant syndrome following seclusion against uncontrollable water intoxication.

Water intoxication in schizophrenia poses a great clinical challenge, and occasionally, behavioral restrictions are unavoidable. A patient with refractory schizophrenia comorbid with severe water intoxication had an apparent weight variation of ,7 kg/day to 65 kg. As he fell twice, when he had been treated with antipsychotic megadose therapy, he was secluded with restricted water access of 3 L/day. Two days later, consciousness level deteriorated significantly with autonomic instability; however, he was treated with intravenous hydration plus dantrolene and recovered completely on the following day. The sodium/chloride levels and serum osmolarity, which had been abnormally low, normalized abruptly. Only after seclusion was it found that his dry weight had been only 52 kg. The first description of such a case was indicative of a potentially aborted neuroleptic malignant syndrome. He is now treated with olanzapine, valproate, and lorazepam, with some success. Caution is required for secluding extreme cases of uncontrollable water intoxication.

Cellular effects of guanylin and uroguanylin.

Ingestion of a salty meal induces secretion of guanylin (GN) and uroguanylin (UGN) into the intestinal lumen, where they inhibit Na+ absorption and induce Cl-, HCO3-, and water secretion. Simultaneously, these hormones stimulate renal electrolyte excretion by inducing natriuresis, kaliuresis, and diuresis. GN and UGN therefore participate in the prevention of hypernatremia and hypervolemia after salty meals. The signaling pathway of GN and UGN in the intestine is well known. They activate enterocytes via guanylate cyclase C (GC-C), which leads to cGMP-dependent inhibition of Na+/H+ exchange and activation of the cystic fibrosis transmembrane regulator. In GC-C-deficient mice, GN and UGN still produce renal natriuresis, kaliuresis, and diuresis, suggesting different signaling pathways in the kidney compared with the intestine. Signaling pathways for GN and UGN in the kidney differ along the various nephron segments. In proximal tubule cells, a cGMP- and GC-C-dependent signaling was demonstrated for both peptides. In addition, UGN activates a pertussis toxin-sensitive G-protein-coupled receptor. A similar dual signaling pathway is also known for atrial natriuretic peptide. Recently, a cGMP-independent signaling pathway for GN and UGN was also shown in principal cells of the human and mouse cortical collecting duct. Because GN and UGN activate different signaling pathways in specific organs and even within the kidney, this review focuses on more recent findings on cellular effects and signaling mechanisms of these peptides and their pathophysiologic implications in the intestine and the kidney.

Treatment of the polydipsia-hyponatremia syndrome with urea.

OBJECTIVE: The polydipsiahyponatremia syndrome is difficult to control in patients with severe mental illness, and there is no established effective therapeutic approach. We investigate the effect of oral daily intake of large amounts of urea to prevent hyponatremic episodes. METHOD: Seven patients were treated during 4 to 18 months with urea (0.3-0.9 g/kg/day). Five of these patients had schizophrenia. Body weight variation between morning and evening was determined before and during the course of therapy in 5 patients. The dose of urea was increased if morning serum sodium level (SNa) was lower than 132 mmol/L. RESULTS: Urea therapy increased mean +/- SD morning SNa (from 127.5 +/- 3.4 mmol/L before initiation of urea treatment to 136.5 +/- 2.4 mmol/L during the second month of urea treatment; p < .01) and mean +/- SD urine osmolality (from 86 +/- 39 mOsm/kg H(2)O to 159 +/- 58 mOsm/kg H(2)O; p < .05), probably without changes in water intake or urine volume excretion as attested by the level of urinary creatinine concentration. Mean +/- SD body weight variation decreased from 4.5% +/- 1.0% before initiation of urea treatment to 2.8% +/- 1.0% during the second month of urea treatment (p < .05). Two patients stopped urea treatment after 1 year and subsequently developed symptomatic hyponatremia. CONCLUSION: These preliminary data show that urea appears to be an effective therapeutic approach for the polydipsiahyponatremia syndrome.

Troubleshooting non-infectious peritoneal dialysis issues.

Peritoneal dialysis is commonly preformed by patients and their caregivers in the home, in nursing homes, and in both acute and rehabilitation hospitals. The success of the therapy requires that the nurse overseeing the care of the patient on peritoneal dialysis in the acute, sub-acute, and chronic settings has the skills and knowledge to identify specific non-infectious issues, choose an appropriate and effective intervention activity, document the findings and outcomes, and educate the patient to assist in the resolution of the non-infectious issues, and avoid future recurrence. This article reviews the most common non-infectious complications that occur in patients on peritoneal dialysis and discusses an organized clinical process to troubleshoot the issues and achieve the desired clinical outcomes.