Does a Reduction in Serum Sodium Concentration or Serum Potassium Concentration Increase the Prevalence of Exercise-Associated Muscle Cramps?

2016 ◽  
Vol 25 (3) ◽  
pp. 301-304 ◽  
Author(s):  
Donal Murray ◽  
Kevin C. Miller ◽  
Jeffrey E. Edwards
Keyword(s):  
Serum Sodium ◽  
Serum Potassium ◽  
Potassium Concentration ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Clinical Scenario ◽  
Clinical Question ◽  
Muscle Cramps ◽  
Serum Potassium Concentration ◽  
Exercise Associated Muscle Cramps

Clinical Scenario:Although exercise-associated muscle cramps (EAMC) are common in ultradistance runners and athletes in general, their etiology remains unclear. EAMC are painful, sudden, involuntary contractions of skeletal muscle occurring during or after exercise and are recognized by visible bulging or knotting of the whole, or part of, a muscle. Many clinicians believe EAMC occur after an imbalance in electrolyte concentrations, specifically serum sodium concentration ([Na+]s) and serum potassium concentration ([K+]s). Studies that have established a link between EAMC occurrence and serum electrolyte concentrations after an athletic event are unhelpful.Focused Clinical Question:Are [Na+]s and [K+]s different in athletes who experience EAMC than noncrampers?

CHANGES IN PLASMA RENIN ACTIVITY AND PLASMA ALDOSTERONE IN THE INDUCED PARALYTIC ATTACK OF THYROTOXIC PERIODIC PARALYSIS

1976 ◽  
Vol 82 (3) ◽  
pp. 715-727 ◽  
Author(s):  
Ryoyu Takeda ◽  
Shinpei Morimoto ◽  
Kenzo Uchida ◽  
Isamu Miyamori
Keyword(s):  
Plasma Renin Activity ◽  
Serum Sodium ◽  
Serum Potassium ◽  
Potassium Concentration ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Serum Sodium Concentration ◽  
Serum Potassium Concentration

ABSTRACT Changes in serum electrolytes, haematocrit, plasma renin activity and plasma aldosterone induced by glucose and insulin (GI) infusion were serially investigated in seven patients with periodic thyrotoxic paralysis. An attack which developed into complete quadriplegia was induced within 90 min after the beginning of the GI infusion in four out of seven patients. Only a slight paralysis of the legs was produced in another two patients and induction of an attack did not materialize in one. In four patients with complete quadriplegia, the mean values of serum sodium and potassium concentrations, haematocrit, plasma renin activity and plasma aldosterone slightly decreased immediately after the beginning of the GI infusion. Induction of a paralytic attack was not accompanied by any significant changes in serum sodium concentration, haematocrit, plasma renin activity and plasma aldosterone either 15 min before or after the onset of attack, while the serum potassium concentration progressively decreased, and an increase in plasma aldosterone associated with an increase of haematocrit and plasma renin activity reached a peak level at the stage of complete quadriplegia. On the other hand, in the three patients in whom an infusion produced slight or no paralysis of the legs, changes in the serum sodium concentration, haematocrit, plasma renin activity and plasma aldosterone were insignificant and the serum potassium concentration was slightly but insignificantly decreased. These results suggest that hyperaldosteronism may not be a trigger for the induced paralytic attack but a phenomenon secondary to volume depletion and a change in potassium homoeostasis induced by GI infusion.

PLASMA ALDOSTERONE CONCENTRATION IN ANEPHRIC CHILDREN

1974 ◽  
Vol 75 (3) ◽  
pp. 561-568 ◽  
Author(s):  
M. Birkhäuser ◽  
C. Godard ◽  
C. Loirat ◽  
M. B. Vallotton
Keyword(s):  
Serum Sodium ◽  
Plasma Cortisol ◽  
Potassium Concentration ◽  
Extracellular Volume ◽  
Sodium Concentration ◽  
Plasma Aldosterone ◽  
Volume Depletion ◽  
Plasma Aldosterone Concentration ◽  
Serum Potassium Concentration ◽  
Postural Changes

ABSTRACT The effect of extractive haemodialysis and of postural changes on the plasma aldosterone concentration has been studied in 5 anephric children. The plasma aldosterone concentration tended to be lower after haemodialysis in spite of the extracellular volume depletion induced. No regular response occurred after orthostatism. There was no correlation between the plasma aldosterone and the plasma cortisol or the serum sodium concentration. A weak positive correlation was found between the plasma aldosterone and serum potassium concentration, suggesting that potassium may play a major role in aldosterone regulation in the anephric state.

Continuous Renal Replacement Therapy: Does Technique Influence Electrolyte and Bicarbonate Control?

2003 ◽  
Vol 26 (4) ◽  
pp. 289-296 ◽  
Author(s):  
H. Morimatsu ◽  
S. Uchino ◽  
R. Bellomo ◽  
C. Ronco
Keyword(s):  
Renal Replacement Therapy ◽  
Continuous Renal Replacement Therapy ◽  
Replacement Therapy ◽  
Serum Sodium ◽  
Serum Potassium ◽  
Potassium Concentration ◽  
Entire Treatment Period ◽  
Serum Potassium Concentration ◽  
The Mean ◽  
Entire Treatment

Background and objectives Different techniques of continuous renal replacement therapy (CRRT) might have different effects on electrolyte and acid-base control. The aim of this study was to determine whether continuous veno-venous hemodiafiltration (CVVHDF) or continuous veno-venous hemofiltration (CVVH) achieve better control of serum sodium, potassium and bicarbonate concentrations. Design Retrospective controlled study. Setting Two tertiary intensive care units. Patients Critically ill patients with acute renal failure (ARF) treated with CVVHDF (n=49) or CVVH (n=50). Interventions Retrieval of daily morning sodium and potassium values and arterial bicarbonate levels from computerized biochemical records before and after the initiation of CRRT for up to 2 weeks of treatment. Statistical comparison of findings. Measurements and results Before treatment, abnormal (high or low) values were frequently observed for sodium (65.1% for CVVHDF vs. 80.0% for CVVH; NS), potassium (45.9% vs. 34.0%; NS), and bicarbonate (73.3% vs. 68.0%; NS). After treatment, however, CVVHDF was more likely to achieve serum sodium concentrations within the normal range (74.1% vs. 62.9%; p=0.0026). Both treatments decreased the mean serum potassium concentration over the first 48 h (p=0.0059 and p <0.0001, respectively), but there was no difference in terms of the normalization of serum potassium concentration during the entire treatment period (88.3% vs. 90.5%; NS). Both treatments increased the mean arterial bicarbonate concentration over the first 48 hours (p=0.011 and p <0.0001, respectively). However, CVVH was associated with a lower incidence of metabolic acidosis (13.8% for CVVH vs. 34.5% for CVVHDF; p <0.0001) and a higher incidence of metabolic alkalosis (38.9% vs. 1.1%; p <0.0001) during the entire treatment period. Conclusions CRRT strategies based on different techniques have a significantly different impact on sodium and bicarbonate control.

scholarly journals A prospective study of serum electrolyte disorders and their clinical manifestation in HIV patients

2018 ◽  
Vol 6 (8) ◽  
pp. 2818
Author(s):  
Ajesh Kumar Damor ◽  
Praful Bala Honta
Keyword(s):  
Hiv Infection ◽  
Clinical Manifestation ◽  
Serum Sodium ◽  
Potassium Concentration ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Electrolyte Imbalance ◽  
Hiv Positive ◽  
Serum Electrolyte ◽  
Electrolyte Disorders

Background: Present study was conducted to evaluate the serum electrolyte disorders and their clinical manifestation in HIV positive patients.Methods: Total 100 patients who were known to be HIV positive or those who were found to be HIV positive were taken. HIV infection was diagnosed by one ELISA and two E/R/S test. All clinical diagnosis medication and routine chemical profiles were recorded along with detailed history and physical examination. Fluid depletion was inferred from the findings like decreased skin turgor, dry mucus membrane; fluid overload was ascertained by presence of jugular venous distension and dependent pulmonary rales. Hyponatremia was defined as a serum sodium concentration less than 135mmol/L and hypokalemia was defined as potassium concentration less than 3.5mmol/L.Results: Eighty percent patients had disorders of electrolyte imbalance. Most common electrolyte was hyponatremia (58%) and hypokalemia (28%). The mean serum sodium concentration was 133.48±7.06 and potassium concentration was 3.87±0.63. Neuromuscular manifestation and neuropsychiatric manifestation were present in 58% and 49% respectively.Conclusions: Patients with HIV infection may develop a bewildering variety of electrolyte and acid-base disturbances. Hyponatremia and hypokalemia from many causes is common and associated with an increased mortality.

scholarly journals Correcting hypokalaemia in a paediatric patient with Bartter syndrome through oral dose of potassium chloride intravenous solution

2021 ◽  
Vol 9 ◽  
pp. 2050313X2110197
Author(s):  
Salman Alasfour ◽  
Haya S Alfailakawi ◽  
Yousif A Shamsaldeen
Keyword(s):  
Paediatric Patient ◽  
Potassium Chloride ◽  
Serum Potassium ◽  
Nasogastric Tube ◽  
Potassium Concentration ◽  
Oral Route ◽  
Bartter Syndrome ◽  
Intravenous Route ◽  
Serum Potassium Concentration ◽  
Main Challenge

Bartter syndrome is a rare autosomal recessive disorder characterized by hypokalaemia. Hypokalaemia is defined as low serum potassium concentration ˂3.5 mmol/L, which may lead to arrhythmia and death if left untreated. The aim of this case report was to normalize serum potassium concentration without the need for intravenous intervention. A 5-month-old male of 2.7 kg body weight diagnosed with Bartter syndrome was admitted to the general paediatric ward with acute severe hypokalaemia and urinary tract infection. The main challenge was the inability to administer drugs through intravenous route due to compromised body size. Therefore, we shifted the route of administration to the nasogastric tube/oral route. A total of 2 mL of concentrated intravenous potassium chloride (4 mEq potassium) were dissolved in distilled water and administered through nasogastric tube. Serum potassium concentration was rapidly normalized, which culminated in patient discharge. In conclusion, shifting drug administration from intravenous to oral route in a paediatric patient with Bartter syndrome includes numerous advantages such as patient convenience, minimized risk of cannula-induced infection, and reduced nurse workload.

Risk factors for hepatic encephalopathy in patients with cirrhosis and refractory ascites: relevance of serum sodium concentration

2010 ◽  
Vol 30 (8) ◽  
pp. 1137-1142 ◽  
Author(s):  
Mónica Guevara ◽  
María E. Baccaro ◽  
Jose Ríos ◽  
Marta Martín-Llahí ◽  
Juan Uriz ◽  
...  
Keyword(s):  
Risk Factors ◽  
Hepatic Encephalopathy ◽  
Serum Sodium ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Refractory Ascites

Serum Sodium Concentration Changes Are Related to Fluid Balance and Sweat Sodium Loss

2010 ◽  
Vol 42 (9) ◽  
pp. 1669-1674 ◽  
Author(s):  
MATTHEW D. PAHNKE ◽  
JOEL D. TRINITY ◽  
JEFFREY J. ZACHWIEJA ◽  
JOHN R. STOFAN ◽  
W. DOUGLAS HILLER ◽  
...  
Keyword(s):  
Fluid Balance ◽  
Serum Sodium ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Concentration Changes ◽  
Sodium Loss ◽  
Sweat Sodium

Disorders of Water Balance

2017 ◽  
Author(s):  
Richard H Sterns ◽  
Stephen M. Silver ◽  
John K. Hix ◽  
Jonathan W. Bress
Keyword(s):  
Water Balance ◽  
Water Intake ◽  
Serum Sodium ◽  
Water Conservation ◽  
Free Water ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Water Losses ◽  
Water Excretion ◽  
Impaired Water

Guided by the hypothalamic antidiuretic hormone vasopressin, the kidney’s ability to conserve electrolyte–free water when it is needed and to excrete large volumes of water when there is too much of it normally prevents the serum sodium concentration from straying outside its normal range. The serum sodium concentration determines plasma tonicity and affects cell volume: a low concentration makes cells swell, and a high concentration makes them shrink. An extremely large water intake, impaired water excretion, or both can cause hyponatremia. A combination of too little water intake with too much salt, impaired water conservation, or excess extrarenal water losses will result in hypernatremia. Because sodium does not readily cross the blood-brain barrier, an abnormal serum sodium concentration alters brain water content and composition and can cause serious neurologic complications. Because bone is a reservoir for much of the body’s sodium, prolonged hyponatremia can also result in severe osteoporosis and fractures. An understanding of the physiologic mechanisms that control water balance will help the clinician determine the cause of impaired water conservation or excretion; it will also guide appropriate therapy that can avoid the life-threatening consequences of hyponatremia and hypernatremia.

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