Disorders of potassium homeostasis

2020 ◽  
pp. 4748-4763
Author(s):  
John D. Firth

Hypokalaemia is defined as a serum potassium concentration lower than 3.5 mmol/litre and is the most common electrolyte abnormality seen in clinical practice, found in about 20% of hospital inpatients. Clinical features and investigation—mild hypokalaemia is asymptomatic, but nonspecific symptoms develop with more severe disturbance, and serious neuromuscular problems sometimes arise at serum potassium concentrations lower than 2.5 mmol/litre. Emergency management is rarely required, but intravenous infusion of potassium should be given in the rare circumstances of life-threatening cardiac arrhythmia or muscular paralysis. There are a very large number of possible causes of hypokalaemia, the most common causes being diuretics (particularly thiazides), vomiting, and diarrhoea. The most common genetic cause is Gitelman’s syndrome. Management is with potassium and magnesium supplements. Other causes of tubular wasting of potassium include Bartter’s syndrome and mineralocorticoid excess. There are several rare conditions in which hypokalaemia is associated with episodes of extreme weakness/paralysis, including thyrotoxic periodic paralysis and familial hypokalaemic periodic paralysis. Hyperkalaemia, defined as a serum potassium concentration of greater than 5.0 mmol/litre, is asymptomatic, and severe hyperkalaemia (>7 mmol/litre) is the most serious of all electrolyte disorders because it can cause cardiac arrest. The electrocardiogram (ECG) is the best guide to the significance of hyperkalaemia in any particular individual. Patients with ECG manifestations more severe than tenting of the T waves should be given intravenous calcium gluconate (10 ml of 10%) followed by intravenous insulin and glucose, or nebulized salbutamol. There are many causes of hyperkalaemia, but by far the most common are renal failure and/or drugs. Other causes include exhaustive exercise, acidosis, drugs, and hyperkalaemic periodic paralysis (very rare).

1996 ◽  
Vol 17 (3) ◽  
pp. 106-106
Author(s):  
Kenneth B. Roberts

Potassium is the major intracellular cation; only a very small fraction of total body potassium is in the intravascular space. Increased potassium concentration in serum is infrequent in pediatrics, but it can be life-threatening because of its effect on membrane potentials, particularly of heart muscle. The serum potassium concentration is affected primarily by the kidney. Potassium is filtered by the glomerulus, then reabsorbed and secreted by the tubule. Processes that interfere with filtration or secretion (eg, acute on chronic glomerulonephritis, interstitial nephritis) may cause hyperkalemia; processes that interfere with reabsorption may cause hypokalemia. The most common cause of an increased serum potassium is "pseudohyperkalemia" due to hemolysis or to tissue hypoxia distal to the placement of a tourniquet.


2014 ◽  
Vol 2014 ◽  
pp. 1-3 ◽  
Author(s):  
Lauren A. Kimmons ◽  
Justin B. Usery

Secondary hyperkalemic paralysis is an uncommon but potentially life-threatening consequence of drug-induced disease. We report a case of a 53-year-old female with history of chronic kidney disease presenting to the emergency department with a one-day history of upper and lower extremity weakness and paresthesias. Serum potassium concentration on admission was greater than 8 mEq/L, and serum creatinine was elevated above baseline. Electrocardiogram showed first-degree atrioventricular block with peaked T waves. The patient reported compliance with daily lisinopril 10 mg, spironolactone 25 mg, and 40 mEq twice daily of potassium chloride. Symptoms and electrocardiogram returned to baseline within 24 hours of presentation and serum potassium returned to 4.2 mEq/L at approximately 36 hours without the need for dialysis. This case emphasizes the importance of including such a condition in the differential diagnosis of patients with ascending paralysis and the importance of close monitoring of patients placed on potassium-elevating agents.


2021 ◽  
Vol 9 ◽  
pp. 2050313X2110197
Author(s):  
Salman Alasfour ◽  
Haya S Alfailakawi ◽  
Yousif A Shamsaldeen

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.


2021 ◽  
Vol 2021 ◽  
pp. 1-4
Author(s):  
Henrik Elenius ◽  
Marie Cesa ◽  
Corina C. Nava Suarez ◽  
Abhishek Nimkar ◽  
Prasanta Basak ◽  
...  

Thyrotoxic periodic paralysis (TPP) is a rare muscular disorder, characterized by muscle weakness and hypokalemia triggered by thyrotoxicosis. In Asian populations, 2% of patients with thyrotoxicosis are affected, compared to only 0.1–0.2% of non-Asians. The vast majority of patients are male. Muscle weakness ranges in severity from very mild to life-threatening, due to respiratory compromise. We present a case of a previously healthy 39-year-old Hispanic male who presented with sudden quadriparesis and quickly recovered after being treated for hypokalemia and thyrotoxicosis. TPP, although unusual, is important to recognize as it is a potentially fatal condition that requires close monitoring and is readily reversible with appropriate therapy. Any cause of thyroid hormone excess can cause TPP, with Graves’ disease being the most common etiology. Acute treatment includes potassium repletion, while long-term management focuses on determining and treating the cause of thyrotoxicosis, since maintaining a euthyroid state will prevent further episodes of TPP.


Diagnostics ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 316 ◽  
Author(s):  
Stefana Bilha ◽  
Ovidiu Mitu ◽  
Laura Teodoriu ◽  
Cristian Haba ◽  
Cristina Preda

Despite its’ life-threatening potential due to cardiac severe dysrhythmia in the context of severe hypokalemia, thyrotoxic periodic paralysis (TPP) often goes unrecognized. Although classically confined to young Asian men, it can occur irrespective of age, sex, and race. We report a short series of three cases of TPP as first presentation of Graves’ disease in a young Caucasian male and in two Caucasian elderly and middle-aged women, respectively. The first patient developed malignant ventricular arrhythmias due to severe hypokalemia and was defibrillated, with recovery after prompt potassium correction and administration of antithyroid agents and propranolol. The other two cases developed persistent hypokalemia despite adequate potassium chloride (KCl) repletion, with slow recovery of motor deficit and serum potassium normalization up to day 5. In the first case, long-term euthyroid state was achieved via total thyroidectomy due to the presence of a suspicious nodule that proved to be malignant. In the other two cases, medical treatment was the choice of therapy for thyrotoxicosis. None experienced recurrent TPP. Thyroid hormone evaluation is mandatory in the presence of hypokalemic paralysis, even in the absence of clinical signs of thyrotoxicosis. If TPP is confirmed, initial therapy should comprise antithyroid drugs and propranolol, besides hypokalemia correction.


1957 ◽  
Vol 189 (3) ◽  
pp. 605-608 ◽  
Author(s):  
W. F. Rosse ◽  
A. L. Bennett ◽  
A. R. McIntyre

Shock was induced in dogs by the release of tourniquets which had been applied to the hind legs for 5 hours. The serum potassium level was followed by spaced sampling. It was seen to rise slightly (from an average of 4.02 mEq/l. to an average of 4.66 mEq/l.) during the prerelease period. Five minutes after the release of the tourniquets, the level had risen to an average of 7.50 mEq/l. and thirty minutes after the release, it had risen to an average of 8.56 mEq/l. At the critical point in the progress of the syndrome (when the mean blood pressure was approximately 50 mm Hg) the average value was 8.46 mEq/l. Ouabain was administered and the level of serum potassium was seen to rise, attaining values as high as 14.67 mEq/l. in one case. The results and significance of these increased levels are briefly discussed as well as an animadversion upon the effects of ouabain on the mean blood pressure.


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