Sodium and potassium condition sheet. Difference between hypo and hyper,

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Scope and normal ranges: The supplied sources define hyponatraemia as serum sodium <135 mmol/L and hypokalaemia as serum potassium <3.5 mmol/L, but do not state upper limits of normal or formal diagnostic thresholds for hypernatraemia or hyperkalaemia. ^1,^2 Hyponatraemia: Hyponatraemia is a disorder of water balance and is classified as mild (130–135 mmol/L), moderate (125–129 mmol/L), or severe (<125 mmol/L), and as acute when present for <48 hours or chronic when present for ≥48 hours. ^1 It may be hypertonic, isotonic/pseudohyponatraemic, or—most commonly—hypotonic true hyponatraemia, which is further divided by volume status into hypovolaemic, euvolaemic, and hypervolaemic forms. ^1 Mechanisms and contributors are often multifactorial and include drugs, especially thiazide diuretics, syndrome of inappropriate antidiuresis, and heart failure, kidney disease, or liver disease. ^1 Hyperglycaemia should be considered as a cause of hypertonic hyponatraemia. ^1 Mild gradual hyponatraemia is often asymptomatic, whereas rapid change or severe hyponatraemia may cause vomiting, headache, drowsiness, seizures, coma, and cardiorespiratory arrest. ^1 Chronic hyponatraemia may cause gait disturbance, falls, impaired concentration, and other cognitive deficits, and symptom severity may not correlate with the sodium concentration. ^1 Major hazards are cerebral oedema in severe or acute hyponatraemia and osmotic demyelination from overly rapid correction in chronic hyponatraemia. ^1,^4 Hypernatraemia: The supplied sources describe hypernatraemia as a consequence of excessive sodium chloride administration, with dehydration of internal organs—particularly the brain—potentially leading to thrombosis and haemorrhage. ^3 Treatment requires careful intravenous hypotonic saline correction, with restoration limited to no more than 10–15 mmol/L per day. ^3 Dialysis may be required with significant renal impairment, a moribund patient, or sodium >200 mmol/L. ^3 Hypokalaemia: Hypokalaemia is usually caused by increased potassium loss or intracellular shift and is rarely due solely to low intake. ^2 It is classified biochemically as mild (3.0–3.4 mmol/L), moderate (2.5–2.9 mmol/L), or severe (<2.5 mmol/L), although clinical severity depends on symptoms and ECG abnormalities as well as the concentration. ^2 Causes and risk factors include thiazide or loop diuretics, beta-agonists, insulin, corticosteroids, primary hyperaldosteronism, hypercortisolism, hypomagnesaemia, vomiting, diarrhoea, alcohol misuse, metabolic alkalosis, thyrotoxicosis, pheochromocytoma, increased insulin secretion, gastrointestinal illness, fasting, hypocaloric or unbalanced diets, and eating disorders. ^2 Manifestations include skeletal-muscle weakness, lethargy, fatigue, myalgia, cramps, paraesthesia, numbness, dyspnoea, rhabdomyolysis, ascending paralysis, respiratory failure, constipation, nausea, vomiting, ileus, polyuria, and cardiac rhythm abnormalities. ^2 Hyperkalaemia: The supplied sources describe hyperkalaemia as potassium intoxication that may follow potassium-containing infusion overdose or occur with renal insufficiency. ^4 Manifestations are predominantly cardiovascular—hypotension, arrhythmia, heart block, ECG abnormalities, and cardiac arrest—and may also include paraesthesiae, weakness, areflexia, muscle or respiratory paralysis, and confusion. ^4 Initial emergency measures include stopping the infusion, ECG monitoring, enhancing urinary potassium excretion where appropriate, and using sodium bicarbonate and insulin with glucose to promote intracellular potassium uptake. ^4 Persistent ECG abnormalities may warrant calcium gluconate to antagonise potassium cardiotoxicity, while haemodialysis or peritoneal dialysis may be required in renal insufficiency. ^4 Primary-care assessment and disposition: For asymptomatic mild hyponatraemia, take a history of acute illness or surgery, fluid intake, thirst, urine output, weight change, medicines, comorbidities, exercise, diet, alcohol, recreational drugs, and prior hyponatraemia. ^1 Assess volume status using pulse, lying and standing blood pressure, JVP, oedema, and signs of dehydration or overload; hypovolaemia includes tachycardia, postural hypotension, dry mucosae, oliguria, low JVP, and reduced skin turgor, while hypervolaemia includes oedema, ascites, weight gain, and raised JVP. ^1 Repeat sodium with potassium, urea, and creatinine, obtain serum osmolality, and send paired urine for osmolality and sodium; consider glucose/HbA1c, renal investigations, and urinalysis where indicated. ^1 Admit urgently for acute-onset, severe, or symptomatic hyponatraemia or signs of hypovolaemia, discuss asymptomatic moderate hyponatraemia with endocrinology, and where appropriate address intercurrent illness, reduce or stop contributing medicines, and monitor sodium in primary care. ^1 For hypokalaemia, assess history including medication use, blood pressure and volume status, ECG abnormalities, and the underlying cause. ^2 Admit immediately if potassium is <2.5 mmol/L, if symptoms occur—particularly dysrhythmia, paralysis, respiratory failure, or severe weakness—or if there is hypovolaemia, thyrotoxic crisis, metabolic acidosis or alkalosis, hyperosmolar hyperglycaemic state, diabetic ketoacidosis, or severe/symptomatic hypomagnesaemia. ^2 Discuss specialist referral for asymptomatic moderate hypokalaemia or concurrent cardiac, renal, or hepatic disease that increases complication risk. ^2 Prognosis: Mild slowly developing sodium or potassium abnormalities may be asymptomatic, but acute or severe derangements can cause neurological, respiratory, or life-threatening cardiac complications. ^1,^2,^4 Hyponatraemia is associated with fragility fractures, osteoporosis, and increased mortality, morbidity, and hospital length of stay. ^1

Sodium and potassium condition sheet. Difference between hypo and hyper,

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