management of hyperkalaemia and hypokalaemia

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Management of Hyperkalaemia and Hypokalaemia

Potassium homeostasis

Obtained through the diet -GI absorption is complete - daily excess intake of about 1 mEq/kg/d (60-100 mEq) - is excreted through the kidneys (90%) and the gut (10%). K homeostasis is maintained predominantly through the regulation of renal excretion. The most important site of regulation is the cortical collecting tubule where aldosterone receptors are present. Excretion is increased by the following:

-Aldosterone -High Na delivery to the distal tubule, eg, diuretics -High urine flow, eg, osmotic diuresis -High serum K level -Delivery of negatively charged ions to the distal tubule, eg, bicarbonate

Excretion is decreased by the following:

-Absence of aldosterone -Low Na delivery to the distal tubule -Low urine flow -Low serum K level -Renal failure

Pathophysiology-Hyperkalaemia

3 pathogenetic mechanisms can cause hyperkalemia. Excessive intake: relatively high K intake in a patient with impaired mechanisms for the intracellular shift of K or renal K excretion. Decreased excretion: renal failure; ingestion of drugs that interfere with K excretion, eg, K-sparing diuretics, ACE-I, NSAIDS; or impaired responsiveness of the distal tubule to aldosterone, eg, type IV renal tubular acidosis observed with DM, sickle cell disease, chronic partial urinary tract obstruction. Shift from intracellular to extracellular space: rhabdomyolysis and tumor lysis. However, more often, insulin deficiency or acute acidosis.

Clinical Features of Hyperkalaemia

Plasma K >6.5mmol/l needs urgent treatment-but 1st ensure its not an artefact (eg. due to hemolysis inside the bottle) Neuromuscular manifestations: Weakness, paraesthesia, areflexia, ascending paralysis Cardiac manifestations: Bradycardia, prolonged of AV conduction, complete heart block, wide complex tachycardia, ventricular fibrillation, and asystole ECG: tall tented T waves, small P waves, depressed ST segments, widened QRS complexes, sine waves (biphasic waves, pre-cardiac arrest) ECG has limitation in predicting cardiac toxicity. Thus patient should be treated even in the absence of ECG changes

Management Goals: -

To protect the heart from effects of K by antagonizing its effects on cardiac conduction (Ca) To shift K from ECF to ICF (Na bicarbonate, insulin & glucose) To reduce total body K (cation exchange resin & dialysis) Treatment is urgent if K>6.5 mmol/L or ECG shows change of hyperkalaemia

RecommendationsMild to moderate hyperK (5.5-6.5mmol/L) with no ECG changes:

low K diet Cation exchange-resins Correction of acidosis in patient with metabolic acisosis +/- Glucose & insulin infusion stop drugs which may cause hyperkalaemia K-sparing diuretics, spironolactone, triamterene, amiloride NSAIDS ACE-I ARB Cyclosporine or tacrolimus Pentamidine Trimethoprim/sulfamethoxazole Heparin Ketoconazole Metyrapone Herbs

Severe Hyperkalaemia (>6.5 mmol/L) or with ECG changes Above treatments Immediate Calcium administration Glucose and insulin infusion Sodium bicarbonate infusion Beta agonist therapy Dialysis

Calcium administration 10ml

of 10% calcium gluconate IV over 2-5 minutes. A 2nd dose can be given after 5 mins if no change in ECG is seen. Effect of calcium occurs within minutes and lasts for 1 hour Slower infusion rates in patients on digitalis to avoid hypercalcaemia-induced digitalis toxicity Calcium should not be given before after bicarbonate in the same IV line to avoid precipitation

Glucose and Insulin infusion Rapid

acting insulin 10u + 50cc of 50% dextrose IV infused over 30-60min (in pt with renal failure, higher dose of glucose needs to be given, e.g. 100-150 ml of dextrose) Onset within 30-60 min & lasts for several hours The above regime can be repeated 6-8 hourly Bolus hypertonic glucose solution may transiently exacerbate hyperK by its osmotic effect on cells After insulin & dextrose infusion, maintain pt. on continuous dextrose infusion, e.g.D5%

Sodium bicarbonate infusion IV

infusion of bicarbonate 100-200 mmol/l over 30 min produces metabolic alkalosis which lowers K in ECF Onset of action occurs within 30 min & lasts for 1-2 hours It is less effective in patients with renal failure

Cation-exchange resins (Resonium A) Bind

potassium in exchange for another cation in GI tract, thereby removing K from body Can be given orally (sodium polystyrebe [Resonium A] 15-30 g 3-4 times daily) or as enemas (Resonium A 30 -60 g in 200 ml 3-4 times daily)

Hemodialysis or peritoneal dialysis When

consvative measures fail, underlying cause is not reversible or in persistent hyperkalaemia

Beta-agonist therapy IV

salbutamol 0.5 mg in 15 min or 10 mg neb ( with or without glucose & insulin infusion) has been shown to be effective in reducing K level (IV is preferred in pt with ESRD) If effective, plasma K will fall by 0.5-1.5 mmol/l in 15-30 min & effect will last for several hours

Pathophysiology -Hypokalaemia

Poor K intake - seen in very elderly individuals unable to cook for themselves or unable to chew or swallow well or in pt.s receiving TPN, where K supplementation may be inadequate for a prolonged period of time. Increased excretion increase renal K losses incl. enhanced Na delivery to the collecting duct, as with diuretics; mineralocorticoid excess, as with primary or secondary hyperaldosteronism; or increased urine flow, as with an osmotic diuresis. GI losses diarrhea,vomiting (produces volume depletion and metabolic alkalosis) Shift from extracellular to intracellular space- Beta-adrenergic stimulation e.g.AMI, beta-agonists, insulin treatment e.g. DKA, exogenous glucose, alkalosis, hypokalaemic periodic paralysis-intermittent weakness lasting up to 72 hours

Clinical Features of Hypokalaemia

If K < 2.5 mmol/L, urgent treatment is required. Note that hypokalaemia exacerbates digoxin toxicity. Malaise, fatigue Neuromuscular disturbances: Weakness, hyporeflexia, paraesthesias, cramps, restless legs syndrome, rhabdomyolysis, paralysis GI : Constipation, ileus Polyuria, plydipsia, metabolic alkalosis ECG changes: small or inverted T waves, prominent U wave, depressed ST segments, prolonged PR intervals Arrhythmias: 1st & 2nd degree heart block, AF, ventricular tachycardia, ventricular fibrillation

Important facts

1g KCL contains 14 mmol (14 mEq) of K If serum K level does not appreciably rise after adequate K therapy (e.g. 72-96 h after oral therapy), concomitant Mg depletion should be suspected. If hypoK & low urinary K excretion (2.5 mmol/L) -Oral KCl 1-2g hrly until return of serum K to at least 3.5 mmol/L -Slow release K (1 tab = 8 mmol) -40-200 mmol daily of KCl may be rqd over periods of days or weeks e.g. 20-40 mmol 2-4 x daily depending on severity of depletion ( as frequent as 2-4 hrly may be rqd) -Monitor K levels closely to prevent hyperK -K-sparing diuretics (e.g. amiloride, triamterene & spironolactone) may be an alternative for pt.s in whom hypoK develops secondary to renal losses

IV therapy -Method of choice in pt.s with severe hypoK ( 10 mmol/hr requires continuous ECG monitoring As soon as ECG normalize, cardiac rhythm returns to normal or respiratory muscle strength is restored, IV infusion is gradually tapered & discontinued. Oral KCl is then initiated.

Complications:Complications of hyperkalemia range from mild ECG changes to cardiac arrest. Weakness is common as well.

Complications of therapy include the following:

Failure to control hyperkalemia Hypokalemia due to excessively aggressive therapy Hypercalcemia due to excessive calcium administration Hypocalcemia from excessive bicarbonate therapy Chest discomfort or tachycardia due to beta-agonist therapy Hypoglycemia or hyperglycemia complicating glucose and insulin administration Metabolic alkalosis and tetany due to excessive sodium bicarbonate administration Volume depletion, metabolic alkalosis, renal insufficiency, hypocalcemia, hypomagnesemia, and hypophosphatemia due to aggressive loop diuretic use Colon perforation due to Kayexalate administration

Complications of Hypokalaemia

Increased susceptibility to cardiac arrhythmias is observed with hypoK in CCF, IHD/ AMI, aggressive therapy of hyperglycemia, such as with DKA,digitalis therapy Low K intake has been implicated as a risk factor for the development of HPT and/or HPT EOD. Muscle weakness, depression of the deep-tendon reflexes, and even flaccid paralysis can complicate hypoK. Rhabdomyolysis can be provoked, especially with vigorous exercise. Abnormalities of renal function often accompany acute or chronic hypoK HypoK decreases gut motility, leading to or exacerbating an ileus. HypoK also is a contributory factor in the development of hepatic encephalopathy in the setting of cirrhosis. HypoK has a dual effect on glucose regulation.

HypoK decreases insulin release. It also decreases peripheral insulin sensitivity.

HypoK has widespread actions in many organ systems, which, over time, result in cardiovascular disease.

Patient Education:Inform patients regarding the following:

Instruct patients on symptoms of hypokalemia or hyperkalemia.

Palpitations or notable cardiac arrhythmias Muscle weakness Increasing difficulty with diabetes control Polyuria

Dietary sources of K, including salt substitutes Medications that impair renal excretion, including ACE-I, ARBs, NSAIDS, and K-sparing diuretics Clinical situations in which pt.s might be at risk for the development of hyperK, which incl.volume depletion and acute renal insufficiency complicating GI fluid losses; increasing doses of ACE-I or K-sparing diuretics; and a

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