Calculate Potassium Deficit Formula

[Paz Warsager]

Hypokalemiais one of the most common water-electrolyte imbalances and affects about 20% of patients admitted to the hospital medical surgical services and about 40% of patients admitted to intensive care units.

The most common causes of hypokalemia defined as a level below 3.5mEq/L (3.5 mmol/L) include vomiting, diarrhea, hypomagnesemia,diuretics such as furosemide, hyperaldosteronism, and less commonlyinadequate intake. Normal potassium levels are between 3.5 and5.0 mEq/L. Mildly low potassium levels (3.0 to 3.5 mEq/L)typically do not cause symptoms, however, may lead to increases inblood pressure and provoke the development of an abnormal heartrhythm. Moderate hypokalemia (serum potassium levels of 2.5 to 3 mEq/L (2.5 -3.0 mmol/L), may cause muscle weakness, tiredness, myalgia, tremor,muscle cramps, and constipation. Severe deficits leading toserum potassium levels below 2.5 mEq/L may be life-threatening andlead to electrocardiographic(ECG) changes such as QRS prolongation, ST-segment and T-wave depression,andU-wave formation. The earliest (ECG) findings in patients withhypokalemia are decreased T waveheight, followed by ST depressions and T inversions as levelscontinue to fall.

Usually, oral potassium chloride is administered when potassium levels need to be replenished, as well as, in patients with ongoing potassium loss (eg, those on thiazide diuretics), when it must be maintained. Potassium-sparing diuretics are generally used only in patients with normal renal function who are prone to significant hypokalemia.

Angiotensin-converting enzyme (ACE) inhibitors, which inhibit renal potassium excretion, can ameliorate some of the hypokalemia that thiazide and loop diuretics can cause. However, ACE inhibitors can lead to lethal hyperkalemia in patients with renal insufficiency who are taking potassium supplements or potassium-sparing diuretics.

Because of the risk associated with potassium replacement, alleviation of the cause of hypokalemia may be preferable to treatment, especially if hypokalemia is mild, asymptomatic, or transient and is likely to resolve without treatment. For example, patients with vomiting who are successfully treated with antiemetics may not require potassium replacement.

Bear in mind, however, that many factors in addition to the total body potassium stores contribute to the serum potassium concentration. Therefore, this calculation could either overestimate or underestimate the true potassium deficit. For example, do not overcorrect potassium in patients with periodic hypokalemic paralysis. This condition is caused by transcellular maldistribution, not by a true deficit.

Patients who have mild or moderate hypokalemia (potassium level of 2.5-3.5 mEq/L) are usually asymptomatic; if these patients have only minor symptoms, they may need only oral potassium replacement therapy. If cardiac arrhythmias or significant symptoms are present, then more aggressive therapy is warranted. This treatment is similar to the treatment of severe hypokalemia.

Higher dosages may increase the risk of cardiac complications. Many institutions have policies that limit the maximum amount of potassium that can be given per hour. Hospital admission or observation in the emergency department is indicated; replacement therapy takes more than a few hours.

Oral potassium is absorbed readily, and relatively large doses can be given safely. Oral administration is limited by patient tolerance because some individuals develop nausea or even gastrointestinal ulceration with enteral potassium formulations.

Intravenous potassium, which is less well tolerated because it can be highly irritating to veins, can be given only in relatively small doses, generally 10 mEq/h. Under close cardiac supervision in emergent circumstances, as much as 40 mEq/h can be administered through a central line. Oral and parenteral potassium can safely be used simultaneously.

Take ongoing potassium losses into consideration by measuring the volume and potassium concentration of body fluid losses. If the patient is severely hypokalemic, avoid glucose-containing parenteral fluids to prevent an insulin-induced shift of potassium into the cells. If the patient is acidotic, correct the potassium first to prevent an alkali-induced shift of potassium into the cells.

Monitor for toxicity of hypokalemia, which generally is cardiac in nature. Monitor the patient if evidence of cardiac arrhythmias is observed, and institute very aggressive replacement parenterally under monitored conditions.

Tailor treatment to the individual patient. For example, if diuretics cannot be discontinued because of an underlying disorder such as heart failure, institute potassium-sparing therapies, such as a low-sodium diet, potassium-sparing diuretics, ACE inhibitors, and angiotensin receptor blockers.

The low-sodium diet and potassium-sparing diuretics limit the amount of sodium reabsorbed at the cortical collecting tubule, thus limiting the amount of potassium secreted. ACE inhibitors and angiotensin receptor blockers inhibit the release of aldosterone, thus blocking the kaliuretic effects of that hormone.

Transfer generally is not required unless patients experience untreatable cardiac arrhythmias, digoxin toxicity, or paralysis and no facilities are available for monitoring. In general, even severe hypokalemia can be treated successfully in most medical centers.

Patients with severe or symptomatic hypokalemia require transfer to an intensive care unit for intravenous potassium supplementation and continuous ECG monitoring. Patients should be transferred only after any cardiac arrhythmias have been treated and the condition has been stabilized. Depending on the level of hypokalemia, an advanced cardiac life support (ACLS) ambulance should be used to allow continuous cardiac monitoring during transport.

Dietary modification may be necessary for patients with excessive potassium losses (eg, diuretic or laxative use) or patients with hypokalemia who are at increased risk, such as those receiving digoxin. In general, a low-sodium and high-potassium diet is appropriate. Avoidance of specific foods (eg, licorice) may also be necessary for high-risk individuals.

Unless the patient has severe underlying cardiac disease, no activity restrictions are necessary in most cases. Instruct patients to discontinue exercise if muscle pain or cramps develop, because this may herald hypokalemia significant enough to produce rhabdomyolysis. Patients with hypokalemic periodic paralysis may need to modify exercise regimens to avoid periods of strenuous exercise.

Patients at risk for hypokalemia from sweat losses should have adequate potassium and fluid available during activities likely to result in significant sweating and should be given anticipatory guidance regarding symptoms of hypokalemia.

Inpatient care includes monitoring serum potassium levels every 1-3 hours and adjusting supplement doses as necessary. Recall that potassium can shift in and out of cells under several influences. Therefore, several determinations of serum potassium level after presumably adequate replacement are indicated to ensure that serum potassium levels achieve normalcy.

After potassium has been replenished, checking again for several days to determine whether potassium has stabilized or has started falling again is equally important. For example, if an individual presents with nausea, vomiting, and hypokalemia, the physician might understandably attribute the hypokalemia to the nausea and vomiting. However, if after replenishment the patient once again develops hypokalemia without nausea and vomiting, then considering other possible causes of hypokalemia is necessary.

Additionally, if a need for ongoing potassium supplementation is anticipated for the patient (eg, a patient on long-term diuresis for hypertension), then ensuring that the prescribed daily potassium supplement is adequate to maintain a normal serum potassium level is important.

Electrocardiographic (ECG) monitoring is imperative for severe hypokalemia (Once a cause has been determined for hypokalemia and the condition has been treated as per the diagnosis, ensuring that treatment plans are adequate is imperative. Evaluate for more unusual secondary causes. If an unusual cause of hypokalemia is suggested, either by specific clinical features or failure to respond to initial therapy, evaluation can at least begin while the patient is hospitalized. However, evaluation often can be completed in an outpatient setting.

If covert diuretic or laxative use is suspected, establishing proof of this is best accomplished in the hospital, with patients in a relatively controlled environment. In this setting, 24-hour urine measurements of sodium and potassium excretion, measurement of serum potassium at frequent intervals, and supervision of intake and output are possible. Ongoing potassium losses in the face of a negative urine and serum screen for diuretics suggest another diagnosis.

Consider an imaging study (eg, renal vascular Doppler, captopril renal scan, or computed tomography [CT] angiography) to investigate the possibility of renal artery stenosis; [59] perform a CT scan of the abdomen to investigate for a possible adrenal adenoma.

A high cortisol level suggests Cushing syndrome. Evaluate for pituitary or adrenal causes. If renin and aldosterone levels are both elevated, this points more strongly to renal artery stenosis. If the index of suspicion is high enough, perform a renal arteriogram and renal vein renin determination to look for significant renal artery stenosis as a cause of hypertension and hypokalemia.

A high aldosterone level with low renin activity suggests primary hyperaldosteronism. If the patient is hypertensive but the aldosterone level is low, this suggests one of the more unusual congenital forms of hypertension, such as Liddle syndrome, in which a mutation in the epithelial sodium channel produces uncontrollable sodium reabsorption or glucocorticoid-remediable hypertension. This scenario also could be produced by licorice ingestion or ingestion of a steroid with mineralocorticoid activity, such as prednisone or fludrocortisone.

3a8082e126