Hypokalemia happens when there’s too little potassium in the extracellular fluid, generally under 3.5 mEq/L and it’s usually due to a low potassium intake, abuse of laxatives, vomiting, metabolic alkalosis and the use of diuretics- both loop and thiazides.
Hypokalemia can be asymptomatic or can cause symptoms like palpitations or smooth muscle weakness leading to an ileus which can cause nausea and vomiting.
In severe cases, there can be muscle weakness in the skeletal muscles, which can lead to diaphragmatic paralysis and difficulty breathing.
Whenever potassium levels are below 3.5 mEq/L, the first thing to do is an EKG.
There may be EKG changes, but they don’t always correlate with the severity and progression of hypokalemia.
The EKG typically shows ST segment depression, a depressed T wave, and an increase in the amplitude of the U wave, best seen in leads V4 to V6.
Sometimes, the T and U waves merge to form a T-U wave which can be mistaken for a prolonged QT interval.
In severe cases, the QRS duration is prolonged, the ST becomes markedly depressed, and the T waves are inverted.
Common causes of hypokalemia are diarrhea, vomiting, or diuretic use. But if these aren’t the cause, then urinary potassium is assessed in order to see if hypokalemia is caused by renal losses.
The best way to do that is to measure the 24-hour urine potassium, but because that takes a full day, in an urgent setting, a spot urine potassium to creatinine ratio can be obtained instead.
Next, an ABG is done to assess acid-base status.
In metabolic acidosis it would show a pH below 7.35 and a bicarbonate-or HCO3 level below 22 mEq/L.
If metabolic acidosis is associated with a low urine potassium to creatinine ratio, then the cause may be gastrointestinal, like laxative abuse.
If metabolic acidosis is associated with a high urine potassium to creatinine ratio, then the cause may be diabetic ketoacidosis or type 1 or 2 renal tubular acidosis.
