Chapter 046. Sodium and Water (Part 15)

Algorithm depicting clinical approach to hypokalemia. TTKG, transtubular K+ concentration gradient; RTA, renal tubular acidosis.
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Chapter 046. Sodium and Water (Part 15) Chapter 046. Sodium and Water (Part 15) Algorithm depicting clinical approach to hypokalemia. TTKG,transtubular K+ concentration gradient; RTA, renal tubular acidosis. After eliminating decreased intake and intracellular shift as potential causesof hypokalemia, examination of the renal response can help to clarify the source ofK+ loss. The appropriate response to K+ depletion is to excrete K+concentration gradient (TTKG). The TTKG is the ratio of the K+ concentrationin the lumen of the CCD ([K+]CCD) to that in peritubular capillaries or plasma([K+]P). The validity of this measurement depends on three assumptions: (1) fewsolutes are reabsorbed in the medullary collecting duct (MCD), (2) K + is neithersecreted nor reabsorbed in the MCD, and (3) the osmolality of the fluid in theterminal CCD is known. Significant reabsorption or secretion of K + in the MCDseldom occurs, except in profound K+ depletion or excess, respectively. WhenAVP is acting (OSMU ≥OSMP), the osmolality in the terminal CCD is the same asthat of plasma, and the K+ concentration in the lumen of the distal nephron can beestimated by dividing the urine K+ concentration ([K+]U) by the ratio of the urineto plasma osmolality (OSM U/OSMP): Hypokalemia: Treatment The therapeutic goals are to correct the K+ deficit and to minimize ongoinglosses. With the exception of periodic paralysis, hypokalemia resulting fromtranscellular shifts rarely requires intravenous K+ supplementation, which can leadto rebound hyperkalemia. It is generally safer to correct hypokalemia via the oralroute. The degree of K+ depletion does not correlate well with the plasma K+concentration. A decrement of 1 mmol/L in the plasma K+ concentration (from 4.0to 3.0 mmol/L) may represent a total body K+ deficit of 200–400 mmol, andpatients with plasma levels under 3.0 mmol/L often require in excess of 600 mmolof K+ to correct the deficit. Furthermore, factors promoting K+ shift out of cells(e.g., insulin deficiency in diabetic ketoacidosis) may result in underestimation ofthe K+ deficit. Therefore, the plasma K+ concentration should be monitoredfrequently when assessing the response to treatment. Potassium chloride is usuallythe preparation of choice and will promote more rapid correction of hypokalemiaand metabolic alkalosis. Potassium bicarbonate and citrate (metabolized to HCO 3–)tend to alkalinize the patient and would be more appropriate for hypokalemiaassociated with chronic diarrhea or RTA. Patients with severe hypokalemia or those unable to take anything bymouth require intravenous replacement therapy with KCl. The maximumconcentration of administered K+ should be no more than 40 mmol/L via aperipheral vein or 60 mmol/L via a central vein. The rate of infusion should notexceed 20 mmol/h unless paralysis or malignant ventricular arrhythmias arepresent. Ideally, KCl should be mixed in normal saline since dextrose solutionsmay initially exacerbate hypokalemia due to insulin-mediated movement of K+into cells. Rapid intravenous administration of K+ should be used judiciously andrequires close observation of the clinical manifestations of hypokalemia(electrocardiogram and neuromuscular examination). Hyperkalemia Etiology Hyperkalemia, defined as a plasma K+ concentration >5.0 mmol/L, occursas a result of either K+ release from cells or decreased renal loss. Increased K +intake is rarely the sole cause of hyperkalemia since the phenomenon of potassiumadaptation ensures rapid K+ excretion in response to increases in dietaryconsumption. Iatrogenic hyperkalemia may result from overzealous parenteral K +replacement or in patients with renal insufficiency. Pseudohyperkalemiarepresents an artificially elevated plasma K+ concentration due to K+ movementout of cells immediately prior to or following venipuncture. Contributing factorsinclude prolonged use of a tourniquet with or without repeated fist clenching,hemolysis, and marked leukocytosis or thrombocytosis. The latter two result in anelevated serum K+ concentration due to release of intracellular K+ following clotformation. Pseudohyperkalemia should be suspected in an otherwiseasymptomatic patient with no obvious underlying cause. If proper venipuncturetechnique is used and a plasma (not serum) K+ concentration is measured, itshould be normal. Intravascular hemolysis, tumor lysis syndrome, andrhabdomyolysis all lead to K+ release from cells as a result of tissue breakdown.