Chapter 046. Sodium and Water (Part 15) pdf

TTKG, transtubular K+ concentration gradient; RTA, renal tubular acidosis.. After eliminating decreased intake and intracellular shift as potential causes of hypokalemia, examination of

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 causes

of hypokalemia, examination of the renal response can help to clarify the source of

K+ loss The appropriate response to K+ depletion is to excrete <15 mmol/d of K+

in the urine, due to increased reabsorption and decreased distal secretion Hypokalemia with minimal renal K+ excretion suggests that K+ was lost via the skin or gastrointestinal tract or that there is a remote history of vomiting or diuretic use As described above, renal K+ wasting may be due to factors that either increase the K+ concentration in the CCD or increase the distal flow rate (or both) The ECF volume status, blood pressure, and associated acid-base disorder may help to differentiate the causes of excessive renal K+ loss A rapid and simple test designed to evaluate the driving force for net K+ secretion is the transtubular

K+concentration gradient (TTKG) The TTKG is the ratio of the K+ concentration

in 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) few solutes are reabsorbed in the medullary collecting duct (MCD), (2) K+ is neither secreted nor reabsorbed in the MCD, and (3) the osmolality of the fluid in the terminal CCD is known Significant reabsorption or secretion of K+ in the MCD seldom occurs, except in profound K+ depletion or excess, respectively When AVP is acting (OSMU ≥OSMP), the osmolality in the terminal CCD is the same as that of plasma, and the K+ concentration in the lumen of the distal nephron can be estimated by dividing the urine K+ concentration ([K+]U) by the ratio of the urine

to plasma osmolality (OSMU/OSMP):

Hypokalemia: Treatment

The therapeutic goals are to correct the K+ deficit and to minimize ongoing losses With the exception of periodic paralysis, hypokalemia resulting from transcellular shifts rarely requires intravenous K+ supplementation, which can lead

to rebound hyperkalemia It is generally safer to correct hypokalemia via the oral route 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 4.0

to 3.0 mmol/L) may represent a total body K+ deficit of 200–400 mmol, and patients with plasma levels under 3.0 mmol/L often require in excess of 600 mmol

of K+ to correct the deficit Furthermore, factors promoting K+ shift out of cells (e.g., insulin deficiency in diabetic ketoacidosis) may result in underestimation of the K+ deficit Therefore, the plasma K+ concentration should be monitored frequently when assessing the response to treatment Potassium chloride is usually the preparation of choice and will promote more rapid correction of hypokalemia and metabolic alkalosis Potassium bicarbonate and citrate (metabolized to HCO3–) tend to alkalinize the patient and would be more appropriate for hypokalemia associated with chronic diarrhea or RTA

Patients with severe hypokalemia or those unable to take anything by mouth require intravenous replacement therapy with KCl The maximum concentration of administered K+ should be no more than 40 mmol/L via a peripheral vein or 60 mmol/L via a central vein The rate of infusion should not exceed 20 mmol/h unless paralysis or malignant ventricular arrhythmias are present Ideally, KCl should be mixed in normal saline since dextrose solutions may initially exacerbate hypokalemia due to insulin-mediated movement of K+ into cells Rapid intravenous administration of K+ should be used judiciously and requires 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, occurs

as 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 potassium

adaptation ensures rapid K+ excretion in response to increases in dietary consumption Iatrogenic hyperkalemia may result from overzealous parenteral K+

replacement or in patients with renal insufficiency Pseudohyperkalemia

represents an artificially elevated plasma K+ concentration due to K+ movement out of cells immediately prior to or following venipuncture Contributing factors include prolonged use of a tourniquet with or without repeated fist clenching, hemolysis, and marked leukocytosis or thrombocytosis The latter two result in an elevated serum K+ concentration due to release of intracellular K+ following clot formation Pseudohyperkalemia should be suspected in an otherwise asymptomatic patient with no obvious underlying cause If proper venipuncture technique is used and a plasma (not serum) K+ concentration is measured, it should be normal Intravascular hemolysis, tumor lysis syndrome, and rhabdomyolysis all lead to K+ release from cells as a result of tissue breakdown