Approach to the patient with electrolyte disorders

Hypokalemia-Hyperkalemia

Zehra Eren, M.D.

LEARNING OBJECTIVES• recall potassium distribution• recall etiology of hypokalemia and hyperkalemia

• describe sing and symptoms of hypokalemia and hyperkalemia

• describe laboratory findings of hypokalemia and hyperkalemia

• explane treatment of hypokalemia and hyperkalemia

POTASSİUM DİSTRİBUTİON

•Gastrointestinal absorption→%98 intracellular%2 extracellular

•NA+K+ ATPase → transports two K+ into cell three Na+ out cell

Hypokalemia 

•Serum K+ < 3.5 mEq/L (mmol/L)

Causes of Hypokalemia • Pseudohypokalemia

-Extreme leukocytosis

• Decreased K intake

• Increased K losses -Nonrenal (skin, gastrointestinal)-Renal

RENAL POTASSİUM LOSS1. Increased distal flow and distal Na+ delivery

-diuretics -osmotic diuresis -salt-wasting nephropathies

2. Increased secretion of potassium - Mineralocorticoid excess: primary

hyperaldosteronism [aldosterone-producing adenomas (APAs)], primary or unilateral adrenal hyperplasia (PAH), idiopathic hyperaldosteronism (IHA) due to bilateral adrenal hyperplasia, and adrenal carcinoma], familial hyperaldosteronism (FH-I, FH-II, congenital adrenal hyperplasias), secondary hyperaldosteronism (malignant hypertension, renin-secreting tumors, renal arterystenosis, hypovolemia), Cushing's syndrome, Bartter's syndrome, Gitelman's syndrome

RENAL POTASSİUM LOSS-Apparent mineralocorticoid excess: genetic

deficiency of 11β-dehydrogenase-2 (syndrome of apparent mineralocorticoid excess), inhibition of 11β-dehydrogenase-2 (glycyrrhetinic/glycyrrhizinic acid and/or carbenoxolone; licorice, food products, drugs), Liddle's syndrome [genetic activation of epithelial Na+ channels (ENaC)]

-Distal delivery of nonreabsorbed anions: vomiting, nasogastric suction, proximal renal tubular acidosis, diabetic ketoacidosis, glue sniffing (toluene abuse), penicillin derivatives (penicillin, nafcillin, dicloxacillin, ticarcillin,oxacillin and carbenicillin)

Causes of Hypokalemia• Redistribution (increased entry into cell)

-Insulin excess-Alkalemia-“Stress” [β2 adrenergic sympathetic activityꜛ: asthma attack,

acute coronary syndrome, trauma, drug intoxication (cocaine) or alcohol withdrawal, B2 adrenergic drugs ]

-α-adrenergic antagonists-Hypokalemic periodic paralysis-Thyrotoxicosis-Barium, Cesium -Hypothermia-Downstream stimulation of NA+/K+ ATPase: theophyline, cafferine

DİAGNOSİS

• Rule out -pseudohypokalemia-redistribution

• Potassium deplettion-renal-gastrointestinal-skin

Clinical manifestations • Cardiovascular:

-Hypertansion (↑BP 5-10mmHg )-Arrhythmias-Digitalis toxicity

• Neuromuscular: 1.Smooth muscle:

-Ileus2.Skeletal muscle:

-Weakness-Paralysis-Rhabdomyolysis

Clinical manifestations• Endocrine:

-Glucose intolerance (↓insulin release and sensitivity)

• Renal: ↓blood flow,↑vascular resistance-Vasopressin resistance-Increased ammonia production-Metabolic alkalosis (retention of Na, Cl, HCO3)-Polyuria, phosphaturia, hypocitraturia

Structural changes: Renal cystsInterstitial changesPT dilation, vacuolization

TREATMENT GOALS

• prevent life-threatening and/or chronic consequences

• replace the associated K+ deficit

• correct the underlying cause and/or mitigate future hypokalemia

TREATMENT

Urgency of therapy depends on -the severity of hypokalemia -associated clinical factors (cardiac disease,digoxin therapy, etc.) -rate of decline in serum K+

Cautions-severe redistributive hypokalemia -concomitant Mg2+ deficiency

TREATMENT•Oral

• İntravenousSafely at a rate of 10 mmol/h

20mmol KCL →↑serum K + ~ 0.25 mmol/L

↑20mmol/h replacement → central venous catheter

Hyperkalemia 

•Serum K ≥5.0 mEq/L (mmol/L)

Causes of Hyperkalemia • Pseudohyperkalemia

-Thrombocytosis-Leukocytosis-Ischemic blood draw

• Redistibution (increased K release from cells)-Exercise, especially in setting of β adrenergic receptor blockage and mineral acidosis-Hyperchloremic metabolic acidosis-Insulin deficiency-Hypertonicity-α adrenergic receptor stimulation

Causes of Hyperkalemia • Excessive intake: rare as sole cause

• Impeared renal K+ excretionGFR <20 mL/min:

-Endogenous or exogenous K+

-Drugs that impair K+ excretion

Clinical manifestations 

• May be disproportionately greater than level of serum K• Cardiovascular

-T-wave abnormalities-Bradyarrhythmias

• Neuromuscular-Ileus-Paresthesias-Weakness-Paralysis

• Renal/electrolyte-Decreased ammonia production-Metabolic acidosis

Case1• A 70-year-old man with advanced prostate cancer develops

bilateral ureteral obstruction and acute on chronic renal failure.

His potassium rises to 7.7 mEq/L with peaked T-waves on electrocardiogram. His medications include digoxin.

Case2• A 72 year old male found collapsed at home on floor of his

bedroom, incontinent of urine and faeces. He complained of significant pain in his right hip with shortening and rotation. His family last had contact with him 3 days prior to his collapse.

• Medical History:CCF , Hypertension , Type 2 DM, Osteoarthritis

• Medication History:His is taking  enlapril for hypertension; spironolactone & metoprolol for his CCF and celebrex for his osteoarthritis.His diabetes is diet controlled.

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