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تاريخ التسجيل : 05/03/2008

مُساهمةموضوع: تمرض الباطنة والجراحة   السبت مارس 15, 2008 9:54 am

Hypokalemia


Hypokalemia is characterized by a serum potassium

concentration of less than 3.5 mEq/L. Ninety-eight percent

of K is intracellular.


I. Pathophysiology of hypokalemia

A. Cellular redistribution of potassium. Hypokalemia

may result from the intracellular shift of potassium by

insulin, beta-2 agonist drugs, stress induced

catecholamine release, thyrotoxic periodic paralysis,

and alkalosis-induced shift (metabolic or respiratory).

B. Nonrenal potassium loss


1. Gastrointestinal loss can be caused by diarrhea,

laxative abuse, villous adenoma, biliary drainage,

enteric fistula, clay ingestion, potassium binding

resin ingestion, or nasogastric suction.

2. Sweating, prolonged low-potassium diet,

hemodialysis and peritoneal dialysis may also

cause nonrenal potassium loss.

C. Renal potassium loss

1. Hypertensive high renin states. Malignant

hypertension, renal artery stenosis, renin-produc-

ing tumors.

2. Hypertensive low renin, high aldosterone

states. Primary hyperaldosteronism (adenoma or

hyperplasia).

3. Hypertensive low renin, low aldosterone states.

Congenital adrenal hyperplasia (11 or 17 hydroxy-

lase deficiency), Cushing's syndrome or disease,

exogenous mineralocorticoids (Florinef, licorice,

chewing tobacco), Liddle's syndrome.



4. Normotensive states

a. Metabolic acidosis. Renal tubular acidosis

(type I or II)

b. Metabolic alkalosis (urine chloride <10

mEq/day). Vomiting

c. Metabolic alkalosis (urine chloride >10

mEq/day). Bartter's syndrome, diuretics, mag-

nesium depletion, normotensive hyperaldo-

steronism

5. Drugs associated with potassium loss includeamphotericin B, ticarcillin, piperacillin, and loop

diuretics.



II. Clinical effects of hypokalemia

A. Cardiac effects. The most lethal consequence of

hypokalemia is cardiac arrhythmia.

Electrocardiographic effects include a depressed ST

segment, decreased T-wave amplitude, U waves,

and a prolonged QT-U interval.

B. Musculoskeletal effects. The initial manifestation of

K depletion is muscle weakness, which can lead to

paralysis. In severe cases, respiratory muscle paraly-

sis may occur.

C. Gastrointestinal effects. Nausea, vomiting, consti-

pation, and paralytic ileus may develop.


III. Diagnostic evaluation
A. The 24-hour urinary potassium excretion should be

measured. If >20 mEq/day, excessive urinary K loss

is the cause. If <20 mEq/d, low K intake, or non-

urinary K loss is the cause.

B. In patients with excessive renal K loss and hyperten-

sion, plasma renin and aldosterone should be mea-

sured to differentiate adrenal from non-adrenal

causes of hyperaldosteronism.

C. If hypertension is absent and serum pH is acidotic,

renal tubular acidosis should be considered. If hyper-

tension is absent and serum pH is normal to alkalotic,

a high urine chloride (>10 mEq/d) suggests

hypokalemia secondary to diuretics or Bartter's

syndrome. A low urine chloride (<10 mEq/d) suggests

vomiting.



IV. Emergency treatment of hypokalemia

A. Indications for urgent replacement.

Electrocardiographic abnormalities, myocardial

infarction, hypoxia, digitalis intoxication, marked

muscle weakness, or respiratory muscle paralysis.

B. Intravenous potassium therapy

1. Intravenous KCL is usually used unless concomi-

tant hypophosphatemia is present, where potas-

sium phosphate is indicated.

2. The maximal rate of intravenous K replacement is

30 mEq/hour. The K concentration of IV fluids

should be 80 mEq/L or less if given via a periph-

eral vein. Frequent monitoring of serum K and

constant electrocardiographic monitoring is recom-

mended when potassium levels are being re-

placed.



V.Non-emergent treatment of hypokalemia

A. Attempts should be made to normalize K levels if

<3.5 mEq/L.

B. Oral supplementation is significantly safer than IV.

Liquid formulations are preferred due to rapid oral

absorption, compared to sustained release formula-

tions, which are absorbed over several hours.

1. KCL elixir 20-40 mEq qd-tid PO after meals.

2. Micro-K, 10 mEq tabs, 2-3 tabs tid PO after me
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