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Etiology by System
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Diagnosis: Clinical signs are weakness, silent distention of the abdomen, dyspnea, cardiac arrythmia, and EKG changes. Serum potassium levels usually low, but may be normal in spite of intracellular depletion (as is common in DKA). Many of the causes are renal; these may be divided into those associated with hypertension (secondary to hyperaldosteronism and hyperreninism) versus normotensive causes which affect tubular function. Symptoms appear when serum K drops below 3. These include: hyperglycemia, CBH intolerance, sodium retention and edema, hyposthenia causing polyuria and polydipsia, and neuromuscular signs such as weakness, paralysis, intestinal ileus, autonomic insufficiency with orthostatic hypotension, lethargy and confusion. Cardiac arrythmias may also develop.
Signifigance: Potassium is necessary for proper nerve conduction. Cardiac arrythmia is the most serious effect.
Treatment: If the K is less than 3, or the patient is symptomatic,
the patient should be placed on a cardiac monitor during treatment.
Urine output should be measured to make sure that urine is produced, and
that K will not accumulate to toxic levels. Unlike treatment of hyponatremia,
K replacement is not a matter of calculating a correction based on serum
K levels, since these are a poor reflection of the overwhelming proportion
of K that is intracellular. Except for emergency management, K replacement
should proceed slowly to allow equilibration. Large intravenous loads
of potassium should be avoided. Replete potassium, up to 100 mEq
per sq meter per 24 hours. Parenteral fluid concentrations of potassium
should not exceed 40 mEq/L. K can also be given by mouth, using 3
mEq/kg/day in addition to maintenance requirements. The citrate salt
is more palatable than the chloride salt.
| Increased Total Potassium | Normal Potassium Stores | |||
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Diagnosis: Characteristic EKG changes include tall, peaked T-waves, prolonged PR interval, disappearance of the P wave, depressed ST segment, widening QRS complex and finally a sine wave pattern followed by ventricular fibrillation. Cardiac changes are usually, but not always, preceeded by weakness and paralysis, usually starting in the lower extremity.
Signifigance: Elevated K depresses the SA node, causes ventricular arrythmias, ventricular fibrillation and asystole.
Treatment: For moderate hyperkalemia (6.5-7) restrict intake of potassium and liberalize dietary sodium. For symptomatic or higher serum potassium, treatment consists of the following: membrane stabilization with calcium gluconate; transfer of potassium into cells by treatment with bicarbonate, glucose and insulin; and removal of potassium from the body using exchange resins or if necessary, peritoneal or hemodialysis. Cardiac monitoring should be used.
If arrythmia is
present, 10% calcium gluconate, 0.5 ml/kg iv over 5 minutes. May
repeat in 10 minutes. Membrane stabilization effect lasts 30 minutes;
there is no effect on serum potassium.
Bicarbonate 2
mEq/kg IV as rapid push over 5-10 minutes (even in absence of acidosis).
Increase ECF to
dilute K concentration: bolus with 20 ml/kg NS unless counterindicated
by patient condition.
Give 0.1 units
per kg insulin with 0.5g/kg of 25% glucose over 30 minutes. Then
begin infusion of 0.5 grams/kg per hour of glucose using D10W or
D25W with 0.1 units of regular insulin per hour. Monitor glucose
q hour.
Kayexalate (polystyrene
sulfonate resin) 0.5 to 1.0 g/kg as retention enema over 30-45 minutes
Administer in sorbitol 20-25%, 3 mL solution per 1 g resin to prevent
constipation and limit stool losses
Repeat q 4-6 hours, watch for hypernatremia secondary to osmotic catharsis
and exchange of Na for K.
Dialysis if necessary.
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