Electrolitos en la Sala de Emergencias
Some electrolyte disturbances may require emergency treatment because they interfere with the electrophysiology of excitable tissues and may produce osmolar disturbances.
Hypokalemia is discussed in another summary of this congress.
Hyperkalemia
Levels of K>5.5 mEq/L result from decreased renal excretion, adrenocortical insufficiency, iatrogenic upload, inadequate distribution and massive cell damage.
Hyperkalemia produces depolarization of neuromuscular membranes, weakness and paresis. 7.5 mEq/L y son más severos cuando se asocia a hiponatremia. Electrocardiographic signs as peaked T waves, prolonged PR and QRS, and if K>7.5 mEq/L, absence of P wave, atrioventicular block and bradycardia is observed. ECG signs are more severe when hyperkalemia is associated with hyponatremia.
Electrocardiographic signs require immediate treatment. Administer 0.5–1.5 ml/kg of 10% calcium gluconate for its immediate cardioprotective effect.
Treat severe shock and hyposmolarity by administering 10–20 ml/kg of 0.9% NaCl boluses in 10 minutes, until adequate resuscitation (EGDT). IV administration of regular insulin 0.5 U/kg + 50% dextrose 4 ml/U added to 0.9% NaCl or RL facilitates potassium movement into the cell and corrects the hyperkalemia.
Although sodium bicarbonate has been indicated to translocate potassium intracellularly, the possibility of inducing cerebrospinal paradoxical acidosis, hyperosmolarity and decrease the ionized calcium neutralizing its cardioprotective effects, makes this drug choice doubtful. Correct uroabdomen or urinary obstruction and renal excretion by dialysis. Furosemide is indicated for massive tissue damage but is ineffective in patients with renal failure.
Hyponatremia
Hyponatremia results from sodium loss or free water gain. The sharp fall of Na<120 mEq/l in 24 hours, reduces serum osmolality creating an osmotic gradient, cerebral edema, depression, irritability, convulsions and coma.
Chronic hyponatremia allows the loss of cellular organic osmoles, if plasmatic correction is faster than >0.5–1.0 mEq/L/hour demyelinating encephalopathy may occur.
The patient presented with severe hyponatremia and hypovolemia would be in shock.
Hyponatremia and fluid overload occurs in patients with CHF, cirrhosis or nephrotic syndrome; they develop edema, ascites and/or pleural effusion. If Na<120 mEq/L and has developed over a period of 48 hours or more, the rate of correction must be <0.5 mEq/L/h and <10–12 mEq/L in 24 hours.
Although there are formulas for calculating the infusion volume and rate for a particular patient and fluid, once free water retention or sodium loss mechanisms are corrected the actual correction speed does not correspond to the calculated one. Thus, strict monitoring and constant reformulation are mandatory.
Infuse 0.9% NaCl 10–20 ml/kg in 10 minutes to correct hypovolemia, repeat as needed to achieve stable hemodynamic parameters. In patients with Na<120 mEq/L, severe acute neurological symptoms and rapid development, 2 ml/kg of 3%NaCl can be administered. The combination with furosemide once blood pressure is restored prevents rapid correction of serum sodium.
In asymptomatic euvolemic patients provide 0.9% NaCl and in euvolemic symptomatic patients a combination of NaCl 3% with furosemide.
Patients with increased ECF require furosemide and judicious salt intake.
Hypernatremia
Hypernatremia is diagnosed when Na>150 mEq/L. It usually results from free water loss or sodium gain. When water loss is the cause, the intracellular and extracellular compartments are reduced.
Causes include excessive diuresis, gastrointestinal losses, diabetes insipidus, hypodipsia, acute renal failure, income excess.
Hypovolemic shock is rare. 190 mEq/L ocasiona daño neurológico severo con hemorragia y trombosis. Plasmatic values of Na>190 mEq/L cause severe neurological damage from hemorrhage and thrombosis, lethargy, confusion, muscle weakness, seizures, coma and myoclonus are observed. Except for cases of diabetes insipidus where hypotonic polyuria is observed, urinary volume decreases whereas urine density increases. Chronic hypernatremia allows intracellular accumulation of non permeable osmoles, therefore acute correction of natremia induces cerebral edema, convulsions and permanent neurological sequelae. Infuse isotonic solutions in hypovolemic patients to correct hypotension, continue with 5% dextrose or 2.5% dextrose in 0.45% saline.
The body water deficit is calculated by the following formula
0.6 x body weight (kg) x [(serum Na/140) – 1]
To avoid potential CNS osmotic damage in chronic cases, after correcting dehydration and hypovolemia changes in serum sodium should be <0.5 mEq/L/h and <12 mEq in 24 hours and the water deficit should be corrected in 48–72 hours.
Hypocalcaemia
Clinical signs usually appear with calcemia<6.5 mg/dl and ionised calcium<1.25 mmol/L in dogs and <1.1 mmol/L in cats.
The most common presentation is postpartum eclampsia, but also hypoparathyroidism, hypoproteinemia, vitamin D deficiency, hyperphosphatemia, acute pancreatitis or chronic kidney disease.
Hypocalcaemia increases membrane permeability to sodium, thus increasing excitation.
Hyperkalemia and hypomagnesemia enhance its adverse effects. Anxiety, muscle weakness, ataxia, tetany and convulsions are observed.
Infuse 10% calcium gluconate 1.0–1.5 ml/kg/IV in 20 minutes, controlling the heart rate.
Perform to effect treatment on eclampsia patients and treat hyperthermia with cold packs. Diazepam may be indicated to reduce the possibility of seizures. Non postpartum cases of hypocalcemia should be treated by infusing 5–10 ml/kg of calcium gluconate in saline or RL solution in 24 hours, or 2 ml/kg in 6 to 8 hours repeating doses at requirement.
Long-term treatment may require the use of vitamin D.
Hypomagnesaemia
The presence of hyponatremia and hypokalemia, as well as hypokalemia and hypocalcemia unresponsive to treatment should increase suspicion of concomitant hypomagnesaemia. Clinical signs relate to its neuromuscular and cardiac conduction function, including weakness, small twitches, dysphagia, dyspnea, and both supraventricular and ventricular arrhythmias. Severe hypomagnesaemia has also been documented in 44% of dogs with eclampsia.
Infuse sulphate or magnesium chloride 0.75–1 mEq/kg/day, decreasing the dose to 0.3–0.5 mEq/kg/day in subsequent days.
For ventricular arrhythmias, administer 0.15–0.3 mEq/kg in 15 to 30 minutes. 50% MgSO4 contains 2 mmol/ml or 4 mEq/ml of magnesium; it should be administered diluted in 0.9% NaCl or 5% Dextrose to obtain a 20% solution.
MgCl is preferred to treat concomitant hypocalcaemia as sulphate is a calcium chelator.
References
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