Guidelines for daily fluid therapy planning: When the going gets tough (Proceedings)


Animals are sometimes presented with such severe abnormalities in important blood constituents that a generic fluid plan does not adequately address the problem.

Animals are sometimes presented with such severe abnormalities in important blood constituents that a generic fluid plan does not adequately address the problem. In these situations specific modifications to the fluids plan are indicated. Designing a fluid plan for a patient with numerous such problems can be difficult, especially if one attempts to address all of the animal's problems with one thought process. Obviously this is not possible, but, more to the point, the fluid plan can be considerably simplified by addressing only one problem at a time. Usually each successive decision will simply fold into the rest of the fluid plan and when you reach the bottom of the page, you have a well-considered, defensible fluid plan. Occasionally one might have to go back and remake a previous decision based on the current problem under consideration, but more often not.

Volume is always the first and foremost consideration; how much dehydration or hypovolemia and how much fluid would you estimate to normalize it. Remember it is not necessarily the objective to totally normalize volume and solute concentrations right away. The immediate objective is to move the animal away from the "death line" and then the remaining therapy can take place over a longer period of time at a more casual, watchful manner. Second priority would be those solute concentration deviations that represent an immediate threat to the life of the patient, such as severe hyperkalemia, severe anemia, hypoglycemia, and severe hypocalcemia. Third priority are the rest of the solute concentration variations that can, or should, be treated over a period of time, such as severe hypokalemia, hypo/hypernatremia, hypercalcemia, hypo/hyperphosphatemia, metabolic acidosis, hypomagnesemia, polycythemia, and hypo/hyperproteinemia.

Severe hypovolemia

Severe hypovolemia is identified by a history of blood loss, the physical exam/imaging findings suggestive of low cardiac preload (dehydration, collapsed jugular veins, low end-diastolic diameter via ultrasound, small postcava via chest radiography), hypotension, vasoconstriction (pale mucous membrane color, prolonged capillary refill time, cool appendages, oliguria/anuria), and metabolic markers of poor tissue oxygenation (low central veous oxygen, lactic acidosis, high oxygen extraction). Since none of these finding are specific to severe hypovolemia, it is important to evaluate as many parameters as are available.

Severe hypovolemia requires the rapid administration of large volumes of fluid. The type of fluid is not so important as long as it is not a low-sodium crystalloid. Iso-osmotic, isotonic, polyionic crystalloids (with a sodium concentration similar to normal ECF and some bicarbonate-like anion [lactate, acetate, gluconate]) (20-40-60-80-100 ml/kg over 5 to 60 minutes, depending upon the magnitude of the hypovolemia), 7.5% hypertonic saline (4-6 ml/kg over 5 minutes), an artificial colloid (6% Dextran 70; 6% Hetastarch) (5-10-15-20-25-30 ml/kg over 5 to 60 minutes), plasma or whole blood (10-30 ml/kg) may be administered. Isotonic crystalloids are most commonly used but might be especially indicated if the animal is also dehydrated or especially not indicated if the animal is edematous (subcutaneous, pulmonary or cerebral). Hypertonic saline may be of use in the field or when time is very short, but realistically, has limited use in most blood volume restoration endeavors. Artificial colloids are more effective blood volume expanders than are isotonic crystalloids and may be especially indicated if the patient is hypoproteinemic, edematous, or if crystalloids have failed to provide a sustained augmentation of blood volume. Plasma is too expensive for routine blood volume support but might be especially indicated if the animal has a coexistent coagulopathy. Whole blood is too expensive for routine blood volume support but might be especially indicated if the animal has a coexistent anemia. Animals that are simultaneously severely hypovolemic and severely anemic are generally better served by the administration of a clear fluid (to augment the effective circulating volume even at the expense of worsening the anemia) until such time as red blood cells can be procured.

Cats have a smaller blood volume than dogs (50-60 ml/kg vs 80-90 ml/kg) and fluid boluses should be proportionately reduced.

Severe hyperkalemia

The plasma potassium measurement defines the magnitude of the hyperkalemia; the ECG changes defines the cardiac electrical problems from it. Hyperkalemia causes membrane hypopolarization which may result in extrasystoles/fibrillation if the resting membrane potential is slightly more negative than threshold potential or asystole when resting membrane potential is slightly less negative. Hyperkalemia also increases potassium permeability which augments the repolarization phases of the electrocardiograph (tall, tented, narrow T-wave) and diminishes the depolarization phases (small P waves; prolonged P-R intervals; bradycardia, and widened QRS complexes). Hyperkalemia may also be associated with peripheral muscle weakness, decreased contractility, and weak pulse quality. Finally there is a blending of the QRS and T waves (a sinusoidal pattern), hypotension, and either ventricular asystole or fibrillation.

Imminently life-threatening hyperkalemia should be treated with calcium (0.2 ml of 10% calcium chloride or 0.6 ml or 10% calcium gluconate per kilogram of body weight , administered intravenously). Calcium effects membrane threshold potential and thereby antagonizes the effect of hyperkalemia. Therapy immediately returns the electrical performance toward normal. The effects of calcium are, however, short-lived, lasting only until the calcium is redistributed. Not so immediately life-threatening hyperkalemia should be treated with insulin and glucose (0.1 to 0.25 units of regular insulin/kg, administered as an intravenous bolus and 0.5 to 1.5 G of glucose/kg, respectively, administered as an intravenous infusion over two hours). Patients should be monitored to make sure that they do not become hypoglycemic.

Bicarbonate will also cause the intracellular redistribution of potassium if it is going to be administered for acidosis. It is not a common choice for the treatment of hyperkalemia because animals commonly do not need to be alkalinized. Sympathomimetic drugs with beta2-agonist activity will also cause the intracellular redistribution of potassium. There are not commonly used for this purpose, however, because their therapeutic margin is narrow. Specific beta2 drugs (terbutaline) are associated with tachycardia and hypotension; while general beta1&2 drugs (epinephrine, dopamine) are associated with tachycardia, arrhythmias, and hypertension.

Severe anemia

In humans, the trigger for a hemoglobin transfusion has traditionally been a hemoglobin concentration of 10 g/dL (a packed cell volume [PCV] of 30%), however recent studies suggest that a more relaxed trigger of 7 g/dL (PCV = 21%) might represent a better benefit:risk ratio. In veterinary medicine, a packed cell volume of 20% (hemoglobin of about 7 gm/dl) has been a common trigger for blood transfusion.

Oxygen delivery is the product of oxygen content (hemoglobin and PO2) and cardiac output. Early compensation for anemia is an increase in cardiac output to maintain oxygen delivery. In situations where the heart is well able to compensate, hemoglobin levels might justifiably be allowed to drop to a lower level (immune mediated anemia), however, in situations where cardiac output is impaired (organic heart disease, circulating cardio-depressants including general anesthetics) blood transfusion triggers should be higher than 7 g/dl. Metabolic markers of poor tissue oxygenation, such as a low PvO2 or a metabolic (lactic) acidosis, may help guide the need for hemoglobin transfusions.

Whole blood may need to be administered in volumes of 10 to 30 ml/kg, depending on the magnitude of anemia and hypovolemia (cats: 5 to 15 ml/kg). These volumes should be halved if packed red blood cell products are used. The rate of administration depends upon the magnitude of the hypovolemia. The amount of blood to administer can also be calculated: (desired PCV - current PCV) x body weight (kg) x 2 ml whole blood (assumes a PCV of about 40%) (or 1 ml packed red blood cells [assumes a PCV of about 80%]).

Severe hypoglycemia

The brain normally lives on glucose and severe hypoglycemia causes seizures, coma, and brain damage. If blood glucose concentration is below about 60 mg/dl, glucose (0.25 g/kg IV) should be administered IV over a minute to restore blood glucose (this dose should increase the ECF blood glucose concentration by 100 mg/dl). A glucose infusion (2.5 to 5% or 0.1 to 0.3 g/kg/hr) should then be started to maintain an acceptable blood glucose concentration (80 to 120 mg/dl by serial measurement).

Severe hypocalcemia

Hypocalcemia lowers (more negative) threshold transmembrane potential and increases the excitability of the nervous system and muscles. This may be manifested by muscle tremors, fasciculations, and twitching; muscle contractions, cramps, and tetany; disorientation, restlessness, hypersensitivity to external stimuli, and parasthesias and facial rubbing; panting and hyperthermia; prolapse of the third eyelid; and arrhythmias and hypotension.

Calcium therapy must be implemented if there are any clinical signs of hypocalcemia. Therapy is also indicated prior to the development of clinical signs when the measured plasma calcium is very low, although there is no broad agreement as to when this should be considered. It seems appropriate to consider calcium therapy when the measured calcium is 20% below normal and to provide therapy when the measured calcium is 30% below normal. This would correspond to about 7.0 and 6.0 mg/dl for total calcium, respectively, and 0.9 and 0.75 mM/L for ionized calcium, respectively. The two common calcium concentrates available for intravenous use are 10% calcium gluconate (9.3 mg Ca/ml; 0.47 mEq/ml) and 10% calcium chloride (27.2 mg Ca/ml; 1.36 mEq/ML). Either form can be used, however calcium chloride can cause tissue necrosis if given undiluted perivascularly or subcutaneously. If the animal is in tetany or a hypotensive crisis, administer 1.0 ml of 10% calcium gluconate/kg intravenously over about one minute. Repeat as necessary to effect. If the animal is not in a crisis, or once the crisis is stabilized, continue with the calcium administration at a rate of 0.5 to 1.0 ml of 10% calcium gluconate/kg per hour. Individual requirements vary widely. It generally does not take more than a few hours to achieve normal blood calcium levels. A maintenance infusion of 0.25 ml 10% calcium gluconate (0.23 mg calcium/kg) per hour may be required to maintain blood calcium concentrations thereafter. Oral supplementation should be implemented, if necessary, as soon as possible.

Severe hypokalemia

Hypokalemia causes membrane hyperpolarization (electrical paralysis) and decreases potassium permeability (diminishes repolarization processes and enhances depolarization processes. Hypokalemia is associated with general muscle weakness (skeletal, gastrointestinal, and myocardial) and may be associated with ECG changes opposite to those of hyperkalemia (although the changes are not as characteristic as they are with hyperkalemia): flattened T-wave, U waves (a positive deflection following the T wave), elevated P wave, increased R wave amplitude, and depressed S-T segment. Hypokalemia is also associated with CNS depression and an impaired ability of the renal nephrons to concentrate urine.

A severely hypokalemic patient (plasma potassium < 2.0 mEq/L) needs to be potassium loaded. The general rule is that potassium should not be administered faster than 0.5 mEq/kg/hour, although this rule is violatable in severe total body potassium depletion (start with 0.5 increase as necessary while monitoring plasma potassium closely). Of the hypokalemia is not life-threatening (>2 mEq/L), the concentration of potassium in the maintenance fluids can be supplemented (generally 20 to 50 mEq/L, depending upon how fast it is administered)(do not supplement fluids that are being rapidly administered) (when in doubt, calculate the potassium infusion rate, monitor the ECG; and make frequent plasma potassium measurements). There are two ways to get into trouble with potassium administration: 1) give too much; 2) give it too fast.

Severe hyponatremia

Hyponatremia causes intracellular edema. Hyponatremia has been associated with obtundation, anorexia, muscle weakness and wasting, and gastrointestinal signs. Common coexisting electrolyte problems include hypochloremia, hyperkalemia, and hyperphosphatemia. Mild hyponatremia requires no special consideration beyond therapy directed to the underlying disease process and volume restoration with any ECF replacement solution. With severe hyponatremia, however, the brain compensates for the cellular edema initially by expelling some of its intracellular potassium (the primary osmotically active intracellular cation) and then with the elimination of the nonionic organic solutes. Rapid correction of severe hyponatremia (<130 mEq/L) may cause myelinolysis (spastic quadriparesis, facial palsy, dysphagia, vocal dysfunction, and mental confusion to coma). Sodium concentration should not be increased faster than 0.5 mEq/L. Within hours of a too rapid correction of hyponatremia, there is an influx of electrolytes into the cells. This would normally be followed, in several days, by the intracellular increase (normalization) of the non-ionic osmoles. The clinical signs of myelinolysis occur 2-7 days after correction of hyponatremia. It is visible by MRI after 2 weeks. The duration is variable and recovery ranges from none to complete.

The regulation of concentrations of brain cell organic osmoles involves carrier-mediated transporters. This involves the synthesis of new transporter proteins. Rapid correction of hyponatremia results in an overshoot of brain sodium and chloride levels and this high intracellular ion concentration may underlie myelinolysis of acute correction.

Volume problems should be addressed first. In severe hypovolemia and hyponatremia, a fluid that contains a sodium concentration identical to that of the patient should be administered, in volumes sufficient to correct most of the hypovolemia. The sodium concentration of lactated ringers ([Na] 130 mEq/L)(or any fluid) can be reduced by admixing the fluid with distilled water or 5% dextrose in water.

Fluid [Na+ ]/Patient's [Na+ ] x 1000 = volume of water to add to one liter

Then the sodium concentration can be corrected by administering 0.3 mEq of sodium/kg per hour (this is calculated to increase the sodium concentration 0.5 mEq/L per hour).

If the patient is not life-threatenly hypovolemic, a fluid with a sodium concentration slightly above (10 mEq/L) (this depends a great deal upon the rate of administration of the fluid)that of the patient could be administered. As the patient's measured sodium concentration increases, the sodium concentration in the fluid can be increased so as to lead the sodium concentration back to normal.

Revolumizing hypovolemic patients eliminates non-osmotic causes of vasopressin release and improves renal blood flow and thus enables such patients to more effectively eliminate the excess free water. Access to oral water should be limited or not permitted. Furosemide should be administered to enhance renal water loss. Furosemide inhibits sodium reabsorption by the ascending loop of henle which diminishes the ability of the kidney to dilute the filtrate and in turn, diminishes medullary hyperosmolality which inhibits the filtrate concentrating ability of the collecting ducts.

Severe hypernatremia

Hypernatremia causes ECF hyperosmolality and intracellular dehydration. The cells first manifesting signs of edema or dehydration are those of the central nervous system (depressed mentation, restlessness, irritability, muscle twitching/tremors, hyper-reflexivity, muscle rigidity/spasticity, ataxia, myoclonus, tonic spasms, coma). Tissue shrinkage can cause intracranial hemorrhage. In time (a day, more or less) the intracellular compartment increases its intracellular osmoles to offset the effects of the extracellular sodium aberration and to restore intracellular water volume toward normal.

In compensation, first there is an accumulation of intracellular electrolytes and then there is an accumulation of organic solutes (phosphocreatinine, myo-inositols, glutamine; glutamic acid and taurine).

Most sodium aberrations are, however, a secondary processes and are not severe. Effective treatment of the underlying disease process and restoration of an effective circulating volume with a neutral sodium solution will allow the animal to correct its own sodium concentration. With severe hypernatremia however (>165 mEq/L), rapid restoration of the water imbalance will cause serious water intoxication problems. Sodium concentrations should be corrected slowly; the general rule is no faster than 1 mEq/L per hour. Severe sodium aberrations may take a day or two to correct.

Volume problems should be addressed first. In severe hypovolemia and hypernatremia, a fluid that contains a sodium concentration identical to that of the patient should be administered, in volumes sufficient to correct most of the hypovolemia. The sodium concentration of saline ([Na] 154 mEq/L)(or any fluid) can be increased by admixing a concentrated sodium solution.

Patients [Na+] - Fluid [Na+] = mEq of sodium to add to one liter

Then the sodium concentration can be corrected by administering 3.7 ml/kg of 5% dextrose in water per hour (this is calculated to decrease the sodium concentration 1 mEq/L per hour).

If the patient is not life-threatenly hypovolemic, a fluid with a sodium concentration slightly below (10 mEq/L) (this depends a great deal upon the rate of administration of the fluid) that of the patient could be administered. As the patient's measured sodium concentration decreases, the sodium concentration in the fluid can be decreased so as to lead the sodium concentration back to normal.

Access to oral water should not be permitted. Furosemide could be administered as a second-order treatment to enhance urinary sodium excretion. DDAVP can be administered (1 drop into the nose or conjunctival sac every 12 hours). If expense is an issue, aqueous vasopressin could be used but it is not as effective. Chlorpropamide (enhances tubule responsiveness to vasopressin) and carbamazepine (enhances vasopressin release) have been used in humans to treat partial diabetes insipidus.

Severe hypercalcemia

Hypercalcemia impairs the function of most cells in the body by decreasing threshold potential (less negative transmembrane potential) for excitable cells (making them less excitable and slows conduction), by increasing the contractile state of smooth and skeletal muscle, by increasing ATP utilization by cell membrane and endoplasmic reticulum membrane calcium pumps, by interfering with ATP production associated with the mitochondrial accumulation of the calcium. This is manifested clinically by obtundation, poor diastolic heart function, increased arteriolar vasomotor tone, impaired nephron concentrating ability, lethargy and muscle weakness, arrhythmias, muscle twitching, and seizures.

The mainstay of hypercalcemia treatment is effective therapy of the underlying disease process. There is no absolute agreement with regard to when more aggressive therapy should be implemented, but one guideline is when the calcium x phosphorous product exceeds 60. Hypercalcemia should be first treated with volume augmentation and saline diuresis. The latter can be augmented by furosemide. Thiazides should be avoided. Life-threatening hypercalcemia could be treated with chelating agents such as sodium or potassium phosphate (0.25 to 0.5 mM/kg IV over 4 hours) , EDTA (50 mg/kg/hr IV to effect), sodium citrate, or calcium-channel blockers. Peritoneal or hemodialysis could also be used to remove calcium from the body. Sodium bicarbonate therapy, notwithstanding alkalemia, will decrease the ionized calcium concentration. Corticosteroids may lower serum calcium if it is elevated due to neoplasia, hypoadrenocorticism, or granulomatous disease. Corticosteroids decrease intestinal resorption and increase renal excretion of calcium, and decrease bone demineralization.

Severe hypophosphatemia

Hypophosphatemia may be associated with depletion of intracellular ATP. In the red blood cell, this accounts for increased cell fragility and hemolysis. Depletion of membrane phospholipids may also contribute. Depletion of erythrocytic 2,3 DPG increases hemoglobin affinity for oxygen (shifts the oxyhemoglobin dissociation curve to the right). Depletion of white blood cell ATP impairs all phases of leucoactivation. There may also be widespread reduced cellular activity, function and integrity leading to a metabolic encephalopathy (progressive obtundation), muscle weakness/cramps; muscle tremors; respiratory and skeletal muscle weakness; myocardial weakness and hypotension; renal tubular dysfunction, platelet dysfunction, and rhabdomyolysis.

Normal serum phosphate concentrations range between 3 and 6 mg/dl in the dog and cat. Therapy should be considered if the measured plasma phosphate is below 2.0 mg/dl and must be implemented if it is below 1.5 mg/dl. Oral sodium or potassium phosphate preparations are available for mild hypophosphatemia; severe hypophosphatemia should be treated intravenously. Intravenous sodium or potassium phosphate is dosed at a rate of 0.02 up to 0.1 mM (0.6 mg]) per kilogram per hour until the plasma phosphate concentrations stabilize, which may take from a few hours to a day to accomplish. Inadvertent hyperphosphatemia may be associated with hypocalcemia and soft tissue mineralization.

Severe hyperphosphatemia

Hyperphosphatemia decreases calcium concentration by a mass action effect promoting soft tissue mineralization. Soft tissue mineralization is reputed to be more likely to occur when the calcium x phosphorous product is greater than 60. Hyperphosphatemia also inhibits 1α-hydroxylase (converts inactive calcidiol to active calcitriol). The resultant decrease in calcitriol levels further decreases serum calcium concentrations and promotes secondary hyperparathyroidism. Hyperphosphatemia is not associated with any specific clinical signs.

The mainstay of treatment for hyperphosphatemia is effective treatment of the underlying disease process. There is no absolute agreement with regard to when more aggressive therapy should be implemented, but one guideline is when the calcium x phosphorous product exceeds 60. Extracellular volume expansion and diuresis enhances phosphaturia. Insulin and glucose therapy (as for hyperkalemia) could temporarily decrease extracellular phosphorous concentration by increasing intracellular redistribution. Oral or rectal phosphate binders could also be administered. Aluminum or calcium and hydroxide, carbonate, or acetate are common phosphate binding compounds. The dosage ranges between 50 and 100 mg/kg/day, divided into 2 or 3 doses.

Severe metabolic acidosis

The treatment of metabolic acidosis should be primarily aimed at correction of the underlying disease process when the pH disturbance is mild to moderate and the underlying disease is readily treatable. If, however, the metabolic acidosis is severe and the underlying disease is difficult to treat, alkalinization therapy may be indicated. In general, alkalinization therapy should be considered if the base deficit is greater than 10 mEq/L or if the bicarbonate concentration is below 14 mEq/L, or if the metabolic acidosis causes the pH to be below 7.2.

Sodium bicarbonate is the most common agent used to treat metabolic acidosis. The mEq of bicarbonate to administer can be calculated. First pick a conservative treatment goal; a base deficit of, say, -5 mEq/L or a bicarbonate of, say, 18 mEq/L. Determine the quantitative difference between the goal value and the measured value; this represents the base deficit or bicarbonate deficit that you wish to treat. Multiply this number by the anticipated volume of distribution of the sodium bicarbonate which is usually considered to be 0.3 x BWkg.

[mEq of bicarbonate to administer = base/bicarbonate deficit x 0.3 x BWkg]

An "off-the-cuff" guideline for dosing sodium bicarbonate is 1 to 5 mEq/kg of body weight, which represent a small to large dose, respectively. This is sufficient to treat a base deficit of approximately 5 to 15 mEq/L, respectively.

These dosages of sodium bicarbonate must not be administered at a rate faster than it can be redistributed from the vascular fluid compartment to the interstitial fluid compartment (20 to 30 minutes). Excessive alkalinization, albeit temporary, of the vascular fluid compartment can cause severe hypotension, restlessness, nausea and vomiting, collapse, and death (in which case it is no longer temporary). The mechanism may be associated with a rapid change in hydrogen ion concentration, a decrease in plasma potassium, or a decrease in plasma ionized calcium. Very small dosages (0.5 mEq/kg) can be rapidly intravenously administered every 5 minutes or so, without problems.

The administration of sodium bicarbonate is also associated with a number of other problems that need to be accommodated. Excessive alkalinization of the patient could be a problem if excessive amounts of sodium bicarbonate are administered; dosages should be calculated carefully and conservatively. The administration of sodium bicarbonate generates carbon dioxide (via carbonic acid) which will result in hypercapnia if the animal is not able to increase its alveolar minute ventilation. Carbon dioxide rapidly diffuses into the intracellular fluid compartment and into the CSF. Once inside, it re-equilibrates across the carbonic acid equilibrium generating an excess of hydrogen ion. Intracellular acidosis may be associated with myocardial and CNS depression. Animals with normal respiratory responsiveness and capability will eliminate this carbon dioxide within a few breaths.

Sodium bicarbonate administration increases plasma sodium concentration and osmolality. The increase is moderate and similar to that associated with the administration of hypertonic saline, when only one or two dosages are administered. Sodium bicarbonate is also very hypertonic (2000 mOsm/kg) and therefore can be irritating to peripheral veins if administered as a continuous infusion; single doses do not cause this problem. If the sodium concentration or osmolality of the solution is a concern, it should be diluted with 5% dextrose in water. One part 7.4 % sodium bicarbonate mixed with 6 parts water will be near isonatremic and iso-osmotic.

There are alternative alkalinizing agents. Tromethamine (THAM)(Abbott) is an organic amine buffer that binds directly with hydrogen ion.

(CH2OH) 3C-NH 2 + H+ (CH2OH) 3C-NH 3+

Tromethamine thus diminishes carbon dioxide concentration. The unionized portion of tromethamine (about 30% of it) is freely diffusable into the cell, and therefore this agent may be a more effective intracellular buffer than is sodium bicarbonate. Tromethamine is also an osmotic diuretic. It is a very alkaline solution (a 0.3 M solution has a pH of 10.6) and is irritating to tissues and small veins (it may cause phlebitis and thrombosis if administered undiluted as a continuous infusion into small peripheral veins). It should be administered via large veins or with significant dilution The dosage is calculated by the formula: base/bicarbonate deficit x 0.4 x BWkg. It is much more expensive than sodium bicarbonate and it is supplied in 500 ml units. Carbicarb is a combination of 0.33 M solution of sodium carbonate and a 0.33 M solution of sodium bicarbonate. This product generates less carbon dioxide than does sodium bicarbonate. There may be some advantages to tromethamine or Carbicarb compared to sodium bicarbonate in certain circumstances, but the problems associated with sodium bicarbonate are not insurmountable and these alternative solutions have not been demonstrated to be superior.


Hypomagnesemia lowers the threshold potential (more negative) for excitable cells which increases their excitability, enhances the release of calcium from stores in the endoplasmic reticulum, facilitates the release of neurotransmitters, inhibition of the Na-K-ATPase membrane pump, enhances the leakage of potassium from the cell (eventually raises resting membrane potential toward or beyond threshold potential), and is generally associated with widespread impaired cellular function. Hypomagnesemia inhibits the release of parathyroid hormone (hypocalcemia) and causes kaliuresis (hypokalemia).

Hypomagnesemia is manifested by neural and neuromuscular excitability: hyperexcitability and noise hypersensitivity; muscle twitching, fasciculations, spasms, and tetany, and eventually coma and muscle paralysis. Hypomagnesemia is usually associated with renal wasting. Hypomagnesemia may be associated with refractory hypokalemia, hypophosphatemia, hyponatremia, and hypocalcemia. It may also be associated with ventricular arrhythmias; ECG changes may be similar to those of hyperkalemia.

Hypomagnesemia should be treated if it is symptomatic. Serum magnesium concentrations less than 1.0 mg/dl (0.4 mM/L) total, or less than 0.2 mM/L (0.45 mg/dl) ionized, should be treated. A test dose of magnesium sulfate (0.2 mEq/Kg) can be slowly administered to see if clinical signs improve. Magnesium sulfate can be administered at a daily dosage of 0.25 to 1.0 mEq/kg/day (3 to 12 mg/kg/day) administered as a continuous rate infusion. There are many oral magnesium supplements available for longer term supplementation.

Related Videos
© 2024 MJH Life Sciences

All rights reserved.