Electrolytes

Electrolyte Replacement Professor Magdy Amin RIAD

Professor of Otolaryngology. Ain shames University Senior Lecturer in OtolaryngologyUniversity of Dundee

PRINCIPLES OF FLUIDS AND ELECTROLYTES

Fluid Compartments Example: 70-kg maleTotal Body Water: 42,000 mol (60% of BW)Intracellular: 28,000 mL (40% of BW)Extracellular: 14,000 mL (20% of BW)Plasma: 3500 mL (5% of BW)Interstitial: 10,500 mL (15% of BW)

Water Balance70-kg male

The minimum obligate water requirement to maintain homeostasis (assuming normal temperature and renal concentrating ability and minimal solute [urea, salt] excretion) is about 800 mL/d, which would yield 500 mL of urine.

Normal IntakeOral liquids: 1500 mLOral solids: 700 mLMetabolic (endogenous): 300 mL

Normal Output:1400-2300 mL/d

Urine: 800-1500 mLStool: 250 mLInsensible loss: 600-900 mL (lungs and skin).

(With fever, each degree above98.6 F adds 2.5 mL/kg/d to insensible loss; insensible losses are decreased if a patientis on a ventilator; free water gain may occur from humidified ventilation.)

Baseline Fluid Requirement

Afebrile 70-kg Adult: 35 mL/kg/24 h

If not a 70-kg Adult: Calculate the water requirement according to Kg Method:

For the first 10 kg of body weight: 100 mL/kg/d plusFor the second 10 kg of body weight: 50 mL/kg/d plusFor the weight above 20 kg: 20 mL/kg/d

Electrolyte Requirements:70-kg adult

Sodium (as NaCl): 80-120 mEq (mmol)/d (Pediatric patients, 3-4 mEq/kg/ 24 h [mmol/kg/24 h])Chloride: 80-120 mEq (mmol)/d, as NaClPotassium: 50-100 mEq/d (mmol/d) (Pediatric patients, 2-3 mEq/kg/24 h [mmol/kg/24 h]).Calcium: 1-3 gm/d, Magnesium: 20 mEq/d (mmol/d).

Electrolyte Requirements

Potassium: In the absence of hypokalemia and with normal renal function, most of this is excreted inthe urine. Of the total amount of potassium, 98% is intracellular, and 2% is extracellular.Thus, assuming the serum potassium level is normal, about 4.5 mEq/L (mmol/L), the totalextracellular pool of K+ = 4.5 ?14 L = 63 mEq (mmol). Potassium is easily interchangedbetween intracellular and extracellular stores under conditions such as acidosis. Potassiumdemands increase with diuresis and building of new body tissues (anabolic states).Calcium: 1? gm/d, most of which is secreted by the GI tract. Routine administration isnot needed in the absence of specific indications.Magnesium: 20 mEq/d (mmol/d). Routine administration is not needed in the absenceof specific indications, such as parenteral hyperalimentation, massive diuresis, ethanolabuse (frequently needed) or preeclampsia.9

Glucose Requirements

100-200 g/d (65-75 g/d/m2). During starvation, caloric needs are supplied by body fat and protein; the majority of protein comes from the skeletal muscles. Every gram of nitrogen in the urine represents 6.25 g of protein broken down. The protein-sparing effect is one of the goals of basic IV therapy. The administration of at least 100 g of glucose/d reduces protein loss by more than one-half. Virtually all IV fluid solutions supply glucose as dextrose (pure dextrorotatory glucose). Pediatric patients require about 100-200 mg/kg/h.

COMPOSITION OF PARENTERAL FLUIDS

Parenteral fluids are generally classified based on molecular weight and oncotic pressure.Colloids have a molecular weight of >8000 and have high oncotic pressure.Crystalloids have a molecular weight of

Potassium

Potassium balance depends on the interaction of internal and external homeostatic mechanisms. Only when one or both systems are disturbed acutely or impaired chronically does plasma K+ change markedly

Internal Balance

Acid-Base

2. Insulin

3. Mineralcorticoids

4. Catecholamines

1. Acid-Base

With increasing extracellular H+ concentration (acidosis), K+ moves from the intracellular to the extracellular compartment in exchange for H+. The increase in plasma K+ concentration is small at first, but increases for a time, as the acidosis continues. However, K+ is lost in the urine, and one sees a lessening of the effect of acidosis on serum K+. The K+ changes seen with metabolic alkalosis are not well understood and are complicated by the kaliuresis that occurs. Some intracellular shift of K+ does occur, but the decrease in serum K+ is mainly due to renal loss.

Internal Balance

2. Insulin Insulin stimulates K+ uptake by muscle and hepatic cells. 3. Mineralcorticoids Aldosterone makes cells more receptive to the uptake of K+ and increases renal excretion of K+.

4. Catecholamines

Epinephrine initially increases plasma K+ because of combined alpha and beta receptor stimulation, which releases K+ from the liver. The response is followed by a decrease in plasma K+ caused by beta-receptor stimulation, which enhances K+ uptake by muscle and liver. The end result is a decrease in serum K+ Propranolol impairs cellular uptake of K+.

External Balance Renal Potassium Excretion

1. Potassium Intake - An acute or chronic increase in K+ intake leads to increased secretion in the distal convoluted tubule. 2. Sodium Intake and Distal Tubular Flow Rate - A sodium load will increase flow past the distal tubule and cause K+ wasting. The converse is true too. 3. Mineralcorticoids - A mineralcorticoid deficiency leads to K+ retention and Na+ wasting, just as excess leads to opposite changes.

External Balance

GI Potassium Excretion Fecal excretion of K+ normally is small, but with diarrhea disorders, K+ loss increases significantly.

SymptomsMuscle weakness, cramps, tetanyPolyuria, polydipsiaSignsDecreased motor strength, orthostatic hypotension, ileusECG changes

Treatment:The therapy depends on the cause.A history of hypertension, GI symptoms, or use of certain medications may suggest the diagnosis.A 24-h urine for potassium may be helpful if the diagnosis is unclear. Levels 20 mEq/d suggest renal losses.

Treatment:A serum potassium level of 2 mEq/L (mmol/L) probably represents a deficit of at least 200 mEq (mmol) in a 70-kg adult; to change potassium from 3 mEq/L (mmol/L) to 4 mEq/L (mmol/L) takes about 100 mEq (mmol) of potassium in a 70-kg adult.Treat underlying cause.Hypokalemia potentiates the cardiac toxicity of digitalis. In the setting of digoxin use, hypokalemia should be aggressively treated.Treat hypomagnesemia if present. It will be difficult to correct hypokalemia in the presence of hypomagnesemia.

Slow Correction.Give KCl orallyAdult: 20-40 mEq two to three times a day (bid or tid)Pediatric patients: 1-2 mEq/kg/d in divided doses

Potassium disordersTreatment of Hypokalemia

The treatment of hypokalemia includes repletion of K+ and removal of the cause of hypokalemia. Emergency situation, in the presence of arrhythmias, K+ can be replaced intravenously by a solution containing 40 to 60 meq/l, infused at a rate of no more than 40 meq/hour. Any magnesium deficiency must be corrected in order to correct the hypokalemia.

Hyperkalemia

Potassium is released from cells at times of stress, injury, acidosis; but the kidney is able to regulate potassium well, and hyperkalemia is rarely a problem. However, in the presence of renal failure hyperkalemia becomes a common problem. It is generally treated if there is an abrupt rise from normal to >6.5 meq/liter or if any level is associated with EKG changes.

Hyperkalemia (K+ >5.2 mEq/L (mmol/L)

Mechanisms: Most often due to iatrogenic or inadequate renal excretion of potassium.Pseudo-Hyperkalemia. Due to leukocytosis, thrombocytosis, hemolysis, poor venipuncture technique (prolonged tourniquet time)

Inadequate Excretion. Renal failure, volume depletion, medications that block potassium excretion (spironolactone, triamterene, others), hypoaldosteronism (including adrenal disorders and hyporeninemic states [such as Type IV renal tubular acidosis], NSAIDs, ACE inhibitors), long-standing use of heparin, digitalis toxicity, sickle cell disease, renal transplant

Redistribution. Tissue damage, acidosis (a 0.1 decrease in pH increases serum K+ approximately 0.5-1.0 mEq/L due to extracellular shift of K+), beta-blockers, decreased insulin, succinylcholine

Excess Administration. Potassium-containing salt substitutes, oral replacement, potassium in IV fluids

Symptoms: Weakness, flaccid paralysis, confusion.Signs:Hyperactive deep tendon reflexes, decreased motor strengthECG changes, such as, peaked T waves, wide QRS, loss of P wave, sine wave,asystoleK+ = 7-8 mEq/L (mmol/L) yields ventricular fibrillation in 5% of casesK+ = 10 mEq/L (mmol/L) yields ventricular fibrillation in 90% of cases

Treatment

Monitor patient on ECG if symptomatic or if K+ >6.5 mEq/L; discontinue all potassium intake, including IV fluids; order a repeat stat potassium to confirm.Pseudo-hyperkalemia should be ruled out. If doubt exists, obtain a plasma potassium in a heparinized tube; the plasma potassium will be normal if pseudo-hyperkalemia is present.

Rapid Correction. These steps only protect the heart from potassium shifts, and total body potassium must be reduced by one of the treatments shown under Slow Correction. Calcium chloride, 500 mg, slow IV push (only protects heart from effect of hyperkalemia)Alkalinize with 50 mEq (1 ampule) sodium bicarbonate (causes intracellular potassium shift)50 mL D50, IV push, with 10-15 units regular insulin, IV push (causes intracellular potassium shift)

Slow Correction

Sodium polystyrene sulfonate (Kayexalate) 20-60 g given orally with 100-200 mL of sorbitolor 40 g Kayexalate with 40 g sorbitol in 100 mL water given as an enema. Repeat doses qid as needed.Dialysis (hemodialysis or peritoneal)

Correct Underlying Cause.Such as stopping potassium-sparing diuretics, ACE inhibitors, mineralocorticoid replacement for hypokalemia

Treatment

Restrict Exogenous K+ Calcium gluconate - 10 to 30 ml of 10% solution over 3 to 5 minutes NaHCO3 - 50 to 100 ml of 7.5% solution Hyperventilation will also create an alkalosis and drive K+ into cells Avoid hypoventilation, Glucose - insulin - 500 ml of 10% dextrose plus 10 units regular insulin or 50 - 100 gm with 10 -20 units regular insulin Lasix, ethacrynic acid, or bumex Oral or rectal sodium or calcium polystyrene with sorbitol Peritoneal dialysis or hemodialysis Transvenous pacemaker

Sodium Physiology1. Sodium and its anions make up about 90% of the total extracellular osmotically active solute. 2. Serum osmolality (mOsm/kg H20) = 2 X [Na+] + [glucose]/18 + [BUN]/2.8 3. For practical purposes, twice the Na+ concentration equals serum osmolality because urea and glucose ordinarily are responsible for less than 5% of the osmotic pressure.

Hyponatremia

Determine serum osmolality to determine if its isotonic, hypertonic, or hypotonic hyponatremia. Most often due to excess body water as opposed to decreased body sodium.

Hyponatremia

Isotonic hyponatremia occurs when plasma solids dilute the Na+. This occurs with hyperproteinemia and hyperlipidemia. b. Hypertonic hyponatremia occurs with uncontrolled diabetes and with the use of mannitol. Treat by correcting the fluid deficit initially with isotonic saline, then give insulin to decrease glucose and hypotonic saline to correct free water deficit. c. True hypotonic hyponatremia is characterized by hypovolemic, hypervolemic, and isovolemic. Differentiation is done by assessing ECF volume: blood pressure, skin turgor, edema, ascites etc

Treatment: Based on determination of volume status.Evaluate volume status by physical examination HR and BP lying and standing after 1 min, skin turgor, edema and by determination of the plasma osmolality. Do not need to treat hyponatremia from pseudo-hyponatremia (increased protein or lipids) or hypertonic hyponatremia (hyperglycemia),

Treatment: Based on determination of volume status.Life-Threatening. (Seizures, coma) 3-5% NS can be given in the ICU setting. Attempt to raise the sodium to about 125 mEq/L with 3-5% NS.Isovolemic Hyponatremia. (SIADH)Restrict fluids (1000-1500 mL/d).Demeclocycline can be used in chronic SIADH.Hypervolemic HyponatremiaRestrict sodium and fluids (1000-1500 mL/d).Treat underlying disorder. CHF may respond to a combination of ACE inhibitor and furosemide.Hypovolemic HyponatremiaGive D5NS or NS.

Hypernatremia

1. Less common than hyponatremia, usually iatrogenic. 2. Occurs with either pure water loss, hypotonic fluid loss, or salt gain. 3. Most commonly we see patients with both water and sodium loss, but water loss exceeds salt loss. 4. Water loss from increased insensible loss, fever, burn, diabetes insipidus 5. Diabetes Insipidus

Hypernatremia (Na+ >144 mEq/L [mmol/L])

Mechanisms: Most frequently, a deficit of total body water.(Hypovolemic hypernatremia). (Isovolemic hypernatremia). (Hypervolemic hypernatremia).

Hypernatremia (Na+ >144 mEq/L [mmol/L])

Mechanisms: Most frequently, a deficit of total body water.Combined Sodium and Water Losses (Hypovolemic hypernatremia). Water loss in excess of sodium loss results in low total body sodium. Due to renal (diuretics, osmotic diuresis due to glycosuria, mannitol, etc) or extrarenal (sweating, GI, respiratory) losses

Hypernatremia (Na+ >144 mEq/L [mmol/L])

Excess Water Loss (Isovolemic hypernatremia). Total body sodium remains normal, but total body water is decreased. Caused by diabetes insipidus ,excess skin losses, respiratory loss, others.

Hypernatremia (Na+ >144 mEq/L [mmol/L])

Excess Sodium (Hypervolemic hypernatremia). Total body sodium increased, caused by iatrogenic sodium administration (ie, hypertonic dialysis, sodium-containing medications) or adrenal hyperfunction (Cushings syndrome, hyperaldosteronism).

HypernatremiaSymptoms: Depend on how rapidly the sodium level has changedConfusion, lethargy, stupor, comaMuscle tremors, seizuresSigns: Hyperreflexia, mental status changes

Hypernatremia:Treatment:

Hypovolemic Hypernatremia. Determine if the patient volume is depleted by determining if orthostatic hypotension is present; if volume is depleted, rehydrate with NS until hemodynamically stable, then administer hypotonic saline (1/2 NS).

Hypernatremia:Treatment:

Euvolemic/Isovolemic. (No orthostatic hypotension) calculate the volume of free water needed to correct the Na+ to normal as follows:Body water deficit = Normal TBW - Current TBWWhere Normal TBW = 0.6 x Body weight in kgAnd Current TBW =Normal serum sodium x TBW / Measured serum sodium

Give free water as D5W, one-half the volume in the first 24 h and the full volume in 48 h.

(Caution: The rapid correction of the sodium level using free water (D5W) can cause cerebral edema and seizures.)

Hypervolemic Hypernatremia

Avoid medications that contain excessive sodium (carbenicillin, etc).

Use furosemide along with D5W.

Treatment of hypernatremia

Hypotonic fluid loss is the most common form of hypernatremia. It is caused by gastroenteritis, osmotic diuresis. Signs of intravascular depletion are evident. Treatment involves replacement volume with normal saline, followed by correction of the free water deficit

HypercalcemiaC a2+ > 10.2 mg/dL (2.55 mmol/L)

MechanismsParathyroid-Related. Hyperparathyroidism with secondary bone resorptionMalignancy-Related. Solid tumors with metastases (breast, ovary, lung, kidney), or paraneoplastic syndromes, (squamous cell, renal cell, transitional cell carcinomas, lymphomas, and myeloma)Vitamin-D-Related. Vitamin D intoxication, sarcoidosis, other granulomatous diseaseHigh Bone Turnover. Hyperthyroidism, Pagets disease, immobilization, vitamin A intoxicationRenal Failure. Secondary hyperparathyroidism, aluminum intoxicationOther. Thiazide diuretics, milk alkali syndrome, exogenous intake

SymptomsStones (renal colic) bones (osteitis fibrosa), moans (constipation), and groans (neuropsychiatric Symptoms e.g confusion), as well as polyuria, polydipsia, fatigue, anorexia, nausea, vomitingSignsHypertension, hyporeflexia, mental status changesShortening of the QT interval on the ECG.

Treatment:Usually emergency treatment if patient is symptomatic and Ca+2 >13 mEq/L (3.24 mmol/L)Use saline diuresis: D5NS at 250-500 mL/h. Give furosemide (Lasix) 20-80 mg or more IV (saline and Lasix will treat most cases).Euvolemia or hypervolemia must be maintained. Hypovolemia results in calcium reabsorption.

Other Second-Line Therapies:

Calcitonin 2-8 IU/kg IV or SQ q6-12h if diuresis has not worked after 2-3hPamidronate 60 mg IV over 24 h (one dose only)Gallium nitrate 200 mg/m2 IV infusion over 24 h for 5 dPlicamycin 25 micg/kg IV over 2-3 h (use as last resort; very potent)Corticosteroids. Hydrocortisone 50-75 mg IV every 6 h.Consider hemodialysis.

HypocalcemiaC a2+ < 8.4 mg/dL (2.1 mmol/L)

Mechanisms: Decreased albumin can result in decreased calciumPTH. Responsible for the immediate regulation of calcium levelsCritical Illness. Sepsis and other ICU-related conditions can cause decreased calcium because of the fall in albumin often seen in critically ill patients, ionized calcium may be normal.PTH Deficiency. Acquired (surgical excision or injury, infiltrative diseases such as amyloidosis or hemachromatosis and irradiation) hereditary hypoparathyroidism (pseudo-hypoparathyroidism), hypomagnesemiaVitamin D deficiency. Chronic renal failure, liver disease, use of phenytoin or phenobarbital, malnutrition, malabsorption (chronic pancreatitis, postgastrectomy)Other. Hyperphosphatemia, acute pancreatitis, osteoblastic metastases, medullary carcinoma of the thyroid, massive transfusion

SymptomsHypertension, peripheral and perioral paresthesia, abdominal pain and cramps, lethargy, irritability (in infants)SignsHyperactive DTRs, carpopedal spasm (Trousseaus sign)Positive Chvosteks sign (facial nerve twitch, can be present in up to 25% of normal adults).Generalized seizures, tetany, laryngospasmProlonged QT interval on ECG

TreatmentAcute Symptomatic

100-200 mg of elemental calcium IV over 10 min in 50-100 mL of D5W followed by an infusion containing 1-2 mg/kg/h over 6-12 h10% calcium gluconate contains 93 mg of elemental calcium.10% calcium chloride contains 272 mg of elemental calcium.Check magnesium levels and replace if low.

Chronic

For renal insufficiency, use vitamin D along with oral calcium supplements

HypermagnesemiaMg2+ > 2.1 mEq/L (mmol/L)

MechanismsExcess Administration. Treatment of preeclampsia with magnesium sulfateRenal Insufficiency. Exacerbated by ingestion of magnesium-containing antacidsOthers. Rhabdomyolysis, adrenal insufficiency

HypermagnesemiaMg2+ > 2.1 mEq/L (mmol/L)

Symptoms and Signs3-5 mEq/L(mmol/L): Nausea, vomiting, hypotension7-10 mEq/L (mmol/L): Hyperreflexia, weakness, drowsiness>12 mEq/L (mmol/L): Coma, bradycardia, respiratory failure

HypermagnesemiaMg2+ > 2.1 mEq/L (mmol/L)

Treatment:

Clinical hypermagnesemia requiring therapy is infrequently encountered in the patient with normal renal function.Calcium gluconate: 10 mL of 10% solution (93 mg elemental calcium) over 10-20 min in 50-100 mL of D5W given IV to reverse symptoms (useful in patients being treated for eclampsia).Stop magnesium-containing medications (hypermagnesemia is most often encountered in patients in renal failure on magnesium-containing antacids).Insulin and glucose as for hyperkalemia ,Furosemide and saline diuresisDialysis