09. Fluids and Electrolytes | Clinicians Pocket Reference, 11th Edition

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Principles of Fluids and Electrolytes

Fluid Compartments

Example: 70-kg man (1 L = 1 kg)

Total Body Water:

42,000 mL (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 in a 70-kg man)

Total Blood Volume

Total blood volume = 5600 mL (8% of BW in a 70-kg man)

Red Blood Cell Mass

Man, 20 36 mL/kg (1.15 1.21 L/m²) Woman, 19 31 mL/kg (0.95 1.0 L/m²)

Water Balance

70-kg man

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

"Normal" Intake:

2500 mL/d (about 35 mL/kg/d baseline)

Oral liquids: 1500 mL
Oral solids: 700 mL
Metabolic (endogenous): 300 mL

"Normal" Output:

1400 2300 mL/d

Urine: 800 1500 mL
Stool: 250 mL
Insensible loss: 600 900 mL (lungs and skin). (With fever, each degree above 98.6 F [37 C] adds 2.5 mL/kg/d to insensible losses; insensible losses are decreased if a patient is undergoing mechanical ventilation; free water gain can 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 the following kg method:

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

Electrolyte Requirements

70-kg adult, unless otherwise specified

Sodium (as NaCl):

80 120 mEq/d (children, 3 4 mEq/kg/24 h)

Chloride:

80 120 mEq/d as NaCl

Potassium:

50 100 mEq/d (children, 2 3 mEq/kg/24 h). In the absence of hypokalemia and with normal renal function, most of this K is excreted in the urine. Of the total amount of K, 98% is intracellular, and 2% is extracellular.

If the serum K level is normal, about 4.5 mEq/L, the total extracellular pool of K⁺ = 4.5 x 14 L = 63 mEq. K is easily interchanged between intracellular and extracellular stores under conditions such as acidemia or alkalemia. K demands increase with diuresis and building of new body tissues (anabolic states).

Calcium:

1 3 g/d, most of which is secreted by the GI tract. Routine administration is not needed in the absence of specific indications.

Magnesium:

20 mEq/d. Routine administration is not needed in the absence of specific indications, such as parenteral hyperalimentation, massive diuresis, ethanol abuse (frequently needed), or preeclampsia.

Glucose Requirements

100 200 g/d (65 75 g/d/m²). During starvation, caloric needs are supplied by body fat and protein; most 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. Administration of at least 100 g/d of glucose reduces protein loss more than one half. Almost all IV fluid solutions supply glucose as dextrose (pure dextrorotatory glucose). Pediatric patients need about 100 200 mg/kg/h.

Composition of Parenteral Fluids

Parenteral fluids are generally classified according to molecular weight and oncotic pressure. Colloids have a molecular weight > 8000 and have high oncotic pressure. Crystalloids have a molecular weight < 8000 and have low oncotic pressure.

Colloids

Albumin (see Table 10 2)
Blood products (eg, RBCs, single-donor plasma) (see Table 10 2)
Plasma protein fraction (Plasmanate) (see Chapter 22)
Synthetic colloids (hetastarch [Hespan], dextran) (see Chapter 22)

Crystalloids

Table 9 1 describes common crystalloid parenteral fluids.

Table 9 1 Composition of Commonly Used Crystalloids

	Electrolytes (mEq/L)^A
Fluid	Glucose (g/L)	Na⁺	Cl	K⁺	Ca²⁺	HCO₃	Mg²⁺	HPO₄²	kcal/L
D₅W (5% dextrose in water)	50								170
D₁₀W (10% dextrose in water)	100								340
D₂₀W (20% dextrose in water)	200								680
D₅₀W (50% dextrose in water)	500								1700
NS (0.45% NaCl)		77	77
3% NS		513	513
NS (0.9% NaCl)		154	154
D₅1/4NS (0.22% NaCl)	50	38	38						170
D₅ NS (0.45% NaCl)	50	77	77						170
D₅NS (0.9% NaCl)	50	154	154						170
D₅LR (5% dextrose in lactated Ringer)	50	130	110	4	3	27			180
Lactated Ringer		130	110	4	3	27			<10
Ionosol MB	50	25	22	20		23	3	3	170
Normosol M	50	40	40	13		16	3		170

^aHCO₃ is administered in these solutions as lactate that is converted to bicarbonate.

Composition of Body Fluids

Table 9 2 gives the average daily production and amount of some of the major electrolytes present in various body fluids.

Table 9 2 Composition and Daily Production of Body Fluids

Electrolytes (mEq/L)
Fluid	Na⁺	Cl	K⁺	HCO₃	Average Daily Production^a (mL)
Sweat	50	40	5	0	Varies
Saliva	60	15	26	50	1500
Gastric juice	60 100	100	10	0	1500 2500
Duodenal fluid	130	90	5	0 10	300 2000
Bile	145	100	5	15	100 800
Pancreatic juice	140	75	5	115	100 800
Ileal fluid	140	100	2 8	30	100 9000
Diarrhea	120	90	25	45

^aIn adults.

Ordering IV Fluids

One of the most difficult tasks to master is choosing appropriate IV therapy for a patient. The patient's underlying illness, vital signs, serum electrolytes, and a host of other variables must be considered. The following are general guidelines for IV therapy. Specific requirements for each patient can vary tremendously from these guidelines.

Maintenance Fluids

The following amounts provide the minimum requirements for routine daily needs:

1. 70-kg Man: 5% dextrose in one-fourth concentration normal saline (D₅ 1/4 NS) with 20 mEq/L KCl at 125 mL/h. (This infusion delivers about 3 L/d of free water.)

2. Other Adult Patients: Also use D₅1/4NS with 20 mEq/L KCl. Determine the 24-h water requirement with the "kg method" (see Baseline Fluid Requirement) and divide by 24 h to determine the hourly rate.

3. Pediatric Patients: Use the same solution as for adults, but determine the daily fluid requirements by either of the following methods:

a. Kg Method: (See Baseline Fluid Requirement)

b. Meter Squared Method: Maintenance fluids are 1500 mL/m²/d. Divide by 24 to get the flow rate per hour. To calculate the surface area, use the "rule of sixes" nomogram (Table 9 3). Formal body surface area charts are in the Appendix.

Table 9 3 "Rule of Sixes" Nomogram for Calculating Fluids in Children^a

Weight (lb)	Body Surface Area (m²)
3	0.1
6	0.2
12	0.3
18	0.4
24	0.5
30	0.6
36	0.7
42	0.8
48	0.9
60^b	1.0

^aOver 100 lb, treat as an adult.

^bAfter 60 lb, add 0.1 for each additional 10 lb.

Specific Replacement Fluids

Fluids are used to replace excessive, nonphysiologic losses.

Gastric Loss (Nasogastric Tube, Emesis):

D₅ NS with 20 mEq/L KCl

Diarrhea:

D₅LR with 15 mEq/L KCl. Use body weight as a replacement guide (about 1 L for each 1 kg, or 2.2 lb, lost).

Bile Loss:

D₅LR with 25 mEq/L ( amp) of sodium bicarbonate milliliter for milliliter

Pancreatic Loss:

D₅LR with 50 mEq/L (1 amp) HCO₃ milliliter for milliliter

Burn Patients:

Use the Parkland or the Rule of Nines formula:

Parkland Formula.

Total fluid required during the first 24 h = (% body burn) x (body weight in kg) x 4 mL

Replace with LR over 24 h. Use

One half of the total over first 8 h (from time of burn)
One fourth of the total over second 8 h
One fourth of the total over third 8 h

Rule of Nines. Used for estimating percentage of body burned in adults. Figure 9 1 shows the calculations for body burn area in adults and children. This system is also useful for determining ongoing fluid losses from a burn until it is healed or grafted.

Figure 9 1.

Tables and graphics for estimating extent of burns in adults (A) and children (B). For adults, another way of estimating percentage of the body surface burned is the rule of nines: Each arm is 9%, each leg is 9%, the head is 9%, the anterior aspect of the body is 9%, the posterior aspect of the body is 9%, and the perineum is 1%. (From: Current Surgical Diagnosis and Treatment, 12th ed., Doherty, GM [editor]. McGraw-Hill, 2006. Used with permission.)

Fluid losses can be estimated as

Loss in mL = (25 x % body burn) x m² body surface area

Determining an IV Rate

Most IV infusions are regulated with infusion pumps. If a mechanical infusion device is not immediately available, use the following formulas to determine the infusion rate.

For a MAXI Drip Chamber:

Use 10 gtt/mL; thus

10 gtt/min = 60 mL/h or
16 gtt/min = 100 mL/h

For a MINI Drip Chamber:

Use 60 gtt/mL; thus

60 gtt/min = 60 mL/h or
100 gtt/min = 100 mL/h

Electrolyte Abnormalities: Diagnosis and Treatment

In all of the following situations, the primary goal is to correct the underlying condition. Unless specified, all dosages are for adults. (See Chapter 4 for the differential diagnosis of laboratory findings.)

Hypernatremia

(Na⁺ > 144 mEq/L)

Mechanisms:

Most frequently, a deficit of total body water.

Combined Sodium and Water Losses (Hypovolemic Hypernatremia). Water loss in excess of Na loss results in low total body Na. Due to renal (eg, diuretics, osmotic diuresis due to glycosuria, mannitol, postobstructive diuresis) or extrarenal (sweating, GI [vomiting, NG suction], respiratory) losses
Excess Water Loss (Isovolemic Hypernatremia). Total body Na remains normal, but total body water is decreased. Caused by diabetes insipidus (central and nephrogenic), excess skin losses, respiratory loss, others
Excess Sodium (Hypervolemic Hypernatremia). Total body Na increased, caused by iatrogenic Na administration (eg, hypertonic dialysis, hypertonic saline enemas, Na-containing medications) and other exogenous sources (seawater ingestion, salt tablets) or adrenal hyperfunction (Cushing syndrome, hyperaldosteronism)

Symptoms:

Depend on the absolute level and also how rapidly the Na⁺ level has changed

Confusion, irritability, lethargy, stupor, coma, muscle twitching, seizures

Signs:

Hyperreflexia, mental status changes

Treatment:

Check the serum Na⁺ levels frequently while attempting to correct hypernatremia.

Hypovolemic Hypernatremia. Determine whether the patient is volume depleted by determining whether orthostatic hypotension is present (see Orthostatic Blood Pressure Measurement); if volume is depleted, rehydrate with NS until patient is hemodynamically stable, then administer hypotonic saline ( NS).
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 TBW

where TBW is total body water and

Normal TBW = 0.6 x Body weight in kg

and

Give free water as D₅W, one half of the volume in the first 24 h and the full volume in 48 h. Caution: Rapid correction of the Na⁺ level using free water (D₅W) can cause cerebral edema and seizures.

Hypervolemic Hypernatremia. Avoid medications that contain excessive Na⁺ (eg, carbenicillin). Use furosemide along with D₅W.

Hyponatremia

(Na⁺ < 136 mEq/L)

Mechanisms:

Most often due to excess body water as opposed to decreased body Na⁺. To define the cause, determine serum osmolality.

Isotonic Hyponatremia. Normal osmolality
Pseudohyponatremia. An artifact caused by hyperlipidemia or hyperproteinemia
Hypertonic Hyponatremia (Dilutional). High osmolality. Water shifts from intracellular to extracellular in response to high concentrations of solutes such as glucose and mannitol. The shift in water lowers the serum Na; however, the total body Na remains the same.
Hypotonic Hyponatremia. Low osmolality. Further classified according to findings at clinical assessment of extracellular volume status

Isovolemic hyponatremia. No evidence of edema; normal BP. Caused by water intoxication (urinary osmolality < 80 mOsm), SIADH, hypothyroidism, hypoadrenalism, thiazide diuretics, beer potomania

Hypovolemic hyponatremia. Evidence of decreased skin turgor and an increase in heart rate and decrease in BP after going from lying to standing position. Due to renal loss (urinary Na > 20 mEq/L) from diuretics, postobstructive diuresis, mineralocorticoid deficiency (Addison disease, hypoaldosteronism), or extrarenal losses (urinary Na < 10 mEq/L) from sweating, vomiting, diarrhea, or third-spacing of fluids (burns, pancreatitis, peritonitis, bowel obstruction, muscle trauma)

Hypervolemic hyponatremia. Evidence of edema (urinary Na < 10 mEq/L). Seen with CHF, nephrosis, renal failure, and liver disease

Excess Water Intake. Primary (psychogenic water drinking) or secondary (large volume of sterile water used in procedures, eg, transurethral resection of the prostate or multiple tap water enemas)

Symptoms:

Usually with Na⁺ < 125 mEq/L; severity of symptoms correlates with rate of decrease in Na⁺

Lethargy, confusion, coma
Muscle twitches and irritability, seizures
Nausea, vomiting

Signs:

Hyporeflexia, mental status changes

Treatment:

Based on determination of volume status. Evaluate volume status by physical examination: HR and BP lying and standing after 1 min, skin turgor, and edema and by determination of plasma osmolality. Not necessary to treat for hyponatremia from pseudohyponatremia (increased protein or lipids) or hypertonic hyponatremia (hyperglycemia); treat for underlying disorder (see above).

Life-Threatening. (Seizures, coma) 3 5% NS can be given in the ICU. Attempt to raise the Na 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 Hyponatremia. Restrict Na and fluids (1000 1500 mL/d). Correct underlying disorder. CHF may respond to a combination of ACE inhibitor and furosemide.
Hypovolemic Hyponatremia. Give D₅NS or NS.

Hyperkalemia

K⁺ > 5.2 mEq/L

Mechanisms:

Most often due to iatrogenic or inadequate renal excretion of K.

Pseudohyperkalemia. Due to leukocytosis, thrombocytosis, hemolysis, poor venipuncture technique (prolonged tourniquet time)
Inadequate Excretion. Renal failure, volume depletion, medications that block K⁺ excretion (eg, spironolactone, triamterene), hypoaldosteronism (due to adrenal disorders and hyporeninemic states [such as type IV RTA], NSAIDs, ACE inhibitors), long-standing use of heparin, digitalis toxicity, sickle cell disease, renal transplantation
Redistribution. Tissue damage, acidosis (a 0.1 decrease in pH increases serum K⁺ approximately 0.5 1.0 mEq/L because of extracellular shift of K⁺), beta-blockers, decreased insulin, succinylcholine
Excess Administration. K-containing salt substitutes, oral replacement, K⁺ in IV fluids

Symptoms:

Weakness, flaccid paralysis, confusion

Signs

Hyperactive deep tendon reflexes, decreased motor strength
ECG changes such as peaked T waves, wide QRS, loss of P wave, sine wave, asystole
K⁺ = 7 8 mEq/L ventricular fibrillation risk: 5%
K⁺ = 10 mEq/L ventricular fibrillation risk: 90%

Treatment

Monitor patient with ECG if symptoms are present or if K⁺ > 6.5 mEq/L; discontinue all K⁺ intake, including IV fluids; order a repeat stat K⁺ to confirm.
Rapid correction. These steps only protect the heart from K⁺ shifts; total body K⁺ must be reduced with one of the treatments described in Slow Correction.

Calcium chloride, 500 mg, slow IV push (only protects heart from effects of hyperkalemia)

Alkalinize with 50 mEq (1 amp) Na bicarbonate (causes intracellular K⁺ shift)

50 mL D₅₀W, IV push, with 10 15 units regular insulin, IV push (causes intracellular K shift)

Slow Correction

Sodium polystyrene sulfonate (Kayexalate) 20 60 g orally with 100 200 mL of sorbitol, or 40 g Kayexalate with 40 g sorbitol in 100 mL water as enema. Repeat doses qid as needed.

Dialysis (hemodialysis or peritoneal dialysis)

Correct Underlying Cause. For example, stop K-sparing diuretics, ACE inhibitors, mineralocorticoid replacement for hypokalemia

Hypokalemia

K⁺ < 3.6 mEq/L

Mechanisms:

Due to inadequate intake, loss, or intracellular shifts

Inadequate Intake. Oral or IV
GI Tract Loss. (Urinary chloride usually < 10 mEq/d; chloride-responsive alkalosis) vomiting, diarrhea, excess sweating, villous adenoma, fistula
Renal Loss. Diuretics and other medications (amphotericin, high-dose penicillins, aminoglycosides, cisplatin), diuresis other than with diuretics (osmotic, eg, hyperglycemia or ethanol induced), vomiting (from metabolic alkalosis due to volume depletion), renal tubular disease (distal or proximal RTA, Bartter syndrome (due to increased renin and aldosterone levels), hypomagnesemia, ingestion of natural licorice, mineralocorticoid excess (primary and secondary hyperaldosteronism, Cushing syndrome, steroid use), and ureterosigmoidostomy
Redistribution (Intracellular Shifts). Metabolic alkalosis (each 0.1 increase in pH lowers serum K⁺ approximately 0.5 1.0 mEq/L; due to intracellular shift of K⁺), insulin administration, beta-adrenergic agents, familial periodic paralysis and therapy for megaloblastic anemia

Symptoms

Muscle weakness, cramps, tetany
Polyuria, polydipsia

Signs

Decreased motor strength, orthostatic hypotension, ileus, ECG changes, such as flattening of T waves, U wave becoming obvious (U wave is the upward deflection after the T wave.)

Treatment:

Therapy depends on the cause.

History of HTN, GI symptoms, or use of certain medications suggests the diagnosis.
A 24-h urine for K⁺ may be helpful if the diagnosis is unclear. Level < 20 mEq/d suggests extrarenal loss or redistribution, > 20 mEq/d suggests renal losses.
A serum K⁺ level of 2 mEq/L represents a deficit of about 300 mEq in a 70-kg adult. To change K⁺ from 3 mEq/L to 4 mEq/L it takes about 100 mEq of K⁺ in a 70-kg adult.
Control 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 is difficult to correct hypokalemia in the presence of hypomagnesemia.
Rapid Correction. Give KCl IV. Monitor heart with replacement > 20 mEq/h. IV K⁺ can be painful and damaging to veins.

Patient < 40 kg: 0.25 mEq/kg/h x 2 h

Patient > 40 kg: 10 20 mEq/h x 2 h

Severe (< 2 mEq/L): Maximum 40 mEq/h IV in adults. In all cases check a stat K⁺ after each 2 4 h of replacement.

Slow Correction. Give KCl orally (see Table 22 8) for K⁺ supplements).

Adults: 20 40 mEq two to three times a day (bid or tid)

Children: 1 2 mEq/kg/d in divided doses

Hypercalcemia

Ca²⁺ > 10.2 mg/dL

Mechanisms

Parathyroid-Related. Hyperparathyroidism with secondary bone resorption
Malignancy-Related. Solid tumors with metastasis (breast, ovary, lung, kidney); paraneoplastic syndromes (squamous cell, renal cell, transitional cell carcinomas, lymphoma, and myeloma)
Vitamin-D Related. Vitamin D intoxication, sarcoidosis, other granulomatous disease
High Bone Turnover. Hyperthyroidism, Paget disease, immobilization, vitamin A intoxication
Renal Failure. Secondary hyperparathyroidism, aluminum intoxication
Other. Thiazide diuretics, milk alkali syndrome, familial hypocalciuric hypercalcemia, exogenous intake

Symptoms

Stones (renal colic), bones (osteitis fibrosa), moans (constipation), and groans (neuropsychiatric symptoms confusion) as well as polyuria, polydipsia, fatigue, anorexia, nausea, vomiting

Signs

HTN, hyporeflexia, mental status changes
Shortening of the QT interval on the ECG

Treatment:

Usually emergency treatment if symptoms are not present and Ca²⁺ > 13 mEq/L

Use saline diuresis: D₅NS at 250 500 mL/h

Give furosemide (Lasix) 20 80 mg or more IV (saline and furosemide correct most cases).

Euvolemia or hypervolemia must be maintained. Hypovolemia results in Ca reabsorption.

Other Second-Line Therapies

Calcitonin 2 8 IU/kg IV or SQ q6 12h if diuresis has not worked after 2 3 h

Pamidronate 60 mg IV over 24 h (one dose only)

Gallium nitrate 200 mg/m² IV infusion over 24 h for 5 d

Plicamycin 25 mcg/kg IV over 2 3 h (use as last resort; very potent)

Corticosteroids. Hydrocortisone 50 75 mg IV q6h

Hemodialysis

Chronic Therapy

Correct underlying condition, discontinue contributing medications (eg, thiazides).

Oral medications (prednisone 30 mg PO bid or phosphorus/K/Na supplement [Neutra-Phos] 250 500 mg PO qid) can be effective chronic therapy for diseases such as breast cancer and sarcoidosis.

Hypocalcemia

Ca²⁺ < 8.4 mg/dL

Mechanisms:

Decreased albumin can result in decreased total Ca (see Calcium, Serum).

PTH. Responsible for the immediate regulation of Ca levels
Critical Illness. Sepsis and other ICU-related conditions can cause decreased Ca because of the decrease in albumin that often occurs in critically ill patients; ionized Ca may be normal.
PTH Deficiency. Acquired (surgical excision or injury, infiltrative diseases such as amyloidosis and hemochromatosis, irradiation), hereditary hypoparathyroidism (pseudohypoparathyroidism), hypomagnesemia
Vitamin D Deficiency. Chronic renal failure, liver disease, use of phenytoin or phenobarbital, malnutrition, malabsorption (chronic pancreatitis, aftermath of gastrectomy)
Other. Hyperphosphatemia, acute pancreatitis, osteoblastic metastasis, medullary carcinoma of thyroid, massive transfusion

Symptoms

Hypertension, peripheral and perioral paresthesia, abdominal pain and cramps, lethargy, irritability in infants

Signs

Hyperactive DTRs, carpopedal spasm (Trousseau sign, see Physical Signs, Symptoms, and Eponyms)
Presence of Chvostek sign (see Physical Signs, Symptoms, and Eponyms) (facial nerve twitch, present in as many as 25% of healthy adults)
Generalized seizures, tetany, laryngospasm
Prolonged QT interval on ECG

Treatment

Acute Symptomatic

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

Chronic

For renal insufficiency, use vitamin D along with oral Ca supplements (see the following lists) and phosphate-binding antacids (eg, Phospho gel, AlternaGEL).

Ca supplements:

Ca carbonate (eg, Os-Cal) 650 mg PO qid (28% Ca)

Ca citrate (eg, Citracal) 950-mg tablets (21% Ca)

Ca gluconate 500- or 1000-mg tablets (9% Ca)

Ca glubionate (eg, Neo-Calglucon) syrup 115 mg/5 mL (6.4% Ca)

Ca lactate 325- or 650-mg tablets (13% Ca)

Hypermagnesemia

Mg²⁺ > 2.1 mEq/L

Mechanisms

Excess Administration. Management of preeclampsia with magnesium sulfate
Renal Insufficiency. Exacerbated by ingestion of magnesium-containing antacids
Others. Rhabdomyolysis, adrenal insufficiency

Symptoms and Signs

3 5 mEq/L: Nausea, vomiting, hypotension, decreased reflexes
7 10 mEq/L: Hyporeflexia, weakness, drowsiness, quadraparesis
> 12 mEq/L: Coma, bradycardia, respiratory failure

Treatment:

Clinical hypermagnesemia necessitating therapy is infrequently encountered in patients with normal renal function.

Ca gluconate: 10 mL of 10% solution (93 mg elemental Ca) 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 common in renal failure patients taking magnesium-containing antacids).
Insulin and glucose as for hyperkalemia. Furosemide and saline diuresis
Dialysis

Hypomagnesemia

Mg²⁺ < 1.5 mEq/L

Mechanisms

Decreased Intake or Absorption. Malabsorption, chronic GI losses, deficient intake (alcoholics), TPN without adequate supplementation
Increased Loss. Diuretics, other medications (gentamicin, cisplatin, amphotericin B, others), RTA, DM (especially DKA), alcoholism, hyperaldosteronism, excessive lactation
Other. Acute pancreatitis, hypoalbuminemia, vitamin D therapy

Symptoms

Weakness, muscle twitches, asterixis, vertigo
Symptoms of hypocalcemia and hypokalemia (hypomagnesemia may cause hypocalcemia and hypokalemia)

Signs

Tachycardia, tremor, hyperactive reflexes, tetany, seizures
ECG may show prolongation of PR, QT, and QRS intervals as well as ventricular ectopy and sinus tachycardia

Treatment

Severe: Tetany or Seizures. Monitor patient with ECG in ICU. 2 g magnesium sulfate in D₅W infused over 10 20 min. Follow with magnesium sulfate: 1 g/h for 3 4 h, watch for DTRs and monitor levels. Repeat replacement if necessary. These patients often have hypokalemic and hypophosphatemic and should be given supplements. Hypocalcemia may also result from hypomagnesemia.
Moderate. Mg²⁺ < 1.0 mEq/L but asymptomatic: Magnesium sulfate: 1 g/h for 3 4 h, monitor levels, and repeat replacement if necessary.
Mild. Magnesium oxide: 1 g/d PO (available over the counter in 140-mg capsules and in 400- and 420-mg tablets). May cause diarrhea.

Hyperphosphatemia

PO₄³ > 4.5 mg/dL

Mechanisms

Increased Intake and Absorption. Iatrogenic, abuse of laxatives or enemas containing phosphorus, vitamin D, granulomatous disease
Decreased Excretion (Most Common Cause). Renal failure, hypoparathyroidism, adrenal insufficiency, hyperthyroidism, acromegaly, sickle cell anemia
Redistribution and Cellular Release. Rhabdomyolysis, acidosis, chemotherapy-induced tumor lysis, hemolysis, plasma cell dyscrasia

Symptoms and Signs:

Mostly related to tetany as a result of hypocalcemia (see Hypocalcemia) caused by the hyperphosphatemia or metastatic calcification (deposition of calcium phosphate in various soft tissues)

Treatment

Low-phosphate diet
Phosphate binders such as aluminum hydroxide gel (eg, Amphojel) or aluminum carbonate gel (eg, Basaljel) orally
Acute, severe cases: Acetazolamide 15 mg/kg q4h or insulin and glucose infusion, dialysis as last resort

Hypophosphatemia

PO₄³ < 2.5 mg/dL

Mechanisms

Decreased Dietary Intake. Starvation, alcoholism, iatrogenic factors (hyperalimentation without adequate supplementation), malabsorption, vitamin D deficiency, phosphate-binding antacids (eg, AlternaGEL)
Redistribution. Conditions associated with respiratory or metabolic alkalosis (eg, alcohol withdrawal, salicylate poisoning), endocrine abnormalities (eg, insulin, catecholamine), anabolic steroids, hyper- or hypothermia, leukemia and lymphoma, hypercalcemia, hypomagnesemia
Renal Losses. RTA, diuretic phase of ATN, hyperparathyroidism, hyperthyroidism, hypokalemia, diuretics, hypomagnesemia, alcohol abuse, poorly controlled DM
Other. Refeeding in the setting of severe protein-calorie malnutrition, severe burns, management of DKA

Symptoms and Signs:

< 1 mg/dL Weakness, muscle pain and tenderness, paresthesia, cardiac and respiratory failure, CNS dysfunction (confusion and seizures), rhabdomyolysis, hemolysis, impaired leukocyte and platelet function

Treatment:

IV therapy is reserved for severe, potentially life-threatening hypophosphatemia (< 1.0 1.5 mg/dL) because too rapid correction can lead to severe hypocalcemia. With mild to moderate hypophosphatemia (1.5 2.5 mg/dL), oral replacement is preferred.

Severe. (< 1.0 1.5 mg/dL) Potassium or sodium phosphate. 2 mg/kg given IV over 6 h. (Caution: Too rapid replacement can lead to hypocalcemic tetany.)
Mild to Moderate. (> 1.5 mg/dL) Sodium potassium phosphate (Neutra-Phos) or potassium phosphate (K-Phos): 1 2 tablets (250 500 mg PO₄ per tablet) PO bid or tid. Sodium phosphate (Fleet Phospho-soda) 5 mL PO₄³ bid or tid (128 mg PO₄³)