5 - Renal, Electrolyte, and Acid Base Disturbances

Editors: Susla, Gregory M.; Suffredini, Anthony F.; McAreavey, Dorothea; Solomon, Michael A.; Hoffman, William D.; Nyquist, Paul; Ognibene, Frederick P.; Shelhamer, James H.; Masur, Henry

Title: Handbook of Critical Care Drug Therapy, 3rd Edition

Copyright 2006 Lippincott Williams & Wilkins

> Table of Contents > Chapter 5 - Renal, Electrolyte, and Acid Base Disturbances

Chapter 5

Renal, Electrolyte, and Acid Base Disturbances

TABLE 5.1. Hypernatremia

Therapy	Dosage	Comments
5% dextrose in water (D5W) or 0.45% NaCl	By calculation: see comment	Free water replacement is based on formula for calculating water deficit: Water deficit (L) = normal total body water - estimated total body water Water deficit = (0.5 body weight [kg]) - [(0.5 body weight [kg]) (140/actual serum Na+)] Replace half of water deficit in the first 24 h and the remainder over the following 2 3 d Monitor serum Na+ q1 2h to ensure gradual correction Correcting too rapidly may produce cerebral edema, seizures, and death
Desmopressin (DDAVP)	Intranasal: 0.1 0.4 ml (10 40 g) qd	Can be administered as a single daily dose or divided into 2 doses
	SC/IV: 0.5 1 ml (2.0 4.0 g) qd	When switching from the intranasal to IV route, the comparable antidiuretic dose is approximately 1/10 of the intranasal dose
Vasopressin	SC/IM: 5 10 U bid-tid	Low cost; however, complications include hypertension and sterile abscesses IV administration not usually recommended
IM, intramuscular; IV, intravenous; SC, subcutaneous Homeostasis of extracellular fluid is more dominant mechanism than maintenance of osmolality. Hypernatremia may be associated with low, normal, or excessive body water. If thirst mechanism is intact, vasopressin replacement is a matter of convenience. Excessive or rapid correction is particularly dangerous if hypernatremia has persisted for more than 24 hours because there is increased central nervous system intracellular osmolality. In this setting, secondary cerebral edema may produce seizures or death.

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TABLE 5.2. Hyponatremia

Therapy	Dosage	Comments
Furosemide	20 200 mg IV q4 6h	Treatment usually required if serum sodium <110 mEq/L or patient is symptomatic
		Aim to bring serum sodium up to 120 125 mEq/L, but raise no more than 12 mEq/L in the first 24 h
0.9% NaCl (154 mEq Na+/L)	By calculation (see comment)	Calculation: Na+ deficit (mEq) = 0.60 lean body wt (kg) (120 - measured Na+)
3% NaCl (513 mEq Na+/L)	By calculation (see comment above)	Only for severe neurologic derangements or seizures Administer very cautiously as overly rapid correction can cause CNS toxicity (central pontine myelinolysis) or volume overload
Demeclocycline	300 mg PO q12h	For patients with SIADH
		Antagonizes ADH action in the distal nephron
ADH, antidiuretic hormone; CNS, central nervous system; PO, by mouth; SIADH, syndrome of inappropriate antidiuretic hormone release Important to exclude spurious hyponatremia caused by hyperglycemia. This occurs because the osmotically active solute, glucose, causes a shift of water from the intracellular compart- ment to the extracellular compartment and dilutes extracellular sodium. For every 62 mg/dl rise in glucose, there is a 1 mEq/L fall in sodium. The rate of correction of hyponatremia should be proportional to its rate of occurrence. Acute correction of hyponatremia should not exceed a 20 mEq/L rise in concentration of serum sodium in the first 48 hours of therapy. Osmolality (mOsm/kg) = 2(Na+ + K+) + (BUN/2.8) + (glucose/18).

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TABLE 5.3. Hyperkalemia

Therapy	Dosage	Onset/Duration	Comments
Acute Management
Sodium bicarbonate (NaHCO3)	1 mEq/kg IV over 3 5 min	Onset: 15 30 minDuration: 1 2 h	Can cause sodium overload and hyperosmolality
Calcium gluconate 10% (100 mg/ml = 9 mg/ml elemental Ca+2, 0.46 mEq/ml)	5 10 ml IV over 2 5 min	Onset: 1 5 min Duration: 1 2 h	Rapid onset, but short-lived Not compatible with NaHCO3; must flush line between infusions Can augment digoxin toxicity
Calcium chloride 10% (100 mg/ml = 27.2 mg/ml elemental Ca+2, 1.36 mEq/ml)	5 10 ml IV over 2 5 min	Onset: 1 5 min Duration: 1 2 h	Rapid onset, but short-lived Not compatible with NaHCO3; must flush line between infusions Can augment digoxin toxicity Preferred preparation when volume is an issue because it contains more elemental calcium per g than calcium gluconate
Dextrose and insulin	Dextrose 0.5 g/kg with 0.3 U regular insulin per g dextrose	Onset: 10 15 min Duration: 3 h	Usual dosing is 25 g dextrose with 6 10 U regular insulin Insulin should be given IV to avoid delayed hypoglycemia that can follow SC insulin; important to administer glucose concurrently
Albuterol	10 20 mg via nebulized aerosol	Onset: 30 min Duration: 2 h	Mechanism is intracellular shunting of potassium by 2-adrenergic agonists Beware of possible angina
Subacute and Chronic Management
Sodium polystyrene sulfonate (SPS)	PO: 15 60 g in 100 200 ml 20% sorbitol q4h PR: 50 g in 50 ml 70% sorbitol added to 100 200 ml water	Onset: PO: 2 h PR: 1 h Duration: 4 h	Resin exchanges sodium for potassium in the gut PO SPS removes 1 mEq KCl/g, PR SPS removes 0.5 mEq KCl/g Be aware of sodium load in patients with heart failure
IV, intravenous; PO, by mouth; PR, per rectum; SC, subcutaneous If conservative methods of therapy fail, up to 50 mEq/h of potassium can be removed by hemodialysis. Peritoneal dialysis removes approximately 10 mEq/h.

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TABLE 5.4. Hypokalemia

Therapy	Dosage	Comments
Potassium chloride (KCl)	See sliding scale for IV infusion (Table 5.5) Maximum infusion rate of 40 mEq/h IV through a central line with continuous cardiac monitoring Solutions should be prepared in non-dextrose containing fluids (i.e., NS or 0.45% NaCl)	Life-threatening hypokalemia usually is caused by gastrointestinal losses (diarrhea) or genitourinary losses (diuretics) Magnitude of deficit can only be approximated Loss of 200 400 mEq of potassium lowers plasma potassium by 1 mEq/L Clinical manifestations are rare when potassium level is 2.5 mEq/L, the exception being patients with cardiac disease The most serious complications are conduction disturbances and arrhythmias; muscle weakness can occur Cautious replacement in oliguric or anuric patients Peripheral IV administration can be painful; pain is less if solutions contain less than 60 mEq KCl/L Rapid IV replacement (greater than 20 mEq/h) warrants continuous cardiac monitoring Check magnesium and supplement if below lower limit of normal
Potassium citrate and citric acid	40 60 mEq PO bid to qid	Solution of 1,100 mg potassium citrate and 334 mg citric acid monohydrate per 5 ml; equivalent to 2 mEq potassium and 2 mEq bicarbonate per ml Dose may be adjusted based on urine pH Useful in renal tubular acidosis, when replacement of both potassium and bicarbonate is required Aggressive treatment of acidosis with bicarbonate alone may aggravate coexisting hypokalemia
NS, normal saline (0.9%); NaCl, sodium chloride. Potassium sparing diuretics may be considered in patients with severe renal losses of potassium; however, they should not be used in patients with renal insufficiency or in conjunction with aggressive potassium supplementation.

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TABLE 5.5. Sliding Scale Algorithm for Potassium Chloride (KCl) Infusion

K+ (mEq/L)	KCl Infusion Rate (mEq/h)
<2.5	20 40
2.5 3.0	15 20
3.1 3.5	10
3.6 4.0	5
>4.1
Potassium level should be checked frequently i.e., every 4 to 6 hours, during IV infusion. Patients receiving 15 mEq/h should have cardiac monitoring. Doses 15 mEq/h should ideally be delivered via central vein because of pain with peripheral administration. (Maximum recommended concentration is 0.4 mEq/ml of solution.)

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TABLE 5.6. Hypercalcemia

Therapy	Dosage	Comments
0.9% NaCl	250 500 ml/h	With or without furosemide 20 mg IV q4 6h Volume expansion in patients with normal renal function leads to urinary calcium losses Calcium loss up to 2 g/24 h Need to monitor magnesium, phosphorus, and potassium
Calcitonin-salmon	Initial: 4 IU/kg SC/IM q12h Repeat: 8 IU/kg SC/IM q12h	Perform skin test for allergy before first dose in patients with suspected sensitivity to calcitonin-salmon Decreases bone reabsorption, but effect is limited and diminishes after several days Maximum dose 8 IU/kg q6h if no response to lower doses May be added to bisphosphonate to achieve normal calcium levels within a few days
Zoledronic acid	4 mg IV as a single dose over at least 15 min	Minimum time period for retreatment is 7 d
Pamidronate disodium	60 mg (for moderate hypercalcemia) or 90 mg (for severe hypercalcemia) as a single IV infusion (diluted in 1 L 0.9% NaCl or D5W) over 24 h	Moderate hypercalcemia: corrected serum calcium 12 13.5 mg/dl; severe hypercalcemia: corrected serum calcium >13.5 mg/dl A minimum of 7 d should elapse to assess response before re-treatment If retreating, dosage is same as initial dose Osteonecrosis of the jaw may occur in patients with cancer
Gallium nitrate	100 mg/M2 IV (for mild hypercalcemia), 150 mg/M2 IV (moderate hypercalcemia), or 200 mg/M2 IV (severe hypercalcemia) in 1 L 0.9% NaCl or D5W infused over 24 h 5 d	If serum calcium is lowered to normal range in less than 5 d, treatment may be discontinued Potential for nephrotoxicity
Hydrocortisone	1 mg/kg IV q8h	Especially effective in patients with sarcoidosis, breast carcinoma, and hematologic malignancies Equivalent doses of other glucocorticoids (dexamethasone or methylprednisolone) may be used (see Table 6.1)
IM, intramuscular; IV, intravenous; SC, subcutaneous

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TABLE 5.7. Hypocalcemia

Therapy	Dosage	Comments
Acute Therapy
Calcium gluconate 10% (100 mg/ml = 9 mg/ml elemental Ca+2, 0.46 mEq/ml)	Initial: 1 g (10 ml) IV over 10 min Infusion: 100 mg/h	Treat as medical emergency if symptomatic (seizures, confusion, tetany, laryngospasm, arrhythmias, hypotension) Therapy of acidosis with bicarbonate lowers ionized serum calcium further Calcium infusion should be continued until elemental calcium level reaches 8 9 mg/dL, then monitor levels and administer as needed Concomitant magnesium supplementation is often required to maintain calcium level
Calcium chloride 10% (100 mg/ml = 27.2 mg/ml elemental Ca+2, 1.36 mEq/ml)	Initial: 1 g (10 ml) IV over 10 min Infusion: 100 mg/h	Preferred preparation when volume is an issue because it contains more elemental calcium per g than calcium gluconate Increased bioavailability in hepatic failure
Chronic Therapy
Calcium carbonate	1.25 5 g PO daily in 3 4 divided doses	1.25 g calcium carbonate contains 500 mg elemental calcium
Ergocalciferol (vitamin D2)	25,000 to 150,000 U/d PO	Used for the treatment of chronic hypocalcemia, rickets, familial hypophosphatemia, and hypoparathyroidism Start therapy with oral calcium Slow acting preparation Long duration of action; if hypercalcemia develops, it may not resolve for weeks Inexpensive
Dihydrotachysterol	0.125 1 mg PO qd	Used for the treatment of chronic hypocalcemia, acute, chronic and latent forms of postoperative tetany and idiopathic tetany, and hypoparathyroidism Fast onset; expensive
Calcitriol	0.5 2 g PO qd	Acute hypocalcemia Rapid onset If hypercalcemia occurs, it is not long lasting
Calcifediol	50 100 g PO gd	Used for the treatment and management of metabolic bone disease or hypocalcemia in patients on chronic renal dialysis Intermediate duration of action
Doxercalciferol	10 g PO 3 times weekly	Used for the management of secondary hyperparathyroidism in patients undergoing chronic renal dialysis Maximum dose 20 g 3 times weekly Intermediate duration of action
Paricalcitol	0.04 1 g/kg IV every other day during hemodialysis	Used for the management of secondary hyperparathyroidism in patients undergoing chronic renal dialysis Intermediate duration of action
IV, intravenous; PO, by mouth Clinically significant hypocalcemia is an uncommon problem, but it may occur after multiple rapid transfusions, parathyroidectomy, thyroidectomy, or severe pancreatitis. Correction for calcium in the setting of hypoalbuminemia: total serum calcium will fall 0.8 g/dl for every 1 g decrease in serum albumin. Consider obtaining measurement of ionized calcium to most accurately determine degree of calcium deficit. Calcium preparations should be diluted to prevent phlebitis and to limit tissue necrosis if extravasated. Do not administer calcium in solutions with either bicarbonate or phosphate; insoluble salts can form.

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TABLE 5.8. Hyperphosphatemia

Therapy	Dosage	Comments
Aluminum hydroxide	30 120 ml PO q4 6h	Can cause constipation
Hemodialysis or peritoneal dialysis
Acetazolamide	15 mg/kg q3 4h
NS infusion
NS, normal saline (0.9%); PO, by mouth Acute, severe hyperphosphatemia in association with symptomatic hypocalcemia can be life threatening. Hyperphosphatemia is associated with tumor lysis, rhabdomyosis, exogenous phosphate administration, lactic, or ketoacidosis.

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TABLE 5.9. Hypophosphatemia

Therapy	Dosage	Comments
Potassium phosphate (K2PO4) or sodium phosphate (Na2PO4)	For mild to moderate hypophosphatemia (PO4 = 1.6 3.0 mg/dL): 0.16 0.32 mmol/kg IV over 6 8 h For severe hypophosphatemia (PO4 = <1.5 mg/dL): 0.64 mmol/kg IV over 6 8 h	Muscle weakness caused by hypophosphatemia can precipitate or exacerbate heart failure, respiratory failure, and neurologic symptoms Intravenous replacement warranted for serum phosphate levels less than 1 mg/dl Be cautious of IV therapy in patients with hypercalcemia because metastatic calcification may occur Maximum phosphate infusion rate is 10 mmol/h (Ann Pharmacother 1997;31:683) Important metabolic replacement in hyperalimentation solutions 1 mmol phosphate = 31 mg phosphate Each ml of potassium phosphate contains phosphate 3 mmol and potassium 4.4 mEq; beware of hyperkalemia and follow potassium levels Each ml of sodium phosphate contains phosphate 3 mmol and sodium 4 mEq
Potassium and sodium phosphate for oral solution	250 500 mg (8 16 mmol) PO qid	Oral therapy is preferred when serum phosphate levels approach 2 mg/dL May require days to replenish intracellular stores of phosphorus, even after serum levels normalize Each capsule/packet contains K+ 7 mEq and Na+ 7 mEq
IV, intravenous; PO, by mouth

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TABLE 5.10. Acidosis

Drug	Dosage	Indications	Comments
Sodium bicarbonate (NaHCO3)	By calculation (see comment below)	Severe nonanion gap metabolic acidosis or hyperkalemia	Generally not given unless pH <7.20 or HCO3- <10 mEq/L Usual rate of administration is 2 5 mEq/h Can cause chemical phlebitis or cellulitis Many drug incompatibilities; flush line after use After cardiac arrest, reversal of acidosis results from adequate ventilation and blood flow. May consider use upon return of spontaneous circulation after long arrest interval (1 mEq/kg IV). Not recommended for routine use after cardiac arrest. May be associated with paradoxical mixed venous acidosis Can cause sodium overload and hyperosmolality Treatment of underlying etiology (i.e., sepsis, hypoperfusion, poisoning) is essential to reverse acidosis
Decision to treat is controversial and depends on clinical situation; indications vary with etiology such as bicarbonate responsive acidosis (e.g., diabetic ketoacidosis). Bicarbonate deficit, an approximation of the amount of bicarbonate replacement needed to return bicarbonate concentration to normal:    HCO3- deficit = body weight (kg) 0.4 (desired [HCO3-] - measured [HCO3-]) In patients with chronic metabolic acidosis caused by chronic renal failure, replace with bicarbonate when bicarbonate concentration is less than 15 mEq/L to prevent osteomalacia. Treatment of lactic acidosis should be directed to the underlying etiology.

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TABLE 5.11. Alkalosis

Therapy	Dosage	Indications	Comments
Potassium chloride (KCl)	Mild alkalosis: 100 150 mEq/d Severe alkalosis: Up to 300 mEq/d	Chloride-responsive alkalosis	Will replete not only chloride, but also potassium deficit, which may be substantial, especially with diuretic-induced alkalosis Spironolactone or potassium-sparing diuretics may be useful in hypokalemic patients
Sodium chloride (NaCl)	Mild alkalosis: 100 150 mEq/d Severe alkalosis: Up to 300 mEq/d	Chloride-responsive alkalosis	Alternative to KCl Use with caution in patients with HF
Acetazolamide	5 mg/kg qd up to qid (PO/IV)	Works well in edematous patients with cirrhosis or HF	Carbonic anhydrase inhibitor; impairs renal sodium and renal bicarbonate resorption, thus reducing net acid excretion Will have diuretic effect and may cause potassium losses
Hydrochloric acid (HCl)	0.1 N HCl by calculation (see comment)	For rapid correction of severe metabolic alkalosis	Concentration is 100 mEq HCl per 1 L sterile water Must administer via a central venous line Amount of H+ needed to correct deficit can be determined by formula: H+ (mEq) = 0.5 weight (kg) (103 - serum chloride)
Ammonium chloride	By calculation (see comment)	Metabolic alkalosis due to significant chloride losses	Ammonium ions are converted to urea in the liver with the generation of hydrogen and chloride ions Should not be given to patients with hepatic failure H+ (mEq) = 0.5 weight (kg) (103 - serum chloride)
HF, heart failure; IV, intravenous; PO, by mouth Correct volume, potassium, and chloride depletions.

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TABLE 5.12. Tumor Lysis Syndrome

Complication	Intervention	Comments
Associated with rapidly growing malignancies (eg. leukemias, lymphomas) that are highly chemo or radio sensitive. Therapy initiated before administration of chemotherapy. Syndrome char- acterized by increases in uric acid, potassium, phosphate, and decreases in calcium that may result in renal failure, arrhythmias, seizures, or sudden death.
Pretreatment Evaluation and Preparation
Volume loading and diuresis	Hypotonic fluids (D5W/0.45% NaCl) 3,000 ml/M2/day	Loop diuretics if necessary to maintain urinary output
Evaluate renal function	Monitor weight, intake and output, and electrolytes	Ultrasound Attempt to relieve obstructive uropathy if present
Control uric acid	Increase clearance (diuresis), prevent uric acid synthesis, increase degradation	Allopurinol 200 400 mg/m2/d IV (max. 600 mg/d) until serum uric acid is normal Rasburicase 0.15 0.2 mg/kd qd 5 d Correct acidosis Alkalinize urine (pH >7.0) with NaHCO3 (100 150 mEq in 1 L D5W or sterile water) is controversial and may promote Ca2PO4 deposition in the kidney, heart, and other organs if hyperphosphatemia is present Alkalinization is not required with a uricase Dialyze if urate nephropathy presents with oliguria
Control phosphate	Initiate oral phosphate binders (aluminum hydroxide) if adequate GI function
Delay chemotherapy if necessary	Until good urine output established and uric acid controlled	Initiate hemodialysis if indicated; oliguria due to acute uric acid nephropathy is very responsive to dialytic therapy
Postchemotherapy Management
Volume replacement and diuresis	Maintain forced diuresis	Omit NaHCO3 from IV solutions because of phosphate crystallization in urine
Monitor electrolytes	Monitor every 4 6 h depending on tumor burden and/or rate of biochemical changes	Monitor ECG for hyperkalemia and/or hypocalcemia
Control uric acid	Allopurinol 200 400 mg/M2/day PO for the first 3 d of chemotherapy, then 200 mg/M2/d PO maintenance Rasburicase 0.15 0.2 mg/kd qd 5 d
Renal failure	Hemodialysis	Indications: Oliguria/azotemia Uncontrolled hyperkalemia Symptomatic hypocalcemia Uric acid nephropathy or rapidly rising uric acid Phosphate nephropathy or rapidly rising phosphate Iatrogenic volume overload in the face of oliguria Continuous arterial or venovenous hemofiltration or hemodiafiltration will control volume status but may not maintain rapid efficient clearance of potassium if tumor lysis is overwhelming
ECG, electrocardiogram; GI, gastrointestinal; IV, intravenous; PO, by mouth

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TABLE 5.13. Diuretics

Site of Action	Type of Diuresis, Onset, and Duration	Usual Dosage	Comments
Loop of Henle	K+ and Na+ wasting, hypo-osmotic or isosmotic urine		Ototoxicity with bumetanide, furosemide, and torsemide in high doses; clinically effective when GFR <25 ml/min
Bumetanide	Onset:    PO: 30 min    IV: <10 min Duration:    PO: 5 6 h    IV: 4 h	Bolus:    0.5 1.0 mg    q2 3 h prn Infusion:    0.08 0.3 mg/h PO: 0.5 2 mg tid-qd	Bumetanide 1 mg furosemide 40 mg Doses >10 mg PO or 20 mg IV may be required in patients with renal failure or in the management of edema or hypertension IV loading dose may be used before starting infusion
Furosemide	Onset:    PO: 60 min    IV: 5 min Duration:    PO: 6 h    IV: 2 h	Bolus:    20 80 mg    q1 2h prn Infusion:    3 12 mg/h PO:    20 80 mg    q6 8h prn	IV doses of 400 mg per bolus or 3 7 g total per day have been used in some patients IV bolus doses are usually doubled until a maximum dose of 400 mg is reached An IV loading dose may be used before starting infusion Furosemide IV dose = 60% to 70% PO dose
Torsemide	Onset:    PO: 60 min    IV: 15 min Duration:    PO: 6 8 h    IV: 6 8 h	Bolus:    25 mg Infusion:    3 10 mg/h PO:    5 40 mg qd	Inject IV dose over 2 min Dose can be titrated upward by doubling the dose until therapeutic effect achieved or maximum dose of 200 mg is attained, although 400 800 mg may be required in patients with acute renal failure Torsemide IV dose = PO dose Torsemide 10 20 mg = furosemide 40 mg = bumetanide 1 mg Patients with CrCl 15 20 ml/min and HF may require an initial infusion rate of 10 mg/h IV loading dose may be used before starting an infusion
Distal Tubule Proximal Tubule	Moderate natriuresis and potassium wasting		May be ineffective when GFR <25 ml/min Commonly used in combination with loop diuretics to enhance efficacy
Chlorothiazide	Onset:    PO: 60 min    IV: 15 min Duration:    PO: 6 8 h    IV: 6 8 h	IV bolus or PO: 500 1,000 mg bid-qid
Hydrochlorothiazide	Onset:    PO: 2 h Duration:    PO: 12 18 h	PO: 25 100 mg qd
Metolazone	Onset:    PO: 1 h Duration:    PO: 12 24 h	PO: 5 20 mg qd	Thiazide type diuretic Administer 30 min before IV diuretic
Collecting Duct (Potassium Sparing)			Weak diuretics; risk of hyperkalemia is relative contraindication
Triamterene	Onset:    PO: 2 4 h Duration:    PO: 12 16 h	PO: 100 200 mg qd	Maximum dose 300 mg/d
Amiloride	Onset:    PO: 2 h Duration:    PO: 24 h	PO: 5 20 mg qd
Spironolactone	Onset:    PO: >24 h Duration:    PO: 48 72 h	PO: 25 200 mg/d given qd or bid	Gradual onset of diuresis with maximal effect on 3rd day
Proximal Tubule
Acetazolamide	Onset:    PO: 30 min    IV: 5 min Duration:    PO: 6 8 h    IV: 4 5 h	For alkalosis:    5 mg/kg/d mg IV/PO qid-qd 2 4 d For edema:    5 mg/kg/d IV/PO divided bid-qid	Carbonic anhydrase inhibitor, causes bicarbonaturia and potassium wasting
CrCl, creatinine clearance; GFR, glomerular filtration rate; HF, heart failure; IV, intravenous; PO, by mouth

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TABLE 5.14. Electrolyte Composition of Common IV Solutions

	mEq/L						Osm	Calories
	Na+	Cl-	K+	HCO3-	Mg+2	Ca+2
Crystalloid
0.9% NaCl (NS)	154	154					292
0.9% NaCl & 5% dextrose in water (D5W/NS)	154	154					565	170
0.45% NaCl (1/2 NS)	77	77					146
0.45% NaCl & 5% dextrose in water (D5W-1/2NS)	77	77					420	170
0.2% NaCl & 5% dextrose (D5W-1/4 NS)	34	34					330	170
5% dextrose in water (D5W)							274	170
10% dextrose in water (D10W)							548	340
Ringer's lactate (RL)	130	109	4	28a		3	277
3% NaCl (hypertonic saline)	513	513					960
Colloid
Hetastarch 6%	154	154					310
Hetastarch 6% in lactated electrolyte injection	143	124	3	28a	9	3	307	340
5% albumin (5 g/100 ml)	145	145
25% albumin (25 g/100 ml)	145	145
aPresent in solution as lactate, which is metabolized to bicarbonate (HCO3-).