Does my patient need maintenance fluids?

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Does my patient need maintenance fluids?

My adult nonacutely ill patient, weighing 70 kg with a glomerular filtration rate (GFR) greater than 60 mL/min/1.73 m2, is admitted to the general medical service. She is to receive nothing by mouth for at least the next 24 hours for testing. Do I need to provide maintenance fluids intravenously?

The question seems like it should have an easy answer. However, there is no consensus either on the type of fluids or the need for them at all.

Mortiz and Ayus1 have described the role of maintenance intravenous (IV) fluids in acutely ill patients and made the case for isotonic saline (0.9% NaCl) to minimize the risk of hyponatremia, while acknowledging that it provides 7 to 10 g of sodium per day.

Recommendations for IV fluids for nonacutely ill hospitalized patients range from isotonic solutions such as 0.9% NaCl and lactated Ringer’s, to hypotonic fluids such as 5% dextrose in water (D5W) in 0.45% NaCl and D5W in 0.2% NaCl.2–5

The 2013 guidelines of the UK National Institute for Health and Care Excellence (NICE) recommend hypotonic fluids to provide 25 to 30 mL/kg/day of water with 1 mmol/kg/day of sodium. For a 70-kg patient (body surface area 1.7 m2), this would be 1,750 to 2,000 mL of water, with a maximum of 70 mEq/L of sodium (35 mEq/L).5 An option would be D5W in 0.2% NaCl, which has 34 mEq/L of sodium.

When choosing maintenance IV fluids, we need to consider the following questions:

  • What is my patient’s volume status?
  • What is the baseline serum sodium and renal function?
  • Are there comorbid conditions that may affect antidiuretic hormone (ADH) status such as physiologic stimulation from volume depletion, drugs, pathologic medical conditions, or syndrome of inappropriate ADH stimulation?
  • Will my patient be receiving strictly nothing by mouth?
  • Are there unusual fluid losses?

SCENARIO 1: ‘USUAL’ MAINTENANCE

If the patient is euvolemic, with a normal serum osmolality, a GFR more than 60 mL/min/1.73 m2, no stimuli for ADH secretion, and no unusual fluid losses, “usual” maintenance would be expected. The usual volume for this patient can be estimated by the following formulas:

  • Maintenance volume: 2,550 mL (1,500 mL × 1.7 m2 body surface area)
  • Holliday-Segar method6: 2,500 mL (1,500 mL plus 20 mL/kg for every kilogram over 20 kg).

The usual sodium can be also estimated by the following formulas:

  • 2 g Na/day = 2,000 mg/day = 87 mEq/day
  • Holliday-Segar6: 3 mEq Na/100 mL and 2 mEq K/100 mL of maintenance fluid.

Maintenance IV fluids for our nonacutely ill adult patient could be:

  • NICE guideline5: D5W in 0.2% NaCl with 20 mEq KCl, to run at 75 mL/hour
  • Holliday-Segar method6: D5W in 0.2% NaCl with 20 mEq KCl, to run at 100 mL/hour.

Twenty-four hours later, assuming no unusual fluid losses or stimulation of ADH secretion, our patient would weigh the same and would have no significant change in serum osmolality.

OTHER OPTIONS

What if I provide 0.9% NaCl instead?

Each 1 L of normal saline provides 154 mEq of sodium, equivalent to 3.5 g of sodium. Thus, for the 24 hours, with administration of 2 to 2.5 L, the patient would receive a sodium load of 7 to 8.75 g. The consequences of this can be debated, but for 24 hours, more than likely, nothing will happen or be noticeable. The kidneys have a wonderful ability to “dump” excess sodium ingested in the diet, as evidenced by the average Western diet with a sodium load in the range of 4 g per day.7,8

What if I provide 0.45% NaCl instead?

Each liter provides 50% of the sodium load of 0.9% NaCl. With the 24-hour administration of 2 to 2.5 L of D5W in 0.45% NaCl, the sodium load would be 3.5 to 4.8 g, and the kidneys would dump the excess sodium.

What if I provide ‘catch-up’ fluids after 24 hours, not maintenance fluids?

Assuming only usual losses and no unusual ADH stimulation except for the physiologic stimuli from volume depletion for 24 hours, our patient would lose 2 kg (1 L fluid loss = 1 kg weight loss) and 87 mEq of sodium. This is approximately 4.5% dehydration; thus, other than increased thirst, no physical findings of volume depletion would be clinically evident.

Table 1. Scenario 1: 24 hours without fluids.

However, serum osmolality and sodium would increase. After 24 hours of nothing by mouth with usual fluid losses, there would be a rise in serum osmolality of 13.5 mOsm/L (a rise in sodium of 6 to 7 mEq/L), which would stimulate ADH in an attempt to minimize further urinary losses. There would be an intracellular volume loss of 1.3 L (Table 1). Clinically, just as with the administration of 0.9% sodium, these changes would not likely be of any clinical consequence in the first 24 hours.

 

 

SCENARIO 2: IMPAIRED WATER EXCRETION, AND FLUIDS GIVEN

Table 2. Scenario 2: Antidiuretic hormone stimulation and 2L of 0.2% NaCl in 24 hours.

If the patient is euvolemic but has or is at risk for ADH stimulation,1,9 providing maintenance IV fluids according to the NICE or Holliday-Segar recommendations (a total of 2 L of 0.2% NaCl = 34 mEq Na/L = 68 mOsm/L) would result in an excess of free water, as an increase in ADH secretion impairs free water clearance. A potential scenario with impaired water excretion is shown in Table 2.

After 24 hours, the patient’s serum osmolality would drop by about 7 mOsm/L, and the serum sodium would decrease by 3 or 4 mEq. The consequence of the intracellular fluid shift would be seen by the expansion of the intracellular volume from 28 to 28.7 L.

If this patient were to have received 2 L of 0.9% NaCl (308 mOsm/L × 2 L = 616 Osm) as suggested by Moritz and Ayus,1 the result would be a serum osmolality of 284 mOsm/L, thus avoiding hyponatremia and intracellular fluid shifts.

THE BOTTOM LINE

Know your patient, answer the clinical questions noted above, and decide.

For a euvolemic patient with normal serum sodium, GFR greater than 60 mL/1.73 m2, and no ADH stimulation, for 24 hours it probably doesn’t matter that much, but a daily reassessment of the continued need for and type of intravenous fluids is critical.

For patients not meeting the criteria noted above such as a patient with systolic or diastolic heart failure, advanced or end-stage renal disease puts the patient at risk for early potential complications of either hyponatremia or sodium overload. For these patients, maintenance intravenous fluids need to be chosen wisely. Daily weights, examinations, and laboratory testing will let you know if something is not right and will allow for early detection and treatment.

References
  1. Mortiz ML, Ayus JC. Maintenance intravenous fluids in acutely ill patients. N Engl J Med 2015; 373(14):1350–1360. doi:10.1056/NEJMra1412877
  2. Feld LG, Neuspiel DR, Foster BA, et al; Subcommittee on Fluid and Electrolyte Therapy. Clinical practice guideline: maintenance intravenous fluids in children. Pediatrics 2018;142(6). doi:10.1542/peds.2018-3083
  3. Sterns RH. Maintenance and replacement fluid therapy in adults. www.uptodate.com/contents/maintenance-and-replacement-fluid-therapy-in-adults. Accessed August 21, 2019.
  4. Shafiee MA, Bohn D, Hoorn EJ, Halperin ML. How to select optimal maintenance intravenous fluid therapy. QJM 2003; 96(8):601–610. doi:10.1093/qjmed/hcg101
  5. National Institute for Health and Care Excellence (NICE). Intravenous fluid therapy in adults in hospital. www.nice.org.uk/guidance/cg174. Accessed August 21, 2019.
  6. Holliday MA, Segar WE. The maintenance need for water in parenteral fluid therapy. Pediatrics 1957; 19(5):823–832. pmid:13431307
  7. Appel LJ, Foti K. Sources of dietary sodium: implications for patients, physicians, and policy. Circulation 2017; 135(19):1784–1787. doi:10.1161/CIRCULATIONAHA.117.027933
  8. Harnack LJ, Cogswell ME, Shikany JM, et al. Sources of sodium in US adults from 3 geographic regions. Circulation 2017; 135(19):1775–1783. doi:10.1161/CIRCULATIONAHA.116.024446
  9. Sterns RH. Pathophysiology and etiology of the syndrome of inappropriate antidiuretic hormone secretion (SIADH). www.uptodate.com/contents/pathophysiology-and-etiology-of-the-syndrome-of-inappropriate-antidiuretic-hormone-secretion-siadh. Accessed August 21, 2019.
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Robert Lichtenberg, MD
Department of Internal Medicine, MacNeal Hospital, Berwyn, IL

Address: Robert Lichtenberg, MD, Department of Internal Medicine, NHS Lothian, 3231 South Euclid Avenue, Suite 203, Berwyn, IL 60402; [email protected]

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Address: Robert Lichtenberg, MD, Department of Internal Medicine, NHS Lothian, 3231 South Euclid Avenue, Suite 203, Berwyn, IL 60402; [email protected]

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My adult nonacutely ill patient, weighing 70 kg with a glomerular filtration rate (GFR) greater than 60 mL/min/1.73 m2, is admitted to the general medical service. She is to receive nothing by mouth for at least the next 24 hours for testing. Do I need to provide maintenance fluids intravenously?

The question seems like it should have an easy answer. However, there is no consensus either on the type of fluids or the need for them at all.

Mortiz and Ayus1 have described the role of maintenance intravenous (IV) fluids in acutely ill patients and made the case for isotonic saline (0.9% NaCl) to minimize the risk of hyponatremia, while acknowledging that it provides 7 to 10 g of sodium per day.

Recommendations for IV fluids for nonacutely ill hospitalized patients range from isotonic solutions such as 0.9% NaCl and lactated Ringer’s, to hypotonic fluids such as 5% dextrose in water (D5W) in 0.45% NaCl and D5W in 0.2% NaCl.2–5

The 2013 guidelines of the UK National Institute for Health and Care Excellence (NICE) recommend hypotonic fluids to provide 25 to 30 mL/kg/day of water with 1 mmol/kg/day of sodium. For a 70-kg patient (body surface area 1.7 m2), this would be 1,750 to 2,000 mL of water, with a maximum of 70 mEq/L of sodium (35 mEq/L).5 An option would be D5W in 0.2% NaCl, which has 34 mEq/L of sodium.

When choosing maintenance IV fluids, we need to consider the following questions:

  • What is my patient’s volume status?
  • What is the baseline serum sodium and renal function?
  • Are there comorbid conditions that may affect antidiuretic hormone (ADH) status such as physiologic stimulation from volume depletion, drugs, pathologic medical conditions, or syndrome of inappropriate ADH stimulation?
  • Will my patient be receiving strictly nothing by mouth?
  • Are there unusual fluid losses?

SCENARIO 1: ‘USUAL’ MAINTENANCE

If the patient is euvolemic, with a normal serum osmolality, a GFR more than 60 mL/min/1.73 m2, no stimuli for ADH secretion, and no unusual fluid losses, “usual” maintenance would be expected. The usual volume for this patient can be estimated by the following formulas:

  • Maintenance volume: 2,550 mL (1,500 mL × 1.7 m2 body surface area)
  • Holliday-Segar method6: 2,500 mL (1,500 mL plus 20 mL/kg for every kilogram over 20 kg).

The usual sodium can be also estimated by the following formulas:

  • 2 g Na/day = 2,000 mg/day = 87 mEq/day
  • Holliday-Segar6: 3 mEq Na/100 mL and 2 mEq K/100 mL of maintenance fluid.

Maintenance IV fluids for our nonacutely ill adult patient could be:

  • NICE guideline5: D5W in 0.2% NaCl with 20 mEq KCl, to run at 75 mL/hour
  • Holliday-Segar method6: D5W in 0.2% NaCl with 20 mEq KCl, to run at 100 mL/hour.

Twenty-four hours later, assuming no unusual fluid losses or stimulation of ADH secretion, our patient would weigh the same and would have no significant change in serum osmolality.

OTHER OPTIONS

What if I provide 0.9% NaCl instead?

Each 1 L of normal saline provides 154 mEq of sodium, equivalent to 3.5 g of sodium. Thus, for the 24 hours, with administration of 2 to 2.5 L, the patient would receive a sodium load of 7 to 8.75 g. The consequences of this can be debated, but for 24 hours, more than likely, nothing will happen or be noticeable. The kidneys have a wonderful ability to “dump” excess sodium ingested in the diet, as evidenced by the average Western diet with a sodium load in the range of 4 g per day.7,8

What if I provide 0.45% NaCl instead?

Each liter provides 50% of the sodium load of 0.9% NaCl. With the 24-hour administration of 2 to 2.5 L of D5W in 0.45% NaCl, the sodium load would be 3.5 to 4.8 g, and the kidneys would dump the excess sodium.

What if I provide ‘catch-up’ fluids after 24 hours, not maintenance fluids?

Assuming only usual losses and no unusual ADH stimulation except for the physiologic stimuli from volume depletion for 24 hours, our patient would lose 2 kg (1 L fluid loss = 1 kg weight loss) and 87 mEq of sodium. This is approximately 4.5% dehydration; thus, other than increased thirst, no physical findings of volume depletion would be clinically evident.

Table 1. Scenario 1: 24 hours without fluids.

However, serum osmolality and sodium would increase. After 24 hours of nothing by mouth with usual fluid losses, there would be a rise in serum osmolality of 13.5 mOsm/L (a rise in sodium of 6 to 7 mEq/L), which would stimulate ADH in an attempt to minimize further urinary losses. There would be an intracellular volume loss of 1.3 L (Table 1). Clinically, just as with the administration of 0.9% sodium, these changes would not likely be of any clinical consequence in the first 24 hours.

 

 

SCENARIO 2: IMPAIRED WATER EXCRETION, AND FLUIDS GIVEN

Table 2. Scenario 2: Antidiuretic hormone stimulation and 2L of 0.2% NaCl in 24 hours.

If the patient is euvolemic but has or is at risk for ADH stimulation,1,9 providing maintenance IV fluids according to the NICE or Holliday-Segar recommendations (a total of 2 L of 0.2% NaCl = 34 mEq Na/L = 68 mOsm/L) would result in an excess of free water, as an increase in ADH secretion impairs free water clearance. A potential scenario with impaired water excretion is shown in Table 2.

After 24 hours, the patient’s serum osmolality would drop by about 7 mOsm/L, and the serum sodium would decrease by 3 or 4 mEq. The consequence of the intracellular fluid shift would be seen by the expansion of the intracellular volume from 28 to 28.7 L.

If this patient were to have received 2 L of 0.9% NaCl (308 mOsm/L × 2 L = 616 Osm) as suggested by Moritz and Ayus,1 the result would be a serum osmolality of 284 mOsm/L, thus avoiding hyponatremia and intracellular fluid shifts.

THE BOTTOM LINE

Know your patient, answer the clinical questions noted above, and decide.

For a euvolemic patient with normal serum sodium, GFR greater than 60 mL/1.73 m2, and no ADH stimulation, for 24 hours it probably doesn’t matter that much, but a daily reassessment of the continued need for and type of intravenous fluids is critical.

For patients not meeting the criteria noted above such as a patient with systolic or diastolic heart failure, advanced or end-stage renal disease puts the patient at risk for early potential complications of either hyponatremia or sodium overload. For these patients, maintenance intravenous fluids need to be chosen wisely. Daily weights, examinations, and laboratory testing will let you know if something is not right and will allow for early detection and treatment.

My adult nonacutely ill patient, weighing 70 kg with a glomerular filtration rate (GFR) greater than 60 mL/min/1.73 m2, is admitted to the general medical service. She is to receive nothing by mouth for at least the next 24 hours for testing. Do I need to provide maintenance fluids intravenously?

The question seems like it should have an easy answer. However, there is no consensus either on the type of fluids or the need for them at all.

Mortiz and Ayus1 have described the role of maintenance intravenous (IV) fluids in acutely ill patients and made the case for isotonic saline (0.9% NaCl) to minimize the risk of hyponatremia, while acknowledging that it provides 7 to 10 g of sodium per day.

Recommendations for IV fluids for nonacutely ill hospitalized patients range from isotonic solutions such as 0.9% NaCl and lactated Ringer’s, to hypotonic fluids such as 5% dextrose in water (D5W) in 0.45% NaCl and D5W in 0.2% NaCl.2–5

The 2013 guidelines of the UK National Institute for Health and Care Excellence (NICE) recommend hypotonic fluids to provide 25 to 30 mL/kg/day of water with 1 mmol/kg/day of sodium. For a 70-kg patient (body surface area 1.7 m2), this would be 1,750 to 2,000 mL of water, with a maximum of 70 mEq/L of sodium (35 mEq/L).5 An option would be D5W in 0.2% NaCl, which has 34 mEq/L of sodium.

When choosing maintenance IV fluids, we need to consider the following questions:

  • What is my patient’s volume status?
  • What is the baseline serum sodium and renal function?
  • Are there comorbid conditions that may affect antidiuretic hormone (ADH) status such as physiologic stimulation from volume depletion, drugs, pathologic medical conditions, or syndrome of inappropriate ADH stimulation?
  • Will my patient be receiving strictly nothing by mouth?
  • Are there unusual fluid losses?

SCENARIO 1: ‘USUAL’ MAINTENANCE

If the patient is euvolemic, with a normal serum osmolality, a GFR more than 60 mL/min/1.73 m2, no stimuli for ADH secretion, and no unusual fluid losses, “usual” maintenance would be expected. The usual volume for this patient can be estimated by the following formulas:

  • Maintenance volume: 2,550 mL (1,500 mL × 1.7 m2 body surface area)
  • Holliday-Segar method6: 2,500 mL (1,500 mL plus 20 mL/kg for every kilogram over 20 kg).

The usual sodium can be also estimated by the following formulas:

  • 2 g Na/day = 2,000 mg/day = 87 mEq/day
  • Holliday-Segar6: 3 mEq Na/100 mL and 2 mEq K/100 mL of maintenance fluid.

Maintenance IV fluids for our nonacutely ill adult patient could be:

  • NICE guideline5: D5W in 0.2% NaCl with 20 mEq KCl, to run at 75 mL/hour
  • Holliday-Segar method6: D5W in 0.2% NaCl with 20 mEq KCl, to run at 100 mL/hour.

Twenty-four hours later, assuming no unusual fluid losses or stimulation of ADH secretion, our patient would weigh the same and would have no significant change in serum osmolality.

OTHER OPTIONS

What if I provide 0.9% NaCl instead?

Each 1 L of normal saline provides 154 mEq of sodium, equivalent to 3.5 g of sodium. Thus, for the 24 hours, with administration of 2 to 2.5 L, the patient would receive a sodium load of 7 to 8.75 g. The consequences of this can be debated, but for 24 hours, more than likely, nothing will happen or be noticeable. The kidneys have a wonderful ability to “dump” excess sodium ingested in the diet, as evidenced by the average Western diet with a sodium load in the range of 4 g per day.7,8

What if I provide 0.45% NaCl instead?

Each liter provides 50% of the sodium load of 0.9% NaCl. With the 24-hour administration of 2 to 2.5 L of D5W in 0.45% NaCl, the sodium load would be 3.5 to 4.8 g, and the kidneys would dump the excess sodium.

What if I provide ‘catch-up’ fluids after 24 hours, not maintenance fluids?

Assuming only usual losses and no unusual ADH stimulation except for the physiologic stimuli from volume depletion for 24 hours, our patient would lose 2 kg (1 L fluid loss = 1 kg weight loss) and 87 mEq of sodium. This is approximately 4.5% dehydration; thus, other than increased thirst, no physical findings of volume depletion would be clinically evident.

Table 1. Scenario 1: 24 hours without fluids.

However, serum osmolality and sodium would increase. After 24 hours of nothing by mouth with usual fluid losses, there would be a rise in serum osmolality of 13.5 mOsm/L (a rise in sodium of 6 to 7 mEq/L), which would stimulate ADH in an attempt to minimize further urinary losses. There would be an intracellular volume loss of 1.3 L (Table 1). Clinically, just as with the administration of 0.9% sodium, these changes would not likely be of any clinical consequence in the first 24 hours.

 

 

SCENARIO 2: IMPAIRED WATER EXCRETION, AND FLUIDS GIVEN

Table 2. Scenario 2: Antidiuretic hormone stimulation and 2L of 0.2% NaCl in 24 hours.

If the patient is euvolemic but has or is at risk for ADH stimulation,1,9 providing maintenance IV fluids according to the NICE or Holliday-Segar recommendations (a total of 2 L of 0.2% NaCl = 34 mEq Na/L = 68 mOsm/L) would result in an excess of free water, as an increase in ADH secretion impairs free water clearance. A potential scenario with impaired water excretion is shown in Table 2.

After 24 hours, the patient’s serum osmolality would drop by about 7 mOsm/L, and the serum sodium would decrease by 3 or 4 mEq. The consequence of the intracellular fluid shift would be seen by the expansion of the intracellular volume from 28 to 28.7 L.

If this patient were to have received 2 L of 0.9% NaCl (308 mOsm/L × 2 L = 616 Osm) as suggested by Moritz and Ayus,1 the result would be a serum osmolality of 284 mOsm/L, thus avoiding hyponatremia and intracellular fluid shifts.

THE BOTTOM LINE

Know your patient, answer the clinical questions noted above, and decide.

For a euvolemic patient with normal serum sodium, GFR greater than 60 mL/1.73 m2, and no ADH stimulation, for 24 hours it probably doesn’t matter that much, but a daily reassessment of the continued need for and type of intravenous fluids is critical.

For patients not meeting the criteria noted above such as a patient with systolic or diastolic heart failure, advanced or end-stage renal disease puts the patient at risk for early potential complications of either hyponatremia or sodium overload. For these patients, maintenance intravenous fluids need to be chosen wisely. Daily weights, examinations, and laboratory testing will let you know if something is not right and will allow for early detection and treatment.

References
  1. Mortiz ML, Ayus JC. Maintenance intravenous fluids in acutely ill patients. N Engl J Med 2015; 373(14):1350–1360. doi:10.1056/NEJMra1412877
  2. Feld LG, Neuspiel DR, Foster BA, et al; Subcommittee on Fluid and Electrolyte Therapy. Clinical practice guideline: maintenance intravenous fluids in children. Pediatrics 2018;142(6). doi:10.1542/peds.2018-3083
  3. Sterns RH. Maintenance and replacement fluid therapy in adults. www.uptodate.com/contents/maintenance-and-replacement-fluid-therapy-in-adults. Accessed August 21, 2019.
  4. Shafiee MA, Bohn D, Hoorn EJ, Halperin ML. How to select optimal maintenance intravenous fluid therapy. QJM 2003; 96(8):601–610. doi:10.1093/qjmed/hcg101
  5. National Institute for Health and Care Excellence (NICE). Intravenous fluid therapy in adults in hospital. www.nice.org.uk/guidance/cg174. Accessed August 21, 2019.
  6. Holliday MA, Segar WE. The maintenance need for water in parenteral fluid therapy. Pediatrics 1957; 19(5):823–832. pmid:13431307
  7. Appel LJ, Foti K. Sources of dietary sodium: implications for patients, physicians, and policy. Circulation 2017; 135(19):1784–1787. doi:10.1161/CIRCULATIONAHA.117.027933
  8. Harnack LJ, Cogswell ME, Shikany JM, et al. Sources of sodium in US adults from 3 geographic regions. Circulation 2017; 135(19):1775–1783. doi:10.1161/CIRCULATIONAHA.116.024446
  9. Sterns RH. Pathophysiology and etiology of the syndrome of inappropriate antidiuretic hormone secretion (SIADH). www.uptodate.com/contents/pathophysiology-and-etiology-of-the-syndrome-of-inappropriate-antidiuretic-hormone-secretion-siadh. Accessed August 21, 2019.
References
  1. Mortiz ML, Ayus JC. Maintenance intravenous fluids in acutely ill patients. N Engl J Med 2015; 373(14):1350–1360. doi:10.1056/NEJMra1412877
  2. Feld LG, Neuspiel DR, Foster BA, et al; Subcommittee on Fluid and Electrolyte Therapy. Clinical practice guideline: maintenance intravenous fluids in children. Pediatrics 2018;142(6). doi:10.1542/peds.2018-3083
  3. Sterns RH. Maintenance and replacement fluid therapy in adults. www.uptodate.com/contents/maintenance-and-replacement-fluid-therapy-in-adults. Accessed August 21, 2019.
  4. Shafiee MA, Bohn D, Hoorn EJ, Halperin ML. How to select optimal maintenance intravenous fluid therapy. QJM 2003; 96(8):601–610. doi:10.1093/qjmed/hcg101
  5. National Institute for Health and Care Excellence (NICE). Intravenous fluid therapy in adults in hospital. www.nice.org.uk/guidance/cg174. Accessed August 21, 2019.
  6. Holliday MA, Segar WE. The maintenance need for water in parenteral fluid therapy. Pediatrics 1957; 19(5):823–832. pmid:13431307
  7. Appel LJ, Foti K. Sources of dietary sodium: implications for patients, physicians, and policy. Circulation 2017; 135(19):1784–1787. doi:10.1161/CIRCULATIONAHA.117.027933
  8. Harnack LJ, Cogswell ME, Shikany JM, et al. Sources of sodium in US adults from 3 geographic regions. Circulation 2017; 135(19):1775–1783. doi:10.1161/CIRCULATIONAHA.116.024446
  9. Sterns RH. Pathophysiology and etiology of the syndrome of inappropriate antidiuretic hormone secretion (SIADH). www.uptodate.com/contents/pathophysiology-and-etiology-of-the-syndrome-of-inappropriate-antidiuretic-hormone-secretion-siadh. Accessed August 21, 2019.
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Human papillomavirus

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To the Editor: I am an active primary care provider. After reading the update on human papillomavirus (HPV) in the March 2019 issue by Zhang and Batur,1 I was hoping for some clarification on a few points.

The statement is made that up to 70% of HPV-related cervical cancer cases can be prevented with vaccination. I have pulled the reference2 but cannot find supporting data for this claim. Is this proven or optimistic thinking based on the decreased incidence of abnormal Papanicolaou (Pap) test results such as noted in the University of New Mexico HPV Pap registry database3? The authors do cite an additional reference4 documenting a decreased incidence of cervical cancer in the United States among 15- to 24-year-olds from 2003–2006 compared with 2011–2014. This study reported a 29% relative risk reduction in the group receiving the vaccine, with the absolute numbers 6 vs 8.4 cases per 1,000,000. Thus, can the authors provide further references to the statement that 70% of cervical cancers can be prevented by vaccination?

The authors also state that vaccine acceptance rates are highest when primary care providers announce that the vaccine is due rather than invite open-ended discussions. At first this shocked me, but then made me pause and wonder how often I do that—and when I do, why. I regularly do it with all the other vaccines recommended by the Advisory Committee on Immunization Practices. When the parent or patient asks for further information, I am armed to provide it. To date, I am struggling to provide data to educate the patient on the efficacy of the HPV vaccine, particularly the claim that it will prevent 70% of cervical cancers. Are there more data that I am missing?

Finally, let me state that I am a “vaccinator”—always have been, and always will be. I discuss the HPV vaccine with my patients and their parents and try to provide data to support my recommendation. However, I am concerned that this current practice regarding the HPV vaccine has been driven by scare tactics and has now turned to “just give it because I say so.” The University of New Mexico Center for HPV prevention reports up to a 50% reduction in cervical intraepithelial neoplasias (precancer lesions) in teens.3 This is exciting information and raises hope for the future successful battle against cervical cancer. I think it is also more accurate than stating to parents and patients that we have proof that we have prevented 70% of cervical cancers. When we explain it in this manner, the majority of parents and patients buy in and, I believe, enjoy and welcome this open-ended discussion.

References
  1. Zhang S, Batur P. Human papillomavirus in 2019: an update on cervical cancer prevention and screening guidelines. Cleve Clin J Med 2019; 86(3):173–178. doi:10.3949/ccjm.86a.18018
  2. Thaxton L, Waxman AG. Cervical cancer prevention: immunization and screening 2015. Med Clin North Am 2015; 99(3): 469-477.
  3. Benard VB, Castle PE, Jenison SA, et al. Population-based incidence rates of cervical intraepithelial neoplasia in the human papillomavirus vaccine era. JAMA Oncol 2017; 3(6):833–837. doi:10.1001/jamaoncol.2016.3609
  4. Guo F, Cofie LE, Berenson AB. Cervical cancer incidence in young US females after human papillomavirus vaccine introduction. Am J Prev Med 2018; 55(2):197–204. doi:10.1016/j.amepre.2018.03.013
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To the Editor: I am an active primary care provider. After reading the update on human papillomavirus (HPV) in the March 2019 issue by Zhang and Batur,1 I was hoping for some clarification on a few points.

The statement is made that up to 70% of HPV-related cervical cancer cases can be prevented with vaccination. I have pulled the reference2 but cannot find supporting data for this claim. Is this proven or optimistic thinking based on the decreased incidence of abnormal Papanicolaou (Pap) test results such as noted in the University of New Mexico HPV Pap registry database3? The authors do cite an additional reference4 documenting a decreased incidence of cervical cancer in the United States among 15- to 24-year-olds from 2003–2006 compared with 2011–2014. This study reported a 29% relative risk reduction in the group receiving the vaccine, with the absolute numbers 6 vs 8.4 cases per 1,000,000. Thus, can the authors provide further references to the statement that 70% of cervical cancers can be prevented by vaccination?

The authors also state that vaccine acceptance rates are highest when primary care providers announce that the vaccine is due rather than invite open-ended discussions. At first this shocked me, but then made me pause and wonder how often I do that—and when I do, why. I regularly do it with all the other vaccines recommended by the Advisory Committee on Immunization Practices. When the parent or patient asks for further information, I am armed to provide it. To date, I am struggling to provide data to educate the patient on the efficacy of the HPV vaccine, particularly the claim that it will prevent 70% of cervical cancers. Are there more data that I am missing?

Finally, let me state that I am a “vaccinator”—always have been, and always will be. I discuss the HPV vaccine with my patients and their parents and try to provide data to support my recommendation. However, I am concerned that this current practice regarding the HPV vaccine has been driven by scare tactics and has now turned to “just give it because I say so.” The University of New Mexico Center for HPV prevention reports up to a 50% reduction in cervical intraepithelial neoplasias (precancer lesions) in teens.3 This is exciting information and raises hope for the future successful battle against cervical cancer. I think it is also more accurate than stating to parents and patients that we have proof that we have prevented 70% of cervical cancers. When we explain it in this manner, the majority of parents and patients buy in and, I believe, enjoy and welcome this open-ended discussion.

To the Editor: I am an active primary care provider. After reading the update on human papillomavirus (HPV) in the March 2019 issue by Zhang and Batur,1 I was hoping for some clarification on a few points.

The statement is made that up to 70% of HPV-related cervical cancer cases can be prevented with vaccination. I have pulled the reference2 but cannot find supporting data for this claim. Is this proven or optimistic thinking based on the decreased incidence of abnormal Papanicolaou (Pap) test results such as noted in the University of New Mexico HPV Pap registry database3? The authors do cite an additional reference4 documenting a decreased incidence of cervical cancer in the United States among 15- to 24-year-olds from 2003–2006 compared with 2011–2014. This study reported a 29% relative risk reduction in the group receiving the vaccine, with the absolute numbers 6 vs 8.4 cases per 1,000,000. Thus, can the authors provide further references to the statement that 70% of cervical cancers can be prevented by vaccination?

The authors also state that vaccine acceptance rates are highest when primary care providers announce that the vaccine is due rather than invite open-ended discussions. At first this shocked me, but then made me pause and wonder how often I do that—and when I do, why. I regularly do it with all the other vaccines recommended by the Advisory Committee on Immunization Practices. When the parent or patient asks for further information, I am armed to provide it. To date, I am struggling to provide data to educate the patient on the efficacy of the HPV vaccine, particularly the claim that it will prevent 70% of cervical cancers. Are there more data that I am missing?

Finally, let me state that I am a “vaccinator”—always have been, and always will be. I discuss the HPV vaccine with my patients and their parents and try to provide data to support my recommendation. However, I am concerned that this current practice regarding the HPV vaccine has been driven by scare tactics and has now turned to “just give it because I say so.” The University of New Mexico Center for HPV prevention reports up to a 50% reduction in cervical intraepithelial neoplasias (precancer lesions) in teens.3 This is exciting information and raises hope for the future successful battle against cervical cancer. I think it is also more accurate than stating to parents and patients that we have proof that we have prevented 70% of cervical cancers. When we explain it in this manner, the majority of parents and patients buy in and, I believe, enjoy and welcome this open-ended discussion.

References
  1. Zhang S, Batur P. Human papillomavirus in 2019: an update on cervical cancer prevention and screening guidelines. Cleve Clin J Med 2019; 86(3):173–178. doi:10.3949/ccjm.86a.18018
  2. Thaxton L, Waxman AG. Cervical cancer prevention: immunization and screening 2015. Med Clin North Am 2015; 99(3): 469-477.
  3. Benard VB, Castle PE, Jenison SA, et al. Population-based incidence rates of cervical intraepithelial neoplasia in the human papillomavirus vaccine era. JAMA Oncol 2017; 3(6):833–837. doi:10.1001/jamaoncol.2016.3609
  4. Guo F, Cofie LE, Berenson AB. Cervical cancer incidence in young US females after human papillomavirus vaccine introduction. Am J Prev Med 2018; 55(2):197–204. doi:10.1016/j.amepre.2018.03.013
References
  1. Zhang S, Batur P. Human papillomavirus in 2019: an update on cervical cancer prevention and screening guidelines. Cleve Clin J Med 2019; 86(3):173–178. doi:10.3949/ccjm.86a.18018
  2. Thaxton L, Waxman AG. Cervical cancer prevention: immunization and screening 2015. Med Clin North Am 2015; 99(3): 469-477.
  3. Benard VB, Castle PE, Jenison SA, et al. Population-based incidence rates of cervical intraepithelial neoplasia in the human papillomavirus vaccine era. JAMA Oncol 2017; 3(6):833–837. doi:10.1001/jamaoncol.2016.3609
  4. Guo F, Cofie LE, Berenson AB. Cervical cancer incidence in young US females after human papillomavirus vaccine introduction. Am J Prev Med 2018; 55(2):197–204. doi:10.1016/j.amepre.2018.03.013
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