Sodium dreadnaught

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Information about Sodium dreadnaught
Health & Medicine

Published on July 21, 2009

Author: nephron

Source: slideshare.net

Description

a comprehensive but too long presentation on sodium

is Hard Joel M. Topf, MD Nephrology Sodium

Sodium is different Most ions must be regulated because of direct effects of the ion. Arrhythmias from high (or low) potassium Weakness from high magnesium Tetany from low calcium Sodium is not like that. The problems with high or low sodium have little to do with direct effects of the ion. Disregulation of sodium causes changes in cell volume.

Most ions must be regulated because of direct effects of the ion.

Arrhythmias from high (or low) potassium

Weakness from high magnesium

Tetany from low calcium

Sodium is not like that.

The problems with high or low sodium have little to do with direct effects of the ion.

Disregulation of sodium causes changes in cell volume.

Osmosis: the thought experiment

The movement of water in the body The movement of water into and out of cells is analogous to the beaker experiment: When tonicity outside of the cells increases, cells shrivel. intracellular compartment extracellular compartment

The movement of water into and out of cells is analogous to the beaker experiment:

When tonicity outside of the cells increases, cells shrivel.

If the concentration of solute in the cells increases the result is predictable: The movement of water in the body When the tonicity inside of cells increases, cells swell.

If the concentration of solute in the cells increases the result is predictable:

Why we care about osmolality Alterations in cell size disrupt tissue function.

Alterations in cell size disrupt tissue function.

So what about sodium? In the dark ages of medicine (50’s – 60’s) Scientists had discovered the importance of osmoregulation but could not reliably measure osmolality. However, flame photometry allowed reliable sodium measurements. Changes in sodium roughly paralleled changes in tonicity.

In the dark ages of medicine (50’s – 60’s)

Scientists had discovered the importance of osmoregulation but could not reliably measure osmolality.

However, flame photometry allowed reliable sodium measurements.

Changes in sodium roughly paralleled changes in tonicity.

Sodium is an indicator of osmolality The clinically important variable is tonicity . We are interested in sodium because it gives a good clue to the tonicity. This is analogous to taking patients temperature: We are interested in whether the patient has an infection. There are better tests for infection but none as convenient as sticking a thermometer in the mouth. There are better tests of tonicity than serum sodium but none as clinically convenient.

The clinically important variable is tonicity .

We are interested in sodium because it gives a good clue to the tonicity.

This is analogous to taking patients temperature:

We are interested in whether the patient has an infection.

There are better tests for infection but none as convenient as sticking a thermometer in the mouth.

There are better tests of tonicity than serum sodium but none as clinically convenient.

Tonicity versus Osmolality Osmolality Total concentration of all particles in solution. Tonicity Concentration of only the osmotically active particles. Only impermeable particles contribute to tonicity. Only impermeable particles cause changes in cell volume.

Osmolality

Total concentration of all particles in solution.

Tonicity

Concentration of only the osmotically active particles.

Only impermeable particles contribute to tonicity.

Summary We are interested in plasma tonicity because: When elevated, water leaves the cells causing dysfunction. When decreased water moves into the cells causing dysfunction. We are interested in sodium because it usually tells us the plasma tonicity.

We are interested in plasma tonicity because:

When elevated, water leaves the cells causing dysfunction.

When decreased water moves into the cells causing dysfunction.

We are interested in sodium because it usually tells us the plasma tonicity.

Low sodium: hyponatremia Hyponatremia is defined as a sodium concentration less than 135 mEq/L. Pseudohyponatremia is when the sodium concentration is low (< 135) but osmolality is high or normal. True hyponatremia is when both the sodium and the osmolality are low.

Hyponatremia is defined as a sodium concentration less than 135 mEq/L.

Pseudohyponatremia is when the sodium concentration is low (< 135) but osmolality is high or normal.

True hyponatremia is when both the sodium and the osmolality are low.

Pseudohyponatremia: high osmolality Elevated glucose (or mannitol) raise plasma tonicity which draws water from the intracellular compartment diluting plasma sodium. Hillier TA, Abbott RD, Barrett EJ. Am J Med 1999; 106: 399-403.

Elevated glucose (or mannitol) raise plasma tonicity which draws water from the intracellular compartment diluting plasma sodium.

Pseudohyponatremia: high osmolality Correcting the sodium for hyperglycemia. Traditional Katz conversion Add 1.6 to the sodium for every 100 mg/dL the glucose is over 100. Example: Na = 126 mEq/L. Glucose = 600 mg/dL: 600 - 100 = 500. So the glucose is five 100’s over 100 5 x 1.6 = 8 126 + 8 =134 True sodium equals 134 mEq/L To remember 1.6 think “Sweet 16”

Correcting the sodium for hyperglycemia.

Traditional Katz conversion

Add 1.6 to the sodium for every 100 mg/dL the glucose is over 100.

Example: Na = 126 mEq/L. Glucose = 600 mg/dL:

600 - 100 = 500. So the glucose is five 100’s over 100

5 x 1.6 = 8

126 + 8 =134

True sodium equals 134 mEq/L

To remember 1.6 think “Sweet 16”

Pseudohyponatremia: high osmolality The only study on this was conducted by Hillier and published in 1999. N=6 Somatstatin infusion prevents endogenous insulin release. D20 0.45 NaCl infused to raise glucose > 600 mg/dL. An insulin gtt then gradually lowers glucose to 140 mg/dL. Glucose and Na measured every 10 minutes. Hillier TA, Abbott RD, Barrett EJ. Am J Med 1999; 106: 399-403.

The only study on this was conducted by Hillier and published in 1999.

N=6

Somatstatin infusion prevents endogenous insulin release.

D20 0.45 NaCl infused to raise glucose > 600 mg/dL.

An insulin gtt then gradually lowers glucose to 140 mg/dL.

Glucose and Na measured every 10 minutes.

Hillier Study on Pseudohyponatremia Na = 140 - 0.016 Glucose Na = 140 - 0.024 Glucose Na = 141 - 0.016 Glucose Na = 151 - 0.04 Glucose

Pseudohyponatremia: high osmolality Conclusion: sodium has a biphasic relationship to glucose. Serum Glucose less than 400 use 1.6 mg per 100mg/dL conversion. For glucose over 400 use 4.0 per 100mg/dL. Alternatively you can 2.4 per 100 mg/dL. Example: Na = 126 mEq/L. Glucose = 600 mg/dL: Using the biphasic relationship: From 100 to 400 the change is 1.6 x 3 = 4.8 From 400 to 600 the change is 4.0 x 2 = 8 4.8 + 8 = 12.8 126 + 12.8 = 149 mEq/L Using the simple relationship From 100 to 600 the change is 2.4 x 5 = 12 126 + 12 =148 mEq/L Compare this to the Katz conversion of 134 mEq/L

Conclusion: sodium has a biphasic relationship to glucose.

Serum Glucose less than 400 use 1.6 mg per 100mg/dL conversion.

For glucose over 400 use 4.0 per 100mg/dL.

Alternatively you can 2.4 per 100 mg/dL.

Example: Na = 126 mEq/L. Glucose = 600 mg/dL:

Using the biphasic relationship:

From 100 to 400 the change is 1.6 x 3 = 4.8

From 400 to 600 the change is 4.0 x 2 = 8

4.8 + 8 = 12.8

126 + 12.8 = 149 mEq/L

Using the simple relationship

From 100 to 600 the change is 2.4 x 5 = 12

126 + 12 =148 mEq/L

Compare this to the Katz conversion of 134 mEq/L

Pseudohyponatremia: Normal osmolality Increased protein or lipids can cause a lab error causing a falsely lowered sodium. Hyperlipidemia Hypercholesterolemia TPN with lipids IV immunoglobulin infusions Susceptible Flame photometry Indirect- potentiometry Over 66% of clinical labs Not Susceptible Direct potentiometry ABG laboratories Participant summary report: surveys 1982-2002. Northfield, Ill.: College of American Pathologists, 1982-2002.

Increased protein or lipids can cause a lab error causing a falsely lowered sodium.

Hyperlipidemia

Hypercholesterolemia

TPN with lipids

IV immunoglobulin infusions

Susceptible

Flame photometry

Indirect- potentiometry

Over 66% of clinical labs

Not Susceptible

Direct potentiometry

ABG laboratories

True hyponatremia Hyponatremia occurs when water intake exceeds water excretion.

Hyponatremia occurs when water intake exceeds water excretion.

True hyponatremia Hyponatremia does not occur when sodium excretion exceeds sodium intake. Negative salt balance causes hypovolemia

Hyponatremia does not occur when sodium excretion exceeds sodium intake.

If a person drinks more water than the kidney is capable of clearing the excess water will dilute the plasma. Causes of hyponatremia: Increased intake To exceed the maximal renal clearance of water an adult needs to drink about 18 liters a day. clearing

If a person drinks more water than the kidney is capable of clearing the excess water will dilute the plasma.

To exceed the maximal renal clearance of water an adult needs to drink about 18 liters a day.

Water clearance Clearance as a general concept: The clearance of any substance is the volume of blood cleared of that substance in a set unit of time. Water clearance Total water clearance is equal to urine output. Not a useful concept.

Clearance as a general concept:

The clearance of any substance is the volume of blood cleared of that substance in a set unit of time.

Water clearance

Total water clearance is equal to urine output. Not a useful concept.

Free water clearance and soup Imagine urine divided into two components A solute component containing all of the solute at the same osmolality as plasma. Loss of this component does not change plasma osmolality Ladle of soup A free water component providing the balance of the volume. Loss of this solute free water will change serum osmolality. Boiling off water from soup In regards to sodium all that matters is the free water component

Imagine urine divided into two components

A solute component containing all of the solute at the same osmolality as plasma.

Loss of this component does not change plasma osmolality

Ladle of soup

A free water component providing the balance of the volume.

Loss of this solute free water will change serum osmolality.

Boiling off water from soup

Free water clearance 0.5 liter free water Solute component (plasma osmolality 284 mOsm/kg) Use clearance to calculate the osmolar clearance 1 liter 142 mOsm/Kg 0.5 liter 284 mOsm/Kg

Free water clearance Solute component (Solute Clearance) ? 0.5 liter Zero mOsm/Kg Free water component (Free water Clearance) The free water component equals urine volume minus the solute component 1 liter 142 mOsm/Kg 0.5 liter 284 mOsm/Kg

Free water clearance 0.5 liter 568 mOsm/Kg 1 liter 284 mOsm/Kg -0.5 liter 568 mOsm/Kg

Free water clearance Solute component (plasma osmolality 284 mOsm/kg) Use clearance to calculate the osmolar clearance 1 liter 284 mOsm/Kg 0.5 liter 568 mOsm/Kg

Free water clearance Solute component (Solute Clearance) ? Free water component (Free water Clearance) 0.5 liter 568 mOsm/Kg – 0.5 liter Zero mOsm/Kg 1 liter 284 mOsm/Kg

Free water clearance: Implications Dilute urine increases serum osmolality Concentrated urine de-creases serum osmolality Dilute urine Solute free water Concentrated urine Negative free water Na + Na +

Free water clearance: The math

Free water clearance: Math Examples

Electrolyte free water clearance Osmolality doesn’t cause problems, rather tonicity causes changes in cell volume which cause clinical syndromes. So free water clearance must be refined to measure clinically significant changes in tonicity.

Osmolality doesn’t cause problems, rather tonicity causes changes in cell volume which cause clinical syndromes.

So free water clearance must be refined to measure clinically significant changes in tonicity.

Electrolyte free water clearance Osmotically active particles (those that contribute to tonicity): Sodium Potassium Albumin, calcium and others Sodium is the dominant osmotically active solute of serum to the point that others can be ignored. Urine has a significant potassium content so in urine sodium and potassium are equal partners in determining urinary tonicity.

Osmotically active particles (those that contribute to tonicity):

Sodium

Potassium

Albumin, calcium and others

Sodium is the dominant osmotically active solute of serum to the point that others can be ignored.

Urine has a significant potassium content so in urine sodium and potassium are equal partners in determining urinary tonicity.

Electrolyte free water clearance Convert the free water clearance calculation to electrolyte free water clearance Substitute urine osmolality with the sum urine Na + K Substitute serum osmolality with serum sodium Free water clearance Electrolyte free water clearance

Convert the free water clearance calculation to electrolyte free water clearance

Substitute urine osmolality with the sum urine Na + K

Substitute serum osmolality with serum sodium

Electrolyte free water clearance: CHF vs. SIADH Heart Failure Urine Osmolality: 800 Serum Osmolality: 270 Urine Volume: 800 Urine Na: 5 Urine K: 40 Serum Na: 125 SIADH Urine Osmolality: 800 Serum Osmolality: 270 Urine Volume: 800 Urine Na: 125 Urine K: 40 Serum Na: 125

Heart Failure

Urine Osmolality: 800

Serum Osmolality: 270

Urine Volume: 800

Urine Na: 5

Urine K: 40

Serum Na: 125

SIADH

Urine Osmolality: 800

Serum Osmolality: 270

Urine Volume: 800

Urine Na: 125

Urine K: 40

Serum Na: 125

Etiology of hyponatremia Hyponatremia occurs when water intake exceeds water excretion. Hyponatremia occurs when water intake exceeds electrolyte free water clearance. Ingestion > EFW clearance

Hyponatremia occurs when water intake exceeds water excretion.

Hyponatremia occurs when water intake exceeds electrolyte free water clearance.

Etiology of hyponatremia Previously stated that the kidney is able to clear 18 liters of water a day Hyponatremia routinely occurs with water intake less than 2 liters So something must prevent the full free water clearance Hyponatremia is primarily due to an inability to produce dilute urine Dilute urine Solute free water

Previously stated that the kidney is able to clear 18 liters of water a day

Hyponatremia routinely occurs with water intake less than 2 liters

So something must prevent the full free water clearance

Etiology of Hyponatremia: 3 steps to generating dilute urine 1. Delivery of water to the diluting segments of the nephron. 2. Functional diluting segments. 3. Collecting tubule impermeable to water (lack of ADH) 1400 285 100 50

1. Delivery of water to the diluting segments of the nephron.

2. Functional diluting segments.

3. Collecting tubule impermeable to water (lack of ADH)

Failure to Generate dilute urine Lack of water delivery to the diluting segments. Renal failure Volume deficiency Cirrhosis Heart failure Nephrotic syndrome

Lack of water delivery to the diluting segments.

Renal failure

Volume deficiency

Cirrhosis

Heart failure

Nephrotic syndrome

Failure to Generate dilute urine Ineffective solute reabsorption diluting segments: Thick ascending limb of the loop of Henle (TALH) Distal convoluted tubule. Diuretics Non-oliguric ATN

Ineffective solute reabsorption diluting segments:

Thick ascending limb of the loop of Henle (TALH)

Distal convoluted tubule.

Diuretics

Non-oliguric ATN

Failure to Generate dilute urine Permeable collecting ducts (ADH) Volume related ADH SIADH Drug induced Paraneoplastic CNS Pulmonary disease Adrenal insufficiency Hypothyroidism

Permeable collecting ducts (ADH)

Volume related ADH

SIADH

Drug induced

Paraneoplastic

CNS

Pulmonary disease

Adrenal insufficiency

Hypothyroidism

ADH is normally used to regulate osmolality The pituitary releases ADH when osmolality rises. ADH causes the kidney to retain water which lowers osmolality. ADH AD ds H ydration to the body.

The pituitary releases ADH when osmolality rises.

ADH causes the kidney to retain water which lowers osmolality.

ADH AD ds H ydration to the body.

ADH is normally used to regulate osmolality We start with an increase in the plasma osmolality This is detected by the brain The brain releases ADH ADH acts on the kidney The kidney reacts by retaining water and producing a small amount of concentrated urine. The retained water goes here not here

ADH is also secreted when there is poor perfusion. With large drops in perfusion/blood pressure (7-15%) the body uses ADH to support perfusion. ADH aids circulating volume by decreasing the excretion of water from the kidney and causing vasoconstriction. When this occurs the body accepts the trade-off of lowered sodium concentration to restore or maintain circulation.

With large drops in perfusion/blood pressure (7-15%) the body uses ADH to support perfusion.

ADH aids circulating volume by decreasing the excretion of water from the kidney and causing vasoconstriction.

When this occurs the body accepts the trade-off of lowered sodium concentration to restore or maintain circulation.

SIADH: ADH release with no physiologic benefit ADH should not be present when: The osmolality is normal or low and Perfusion is normal. The release of ADH under these conditions is inappropriate. Syndrome of Inappropriate ADH (SIADH) 4 Criteria for the diagnosis of SIADH: Low serum Na and low serum osmolality Clinically euvolemic Urine osmolality 200 more than serum osmolality Urine sodium over 20 mmol/L Also must have normal adrenal and thyroid axis

ADH should not be present when:

The osmolality is normal or low and

Perfusion is normal.

The release of ADH under these conditions is inappropriate.

Syndrome of Inappropriate ADH (SIADH)

4 Criteria for the diagnosis of SIADH:

Low serum Na and low serum osmolality

Clinically euvolemic

Urine osmolality 200 more than serum osmolality

Urine sodium over 20 mmol/L

Also must have normal adrenal and thyroid axis

Causes of SIADH MDMA (Ecstasy) Neurological: Meningitis Tumors Trauma SAH Pulmonary disease: Asthma Mechanical ventilation Pneumonia TB Stress Pain Vomiting Post-surgical Medication Antipsychotics SSRI First generation sulfonylureas Pitocin/Oxytocin Narcotics Cyclophosphamide AIDS

MDMA (Ecstasy)

Neurological:

Meningitis

Tumors

Trauma

SAH

Pulmonary disease:

Asthma

Mechanical ventilation

Pneumonia

TB

Stress

Pain

Vomiting

Post-surgical

Medication

Antipsychotics

SSRI

First generation sulfonylureas

Pitocin/Oxytocin

Narcotics

Cyclophosphamide

AIDS

 

The response to hyponatremia Low sodium concentration causes water to move into the cells. In the brain this causes an increase in ICP. Compensated chronic hyponatremia is essentially asymptomatic.

The problem with compensation The starting point is after compensation has reduced the amount of intracellular solute and the ICP Now, an over-eager intern sees the low sodium and starts an infusion of 3% NaCl to raise the sodium to normal. Sodium 108 The sodium draws water from the inside of the cells causing the brain to shrivel. The problem with interns Sodium 134

Central pontine myelinolysis This brain shrinkage can cause central pontine myelinolysis: Quadriplegia Respiratory paralysis Mental status changes Usually fatal within three to five weeks Risk factors: Hyponatremia for > 24 hours Over-correction of hyponatremia (> 25 mEq/L/day) Rapid correction (greater than 1–2 meq/hr) Alcoholism Malnutrition Liver disease

This brain shrinkage can cause central pontine myelinolysis:

Quadriplegia

Respiratory paralysis

Mental status changes

Usually fatal within three to five weeks

Risk factors:

Hyponatremia for > 24 hours

Over-correction of hyponatremia (> 25 mEq/L/day)

Rapid correction (greater than 1–2 meq/hr)

Alcoholism

Malnutrition

Liver disease

Damned if you do. Damned if you don’t Without treatment patients have cerebral edema. With mistreatment patients are at risk of CPM.

Without treatment patients have cerebral edema.

With mistreatment patients are at risk of CPM.

 

Symptomatic vs. Asymptromatic Uncompensated, symptomatic hyponatremia Treat aggressively with 3% saline. Compensated, asymptomatic hyponatremia Treat conservatively Symptoms Mental status changes Nausea Vomitting Head ache Movement abnormalities Seizures Hypoxia/respiratory failure

Uncompensated, symptomatic hyponatremia

Treat aggressively with 3% saline.

Compensated, asymptomatic hyponatremia

Treat conservatively

Symptoms

Mental status changes

Nausea

Vomitting

Head ache

Movement abnormalities

Seizures

Hypoxia/respiratory failure

Symptomatic vs. Asymptromatic Use the etiology of hyponatremia as a clue to duration of hyponatremia Patients with which are long standing disease processes are more likely to be chronic: SIADH CHF Cirrhosis Likely to cause acute hyponatremia: Psychogenic polydipsia Thiazide diuretics Post-operative hyponatremia

Use the etiology of hyponatremia as a clue to duration of hyponatremia

Patients with which are long standing disease processes are more likely to be chronic:

SIADH

CHF

Cirrhosis

Likely to cause acute hyponatremia:

Psychogenic polydipsia

Thiazide diuretics

Post-operative hyponatremia

Symptomatic vs. Asymptromatic The clock and calendar are unreliable measures of chronicity. The text books say compensation should be complete by 24 to 48 hours. Ayuf and Arief would argue otherwise. Prospectively collected case series of 53 postmenopausal women. Average duration of hyponatremia: 5.2 days All had severe neurologic symptoms. Ayus JC, Arieff AI. JAMA 1999; 281: 2299-2304.

The clock and calendar are unreliable measures of chronicity.

The text books say compensation should be complete by 24 to 48 hours.

Ayuf and Arief would argue otherwise.

Prospectively collected case series of 53 postmenopausal women.

Average duration of hyponatremia: 5.2 days

All had severe neurologic symptoms.

Chronic or acute hyponatremia

 

Conservative therapy for asymptomatic hyponatremia Do no harm. Fluid restrict the patient. Check the urine Na and K and calculate the free water clearance. Restrict water intake below this free water clearance (add 1 liter of insensible losses) and the sodium will rise. 0.5 mmol/L/hr No more than 12 mmol in the first day.

Do no harm.

Fluid restrict the patient.

Check the urine Na and K and calculate the free water clearance.

Restrict water intake below this free water clearance (add 1 liter of insensible losses) and the sodium will rise.

0.5 mmol/L/hr

No more than 12 mmol in the first day.

Conservative therapy for asymptomatic hyponatremia Take a typical patient with SIADH Urine Na 140 Urine K 40 Volume 800 mL Serum Na 115 C EFW = –452 Hard to restrict the free water to less than zero.

Take a typical patient with SIADH

Urine Na 140

Urine K 40

Volume 800 mL

Serum Na 115

C EFW = –452

Hard to restrict the free water to less than zero.

Water restriction is ineffective

Cool furosemide trick Give Mr. SIADH 20 mg of furosemide BID Makes the urine like 0.45NS. Recheck free water clearance Conservative therapy for asymptomatic hyponatremia

Cool furosemide trick

Give Mr. SIADH 20 mg of furosemide BID

Makes the urine like 0.45NS.

Recheck free water clearance

Acute symptomatic hyponatremia In patients with neurologic symptoms due to hyponatremia: 3%. Increase sodium until symptoms abate or 6 mmol/L, which ever comes first. Increase Na < 25 mmol/L in the first 24 hours. Use the change of sodium formula.

In patients with neurologic symptoms due to hyponatremia: 3%.

Increase sodium until symptoms abate or 6 mmol/L, which ever comes first.

Increase Na < 25 mmol/L in the first 24 hours.

Use the change of sodium formula.

Change in sodium formula The formula predicts serum sodium following any infusion. Works equally well in hyponatremia and hypernatremia. comes in two varieties: Simple General Change in sodium following one liter of any IVF. TBW = kg x 0.7 or 0.6 or 0.5 or 0.4 Na in 3%: 513 Na in 0.9%: 154 Na in 0.45%: 77 Na in 0.225%: 39

The formula predicts serum sodium following any infusion.

Works equally well in hyponatremia and hypernatremia.

comes in two varieties:

Simple

General

Change in Sodium Formula: Examples 66 yo AA female 3 days post-op from TAH develops seizures and is unresponsive. Na = 108 K = 2.8 Weight = 65 kg Raise Na 6 mEq in 2 hours give 300 ml/hr for 2 hours or until symptoms resolve. After that 100mL will increase serum Na by 1mmol/L. Check frequent serum Na, recheck change in Na calc. The speed limit is less than 25 mmol/L in first day

66 yo AA female 3 days post-op from TAH develops seizures and is unresponsive.

Na = 108

K = 2.8

Weight = 65 kg

Raise Na 6 mEq in 2 hours give 300 ml/hr for 2 hours or until symptoms resolve.

After that 100mL will increase serum Na by 1mmol/L.

Check frequent serum Na, recheck change in Na calc.

The speed limit is less than 25 mmol/L in first day

Hyponatremia: Summary Hyponatremia is a sodium < 135 mEq/L Rarely, it is associated with a normal or high osmolality and is called pseudohyponatremia. Otherwise, it is due to an imbalance in the intake and excretion of water. It increases the icp but after 24 hours the body compensates. Treatment of acute hyponatremia can occur at 1.5-2.0 mEq/L per hour. Treatment of chronic hyponatremia must be at 0.5 mEq/L per hour at the fastest.

Hyponatremia is a sodium < 135 mEq/L

Rarely, it is associated with a normal or high osmolality and is called pseudohyponatremia.

Otherwise, it is due to an imbalance in the intake and excretion of water.

It increases the icp but after 24 hours the body compensates.

Treatment of acute hyponatremia can occur at 1.5-2.0 mEq/L per hour.

Treatment of chronic hyponatremia must be at 0.5 mEq/L per hour at the fastest.

Hypernatremia Hypernatremia is defined as a sodium > 145 mEq/L. Hypernatremia is associated with increased hospital mortality. Patients who present with hypernatremia typically get appropriate therapy. In patients who develop hypernatremia while hospitalized don’t get therapy as often.

Hypernatremia is defined as a sodium > 145 mEq/L.

Hypernatremia is associated with increased hospital mortality.

Patients who present with hypernatremia typically get appropriate therapy.

In patients who develop hypernatremia while hospitalized don’t get therapy as often.

Causes of hypernatremia Water excretion exceeds water intake Two step process Generation Generation Gain of sodium Loss of water Maintenance Maintenance Inability to ingest water Without both of these processes there cannot be hypernatremia.

Water excretion exceeds water intake

Two step process

Generation

Gain of sodium

Loss of water

Maintenance

Inability to ingest water

Without both of these processes there cannot be hypernatremia.

70 kg man with Na of 140 Receives 5 amps (500 mL) of bicarb during a code. Generation – Gain of sodium Ingestion of excessive sodium can generate hypernatremia. Causes of this include: Use of 3% saline Use of bicarbonate infusions Overdose of salt tablets If he received a liter the Na would be 160, but with 500mL it rises to 150.

70 kg man with Na of 140

Receives 5 amps (500 mL) of bicarb during a code.

Ingestion of excessive sodium can generate hypernatremia.

Causes of this include:

Use of 3% saline

Use of bicarbonate infusions

Overdose of salt tablets

If he received a liter the Na would be 160, but with 500mL it rises to 150.

Generation – Loss of water Water losses: Extra-renal Diarrhea Vomiting Losses through the skin with burns Renal losses Osmotic diuresis Hyperglycemia Mannitol Post-obstructive Post-ATN (diuretic phase) Diabetes insipidis Renal losses are cases of high electrolyte free water clearance Electrolyte free water clearance

Water losses:

Extra-renal

Diarrhea

Vomiting

Losses through the skin with burns

Renal losses

Osmotic diuresis

Hyperglycemia

Mannitol

Post-obstructive

Post-ATN (diuretic phase)

Diabetes insipidis

Renal losses are cases of high electrolyte free water clearance

Diabetes insipidis Diabetes insipidus generates hypernatremia by allowing large renal water losses. Diabetes insipidus is due to the lack of ADH activity. Central diabetes insipidus: ADH is not being released. Nephrogenic diabetes insipidus: End organ (kidney) resistance to ADH

Diabetes insipidus generates hypernatremia by allowing large renal water losses.

Diabetes insipidus is due to the lack of ADH activity.

Central diabetes insipidus: ADH is not being released.

Nephrogenic diabetes insipidus: End organ (kidney) resistance to ADH

Diabetes insipidis Central CNS disease Neurosurgery Pituitary disease Tumor Infiltrative disease Autoimmune/idiopathic Pregnancy Nephrogenic Lithium Demeclocycline Congenital Hypokalemia Hypercalcemia Sickle cell disease Sjorgrean’s syndrome

Central

CNS disease

Neurosurgery

Pituitary disease

Tumor

Infiltrative disease

Autoimmune/idiopathic

Pregnancy

Nephrogenic

Lithium

Demeclocycline

Congenital

Hypokalemia

Hypercalcemia

Sickle cell disease

Sjorgrean’s syndrome

Maintenance of hypernatremia The body rapidly corrects hypernatremia following generation by ingesting water.

The body rapidly corrects hypernatremia following generation by ingesting water.

Inability to drink

Inability to drink For hypernatremia to persist there must be an inability to drink: No water available Too small to express thirst: Babies Unconscious/mental status changes Vomiting On tube or IV feedings with an inadequate amount of water For hypernatremia to persist there must be an inability to drink: No water available Too small to express thirst: Babies Unconscious/mental status changes Vomiting On tube or IV feedings with an inadequate amount of water

For hypernatremia to persist there must be an inability to drink:

No water available

Too small to express thirst: Babies

Unconscious/mental status changes

Vomiting

On tube or IV feedings with an inadequate amount of water

For hypernatremia to persist there must be an inability to drink:

No water available

Too small to express thirst: Babies

Unconscious/mental status changes

Vomiting

On tube or IV feedings with an inadequate amount of water

Summary of hypernatremia Generation Addition of sodium IV Bicarbonate Salt in formula Salt tablet ingestion Loss of water Vomiting Diarrhea Skin losses Diabetes insipidus Osmotic diuresis Maintenance Inability to drink water No water available Too small to get water Mental status changes Improper TPN or tube feedings Hypernatremia is a sodium concentration > 145 mEq/L The development of hypernatremia is a two part processes:

Generation

Addition of sodium

IV Bicarbonate

Salt in formula

Salt tablet ingestion

Loss of water

Vomiting

Diarrhea

Skin losses

Diabetes insipidus

Osmotic diuresis

Maintenance

Inability to drink water

No water available

Too small to get water

Mental status changes

Improper TPN or tube feedings

Consequences and compensation

Symptoms of hypernatremia The movement of water from the brain cells causes the brain to shrink. This can cause rupture of the cerebral veins leading to intracerebral and subarachnoid hemorrhages. Symptoms begin with lethargy, weakness and irritability. Worsening disease is characterized by twitching, seizures and coma. Insulin resistance and hyperglycemia

The movement of water from the brain cells causes the brain to shrink.

This can cause rupture of the cerebral veins leading to intracerebral and subarachnoid hemorrhages.

Symptoms begin with lethargy, weakness and irritability.

Worsening disease is characterized by twitching, seizures and coma.

Insulin resistance and hyperglycemia

Consequences of mismanagement This compensation prevents rapid treatment of chronic hypernatremia, just as with low sodium.

This compensation prevents rapid treatment of chronic hypernatremia, just as with low sodium.

Treatment Provide electrolyte free water to disrupt the maintenance of hypernatremia Enteral water is preferred D 5 W results in hyperglycemia Note on D 5 W, since D 5 W distributes through the total body water 1 liter of D 5 W increases the intravascular space by only 83 mL

Provide electrolyte free water to disrupt the maintenance of hypernatremia

Enteral water is preferred

D 5 W results in hyperglycemia

Note on D 5 W, since D 5 W distributes through the total body water 1 liter of D 5 W increases the intravascular space by only 83 mL

Use the change in sodium formula to calculate the fluid volume. The amount of fluid TBW= kg x % body water 0.6 for well hydrated males 0.5 for well hydrated females reduce by 0.1 for: Obesity Elderly Dehydration Each liter of D5 or free water lowers Na 4, so 6 liters will reduce the Na to 144.

Use the change in sodium formula to calculate the fluid volume.

TBW= kg x % body water

0.6 for well hydrated males

0.5 for well hydrated females

reduce by 0.1 for:

Obesity

Elderly

Dehydration

Each liter of D5 or free water lowers Na 4, so 6 liters will reduce the Na to 144.

The rate of correction There are two speed limits for correction Chronic asymptomatic should be corrected no faster than 0.5 mmol/L per hour. Acute symptomatic hypernatremia can be corrected at 1.0 mmol/L per hour. Using the prior example of 6 liters to correct 24 mmol, give that volume over 24 hours for acute hypernatremia: 250 mL/hr.

There are two speed limits for correction

Chronic asymptomatic should be corrected no faster than 0.5 mmol/L per hour.

Acute symptomatic hypernatremia can be corrected at 1.0 mmol/L per hour.

Using the prior example of 6 liters to correct 24 mmol, give that volume over 24 hours for acute hypernatremia: 250 mL/hr.

Accounting for ongoing losses Patients with NDI have large ongoing free water losses (200-300 mL/hr). Failing to account for these losses will result in a failure to correct the hypernatremia. Patient in the recovery phase of ATN may make 300mL/hr calculating the C EFW will reveal ongoing losses of 150 mL of EFW. Add 150 to the calculated rate. 250 + 150 = 400 mL/hr.

Patients with NDI have large ongoing free water losses (200-300 mL/hr).

Failing to account for these losses will result in a failure to correct the hypernatremia.

Patient in the recovery phase of ATN may make 300mL/hr calculating the C EFW will reveal ongoing losses of 150 mL of EFW.

Add 150 to the calculated rate.

250 + 150 = 400 mL/hr.

Treating hypernatremic patients Some tid-bits about treating these patients: Many of these patients have poor perfusion or early stage shock. Treat shock and compromised perfusion as you would with a normal sodium. After perfusion is restored treat the hypernatremia.

Some tid-bits about treating these patients:

Many of these patients have poor perfusion or early stage shock.

Treat shock and compromised perfusion as you would with a normal sodium.

After perfusion is restored treat the hypernatremia.

Hypernatremia summary Hypernatremia is defined as a sodium > 145. There are always two processes causing hypernatremia: Generation: ingestion of sodium or loss of water. Maintenance: Inability to drink water. Symptoms are primarily neurologic from the decrease in cell volume in the brain. The brain compensates for this loss of volume by adding solutes inside the cells.

Hypernatremia is defined as a sodium > 145.

There are always two processes causing hypernatremia:

Generation: ingestion of sodium or loss of water.

Maintenance: Inability to drink water.

Symptoms are primarily neurologic from the decrease in cell volume in the brain.

The brain compensates for this loss of volume by adding solutes inside the cells.

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