Disorders of Water BalanceHypo/Hypernatremia

Water-drinking contestants say they weren't told of health risks

From Associated Press7:18 PM PST, January 15, 2007

SACRAMENTO (AP) -- Two people who competed in a radio station's water drinking contest with a 28-year-old mother of three who later died said they were never warned they were putting their health at

risk, a newspaper reported Monday.

Gina Sherrod said that family members listening in on KDND-FM's "Hold Your Wee for a Wii" contest told her that a nurse called into the

program to warn that drinking too much water was dangerous, but that she did not worry until she learned of Jennifer Lea Strange's

death.

Outline

• Hyponatremia: Physiology, differential, treatment. Case.

• Hypernatremia. Physiology, differential, treatment.

• Case

Question

• How is water balance achieved in the face of increased water intake?

• By the excretion of dilute urine.

Changes in Urinary Volume and Osmolality along the Nephron

Defense against hyponatremia

Control of Serum Na

Retain 1L Water

Serum Na Falls by 5meq/l

Decreases Vasopression Release

Approach to the hyponatremic patient

Hyponatremia

High Osmolality Normal Osmolality Low Osmolality

Hyponatremia with high or Nml Osmolality

• TRANSLOCATION• GLUCOSE• MANNITOL• GLYCINE• MALTOSE

• PSEUDOHYPONATRE• PROTEIN• LIPIDS

Pseudohyponatremia

• Normally serum is 93%water and 7% lipids.• If non aqueous portion of serum rose to 20%• Serum measured Na would be:• 150x0.8=120 as opposed to 150x0.93

Pseudohyponatremia

Approach to the hyponatremic patient with Low plasma osm

Hyponatremia with low Osm

Normally Dilute urine<100mosm

Uosm>100mosm

Psychogenic Polydipsia Low Solute intake

Low Solute intake

Urine flow= urinary solute excretionurinary osmolality

Sources of urinary solutes

Psychogenic Polydipsia

• Usually acute• Common in institutionalized schizophrenics• Abnormal weight gains (as much as 10%)• Episodic symptoms that resolve with water

restriction

Beer Potomania

• Large intake of fluid with beer as sole source of nutrition

• Beer sodium content <2meq/L• Beer Potassium content 10-12meq/L

Beer Potomania

• Assume Beer consumption of 5L• Na intake 10mM• K intake 50mM• Obligatory urea excre 80mM

• V=Soluteexcretion 5=200• Uosm 40

Approach to the hyponatremic patient with low plasma osm

Low plasma osm

Normally dilute urineUosm<100

Uosm>100mosmAlmost always vasopressin

mediated

Diuretic Induced Hyponatremia

• Thiazides block diluting segment• May appear euvolemic• Most common in small elderly women• Associated with increased water intake and

low protein intake

Hyponatremia in Edematous disorders

• Reflects advanced disease and poor prognosis• Decreased delivery to diluting sites• Increased vasopressin levels• Increased AQP2 expression

Cerebral Salt wasting

• Most common in subarachnoid hemorrhage• Increased ANP and BNP• Loss of sodium, volume depletion which then

leads to increased ADH.• Different from SIADH as volume depleted.• Treat with saline

Hyponatremia and SSRIs

• Four fold higher incidence than non users• First 2 weeks• More common in elderly• Not related to drug levels

Features of SIADH

• Clinically euvolemic• Uosm>100mosm• Una=Na intake usually >20meq/L• Low bun and Uric acid

Malignancies and SIADH

• Most common with small cell lung ca (10-15%)• mRNA for AVP in tumor• Head and neck tumors• Other isolated cases

Treatment of Hyponatremia

Treatment of Hyponatremia

• Three key Questions• How long has the hyponatremia been

present?• Does the patient have symptoms?• Does the patient have risk factors for the

development of neurologic complications?

Duration of Hyponatremia acute

• <48hrs• Severe brain edema• Rapid correction is well tolerated• BUT WHEN IN DOUBT…Treat as chronic

SXS of Hyponatremia

• Seizures• Herniation• Coma• Respiratory depression• death

Patients at increased risk for neurologic complications

• Post op menstruant females• Elderly women on HCTZ• Children• Hypoxemic patients• Psychogenic polydipsia

Duration of Hyponatremia Chronic

• 48hrs or unknown duration• Mild cerebral edema <10%• Sensitive to correction

SXS of Chronic hyponatremia

• Nausea and vomitting• Muscle cramps and weakness• Ataxia• Confusion and personality changes• Seizure

Symptomatic vs Asymptomatic

• Symptomatic hyponatremia warrents aggressive correction. (sz, severe neuro abnormalities). Most likely to occur in acute setting such as:

• Post op menstruating females• Exercise induced hyponatremia• Hyponatremia associated with ecstasy• Hyponatremia in patients with intracerebral

pathology, • Self induced water intoxication

Symptomatic hyponatremia

• Aggressive correction at a rate of 1.5-2meq/L per hour for 3-4 hrs or until sxs resolve.

• Usually with hypertonic saline at 0.5ml/kg/hr• However no more than 10-12meq/24hrs and

18meq/48hrs.

Asymptomatic but <115 or 110

• Such patient if they have sxs such as confusion, lethargy, gait disturbances will benefit from rise of 1meq/L/hr for 3-4 hrs but no faster than 8meq/24hrs.

• IF asymptomatic and >120meq/L then would benefit from free water restriction or treatment of volume depletion but no faster than 6-8meq/24hrs.

Risk factors for Development of Osmotic demyelination

• Alcoholism• Malnutrition• Burns• Severe Potassium depletion• Elderly women on thiazide diuretics

Case: acute Hyponatremia

• 31 yo female weighing 60Kg was admitted for elective hysterectomy. Normal preop exam and electrolytes. Underwent surgery with minimal intraop blood loss. During a 4 hr course in recovery she received 2 L NS and then ½ NS at 125cc/hr. At 12 hrs post op she made 1500cc urine. She complained of nausea and vomitting complicated by pain for which she received demerol. No record of oral intake. ½ NS continued.

Case: acute Hyponatremia

• 30 hrs post op mental status changes developed. Serum Na was measured at 114meq/L. IV changed to NS at 200cc/hr for 5hrs during which she put out 750cc of urine. Una was 140meq and Uk was 52meq/L. The patient had a sz with respiratory arrest and death. Repeat Na was 112 meq/L

Urine flow= urinary solute excretionurinary osmolality

V2 Receptor antag

• Conivaptan is the only IV antagonist available in the US

• FDA approved for hospitalized euvolemic SIADH• Unclear of the rate of rise • Suggest use with 3% saline is symptomatic

hyponatremia.• Contraindicated in Liver patients as increased

variceal bleed and hypotension

Hypernatremia

Causes of hypernatremia

• 1. Inappropriately high water losses• 2. Insufficient water intake• 3. High Na intake without adequate water• 4. Thirst center/osmoreceptor lesion

4. Impaired thirst or osmoreceptors

• Causes usually tumor, granulomatous dz, ischemia, primary aldosteronism, age.

• Na>146 but not thirsty. Dilute urine after any H20 with impaired osmoreceptors

3. High NaCl intake without water

• Rare• Seawater ingestion• NaCl poisoning• Hypertonic Na or bicarb boluses.

2. Insufficient water Intake

• Usually when ill or in the hospital setting• Inadequate Free water• Common after surgery, high nutrient intake

1. Inappropriately high water losses

Sites of water loss1. insensible (sweat, breath)2. GI (vomitting, NG, Diarrhea)3. Kidney

1. Inappropriately high water losses

• Renal losses• Osmotic diuresis- urea, mannitol, glucose,

diuretics• DI

DI

• Vasopressinase production• Central (neurogenci) DI• Nephrogenic DI

Vasopressin (ADH) Receptors

• V2 • Makes collecting duct permeable to water• V1• Increases systemic BP• Expressed in vasculature, liver and brain

DI – lack of vasopressin

• Gestational DI• Central DI

Gestational DI

• 1 in 300,000 pregnancies• Increased action of vasopressinase normally

from the placenta• Vasopressinase does not attack DDAVP as

rapidly

Central (neurogenic) DI

• Acquired- tumor, trauma, autoimmune, granulomatous, vascular

• Congenital- autosomal dominant

Nephrogenic

• Congenital• Acquired• Drugs- LI, demeclocycline• Hypercalcemia• Hypokalemia• Uretral obstruction• Renal insufficiency

Treatment

• Acute<24hrs• Osmotic loss of brain water• Accumulation of electrolytes: Na, K• Chronic >24hrs• Accumulation of organic solutes such as myo-

inositol, sorbitol, others.

Conclusions

• Hyponatremia and hypernatremia are critical. • Understand the physiology.• Slower correction unless the patient is

decompensting.• Always assume chronic when in doubt.• Multiple formulas but always recheck values at

several time points.• New drugs on the horizon. Unclear of benefit.