diagnosis and treatment of hyponatremia acute: symptomatic chronic: asymptomatic thomas dubose,m.d....
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Diagnosis and Treatment of Hyponatremia
Diagnosis and Treatment of Hyponatremia
Acute: SymptomaticChronic: Asymptomatic
Thomas DuBose,M.D.Professor and Chair, Internal
MedicineWake Forest University School of
Medicine
Hyponatremia: ICUHyponatremia: ICU Pseudohyponatremia
• Hyperglycemia, Hyperlipidemia Post-operative Hyponatremia SIADH Cerebral Salt Wasting Mechanical Ventilation Cirrhosis Congestive Heart Failure SIRS/MODS Loop diuretics with hypotonic fluid
replacement Certain drug intoxications Agents that enhance ADH release or action
Major Causes of Hyponatremia
Major Causes of Hyponatremia
EIVF Depletion True Volume Depletion CHF or Cirrhosis
SIADH Hormone mediated
Adrenal Insufficiency Hypothyroidism Pregnancy
Disorders in which ADH levels may be appropriately suppressed Advanced renal failure Primary polydipsia Beer drinker’s potomania
Pseudohyponatremia High plasma osmolality: hyperglycemia, mannitol,
urea Normal plasma osmolality: hyperlipidemia,
hyperproteinemia, glycine infusion.
Steps in the Evaluation of Hyponatremia
Calculate plasma osmolality Measure plasma osmolality
• When low; defines true hypo-osmolal state or clinical hyponatremia
• Consider plasma glucose, protein and lipids Evaluate volume status of patient
• Volume depletion• Volume expansion• Euvolemia
Measure urine sodium
Estimating the Serum Osmolality
Estimating the Serum Osmolality
In Spurious Hyponatremia:
Calculated OSMp < Determined OSMp
Spurious Hyponatremia (hyperlipemia, hyperproteinemia) is not a hypoosmolar state.
2[Na]p BUN
2.8 GLUCOSE
18
Causes of Hypoosmolality Volume Depletion
• GI, lung or skin losses • Third space sequestration • Adrenal insufficiency• Renal salt wasting• Cerebral salt wasting
Volume Expansion• CHF, cirrhosis with ascites, nephrotic
syndrome Euvolemic
• SIADH, water intoxication, reset osmostat, drugs
Antidiuretic DrugsAntidiuretic DrugsAntidiuretic hormones:Antidiuretic hormones: Vasopression
OxytocinDiuretics:Diuretics: Thiazides
FurosemideEthacrynic acid
CNS-active drugs:CNS-active drugs: VincristineCarbamazepinePsychotropic drugs
Inhibitors of prostaglandin synthesis:Inhibitors of prostaglandin synthesis: ChlorpropamideSalicylatesAcetaminophenNonsteroidal anti-inflammatory agentsCOX 2 inhibitors
Others:Others: ClofibrateCyclophosphamideSomatostatinEcstasy
Syndrome of Inappropriate ADH Release (Bartter’s
Criteria)
Syndrome of Inappropriate ADH Release (Bartter’s
Criteria)Hyponatremia and true hypoosmolality by
definitionEuvolemia clinicalUrine less than maximally dilute (urinary
osmolality usually > 200 mOsm/kg of H2O)Normal renal, cardiac, hepatic, adrenal,
pituitary, and thyroid functionNo history of antidiuretic drugsNo emotional or physical stressUrinary sodium > 20 mEq/litera
a Urinary sodium may be <20 mEq/liter if the patient is volume
deleted or on low sodium intake.
Disorders Associated With SIADH
Disorders Associated With SIADH
Carcinomas
Pulmonary disorders
Central nervous system disorders
Most Common Causes of SIADH in Elderly (CDP and
NHR)*
Most Common Causes of SIADH in Elderly (CDP and
NHR)*
MedicationsIdiopathic formMalignancies
*Aging Clin Exp Res 2003, 15:6-11.
Small cell carcinoma of the lungCarcinoma of the duodenumCarcinoma of the pancreasThymomaLymphomaEwing’s sarcomaMesotheliomaCarcinoma of the bladderProstatic carcinomaOlfactory neuroblastoma
Disorders Associated With SIADH: Carcinomas
Disorders Associated With SIADH: Carcinomas
Disorders Associated With SIADH: Pulmonary
Disorders
Disorders Associated With SIADH: Pulmonary
DisordersViral pneumoniaBacterial pneumoniaPulmonary abscessTuberculosisAspergillosisPositive-pressure breathingAsthmaPneumothoraxCystic fibrosisLung cancers
Disorders Associated With SIADH: Central Nervous
Disorders
Disorders Associated With SIADH: Central Nervous
DisordersEncephalitis (viral or
bacterialMeningitis (viral,
bacterial, tuberculosis, fungal)
Head traumaBrain abscessBrain tumorsGuillain-Barré syndromeAcute intermittent
porphyriaSubarachnoid
hemorrhage or subdural hematoma
Cerebellar and cerebral atrophy
Cavernous sinus thrombosis
Neonatal hypoxiaHydrocephalusShy-Drager syndromeRocky Mountain spotted
feverDelirium tremensCerebrovascular accident
(cerebral thrombosis or hemorrhage)
Acute psychosisPeripheral neuropathyMultiple sclerosis
Guiding Principles in the Treatment of Hyponatremia
Guiding Principles in the Treatment of Hyponatremia1. Neurologic disease can follow both the
failure to promptly treat as well as injudiciously rapid treatment of hyponatremia.
2. Presence or absence of significant neurologic signs and symptoms must guide treatment.
3. Acuity or chronicity of the electrolyte disturbance impacts the rate at which the correction should be undertaken.
A Prudent Approach to the Treatment of Hyponatremia
- 1
A Prudent Approach to the Treatment of Hyponatremia
- 1Acute Symptomatic Hyponatremia (duration <
48 hours)
1. Risk for complication of cerebral edema greater than risk of treatment of complication.
2. Treat with hypertonic NaCl: 3% NaCl @ 1-2 mL/kg/hr or 2 mEq/L/hr. until convulsions subside. Usually means increasing [Na+] by 10%.
3. Alternative: furosemide and hypertonic NaCl
4. Full correction is dangerous. Correct by 10% or to 120-122 mEq/L slowly.
5. Then initiate water restriction.
A Prudent Approach to the Treatment of Hyponatremia
- 2
A Prudent Approach to the Treatment of Hyponatremia
- 2Symptomatic Hyponatremia (Chronic
or Unknown Duration)1. Increase serum sodium by 10%, that is,
approximately 10 mEq/L and then water restrict. Usually 1 -2 mL/kg/hr of hypertonic saline.
2. Do not exceed a correction rate of 1.5 mEq/L/hr at any given time.
3. Do not increase serum sodium by more than 15 mEq/day.
4. Long-term• H2O restriction• Demeclocycline 300 - 600 mg bid• V2 receptor antagonist? Aquaretics
Therapeutic Strategy Based On
Therapeutic Strategy Based On
Volume Status of Patient Presence of Absence of Symptoms Duration of Hypoosmolality Presence of absence of risk factors
for development of neurological complication Osmotic demyelination is rare in
patients with initial Na+ > 120mEq/L
A Prudent Approach to the Treatment of Hyponatremia
- 3
A Prudent Approach to the Treatment of Hyponatremia
- 3
Asymptomatic Hyponatremia
1.Almost always chronic.
2.Treat with water restriction regardless of how low the serum sodium.
Calculating Sodium Requirement in Hyponatremia
Calculating Sodium Requirement in Hyponatremia
In correcting hyponatremia the approximate expansion of total body water must be determined first by calculating the volume of water which was required to dilute the serum sodium concentration to its observed value. For example, in a 70 kg patient with a serum Na+ concentration of 120 mEq/L rather than 140 mEq/L, this calculation is made as follows:
Body water in normal state = (70 kg) (0.60) = 42 LBody water in abnormal state = (x) (120) = (42)(140) =
49LExcess body water = 7 L
The amount of Na+ in milliequivalents required for correction can then be calculated; again it is necessary to assume Na+ is distributed throughout the total body water.(140-patient’s - Na+) (calculated total body water) = total Na+ requirement.
How to predict the effect of therapy on the patient’s serum
sodium
How to predict the effect of therapy on the patient’s serum
sodium
The Bottle:
0.9% = 154 mEq/L
Ringer’s = 130 mEq/L
0.45% = 77 mEq/L
3% = 513 mEq/L
[Na]Patient
[Na ]Bot [Na ]Patient
TBW 1
Diagnosis and Treatment of
Hypernatremia
Diagnosis and Treatment of
Hypernatremia
Steps in Evaluation of Hypernatremia
Establish history of water intake, and integrity of thirst mechanism Severe hypernatremia is unusual
unless thirst mechanism is defective or water is not available to the patient.
Determine patient’s volume status Measure urine sodium
concentration
Causes of HypernatremiaCauses of Hypernatremia Volume Depletion
Urine Na+ < 20: sweating, diarrhea, burns Urine Na+ > 20: Renal losses:
Hyperglycemia, mannitol, urea (osmotic diuresis), or intrinsic renal disease
Volume Expansion Urine Na+ > 20: Salt loading, Cushing’s
syndrome, NaHCO3, hypertonic dialysis Eulovemic
Urine Na+ < 20: Fever, heat exhaustion, hypermetabolic state
Urine Na+ variable or > 20: Central DI, Nephrogenic DI
Alcohol Diphenylhydantoin Lithium Demeclocycline Acetohexamde Tolazamide
Glyburide Propoxyphene Amphotericin Methoxyflurane Norepinephrine
Diuretic DrugsDiuretic Drugs
Patient Groups at Increased Risk for
Hypernatremia
Patient Groups at Increased Risk for
Hypernatremia Post craniotomy (sellar tumors) Elderly, nursing home residents Hypertonic infusions Tube feedings Osmotic diuretics Lactulose Mechanical ventilation Diabetes mellitus with poor glycemic
control Polyuric disorders
Diabetes Insipidus
Central DI Failure to synthesize or secrete ADH
Unable to concentrate urine with water deprivation (caution !)
– 3% decrease in BW or increase in Posm to 295 normally results in increase in Uosm > 700
– Submaximal response: give ADH Central DI Uosm will increase by 100%
or more
Therapeutic Regimens for the Treatment of Diabetes
Insipidus
Therapeutic Regimens for the Treatment of Diabetes
Insipidus Drug Dose
Complete central diabetes insipidus
dDAVP 10-20 mg intranasally q 12-24 hr
Vasopressin tannate
2-5 U IM q 24-48 hr
Aqueous vasopressin
5-10 U SQ q 4-6 hr
Chlorpropamide 250-500 mg/ day
Clofibrate 500 mg tid-qid
Partial central diabetes insipidus
Carbamazepine 400-600 mg/ day
Thiazide diuretics
Conventional doses
NSAIDS Conventional doses
Nephrogenic diabetes insipidus (NDI)
Amiloride (for lithium-related NDI)
5 mg qd
Nephrogenic Diabetes Insipidus
Nephrogenic Diabetes Insipidus
Does not respond to AVP Causes:
Congenital NDI - AVPR2 or AQP2 mutation
Hypokalemia Hypercalcemia Drugs: Lithium, demeclocycline,
glyburide, colchicine, amphotericin B Treatment:
Thiazides Reduce solute intake (low Na+ diet) NSAIDS
Treatment of Symptomatic Hypernatremia
Treatment of Symptomatic Hypernatremia
1.Drop Na+S by 2 mEq/L/hr.
2.Replace 50% of water deficit over 12-24 hrs.
3.Replace rest over next 24 hrs.
4.Perform serial neurological exams.
5.Decrease rate of correction when patient improved.
6.Measure Na+ in serum and urine q 12 hrs.