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Hyponatremia resident survival guide
Introduction
Causes
Causes
Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. Severe hyponatremia ( <115 mEq/L) is by itself life threatening and should be treated as such irrespective of the cause.[2]
Common Causes
Hypovolemic hyponatremia:
- Cerebral salt wasting syndrome
- Adrenal failure[3][4]
- Thiazide diuretics[5]
- Vomiting or diarrhea treated with free water replacement
Euvolemic hyponatremia:
- SIADH
- Primary polydipsia
- Exercise associated hyponatremia
- Glucocorticoid deficiency
- Hypothyroidism
- Nephrogenic syndrome of inappropriate antidiuresis
- Low sodium intake
Hypervolemic hyponatremia:
Causes of Hyponatremia based upon Serum Osmolality:
| Serum Osmolality | Etiology |
|---|---|
| Hypertonic Hyponatremia | Hyperglycemia |
| Mannitol | |
| Glycerol | |
| Sorbitol | |
| Isotonic Hyponatremia | Lab/blood draw error |
| Hyperparaproteinemia | |
| Hyperlipidemia | |
| Post TURP (bladder irrigation with osmotic solutions) | |
| Hypotonic Hyponatremia | Etiology depends upon volume status (Hypervolemic/ Euvolemic/ Hypovolemic |
Classification
Classification
Hyponatremia is defined as serum sodium less than 135 mEq/L (mmol/L).There are different classifications for hyponatremia based on duration, severity, volume status and ADH level.
Hyponatremia is classified based on serum sodium level to :
- Mild : Serum sodium 130– 135 mmol/L
- Moderate: Serum sodium ≤125–129 mmol/L
- Severe: Serum sodium <124 mmol/L
Classification based on duration[7] :
- Hyperacute: Develops in a few hours, excess water intake, impaired water excretion, runners, users of the recreational drug (Ecstasy)
- Acute: Rapid onset <48 hours, surgeries, colonoscopy preparation, polydipsia, diuretics
- Chronic: Gradual onset >48 hours, caused by chronic disease ( including cardiac, renal, hepatic and other conditions)
Classification based on ADH level :
- ↑ ADH: Volume depletion (GI loss, Renal loss) , decreased perfusion ( CHF, Cirrhosis), increased ADH secretion, reset osmostat
- ↓ ADH: Primary polydipsia, ↓ dietary solute intake, advanced renal failure
According to volume status :
| Volume status | Sodium status |
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|---|---|---|
| Hypovolemic
Hyponatremia |
| |
| Hypervolemic
Hyponatremia |
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| Euvolemic
Hyponatremia |
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|
FIRE
FIRE
| Serum Na ≤ 135 meq/L | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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| Hypotonicity <275 mOsm/kg | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| UOsm < 100mOsm/kg | UOsm > 200mOsm/kg | UOsm 100–200mOsm/kg | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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| Hypovolemia Based on history & physical exam | Hypervolemia | Euvolemia | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| UNa < 30 mEq/L | Variable UNa | UNa > 30 mEq/L | UNa < 30 mEq/L | UNa > 30 mEq/L | Variable UNa | UNa < 20 mEq/L | > 20 UNa < 40 mEq/L | UNa > 40 mEq/L | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Variable UNa •Diuretic use Discontinue diuretics if UNa is still abnormal |
|
|
| Discontinue diuretics if PNa normalize it’s not SIAD if it’s not normalized | Probable hypovolemia | Hypovolemia or euvolemia | •Probable euvolemia •SIAD •Cortisol deficiency •Hypothyroidism | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Administer 0.9% saline | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Normalize PNa | Administer 1–2 L 0.9% saline | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Failure to normalize PNa | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Hypovolemia | PNa decreases or no change | PNa increases | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Decreasing UOsm | No change in UOsm but UNa increases | SIAD | No change in UOsm but UNa increases | Decreased UNa | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Hypovolemia | Salt-depleted SIAD | Hypovolemia | Decreasing Uosm | Administer additional saline | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| No change in UOsm but UNa increases | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Salt-depleted SIAD | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Management
Management
Diagnostic Approach
Shown below is an algorithm depicting the diagnostic management of hyponatremia based on Diagnosis, Evaluation, and Treatment of Hyponatremia: Expert Panel Recommendations (2013).[8]
Characterize the symptoms: ❑ Nausea and vomiting ❑ Headache ❑ Confusion ❑ Lethargy, fatigue, loss of appetite ❑ Restlessness and irritability ❑ Muscle weakness, spasms, cramps ❑ Seizures ❑ Decreased consciousness or coma[9] Hyponatremic encephalopathy: (sodium < 115 meq/L) ❑ Decorticate or decerebrate posturing ❑ Respiratory arrest ❑ Non-cardiogenic pulmonary edema | |||||||||||||||||||||||||||||||||||||||||
Examine the patient: ❑ Orthostatic vital signs ❑ Mental status examination (low score) ❑ Jugular venous pressure ↑/↓ ❑ Peripheral edema | |||||||||||||||||||||||||||||||||||||||||
Check labs: ❑ Plasma osmolality ❑ Urine osmolality ❑ Urinary sodium concentration ❑ Serum uric acid/creatinine ❑ Thyroid stimulating hormone (TSH) ❑ Serum cortisol level ❑ Serum proteins ❑ Triglyceride ❑ Random blood sugar | |||||||||||||||||||||||||||||||||||||||||
Consider alternative diagnosis: ❑ Adrenal crisis ❑ Alcoholism ❑ Hypothyroidism ❑ Pulmonary/cardiogenic edema | |||||||||||||||||||||||||||||||||||||||||
❑ Check serum osmolality Serum osmolality (mmol/kg) = (2 x serum sodium concentration) + (serum glucose concentration/18) + (blood urea nitrogen/2.8) | |||||||||||||||||||||||||||||||||||||||||
Isotonic hyponatremia (Serum osmolality 280-295 mOsm/kg) | Hypotonic hyponatremia (Serum osmolality < 280 mOsm/kg) | Hypertonic hypernatremia (Serum osmolality > 295 mOsm/kg) | |||||||||||||||||||||||||||||||||||||||
| Pseudohyponatremia | Assess volume status | Hyperglycemia Mannitol infusion | |||||||||||||||||||||||||||||||||||||||
| Hypovolemia | Euvolemia | Hypervolemia | |||||||||||||||||||||||||||||||||||||||
| Urine sodium levels | Urine sodium levels | Urine sodium levels | |||||||||||||||||||||||||||||||||||||||
| >20 mEq/L | ≤ 20 mEq/L | >20 mEq/L | >20 mEq/L | ≤ 20 mEq/L | |||||||||||||||||||||||||||||||||||||
❑ Vomiting & diarrhea treated with free water replacement | ❑ SIADH ❑ Primary polydipsia ❑ Exercise associated hyponatremia ❑ Nephrogenic syndrome of inappropriate antidiuresis ❑ Glucocorticoid deficiency ❑ Hypothyroidism ❑ Low solute intake | ||||||||||||||||||||||||||||||||||||||||
Therapeutic Approach
Initial Management
Shown below is an algorithm depicting the initial management of symptomatic hyponatremia based on Diagnosis, Evaluation, and Treatment of Hyponatremia: Expert Panel Recommendations (2013).[8]
| Symptomatic hyponatremia | |||||||||||||||||||||||||||||||||||||||||||||||||||
| Acute hyponatremia (< 48 hours) | Chronic hyponatremia | ||||||||||||||||||||||||||||||||||||||||||||||||||
Goals of treatment: ❑ Target sodium levels = 125-130 mEq/L[10] ❑ Daily ↑ in sodium levels by 4-6 mmol/L | Goals of treatment: ❑ Target sodium levels = 125-130 mEq/L ❑ Daily ↑ in sodium levels by 4-8 mmol/L if low risk of ODS ❑ Daily ↑ in sodium levels by 4-6 mmol/L if high risk of ODS | ||||||||||||||||||||||||||||||||||||||||||||||||||
| Mild to moderate symptoms | Severe symptoms | Mild to moderate symptoms | Severe symptoms | ||||||||||||||||||||||||||||||||||||||||||||||||
❑ Administer 0.9% NaCl to achieve target sodium levels, or ❑ Administer vaptans | ❑ Administer 3% NaCl (100 ml infused over 10 minutes and repeated once if needed) ❑ Shift to 0.9% NaCl/vaptans at sodium levels > 125 mEq/L | ❑ Administer 0.9% NaCl to achieve target sodium levels, or ❑ Administer vaptans | ❑ Administer 3% NaCl (100 ml infused over 10 minutes and repeated once if needed) ❑ Achieve 1st day target in 1st 6 hours and withhold any more fluids for the day ❑ Shift to 0.9% NaCl/vaptans at sodium levels > 125 mEq/L | ||||||||||||||||||||||||||||||||||||||||||||||||
Administer vaptans (contraindicated for hypovolemic hyponatremia) ❑ Conivaptan:
| |||||||||||||||||||||||||||||||||||||||||||||||||||
Additional Management
Shown below is an algorithm depicting the management of symptomatic and asymptomatic hyponatremia based on underlying etiology based on Diagnosis, Evaluation, and Treatment of Hyponatremia: Expert Panel Recommendations (2013).[8]
| Etiology based management | |||||||||||||||||||||||||||||||||||||||||||||||||||
| Hypovolemia | Euvolemia | Hypervolemia | |||||||||||||||||||||||||||||||||||||||||||||||||
| Urine sodium level > 20 mEq/L | Urine sodium level ≤ 20 mEq/L | Urine sodium level > 20 mEq/L | Urine sodium level > 20 mEq/L | Urine sodium level ≤ 20 mEq/L | |||||||||||||||||||||||||||||||||||||||||||||||
Cerebral salt wasting syndrome: ❑ Fluid restriction is not advised Adrenal failure: Thiazide like diuretics: ❑ Stop thiazide diuretics ❑ Monitor the rate of rise of Na+ ❑ Monitor urine osmolality & volume to detect hypercorrection ❑ Follow K+ levels, as they may drop with therapy | Gastrointestinal losses: ❑ Correct K+ levels as appropriate ❑ Administer bicarbonate if acidosis develops ❑ Start antiemetics and specific therapy as indicated | ❑ SIADH: ❑ Restrict water
Nephrogenic syndrome of inappropriate antidiuresis: Hypothyroidism: Glucocorticoid def.: Exercise associated hyponatremia: Low solute intake: Primary polydipsia: ❑ Restrict water | Acute kidney injury: ❑ Restrict water | Heart failure: ❑ Initiate treatment with fluid restriction ❑ Administer loop diuretics ❑ Consider vaptans Liver cirrhosis: ❑ Use tolvaptan restrictively based on LFT’s | |||||||||||||||||||||||||||||||||||||||||||||||
ADH: Anti diuretic hormone; SIADH: Syndrome of inappropriate antidiuretic hormone secretion; NaCl: Sodium chloride; LFT: Liver function test;IV: Intravenous; PO: Per oral; ECF:Extra cellular fluid; HPE:History and physical examination; ODS: Osmotic demyelination syndrome
Do’s
Do’s
- Do the following to prevent over correction of sodium levels:
- Replace water losses or administer desmopressin after correction by 6-8 mmol/L during the first 24 hours of therapy.
- Withhold the next dose of vaptans if the correction is >8 mmol/L.
- Consider therapeutic lowering of serum sodium if correction exceeds therapeutic limits.
- Consider administration of high-dose glucocorticoids (eg, dexamethasone, 4 mg every 6 hours) for 24-48 hours following the excessive correction.
- Follow these steps to lower serum sodium, if correction exceeds therapeutic limits:
- Administer desmopressin to prevent further water losses: 2-4 mg every 8 hours parenterally.
- Replace water orally or as 5% dextrose in water intravenously at the rate of 3 mL/kg/h.
- Recheck serum sodium hourly and continue therapy infusion until serum sodium is reduced to goal.
- Initiate vaptans treatment only in hospital setting, so as to regularly monitor serum sodium levels.
- Fluid restrictions:
- Restrict all intake that is consumed by drinking, not just water.
- Aim for a fluid restriction that is 500 mL/d below the 24-hour urine volume.
- Do not restrict sodium or protein intake unless indicated.
- Gastrointestinal losses:
- Measure urine chloride, if vomiting is present to confirm the presence of solute and volume depletion.
- Treat typically as a chronic hyponatremia.
- Thiazide diuretic induced:
- Treat typically as chronic hyponatremia.
- Be vary of rapid correction.
- Serially follow changes in urine osmolality together with urine volume.
- Measure serum sodium every 6 hours to begin with.
- Adjust potassium levels in fluids as needed.
Dont’s
Dont’s
- Do not use to treat hypovolemic hyponatremia.
- Do not use in conjunction with other treatments for hyponatremia.
- Do not use immediately after cessation of other treatments for hyponatremia, particularly 3% NaCl.
- Do not use for severe, symptomatic hyponatremia, as 3% NaCl provides a quicker and more certain correction of serum sodium than vaptans.
- Do not use isotonic normal saline as primary therapy for SIADH.
References
References
- ↑ Laczi, F. (2008). “[Etiology, diagnostics and therapy of hyponatremias]”. Orv Hetil. 149 (29): 1347–54. doi:10.1556/OH.2008.28409. PMID 18617466. Unknown parameter
|month=ignored (help) - ↑ Clayton, JA.; Le Jeune, IR.; Hall, IP. (2006). “Severe hyponatraemia in medical in-patients: aetiology, assessment and outcome”. QJM. 99 (8): 505–11. doi:10.1093/qjmed/hcl071. PMID 16861720. Unknown parameter
|month=ignored (help) - ↑ Schmitz, PH.; de Meijer, PH.; Meinders, AE. (2001). “Hyponatremia due to hypothyroidism: a pure renal mechanism”. Neth J Med. 58 (3): 143–9. PMID 11246114. Unknown parameter
|month=ignored (help) - ↑ Macaron, C.; Famuyiwa, O. (1978). “Hyponatremia of hypothyroidism. Appropriate suppression of antidiuretic hormone levels”. Arch Intern Med. 138 (5): 820–2. PMID 417689. Unknown parameter
|month=ignored (help) - ↑ Leung, AA.; Wright, A.; Pazo, V.; Karson, A.; Bates, DW. (2011). “Risk of thiazide-induced hyponatremia in patients with hypertension”. Am J Med. 124 (11): 1064–72. doi:10.1016/j.amjmed.2011.06.031. PMID 22017784. Unknown parameter
|month=ignored (help) - ↑ Oren, RM. (2005). “Hyponatremia in congestive heart failure”. Am J Cardiol. 95 (9A): 2B–7B. doi:10.1016/j.amjcard.2005.03.002. PMID 15847851. Unknown parameter
|month=ignored (help) - ↑ Sterns, Richard H.; Ingelfinger, Julie R. (2015). “Disorders of Plasma Sodium — Causes, Consequences, and Correction”. New England Journal of Medicine. 372 (1): 55–65. doi:10.1056/NEJMra1404489. ISSN 0028-4793.
- ↑ 8.0 8.1 8.2 Verbalis, JG.; Goldsmith, SR.; Greenberg, A.; Korzelius, C.; Schrier, RW.; Sterns, RH.; Thompson, CJ. (2013). “Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations”. Am J Med. 126 (10 Suppl 1): S1–42. doi:10.1016/j.amjmed.2013.07.006. PMID 24074529. Unknown parameter
|month=ignored (help) - ↑ “Sign In” (PDF). Retrieved 28 January 2014.
- ↑ Gross, P.; Reimann, D.; Neidel, J.; Döke, C.; Prospert, F.; Decaux, G.; Verbalis, J.; Schrier, RW. (1998). “The treatment of severe hyponatremia”. Kidney Int Suppl. 64: S6–11. PMID 9475480. Unknown parameter
|month=ignored (help)
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Iqra Qamar M.D.[2] Priyamvada Singh, M.D. [3]Vidit Bhargava, M.B.B.S [4] Saeedeh Kowsarnia M.D.[5]
