Rosen & Barkin's 5-Minute Emergency Medicine Consult (692 page)

Read Rosen & Barkin's 5-Minute Emergency Medicine Consult Online

Authors: Jeffrey J. Schaider,Adam Z. Barkin,Roger M. Barkin,Philip Shayne,Richard E. Wolfe,Stephen R. Hayden,Peter Rosen

Tags: #Medical, #Emergency Medicine

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SIGNS AND SYMPTOMS
  • Serum sodium <135 mEq/L:
    • May be asymptomatic
  • Serum sodium <130 mEq/L:
    • Weakness/lethargy
    • Weight gain
    • Headache
    • Anorexia
  • Sodium serum <120 mEq/L:
    • Altered mental status
    • Seizure/coma
  • Chronic hyponatremia: 50% asymptomatic
  • High mortality in acute hyponatremia
History
  • Thorough medication history
  • Course of illness (acute, subacute, or chronic)
Physical-Exam
  • Volume status
  • Mental status
  • Stigmata of malignancy
ESSENTIAL WORKUP
  • Diagnosis is 1 of exclusion, need to evaluate for other causes of:
    • Depletional or dilutional hyponatremia
  • Electrolytes, BUN, Cr, glucose, protein, lipids:
    • Hyponatremia (serum Na <135 mmol/L)
    • Serum hyposmolality (serum Osm <275 mOsm/kg)
  • Urine osmolality:
    • Inability to excrete dilute urine
    • Urine osmolality >100 mOsm/kg
  • Urine sodium:
    • Continued urinary excretion of sodium
    • Urinary sodium >20 mEq/L
DIAGNOSIS TESTS & NTERPRETATION
Lab
  • Serum protein levels
  • Lipid levels
  • Glucose levels
  • Serum osmolality
  • LFT and thyroid function test
  • Morning cortisol level
Imaging

Consider imaging (CXR, CT head) to screen for pathology causing SIADH (tumors/masses)

DIFFERENTIAL DIAGNOSIS
Causes of Hyponatremia
  • See etiologies above
  • Increased extracellular fluid (dilutional hyponatremia):
    • Renal failure/insufficiency
    • CHF
    • End-stage liver disease
  • Normal extracellular fluid (dilutional hyponatremia):
    • SIADH
    • Myxedema
    • Sheehan syndrome (postpartum hypopituitarism)
    • Reset osmostat syndromes (dilute urine at lower than normal sodium levels)
  • Decreased extracellular fluid (depletional hyponatremia):
    • Increased losses:
      • Excessive sweating (endurance sports)
      • GI losses (vomiting, diarrhea)
    • 3rd-space sequestration
    • Diuretic use
    • Aldosterone deficiency:
      • Addison disease
    • Salt-losing nephropathies:
      • Renal tubular acidosis
  • Pseudohyponatremia (seen in hyperglycemia, hyperproteinemia, hyperlipidemia)
TREATMENT
PRE HOSPITAL
  • In patients with altered mental status, maintenance and protection of the airway are paramount.
  • When hypovolemia is suspected, appropriate fluid resuscitation should be initiated.
  • Rapid patient evaluation and transport are essential.
INITIAL STABILIZATION/THERAPY
  • Severe symptomatic hyponatremia with CNS manifestations
  • Endotracheal intubation for patients in need of airway protection
  • Identify/treat other causes of altered mental status
  • Treat seizures with benzodiazepines
  • Proceed to hyponatremia treatment
ED TREATMENT/PROCEDURES
  • Most effective treatment of SIADH is successful
    eradication of the underlying cause
    .
  • Initial treatment of hyponatremia caused by SIADH is the same for all causes of euvolemic/hypervolemic hyponatremia.
Mildly Symptomatic Hyponatremia, Chronic Hyponatremia with Minimal Symptoms, Asymptomatic Hyponatremia
  • Serum sodium usually >125 mEq/L
  • Fluid restriction 800–1,000 mL/day alone or in conjunction with:
    • 0.9% NS infusion and/or IV furosemide
  • Correct serum sodium by no more than 0.5 mEq/L/hr (5–6 mEq/day):
    • Too rapid correction of serum sodium levels can induce
      central pontine myelinolysis
      , associated with development of bulbar palsy, quadriplegia, seizures, coma, and death.
Severe Hyponatremia
  • Symptomatic patient, serum sodium <125 mEq/L
  • Increase serum sodium by no more than 12 mEq/L in 1st 24 hr at a rate of 1 mEq/L/hr (8–12 mEq/day when serum sodium below 125 mEq/L and slow to 5–6 mEq/day when serum sodium rises to 125 mEq/L).
  • Target level: 125 mEq/L
  • Treat patients with significant neurologic symptoms with 3% saline solution.
  • Serum sodium lab testing every 1–2 hr
Acute Life-threatening Hyponatremia
  • Serum sodium usually <120 mEq/L
  • Associated with seizures or coma
  • Clinical goal: Stop seizure and improve neurologic status
  • Therapeutic goal: Same as for severe hyponatremia
  • Administer hypertonic saline solution (3%)
  • Stop hypertonic saline when symptoms (i.e., seizures) resolve and transition to NS.
  • IV furosemide to promote diuresis and induce a negative fluid balance.
  • Once serum sodium = 125 mEq/L, further IV fluid should be in the form of 0.9% saline solution.
  • Restoration of serum sodium to normal levels should take place over ≥48 hr.
  • Drugs that inhibit the secretion/effects of ADH:
    • Indicated when SIADH not self-limited and cause cannot be removed
    • Demeclocycline (blocks effect of ADH)
MEDICATION
  • Conivaptan 20 mg IV over 30 min (for severe hyponatremia in concert with admitting physician)
  • Demeclocycline: 300 mg PO BID–QID
  • Hypertonic saline solution (3% NaCl): 250–500 mL (max. initial dose 5 mL/kg):
    • 25–100 mL/hr
    • Limit rate in rise of serum sodium to 0.5–1 mEq/L/h.
    • Discontinue when seizure resolves or serum sodium of 125 mEq/L is reached.
    • Rise in serum sodium by 4–6 mEq/L is usually sufficient to stop seizures.
  • 0.9% NS: Maintenance rates
  • Lasix: 1 mg/kg up to 20–40 mg IV
FOLLOW-UP
DISPOSITION
Admission Criteria
  • Severe life-threatening hyponatremia
  • Symptomatic hyponatremia
  • Serum sodium <125 mEq/L regardless of symptoms
  • New-onset SIADH in which underlying cause or complications must be diagnosed and treated
  • Patient’s compliance an issue
Discharge Criteria
  • Asymptomatic chronic hyponatremia
  • Serum sodium >125 mEq/L
  • No unstable comorbid factors
  • Known diagnosis of SIADH
FOLLOW-UP RECOMMENDATIONS

All patients with hyponatremia that meet discharge criteria still require follow-up to check for resolution, monitoring, and/or diagnosis of the underlying cause of the SIADH/hyponatremia.

PEARLS AND PITFALLS
  • SIADH is a diagnosis of exclusion.
  • Must evaluate for other causes as well as renal, thyroid, adrenal, cardiac, and hepatic dysfunction.
  • Take a thorough medication history.
ADDITIONAL READING
  • Balasubramanian A, Flareau B, Sourberr J. Syndrome of inappropriate antidiuretic hormone secretion.
    Hospital Physician
    . 2007;39:33–36.
  • Brimioulle S, Orellana-Jimenez C, Aminian A, et al. Hyponatremia in neurological patients: Cerebral salt wasting versus inappropriate antidiuretic hormone secretion.
    Intensive Care Med
    . 2008;34:125–131.
  • Ellison DH, Berl T. Clinical practice. The syndrome of inappropriate antidiuresis.
    N Engl J Med
    . 2007;356(20):2064–2072.
  • Gross P. Clinical management of SIADH.
    Ther Adv Endocrinol Metab.
    2012;3(2):61–73.
  • Verbalis JG. Managing hyponatremia in patients with syndrome of inappropriate antidiuretic hormone secretion.
    J Hosp Med.
    2010;5(suppl 3):S18–S26.
See Also (Topic, Algorithm, Electronic Media Element)

Hyponatremia

The author gratefully acknowledges the contribution of Arunachalam Einstein on previous editions of this chapter.

CODES
ICD9
  • 253.6 Other disorders of neurohypophysis
  • 276.1 Hyposmolality and/or hyponatremia
ICD10
  • E22.2 Syndrome of inappropriate secretion of antidiuretic hormone
  • E87.1 Hypo-osmolality and hyponatremia
SYNOVITIS, TOXIC
Daniel A. Popa

Ian R. Grover
BASICS

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