An 18 year old female presents to the ED with vague symptoms of lower back pain. She exhibited inappropriate and erratic behavior that seemed more than just teenage angst. The patient was thin in NAD and had a grossly normal musculoskeletal, motor and neuro exam, no red flags. Labs were drawn and she had a sodium of 118. On further questioning the patient admitted that she is in an anorexia outpatient program and she had been aggressively drinking water the past 2 days in order for her to meet her weight goal.
Causes of hyponatermia
Hypovolemic: Vomiting, diarrhea, rental tubular acidosis, renal losses (thiazide, loop diuretics). Vomiting will result in metabolic alkalosis. Diarrhea and renal tubular acidosis both result in non anion gap metabolic acidosis.
Euvolemic: SIADH 2/2 intracerebral pathology, tumors, adrenal insufficiency, hypothyroidism, drugs (ex MDMA intoxication), and the release of HCG in pregnancy. Other causes: primary polydipsia, low dietary solute intake and pseudohyponatremia. Pseudohyponatremia occurs in hyperglycemia (for every 100 incr in [glucose] [Na] should fall by 1.6), hyperlipidemia (uncontrolled DM), hyperprotinemia (multiple myeloma) or mannitol intake.
Hypervolemic: heart failure, cirrhosis, renal failure. Decreased intravascular volume is sensed by the carotid sinus baroreceptors and causes an increase in ADH excretion. The rise in serum ADH levels varies with the severity of the disease, making hyponatremia an important prognostic sign.
Treatment:
– Goal to increase Na by 4 to 6 meq/L in 24 hours, every effort should be made so that the increase in Na is less than 9 meq/L. In patients with chronic hyponatremia (more than 1-2 days) avoid rapid correction to avoid central pontine myelinolysis.
asymptomatic, no CNS findings: Fluid resuscitation for hypovolemic states; restoration of euvolemia will suppress the release of ADH. For hypervolemic states treat the underlying disease with diuresis, paracentesis, dialysis, as appropriate. For euvolemic states fluid restriction is primary treatment. Monitor electrolytes closely
symptomatic, +mild to moderate CNS findings: (eg, fatigue, nausea, dizziness, gait disturbances, forgetfulness, confusion, lethargy, and muscle cramps): correction with isotonic NS and oral salt tablets. Initial hypertonic saline therapy to raise the serum sodium at rates of 0.5 to 1 meq/L per hour may be justified in the first four hours.
symptomatic, +severe CNS findings: (eg, unstable vitals, findings of impending brain herniation, or actively seizing): use 100 mL of 3% NS as IV bolus, which should raise the [Na] by 1.5-2 meq/L. If neuro symptoms persist or worsen, a 100mL bolus of 3% NS can be repeated 1-2 more times at 10min intervals. The use of vasopressin antagonists, tolvaptan (oral) and conivaptan (IV) are approved for euvolemic hyponatremia, mostly due to SIADH. Tolvaptan is approved for hypervolemic states, like heart failure. Do not use vasopressin antagonists in volume depleted patients, volume repletion should be primary therapy.
Thanks Bell for an awesome morning report case which this case was inspired from.
