understand electrolyte disorders

 

ELECTROLYTE DISORDERS

 

HYPONATREMIA: is an excess of water relative to sodium, almost always 2/2 elevated ADH (appropriate vs inappropriate)

 

History/PE

• The patient may be asymptomatic or may present with confusion, lethargy, muscle cramps or nausea.  Hyponatremia can progress to seizures, status epilepticus
• on physical exam look for signs to help assess volume status (vital signs, orthostatics, JVP, skin turgor, mucous membranes, peripheral edema); careful mental status assessment

 

Workup:

• measure plasma osmolality, BUN and creatnine, uric acid
• urine osm generally not helpful because almost always >300 (although Uosm <100 generally seen in primary polydipsia)

 

Now try to determine if the patient has hypovolemic hyponatremia, euvolemic hyponatremia or hypervolemic hyponatremia

 

Etiology and Treatment:

Hypovolemic hyponatremia may be from renal losses (diuretics, salt wasting nephropathy, cerebral salt wasting, mineralcorticoid deficiency) or extrarenal losses (GI losses, third spacing, inadequate intake, insensible losses).  It is generally treated by volume repletion with normal saline.

 

Euvolemic hyponatremiamay be from SIADH (can be triggered by pulmonary processes, intracranial disorders, certain drugs), endocrinopathies (glucocorticoids deficiency or hypothyroidism), psychogenic polydipsia, low solute diet, or reset osmostat.    SIADH is treated with sodium and restriction and free water restriction as well as treatment of the underlying cause.  If that doesn’t work you may have to treat the patient with hypertonic saline +/- loop diuretics.

 

Hypervolemic hyponatremia can be seen in CHF, cirrhosis, nephritic syndrome, and advanced renal failure.  It is generally treated with sodium restriction and free water restriction.

 

Remember: Avoid rapid correction of hyponatremia as it can lead to central pontine myelinolysis (spastic quadriplegia, dysarthria, dysphagia).  Be especially cautious if you suspect that the patient is chronically hyponatremic.  If the pt is asymptomatic, aim for Na correction at a rate of <= .5 mEq/L/h.  If they are symptomatic they will need initial rapid correction of Na (2meq/l/hr for the first 2-3 hours) util their sxs resolve.  Do not correct the Na more than 10-12 mEq/L/day.

 

HYPERNATREMIA is defined as a deficit of water relative to sodium (Na >145 mEq/L)

 

History/PE:

• Pts may report thirst and oliguria or polyuria (depending on the etiology) as well as mental status changes, weakness, focal neurologic deficits and seizures. 
• Physical exam may reveal doughy skin; you want to check their volume status (vital signs, orthostatics, JVP, skin turgor, mucous membranes, peripheral edema)

 

Workup:

• check BUN and creatnine
• check Uosm and UNa

 

Etiology and Treatment:

Hypovolemic hypernatremia:

• renal H2O losses: Uosm 300-600, UNa >20; can be due to loop diuretics, osmotic diuresis
• extrarenal H20 losses: Uosm>600, UNa <20; caused by diarrhea, insensible losses (fever, exercise)
• treat the underlying causes and replace free water deficit with hypotonic salne, D5W or oral water depending on volume status.  Correction should occur gradually over 48-72 hours to precent neurologic damage secondary to cerebral edema.

 

Euvolemic hypernnatremia:

• central diabetes insipidus: caused by ADH deficiency, Uosm <300-600; etiologies include congenital, trauma/surgery, tumors, infiltrative disease of hypothalamus or posterior pituitary, idiopathic, hypoxia, encephalopathy, anorexia
• nephrogenic diabetes insipidus: caused by ADH resistance, Uosm <300-600; etiologies include drugs (lithium, amphotericin, demeclocycline, foscarnet, cidofovir), metabolic (hypercalcemia, severe hypokalemia, protein malnutrition, congenital), tubulointerstitial (postobstructive, recovery phase of ATN, PCKD, sickle cell, sjogrens, amyloid, pregnancy
• Seizures or exercise: Uosm >600; increased intracellular osmoles -> H2O shift -> transient elevation in serum sodium
• Central DI can be treated with desmopressin while nephrogenic DI is treated by treating the underlying cause; you can also try sodium restriction with a thiazide

 

Hypervolemic hypernatremia:

• Hypertonic saline administration (eg. Cardiac arrest resuscitation with NaHCO3)
• Mineralcorticoid excess: usually presents as mild hypernatremia caused by ADH suppression
• treat with D5W and a loop diuretic

 

HYPOKALEMIA is when the serum potassium is <3.5 mEq/L

 

Etiology:

• Transcellular shifts: Insulin. B-agonists, alkalosis, periodic paralysis (Ca channelopathy), acute increase in hematopoiesis (megaloblastic anemia txd with B12, AML crisis)
• GI losses plus metabolic acidosis: diarrhea, laxative abuse, villous adenoma
• Renal potassium losses: diuretics, primary mineralocorticoid excess or sevondary hypoeraldosteronism, DKA, RTA, hypomagnesemia

 

History/PE:

• May present with nausea/vomiting, fatigue, muscle weakness or cramps, ileus, hyporeflexia, paresthesias, flaccid paralysis

 

Workup:

• 24 hour or spot urine potassium can help differentiate renal from GI losses
• EKG may reveal T-wave flattening, U waves, and ST depression followed by AV block and subsequent cardiac arrest

 

Tx:

• potassium repletion: KCl 4 mEq po q4-6h if non-urgent, KCl 10 meq/h IV if urgent; recheck K frequently
• beware of excessive potassium repletion if transcellular shift is the cause of hypokalemia
• treat underlying cause
• replete Mg as necessary

HYPERKALEMIA: Serum potassium >5 mEq/L

 

Etiologies:

• transcellular shifts: acidosis, insulin deficiency, B-blockers, dig toxicity, massive cellular necrosis (tumor lysis, rhabdo, ischemic bowel) hyperkalemic period paralysis (Na channelopathy)
• Decreased GFR: any cause of oligo- or anuric acute renal failure or any cause of end-stage renal disease
• Normal GFR but with decreased renal K excretion: CHF, cirrhosis, nephropathy (diabetic, HIV), chronic interstitial nephritis, primary adrenal disorders, drugs (NSAIDS, ACEI/ARBSm potassium sparing diuretics, bactrim), systemic disorders that cause tubulointerstitial disease  (sickle cell, SLE, amyloid)
• Iatrogenic (over-repletion of hypokalemia)

 

History/PE:

• pts may be asymptomatic or may present with nausea, vomiting, weakness, paresthesias, palpitations
• PE may reveal areflexia, flaccid paralysis, paresthesias

 

Workup:

• verify hyperkalemia with repeat blood draw (unless already have high index of suspicion)
• check EKG: findings may include tall peaked T waves, PR prolongations, wide QRS, loss of P waves and eventual progression to sine waves, v fib and cardiac arrest!

 

Treatment:

• values of >6.5 mEq/L or EKG changes (especially PR prolongation or wide QRS) require immediate treatment
• calcium gluconate 1-2 amps IV for cardiac cell membrane stabilization
• insulin 10U IV with 1-2 amps D50W to transiently drive K into cells
• Bicarbonate 1-3 amps to transiently drive K into cells
• B2 agonist (albuterol) to transiently drive K into cells
• Kayexalate 30-90 g po/pr to decrease total body K
• loop diuretic (lasix 40 mg IV) to decrease total body K
• dialysis

 

ACID-BASE ABNORMALITIES

 

	pH	PCO2	[HCO3]	Cause	Compensatory Response
Metabolic acidosis	Decreased	Decreased	Decreased	Diabetic ketoacidosis, diarrhea, lactic acidosis, salylate OD, acetazolamide	Hyperventilation
Respiratory acidosis	Decreased	Increased	Increased	COPD, airway obstruction	Renal [HCO3] reabsorption
Respiratory alkalosis	Increased	Decreased	Decreased	High altitude, hyperventilation	Renal [HCO3] secretion
Metabolic alkalosis	Increased	Increased	Increased	Vomiting	hypoventilation

 

 

 

ELECTROLYTES/ACID-BASE CASES

 

1.  A 39 yo M comes to the ER experiencing labored breathing and mental obtundation.  PE is unremarkable.  Labs reveal Na 144, K 3.7, chloride 97, bicarb 16, arterial pH 7.38, PCO2 21.  The acid base disturbance is:

-what is the patient’s acid-base disturbance?  Is it a single disturbance or mixed disturbance?

 

a)  what is the patient’s anion gap?

b)  what are some possible causes of his acid-base derangement?

 

 

2. A 60 yo M is admitted c/o nausea, weakness and confusion x 1 week.  He has HTN and congestive heart failure and is on lasix and digoxin.  PE reveals BP 145/90, +JVD, bilateral basilar rales and 2+ ankle edema.  Labs reveal the following: Na 120, BUN 93, glucose 135, plasma osm 252, urine osm 690.

 

c)  what is the most likely cause of the patient’s hyponatremia?

d)  how would you treat the patient?

 

 

3.  A 58 yo M is admitted c/o nausea, vomiting, weakness, and palpitations.  He has known portal hypertension and ascites and was recently started on aldactone.  His labs reveal a potassium of 6.2.

 

e)  list 4 EKG findings you might find in patients with hyperkalemia

f)  list 4 treatment options to treat the patient’s hyperkalemia

 

Answers

 

a)      AG = 144 - (97+16) = 31

b)      Mixed AG metabolic acidosis & respiratory alkalosis (PCO2 is lower than expected compensation for met acidosis).  Possible etiologies include: salicylate intoxication, lactic or ketoacidosis, renal failure, etc.

c)      Hyponatremia likely due to volume overload/CCF

d)     Diurese aggressively

e)      Peaked T waves, prolonged PR interval, junctional bradycardia, widening of QRS

f)       Treat hyperkalemia with ECG changes with: calcium gluconate, IV insulin & dextrose, albuterol or another short-acting beta-agonist bronchodilator, kayexalate if available, consider using lactulose if kayexalate unavailable (has some ability to reduce K through osmotic diarrhea).  Other treatment modalities include: bicarbonate, furosemide, & dialysis.