|
|
| Line 23: |
Line 23: |
| ==[[Hypokalemia differential diagnosis|Differential diagnosis]]== | | ==[[Hypokalemia differential diagnosis|Differential diagnosis]]== |
|
| |
|
| ==Diagnosis== | | ==[[Hypokalemia diagnosis | Diagnosis]]== |
| === Symptoms ===
| |
| The severity of symptoms depends on the degree of hypokalemia, but keep in mind that there is marked individual variability.
| |
| ==== Constitutional ====
| |
| * [[Ddx:Fatigue|Fatigue]]
| |
| * Weakness
| |
| * [[Ddx:Nausea and Vomiting|Vomiting]]
| |
| * [[Ddx:Constipation|Constipation]]
| |
| * Muscle cramps and paralysis (the lower extremity muscles are most commonly involved) which may involve the intestine and cause ileus
| |
| * Respiratory muscle weakness leading to respiratory failure
| |
| ==== Cardiac ==== | |
| * Hypertension
| |
| * Arrhythmias including premature atrial and ventricular complexes, paroxysmal atrial or junctional tachycardia and even ventricular tachycardia or fibrillation
| |
| * Heart block
| |
| * Digoxin therapy, CAD and left ventricular hypertrophy potentiate hypokalemia effects on the heart
| |
| ==== Renal ====
| |
| *Nephrogenic diabetes insipidus due to decreased concentrating ability. As a consequence, the patient presents with polyuria and polydipsia
| |
| *Increased bicarbonate reabsorption
| |
| *Increased ammonia formation which may precipitate hepatic encephalopathy in cirrhotic patients
| |
| *Decreased sodium reabsorption resulting in hyponatremia
| |
| ==== Other ====
| |
| * Rhabdomyolysis
| |
| * [[Ddx:Hyperglycemia|Hyperglycemia]]
| |
|
| |
|
| === History === | | ==[[Hypokalemia history and symptoms | History and Symptoms ]]== |
| A detailed history can help depict the cause of hypokalemia.
| |
|
| |
|
| ==== Dietary history ==== | | ==[[Hypokalemia laboratory tests | Lab Tests]]== |
| Malnutrition: lack of meat and fruit intake
| |
|
| |
|
| ==== Medication history ==== | | ==[[Hypokalemia electrocardiogram | Electrocardiogram]]== |
| *Diuretics (loop and thiazides)
| |
| *Beta agonists
| |
| *Chloroquine
| |
| *Theophylline
| |
| *Insulin
| |
| *Corticosteroids
| |
| *Licorice
| |
| *Nephrotoxic drugs (platinum-based chemotherapy, aminoglycosides)
| |
| *Laxatives
| |
|
| |
|
| ==== Past medical history ==== | | ==[[Hypokalemia medical therapy| Treatment]]== |
| *Uncontrolled diabetes
| |
| *Hyperthyroidism
| |
| *Pernicious anemia
| |
| *COPD (treated with Beta agonists and theophylline)
| |
| *Cushing’s disease
| |
| *Periodic paralysis
| |
| *Ileostomy/short bowel
| |
| *Primary hyperaldosteronism
| |
| *Liddle syndrome
| |
| *Bartter and Gitelman syndrome
| |
| *Prolonged starvation
| |
| *Cancer
| |
| *Renal tubular acidosis type I and type II
| |
| | |
| == Laboratory Findings ==
| |
| * Complete blood count (CBC)
| |
| * Blood urea nitrogen (BUN)/creatinine
| |
| * Calcium
| |
| * Magnesium
| |
| * Glucose
| |
| * Arterial blood gases
| |
| * Aldosterone level
| |
| * Renin levels
| |
| * Urinary sodium
| |
| * Urine potassium
| |
| ** Levels <25 meq/'''day''' (or <15 meq/L on urine '''spot''') rule out a renal cause of hypokalemia and suggest extrarenal potassium loss or transcellular shift
| |
| ** Higher potassium excretion suggest renal losses.
| |
| * Transtubular potassium gradient (TTKG)
| |
| ** TTKG= (Urine K x Plasma osmolarity)/(Plasma K x Urine osmolarity)
| |
| ** A TTKG less than 2-3 indicates renal potassium conservation in a hypokalemic patient
| |
| ** A urine osmolality less than plasma osmolality or urine sodium <20 mEq/L, the formula is not applicable
| |
| * Urine chloride
| |
| ** <25 meq/L: vomiting or remote diuretic use
| |
| ** >40 meq/L: diuretics, Bartter's, Gitelman's and mineralocorticoid excess
| |
| | |
| == Electrocardiography ==
| |
| ==== Overview ====
| |
| *Caused mainly by delayed ventricular repolarization
| |
| *Seen at potassium levels <3 meq/L (90% of patients with potassium levels <2.7 meq/L have abnormal ECG findings)
| |
| *Rapidly reversible with potassium repletion
| |
| | |
| ==== ECG changes ====
| |
| # ST segment depression, decreased T wave amplitude, prominent U waves
| |
| #* seen in 78% of patients with a K < 2.7 meq
| |
| #* seen in 35% of patients with a K > 2.7 and < 3.0
| |
| #* seen in 10% of patients with a K > 3.0 and < 3.5
| |
| #* U waves are also prominent in bradycardia and LVH
| |
| # Prolongation of the QRS duration
| |
| #* uncommon except in severe hyperkalemia
| |
| # Increase in the amplitude and duration of the P-wave
| |
| # Cardiac arrhythmias and AV block
| |
| # Contrary to popular belief there is not prolongation of the QTc, this is artifactually prolonged due to the U wave. In some cases there is fusion of the T and the U wave making interpretation impossible.
| |
| | |
| <div align="center">
| |
| <gallery heights="175" widths="175">
| |
| Image:Hypokalemia.jpg|Long QT interval, ST segment depression, low T waves amplitude and TU wave fusion in a hypokalemic patient.
| |
| Image:KJcasu18-3.jpg|Consecutive ECGs of a patient with hypokalemia. ECG1
| |
| </gallery>
| |
| </div>
| |
| | |
| | |
| <div align="center">
| |
| <gallery heights="117" widths="117">
| |
| Image:KJcasu18-2.jpg|Consecutive ECGs of a patient with hypokalemia. ECG2
| |
| Image:KJcasu18-1.jpg|Consecutive ECGs of a patient with hypokalemia. After correction of potassium levels.
| |
| Image:V10.ht14.jpg|Hypokalemia with LVH. Image courtesy of Dr Jose Ganseman
| |
| </gallery>
| |
| </div>
| |
| | |
| ==Treatment==
| |
| The most important step in severe hypokalemia is removing the cause, such as treating [[diarrhea]] or stopping offending medication.
| |
| | |
| * Patients treated with loop or thiazide diuretics can be offered medications that counteract their kaliuretic effect such as aldosterone antagonists (spironolactone and eplerenone) or distal sodium channel blockers (eg, amiloride).
| |
| * The combination of thiazide and loop diuretics should be avoided.
| |
| * Oral potassium administration is safer than the IV route.
| |
| * An oral dose should '''not''' exceed 20-40 mEq.
| |
| * IV potassium infusion should be reserved for symptomatic patients with severe hyperkalemia and patients who can't take oral supplements.
| |
| | |
| === Mild hypokalemia ===
| |
| * Potassium levels in the range 3.0-3.5 mEq/L.
| |
| * Represent potassium deficit of 200-400 mEq.
| |
| * May be treated with oral potassium salt supplements: potassium chloride KCl (Sando-K®, Slow-K®) or potassium bicarbonate KHCO3 (which can be generated from the metabolism of many organic salts eg, potassium citrate, potassium gluconate, etc).
| |
| * Potassium-containing foods may be recommended, such as tomatoes, oranges or bananas, but they are less effective than oral supplements.
| |
| * Both dietary and pharmaceutical supplements are used for people taking diuretic medications (see '''Causes''', above).
| |
| * KCl is the most effective replacement for metabolic alkalosis-associated hypokalemia.
| |
| * KHCO3 and the organic "alkalinizing" salts K-citrate and K-gluconate are recommended for hypokalemia associated with metabolic acidosis (chronic diarrhea, renal tubular acidosis,etc).
| |
| | |
| === Severe hypokalemia === | |
| * Potassium levels below 3.0 mEq/L
| |
| * Potassium levels between 2.0 and 3.0 correspond to 400-800 mEq deficit.
| |
| * It may require [[intravenous]] supplementation. Typically, [[saline (medicine)|saline]] is used, with 20-40 mEq KCl per liter over 3-4 hours (ie, at an infusion rate of 10 mEq/L/h)
| |
| * '''Giving IV potassium at faster rates may predispose to [[ventricular tachycardia]]s and requires intensive ECG monitoring.'''
| |
| * '''Giving IV KCl at doses >60 mEq/L are painful and can cause venous necrosis.'''
| |
| * Difficult or resistant cases of hypokalemia may be amenable to [[amiloride]], a potassium-sparing diuretic, or [[spironolactone]].
| |
| * When replacing potassium intravenously, infusion via central line is encouraged to avoid the frequent occurrence of a burning sensation at the site of a peripheral IV and the aforementioned venous necrosis. When peripheral infusions are necessary, the burning can be reduced by diluting the potassium in larger amounts of IV fluid, or mixing 3 ml of 1% lidocaine to each 10 meq of kcl per 50 ml of IV fluid. The practice of adding lidocaine, however, raises the likelihood of serious medical errors [http://www.ismp.org/newsletters/acutecare/articles/20040212_2.asp].
| |
| * Potassium infusions via a central line can reach 200 mEq/L (20 mEq in 100 mL of '''isotonic saline''' (see below)) but '''the administration rate should not be greater than 10–20 mEq per hour.'''
| |
| * Saline solutions are preferred to prevent potassium transcellular shifting that is triggered by dextrose-induced insulin release!
| |
|
| |
|
| ==See also== | | ==See also== |
