Rosen & Barkin's 5-Minute Emergency Medicine Consult (380 page)

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

Tags: #Medical, #Emergency Medicine

BOOK: Rosen & Barkin's 5-Minute Emergency Medicine Consult
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DESCRIPTION
  • Defined as a serum potassium level <3.5 mEq/L:
    • Mild: 3–3.5 mEq/L
    • Moderate: 2.5–3 mEq/L
    • Severe: <2.5 mEq/L
  • Frequency:
    • Up to 20% of inpatients have documented hypokalemia (5% have levels <3 mEq/L).
    • Up to 14% of outpatients are mildly hypokalemic (most are related to diuretics or GI loss).
    • 5% of geriatric patients have K <3 mEq/L.
  • Potassium is the major intracellular cation:
    • Gradient is maintained by Na–K ATPase activity (enhanced by insulin and β-agonists) and mineralocorticoids.
  • Total body potassium is ∼55 mEq/kg of body weight (98% ICF, 2% ECF).
  • Electrophysiologic effects of hypokalemia:
    • Increase in the normal intracellular to extracellular potassium gradient:
      • Alters the depolarization threshold for muscles and nerves
      • Inhibits the termination of action potentials
    • Alterations in intracellular potassium directly affect cellular function.
ETIOLOGY
Renal Losses
  • Diuretics (thiazides, loop diuretics, carbonic anhydrase inhibitors), usually associated with loss of other cations (Mg
    2+
    , Ca
    2+
    , P
    3+
    , Na
    +
    )
  • Renal tubular damage:
    • Primary renal tubular disorders (RTA type I and II)
    • Interstitial nephritis, analgesic nephropathy, drug toxicity (amphotericin, gentamicin, toluene, cisplatin), myeloma kidney
    • Overdose toxicity: Acetaminophen, NSAIDs, hydroxychloroquine
  • Hyperaldosteronism:
    • Primary (primary hyperaldosteronism, Cushing, pituitary tumor-producing ACTH, congenital adrenal hyperplasia)
    • Secondary (volume depletion, CHF, cirrhosis, nephrotic)
    • Exogenous (steroids; fludrocortisone, glycyrrhizic acid [licorice]) hyperrenin state in renal artery stenosis
  • Hypomagnesemia (increased secretion)
  • Polyuria:
    • Osmotic diuresis (mannitol, hyperglycemia)
    • Psychogenic polydipsia
  • Congenital disorders:
    • Bartter and Gitelman syndromes—hypokalemic metabolic alkalosis and low BP
    • Liddle syndrome is the same but with hypertension.
  • Delivery of nonreabsorbable anions such that sodium is reabsorbed and potassium is exchanged out and excreted:
    • Bicarbonate in metabolic alkalosis
    • β-hydroxybutyrate in DKA
    • Hippurate in toluene abuse
    • Penicillins—high dose IV therapy
GI Losses
  • Diarrhea:
    • Proportional to volume and duration
    • Villous adenomas
    • Laxative abuse
  • Vomiting and nasogastric suction result in volume depletion and metabolic alkalosis, which increases renal losses of potassium from bicarbonaturia and hyperaldosteronism.
  • Ureterosigmoidostomy
  • Intestinal fistulae, ileostomy
  • Cystic fibrosis
Intracellular Shift of Potassium
  • Alkalosis (metabolic or respiratory)
  • Insulin:
    • Insulin administration
    • Stimulation of insulin release by IV glucose or massive sweetened beverage intake
    • Refeeding in prolonged starvation
  • Adrenergic excess:
    • Severe stress (trauma, MI, sepsis)
    • Treatment of asthma (frequent β-agonists and theophylline toxicity)
    • Cocaine, amphetamines, caffeine excess
    • Dobutamine, dopamine, pseudoephedrine
  • Hypokalemic periodic paralysis:
    • Familial
    • Thyrotoxic
  • B
    12
    administration in severely deficient patient
  • Hypothermia
  • Drugs: GM-CSF, quetiapine, risperidone
Poor Intake (Rare as a Sole Cause)
  • Nutritional (poverty, pica, dementia)
  • Eating disorders
  • Dental problems/oral lesions
  • Esophageal disease
DIAGNOSIS
SIGNS AND SYMPTOMS
History
  • Neuromuscular:
    • Severe weakness (K <2.5 mEq/L):
      • Begins in the lower extremities and progresses cephalad
    • May progress to paralysis if K <2 mEq/L and rapid development
    • Muscle cramps, tetany, and tenderness
    • Rhabdomyolysis
    • Paresthesias
    • Generalized fatigue and malaise
  • GI:
    • Constipation
    • Ileus
  • Cardiovascular (heart disease increases risk):
    • Ventricular and atrial premature beats
    • AV block, atrial or junctional tachycardias
    • Ventricular tachycardia (VT) or fibrillation
    • Potentiation of digoxin toxicity
  • Renal:
    • Impaired urinary concentrating ability resistant to ADH (polyuria, polydipsia)
    • Increased renal bicarbonate reabsorption and ammonia production (worsens alkalosis)
Physical-Exam
  • HTN—renal artery stenosis, primary hyperaldosteronism, licorice, congenital adrenal hyperplasia, Liddle syndrome, glucocorticoid use
  • Hypotension—GI losses, diuretic use, Bartter and Gitelman syndromes
  • Neuromuscular—muscle weakness, decreased reflexes, muscle tenderness
DIAGNOSIS TESTS & NTERPRETATION
Lab
  • Electrolytes, BUN, creatinine, glucose:
    • High HCO
      3
      suggests diuretic abuse, vomiting, mineralocorticoid excess, Bartter, Gitelman.
    • Low HCO
      3
      suggests renal tubular disease or diarrhea
    • Low serum sodium suggests diuretic use or marked volume depletion from GI losses
    • High serum sodium suggests nephrogenic diabetes insipidus or primary hyperaldosteronism
  • Urine K (spot sample):
    • <20 mEq/L suggests GI loss, potassium shift into cells, poor intake.
    • >20 mEq/L suggests renal loss.
  • Urine K to creatinine ratio is more precise
    • <13 mEq/g or 1.5 mEq/mmol (nonrenal)
    • >13 mEq/g or >1.5 mEq/mmol (renal loss)
  • Urine Na:
    • <20 mEq/L with elevated urine K suggests secondary hyperaldosteronism.
  • Plasma renin if hypertensive:
    • High renin: Secondary hyperaldosteronism, renal artery stenosis
    • Low renin: Primary hyperaldosteronism
  • TSH and free T4 if Asian male
ECG Findings
  • Low-voltage T-waves
  • Sagging of the ST segments
  • U-waves:
    • In severe hypokalemia, the T disappears and the U-wave predominates, giving the illusion of dramatic QT prolongation.
  • Diminutive P-waves (appears nodal)
  • Dysrhythmias (very prevalent if underlying cardiomyopathy or digoxin toxic):
    • Atrial: Premature atrial contractions (PACs), atrial fibrillation (Afib)
    • Ventricular: Premature ventricular contractions (PVCs), VT, torsade
DIFFERENTIAL DIAGNOSIS
  • Intrinsic cardiac disease with dysrhythmias
  • Causes of muscular weakness:
    • Neuromuscular junction disease (myasthenia gravis, organophosphate poisoning, botulism)
    • Spinal cord disease
    • Polyneuropathies
    • Primary acute myopathies
    • Cataplexy
TREATMENT
INITIAL STABILIZATION/THERAPY
  • Establish IV access/volume resuscitation
  • ABCs
  • Cardiac monitoring
ED TREATMENT/PROCEDURES
  • Total body deficit is 200–300 mEq per 1 mEq/L decrement in serum potassium level.
  • Rate of replacement and route dependent on presence of symptoms, severity of hypokalemia, and comorbidities.
  • Complete replacement over several days
  • Oral potassium preferable to IV therapy whenever possible
  • Identify and prevent ongoing K losses:
    • Hold diuretics or laxatives
    • Treat vomiting or diarrhea
    • Minimize nasogastric suction losses by administering H2 blockers or PPIs
    • Avoid glucose-containing fluids
MEDICATION
  • Oral potassium chloride:
    • Preferred replacement in almost all cases
    • Liquid (or powder dissolved in water or juice) is more bioavailable, but nausea may occur:
      • 10–40 mEq per dose
      • Rapid rise in K, but will drop after 4 hr from transcellular shift
    • Tablets (wax matrix and microencapsulated):
      • More palatable, more sustained effect
      • Slowly absorbed
      • Potential for small bowel ulceration.
    • Dosage for hypokalemia:
      • Mild to moderate: 10–20 mEq q6–12h
      • Moderate to severe: 40–60 mEq q8–12h
      • Continue until K remains 3–3.5 mEq/L
  • Oral potassium gluconate or citrate:
    • Use in acidotic patients (e.g., RTA)
    • Ineffective if accompanying metabolic alkalosis
    • Less effective than KCl
    • Can be used as prophylaxis of calcium oxalate renal stones or may dissolve uric acid stones
  • IV potassium:
    • Recommended if neuromuscular symptoms, cardiac arrhythmias, ongoing GI losses, or severe hypokalemia
    • Potassium chloride is the preferred replacement:
      • Potassium phosphate is used only if accompanying severe hypophosphatemia.
    • Administration:
      • A potassium rider at 10 mEq/h piggybacked into maintenance 0.9 NS is safest and best tolerated (peds: 0.1–0.2 mEq/kg/h)
      • 15–20 mEq/h are feasible by peripheral vein but not recommended due to risk of phlebitis and pain
      • If K is added to maintenance fluids, the concentration should not be >40 mEq/L and dextrose solutions should be avoided
      • If sustained life-threatening dysrhythmias, 20–40 mEq/h by central line or 2 peripheral lines can be considered.
      • If cardiac arrest occurs in a patient with known severe hypokalemia, 20 mEq could be given IV over 2–3 min
      • Monitor serum potassium after every 40 mEq IV
    • Hypokalemic periodic paralysis and other situations in which there is significant transcellular K shifts (adrenergic excess):
      • Small amounts of K are effective (20 mEq IV).
      • More zealous administration may lead to rebound hyperkalemia.
  • Electrolyte corrections:
    • Magnesium:
      • Consider if hypokalemia is resistant to K replacement.
      • Magnesium sulfate 2 g slow IV infusion
    • Chloride:
      • Hypokalemia with alkalosis is resistant to replacement unless volume depletion and hypochloremia is corrected by saline administration.

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