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

BOOK: Rosen & Barkin's 5-Minute Emergency Medicine Consult
12.53Mb size Format: txt, pdf, ePub
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.

Other books

Toad Words by T. Kingfisher
Shadow Of A Mate by SA Welsh
I Love You by Brandy Wilson
Owning Corey by Maris Black
Gray Matters by William Hjortsberg
False Gods by Graham McNeill
The Rule of Nine by Steve Martini
Luckstones by Madeleine E. Robins
The Forgiving Hour by Robin Lee Hatcher
An Air That Kills by Andrew Taylor