hypokalemia, diagnosis and management
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Transcript of hypokalemia, diagnosis and management
HYPOKALEMIA
Sheila Perillo, MDObstetrics and Gynecology
Less than 3.5 mEq/L- (3.5 mmol/L) Moderate hypokalemia- 2.5-3 mEq/L Severe hypokalemia- less than 2.5
mEq/L
POTASSIUM -most abundant intracellular cation- important to normal cellular function
particularly of nerve and muscle cells-regulated by specific ion-exchange pumps,
primarily by cellular, membrane-bound, sodium-potassium adenosine triphosphatase (ATPase) pumps
-obtained through the diet -excreted via the kidney. -Potassium homeostasis is maintained
predominantly through the regulation of renal excretion
HYPOKALEMIA
inadequate potassium intake increased potassium excretion- most
common shift of potassium from the extracellular
to the intracellular space
Common findings include weakness, fatigue, constipation, ileus, and respiratory muscle dysfunction.
Symptoms seldom occur unless plasma K+ is less than 3.0 mmol/L.
ECG changes
THE TREATMENT OF HYPOKALEMIA HAS 4 FACETS
Reduction of potassium losses Replenishment of potassium stores Evaluation for potential toxicities Determination of the cause to prevent
future episodes
PATHOPHYSIOLOGY
Daily excess intake of approximately 1 mEq/kg/day (60-100 mEq):Ninety percent is excreted through the
kidneys10% is excreted through the gut
Potassium homeostasis is maintained predominantly through the regulation of renal excretion (collecting duct)
POTASSIUM EXCRETION IS INCREASED BY THE FOLLOWING FACTORS: Aldosterone High sodium delivery to the collecting
duct (eg, diuretics) High urine flow (eg, osmotic diuresis) High serum potassium levels Delivery of negatively charged ions to
the collecting duct (eg, bicarbonate)
POTASSIUM EXCRETION IS DECREASED BY THE FOLLOWING FACTORS: Absolute aldosterone deficiency or
resistance to aldosterone effects Low sodium delivery to the collecting
duct Low urine flow Low serum potassium levels Renal failure
increase in osmolality exit from cells
acute cell/tissue breakdown releases potassium into extracellular space
RENAL FACTORS IN POTASSIUM HOMEOSTASIS
Kidneys adapt to acute and chronic alterations in potassium intake: When potassium intake is chronically high,
potassium excretion likewise is increased. obligatory renal losses are 10-15 mEq/day
The kidney maintains a central role in the maintenance of potassium homeostasis, even in the setting of chronic renal failure.
In the presence of renal failure, the proportion of potassium excreted through the gut increases.
The colon is the major site of gut regulation of potassium excretion.
POTASSIUM DISTRIBUTION
Potassium is predominantly an intracellular cation; therefore, serum potassium levels can be a very poor indicator of total body stores.
SEVERAL FACTORS THAT REGULATE THE DISTRIBUTION OF POTASSIUM BETWEEN THE INTRACELLULAR AND EXTRACELLULAR SPACE
Glycoregulatory hormones: (1) Insulin enhances potassium entry into cells (2) glucagon impairs potassium entry into cellsAdrenergic stimuli: (1) Beta-adrenergic stimuli enhance potassium
entry into cells (2) alpha-adrenergic stimuli impair potassium
entry into cellspH: (1) Alkalosis enhances potassium entry into cells (2) acidosis impairs potassium entry into cells
PATHOGENIC MECHANISMS Hypokalemia can occur via the following
pathogenetic mechanisms:Deficient intake Increased excretionA shift from the extracellular to the
intracellular space Although poor intake or an intracellular
shift by itself is a distinctly uncommon cause
INCREASED EXCRETION
The most common mechanisms leading to increased renal potassium losses include the following:Enhanced sodium delivery to the
collecting duct, as with diureticsMineralocorticoid excess, as with
primary or secondary hyperaldosteronism
Increased urine flow, as with an osmotic diuresis
Gastrointestinal losses: Diarrhea Vomiting nasogastric suctioning, also are common
causes of hypokalemia Volume depletion leads to secondary
hyperaldosteronism enhanced cortical collecting tubule secretion of potassium in response to enhanced sodium reabsorption
Metabolic alkalosis increases collecting tubule potassium secretion
EXTRACELLULAR/INTRACELLULAR SHIFT Shift from extracellular to intracellular
spaceoften accompanies increased excretion
potentiation of the hypokalemic effect of excessive loss
Intracellular shifts of potassium often are episodic frequently are self-limited (ie., acute insulin
therapy for hyperglycemia)
COMPLICATIONS
Cardiovascular complicationsAtrial and ventricular arrhythmias Increased susceptibility to cardiac
arrhythmias is observed with hypokalemia in the following settings: Congestive heart failure Underlying ischemic heart disease/acute
myocardial ischemia Aggressive therapy for hyperglycemia, such as
with diabetic ketoacidosis Digitalis therapy Methadone therapy Conn syndrome
Low potassium intakehypertension and/or hypertensive end-
organ damagealtered vascular reactivity
vasoconstriction and impaired relaxation Treatment of hypertension with diuretic
exacerbates the development of end-organ damage by fueling the metabolic abnormalities
high risk for lethal hypokalemia under stress conditions such as myocardial infarction, septic shock, or diabetic ketoacidosis
MUSCULAR COMPLICATIONS Muscle weakness Depression of the deep-tendon reflexes Flaccid paralysis Rhabdomyolysis (severe hypokalemia)
RENAL COMPLICATIONS
Nephrogenic diabetes insipidus- Abnormalities of renal function often
accompany acute or chronic hypokalemia Metabolic alkalosis from impaired
bicarbonate excretion Cystic degeneration Interstitial scarring
GASTROINTESTINAL COMPLICATIONS Decreased gut motility, which can lead
to or exacerbate an ileus
Hepatic encephalopathy in the setting of cirrhosis
METABOLIC COMPLICATIONS
Dual effect on glucose regulation by decreasing insulin release and peripheral insulin sensitivity
Thiazide-associated diabetes mellitus
ETIOLOGY Inadequate potassium intake Increased potassium excretion ** Shift of potassium from the extracellular
to the intracellular space
INADEQUATE POTASSIUM INTAKE
Eating disorders : Anorexia, bulimia, starvation, pica, and alcoholism
Dental problems: Impaired ability to chew or swallow
Poverty: Inadequate quantity or quality of food (eg, "tea-and-toast" diet of elderly individuals)
Hospitalization: Potassium-poor TPN
INCREASED POTASSIUM EXCRETION Mineralocorticoid excess (endogenous
or exogenous) Hyperreninism from renal artery
stenosis Osmotic diuresis: Mannitol and
hyperglycemia can cause osmotic diuresis
Increased gastrointestinal losses Drugs Genetic disorders
GASTROINTESTINAL LOSS OF POTASSIUM Vomiting Diarrhea Small intestine drainage
DRUGS THAT CAN CAUSE HYPOKALEMIA INCLUDE THE FOLLOWING: Diuretics (carbonic anhydrase inhibitors, loop diuretics,
thiazide diuretics): Increased collecting duct permeability or increased gradient for potassium secretion can result in losses
Methylxanthines (theophylline, aminophylline, caffeine) Verapamil (with overdose) Quetiapine (particularly in overdose) Ampicillin, carbenicillin, high-dose penicillins Bicarbonate Antifungal agents (amphotericin B, azoles, echinocandins) Gentamicin Cisplatin Ephedrine (from Ephedra; banned in the United States, but
available over the Internet) Beta-agonist intoxication
GENETIC DISORDERS Congenital adrenal hyperplasia (11-beta
hydroxylase or 17-alpha hydroxylase deficiency) Glucocorticoid-remediable hypertension Bartter syndrome Gitelman syndrome Liddle syndrome Gullner syndrome Glucocorticoid receptor deficiency Hypokalemic period paralysis Thyrotoxic periodic paralysis (TTPP) Seizures, sensorineural deafness, ataxia, mental
retardation, and electrolyte imbalance (SeSAME syndrome)
SHIFT OF POTASSIUM FROM EXTRACELLULAR TO INTRACELLULAR SPACE Alkalosis (metabolic or respiratory) Insulin administration or glucose
administration (the latter stimulates insulin release)
Intensive beta-adrenergic stimulation Hypokalemic periodic paralysis Thyrotoxic periodic paralysis Refeeding: This is observed in prolonged
starvation, eating disorders, and alcoholism Hypothermia
OTHER FACTORS ASSOCIATED WITH A HIGH INCIDENCE OF HYPOKALEMIA INCLUDE THE FOLLOWING: Eating disorders (incidence of 4.6-19.7%
in an outpatient setting) AIDS (23.1% of hospitalized patients) Alcoholism (incidence reportedly as high
as 12.6% [33] in the inpatient setting), likely from a hypomagnesemia-induced decrease in tubular reabsorption of potassium
Bariatric surgery
TREATMENT Therapeutic goals
Prevent life-threatening complications (arrhythmias, respiratory failure, hepatic encephalopathy)
Correct the K+ deficitMinimize ongoing lossesTreat the underlying cause
TREATMENT K deficit= (desired k- actual k) x 100% 0.27
Estimation of K+ deficit3.0 meq/L= total body K+ deficit of 200-400
meq/70kg2.5 meq/L = 500 meq/70kg2.0 meq/L = 700 meq/70kg
TREATMENT Oral therapy
Generally saferDegree of K+ depletion does not correlate
well with the plasma K+KCl is usually the preparation of choiceKalium durule: 1 durule = 10 meqs KClKCl syrup: 1meq/mL
TREATMENT IV therapy
For severe hypokalemia or those who are unable to take anything by mouth
Maximum rate at which potassium is infused into peripheral veins is usually 10 meq/hr
Central – 20 meq/hrRate of infusion should not exceed 20
meq/hour unless paralysis or malignant ventricular arrhythmias are present
TO GOD BE THE GLORY!