Download Approach to the patient with electrolyte disorders

Approach to the patient with
electrolyte disorders
Hypokalemia-Hyperkalemia
Zehra Eren, M.D.
LEARNING OBJECTIVES
• recall potassium distribution
• recall etiology of hypokalemia and hyperkalemia
• describe sing and symptoms of hypokalemia and
hyperkalemia
• describe laboratory findings of hypokalemia and
hyperkalemia
• explane treatment of hypokalemia and
hyperkalemia
POTASSİUM DİSTRİBUTİON
• Gastrointestinal absorption→
%98 intracellular
%2 extracellular
• NA+K+ ATPase → transports
two K+ into cell
three Na+ out cell
Hypokalemia
• Serum K+ < 3.5 mEq/L (mmol/L)
Causes of Hypokalemia
• Pseudohypokalemia
-Extreme leukocytosis
• Decreased K intake
• Increased K losses
-Nonrenal (skin, gastrointestinal)
-Renal
RENAL POTASSİUM LOSS
1. Increased distal flow and distal Na+ delivery
-diuretics
-osmotic diuresis
-salt-wasting nephropathies
2. Increased secretion of potassium
- Mineralocorticoid excess: primary
hyperaldosteronism [aldosterone-producing adenomas (APAs)],
primary or unilateral adrenal hyperplasia (PAH), idiopathic
hyperaldosteronism (IHA) due to bilateral adrenal hyperplasia, and
adrenal carcinoma], familial hyperaldosteronism (FH-I, FH-II,
congenital adrenal hyperplasias), secondary hyperaldosteronism
(malignant hypertension, renin-secreting tumors, renal
arterystenosis, hypovolemia),
Cushing's syndrome, Bartter's syndrome, Gitelman's syndrome
RENAL POTASSİUM LOSS
-Apparent mineralocorticoid excess: genetic
deficiency of 11β-dehydrogenase-2 (syndrome of apparent
mineralocorticoid excess), inhibition of 11β-dehydrogenase-2
(glycyrrhetinic/glycyrrhizinic acid and/or carbenoxolone; licorice,
food products, drugs), Liddle's syndrome [genetic activation of
epithelial Na+ channels (ENaC)]
-Distal delivery of nonreabsorbed anions:
vomiting, nasogastric suction, proximal renal tubular acidosis,
diabetic ketoacidosis, glue sniffing (toluene abuse), penicillin
derivatives (penicillin, nafcillin, dicloxacillin, ticarcillin,oxacillin and
carbenicillin)
Causes of Hypokalemia
• Redistribution (increased entry into cell)
-Insulin excess
-Alkalemia
-“Stress” [β2 adrenergic sympathetic activityꜛ: asthma attack, acute
coronary syndrome, trauma, drug intoxication (cocaine) or alcohol
withdrawal, B2 adrenergic drugs ]
-α-adrenergic antagonists
-Hypokalemic periodic paralysis
-Thyrotoxicosis
-Barium, Cesium
-Hypothermia
-Downstream stimulation of NA+/K+ ATPase: theophyline, cafferine
DİAGNOSİS
• Rule out
-pseudohypokalemia
-redistribution
• Potassium deplettion
-renal
-gastrointestinal
-skin
Clinical manifestations
• Cardiovascular:
-Hypertansion (↑BP 5-10mmHg )
-Arrhythmias
-Digitalis toxicity
• Neuromuscular:
1.Smooth muscle:
-Ileus
2.Skeletal muscle:
-Weakness
-Paralysis
-Rhabdomyolysis
Clinical manifestations
•
Endocrine:
-Glucose intolerance (↓insulin release and sensitivity)
•
Renal: ↓blood flow,↑vascular resistance
-Vasopressin resistance
-Increased ammonia production
-Metabolic alkalosis (retention of Na, Cl, HCO3)
-Polyuria, phosphaturia, hypocitraturia
Structural changes:
Renal cysts
Interstitial changes
PT dilation, vacuolization
TREATMENT GOALS
• prevent life-threatening and/or chronic consequences
• replace the associated K+ deficit
• correct the underlying cause and/or mitigate future
hypokalemia
TREATMENT
Urgency of therapy depends on
-the severity of hypokalemia
-associated clinical factors (cardiac disease,digoxin
therapy, etc.)
-rate of decline in serum K+
Cautions
-severe redistributive hypokalemia
-concomitant Mg2+ deficiency
TREATMENT
• Oral
• İntravenous
Safely at a rate of 10 mmol/h
20mmol KCL →↑serum K + ~ 0.25 mmol/L
↑20mmol/h replacement →
central venous catheter
Hyperkalemia
• Serum K ≥5.0 mEq/L (mmol/L)
Causes of Hyperkalemia
• Pseudohyperkalemia
-Thrombocytosis
-Leukocytosis
-Ischemic blood draw
• Redistibution (increased K release from cells)
-Exercise, especially in setting of β adrenergic receptor blockage and
mineral acidosis
-Hyperchloremic metabolic acidosis
-Insulin deficiency
-Hypertonicity
-α adrenergic receptor stimulation
Causes of Hyperkalemia
• Excessive intake: rare as sole cause
• Impeared renal K+ excretion
GFR <20 mL/min:
-Endogenous or exogenous K+
-Drugs that impair K+ excretion
Clinical manifestations
• May be disproportionately greater than level of serum K
• Cardiovascular
-T-wave abnormalities
-Bradyarrhythmias
• Neuromuscular
-Ileus
-Paresthesias
-Weakness
-Paralysis
• Renal/electrolyte
-Decreased ammonia production
-Metabolic acidosis
Case1
• A 70-year-old man with advanced prostate cancer develops
bilateral ureteral obstruction and acute on chronic renal
failure.
His potassium rises to 7.7 mEq/L with peaked T-waves on
electrocardiogram. His medications include digoxin.
Case2
• A 72 year old male found collapsed at home on floor of his
bedroom, incontinent of urine and faeces. He complained of
significant pain in his right hip with shortening and rotation.
His family last had contact with him 3 days prior to his
collapse.
• Medical History:CCF , Hypertension , Type 2 DM,
Osteoarthritis
• Medication History:His is taking enlapril for hypertension;
spironolactone & metoprolol for his CCF and celebrex for his
osteoarthritis.His diabetes is diet controlled.