A 62 y/o M diabetic with chronic kidney disease and a creatinine of 3.5 mg/dl and an estimated GFR of 15 ml/min consults due to the inability to lift himself from a chair. He had been eating fruits with each meal for the past two weeks. On PE there is marked proximal weakness and decreased skin turgor. The ECG revealed peaked T waves and widening of the P wave and QRS complex.
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A 62 y/o M diabetic with chronic kidney disease and a creatinine of 3.5 mg/dl and an estimated GFR of 15 ml/min consults due to the inability to lift himself from a
chair. He had been eating fruits with each meal for the past two weeks. On PE there
is marked proximal weakness and decreased skin turgor. The ECG revealed peaked T waves and widening of the P
wave and QRS complex.
Salient Features
• 62 M• CKD• Diabetic• CC: inability to lift himself from a chair• Creatinine of 3.5 mg/dl• GFR of 15 ml/min – Low• Decreased skin turgor and marked proximal weakness• ECG: Peaked T waves and widening of P wave and
QRS complex
Laboratory ResultsParameters Patient Normal Values
Plasma Na 130 meq/L 136-146 meq/L
K 8.5 meq/L 3.5-5.0 meq/L
Cl 98 meq/L 102-109 meq/L
HCO3 17 meq/L 22-30 meq/L
Creatinine 2.7 meq/L 0.6-1.2 meq/L
pH 7.32 7.35-7.45
Capillary Blood Glucose 400 mmol/L 3.9-6.7 mmol not more than 125 mg/dl
Serum Acetone + -
1. What are the most likely factors responsible for the elevation of the plasma potassium?
Most likely causes of Hyperkalemia in the patient
1. ) The patient has chronic kidney disease and is in renal failure – GFR 15 ml/min– Compensatory mechanism for increasing distal
flow rate and K secretion per nephron is decreased because there is decreased renal mass in chronic renal insufficiency
2.) The patient has diabetes- Insulin deficiency and hypertonicity promote K shift from the ICF to the ECF.
3. Intake of fruits does not necessarily cause hyperkalemia.
- Huge amount of parenteral K can elicit hyperkalemia.
4. Acidosis causes shift of potassium from intracellular space into extracellular space.
2. Is this pseudohyperkalemia? Why or why not?
PSEUDOHYPERKALEMIA• Artificially elevated plasma K+ concentration due to
K + movement out of cells immediately prior to or following venipuncture
• Contributing factors: prolonged use of tourniquet with or without repeated fist clenching, hemolysis, and marked leukocytosis or thrombocytosis
• marked leukocytosis or thrombocytosis results in an elevated serum K + concentration due to release of intracellular K + following clot formation
Harrison’s Principles of Internal Medicine 17th ed.Onyekachi Ifudu, Mariana S. Markell, Eli A. Friedman. Unrecognized Pseudohyperkalemia as a Cause of Elevated Potassium in Patients with Renal Disease
PSEUDOHYPERKALEMIA
• serum to plasma potassium difference of more than 0.4 mmol/l
• occurs when platelets, leukocytes or erythrocytes release intracellular potassium in vitrofalsely elevated serum values.
excitability• Since the resting membrane potential is related to the
ratio of the ICF to ECF K+ concentration, hyperkalemia partially depolarizes the cell membrane
– It may progress to flaccid paralysis and hypoventilation if the respiratory muscles are involved
• Metabolic acidosis– Net acid excretion is impaired• Inhibition of renal ammoniagenesis and reabsorption of
NH4+ in the TALH
– It may exacerbate the hyperkalemia due to K+ movement out of cells
• Cardiac toxicity– Increased T-wave amplitude, or peaked T waves– Prolonged PR interval and QRS duration,
atrioventricular conduction delay, and loss of P waves• More severe degrees of hyperkalemia
– Sine wave pattern• Progressive widening of the QRS complex and merging
with the T wave– The terminal event is usually ventricular fibrillation or
asystole
How would you manage this case?
Management
• Most important consequence of Hyper K is altered Cardiac Conductance– With the risk of bradycardia and cardiac arrest
• The patient should be treated as an emergency case and warrants emergency treatment– + ECG changes and K > 6.0 mM (Px= 8.5 mM)
Urgent Management
• 12- lead ECG• Admission to the hospital• Continuous cardiac monitoring• Immediate treatment
Treatment
• Antagonism of the cardiac effect of hyperkalemia– Stabilize membrane potential• Calcium Therapy 10% Ca gluconate, 10 mL over 10
mins or Calcium chloride 5 mL of 10% sol IV over 2 min• Stop infusion if bradycardia develops
• Rapid reduction in K+ by redistribution into cells– Cellular K+ uptake• Insulin 10 U R (CBG= 400 mmol/L)• B2-agonist nebulize albuterol, 10-20 mg in 4mL saline
Treatment
• Removal of K+ from the body– Furosemide 20-250 mg IV– Kayexalate 30-60 g mixed with 100 mL of 20% sorbitol