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
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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 Results
Parameters
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
7.32
7.35-7.45
pH
Capillary Blood Glucose
Serum Acetone
400 mmol/L
+
3.9-6.7 mmol
not more than 125 mg/dl
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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
vitrofalsely elevated serum values.
• Observed in:
– Myeloproliferative disorders including leukemia
– Infectious mononucleosis
– Rheumatoid arthritis
2. Is this pseudohyperkalemia?
Why or why not?
NO… this is not pseudohyperkalemia since there are no
enough evidence of blood count differentials as well as no
history predisposing the patient to develop such.
Also, the presence of ECG abnormalities which require
emergency therapy is not a common indication in
pseudohyperkalemia
3. What are the clinical
manifestations of hyperkalemia in
this patient? Explain the
pathophysiology.
HYPERKALEMIA
• Excessive intake
– Uncommon cause of hyperkalemia
– Most often, hyperkalemia is caused by a relatively
high potassium intake in a patient with impaired
mechanisms for the intracellular shift of
potassium or for renal potassium excretion
• Decreased excretion
– Most common cause of hyperkalemia
• Decreased excretion of potassium, especially coupled with
excessive intake
– Decreased renal potassium excretion
• Renal failure
• Ingestion of drugs that interfere with potassium excretion
– Potassium-sparing diuretics, angiotensin-convening enzyme
inhibitors, nonsteroidal anti-inflammatory drugs
• Impaired responsiveness of the distal tubule to aldosterone
– Type IV renal tubular acidosis observed with diabetes mellitus,
sickle cell disease, or chronic partial urinary tract obstruction
• Shift from intracellular to extracellular space
– Uncommon cause of hyperkalemia
– Exacerbate hyperkalemia produced by a high intake or
impaired renal excretion of potassium.
– Clinical situations in which this mechanism is the
major cause of hyperkalemia includes
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Hyperosmolality
Rhabdomyolysis
Tumor lysis
Succinylcholine administration
– Depolarizes the cell membrane and thus permits potassium to
leave the cells
CLINICAL MANIFESTATIONS
• Weakness
– Prolonged depolarization impairs membrane
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
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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
PO
– Hemodialysis (if necessary)
• Intractable Acidosis
• Uncontrollable Hyperkalemia
• Sodium Bicarbonate
– 1 mEq/kg slow IV push or continuous IV drip