Hyperkalemia prof. ahmed hassan

Dr. Ahmed Hassan MD
ASS. Prof. of Nephrology
National Institute Of Urology & Nephrology
ESNT- EFS. Cairo Sep 12/9/2018

National Institute Of Urology And
Nephrology

Identify the causes of hyperkalemia
Discuss the pathophysiology of hyperkalemia
Clarify the possible clinical manifestation
Enumerate possible diffrential diagnosis
Identify diagnostic measures of hyperkalemia
Thinking about the proper measures of treatment
of hyperkalemia
Objectives

Hormonal effect sites

 Ineffective elimination
Excessive release from cells
Excessive intake
Pseudohyperkalemia
Familial pseudohyperkalaemia

Renal insufficient
Medication
Mineralocorticoid deficiency or resistant.
Type IV renal tubular acidosis (resistance of
renal tubules to aldosterone)
Gordon's syndrome
(pseudohypoaldosteronism type II) (familial
hypertension with hyperkalemia).

Hyperkalemia
K sparing diuretics
ACEI
Heparin
Antineoplastic agents
Isonaizid
NSAIDS
Lithium
B Blockers
Tetracycline
Ciclosporine

Rhabdomyolysis
Burns
Tumor lysis syndrome.
Massive blood transfusion
Massive hemolysis
Shifts(transport out of cells = redistributional)
acidosis,
low insulin levels,
beta-blocker therapy
Excessive Release From Cells

Excessive intake with salt-substitute,
potassium-containing dietary supplements, or
potassium chloride (KCl) infusion.
a person with normal kidney function and
normal elimination, hyperkalemia seen only
with large infusions of KCl or oral doses of
several hundred milliequivalents of KCl.
Excessive Intake

Due to excessive leakage of potassium from
cells, during or after blood is drawn (a
laboratory artifact ).
Hemolysis during venipuncture
Excessive tourniquet time
A delay in the processing of the blood specimen
Platelets (>500,000/mm³
Leukocytes (> 70 000/mm³)
Erythrocytes (hematocrit > 55%).
Pseudohyperkalemia

 Adominant red-cell trait
 Due to mutations in Langereis blood group
antigen (ABCB6 gene, is located on the long
arm of chromosome 2) , which encodes an
erythrocyte membrane porphyrin transporter.
Characterized by increased serum potassium
in whole blood stored at or below room
temperature.
Familial Pseudohyperkalaemia

 Asymptomatic
Frank muscle paralysis (weakness)
Dyspnea
Palpitations (bradycardia)
Chest pain
Nausea or vomiting/Hypoactive or absent
bowel sounds (ileus)
Paresthesias/depressed or absent deep tendon
reflexes.
Clinical Manifestation

Acidosis, Metabolic
Acute Tubular Necrosis
Burns, Electrical/ Thermal
Congenital Adrenal Hyperplasia
Head Trauma
Hypocalcemia
Rhabdomyolysis
Tumor Lysis Syndrome
Differential Diagnoses

Diagnoses

Repeated samples of potassium (normal
serum level of potassium is 3.5 to 5 mEq/L).
Electrocardiography (EKG/ECG) to determine
cardiac arrhythmias.
Renal function (creatinine, blood urea
nitrogen)
Renal ultrasound.

CBC ( hemolysis / pseudohyperkalemia)
LDH, uric acid, phosphate, and ALT levels
(tissue breakdown)
Decreased serum cortisol, renin, & aldosterone
Glucose level – (diabetes mellitus).
Arterial or venous blood gas
CPK and calcium measurements
Urine myoglobin test
Diagnosis

Measuring elevated plasma 11-deoxycortisol
levels or urinary tetrahydro-ll-deoxycortisol
levels
 Measurement of elevated 17-hydroxy-
progesterone levels (generally 90-1200 nmol/L)
in blood.
Diagnosis

TTKG = (urine potassium X serum osmolarity)
/ (serum potassium X urine osmolarity)
A TTKG < 7 suggests a lack of aldosterone effect
on the collecting tubules .
A TTKG >7 suggests an adequate aldosterone
effect.
Diagnosis
TTKG= transtubular K gradient

ECG Changes In Hyperkalemia

Serum K : 5-6.5 mEq/L

Serum K : 6.5 -8 mEq/L

Serum K : > 8 mEq/L

Treatment

The first step is to administer IV calcium to
ameliorate cardiac toxicity.
The second step is to identify and remove
sources of potassium intake.
Discontinue oral and parenteral potassium
supplements.
Remove potassium-containing salt substitutes.
Change the diet to a low-potassium diet.
Treatment

The third step is to enhance K uptake by cells.:
Parenteral glucose + insulin infusions.
The onset of action is within 20-30 minutes,
The duration is variable, (2 to 6 hours).
Beta-adrenergic agonists : nebulized albuterol.
The dose for treating hyperkalemia, 10 mg.
Sodium bicarbonate to Correct metabolic
acidosis (less effective and less predictable).
Treatment

The fourth step is to increase K excretion from the
body:
IV saline accompanied by a loop diuretic.
Discontinue potassium-sparing diuretics, ACE,
ARBs, and other drugs that inhibit renal potassium
excretion.
fluorohydrocortisone acetate adminsteration in
patients with hyporeninemia or hypoaldosteronism
cation exchange resins such as sodium
polystyrene sulfonate orally or rectaly (GIT
excretion).
Treatment

The fifth step:
Emergency dialysis:
unresponsive to more conservative measures
for patients who have complete renal failure
Finally, it is important to determine the cause
of hyperkalemia in order to prevent future
episodes.
Treatment

Summary
Potassium is critical for the normal
functioning of the muscles, heart, and nerves. It
plays an important role in controlling activity of
smooth muscle (such as the muscle found in the
digestive tract) and skeletal muscle (muscles of
the extremities and torso), as well as the muscles
of the heart. It is also important for normal
transmission of electrical signals throughout the
nervous system within the body.

Summary
hyperkalemia means an abnormally elevated level of
potassium in the blood (> 5 mEq/L).
it is diagnosed in up to 8% of hospitalized patients.
 Any condition causing mild hyperkalemia should be
treated to prevent progression into more severe
hyperkalemia.
Severe hyperkalemia can lead to cardiac arrest and
death (a mortality rate of about 67% if not recognised
and treated properly).

On which of the following does aldosterone
exert its greatest effect?
A. Glomerulus
B. Proximal tubule
C. Thin portion of the loop of Henle
D. Thick portion of the loop of Henle
E. Cortical collecting duct
MCQ QUESTIONS
Answer E

Which of the following causes hyperkalemia?
A. Exercise
B. Alkalosis
C. Insulin injection
D. Decreased serum osmolarity
E. Treatment with β-agonists
MCQ QUESTIONS
Answer A

All of the following may occur due to
hyperkalemia except?
A. Prolonged PR interval
B. Prolonged QRS interval
C. Prolonged QT interval
D. Ventricular asystole
E. Shortening QT interval
MCQ QUESTIONS
Answer C

Cardiotoxic effect of hyperkalemia increased
by:
A. Hypernatremia
B. Hypercalcemia
C. Hypocalcemia
D. Alkalosis
E. Hypermagnesemia
MCQ QUESTIONS
Answer: C

In a patient who has developed severe hyperkalemia
and associated changes on ECG (peaked T waves,
widened QRS complex).
Administration of which of the following is the
most appropriate initial therapy?
A. A ß2-agonist, via a nebulizer
B. IV Calcium gluconate
C. IV Insulin plus glucose
D. Urgent hemodialysis
E. Sodium polystyrene sulfonate, orally
MCQ QUESTIONS
Answer B

A patient with long standing diabetic renal disease
and hyperkalemia and recent onset congestive heart
failure requires a diuretic
Which of the followingwould be LEAST harmful in a
patient with Hyperkalemia?
A. Amiloride
B. Hydrochlorothiazide
C. Spironolactone
D. Triamterene
MCQ QUESTIONS
Answer B

A 65-year-old diabetic with a creatinine of 1.6 was
started on an ACEI for hypertension and presents to the
emergency room with weakness. His other medications
include a statin for hypercholesterolemia, a beta
blocker and spironolactone for congestive heart
failure, insulin for diabetes, and aspirin. Laboratory
examinations include: K: 7.2 meq/L Creatinine: 1.8
Glucose: 400 mg/dL CPK: 400 IU/L.
MCQ QUESTIONS

A- Worsening renal function
B- Uncontrolled diabetes
C- Statin-induced rhabdomyolysis
D- Drug-induced defects in the renin-
angiotensin-aldosterone system
Which is the most important cause of
hyperkalemia in this patient?
Answer D

Thank you

Hyperkalemia prof. ahmed hassan

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