1. This lecture was conducted during the Nephrology Unit Grand Ground by Medical Student under Nephrology Division under the supervision and administration of Prof. Jamal Al Wakeel, Head of Nephrology Unit, Department of Medicine and Dr. Abdulkareem Al Suwaida, Nephrology Consultant. Nephrology Division is not responsible for the content of the presentation for it is intended for learning and /or education purpose only.

2. Hyperkalemia
Dr: fatimah al-faraj

3. Potassium homeostasis
-Gastrointestinal absorption is complete, resulting in daily excess intake of about 1 mmol/kg/d
this excess is
(10%) through the gut
(90%) excreted through the kidneys
- The most important site of regulation is the distal nephron, including the distal convoluted tubule, the connecting tubule, and the cortical collecting tubule

4. Excretion is increased by the following:
-Aldosterone
-High sodium delivery to the distal tubule (eg, diuretics)
-High urine flow (eg, osmotic diuresis)
-High serum potassium level
-Delivery of negatively charged ions to the distal
tubule (eg, bicarbonate)

5. Excretion is decreased by the following:
-Absence of aldosterone
-Low sodium delivery to the distal tubule
-Low urine flow
-Low serum potassium level
-Renal failure

6. Function of Potassium in the Body
muscle contraction
regulation of the heart contractility
important for the kidney to function normally

7. -The normal serum level of potassium is 3.5 to 5 mmol/L
-Daily Requirements 1-1,5 mmol/kg
-Dietary sources include dried fruits; legumes; meats; poultry; fish; soy; bananas; citrus fruits; potatoes; tomatoes; broccoli; mushrooms; dark, leafy green vegetables

8. Hyperkalemia
Hperkalemia is defined as a condition in which serum potassium greater than 5.3 mEq/L

9. Pseudohyperkalemia
-is the term applied to the clinical situation in which in vitro lysis of cellular contents leads to the measurement of a high serum potassium level not reflective of the true in vivo level.
-condition occurs most commonly with
red cell hemolysis during the blood draw (tourniquet too tight or the blood left sitting too long),

10. causes Excessive intake Decreased excretion
Shift from intracellular to extracellular space

11. Excessive intake - uncommon cause of hyperkalemia.
-The mechanisms for shifting potassium intracellularly and for renal excretion allow a person with normal potassium homeostatic mechanisms to ingest virtually unlimited quantities of potassium in healthy individuals.
-Most often, it is caused in a patient with impaired mechanisms for the intracellular shift of potassium or for renal potassium excretion

12. Decreased excretion -is the most common cause
-The causes of decreased renal potassium excretion include:
renal failure
diabetes mellitus
sickle cell disease
medications (eg, potassium-sparing diuretics, NSAID,angiotensin-convening enzyme inhibitors)

13. Shift from intracellular to extracellular space
- uncommon alone
-but can exacerbate hyperkalemia produced by a high intake or
impaired renal excretion of potassium.
-It can be the major cause of hyperkalemia in
hyperosmolalit,
rhabdomyolysis,
tumor lysis,
succinylcholine administration,
insulin deficiency or acute acidosis.

14. Causes Shift from (ICF to ECF) Decreased renal excretion
Excessive intake
Hyperosmolality
rhabdomyolysis
tumor lysis
Succinylcholin
insulin deficiency
acute acidosis.
Diabetes mellitus (esp diabetic nephropathy
Renal failure
Congestive heart failure
SLE
Sickle cell anemia
NSAID
ACE Inhibitor
Potassium sparing Diuretics
Multiple Myeloma
chronic partial urinary tract obstruction
Oral or IV Potassium Supplementation
Salt substitute
Blood transfusion

15. Symptoms weakness and fatigue(most common) frank muscle paralysis
shortness of breath
palpitations

16. Physical -vital signs generally are normal except
bradycardia due to heart block
or tachypnea due to respiratory muscle weakness.

17. Lab Assess renal function.
Check serum BUN and creatinine levels to determine whether renal insufficiency is present
Check 24-hour urine for creatinine clearance
Estimate the glomerular filtration rate (GFR)

18. Measure complete blood count.
-A low hemoglobin and hematocrit or abnormal red cell morphology may suggest hemolysis.
-Severe leukocytosis or thrombocytosis raises the possibility
of pseudohyperkalemia.

19. ECG Changes occur when Serum Potassium >6.0 mmol /L A-Initial
T Waves peaked or Tented
B-Next
ST depression
loss of P Wave
QRS widening
C-Final
Biphasic wave (sine wave) QRS and T fusion

23. Measure complete metabolic profile
-Low bicarbonate may suggest hyperkalemia due to metabolic acidosis.
-Hyperglycemia suggests diabetes mellitus.

24. -A creatine kinase (CK) elevation suggests rhabdomyolysis.
-Elevated lactic dehydrogenase (LDH), uric acid, phosphate, and alanine aminotransferase (ALT) may suggest tissue breakdown, as occurs in hemolysis, rhabdomyolysis, or
tumor lysis.

25. Treatment The first step -determine life-threatening toxicity.
By Perform an ECG to look for cardiotoxicity.
- if present
Administer Iv Calcium Gluconate to ameliorate cardiac toxicity.
-Initial dose: 10 ml over 2-5 minutes
Second dose after 5 minutes if no response
-Effect occurs in minutes and lasts for minutes
Anticipate EKG improvement within 3 minutes

26. The second step
-is to identify and remove sources of potassium intake
-Change the diet to a low-potassium diet.

27. The third step -Potassium shift from intravascular to intracellular
-Glucose and Insulin Infusion
Insulin Regular 10 units IV
50 ml 50% of dextrose
Every mints
-Measure glucose and potassium every 2 hours
-Correct metabolic acidosis with sodium bicarbonate. 50ml 50% bolus

28. -is to increase potassium excretion from the body
The fourth step
-is to increase potassium excretion from the body
-in normal kidney function by the administration of parenteral saline accompanied by a loop diuretic, such as furosemide Dose: mg IV.

29. -Discontinue potassium-sparing diuretics, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and other drugs that inhibit renal potassium
excretion.
Monitor volume status and aim to maintain euvolemia.
-in patients with hyporeninemia or hypoaldosteronism Renal excretion can be enhanced by administration of an aldosterone analogue, such as 9-alpha fluorohydrocortisone acetate (Florinef).

30. Emergency dialysis
is a final recourse for unresponsive hyperkalemia with renal failure.

32. thanks