Transcript Hyperkalemia

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.
Hyperkalemia
Dr: fatimah al-faraj
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
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)
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
Function of Potassium in the Body
muscle contraction
regulation of the heart contractility
important for the kidney to function normally
-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
Hyperkalemia
Hperkalemia is defined as a condition in which
serum potassium greater than 5.3 mEq/L
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),
causes
Excessive intake
Decreased excretion
Shift from intracellular to extracellular space
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
Decreased excretion
-is the most common cause
-The causes of decreased renal potassium excretion include:-
renal failurediabetes mellitus
sickle cell disease
medications (eg, potassium-sparing diuretics,
NSAID,angiotensin-convening enzyme inhibitors)
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.
Causes
Excessive intake
Decreased renal excretion
Shift from (ICF to
ECF)
Oral or IV
Potassium
Supplementation
Diabetes mellitus (esp diabetic
nephropathy
Hyperosmolality
rhabdomyolysis
Renal failure
tumor lysis
Salt substitute
Congestive heart failure
Succinylcholin
SLE
Blood transfusion
insulin deficiency
Sickle cell anemia
acute acidosis.
NSAID
ACE Inhibitor
Potassium sparing Diuretics
Multiple Myeloma
chronic partial urinary tract obstruction
Symptoms
weakness and fatigue(most common)
frank muscle paralysis
shortness of breath
palpitations
Physical
-vital signs generally are normal
except
bradycardia due to heart block
or tachypnea due to respiratory muscle weakness.
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)
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.
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
Measure complete metabolic profile
-Low bicarbonate may suggest hyperkalemia due to
metabolic acidosis.
-Hyperglycemia suggests diabetes mellitus.
-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.
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 30-60 minutes
Anticipate EKG improvement within 3 minutes
The second step
-is to identify and remove sources of potassium intake
-Change the diet to a low-potassium diet.
The third step
-Potassium shift from intravascular to intracellular
-Glucose and Insulin Infusion
Insulin Regular 10 units IV
50 ml 50% of dextrose
Every 15- 30 mints
-Measure glucose and potassium every 2 hours
-Correct metabolic acidosis with sodium bicarbonate.
50ml 50% bolus
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: 20-40 mg IV.
-Discontinue potassium-sparing diuretics, angiotensinconverting 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).
Emergency dialysis
is a final recourse for unresponsive
hyperkalemia with renal failure.
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