Hyperkalemia final

HYPERKALEMIA
Presenter: Dr. Nikhil

DEFINITION
 It is defined as a serum potassium concentration greater than
5.5mEq/L.
 The normal serum concentration range for potassium is 3.5-
5.0mEq/L

CAUSES OF HYPERKALEMIA :
I. Pseudohyperkalemia
II. Intra- to extracellular shift
III. Inadequate excretion

I. Pseudohyperkalemia
• Factitious hyperkalemia
•Artifactual increase in serum K+ due to the release of K+ during or after
venipuncture.
• Causes :
(a) In-vitro hemolysis.
(b) Marked leukocytosis or thrombocytosis

II. Intra- to extracellular shift
A. Acidosis
B. Hypertonicity
C. Digoxin and related glycosides (yellow oleander)
D. Succinylcholine; thermal trauma, neuromuscular injury, disuse
atrophy, mucositis, or prolonged immobilization
E. Rapid tumor lysis

(A) ACIDOSIS :
Acidemia → cellular uptake of H+ → efflux of K+
(B) HYPEROSMOLALITY
- Due to osmotic gradient ("solvent drag" effect)
-Hyperkalemia due to hypertonic mannitol, hypertonic saline, and
intravenous immune globulin is due to osmotic gradient.
-Diabetics are also prone to osmotic hyperkalemia in response to
intravenous hypertonic glucose, when given without adequate insulin.

(C) DIGOXIN
• Digoxin → inhibits Na+/K+-ATPase → impairs uptake of K+ so, digoxin
overdose → hyperkalemia.
• Structurally related glycosides found in yellow oleander or foxglove

• (D) SUCCINYLCHOLINE
• SCh → depolarizes muscle cells→ efflux of K+ through
acetylcholine receptors (AChRs).
• Contraindicated in patients who have sustained thermal
trauma, neuromuscular injury, disuse atrophy, mucositis, or
prolonged immobilization because it leads to an exaggerated
efflux of K+ causing acute hyperkalaemia.

(F) EXCESS INTAKE OR TISSUE NECROSIS
Following conditions provoke severe hyperkalemia in
susceptible patients :
Foods rich in potassium include tomatoes, bananas, and citrus
fruits;
 Red cell transfusion, typically massive transfusions.
Finally, severe tissue necrosis, as in acute tumor lysis
syndrome and rhabdomyolysis.

• III. Inadequate excretion
A.Inhibition of RAAS; ↑ risk of hyperkalemia when used in combination :
 ACE inhibitors, ARBs, Mineralocorticoidreceptor
blockers, Blockade of the ENaC
B. Decreased distal delivery eg., CHF
C. Hyporeninemic hypoaldosteronism
1. Tubulointerstitial diseases: SLE, sickle cell anemia
2. Diabetes, diabetic nephropathy
3. Drugs: NSAIDs, β-blockers, cyclosporine
4. Chronic kidney disease, advanced age

D. Advanced renal insufficiency eg., CKD, ESRD
E. Primary adrenal insufficiency
1. Autoimmune: Addison’s disease
2. Infectious: HIV, CMV, TB
3. Infiltrative: amyloidosis, malignancy
4. Drug-associated: heparin, LMWH
5. Hereditary: adrenal hypoplasia congenita

CLINICAL FEATURES
-Medical emergency due to its effects on heart, i.e., cardiac
arrhythmias.
 Most of Hyperkalemic individuals are asymptomatic.
 If present- symptoms are nonspecific and predominantly related to
muscular or cardiac functions.
 The most common - weakness and fatigue.
 Occasionally,frank muscle paralysis or shortness of breath.
 Patients also may complain of palpitations or chest pain.
 Arrythmias occur- Sinus Brady, Sinus arrest, VT, VF,
Asystole
 Patients may report nausea, vomiting, and paresthesias

DIAGNOSTIC APPROACH
•First priority is to assess the need for emergency treatment, followed
by a comprehensive workup to determine the cause.

Trans-tubular potassium gradient (TTKG) :
- index reflecting the conservation of potassium in the cortical
collecting ducts (CCD) of the kidneys.

TREATMENT :
The treatment of hyperkalemia is divided into three stages:
1.Immediate antagonism of the cardiac effects of hyperkalemia
- Intravenous calcium
2.Rapid reduction in plasma K+ concentration by redistribution
into cells
• Insulin
• β2-agonists (most commonly albuterol)
3. Removal of potassium
- using cation exchange resins, diuretics, and/or dialysis.
- Hemodialysis is the most effective and reliable method to reduce
plasma K+ concentration.

Drugs Dosage ONSET
Length of MOA
effect
Cautions
Ca2+
gluconate
10 mL of
10% solution
IV over 10
minutes
Immediate 30 minutes
from toxic
effects of
Ca2+
Protects Can worsen
myocardium digoxin
toxicity
Insulin Regular
insulin 10
units IV with
50 mL of
50% glucose
15-30
minutes
2-6 hrs. Shifts K+ out
of the
vascular
space and
into the cells
Consider 5% Dextrose solution infusion at 100 mL/hr to prevent hypoglycemia
with repeated doses. Glucose unnecessary if blood sugar elevated above
250mg/dL
Albuterol
(Ventolin)
10-20 mg by
nebulizer
over 10
minutes (use
conc. form,
5mg/mL)
15-30 2-3 hrs.
minutes
Shifts K+
into the
cells,
additive to
the effect of
insulin
May cause a
brief initial
rise in
serum
potassium

Drugs Dosage Onset Length of
effect
MOA Cautions
Furosemide
(Lasix)
20-40 mg IV,
give with
saline if
volume
depletion is a
15 min. - 1
hr.
4 hrs. Increases
renal
excretion of
potassium
Only
effective if
adequate
renal
response to
concern loop diuretic
Sodium
polystyrene
sulfonate
(Kayexalate)
Oral : 50 g in
30 mL of
sorbitol
solution
Rectal : 50 g
in a retention
1-2 hrs.
(Rectal
route is
faster)
4-6 hrs. Removes
potassium
from the gut
in exchange
for sodium
Sorbitol may
be
associated
with Bowel
necrosis.
enema

Hyperkalemia final

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