MANAGEMENT OF

HYPERKALEMIA
BY DR. ORBUNDE PRECIOUS WASHIMA
UNIT PRESENTATION

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OUTLINE
Introduction
Physiology
Pathophysiology
Definition
Classification
Causes
Clinicalfeatures
Investigation
Treatment
Conclusion
References

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INTRODUCTION

The most common and most serious

electrolyte derangement emergency in
clinical practice!!!
As a result of serum K concentration
greater than the upper limit (normal range
3.5-5.0mEq/L)
It is important for normal functioning of
neurones and myocyte
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PHYSIOLOGY
Potassium is a major intracellular cation
Total body K+ content in a normal adult
3000-4000mEq
98% intracellular, 2% in ECF.
Normal homeostatic mechanisms
maintain the serum K level within a
narrow range (3.5-5.0mEq/L).

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The primary mechanisms maintaining this
balance are the buffering of ECF
potassium against a large ICF potassium
pool ( via the Na – K pump)
Na+ – K+ ATPase pump actively
transports Na+ out of the cell and K+ into
the cell in a ratio 3:2 ratio.
Renal excretion – Major route of excess
K+ elimination
Approx 90% of K+ excretion occurs in
the urine.
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Less than 10% excreted through sweat or
stool.
Within the kidneys, K+ excretion occurs
mostly in the principal cells of the cortical
collecting duct (CCD).

Urinary K+ excretion depends on:

1.) Luminal Na+ delivery to the DCT and the
CCD.
2.) Effect of Aldosterone and other adrenal
corticosteroids with mineralocorticoid
activity.
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PATHOPHYSIOLOGY
Hyperkalemia may occur either because of
 Redistribution of potassium between the ICF and ECF
 Intake exceeds excretion.
The redistribution of potassium from ICF to
the ECF may occur in the presence of
systemic acidosis or when the circulating
level of insulin, catecholamines and
aldosterone are reduced or when the effects
of these hormones are blocked.

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High potassium intake may contribute to
hyperkalemia but seldom the only
explanation unless renal excretion
mechanisms are impaired.
Intake; Exogenous (diet, IV therapy)
Endogenous (haemolysis,
rbadomyolysis)

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HYPERKALEMIA
Defined
as plasma potassium level of
>5.5mEq/L.

Severe hyperkalemia when serum

potassium levels are >6.5mEq/L.

Decrease in renal excretion is the most

frequent cause.

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CLASSIFICATION
Hyperkalemia could be
Mild
Moderate
Severe

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CAUSES
Increased intake (oral / IV )
a. Dietary : banana, plantain, green vegetable,
potash, fruits.
b. Medication : K sparing drugs (S A T )
ACE inhibitors (captopril, enapril)
NSAID’s (aspirin-salisylic acid)
Angiotensin II receptor blockers
(losartan)
Anticoagulants (heparin)
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CAUSES
Increased endogenous production :
a. severe burns
b. crush injury
c. cellular damage(rhabdomyolysis) –

excess blood transfusion, haemolysis,

leucocytosis

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CAUSES
Renal causes :
a. Insufficient Na exchange
(Acute/Chronic renal failure )
b. Decreased Na/K exchange –
hypoaldosteronism (Addison’s)
pseudohypoaldosteronism

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CAUSES
Redistribution causes :
Acidosis
Hypoxia
Severe tissue damage
Alpha adrenergic stimulants

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CAUSES
Iatrogenic / pseudohyperkalemia
prolonged tourniquet time
delayed separation time
K EDTA containers
fisting of the hand
Familial hyperkalemic periodic
paralysis

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FEATURES
Neuromuscular:
weakness, paraesthesia, flaccid paralysis,
hyporeflexia, hypotonia, decreased
respiratory tone
GIT :
nausea, vomiting, ileus, obstruction
(distension, pain, constipation)
CNS :
lethargy, confusion, mental retardation
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FEATURES
CVS:
bradycardia, arrhythmias, conduction
defects, peripheral vascular collapse,
cardiac arrest @ DIASTOLE
ECG changes :
wide QRS complex
wide PR interval
tall tented T-waves
ventricular arrhythmias
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ECG FINDINGS OF HYPERKALEMIA

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INVESTIGATIONS
AIMS :
to determine severity
to determine the cause
1. Serum U&E (K: 3.6-5.2mmol/L)
2. Urinalysis
3. ECG (wide QRS complex, tall T-waves)
4. Serum glucose (r/o DM, insulinoma)
5. Hormone analysis (cortisol, aldosterone)
6. TTKG – transtubular K gradient
= urinary K X plasma osmolality
plasma K X urine osmolality
if < 3, mineralocorticoid deficiency
If > 3, on potassium supplements or high intake

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Rule out artefactual causes – Prolonged
tourniquet, contaminated bottles, use of
supplements, hemolytic causes, diuretics,
hypoxia, severe trauma

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TREATMENT
AIMS:
To return plasma K level to normal
To treat the underlying cause
PRINCIPLES:
Stabilize cell membrane
shift potassium into cells
remove excess from the body

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TREATMENT
Stabilize cell membrane •10% Ca gluconate 10mls over
10mins (for severe hyperkalemia)
Shift potassium into cells •Inhaled beta 2 adrenergic agonists –
salbutamol
•Insulin with glucose – 50mls of 50%
soln (IV)
•NaHCO3 – 100mls
Remove excess potassium •Frusemide & N/S (IV)
•Ion exchange resin – Resonium A
oral or enema
•Dialysis

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CONCLUSION
Hyperkalemia remains a common
problem encountered in clinical practice.
It can present in a myriad of ways, most
of which are often non-specific and an
understanding of these is valuable to the
clinician
Early identification and appropriate
correction can help prevent significant
morbidity and mortality
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REFERENCES
Encyclopedia of Human Nutrition (Third
Edition) by L J Appel, 2013
Kapoor R, Moseley RH, Kapoor JR, et al.
Clinical problem-solving. Needle in a
haystack. N Engl J Med. 2009 Feb 5.
360(6):616-21. [Medline]
Zacchia M, Abategiovanni ML, Stratigis S,
Capasso G. Potassium: From Physiology to
Clinical Implications. Kidney Dis (Basel).
2016 Jun. 2 (2):72-9. [Medline].
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THANK YOU!!!!

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