Hyperkalemia
– an emergency?
Shaila Sukthankar
Paediatric Nephrology Study Day
22.06.12
RMCH
Hyperkalemia

Overview

Clinical cases

Emergency Management
Hyperkalemia - causes
Spurious/ pseudohyperkalemia
 Increased intake
 Trans-cellular shift
 Decreased renal tubular excretion

– Renal
– Endocrine
– Drugs
Investigations

Renal
– U&Es, acid base balance, urinalysis
– TTKG (urine K X P osmol/ plasma K X U osmol)

Endocrine
– For another meeting!
– Renin, aldosterone, urinary steroids, 17-OHP

Others
– FBC, blood film, urate, CK, calcium, phosphate
Case 1
ER, 15 years old girl
 Known to have IDDM for several years
 Difficult family circumstances but ER very well
engaged and compliant
 Recent annual diabetes review 3 months before
admission - good glycaemic control
 Blood tests unremarkable, urine microalbumin/
creatinine ratio normal
 Growth – weight and height 2nd to 9th and
postpubertal

Clinical Presentation
Diarrhoeal illness for 1 week – mucus, no
blood. Initially polyuric and nocturic, now
decreased urine output
 Parents noticed her to be pale and tired lately
 Examination – pale, BP 130/ 86, hydration
and perfusion normal
 Urine 3+ glucose, ketones ++

Initial investigations
CBG: pH 7.2, BE –10, Bicarb 15
 Na 128, K 6.5, urea 23
 Hb 9.8, WCC 5.8
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Further investigations
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Platelet 240
Glucose 7.8
Creatinine 210
Ca 1.9, Pi 2.8
Blood film – normal RBC and platelet
morphology
Urine 2+ protein, 3+ blood with casts
Immediate measures
Stop external sources of K
 Stabilise myocardium

– IV calcium gluconate

Enhance intracellular shift of K
– Nebulised Salbutamol
– Sodium Bicarbonate
– Glucose Insulin infusion

Increase excretion
– Ion exchange resin
– Dialysis
Calcium Gluconate
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If K >7 mmol/ L or ECG changes
10% solution
0.5 ml/ Kg (maximum 20ml) over 10 minutes
With ECG control via large peripheral or
central line
Protects myocardium from acute dysrhythmia,
no effect on K levels
Salbutamol
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First line treatment – nebulised
2.5mg up to 5 years age, 5mg there after
Can be repeated up to 3 times
Alternatively, if access available, IV
salbutamol
–
–
–
–

4mcg/ kg
diluted with normal saline or glucose
50mcg/ml concentration
Over 5 min as slow bolus
Does not lower net K, shifts from ECF to ICF
Sodium Bicarbonate
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In presence of acidosis
8.4% solution
1ml (1mmol)/ Kg
Diluted to minimum 1:10 with normal saline/
glucose for peripheral venous use (1:5 for
central access)
Infusion over 30 minutes
Shifts K from ECF to ICF
Glucose Insulin infusion
Soluble short acting insulin (0.1 U/ Kg)
 Mixed in 5 – 10 ml/ Kg of 10% dextrose for
peripheral use (2.5 to 5 ml of 20% dextrose
for central access)
 Infused over 30 minutes
 Check BM every 15 minutes by POCT – until
15 minutes after infusion

Calcium Resonium
Oral (not neonates) or rectal
 125-250 mg/ kg qds (maximum 15gm per
dose)
 If given orally, also use lactulose
 Lowers total body K by excretion in stools

Further management
Treatment of underlying cause – DKA
management, endocrine, renal etc
 Renal replacement modalities

– Haemodialysis for rapid effective reduction in K
levels
– Peritoneal dialysis is as effective but over longer
duration
– Haemofiltration – if already on ICU
After emergency treatment…

Recheck U&Es after 15 minutes of initial
intervention to ensure
– treatment is effective
– Level is reaching safe range
Recheck after 1 – 2 hours to detect rebound
hyperkalemia
 Look for underlying cause

ER - update
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Required nebulised salbutamol and Ca
gluconate at local DGH
Transferred to RMCH and started on dialysis
the same day
Had immune work up and renal biopsy
GFR reduced to <10 (ESRD) – CKD5
management
On dialysis
Had living related donor kidney transplant
Case 2
3 years, boy, previously well
 Presented with fever and frequent URI
 Growth, examination normal
 Blood tests
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–
–
–
–
FBC normal, mild iron deficiency
Na 135, K 6.8, U 4.5, Creatinine 35
pH 7.3 BE – 8, sugar 4.8, urine NAD
ECG nSR
Case 2 continues…
Plasma renin and aldosterone low
 Synacthen test and 17-OHP normal
 Diagnosis??

– Hyporeninemic hypoaldosteronism
– Pseudohypoaldosteronism
Gordon’s syndrome (PHA 2)
Tubulopathy affecting chloride channels,
decreased potassium excretion (WNK1, WNK4
AR mutation)
 Responded well to thiazide diuretics
 Younger twin siblings also affected
 All currently well with normal K levels on
thiazide treatment

Summary

Acute, severe, true hyperkalemia
– is a medical emergency
– requires prompt recognition and optimum
treatment
Not all hyperkalemia is renal in origin
 Specialist input required to establish etiology
and long term management

Specialist Input
Assessment
Action
Abnormal renal function
D/w Nephrology
Massive hemolysis/
rhabdomyolysis or tumor
lysis
Normal renal function
D/w Nephrology
(+ hemato-oncology)
Uncertain
D/w All
D/w Endocrinology (+/nephrology)