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| Journal of the New Zealand Medical Association,
29-April-2011, Vol 124 No 1333
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Hyperkalaemic paralysis
David Hamilton, Sergej Cicovic, Mark Rassie
Hyperkalaemia is associated with cardiac manifestations with
characteristic electrocardiogram (ECG) changes. It rarely presents with acute
tetra-paralysis. We present a case of secondary hyperkalaemic paralysis.
Case reportA 46-year-old gentleman presented with lethargy, nausea,
vomiting and acute ascending weakness. He had end-stage renal failure secondary
to diabetes and was on home haemodialysis. He dialysed every second day. He had
Type 2 diabetes (on insulin), hypertension (on quinapril and metoprolol),
anxiety and depression (on citalopram). Other medications were alphacalcidol,
calcium carbonate, aluminium hydroxide, erythropoietin, simvastatin, frusemide
and ranitidine.
He was transported to the hospital via ambulance. He
complained of weakness in his legs. He had not completed his most recent
haemodialysis which was due 3 days previously. On route he became hypotensive
(60 mmHg systolic) and bradycardic (35/min). Intravenous adrenalin was commenced
and systolic blood pressure improved to 100 mmHg systolic.
On presentation to hospital the weakness ascended and
involved his upper limbs. He was afebrile, had a blood pressure of 136/70 mmHg,
pulse rate of 30/min and O₂ saturation of 100% on air. JVP was at the
angle of the jaw. There was bilateral, symmetrical weakness of the upper and
lower limbs (power 1-2/5). Reflexes and plantar responses were reduced.
Venous blood gas analysis showed a pH of 7.24, bicarbonate
of 15.0 and a base excess of -9.8. ECG showed a junctional bradycardia with
peaked T-waves. Blood tests revealed blood glucose 5.9, serum sodium 130, serum
potassium 7.9, haemoglobin 126, WBC 11.7, platelets 270, urea 43.6, creatinine
1390, calcium 2.29 and phosphate 2.38.
His hyperkalaemia was initially managed with calcium
gluconate and intravenous insulin. He was transferred to the renal ward where
haemodialysis was commenced. He was dialysed for 4 hours and throughout the
procedure his tetraparesis gradually improved—this was correlated with a
reduction in repeated serum potassium (5.0). A repeat ECG showed normal sinus
rhythm. His power was 5/5 universally. He received haemodialysis the following
day and was asymptomatic for the remainder of admission.
He had two further presentations of tetra-paresis. Both were
associated with hyperkalaemia and improved during haemodialysis. The episodes
were due to chronic renal failure and non-compliance with haemodialysis.
DiscussionThere are primary and secondary forms of hyperkalaemic
paralysis.
Primary hyperkalaemic paralysis involves a genetically
determined defect in sodium ion channels of muscle fibre plasma
membranes.1,2 Presentations of flaccid
paralysis happen in the first decade. The attacks last from a few minutes to
hours but rarely exceed 4 hours. The attacks are initially infrequent and tend
to increase in frequency and severity over
time.1 Common triggers include rest after
exercise and intake of potassium.1,2
Salbutamol, intravenous calcium gluconate and acetazolamide all successfully
treat attacks.1,2
The exact mechanism of secondary hyperkalaemic paralysis is
not known. It may be due to potassium directly affecting the muscle cell
membrane or the peripheral nerves.3 Patients
present later in life. Evers et al described 18 cases.
4 Presentation classically involved an
ascending flaccid paralysis with mild or no sensory deficit and spared cranial
nerves. It may be mistaken for Guillain-Barré
syndrome.4
Attacks are usually precipitated by chronic renal
failure4 but have also been reported secondary
to potassium sparing diuretics,5 ACE
inhibitors,6 nonsteroidal
anti-inflammatories,7 postoperative renal
impairment8 and traumatic rupture of the
bladder.9
Management involves correcting physiological disturbance,
repeated ECGs and monitoring serum potassium. Treatment is through correcting
hyperkalaemia through calcium infusion, insulin, salbutamol or dialysis.
Long-term management involves reducing dietary potassium, avoidance of
predisposing medications and compliance with dialysis.
The prognosis for secondary hyperkalaemic paralysis is good
if recognised and managed appropriately; reported deaths were due to
arrhythmias.4 There have been reports where no
ECG changes have been present.5 Therefore both
an ECG and serum potassium levels should be obtained in patients presenting with
acute paralysis.
There must be a universal awareness because if not
recognised, secondary hyperkalaemic paralysis can be a fatal condition.
Author information: David Hamilton,
Nephrologist; Sergej Cicovic, Trainee Intern; Mark Rassie, Trainee Intern;
University of Auckland
Correspondence: Sergej Cicovic, Trainee
Intern, University of Auckland, Private Bag 92019, Victoria Street West,
Auckland, New Zealand. Email: scic001@aucklanduni.ac.nz
References:
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