A Simple and Rapid Approach to Hypokalemic Paralysis in

Emergency Department -Three Cases Report

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Introduction
Acute muscle weakness with severe hypokalemia is not unusually encountered in the
emergency department. The first step is to clarify two different etiologies. The one is
hypokalemic periodic paralysis(HPP), which is due to an acute shift of K

into cells
without total !ody K

deficit. The other is non"HPP, primarily due to e#cessive
e#cretion of K

. $ailure to clarify these two different etiologies may give to improper

management. The therapy of HPP re%uires only small doses of potassium replacement
to avoid re!ound hyperkalemia. As the clinical presentations !etween them are almost
similar, the use of spot urine for K

e#cretion rate and evaluation of !lood acid"!ase

status may !e clinically !eneficial in the diagnosis and management.
Case reports
Case 1: Hypokalemia, weakness, and a normal acid-base state
A &'"year"old male presented with sudden onset of general muscular weakness of
all e#tremities and ina!ility to am!ulate upon awakening. (o significant findings
were found on his medical and family history. )n physical e#amination, his !lood
pressure was high(*+,-,. mmHg), as was his heart rate(*', !eats-min). The principal
findings were diffusely enlarged thyroid gland and total paralysis of all e#tremities.
/iochemical studies are shown in ta!le *. He did not have an acid"!ase disorder and
K
+
e#cretion was low and transtu!ular potassium gradient(TTK0) of *.1.
He was treated with intravenous K23 at a rate of *4 mmol-hr. However,
hyperkalemia +.' mmol-3 was o!served two hours after recovery.His T& and T.
levels were elevated while T5H was suppressed. His hyperthyroidism was treated
with oral propylthiouracil and propranolol. His thyroto#ic periodic paralysis did not
recur and he has remained clinically euthyroid through the following half an year
follow up.
Case 2: Hypokalemia, weakness , and metabolic acidosis
A '1"year"old female was !rought to the emergency room !ecause of an ina!ility to
am!ulate for several hours. 5he noticed mild weakness of her lower e#tremities for
one week. 5he denied anore#ia, nausea, vomiting, or diarrhea. There were no
significant findings on physical e#amination e#cept total paralysis of her lower
e#tremities with a!sent refle#es.The !iochemical studies are shown in Ta!le *.
Although her 6k was low, the spot urine 6
K
-6
2r
of '., was higher than e#pected,
suggesting renal K
+
wasting. 5he had meta!olic acidosis(pH 7.'7) and a normal
plasma anion gap. A diagnosis of 8TA was esta!lished. Aggressive replacement
therapy with K23(mmol-hr) was given to treat her HP.
9mmunologic surveys revealed elevated rheumatoid factor, positive anti"8o and 3a
anti!odies, and positive 5chimer:s test for dry eyes.5he proved to have 5;ogren
syndrome. 5he was placed on oral potassium citrate, active vitamin <& and steroid
therapy.
Case 3: Hypokalemia,weakness, and metabolic alkalosis
A '4"year"old male presented to emergency department with muscular weakness
that progressed to paralysis involving all e#tremities= he was una!le to walk for hours.
He denied nausea, vomiting, diarrhea, or use of diuretics. There were no significant
findings on physical e#amination e#cept a symmetric flaccid paralysis with arefle#ia
in the upper and lower e#tremities.
Hypokalemia was the most striking !iochemical a!normality(*., mmol-3)= it was
accompanied !y meta!olic alkalosis(Ta!le *). 6rinary e#cretion of K

was
considering his hypokalemia(6k **mmol-3, 6
K
-6
2r
'.,). A /artter:s"like syndrome
was tentatively diagnosed. Aggressive replacement therapy with K23('4 mmol-hr)
was initiated to treat his HP. 9ntravenous magnesium sulfate , gm for his
accompa%nying hypomagnesium was also administered over four hours.
Ta!le *. /iochemical investigations on admission
Case 1 2 3
Plasma
5odium (mmol-3) *.* *&> *.*
Potassium (mmol-3) '.4

*.,

*.7

2hloride (mmol-3) *4+ **.

11
H2)&? (mmol-3) '. *'

&4

pH 7.&1 7.'7

7..+

9norganic phosphate(mmol-3) 4.>

4.>

*.&
@agnesium (mmol-3) 4.7 4., 4.>

/6( (mg-dl) ** *+ *.
2reatinine (mg-dl) 4.7 *.4 4.,
Urine
5odium (mmol-3) *++ .. 14
Potassium (mmol-3) *' 1 **
2hloride (mmol-3) *>, .+ ,4
2reatinine (mmol-3) ** '., &.7
)smolality (mosm-Kg.H')) ,1. *+. '.*
K-creatinine mmol-mmol 4.7 '.,A '..A
TTK0 '.* " "..
Adenotes a!normal values
Conclusions
A severe degree of hypokalemia with paralysis is a potential life"medical
emergency. The causes of hypokalemia paralysis are usually not evident from the
history. Bmergency physicians should first evaluate whether renal wasting is
contri!uting to the hypokalemic paralysis. Three measurements including 6k(C*>"'4
mmol-3,might !e misleading), 6
K
-6
2r
ratio(D'), and TTK0(D&) may indicate renal
wasting. The 6
K
-6
2r
reflects a corrected K e#cretion at the time. The TTK0 is a
semi"%uantitative inde# for 6k that ad;usts for the Pk and for water rea!sorptionin the
medullary collecting ducts.
At B8, a simple approach is necessary to clarify its etiologies and su!se%uently can
give correctly rapid potassium replacement and management. Ee can differentiate
hypokalemic paralysis simply !ased on the patient:s acid"!ase status on presentation
to emergency department.(Ta!le ' and $igure *)
Table2 -./012
345678(HPP)
( 9 )
:;<=>(non-HPP)
(
)
/0
? @A:BCD ?E @A:FCD
(thyrotoxic periodic paralysis)
/0
(familial periodic paralysis)
/0
(sporadic periodic paralysis)
/0
(hypernatremic hypokalemic
paralysis)


(barium poisoning)

!"# $% G
(primary &secondary
aldosteronism ,licorice ingestion
,glucocorticoid excess)
&'()*
(Liddles syndrome ,Batters or
Gitelman syndrome)
+,-
(diuretics)
./
A!"
01
H!
"
HI
23&'(4

(medullary sponge kidney,
#$ogrens syndrome)
53&'(4
%anconi syndrome
EH!
"
HI
67

(diarrhea state)

8,(9:
(ureteral di&ersion)

;<

(toluene abuse)
9n patients with HPP, there is no o!vious acid"!ase disorder and the 6
K
-6
2r
ratio is
less than ', while in non"HPP there is associated with a!normal acid"!ase disorder
and the 6
K
-6
2r
ratio is more than '.
Ehen treating patients with HPP, the dose of K23 should !e as small as possi!le
to avoid re!ounding hyperkalemia. 9n contrast, non"HPP due to e#cessive renal K
e#cretion re%uires large doses of K23 to correct the deficit in total !ody K.
$inally, close monitoring the plasma potassium, B20 and muscle strength is
a!solutely necessary in the management of patient with HP.
JKLM
'()unlap "%,*epler +,( A syndrome resembling familial periodic paralysis
occurring in the course of exophthalmic goiter( +ndocrinology '-.'/'0102'34(
5(#ted6ell 7+, Allen *8, Binder L#( "ypokalemic paralyses1 A re&ie6 of the
etiologies, patholphysiology, presentation , and therapy( Am , +merg 8ed
'--5/ '91'2.3:(
.(8c%ad;ean A,#, <eung 7( =eriodic paralysis complicating thyrotoxicosis in
hinese( Br 8ed , '-4>/ '120'30(
2(8anoukian 8A, %oote ,A, rapo L8( linical and metabolic features of
thyrotoxic periodic paralysis in 52 episodes( Arch ?ntern 8ed '---/ '0-149'34(
0(Lin #", Lin <%, "alperin 8L( "ypokalaemia and paralysis( @,8 599'/ -21'..3
-(
4(Ahla6at #*, #achde& A( "ypokalaemic paralysis( =ostgrad 8ed , '---/>01'-.3
>(
>(*o G!, ho6 , <eung A!%, han ""L, Li ,*<, ockran #( !hyrotoxic
periodic paralysis in a hineses population( @,8 '--4/ 4124.3:(
:(Lin #", hiu ,#, "su B, hau !( A simple and rapid approach to hypokalemic
paralysis( Am , +merg 8ed 599. (?n =ress)
-(Lin <%, Lin #", !sai B#, )a&ids 87,"alperin 8L( #e&ere hypokalaemia in a
hinese male( @,8 5995 '914-03>92(
'9(Lin <%, Bu , =ei ), hu #,, Lin #"( )iagnosing thyrotoxic periodic
paralysis in the +)( Am , +merg 8ed 5995 (?n =ress)
''(Lin #", Lin <%# =ropranolol rapidly re&erses paralysis,hypokalemia,and
hypophosphatemia in thyrotoxic periodic paralysis# Am , *idney )is 599'/
.145935.#
%igure ' linical algorithm for the approach to patients 6ith hypokalemic paralysis
Abbre&iation1 !==1 thyrotoxic periodic paralysi/ %==1 familial periodic paralysis/
#==1 sporadic periodic paralysis/ 7!A1 renal tubular acidosis/ G#/ GitelmanCs
syndrome/ B#1BartterCs syndrome


Shi$t De$icit

Acid3base state

Blood pressure
Dormal "igh




Hypokalemia and Paralysis
Lo6 *E excretion and normal acid3base "igh *E excretion and abnormal acid3base
%ari&m poisoning 8etabolic acidosis 8etabolic alkalosis
Tol&ene ab&se
Pro$o&nd diarrhea
RTA 'S or %S
Di&retics
(omiting
)ineralocorticoid
e*cess