A Simple and Rapid Approach to Hypokalemic Paralysis in
Emergency Department -Three Cases Report
急診之簡單和快速評估低血鉀麻痺症-三病例報告
許金旺 1 林石化 2 陳建生 1 朱士傑 1 劉敏英 1
三軍總醫院急診部 1 三軍總醫院內科部腎臟科 2
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 body K+ deficit.
The other is non-HPP, primarily due to excessive excretion of K+. Failure
to clarify these two different etiologies may give to improper management.
The therapy of HPP requires only small doses of potassium replacement to
avoid rebound hyperkalemia. As the clinical presentations between them
are almost similar, the use of spot urine for K+ excretion rate and
evaluation of blood acid-base status may be clinically beneficial in the
diagnosis and management.
Case reports
Case 1: Hypokalemia, weakness, and a normal acid-base state
A 32-year-old male presented with sudden onset of general muscular
weakness of all extremities and inability to ambulate upon awakening. No
significant findings were found on his medical and family history. On
physical examination, his blood pressure was high(168/84 mmHg), as was
his heart rate(128 beats/min). The principal findings were diffusely
enlarged thyroid gland and total paralysis of all extremities.
Biochemical studies are shown in table 1. He did not have an acid-base
+
disorder and K excretion was low and transtubular potassium gradient(TTKG)
of 1.9.
He was treated with intravenous KCL at a rate of 10 mmol/hr. However,
hyperkalemia 6.2 mmol/L was observed two hours after recovery.His T3 and
T4 levels were elevated while TSH was suppressed. His hyperthyroidism was
treated with oral propylthiouracil and propranolol. His thyrotoxic
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 29-year-old female was brought to the emergency room because of an
inability to ambulate for several hours. She noticed mild weakness of her
lower extremities for one week. She denied anorexia, nausea, vomiting,
or diarrhea. There were no significant findings on physical examination
except total paralysis of her lower extremities with absent reflexes.The
biochemical studies are shown in Table 1. Although her Uk was low, the
spot urine UK/UCr of 2.8 was higher than expected, suggesting renal K+
wasting. She had metabolic acidosis(pH 7.27) and a normal plasma anion
gap. A diagnosis of RTA was established. Aggressive replacement therapy
with KCL(mmol/hr) was given to treat her HP.
Immunologic surveys revealed elevated rheumatoid factor, positive
anti-Ro and La antibodies, and positive Schimer”s test for dry eyes.She
proved to have Sjogren syndrome. She was placed on oral potassium citrate,
active vitamin D3 and steroid therapy.
Case 3: Hypokalemia,weakness, and metabolic alkalosis
A 20-year-old male presented to emergency department with muscular
weakness that progressed to paralysis involving all extremities; he was
unable to walk for hours. He denied nausea, vomiting, diarrhea, or use
of diuretics. There were no significant findings on physical examination
except a symmetric flaccid paralysis with areflexia in the upper and lower
extremities.
Hypokalemia was the most striking biochemical abnormality(1.8 mmol/L);
it was accompanied by metabolic alkalosis(Table 1). Urinary excretion of
K+ was considering his hypokalemia(Uk 11mmol/L, UK/UCr 2.8). A
Bartter”s-like syndrome was tentatively diagnosed. Aggressive
replacement therapy with KCL(20 mmol/hr) was initiated to treat his HP.
Intravenous magnesium sulfate 8 gm for his accompaqnying hypomagnesium
was also administered over four hours.
Table 1. Biochemical investigations on admission
Case
1
2
3
Plasma
Sodium
(mmol/L)
Potassium
(mmol/L)
Chloride
(mmol/L)
HCO3¯
(mmol/L)
pH
Inorganic phosphate(mmol/L)
141
2.0＊
106
24
7.39
0.5＊
135
1.8＊
114＊
12＊
7.27＊
0.5＊
141
1.7＊
99
30＊
7.46＊
1.3
Magnesium
BUN
Creatinine
(mmol/L)
(mg/dl)
(mg/dl)
0.7
11
0.7
0.8
16
1.0
0.5＊
14
0.8
Urine
Sodium
Potassium
Chloride
Creatinine
Osmolality
K+/creatinine
(mmol/L)
(mmol/L)
(mmol/L)
(mmol/L)
(mosm/Kg.H2O)
mmol/mmol
166
12
158
11
894
0.7
44
9
46
2.8
164
2.8*
90
11
80
3.7
241
2.4*
2.1
-
-..
TTKG
*denotes abnormal 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. Emergency physicians should first evaluate
whether renal wasting is contributing to the hypokalemic paralysis. Three
measurements including Uk(<15-20 mmol/L,might be misleading), UK/UCr
ratio(>2), and TTKG(>3) may indicate renal wasting. The UK/UCr reflects
a corrected K+ excretion at the time. The TTKG is a semi-quantitative index
for Uk that adjusts for the Pk and for water reabsorptionin the medullary
collecting ducts.
At ER, a simple approach is necessary to clarify its etiologies and
subsequently can give correctly rapid potassium replacement and
management. We can differentiate hypokalemic paralysis simply based on
the
patient”s
acid-base
status
on
presentation
to
emergency
department.(Table 2 and Figure 1)
Table2 常見低血鉀癱瘓之原因
自細胞之間轉移(HPP)
急性鉀離子缺乏(non-HPP)
(全身鉀離子有缺乏)
(全身鉀離子並未缺乏)
甲狀腺高能症週期性癱瘓
(thyrotoxic periodic paralysis)
家族性週期性癱瘓
(familial periodic paralysis)
偶發性週期性癱瘓
(sporadic periodic paralysis)
高血鈉低血鉀癱瘓
(hypernatremic hypokalemic
paralysis)
鋇中毒
(barium poisoning)
有低血氯代謝性鹼中毒
嚴重嘔吐
礦物皮質酮過量
有高血氯代謝性酸中毒
低 NH4+ 分泌
遠端腎小管酸中毒
(primary &secondary
(medullary sponge kidney,
aldosteronism ,licorice
Sjogren’s syndrome)
ingestion ,glucocorticoid excess)
腎小管疾病
近端腎小管酸中毒
(Liddle’s syndrome ,Batter’s or
Fanconi syndrome
Gitelman’ syndrome)
利尿劑 (diuretics)
高 NH4+ 分泌
異位性 ACTH 症候群
腹瀉
(diarrhea state)
輸尿管分流
(ureteral diversion)
濫用甲苯
(toluene abuse)
In patients with HPP, there is no obvious acid-base disorder and the
UK/UCr ratio is less than 2, while in non-HPP there is associated with
abnormal acid-base disorder and the UK/UCr ratio is more than 2.
When treating patients with HPP, the dose of KCL should be as small
as possible to avoid rebounding hyperkalemia. In contrast, non-HPP due
to excessive renal K+ excretion requires large doses of KCL to correct
the deficit in total body K+.
Finally, close monitoring the plasma potassium, ECG and muscle
strength is absolutely necessary in the management of patient with HP.
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Figure 1 Clinical algorithm for the approach to patients with hypokalemic paralysis
Abbreviation: TPP: thyrotoxic periodic paralysi; FPP: familial periodic paralysis;
SPP: sporadic periodic paralysis; RTA: renal tubular acidosis; GS; Gitelman”s
syndrome; BS:Bartter”s syndrome
Hypokalemia and Paralysis
Shift
Deficit
Low K+ excretion and normal acid-base
High K+ excretion and abnormal acid-base
Acid-base state
TPP
FPP
Barium poisoning
SPP
Metabolic acidosis
Metabolic alkalosis
Blood pressure
Normal
Toluene abuse
Profound diarrhea
High
RTA
GS or BS
Diuretics
Vomiting
Mineralocorticoid
excess