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Cited by 173Potassium and Related DisordersCardiac electrophysiology and arrhythmiasIon Transport and Channel Regulation

Hypokalaemia and paralysis

Lin, S.-H.·2001·QJM
DOI 10.1093/qjmed/94.3.133
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Abstract

It is not uncommon for patients to present to the emergency room with severe weakness and a markedly low plasma potassium concentration. We attempted to identify useful clues to the diagnosis of hypokalaemic periodic paralysis (HPP), because its acute treatment aims are unique. We retrospectively reviewed charts over a 10-year period: HPP was the initial diagnosis in 97 patients. Mean patient age was 29+/-1.1 and the male:female ratio was 77:20. When the final diagnosis was HPP (n=73), the acid-base state was normal, the urine K(+) concentration was low, and the transtubular K(+) concentration gradient (TTKG) was <3. In patients with thyrotoxic periodic paralysis (TPP) (n=39), hypokalaemia was very commonly accompanied by hypophosphataemia (1.9+/-0.1 mg/dl). A clinical diagnosis of sporadic periodic paralysis (SPP) was made if hyperthyroidism and a family history of HPP were both absent (n=29). One subgroup of patients with HPP had a severe degree of hypernatraemia (167+/-5.0 mmol/l, n=3). There were only two patients with familial periodic paralysis (FPP). In 24 patients, the initial diagnosis was HPP, but subsequent studies failed to confirm this diagnosis. Each of these patients had an acid-base disorder, a high rate of renal K(+) excretion in the presence of hypokalaemia, and a TTKG of close to 7. With respect to therapy, much less K(+) was given to patients with HPP, yet 1:3 subsequently had a plasma K(+) concentration that eventually exceeded 5.0 mmol/l. Using plasma acid-base status, phosphate and K(+) excretion parameters allows a presumptive diagnosis of HPP with more confidence in the emergency room.

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  • In one series, tachycardia (mean heart rate = 105 bpm) was noted at presentation and distinguished TPP patients from those with familial hypokalemic periodic paralysis.

    “In one series, tachycardia (mean heart rate = 105 bpm) was noted at presentation and distinguished these patients from those with familial hypokalemic periodic paralysis [22].”

    From Thyrotoxic Periodic Paralysis: Clinical Challenges (2014) · cites this paper as [22]

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Authors
Lin, S.-H.
Affiliations
Tri-Service General Hospital (TW)
Corresponding author
Lin, S.-H.
ORCID
Lin, S.-H.
Venue
QJM
Publisher
Oxford University Press (OUP)
Published
2001-03-01
Volume
94
Issue
3
Pages
133-139
ISSN
  • 0033-5622 (ISSN-L)
  • 1460-2393
DOI
10.1093/qjmed/94.3.133
OpenAlex
W2159477041
Cited by
173
References
50
Citations by year
2026: 1 · 2025: 4 · 2024: 5 · 2023: 5 · 2022: 6 · 2021: 4 · 2020: 5 · 2019: 5 · 2018: 6 · 2017: 9 · 2016: 4 · 2015: 10 · 2014: 7 · 2013: 3 · 2012: 11
FWCI
7.63
Type
journal article
Language
en
Open access
closed
Locations
  • QJM (publishedVersion)
  • PubMed (publishedVersion)
  • HighWire Press Open Archive (submittedVersion)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Potassium and Related Disorders
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Keywords
hypokalemic periodic paralysis, thyrotoxic periodic paralysis, familial periodic paralysis, hypokalemia, paralysis, hypophosphatemia, hypernatremia, acid-base status, renal potassium excretion, potassium replacement therapy, emergency diagnosis
MeSH terms
Acid-Base Equilibrium, Adolescent, Adult, Aged, Analysis of Variance, Diagnosis, Differential, Female, Humans, Hypernatremia, Hypokalemia, Male, Middle Aged, Paralysis, Potassium, Retrospective Studies, Thyrotoxicosis, Hypophosphatemia, Genetic Predisposition to Disease

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