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Life-Threatening Hypokalemic Paralysis in a Young Bodybuilder







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Journal ListCase Rep Endocrinolv.2014; 2014PMC3934379












Case Rep Endocrinol. 2014; 2014: 483835. Published online 2014 Feb 11. doi:  10.1155/2014/483835PMCID: PMC3934379Life-Threatening Hypokalemic Paralysis in a Young BodybuilderKitty K. T. Cheung,* Wing-Yee So, Alice P. S. Kong, Ronald C. W. Ma, and Francis C. C. ChowDepartments
of Medicine and Therapeutics, Prince of Wales Hospital, The Chinese
University of Hong Kong, 30-32 Ngan Shing Street, Shatin, New
Territories, Hong Kong*Kitty K. T. Cheung: Email: kh.ude.khuc@gnuehctkyttikAcademic Editors: B. K. Irons and X. ZhangAuthor information �
� Article notes �
� Copyright and License information �
�Received 2013 Dec 3; Accepted 2014 Jan 8.Copyright © 2014 Kitty K. T. Cheung et al.This
is an open access article distributed under the Creative Commons
Attribution License, which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly
cited.Go to:AbstractWe
report a case of life-threatening hypokalemia in a 28-year-old
bodybuilder who presented with sudden onset bilateral lower limbs
paralysis few days after his bodybuilding competition. His
electrocardiogram (ECG) showed typical u-waves due to severe hypokalemia
(serum potassium 1.6mmol/L, reference range (RR) 3.5–5.0mmol/L).
He was admitted to the intensive care unit (ICU) and was treated with
potassium replacement. The patient later admitted that he had exposed
himself to weight loss agents of unknown nature, purchased online, and
large carbohydrate loads in preparation for the competition. He made a
full recovery after a few days and discharged himself from the hospital
against medical advice. The severe hypokalemia was thought to be caused
by several mechanisms to be discussed in this report. With the ever
rising number of new fitness centers recently, the ease of online
purchasing of almost any drug, and the increasing numbers of youngsters
getting into the bodybuilding arena, clinicians should be able to
recognize the possible causes of sudden severe hypokalemia in these
patients in order to revert the pathophysiology.Go to:1. IntroductionSevere
hypokalemia can be life threatening. It can be caused by genuine
diseases or iatrogenic. Either way, prompt recognition of the condition
and the underlying causes is needed for effective management of the
patients. With the ever rising number of new fitness centers recently,
the ease of online purchasing of almost any drug, and the increasing
numbers of youngsters getting into the bodybuilding arena, clinicians
should be able to recognize the possible iatrogenic causes of sudden
severe hypokalemia in this group of patients.Go to:2. Case PresentationA
28-year-old Chinese man with good past health and no significant family
history presented to the Accident and Emergency Department (AED) due to
sudden onset bilateral lower limb paralysis (Medical Research Council
power grading 2/5) on August 13, 2013. The patient reported no recent
head, neck, or spine injury and remained conscious all along. Physical
exam revealed a muscular young man with no features of dehydration,
hyperthyroidism, or Cushing's syndrome. Urgent imaging including plain
computer tomography (CT) of brain and X-ray spine showed no abnormality.
ECG showed typical u-waves and serum biochemistries came back to show
severe hypokalemia (1.6mmol/L, RR 3.5–5.0mmol/L) (Figure 1).
His serum creatinine, magnesium, thyroid stimulating hormone, and pH
levels were all normal. He was therefore admitted to the ICU and was
commenced on oral and intravenous potassium replacement. Spot urine for
potassium (14mmol/L) was only saved after the start of potassium replacement when the paired serum potassium was 2.2mmol/L. In total, 20mmol of intravenous and 10mmol of oral potassium chloride were given, and his serum potassium was stabilized at 3.7–4mmol/L eighteen hours after admission. Urine for toxicology screen was saved and the report was pending at that time.Figure 1ECG of the patient showing typical u-waves of hypokalemia.Upon
further questioning, the patient admitted to have taken some weight
loss agents of unknown nature which he had purchased over the Internet
until the date of his competition. He then disclosed that, in
preparation for the bodybuilding competition, he had been taking heavy
loads of carbohydrate for muscle building and restricting salt and fluid
intake a few days prior to the presentation. He denied any recent use
of anabolic steroid. The patient recovered fully from his paralysis a
couple of days later and discharged himself from the hospital against
medical advice on August 15, 2013. His latest serum potassium prior to
discharge was 4.4mmol/L.The
urine toxicology screen came back two weeks after the patient's
presentation showing rhein, emodin, aloe-emodin, and physcion.
Unexpectedly, mycophenolate mofetil (MMF) and diltiazem were also
identified although the patient denied having any prescribed
medications. The patient was phoned up and the urine toxicology results
were explained to him, with emphasis on the potential adverse effects of
taking drugs without prescription from doctors.Go to:3. DiscussionIt
is well known that in preparation for bodybuilding competitions,
bodybuilders, in addition to hard muscle training, very often engage
themselves in dietetic manipulations. Three phases have been described.
The first phase involves few months of hypercaloric nutrition rich in
proteins, for the build-up of muscle mass. The second phase is a period
of reduced caloric intake to reduce subcutaneous fat. The third phase,
during the last week of preparations, includes simultaneous extreme
carbohydrate intake to load muscles with glycogen, sodium, and water
restriction to produce subcutaneous volume deficit and better definition
of muscle contours. Hypokalemia and flaccid paralysis often result
during the course of these dietetic manipulations [1].Our
patient appeared to have been following these phases in preparation for
his bodybuilding competition and suffered from the resulting
hypokalemic paralysis. The intake of extreme carbohydrate loads had led
to an intracellular shift of the potassium from extracellular to
intracellular space through stimulating endogenous insulin release,
which in turn promoted the entry of potassium into skeletal muscle and
liver cells by activating the Na-K-ATPase pump [2]. The quick reversal of his potassium level with just 20mmol of intravenous and 10mmol
of oral potassium chloride made this a possible explanation as it is
classical for hypokalemia due to intracellular shift to be reverted
quickly without large amount of potassium replacement.The
use of �śweight loss agents” might have included diuretics, such as
spironolactone or other mineralocorticoid antagonists, which competed
with aldosterone for receptor sites in the distal renal tubules,
increasing in sodium chloride and water excretion while conserving
potassium and hydrogen ions. The sudden withdrawal of spironolactone
right after the competition might have caused a relative
mineralocorticoid excess, since mineralocorticoid was previously
overstimulated due to its action being blocked in the renal tubules.
This relative mineralocorticoid excess therefore contributed to the
hypokalemia. Since the half-life of spironolactone in serum is only
78–84 minutes and is only found in the body for two-three days after
ingestion, this might be the reason for it not being detected in the
urine toxicology screen [3].Rhein,
emodin, aloe-emodin, and physcion are anthraquinones with laxative
effect, and using these chronically may cause hypokalemia [4].
Therefore, these, most likely constituents of the �śweight loss agents”
from over the Internet, serve as the third possible cause of his severe
hypokalemia. Although MMF and diltiazem could not be accounted for the
life-threatening hypokalemia, they serve to remind all clinicians that
everything could be present in over the Internet drugs, including those
which should not be supplied without doctor's prescription.In
conclusion, we report here a young bodybuilder who presented with
life-threatening hypokalemic paralysis few days after his bodybuilding
competition. Three possible mechanisms for the severe hypokalemia were
identified: (1) intracellular potassium shift due to extreme
carbohydrate loads (2) suspected spironolactone, or other
mineralocorticoid antagonists, content in the �śweight loss agents”
purchased by patient over the Internet leading to relative
mineralocorticoid excess shortly after withdrawal (3) anthraquinones
with laxative effect leading to gastrointestinal loss of potassium. With
the ever rising number of new fitness centers recently, the ease of
online purchasing of almost any drug, and the increasing numbers of
youngsters getting into the bodybuilding arena, clinicians should be
able to recognize the possible causes of sudden severe hypokalemia in
these patients in order to treat and advise the patients efficiently.Go to:Conflict of InterestsThe authors declare that there is no conflict of interests regarding the publication of this paper.Go to:References1. Britschgi F, Zund G. Body building: hypokalemia and hypophosphatemia. Schweizerische Medizinische Wochenschrift. 1991;121(33):1163–1165. [PubMed]2. Mount DB. Clinical manifestations and treatment of hypokalemia. In: Basow DS, editor. UpToDate. Waltham, Mass, USA: UpToDate; 2013. 3. Basow DS, editor. UpToDate. Waltham, Mass, USA: UpToDate; 2013. Spironolactone: drug information.4. Chen D, Xiong Y, Wang L, Lv B, Lin Y. Characteristics of emodin on modulating the contractility of jejunal smooth muscle. Canadian Journal of Physiology and Pharmacology. 2012;90(4):455–462. [PubMed]Abstract1. Introduction2. Case Presentation3. DiscussionConflict of InterestsReferencesArticles from Case Reports in Endocrinology are provided here courtesy of Hindawi Publishing Corporation














Formats:Article | PubReader | ePub (beta) | PDF (961K) | CitationRelated citations in PubMedHypokalemic paralysis in a professional bodybuilder.[Am J Emerg Med. 2012]Mayr FB, Domanovits H, Laggner AN. Am J Emerg Med. 2012 Sep; 30(7):1324.e5-8. Epub 2011 Aug 25.Clinical and metabolic features of thyrotoxic periodic paralysis in 24 episodes.[Arch Intern Med. 1999]Manoukian MA, Foote JA, Crapo LM. Arch Intern Med. 1999 Mar 22; 159(6):601-6. Unilateral paralysis associated with profound hypokalemia.[Am J Emerg Med. 2012]Chiang WF, Yeh FC, Lin SH. Am J Emerg Med. 2012 Nov; 30(9):2100.e5-7. Epub 2012 Mar 29.Hypokalemic periodic paralysis: a case series, review of the literature and update of management.[Eur J Emerg Med. 2010]Alkaabi JM, Mushtaq A, Al-Maskari FN, Moussa NA, Gariballa S. Eur J Emerg Med. 2010 Feb; 17(1):45-7. Hypokalemic paralyses: a review of the etiologies, pathophysiology, presentation, and therapy.[Am J Emerg Med. 1992]Stedwell RE, Allen KM, Binder LS. Am J Emerg Med. 1992 Mar; 10(2):143-8. See reviews...See all...LinksPubMedPubMedPubMed citations for these articlesRecent ActivityClearTurn OffTurn OnLife-Threatening Hypokalemic Paralysis in a Young BodybuilderLife-Threatening Hypokalemic Paralysis in a Young BodybuilderCase Reports in Endocrinology. 2014; 2014()Injuries and overuse syndromes in powerlifting.Injuries and overuse syndromes in powerlifting.Int J Sports Med. 2011 Sep ;32(9):703-11. doi: 10.1055/s-0031-1277207. Epub 2011 May 17 .PubMedinjuries powerlifting (12)PubMedAcute myocardial infarction and renal infarction in a bodybuilder using anabolic...Acute myocardial infarction and renal infarction in a bodybuilder using anabolic steroids.Turk Kardiyol Dern Ars. 2010 Jun ;38(4):275-8.PubMedLife-threatening hypokalemic paralysis in a young bodybuilder.Life-threatening hypokalemic paralysis in a young bodybuilder.Case Rep Endocrinol. 2014 ;2014:483835. doi: 10.1155/2014/483835. Epub 2014 Feb 11 .PubMedYour browsing activity is empty.Activity recording is turned off.Turn recording back onSee more...


[Bodybuilding: hypokalemia and hypophosphatemia].[Schweiz Med Wochenschr. 1991]Britschgi F, Z�źnd GSchweiz Med Wochenschr. 1991 Aug 17; 121(33):1163-5.Characteristics of emodin on modulating the contractility of jejunal smooth muscle.[Can J Physiol Pharmacol. 2012]Chen D, Xiong Y, Wang L, Lv B, Lin YCan J Physiol Pharmacol. 2012 Apr; 90(4):455-62.



















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[Bodybuilding: hypokalemia and hypophosphatemia].Britschgi F, Z�źnd GSchweiz Med Wochenschr. 1991 Aug 17; 121(33):1163-5.[PubMed] [Ref list]2. Mount DB. Clinical manifestations and treatment of hypokalemia. In: Basow DS, editor. UpToDate. Waltham, Mass, USA: UpToDate; 2013. [Ref list]3. Basow DS, editor. UpToDate. Waltham, Mass, USA: UpToDate; 2013. Spironolactone: drug information. [Ref list]Characteristics of emodin on modulating the contractility of jejunal smooth muscle.Chen D, Xiong Y, Wang L, Lv B, Lin YCan J Physiol Pharmacol. 2012 Apr; 90(4):455-62.[PubMed] [Ref list]




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