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International Journal of Trend in Scientific Research and Development (IJTSRD)
Volume: 3 | Issue: 3 | Mar-Apr 2019 Available Online: www.ijtsrd.com e-ISSN: 2456 - 6470
@ IJTSRD | Unique Paper ID - IJTSRD21658 | Volume – 3 | Issue – 3 | Mar-Apr 2019 Page: 216
Hypokalemic Periodic Paralysis: A Case Report
Blessy Rachal Boban, Cillamol K. J, Elena Cheruvil, Sheffin Thomas, Tony Abraham
PHARM.D (Doctor of Pharmacy) Interns, Pushpagiri Medical College Hospital, Thiruvalla, Kerala, India
How to cite this paper: Blessy Rachal
Boban | Cillamol K. J | Elena Cheruvil |
Sheffin Thomas | Tony Abraham
"Hypokalemic PeriodicParalysis: A Case
Report" Published in International
Journal of Trend in Scientific Research
and Development
(ijtsrd), ISSN: 2456-
6470, Volume-3 |
Issue-3, April 2019,
pp.216-217, URL:
http://www.ijtsrd.co
m/papers/ijtsrd216
58.pdf
Copyright © 2019 by author(s) and
International Journal of Trend in
Scientific Research and Development
Journal. This is an Open Access article
distributed under
the terms of the
Creative Commons
Attribution License (CC BY 4.0)
(http://creativecommons.org/licenses/
by/4.0)
ABSTRACT
Hypokalemic periodic paralysis (HPP) is a medical emergency with prevalence of 1 in
100,000.Rapidmanagementisveryimportant;since,verylowpotassiumlevelscanlead
to cardiac complications . In this case, a twenty four year-old female without a similar
historyinthefamily,havinghypokalemiaperiodicparalysisattackispresented.Thiscase
report study has been presented for the consideration of the rare HPP in patients
presentingwithsuddenmuscleweakness.
Keywords: Hypokalemia, paralysis, potassium, weakness, complications
INTRODUCTION
Hypokalemic periodic paralysis (HPP), the most common
form of periodic paralysis, is reasonably rare with an
approximated prevalence of 1 in 100,000 [1]. HPP is a
condition in which affected individuals may experience
flaccid paralytic episodes with concomitant hypokalemia.
The clinical features of the syndrome vary somewhat
depending on the underlying etiology but the most striking
feature is the sudden onset of weakness ranging in severity
from mild, transient weakness to severe disability resulting
in life-threatening respiratory failure. A perturbation of
sodium and calcium ion channels results in low potassium
levels and muscle dysfunction [2]. Although the serum
potassium level is often alarmingly low, other electrolytes
are usually normal. Indeed, total body potassium is actually
normal with the change in the serum level reflecting a shift
of potassium into cells [3]. Electrocardiographicchanges are
common. Majority of the cases are characterized as familial
or primary HPP, whereas sporadic cases are associatedwith
various other conditions such as barium poisoning,
hyperthyroidism, renal disorders, endocrinopathies and
gastrointestinal potassium losses. Respiration, deglutition
and ocular motility are usually affected only in severe
attacks. Furthermore, studies have shown HPP does not
affect the heart, but can trigger cardiac arrhythmias. Very
rarely, patients can develop permanent weakness but this
phenomenon is usually observed in young adults [4]. In
hypokalemia familial periodic paralysis, the factors that
trigger weakness or paralysis are anesthesia, surgery,
pregnancy, insulin, alcohol, strenuous exercise, and
steroids. [5,6]. The guidelines for care include control of
plasma potassium, avoidance of large glucose and salt loads,
maintenance of body temperature, acid–base balance, and
careful use of neuromuscular blocking agents.[7,8] .
Approximately one-third of cases represent new mutations
[9]. Treatment consists of diet changes and avoiding things
that trigger your attacks. Carbonic anhydrase inhibitors:
These medications increase the flow of potassium. Common
options include dichlorphenamide (Keveyis) and
acetazolamide (Diamox). Potassium supplements: Oral
potassium supplements may be given to help stop an attack
that’s in progress. Your doctor will advise you on proper
dosage [10].
CASE REPORT
A 24 year-old female with significant past medical history
presented to the emergency room with sudden onset
paralysis. The patient had gone to bed at 11 pm with no
weakness and awoke at 3 a.m found unable to move her
upper or lower extremities. The weakness was bilateral and
involved both the proximal muscles of the shoulders and
hips as well as the distal extremities. She had no respiratory
or swallowing difficulty and was able to move her neck and
facial muscles. She denied any pain or paresthesia. She had
her first episode 10 years ago and it was repeated for 21
times till 2019.Prior to this episode,thepatienthadtaken ice
cream as a part of colleague’s treat. Usually the episodic
IJTSRD21658
International Journal of Trend in Scientific Research and Development (IJTSRD) @ www.ijtsrd.com eISSN: 2456-6470
@ IJTSRD | Unique Paper ID - IJTSRD21658 | Volume – 3 | Issue – 3 | Mar-Apr 2019 Page: 217
weakness get relieved with I.V infusion but this time, the
weakness was prolonged and taken to a localhospitalwhere
her potassium correction was made .But repeat potassium
was low (1.9) .Hence referred to Pushpagiri Medical
College.She did report several episodes of weakness after
consuming ice creams. Her mother had been diagnosedwith
hepatic cellular carcinoma and died 3 years ago.
On examination, the patient's blood pressure was 100/60.
No jugular venous distension, goiter or lymphadenopathy
were appreciated. Cardiac exam revealed tachycardiawith a
regular rhythm and no murmurs. Examination of the lungs
and abdomen wereunremarkable. Neurologicexam revealed
Grade 2 power. Routine chemistry, liver enzymes and
complete blood count were normal except for a potassium
level of 1.9(3.5–5 mmol/L),ESR- 52,ALP-122. Two hours
after initiation of intravenous potassium replacement, the
patient's symptoms had completely resolved. Thyroid
stimulating hormone (TSH), triiodothyronine (T3) and
thyroxine (T4) levels were obtained and revealed a
markedly normal value.
DISCUSSION
There are several types of Periodic Paralysis associatedwith
metabolic and electrolyte abnormalities. Of these,
Hypokalemic Periodic Paralysis (HPP) is the most common.
Electromyography reveals abnormalities in some patients
but is often normal, especially between episodes when no
clinically detectable weakness is present. HPP occurs in
several settings and the diagnosis may require an extensive
search for the underlying etiology since thetreatment varies
according to the cause. Rarely, HPP can result from
substantial gastrointestinal or renal potassium
losses. Acetazolamide may prevent the paralytic episodes
and antiarrhythmics or beta-blockers may prevent
ventricular ectopy, but there is little data available.Most
patients do not require treatment but areinstructedto avoid
paralysis-inducing situations.
CONCLUSION
This patient presented with sudden onset paralysis and
markedly abnormal potassium, ESR. This presentation is
typical of Familial Hypokalemic Periodic Paralysis. The
paralysis resolved completely following potassium
replacement and she began a course of Acetazolamide 250
mg prior to being discharged from the hospital. At the time
of discharge, she had no neurologic findings and a normal
blood pressure. She has not suffered anyfurther episodes of
paralysis .Periodic Paralysis is important to consider when
seeing a patient with sudden onset weakness or paralysis,
especially those with no history or evidence of other
diseases and no significant risk factors for stroke. Failure to
properly diagnose and treat Periodic Paralysis can be fatal,
but rapid correction of potassium abnormalities can resolve
the symptoms quickly and completely. When possible, the
underlying cause must be adequately addressed to prevent
the persistence or recurrence of paralysis.
REFERENCES
[1] Fontaine B. Chapter 1 Periodic Paralysis. Advances in
Genetics. 63: Academic Press; 2008. p. 3-23.
[2] Jurkat-Rott K, Lerche H, Lehmann-Horn F. Skeletal
muscle channelopathies. J Neurol. 2002; 249:1493–
1502. doi: 10.1007/s00415-002-0871-5.
[3] Lin SH, Lin YF, Chen DT, Chu P, Hsu CW, Halperin ML.
Laboratory tests to determine the cause of
hypokalemia and paralysis. Arch Intern Med. 2004;
164:1561–1566. doi: 10.1001/archinte.164.14.1561.
[4] Fontaine B. Chapter 1 Periodic Paralysis. Advances in
Genetics. 63: Academic Press; 2008. p. 3-23
[5] Melnick B, Chang J, Larson CE, Bedger R. Hypokalemic
familial periodic paralysis. Anesthesiology. 1983;
58:263–5
[6] 6. Griggs RC, Resnick J, Engel WK. Intravenous
treatment of hypokalemic periodic paralysis. Arch
Neurol. 1983;40:539–40
[7] Rollman JE, Dickson CM. Anesthetic management of a
patient with hypokalemic periodic paralysis for
coronary artery bypass surgery. Anesthesiology.
1985;63:526–527
[8] 8. Levitt JO. Practical aspects in the management of
hypokalemic periodic paralysis. J Transl Med.
2008;6:18.
[9] https://www.uptodate.com/contents/hypokalemic-
periodic-paralysis/abstract/10
[10] www.healthline.com/health/hypokalemic-periodic-
paralysis

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Hypokalemic Periodic Paralysis A Case Report

  • 1. International Journal of Trend in Scientific Research and Development (IJTSRD) Volume: 3 | Issue: 3 | Mar-Apr 2019 Available Online: www.ijtsrd.com e-ISSN: 2456 - 6470 @ IJTSRD | Unique Paper ID - IJTSRD21658 | Volume – 3 | Issue – 3 | Mar-Apr 2019 Page: 216 Hypokalemic Periodic Paralysis: A Case Report Blessy Rachal Boban, Cillamol K. J, Elena Cheruvil, Sheffin Thomas, Tony Abraham PHARM.D (Doctor of Pharmacy) Interns, Pushpagiri Medical College Hospital, Thiruvalla, Kerala, India How to cite this paper: Blessy Rachal Boban | Cillamol K. J | Elena Cheruvil | Sheffin Thomas | Tony Abraham "Hypokalemic PeriodicParalysis: A Case Report" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456- 6470, Volume-3 | Issue-3, April 2019, pp.216-217, URL: http://www.ijtsrd.co m/papers/ijtsrd216 58.pdf Copyright © 2019 by author(s) and International Journal of Trend in Scientific Research and Development Journal. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0) (http://creativecommons.org/licenses/ by/4.0) ABSTRACT Hypokalemic periodic paralysis (HPP) is a medical emergency with prevalence of 1 in 100,000.Rapidmanagementisveryimportant;since,verylowpotassiumlevelscanlead to cardiac complications . In this case, a twenty four year-old female without a similar historyinthefamily,havinghypokalemiaperiodicparalysisattackispresented.Thiscase report study has been presented for the consideration of the rare HPP in patients presentingwithsuddenmuscleweakness. Keywords: Hypokalemia, paralysis, potassium, weakness, complications INTRODUCTION Hypokalemic periodic paralysis (HPP), the most common form of periodic paralysis, is reasonably rare with an approximated prevalence of 1 in 100,000 [1]. HPP is a condition in which affected individuals may experience flaccid paralytic episodes with concomitant hypokalemia. The clinical features of the syndrome vary somewhat depending on the underlying etiology but the most striking feature is the sudden onset of weakness ranging in severity from mild, transient weakness to severe disability resulting in life-threatening respiratory failure. A perturbation of sodium and calcium ion channels results in low potassium levels and muscle dysfunction [2]. Although the serum potassium level is often alarmingly low, other electrolytes are usually normal. Indeed, total body potassium is actually normal with the change in the serum level reflecting a shift of potassium into cells [3]. Electrocardiographicchanges are common. Majority of the cases are characterized as familial or primary HPP, whereas sporadic cases are associatedwith various other conditions such as barium poisoning, hyperthyroidism, renal disorders, endocrinopathies and gastrointestinal potassium losses. Respiration, deglutition and ocular motility are usually affected only in severe attacks. Furthermore, studies have shown HPP does not affect the heart, but can trigger cardiac arrhythmias. Very rarely, patients can develop permanent weakness but this phenomenon is usually observed in young adults [4]. In hypokalemia familial periodic paralysis, the factors that trigger weakness or paralysis are anesthesia, surgery, pregnancy, insulin, alcohol, strenuous exercise, and steroids. [5,6]. The guidelines for care include control of plasma potassium, avoidance of large glucose and salt loads, maintenance of body temperature, acid–base balance, and careful use of neuromuscular blocking agents.[7,8] . Approximately one-third of cases represent new mutations [9]. Treatment consists of diet changes and avoiding things that trigger your attacks. Carbonic anhydrase inhibitors: These medications increase the flow of potassium. Common options include dichlorphenamide (Keveyis) and acetazolamide (Diamox). Potassium supplements: Oral potassium supplements may be given to help stop an attack that’s in progress. Your doctor will advise you on proper dosage [10]. CASE REPORT A 24 year-old female with significant past medical history presented to the emergency room with sudden onset paralysis. The patient had gone to bed at 11 pm with no weakness and awoke at 3 a.m found unable to move her upper or lower extremities. The weakness was bilateral and involved both the proximal muscles of the shoulders and hips as well as the distal extremities. She had no respiratory or swallowing difficulty and was able to move her neck and facial muscles. She denied any pain or paresthesia. She had her first episode 10 years ago and it was repeated for 21 times till 2019.Prior to this episode,thepatienthadtaken ice cream as a part of colleague’s treat. Usually the episodic IJTSRD21658
  • 2. International Journal of Trend in Scientific Research and Development (IJTSRD) @ www.ijtsrd.com eISSN: 2456-6470 @ IJTSRD | Unique Paper ID - IJTSRD21658 | Volume – 3 | Issue – 3 | Mar-Apr 2019 Page: 217 weakness get relieved with I.V infusion but this time, the weakness was prolonged and taken to a localhospitalwhere her potassium correction was made .But repeat potassium was low (1.9) .Hence referred to Pushpagiri Medical College.She did report several episodes of weakness after consuming ice creams. Her mother had been diagnosedwith hepatic cellular carcinoma and died 3 years ago. On examination, the patient's blood pressure was 100/60. No jugular venous distension, goiter or lymphadenopathy were appreciated. Cardiac exam revealed tachycardiawith a regular rhythm and no murmurs. Examination of the lungs and abdomen wereunremarkable. Neurologicexam revealed Grade 2 power. Routine chemistry, liver enzymes and complete blood count were normal except for a potassium level of 1.9(3.5–5 mmol/L),ESR- 52,ALP-122. Two hours after initiation of intravenous potassium replacement, the patient's symptoms had completely resolved. Thyroid stimulating hormone (TSH), triiodothyronine (T3) and thyroxine (T4) levels were obtained and revealed a markedly normal value. DISCUSSION There are several types of Periodic Paralysis associatedwith metabolic and electrolyte abnormalities. Of these, Hypokalemic Periodic Paralysis (HPP) is the most common. Electromyography reveals abnormalities in some patients but is often normal, especially between episodes when no clinically detectable weakness is present. HPP occurs in several settings and the diagnosis may require an extensive search for the underlying etiology since thetreatment varies according to the cause. Rarely, HPP can result from substantial gastrointestinal or renal potassium losses. Acetazolamide may prevent the paralytic episodes and antiarrhythmics or beta-blockers may prevent ventricular ectopy, but there is little data available.Most patients do not require treatment but areinstructedto avoid paralysis-inducing situations. CONCLUSION This patient presented with sudden onset paralysis and markedly abnormal potassium, ESR. This presentation is typical of Familial Hypokalemic Periodic Paralysis. The paralysis resolved completely following potassium replacement and she began a course of Acetazolamide 250 mg prior to being discharged from the hospital. At the time of discharge, she had no neurologic findings and a normal blood pressure. She has not suffered anyfurther episodes of paralysis .Periodic Paralysis is important to consider when seeing a patient with sudden onset weakness or paralysis, especially those with no history or evidence of other diseases and no significant risk factors for stroke. Failure to properly diagnose and treat Periodic Paralysis can be fatal, but rapid correction of potassium abnormalities can resolve the symptoms quickly and completely. When possible, the underlying cause must be adequately addressed to prevent the persistence or recurrence of paralysis. REFERENCES [1] Fontaine B. Chapter 1 Periodic Paralysis. Advances in Genetics. 63: Academic Press; 2008. p. 3-23. [2] Jurkat-Rott K, Lerche H, Lehmann-Horn F. Skeletal muscle channelopathies. J Neurol. 2002; 249:1493– 1502. doi: 10.1007/s00415-002-0871-5. [3] Lin SH, Lin YF, Chen DT, Chu P, Hsu CW, Halperin ML. Laboratory tests to determine the cause of hypokalemia and paralysis. Arch Intern Med. 2004; 164:1561–1566. doi: 10.1001/archinte.164.14.1561. [4] Fontaine B. Chapter 1 Periodic Paralysis. Advances in Genetics. 63: Academic Press; 2008. p. 3-23 [5] Melnick B, Chang J, Larson CE, Bedger R. Hypokalemic familial periodic paralysis. Anesthesiology. 1983; 58:263–5 [6] 6. Griggs RC, Resnick J, Engel WK. Intravenous treatment of hypokalemic periodic paralysis. Arch Neurol. 1983;40:539–40 [7] Rollman JE, Dickson CM. Anesthetic management of a patient with hypokalemic periodic paralysis for coronary artery bypass surgery. Anesthesiology. 1985;63:526–527 [8] 8. Levitt JO. Practical aspects in the management of hypokalemic periodic paralysis. J Transl Med. 2008;6:18. [9] https://www.uptodate.com/contents/hypokalemic- periodic-paralysis/abstract/10 [10] www.healthline.com/health/hypokalemic-periodic- paralysis