Hypokalemic periodic paralysis is anautosomal dominantdisease characterized by muscle

weakness or paralysis with a matching fall in blood potassium levels. Paralysis attacks

often occur in adolescence and are induced by strenuous exercise followed by rest,

high carbohydrateor high sodiummeal content, sudden changes in temperature, and

even excitement, noise, flashing lights and cold temperatures. Despite global daily use

of intravenous and oral potassium in the treatment of patients, data about intravenous

bolus potassium is rare. Here we report a 29-year-old man complaining of weakness in the

upper and lower limbs. By initial diagnosis of periodic hypokalemic paralysis, potassium

chloride was ordered by oral route. After a few minutes, we heard patient screaming in

pain. He complained of severe acute pain in peripheral intravenous line, palpitation and

dyspnea. We noticed that potassium chloride vial was infused directly via cubital vein in

few minutes erroneously. Physical exam revealed sinus tachycardia and hypertension. We

began hyperkalemia treatment immediately. With appropriate treatment,the patient was

discharged with good condition after 12 hours of admission.

Keywords: Hypokalemic paralysis, Hyperkalemia, Potassium chlorid

Seyed Hesam Rahmani1* , Gholamreza Faridaalaee2,

English

Simorgh Research Repository

Journal of Emergency Practice and TraumaIntroductionHypokalemic periodic paralysis is an autosomal dominant disease characterized by muscle weakness or paralysis with a matching fall in serum potassium levels. Attacks often occur in adolescence and are induced by strenuous exercise, high carbohydrate or high sodium meal content, sudden changes in temperature and cold temperatures. Weakness may be mild and limited to certain muscle groups, or more severe full body paralysis. Attacks may last for a few hours or several days. Some people only develop symptoms of periodic paralysis due to hyperthy-roidism (1). People with hypokalemic periodic paralysis maybe misdiagnosed as having a conversion disorder since the weakness is muscle-based and does not corre-spond to any nerve or spinal root distributions (2). Treat-ment of hypokalemic periodic paralysis focuses on reliev-ing acute symptoms and preventing further attacks by avoiding carbohydrate-rich meals and strenuous exercise. Paralysis attacks can be managed by drinking one of vari-ous potassium salts dissolved in water. Rapidly absorbed boluses of liquid potassium are generally needed to stop an attack, but some patients also find maintenance results with time-released tablets. Intravenous potassium is sel-dom justified unless the patient is unable to swallow (3). Potassium chloride is extensively used as a potassium sup-plement, mostly in the form of salt substitute. Therapeuti-cally, both oral and intravenous forms of potassium are used. Treatment of hypokalemia in stable patients who are able to tolerate oral intake can be done orally by food rich in potassium, salt substitutes and potassium supplements. IV replacement is appropriate for severe hypokalemia and infusion rate should be no greater than 40 mEq/h. Cardiac manifestations are the most serious side effect of hyperka-lemia and rapid KCL infusion, cardiac dysrhythmia such as VF, complete heart block and asystol may also occur (4). Here, we present the case of intravenous bolus injec-tion of potassium chloride into cubital vein in a young man with hypokalemic periodic paralysis.Case reportA 29-year-old healthy man was admitted to the emer-gency department (bodyweight, 78 kg) complaining of     Case ReportVolume 5, Issue 1, 2019, p. 29-31Accidental  intravenous bolus infusion of potassium chloride in a young man with hypokalemic periodic paralysis© 2019 The Author(s). Published by Kerman University of Medical Sciences. This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Seyed Hesam Rahmani1*, Gholamreza Faridaalaee21Emergency Medicine Department, Imam Khomeini Hospital, Urmia University of Medical Sciences, Urmia, Iran 2 Emergency Medicine Department, Maragheh University of Medical Sciences, Maragheh, IranReceived: 8 September 2017Accept: 12 November 2017Published online: 21 November 2017*Corresponding author: Seyed Hesam Rahmani, Emergency Medicine Department, Imam Khomeini Hospital, Urmia university of Medical Sciences, Urmia, Iran. Tel: +989121167809;Fax: 041133858859; Email: rahmani_h@umsu.ac.irCompeting interests: None.Funding information: None.Citation: Rahmani SH, Faridaalaee G. Accidental  intravenous bolus infusion of potassium chloride in a young man with hypokalemic periodic paralysis. Journal of Emergency Practice and Trauma 2019; 5(1): 29-31. doi: 10.15171/jept.2017.34AbstractHypokalemic periodic paralysis is anautosomal dominantdisease characterized by muscle weakness or paralysis with a matching fall in blood potassium levels. Paralysis attacks often occur in adolescence and are induced by strenuous exercise followed by rest, high carbohydrateor high sodiummeal content, sudden changes in temperature, and even excitement, noise, flashing lights and cold temperatures. Despite global daily use of intravenous and oral potassium in the treatment of patients, data about intravenous bolus potassium is rare. Here we report a 29-year-old man complaining of weakness in the upper and lower limbs. By initial diagnosis of periodic hypokalemic paralysis, potassium chloride was ordered by oral route. After a few minutes, we heard patient screaming in pain. He complained of severe acute pain in peripheral intravenous line, palpitation and dyspnea. We noticed that potassium chloride vial was infused directly via cubital vein in few minutes erroneously. Physical exam revealed sinus tachycardia and hypertension. We began hyperkalemia treatment immediately. With appropriate treatment,the patient was discharged with good condition after 12 hours of admission.Keywords: Hypokalemic paralysis, Hyperkalemia, Potassium chlorideJepthttp://jept.irOpen AccessPublish Freedoi 10.15171/jept.2017.34Rahmani and FaridaalaeeJournal of Emergency Practice and Trauma, 2019, 5(1), 29-3130the weakness in the upper and lower limbs. On arrival, the patient was hemodynamically stable. Oral tempera-ture was 37.5°C (99.5°F), pulse rate 78 bpm with a sinus rhythm, blood pressure 125/75 mm Hg, and his respira-tory rate was 14 breaths per minute. The abdomen and bowel sounds were normal. The initial oxygen saturation was 94% (in room air). He was alert and awake with no apparent distress. In clinical examination, forces of up-per limbs were 3/5 but lower limbs were 4/5. Weakness of upper limbs was more significant. By initial diagnosis of periodic hypokalemic paralysis,potassium chloride (50 cc of 15 % [7.5 g]) was ordered by oral route. After a few minutes, we heard patient screaming in pain. We quickly attended the patient’s bed and it was very surprising to see him severely agitated with severe acute pain in peripheral IV line, palpitation and dyspnea. Immediately, we found that all of potassium chloride vial was infused directly via right cubital vein in few minutes erroneously. After that, the patient was transferred to CPR part immediately. He went under cardiac monitoring and received oxygen by nasal canola. He had sinus tachycardia (HR = 140), HTN (160/90) and tachypnea (RR: 28). Calcium gluconate solu-tion (10 cc of 10%) was intravenously injected in 2 min-utes and one litre of normal saline was immediately in-fused. Only 15-20 minutes after injection of calcium glu-conate and serum, dyspnea and palpitation became better, but 20 minutes latter symptoms of the patient flared up. Due to this situation another calcium gluconate solution was intravenously reinjected and one litre of normal saline was ordered again for one hour. The color Doppler sonog-raphy of the right upper extremity showed no thrombosis in superficial veins. Muscle weakness was healed in the first few minutes. A 12-lead electrocardiogram revealed sinus tachycardia at a rate of 140 bpm (Figure 1). Lab data in admission time: a complete blood count in patient was normal except for a mildly elevated white blood cell count of 11.2× 103/µL (11.2× 109/L), with 50% neutrophils, 48% lymphocytes, 1% monocytes, and 1% eosinophils, hemo-globin 15.3 g/dL, hematocrit 44.5%. His serum blood urea nitrogen, creatinine, creatinine kinase, and liver function tests were normal (sodium 141 mEq/L, potassium 3.2 mEq/L, calcium [total] 9 mg/dL, magnesium 1.7 mg/dL). Serum glucose was 130 mg/dL. In the blood sample taken after the first injection of calcium gluconate, potassium was 4 and 3 hours before discharge, potassium level was 3.8. Patient was discharged 12 hours after admission by diagnosis of periodic hypokalemic paralysis with recom-mendation of low carbohydrate and high potassium diet. He was advised to apply warm compress and ibuprofen 400 mg orally every 6 hours was prescribed as well.DiscussionIntentional intravenous potassium intoxication or intoxi-cation due to medical treatment is a rare and very dan-gerous condition. The risks of intravenous potassium chloride injections are well known. Rapid or high dose injection can cause cardiac arrest within minutes. The ef-fect of hyperkalemia on the heart is complex – virtually any arrhythmia may be observed (5). Hyperkalemia cause various electrocardiography (ECG) changes, depending on potassium serum concentration. So, ECG is essential to detect and follow these abnormalities. There is a close cor-relation between plasmatic potassium concentration and ECG changes with great variability (6). Rapid diagnosis and treatment of intravenous potassium poisoning by ad-ministration of calcium gluconate and other medications as beta-2-adrenergic agonists and insulin-glucose im-proved outcome (6). The ion exchange resins and diuret-ics have no role in this type of care. Their delayed effect dedicate them to the treatment of chronic moderate hy-perkalemia. Hemodialysis performed in emergency is the standard treatment of hyperkalemia, particularly in cases of severe hyperkalemia which quickly set up or with high risk of reconstitution (hemolysis, tissue catabolism) (6). Most toxic hyperkalemia described in texts and case re-ports are due to sustained-release potassium supplements, side effects, or overdose of medical treatments (7-9).The true incidence of potassium-related fatalities and incidents is unknown. Fatal intravenous injection of potassium pro-duces no specific anatomic changes and if any findings, it is subtle (10). Nilsson et al reported a case of a 30-year-old woman who was admitted to the emergency depart-ment due to the ingestion of 300 slow-release tablets of potassium-chloride. Her serum potassium was 9.5 mmol/l and cardiovascular function was poor. Despite intensive medical treatment and gastric lavage, serum potassium re-mained very high (9 mmol/l). Although hemodialysis was initiated but despite ongoing dialysis, potassium increased to 10.3 mmol/l. A parallel dialysis was started and after 4 hours of parallel dialysis, serum potassium decreased to 6.4 mmol/l. An x-ray revealed large amounts of pills re-maining in the stomach and the surgeon removed about 200 pills with laparotomy. The patient recovered slowly thereafter, but later developed a gastric stricture and PTE (11). Battefort et al in 2012 reported a case of a 20-year-old nurse student with IV injection of four vials of potassium chloride (20 mL, 10%) and subsequent cardiac arrest with asystol rhythm. Initial resuscitation with epinephrine and sodium bicarbonate resulted in the recovery and effective cardiac activity without any squeal. They concluded that the advanced resuscitation with the use of a specific treat-ment helped to resuscitate the patient (12). Bertol et al in 2012 reported a case of a 41-year-old man who died due Figure 1. Twelve-lead electrocardiogram revealed sinus tachycardia.Rahmani and FaridaalaeeJournal of Emergency Practice and Trauma, 2019, 5(1), 29-31 31to intravenous injection of potassium chloride (13). In our case with underlying hypokalemia, sins tachycardia and no renal dysfunction it seems that hyperkalemia will be transient and we prefer to use just calcium gluconate to protect cardiac cell and hydration. We avoid using other treatment options such as insulin–glucose, beta-2-adren-ergic agonists and bicarbonate or the ion exchange resins, diuretics and hemodialysis.ConclusionThere are some case reports of life-threatening dysrhyth-mia and death due to rapid IV potassium infusion and oral high dose ingestion. Immediate recognition and spe-cific treatment are vital to survive patients.Ethical issuesConfidentiality of patient information was maintained. References1. Kung AW. Clinical review: thyrotoxic periodic paralysis: a diagnostic challenge. J Clin Endocrinol Metab 2006; 91(7): 2490-5. doi: 10.1210/jc.2006-0356. 2. Segal MM, Jurkat-Rott K, Levitt J, Lehmann-Horn F. Hypokalemic periodic paralysis - an owner’s manual. Available from: http://simulconsult.com/resources/hypopp.html.3. Kim JB, Kim MH, Lee SJ, Kim DJ, Lee BC. The genotype and clinical phenotype of Korean patients with familial hypokalemic periodic paralysis. J Korean Med Sci 2007; 22(6): 946-51. doi: 10.3346/jkms.2007.22.6.946.4. Tintinalli JE, Stapczynski JS, Ma OJ, Yealy DM, Meckler GD, Cline DM. Tintinalli’s Emergency Medicine. 7th ed. New York: McGraw-Hill Medical; 2011. p. 121-122.5. Rardon DF, Fisch C. Electrolytes and the heart. In: Schlant RC, Alexander RW, eds. Hurst’s the Heart. 8th ed. New York: McGraw-Hill; 1994. p. 759-74.6. Alfonzo AV, Isles C, Geddes C, Deighan C. Potassium disorders--clinical spectrum and emergency management. Resuscitation 2006; 70(1): 10-25. doi:10.1016/j.resuscitation.2005.11.002.7. McCann B, Hunter R, McCann J. Cocaine/heroin induced rhabdomyolysis and ventricular fibrillation. Emerg Med J 2002; 19(3): 264-5.8. Ochoa-Gómez J, Villar-Arias A, Aresti I, Marco-Aguilar P. A case of severe hyperkalaemia and compartment syndrome due to rhabdomyolysis after drugs abuse. Resuscitation 2002; 54(1): 103-5.9. Nathan A, Ganesh A, Godinez RI, Nicolson SC, Greeley WJ. Hyperkalemi cardiac arrest after cardiopulmonary bypass in a child with Duchenne muscular dystrophy. Anesth Analg 2005; 100(3): 672-4. doi: 10.1213/01.ANE.0000146533.21771.2F.10. Wetherton AR, Corey TS, Buchino JJ, Burrows AM. Fatal intravenous injection of potassium in hospitalized patients. Am J Forensic Med Pathol 2003; 24(2): 128-31. doi: 10.1097/01.paf.0000068224.31539.a9.11. Nilsson TS, Malmgren J, Knudsen K. Parallel haemodialysis and surgery saves a life after massive overdose of potassium pills. BMJ Case Rep 2012. doi: 10.1136/bcr.02.2012.5773.12. Battefort F, Dehours E, Vallé B, Hamdaoui A, Bounes V. Suicide attempt by intravenous potassium self-poisoning: a case report. Case Rep Emerg Med 2012; 2012: 323818. doi: 10.1155/2012/323818.13. Bertol E, Politi L, Mari F. Death by potassium chloride intravenous injection: evaluation of analytical detectability. J Forensic Sci 2012; 57(1): 273-5. doi: 10.1111/j.1556-4029.2011.01907.x. 

Accidental intravenous bolus infusion of potassium

chloride in a young man with hypokalemic periodic

paralysis

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Accidental intravenous bolus infusion of potassium chloride in a young man with hypokalemic periodic paralysis

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