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Journal articles on the topic 'Hyperkalaemia'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Cornes, Michael P., Clare Ford, and Rousseau Gama. "Spurious hyperkalaemia due to EDTA contamination: common and not always easy to identify." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 45, no. 6 (September 9, 2008): 601–3. http://dx.doi.org/10.1258/acb.2008.007241.

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Background To study the detection and prevalence of spurious hyperkalaemia due to potassium ethylenediaminetetra-acetic acid (kEDTA) contamination. Methods In a one-month prospective study, serum EDTA, zinc, calcium, magnesium concentrations and alkaline phosphatase activity were measured in samples with serum potassium ≥6.0 mmol/L. Results Twenty-eight out of 117 hyperkalaemic samples were contaminated with EDTA. Only serum zinc values below the reference range had 100% sensitivity for indicating EDTA contamination, but even at an optimal specificity of 89% at least 12 potentially genuine hyperkalaemic samples would be rejected. Conclusion Spurious hyperkalaemia due to kEDTA contamination is common. Gross kEDTA contamination is obvious by marked unexpected hyperkalaemia, hypocalcaemia, hypomagnesaemia and hypozincaemia. Spurious hyperkalaemia due to low concentrations of kEDTA contamination can only be confidently detected by measurement of serum EDTA.

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2

McFadzean, Will, Paul Macfarlane, Latifa Khenissi, and Joanna C. Murrell. "Repeated hyperkalaemia during two separate episodes of general anaesthesia in a nine-year-old, female neutered greyhound." Veterinary Record Case Reports 6, no. 3 (September 2018): e000658. http://dx.doi.org/10.1136/vetreccr-2018-000658.

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There is an increasing awareness of the development of hyperkalaemia during anaesthesia in otherwise healthy veterinary patients. In the human literature 63 per cent of in-hospital hyperkalaemic episodes are associated with drug administration. Anecdotal veterinary reports have suggested that a genetic component may also play a role, with greyhounds seemingly more susceptible to the development of hyperkalaemia under anaesthesia. This case report identifies the repeated development of hyperkalaemia, and its treatment, during two separate episodes of general anaesthesia in a nine-year-old, female neutered greyhound. The first episode of hyperkalaemia (7.89 mmol/l) was identified due to bradycardia and second-degree atrioventricular block on electrocardiogram. Treatment was with intravenous calcium gluconate, insulin, glucose and fluid therapy. The second episode (6.60 mmol/l) was associated with spiked T-waves, and treatment was with insulin and glucose infusions to allow completion of the anaesthetic and surgery. Possible causes and treatments are discussed, and the need for reporting of such cases is highlighted.

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3

McNeill, Holly, and Chris Isles. "Electrocardiographic recognition of life-threatening hyperkalaemia: the hyperkalaemic Brugada sign." JRSM Open 10, no. 9 (September 2019): 205427041983424. http://dx.doi.org/10.1177/2054270419834243.

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Lesson Consider life-threatening hyperkalaemia if the ECG shows high take-off with coved ST segment elevation and negative T wave in lead V1 superimposed on other ECG signs of hyperkalaemia and treat with calcium gluconate while waiting for blood chemistry results.

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4

Nyirenda, M. J., J. I. Tang, P. L. Padfield, and J. R. Seckl. "Hyperkalaemia." BMJ 339, oct23 1 (October 23, 2009): b4114. http://dx.doi.org/10.1136/bmj.b4114.

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5

R, Manasa, Aksa Johnson, Presly Thomas Augustine, and Anjana Tom. "Assessment of Predictors of Hyperkalemia in Cardiovascular Diseased Patients." Journal of Drug Delivery and Therapeutics 11, no. 2 (March 15, 2021): 51–54. http://dx.doi.org/10.22270/jddt.v11i2.4587.

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Purpose: The objective is to determine the predictors of hyperkalaemia, severity of hyperkalaemia and to access the prevalence of cardiovascular diseases Methodology: A cross sectional observational study was conducted on the predictors of hyperkalaemia in CVD patients, in a tertiary care teaching hospital for a period of 6 months. Results: Among 105 patients, there were 83 males and 22 females, the age group from 41-60 year shows more CVDs and 61-80 years aged patients are more prone to hyperkalaemia and shows more prevalent when compared to other age groups. The major risk factors of hyperkalaemia were Drugs (30.23%), Disease (58.13%), and Drug interactions (11.62%).Among the cardiovascular diseases, Myocardial Infarction (38%) were the most common type of CVD, while in hyperkalaemia Ischemic Heart Disease (48.83%) were more prevalent. The severity of hyperkalaemia is measured as Mild (60.46%), Moderate (37.20%), and Severe (2.32%). Conclusion: The present study was carried out in order to assess the predictors, prevalence and severity of hyperkalaemia in cardiovascular disease patients. Our study concluded that patients with cardiovascular disease can have an increased risk of hyperkalaemia. Keywords: CVD, Hyperkalaemia, Cross sectional observational study, Predictors, Prevalence, Severity.

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6

Gross, P., and F. Pistrosch. "Hyperkalaemia: again." Nephrology Dialysis Transplantation 19, no. 9 (August 6, 2004): 2163–66. http://dx.doi.org/10.1093/ndt/gfh284.

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7

Cheng, C. J., C. S. Lin, L. W. Chang, and S. H. Lin. "Perplexing hyperkalaemia." Nephrology Dialysis Transplantation 21, no. 11 (September 12, 2006): 3320–23. http://dx.doi.org/10.1093/ndt/gfl389.

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8

Lexchin, Joel. "Treating hyperkalaemia." Lancet 361, no. 9357 (February 2003): 616. http://dx.doi.org/10.1016/s0140-6736(03)12544-5.

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9

Hoye, Angela, and Andrew Clark. "Iatrogenic hyperkalaemia." Lancet 361, no. 9375 (June 2003): 2124. http://dx.doi.org/10.1016/s0140-6736(03)13724-5.

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10

Taylor, Polly, Caroline Prymak, John Hird, Sophie Adamantos, Paul MacFarlane, and Will McFadzean. "Unanticipated hyperkalaemia." Veterinary Record 182, no. 3 (January 19, 2018): 84.2–84. http://dx.doi.org/10.1136/vr.k206.

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11

Smellie, W. Stuart A. "Spurious hyperkalaemia." BMJ 334, no. 7595 (March 29, 2007): 693–95. http://dx.doi.org/10.1136/bmj.39119.607986.47.

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12

Louro, Luís Filipe, Joanna Raszplewicz, and Briony Alderson. "Hyperkalaemia during general anaesthesia: six cases." Veterinary Record Case Reports 8, no. 3 (July 2020): e001075. http://dx.doi.org/10.1136/vetreccr-2020-001075.

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The objective of this case series is to describe the clinical course, treatment and outcome in six dogs following acute hyperkalaemia during general anaesthesia. A total of six dogs were presented for routine surgical and/or imaging procedures requiring general anaesthesia. All patients developed hyperkalaemia (ranging from 7.0 to 8.7 mmol/L, reference interval: 3.4–4.9 mmol/L), and electrocardiographic changes were seen in all but one case. The prognosis for treatment of hyperkalaemia during general anaesthesia appears to be excellent as all dogs fully recovered following treatment. To the authors’ knowledge, this is the first reported case series of hyperkalaemia during general anaesthesia in dogs. Our objective is to provide further information regarding possible causes for the development of hyperkalaemia in dogs under general anaesthesia.

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13

Maxwell, AP, K. Linden, S. O'Donnell, PK Hamilton, and GE McVeigh. "Management of hyperkalaemia." Journal of the Royal College of Physicians od Edinburgh 43, no. 3 (September 30, 2013): 246–51. http://dx.doi.org/10.4997/jrcpe.2013.312.

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14

Perazella, Mark A. "Trimethoprim-Induced Hyperkalaemia." Drug Safety 22, no. 3 (2000): 227–36. http://dx.doi.org/10.2165/00002018-200022030-00006.

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15

Morton, A. R., and S. A. Crook. "HYPERKALAEMIA AND SPIRONOLACTONE." Lancet 330, no. 8574 (December 1987): 1525. http://dx.doi.org/10.1016/s0140-6736(87)92658-4.

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16

KIRMIZIS, DIMITRIOS, and KAMILLA BIEDERMANN. "POST-DIALYSIS HYPERKALAEMIA." Nephrology 12, no. 2 (April 2007): 205–6. http://dx.doi.org/10.1111/j.1440-1797.2007.00765.x.

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17

Yentis, S. M. "Suxamethonium and Hyperkalaemia." Anaesthesia and Intensive Care 18, no. 1 (February 1990): 92–101. http://dx.doi.org/10.1177/0310057x9001800114.

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18

Gill, Denis G. "Hyperkalaemia or potassophobia?" Archives of Disease in Childhood 97, no. 12 (September 22, 2012): 1103. http://dx.doi.org/10.1136/archdischild-2012-302414.

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19

Panneerselvam, Arunkumar. "ECG in hyperkalaemia." Postgraduate Medical Journal 94, no. 1115 (April 26, 2018): 537. http://dx.doi.org/10.1136/postgradmedj-2018-135735.

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20

Bacon, N. C. "Hospital-acquired hyperkalaemia." Postgraduate Medical Journal 73, no. 861 (July 1, 1997): 433–34. http://dx.doi.org/10.1136/pgmj.73.861.433.

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21

Rastergar, A., and M. Soleimani. "Hypokalaemia and hyperkalaemia." Postgraduate Medical Journal 77, no. 914 (December 1, 2001): 759–64. http://dx.doi.org/10.1136/pgmj.77.914.759.

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22

Gama, R., M. Cornes, and C. Ford. "Avoiding spurious hyperkalaemia." BMJ 339, no. 17 2 (November 17, 2009): b4823. http://dx.doi.org/10.1136/bmj.b4823.

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23

Masters, P. W., A. A. A. Ismail, N. J. Gourlay, and C. McArthur. "Minimising factitious hyperkalaemia." BMJ 315, no. 7101 (July 19, 1997): 190. http://dx.doi.org/10.1136/bmj.315.7101.190a.

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24

Lim, YH, and J. Hendricks. "A Case of Nonfatal Non-Collapsed Patient with Extreme Hyperkalaemia." Hong Kong Journal of Emergency Medicine 14, no. 4 (October 2007): 228–32. http://dx.doi.org/10.1177/102490790701400407.

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This is a report of a non-collapsed patient with nonfatal, extreme hyperkalaemia of 10.7 mmol/L. The patient's hyperkalaemia was initially treated in the Emergency Department and then transferred to the Department of Renal Medicine of another hospital for further stabilisation. There have only been a few reported cases of successful management of extreme hyperkalaemia in excess of 10.0 mmol/L.

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25

Campbell, Patricia, Paul McKeveney, Kay Donegan, Charlie Ataliotis, Carol Patton, and Robert Mullan. "Practical guidance for the use of potassium binders in the management of hyperkalaemia in patients with heart failure and/or chronic kidney disease." British Journal of Hospital Medicine 82, no. 4 (April 2, 2021): 1–11. http://dx.doi.org/10.12968/hmed.2021.0215.

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Given the critical physiological role of potassium, it is understandable that the development of severe hyperkalaemia requires effective management to reduce its effects, which include muscle weakness, paralysis and cardiac arrhythmias. Hyperkalaemia most often results from the failure of renal adaptation to potassium imbalance. Patients who are most susceptible to the development of hyperkalaemia include those with chronic kidney disease and those with heart failure. These patients are often treated with renin–angiotensin–aldosterone system (RAAS) inhibitors, such as angiotensin-converting enzyme inhibitors and angiotensin II-receptor blockers, but the development of hyperkalaemia can require down-titration or cessation of RAAS inhibitors. This presents a significant challenge to nephrologists, cardiologists and healthcare professionals treating these patients as this can prevent them from receiving maximum guideline-directed RAAS inhibitor therapy. Panellists in this roundtable discussion shared their clinical experiences of using potassium binders to manage hyperkalaemia in patients with chronic kidney disease and patients with heart failure (illustrated with case studies) in Northern Ireland and considered recommendations for the implementation and maintenance of chronic potassium-lowering treatment.

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26

Jarman, PR, AM Kehley, and HM Mather. "Hyperkalaemia and apple juice." Lancet 358, no. 9284 (September 2001): 841. http://dx.doi.org/10.1016/s0140-6736(01)05986-4.

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27

Sowinski, Kevin M., and Bruce A. Mueller. "Hyperkalaemia and apple juice." Lancet 358, no. 9284 (September 2001): 841–42. http://dx.doi.org/10.1016/s0140-6736(01)05987-6.

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28

Fulop, Milford. "Hyperkalaemia and apple juice." Lancet 358, no. 9284 (September 2001): 842. http://dx.doi.org/10.1016/s0140-6736(01)05988-8.

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29

Newstead, C. G., Jon Friedland, David Paterson, and A. Waise. "HYPERKALAEMIA—SILENT AND DEADLY." Lancet 333, no. 8652 (June 1989): 1447. http://dx.doi.org/10.1016/s0140-6736(89)90148-7.

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30

Hata, Toshiyuki, Kohkichi Hata, and Takae Kawamura. "Severe hyperkalaemia with nafarelin." Lancet 347, no. 8997 (February 1996): 333. http://dx.doi.org/10.1016/s0140-6736(96)90514-0.

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31

Masterson, G. R. "Hyperkalaemia, suxamethonium and malignancy." Anaesthesia 51, no. 10 (October 1996): 991b—992b. http://dx.doi.org/10.1111/j.1365-2044.1996.tb14983.x.

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32

Martyn, J. A. J., and D. R. Goldhill. "Cold injury and hyperkalaemia." Anaesthesia 42, no. 5 (May 1987): 561. http://dx.doi.org/10.1111/j.1365-2044.1987.tb04074.x.

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33

Noble, K. "Hyperkalaemia causing profound bradycardia." Heart 92, no. 8 (August 1, 2006): 1063. http://dx.doi.org/10.1136/hrt.2005.071803.

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34

CHAUHAN, S., and P. TEWARI. "Paralysis caused by hyperkalaemia." British Journal of Anaesthesia 72, no. 3 (March 1994): 369. http://dx.doi.org/10.1093/bja/72.3.369.

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35

Thomas, N. "Hyperkalaemia in the elderly." QJM 90, no. 11 (November 1, 1997): 726a. http://dx.doi.org/10.1093/qjmed/90.11.726a.

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36

Butler, Javed, Shilpa Vijayakumar, and Bertram Pitt. "Revisiting hyperkalaemia guidelines: rebuttal." European Journal of Heart Failure 20, no. 9 (September 2018): 1255. http://dx.doi.org/10.1002/ejhf.1249.

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37

Murthy, B. V. S., H. D. Waiker, K. Neelakanthan, and K. M. Das. "Hyperkalaemia following blood transfusion." Postgraduate Medical Journal 75, no. 886 (August 1, 1999): 501–3. http://dx.doi.org/10.1136/pgmj.75.886.501.

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38

Strange, Barnaby. "Prehospital treatment of hyperkalaemia." Journal of Paramedic Practice 2, no. 5 (May 28, 2010): 194–99. http://dx.doi.org/10.12968/jpar.2010.2.5.48159.

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39

Crook, M. A. "Pseudohyperkalaemia or spurious hyperkalaemia." Annals of Clinical Biochemistry: An international journal of biochemistry and laboratory medicine 50, no. 2 (March 1, 2013): 180–81. http://dx.doi.org/10.1177/0004563213479210.

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40

Rees, Richard N., Joe Barnett, Daniel JB Marks, and Marc J. George. "Coconut water-induced hyperkalaemia." British Journal of Hospital Medicine 73, no. 9 (September 2012): 534. http://dx.doi.org/10.12968/hmed.2012.73.9.534.

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41

Tomcsányi, János, and Béla Bózsik. "Hyperkalaemia and cardiac pacing." Journal of Electrocardiology 51, no. 6 (November 2018): 1154. http://dx.doi.org/10.1016/j.jelectrocard.2018.08.015.

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42

Patel, M. C. "Trimethoprim related Hyperkalaemia in a Trimethoprim related Hyperkalaemia in acidosis type 4." Acute Medicine Journal 8, no. 3 (July 1, 2009): 117–18. http://dx.doi.org/10.52964/amja.0249.

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Hyperkalaemia is a common, treatable, medical emergency, often with an iatrogenic cause. This case illustrates the vulnerability of patients with pre-existing renal tubular acidosis type 4 to medications that further inhibit renin-aldosterone action. The case also illustrates the danger of keeping entirely separate case notes between different hospital disciplines.

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43

Van Elslande, Jan, Toon Dominicus, Jaan Toelen, Glynis Frans, and Pieter Vermeersch. "A case of severe pseudohyperkalaemia due to muscle contraction." Biochemia medica 30, no. 2 (June 14, 2020): 331–37. http://dx.doi.org/10.11613/bm.2020.021004.

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Introduction: Severe hyperkalaemia is a serious medical condition requiring immediate medical attention. Before medical treatment is started, pseudohyperkalaemia has to be ruled out. Case description: A 10-month old infant presented to the emergency department with fever and coughing since 1 week. Routine venous blood testing revealed a severe hyperkalaemia of 6.9 mmol/L without any indication of haemolysis. Reanalysis of the plasma sample confirmed the hyperkalaemia (7.1 mmol/L). Based on these results, the clinical pathologist suggested to perform a venous blood gas analysis and electrocardiogram (ECG) which revealed a normal potassium of 3.7 mmol/L and normal ECG, ruling out a potentially life-treating hyperkalaemia. The child was diagnosed with pneumonia. The paediatrician had difficulty to perform the first venous blood collection due to excessive movement of the infant during venipuncture. The muscle contractions of the child in combination with venous stasis most probably led to a local increase of potassium in the sampled limbs. The second sample collected under optimal preanalytical circumstances had a normal potassium. Since muscle contraction typically does not cause severe hyperkalaemia, other causes of pseudohyperkalaemia were excluded. K3-EDTA contamination and familial hyperkalaemia were ruled out and the patient did not have extreme leucocytosis or thrombocytosis. By exclusion a diagnosis of pseudohyperkalaemia due to intense muscle movement and venous stasis was made. Conclusion: This case suggests that intense muscle contraction and venous stasis can cause severe pseudohyperkalemia without hemolysis. Once true hyperkalemia has been ruled out, a laboratory work-up can help identify the cause of pseudohyperkalaemia.

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44

Wight, J. P., S. Laurence, S. Holt, and A. R. W. Forrest. "Rhabdomyolysis with Hyperkalaemia after Aminophylline Overdose." Medicine, Science and the Law 27, no. 2 (April 1987): 103–5. http://dx.doi.org/10.1177/002580248702700207.

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A case of rhabdomyolysis associated with hyperkalaemia and renal failure following an overdose of Aminophylline is reported. Whilst rhabdomyolysis has been reported previously in a patient without hyperkalaemia who survived, it is not a recognized complication of Aminophylline overdose but may have fatal results.

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45

Abdelaal Ahmed Mahmoud, Ahmed, Mark Campbell, and Margarita Blajeva. "Can ACE-I Be a Silent Killer While Normal Renal Functions Falsely Secure Us?" Case Reports in Anesthesiology 2018 (July 9, 2018): 1–4. http://dx.doi.org/10.1155/2018/1852016.

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The current case report represents a warning against serious hyperkalaemia and acidosis induced by ACE-I during surgical stress while normal renal function could deceive the attending anaesthetist. Arterial gas analysis for follow-up of haemoglobin loss accidentally discovered hyperkalaemia and acidosis. Glucose-insulin and furosemide successfully corrected hyperkalaemia after 25 minutes and acidosis after 3 hours. These complications could be explained by a deficient steroid stress response to surgery secondary to suppression by ACE-I. Event analysis and database search found that ACE-I induced aldosterone deficiency aggravated by surgical stress response with an inadequate increase in aldosterone secretion due to angiotensin II deficiency as a sequel of ACE-I leading to defective secretion of H+ and K+. Furosemide is recommended to secrete H+ and K+ compensating for aldosterone deficiency in addition to other antihyperkalaemia measures. Anaesthetising an ACE-I treated patient requires considering ACE-I as a potential cause of hyperkalaemia and acidosis.

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46

Linton, RAF, and DM Band. "Potassium and Breathing." Physiology 5, no. 3 (June 1, 1990): 104–7. http://dx.doi.org/10.1152/physiologyonline.1990.5.3.104.

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Potassium is lost from exercising muscle into extracellular fluid and causes hyperkalaemia. Intravenous administration of KCl in anesthetized cats to produce similar levels of arterial hyperkalaemia causes peripheral chemoreceptor stimulation, which produces an increase in ventilation. Interactions of arterial PO2, PCO2, and (K+) as drives to breathing are discussed.

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47

Lainscak, Mitja. "How to Improve Adherence to Life-saving Heart Failure Treatments with Potassium Binders." Cardiac Failure Review 03, no. 01 (2017): 33. http://dx.doi.org/10.15420/cfr.2017.2.1.

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Medications that affect the renin–angiotensin–aldosterone system (RAAS) form the mainstay of current heart failure (HF) therapy in patients with reduced ejection fraction. Concerns about the risk of hyperkalaemia have created a significant barrier to optimal RAAS inhibitor therapy in patients with HF, however, and many patients are discontinuing or receiving suboptimal doses of these lifesaving therapies. This has serious health and economic implications due to adverse renal and cardiovascular events. There is therefore an important unmet need for novel therapeutic options for the long-term management of patients with, and at risk for, hyperkalaemia. Two new potassium-binding agents, patiromer and ZS-9, have been shown to be effective and safe for the treatment of hyperkalaemia, as well as the maintenance of normokalaemia, without dose reduction or discontinuation of RAAS inhibitors. In addition, the fast onset of ZS-9 action suggests that it may be useful in the treatment of acute hyperkalaemia. These agents may allow for dose optimisation of RAAS inhibitors for the long-term maintenance and protection of the renal and cardiovascular system.

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48

van Vlijmen, Nicole, Robert Hoekstra, Albert-Jan Aarnoudse, and Donna van den Bersselaar. "Acute life-threatening hyperkalaemia in a patient with giant hydronephrosis: a case report." BMJ Case Reports 14, no. 4 (April 2021): e240946. http://dx.doi.org/10.1136/bcr-2020-240946.

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A 52-year-old man with a history of urolithiasis presents to the emergency department with a sudden, sharp, continuous right flank colicky pain. Laboratory workup demonstrates acute kidney injury with a mild hyperkalaemia. During the observation period, the patient develops an atypical broad complex sinus bradycardia and eventually short asystolic periods. This was caused by a severe therapy-resistant hyperkalaemia, wherefore emergency haemodialysis was necessary. Radiographic results showed a giant hydronephrosis with a blowout of the right kidney and an obstructing calculi of 21 mm in the distal ureter. We will discuss the mechanism of reversed intraperitoneal dialysis causing the refractory hyperkalaemia and the need of close ECG monitoring in patients where kidney blowout is considered.

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49

Provenzano, Michele, Roberto Minutolo, Paolo Chiodini, Vincenzo Bellizzi, Felice Nappi, Domenico Russo, Silvio Borrelli, et al. "Competing-Risk Analysis of Death and End Stage Kidney Disease by Hyperkalaemia Status in Non-Dialysis Chronic Kidney Disease Patients Receiving Stable Nephrology Care." Journal of Clinical Medicine 7, no. 12 (December 1, 2018): 499. http://dx.doi.org/10.3390/jcm7120499.

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Hyperkalaemia burden in non-dialysis chronic kidney disease (CKD) under nephrology care is undefined. We prospectively followed 2443 patients with two visits (referral and control with 12-month interval) in 46 nephrology clinics. Patients were stratified in four categories of hyperkalaemia (serum potassium, sK ≥ 5.0 mEq/L) by sK at visit 1 and 2: Absent (no-no), Resolving (yes-no), New Onset (no-yes), Persistent (yes-yes). We assessed competing risks of end stage kidney disease (ESKD) and death after visit 2. Age was 65 ± 15 years, eGFR 35 ± 17 mL/min/1.73 m2, proteinuria 0.40 (0.14–1.21) g/24 h. In the two visits sK was 4.8 ± 0.6 and levels ≥6 mEq/L were observed in 4%. Hyperkalaemia was absent in 46%, resolving 17%, new onset 15% and persistent 22%. Renin-angiotensin-system inhibitors (RASI) were prescribed in 79% patients. During 3.6-year follow-up, 567 patients reached ESKD and 349 died. Multivariable competing risk analysis (sub-hazard ratio-sHR, 95% Confidence Interval-CI) evidenced that new onset (sHR 1.34, 95% CI 1.05–1.72) and persistent (sHR 1.27, 95% CI 1.02–1.58) hyperkalaemia predicted higher ESKD risk versus absent, independently from main determinants of outcome including eGFR change. Conversely, no effect on mortality was observed. Results were confirmed by testing sK as continuous variable. Therefore, in CKD under nephrology care, mild-to-moderate hyperkalaemia status is common (37%) and predicts per se higher ESKD risk but not mortality.

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50

Strachan, Jamie, and Matthew Frise. "Life-threatening hyperkalaemia after succinylcholine." Lancet 395, no. 10219 (January 2020): e9. http://dx.doi.org/10.1016/s0140-6736(19)32493-6.

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