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Adverse drug event of hypokalaemia-induced cardiotoxicity secondary to the use of laxatives: A systematic review of case reports

Khan S, Khan SU

J Clin Pharm Ther, 2020 Oct;45(5):927-936.

PMID: 32672366 DOI: 10.1111/jcpt.13204

WHAT IS KNOWN AND OBJECTIVE: The imbalance in serum potassium caused by laxatives can negatively affect the cardiovascular system, leading to life-threatening consequences. Our objective was to evaluate the reported evidence of adverse events related to the cardiac system due to laxative-induced hypokalaemia from case reports.

METHODS: A systematic electronic literature search of PubMed, Embase, the Cochrane Library and Science Direct was conducted for the period 1995-2019. In these databases, search terms describing hypokalaemia and cardiotoxicity were combined with the term laxative use.

RESULTS AND DISCUSSION: Over the 23 years, 27 incidents were identified in 12 countries. There were 19 female and eight male patients, with ages ranging from 1 month to 93 years. The frequency of reported cases according to severity was the following: severe hypokalaemia 48%, moderate hypokalaemia 44.4% and mild hypokalaemia 7.4%. In 70% of patients, the effect of laxative on the heart was typical hypokalaemic electrographic changes, 7.4% showed abnormal changes in cardiac rhythm, whereas in 18.5%, the cardiotoxicity observed was a very serious kind. Two patients died due to severe cardiac effects.

WHAT IS NEW AND CONCLUSION: The laxatives-along with the involvement of some other contributing factors-caused mild-to-severe hypokalaemic cardiotoxicity. These factors were non-adherence of the patient to the recommended dosage, laxative abuse, drug-drug and drug-disease interactions, non-potassium electrolyte imbalances and the use of herbal laxatives. We recommend that laxatives and aggravating factors should be taken into account in the assessment of patients with suspected hypokalaemic cardiotoxicity.

Matched MeSH terms: Hypokalemia/complications

Fulltext Torsade de pointes and sudden death associated with diabetic autonomic diarrhoea--a case report

Quek DK, H'ng PK

Singapore Med J, 1993 Jun;34(3):266-70.

PMID: 8266190

A 68-year-old diabetic and hypertensive woman presented with chronic autonomic diarrhoea, syncope and palpitations which were associated with QT prolongation and recurrent episodes of torsade de pointes. She was on glibenclamide, indapamide and probucol (for type V hyperlipidaemia). Despite intravenous infusions of potassium, lignocaine and amiodarone, the unstable rhythm persisted. However, intravenous magnesium sulphate with small doses of intravenous propranolol terminated the torsade de pointes. She was stabilised but following discharge she relapsed, and upon re-admission, succumbed to intractable ventricular fibrillation. Early recognition and aggressive treatment of this condition is emphasised. Multiple aggravating factors ie autonomic diarrhoea resulting in severe potassium and magnesium depletion, kaliuretic effect of indapamide, probable QT prolongation associated with diabetic autonomic neuropathy and probucol; probable underlying coronary artery disease and heightened emotional and sympathetic discharge could have contributed to this very unstable ventricular arrhythmia and sudden death.

Matched MeSH terms: Hypokalemia/complications

Thyrotoxic periodic paralysis and intravenous propranolol in the emergency setting

Birkhahn RH, Gaeta TJ, Melniker L

J Emerg Med, 2000 Feb;18(2):199-202.

PMID: 10699522

A 27-year-old male of Malaysian descent presented to the Emergency Department (ED) with rapidly progressive flaccid paralysis that quickly compromised his respiratory effort. The patient was found to have a serum potassium of 1.9 meq/L, and was diagnosed as having an acute paralytic episode secondary to thyrotoxic periodic paralysis. The paralytic attack was aborted with a combination of potassium replacement and parenteral propranolol in large doses. We report the use of a rarely described, yet possibly more effective, therapy for an acute attack of thyrotoxic periodic paralysis.

Matched MeSH terms: Hypokalemia/complications

Fulltext Rhabdomyolysis associated with hypokalaemic periodic paralysis of renal tubular acidosis

Hanip MR, Cheong IK, Chin GL, Khalid BA

Singapore Med J, 1990 Apr;31(2):159-61.

PMID: 2371581

Two cases of hypokalaemia with serum potassium levels of 1.4 mmol/L and 1.9 mmol/L causing severe periodic paralysis since childhood are presented. There were associated with muscular aches and markedly raised muscle enzymes suggesting massive rhabdomyolysis. These abnormalities were due to renal tubular acidosis with markedly acidic arterial pH. The hypokalaemia and rhabdomyolysis responded to potassium and bicarbonate replacement. We postulate these patients had sporadic distal type of renal tubular acidosis and that the hypokalaemia and acidosis had caused the rhabdomyolysis.

Matched MeSH terms: Hypokalemia/complications*

High prevalence of hypokalemia after acute acetaminophen overdose: impact of psychiatric illness

Zyoud SH, Awang R, Syed Sulaiman SA, Al-jabi SW

Hum Exp Toxicol, 2010 Sep;29(9):773-8.

PMID: 20144962 DOI: 10.1177/0960327110361759

Hypokalemia is not an isolated disease but an associated finding in a number of different diseases. It is also a commonly neglected condition among patients with acute acetaminophen overdose.

Matched MeSH terms: Hypokalemia/complications*

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