Hypokalaemia associated with excessive cola-flavoured drinks consumption.

We present a case involving a male patient in his 30s who was admitted to hospital due to recurrent episodes of hypokalaemia over the past 5 years. His medical history revealed hypertension, attention deficit hyperactivity disorder (ADHD), autism, and paranoia. He was taking citalopram, ramipril, amlodipine, and pramipexole. Tests indicated normal levels of aldosterone/renin ratio and plasma metanephrines. On reviewing his dietary history, it was noted that he consumed 3 to 3.5 L of cola-flavoured drinks on a daily basis. Normal potassium levels were achieved after a significant reduction in cola-flavoured drinks intake and potassium replacement. Subsequent outpatient clinic follow-up revealed that normal potassium levels were maintained even after the patient ceased taking potassium replacement tablets. Given the rarity of hypokalaemia associated with fizzy drinks, the underlying mechanism for this association remains unclear. In this case report, we attempt to provide a possible explanation for the involved mechanisms.

Initial eGFR Changes with SGLT2 Inhibitor in Patients With Type 2 Diabetes and Associations With the Risk of Abnormal Serum Potassium Level.

BACKGROUND: Both high and low levels of serum potassium measurements are linked with a higher risk of adverse clinical events among patients with type 2 diabetes. The study was aimed at evaluating the implications of the various degrees of initial estimated glomerular filtration rate (eGFR) change on subsequent serum potassium homeostasis following sodium-glucose cotransporter-2 inhibitor (SGLT2i) initiation among patients with type 2 diabetes. METHODS AND RESULTS: We used medical data from a multicenter health care provider in Taiwan and recruited 5529 patients with type 2 diabetes with baseline/follow-up eGFR data available after 4 to 12 weeks of SGLT2i treatment from June 1, 2016, to December 31, 2018. SGLT2i treatment was associated with an initial mean (SEM) eGFR decline of -3.5 (0.2) mL/min per 1.73 m2 in overall study participants. A total of 36.7% (n=2028) of patients experienced no eGFR decline, and 57.9% (n=3201) and 5.4% (n=300) of patients experienced an eGFR decline of 0% to 30% and >30%, respectively. Patients with an initial eGFR decline of >30% were associated with higher variability in consequent serum potassium measurement when compared with those without an initial eGFR decline. Participants with a pronounced eGFR decline of >30% were associated with a higher risk of hyperkalemia ≥5.5 (adjusted hazard ratio,4.59 [95% CI, 2.28-9.26]) or use of potassium binder (adjusted hazard ratio, 2.65 [95% CI, 1.78-3.95]) as well as hypokalemia events <3.0 mmol/L (adjusted hazard ratio, 3.21 [95% CI, 1.90-5.42]) or use of potassium supplement (adjusted hazard ratio, 1.87 [95% CI, 1.37-2.56]) following SGLT2i treatment after multivariate adjustment. CONCLUSIONS: Physicians should be aware that the eGFR trough occurs shortly, and consequent serum potassium changes following SGLT2i initiation.

Polymorphic ventricular tachycardia and cardiac arrest from abiraterone-induced hypokalemia: a case report.

BACKGROUND: Polymorphic ventricular tachycardia (PMVT) is an unstable and often fatal cardiac tachyarrhythmia. While there are many causes of this rhythm, including electrolyte imbalances, ischemia, and genetic disorders, iatrogenic etiologies are important to recognize. Abiraterone is an androgen synthesis antagonist effective in treating prostate cancer, but here we describe a case of severe hypokalemia secondary to abiraterone resulting in polymorphic ventricular tachycardia and cardiac arrest. While this is a potential adverse effect of the medication, severe hypokalemia causing polymorphic ventricular tachycardia and cardiac arrest, as seen in our patient's case, has not been described. CASE PRESENTATION: A 78-year-old African-American man with history of prostate cancer presents with polymorphic ventricular tachycardia and cardiac arrest. After resuscitation, he was found to be severely hypokalemic and refractory to large doses of repletion. Evaluation of secondary causes of hypokalemia identified the likely culprit to be adverse effects from prostate cancer treatment. CONCLUSION: A broad differential diagnosis for polymorphic ventricular tachycardia is essential in identifying and treating patients presenting in this rhythm. Here we present a case of iatrogenic polymorphic ventricular tachycardia secondary to oncologic treatment.

[Flucloxacillin-induced hypokalemia]. / Door flucloxacilline geïnduceerde hypokaliëmie.

Flucloxacillin-induced hypokalaemia can be progressive and life-threatening, despite of potassium supplementation. In this case description, a high dose of intravenous flucloxacillin was started after a 68-year-old patient presented with an infected knee replacement. After two days, hypokalaemia was noted with an inadequate response to potassium supplementation. It was decided to change antibiotics and increase potassium supplementation, with good results. It is advisable to include monitoring of potassium levels in local treatment protocols when flucloxacillin is prescribed.

Outcomes associated with a variable rate insulin infusion diabetic ketoacidosis protocol.

AIMS: To relate adverse events with glucose correction rates in diabetic ketoacidosis (DKA) using variable rate intravenous insulin-infusions (VRIII). METHODS: Retrospective, observational study in adults with DKA who received insulin infusions between 2012 and 2017 at St Vincent's Hospital, Melbourne. Early correction of hyperglycaemia (<10 mmol/L) was evaluated for association with hypoglycaemia (<4.0 mmol/L), hypokalaemia (potassium <3.3 mmol/L) and clinical outcomes via regression analysis. RESULTS: The study involved 97 patients, with 93 % having type 1 diabetes. The mean age was 38 years, 47 % were women and 35 % were admitted to intensive care. Hypoglycaemia rates during 12 and 24 h of treatment were 6.2 % and 8.2 %, respectively with 58 % of patients recording their first BGL <10 mmol/L within 12 h and 88 % within 24 h. Ketone clearance time averaged at 15.6 h. Hyperglycaemia correction rates to <10 mmol/L were not different in those with/without hypoglycaemia at 12/24 h, in multivariate analysis including admission BGL. Hypokalaemia occurred in 40.2 % of patients and was associated with lower pH but not BGL correction rates. CONCLUSION: The VRIII protocol achieved early hyperglycaemia correction and ketoacidosis reversal with low hypoglycaemia risk. However, high hypokalaemia rates suggest the need for aggressive potassium replacement, especially in markedly acidotic patients.

Perianesthetic metabolic acidosis is associated with 2% dorzolamide eye drops in dogs that underwent ophthalmic surgery: a retrospective study (2019-2022).

OBJECTIVE: To evaluate whether the administration of 2% dorzolamide ophthalmic solution in dogs undergoing ophthalmic surgery is associated with perianesthetic metabolic acidosis. ANIMALS: 60 dogs, with or without dorzolamide administration, underwent arterial blood gas analysis immediately after anesthesia for ophthalmic surgery between 2019 and 2022; a total of 60 surgeries were evaluated. METHODS: This was a retrospective cross-sectional study. Logistic regression analysis was performed to investigate the association between the administration of 2% dorzolamide ophthalmic solution in dogs and the development of metabolic acidosis. Additionally, the influence of various potential risk factors, including age, body weight, sex, use of topical or systemic NSAIDs, and preoperative medications on the occurrence of metabolic acidosis, was evaluated. RESULTS: A significant association was found between the use of 2% dorzolamide ophthalmic solution and perianesthetic metabolic acidosis (OR, 6.79; 95% CI, 2.00 to 23.02; P = .002). Furthermore, topical dorzolamide administration was significantly associated with both perianesthetic hypokalemia (OR, 3.52; 95% CI, 1.11 to 11.20; P = .033) and perianesthetic hyperchloremia (OR, 9.25; 95% CI, 1.71 to 50.01; P = .010). CLINICAL RELEVANCE: The use of 2% dorzolamide ophthalmic solution is associated with perianesthetic metabolic acidosis, hypokalemia, and hyperchloremia in dogs. It is prudent to be aware of these risks, especially before anesthesia.

Risk of hyperkalaemia in patients with type 2 diabetes mellitus prescribed with SGLT2 versus DPP-4 inhibitors.

AIMS: To investigate the risk of hyperkalaemia in new users of sodium-glucose cotransporter 2 (SGLT2) inhibitors vs. dipeptidyl peptidase-4 (DPP-4) inhibitors among patients with type 2 diabetes mellitus (T2DM). METHODS AND RESULTS: Patients with T2DM who commenced treatment with an SGLT2 or a DPP-4 inhibitor between 2015 and 2019 were collected. A multivariable Cox proportional hazards analysis was applied to compare the risk of central laboratory-determined severe hyperkalaemia, hyperkalaemia, hypokalaemia (serum potassium ≥6.0, ≥5.5, and <3.5 mmol/L, respectively), and initiation of a potassium binder in patients newly prescribed an SGLT2 or a DPP-4 inhibitor. A total of 28 599 patients (mean age 60 ± 11 years, 60.9% male) were included after 1:2 propensity score matching, of whom 10 586 were new users of SGLT2 inhibitors and 18 013 of DPP-4 inhibitors. During a 2-year follow-up, severe hyperkalaemia developed in 122 SGLT2 inhibitor users and 325 DPP-4 inhibitor users. Use of SGLT2 inhibitors was associated with a 29% reduction in incident severe hyperkalaemia [hazard ratio (HR) 0.71, 95% confidence interval (CI) 0.58-0.88] compared with DPP-4 inhibitors. Risk of hyperkalaemia (HR 0.81, 95% CI 0.71-0.92) and prescription of a potassium binder (HR 0.74, 95% CI 0.67-0.82) were likewise decreased with SGLT2 inhibitors compared with DPP-4 inhibitors. Occurrence of incident hypokalaemia was nonetheless similar between those prescribed an SGLT2 inhibitor and those prescribed a DPP-4 inhibitor (HR 0.90, 95% CI 0.81-1.01). CONCLUSION: Our study provides real-world evidence that compared with DPP-4 inhibitors, SGLT2 inhibitors were associated with lower risk of hyperkalaemia and did not increase the incidence of hypokalaemia in patients with T2DM.

SGLT2 Inhibition and Kidney Potassium Homeostasis.

Pharmacologic inhibition of the sodium-glucose transporter 2 (SGLT2) in the proximal tubule brings about physiologic changes predicted to both increase and decrease kidney K + excretion. Despite these effects, disorders of plasma K + concentration are an uncommon occurrence. If anything, these drugs either cause no effect or a slight reduction in plasma K + concentration in patients with normal kidney function but seem to exert a protective effect against hyperkalemia in the setting of reduced kidney function or when given with drugs that block the renin-angiotensin-aldosterone axis. In this review, we discuss the changes in kidney physiology after the administration of SGLT2 inhibitors predicted to cause both hypokalemia and hyperkalemia. We conclude that these factors offset one another, explaining the uncommon occurrence of dyskalemias with these drugs. Careful human studies focusing on the determinants of kidney K + handling are needed to fully understand how these drugs attenuate the risk of hyperkalemia and yet rarely cause hypokalemia.

Evaluation of the pharmacokinetics of liposomal amphotericin B and analysis of the relationship between pharmacokinetics, efficacy and safety in patients with hematological diseases.

INTRODUCTION: This study aimed to identify factors responsible for changes in blood concentrations of a liposomal formulation of amphotericin B (AMPH-B, L-AMB) and analyze the relationships between blood concentrations and efficacy or toxicity. METHODS: L-AMB was administered to 30 patients being treated for hematological diseases. AMPH-B plasma concentrations were determined right before the initiation (Cmin) and at the end (Cmax) of infusion on at least 1 day, beginning on Day 3 of L-AMB treatment. The relationships of Cmin divided by dose (C/D ratio) to body weight, age, hepatic function, renal function, serum albumin, C-reactive protein (CRP), response, hypokalemia, and renal impairment were evaluated. RESULTS: C/D ratio was not correlated with age, hepatic function, renal function, or serum albumin. Body weight adjusted C/D ratio was negatively correlated with CRP. Cmax and Cmin were compared between responders and non-responders, those with or without hypokalemia, and those with or without renal impairment. A higher Cmax in patients with hypokalemia was the only significant difference seen. CONCLUSIONS: The negative correlation between CRP and plasma concentrations was likely caused by higher distribution of L-AMB from the blood to infected tissue in patients with a greater degree of infection, with a resulting decrease in plasma concentrations. AMPH-B plasma concentrations were not related to response. Higher Cmax of AMPH-B were observed in patients with hypokalemia, but no relationship between plasma concentration and renal toxicity was observed, suggesting that AMPH-B plasma concentrations appear to be minimally related to PD when used as L-AMB.

Comparison of Class-Specific Side Effects Across Preventative Pharmacologic Therapies for Kidney Stone Disease.

INTRODUCTION: Clinical guidelines recommend monitoring for metabolic derangements while on preventive pharmacologic therapy for kidney stone disease. The study objective was to compare the frequency of side effects among patients receiving alkali citrate, thiazides, and allopurinol. METHODS: Using claims data from working-age adults with kidney stone disease (2008-2019), we identified those with a new prescription for alkali citrate, thiazide, or allopurinol within 12 months after their index stone-related diagnosis or procedure. We fit multivariable logistic regression models, adjusting for cohort characteristics like comorbid illness and medication adherence, to estimate 2-year measured frequencies of claims-based outcomes of acute kidney injury, falls/hip fracture, gastritis, abnormal liver function tests/hepatitis, hypercalcemia, hyperglycemia/diabetes, hyperkalemia, hypokalemia, hyponatremia, and hypotension. RESULTS: Our cohort consisted of 1776 (34%), 2767 (53%), and 677 (13%) patients prescribed alkali citrate, thiazides, or allopurinol, respectively. Comparing unadjusted rates of incident diagnoses, thiazides compared to alkali citrate and allopurinol were associated with the highest rates of hypercalcemia (2.3% vs 1.5% and 1.0%, respectively, P = .04), hypokalemia (6% vs 3% and 2%, respectively, P < .01), and hyperglycemia/diabetes (17% vs 11% and 16%, respectively, P < .01). No other differences with the other outcomes were significant. In adjusted analyses, compared to alkali citrate, thiazides were associated with a higher odds of hypokalemia (OR=2.01, 95% CI 1.44-2.81) and hyperglycemia/diabetes (OR=1.52, 95% CI 1.26-1.83), while allopurinol was associated with a higher odds of hyperglycemia/diabetes (OR=1.34, 95% CI 1.02-1.75). CONCLUSIONS: These data provide evidence to support clinical guidelines that recommend periodic serum testing to assess for adverse effects from preventive pharmacologic therapy.

Rebound hyperkalemia in a dog with albuterol toxicosis after cessation of potassium supplementation.

OBJECTIVE: To describe the presentation of rebound hyperkalemia as a delayed side effect of albuterol toxicity in a dog. CASE SUMMARY: A 3-year-old female neutered mixed-breed dog was presented for albuterol toxicosis that led to a severe hypokalemia, hyperlactatemia, and hyperglycemia. The dog also experienced sinus tachycardia and generalized weakness. Treatment was instituted with intravenous fluid therapy and potassium supplementation, and the dog was monitored with a continuous electrocardiogram. Resolution of hypokalemia was documented 12 hours after initial presentation, at which time fluid therapy and potassium supplementation were discontinued. There were no further periods of sinus tachycardia, but instead the dog developed ventricular ectopy with rapid couplets (instantaneous rates of 300/min). An echocardiogram revealed normal cardiac size and function. Twenty-four hours after presentation, the patient developed severe hyperkalemia, despite discontinuation of fluids and potassium supplementation for 12 hours. Serial venous and urinary electrolytes were performed for determination of the fractional excretion of electrolytes. These data confirmed rebound hyperkalemia (7.0 mmol/L), consistent with a markedly increased fractional excretion of potassium, and secondary to the release of potassium from inside the cells. Fluid therapy with dextrose supplementation was provided until 36 hours postpresentation. The hyperkalemia resolved, and the dog was discharged after 44 hours of hospitalization. NEW OR UNIQUE INFORMATION PROVIDED: This case documents rebound hyperkalemia following treatment of albuterol toxicosis in a dog. This case highlights the importance of understanding the distribution of total body potassium when treating serum hypokalemia. Transcellular shifts of potassium, as in the case of albuterol toxicosis, can lead to rebound hyperkalemia even after discontinuation of potassium supplementation. This case further explores the utility of fractional excretion of electrolytes in elucidating the etiology and management of electrolyte disturbances.

Ogilvie Syndrome Secondary Due To Underlying Hypokalaemia And Anticholinergics: Case Report And Brief Review Of The Literature.

Ogilvie's syndrome is a rare but potentially life-threatening condition characterised by massive dilation of the colon without a mechanical obstruction. It typically affects older adults and those with underlying medical conditions, such as neurological or cardiovascular diseases, and may result in severe complications such as perforation or sepsis. Diagnosis is based on clinical presentation and radiological studies, and treatment involves a combination of conservative measures, such as bowel rest and pharmacological agents, and interventional procedures, such as endoscopic decompression or surgery. Here we present the case of a 67 year old male who presented with Ogilvie's syndrome after changes in his antipsychotic medications. He was given laxatives which led to persistent hypokalemia contributing to worsening distention. This case report highlights the important aspects in management such as cautious use of secretory laxatives (causing worsening Hypokalemia) and combination of motility agents in pseudo colonic obstruction.

Liquorice Toxicity: A Comprehensive Narrative Review.

BACKGROUND: Renowned since ancient times for its medical properties, liquorice is nowadays mainly used for flavoring candies or soft drinks. Continuous intake of large amounts of liquorice is a widely known cause of pseudo-hyperaldosteronism leading to hypertension and hypokalemia. These manifestations are usually mild, although in some cases may generate life-threatening complications, i.e., arrhythmias, muscle paralysis, rhabdomyolysis, and coma. In addition, liquorice has an important estrogenic-like activity. METHODS: We summarized the current knowledge about liquorice and reviewed 104 case reports in both the English and Italian languages from inception to June 2023 concerning complications due to an excess of liquorice intake. RESULTS: In contrast to most published data, female sex and old age do not appear to be risk factors. However, hypertension and electrolyte imbalance (mainly hypokalemia) are prevalent features. The detection of glycyrrhetinic acid in blood is very uncommon, and the diagnosis is essentially based on an accurate history taking. CONCLUSIONS: Although there is not a significant mortality rate, liquorice toxicity often requires hospitalization and therefore represents a significant health concern. Major pharmaceutical drug regulatory authorities should solicit public awareness about the potentially dangerous effects caused by excessive use of liquorice.

Hypokalemia after rituximab administration in nephrotic syndrome: two case reports.

Rituximab, a chimeric anti-CD20 monoclonal antibody, is an effective treatment for nephrotic syndrome. Hypokalemia is a rare adverse reaction among patients treated with rituximab although there have been extensive reports of acute and chronic adverse events with the administration of rituximab. We herein report two cases of symptomatic hypokalemia after intravenous rituximab administration in our center, to help health professionals consider the possibility of acute hypokalemia after rituximab administration, monitor potassium timely and develop an appropriate treatment plan.

Association between RCT methodology and disease indication with mineralocorticoid-related toxicity for patients receiving abiraterone acetate for advanced prostate cancer: A meta-analysis of RCTs.

INTRODUCTION: While abiraterone acetate (AA) has demonstrated survival benefit in advanced prostate cancer (APC), meaningful cardiotoxicity is observed. It is unclear whether the magnitude differs based on disease indication and concurrent steroid administration. METHODS: We performed a systematic review and meta-analysis of phase II/III RCTs of AA in APC published as of August 11, 2020. Primary outcomes examined were all- and high-grade (grade ≥ 3) hypokalemia and fluid retention, and secondary outcomes included hypertension and cardiac events. We performed random effects meta-analysis comparing intervention (AA + steroid) and control (placebo ± steroid), stratified by treatment indication and whether patients received steroids. RESULTS: Among 2,739 abstracts, we included 6 relevant studies encompassing 5901 patients. Hypokalemia and fluid retention were observed more frequently among patients receiving AA (odds ratio [OR] 3.10 [95% CI 1.69-5.67] and 1.41 [95% CI 1.19-1.66]). This was modified by whether patients in the control received steroids: trials where control patients did not demonstrated a larger association between AA and hypokalemia (OR 6.88 [95% CI 1.48-2.36] versus OR 1.86 [95% CI 4.97-9.54], P < .0001) and hypertension (OR 2.53 [95% CI 1.91-3.36] vs. OR 1.55 [95% CI 1.17-2.04], P = .1) than those where steroids were administered. We observed heterogeneity due to indication: there were greater effects on hypokalemia (P < 0001), hypertension (P = .03), and cardiac disorders (P = .01) among patients treated for mHSPC than mCRPC. CONCLUSIONS: The magnitude of cardiotoxicity with AA differs based on trial design and disease indication. These data are valuable in treatment decisions and highlight utilization of appropriate data for counseling.

Electrolytes Play a Role in Detecting Cisplatin-Induced Kidney Complications and May Even Prevent Them-Retrospective Analysis.

Background and Objective: Cisplatin is a chemotherapy drug used to treat several types of malignancies. It is a platinum-based compound that interferes with cell division and DNA replication. Cisplatin has been associated with renal damage. This study evaluates the early detection of nephrotoxicity through routine laboratory tests. Materials and Methods: This is a retrospective chart review based on the Saudi Ministry of National Guard Hospital (MNGHA). We evaluated deferential laboratory tests for cancer patients treated with cisplatin between April 2015 and July 2019. The evaluation included age, sex, WBC, platelets, electrolytes, co-morbidities and interaction with radiology. Results: The review qualified 254 patients for evaluation. Around 29 patients (11.5%) had developed kidney function abnormality. These patients presented with abnormally low magnesium 9 (31%), potassium 6 (20.7%), sodium 19 (65.5%) and calcium 20 (69%). Interestingly, the whole sample size had abnormal electrolytes presenting magnesium 78 (30.8%), potassium 30 (11.9%), sodium 147 (58.1%) and calcium 106 (41.9%). Some pathological features were detected, such as hypomagnesemia, hypocalcemia and hypokalemia. In addition, infections that needed antibiotics were dominant in patients treated with cisplatin alone, representing 50% of this group. Conclusions: We report that an average of 15% of patients with electrolyte abnormalities develop renal toxicity and reduced function. Moreover, electrolytes may serve as an early indicator for renal damage as part of chemotherapy complication. This indication represents 15% of renal toxicity cases. Changes in electrolyte levels have been reported with cisplatin. Specifically, it has been linked to hypomagnesemia, hypocalcemia and hypokalemia. This study will help reduce the risk of dialysis or the need for kidney transplant. It is also important to manage any underlying conditions and control patients' intake of electrolytes.

Zonisamide-induced distal renal tubular acidosis and critical hypokalaemia.

A woman in her 20s presented with rapidly progressive muscle weakness and a 1-month preceding history of fatigability, nausea and vomiting. She was found to have critical hypokalaemia (K+ 1.8 mmol/L), a prolonged corrected QT interval (581 ms) and a normal anion gap metabolic acidosis (pH 7.15) due to zonisamide-induced distal (type 1) renal tubular acidosis. She was admitted to the intensive care unit for potassium replacement and alkali therapy. Clinical and biochemical improvement ensued, and she was discharged after a 27-day inpatient stay.

Steroid-induced hypokalemic periodic paralysis: a case report and literature review.

BACKGROUND: Hypokalemic periodic paralysis (HPP) is a rare channelopathy characterized by episodic attacks of acute muscle weakness concomitant with hypokalemia. The etiology of hypokalemia is the shift of potassium into the cells, and the clinical symptoms resolve when potassium starts to leak back to the serum. Most of the time, the underlying ion channel defects are well compensated, and an additional trigger is often required to initiate an attack. Well-known trigger factors include carbohydrate-rich meals, exercise followed by rest, stress, cold weather, and alcohol consumption. CASE PRESENTATION: Here, we present the case of a 26-year-old Asian man who suffered from an acute onset of bilateral lower limb weakness with hypokalemia following dexamethasone injection. He was diagnosed with HPP. CONCLUSIONS: We would like to remind physicians to think of steroids as an unusual precipitating factor while managing patients with HPP, per results of this case study.

[Intraoperative management of potentially fatal arrhythmias after anesthesia induced by severe hypokalemia: A case report].

Severe hypokalemia is defined as the concentration of serum potassium lower than 2.5 mmol/L, which may lead to serious arrhythmias and cause mortality. We report an unusual case of potentially fatal ventricular arrhythmias induced by severe hypokalemia in a patient undergoing laparoscopic partial nephrectomy in Peking University Third Hospital due to irregular use of indapamide before operation. Indapamide is a sulfonamide diuretic with vasodilative and calcium antagonistic effects, which enhances sodium delivery to the renal distal tubules resulting in a dose-related increase in urinary potassium excretion and decreases serum potassium concentrations. The electrolyte disorder caused by the diuretic is more likely to occur in the elderly patients, especially those with malnutrition or long-term fasting. Hence, the serum potassium concentration of the patients under indapamide therapy, especially elderly patients, should be monitored carefully. Meanwhile, the potassium concentration measured by arterial blood gas analysis is different from that measured by venous blood or laboratory test. According to the previous research, the concentration of potassium in venous blood was slightly higher than that in arterial blood, and the difference value was 0.1-0.5 mmol/L. This error should be taken into account when rapid intravenous potassium supplementation or reduction of blood potassium level was carried out clinically. In the correction of severe hypokalemia, the standard approach often did not work well for treating severe hypokalemia. The tailored rapid potassium supplementation strategy shortened the time of hypokalemia and was a safe and better treatment option to remedy life-threatening arrhythmias caused by severe hypokalemia with a high success rate. Through the anesthesia management of this case, we conclude that for the elderly patients who take indapamide or other potassium excretion diuretics, the electrolyte concentration and the general volume state of the patients should be comprehensively measured and fully evaluated before operation. It may be necessary for us to reexamine the serum electrolyte concentration before anesthesia induction on the morning of surgery in patients with the history of hypokalemia. For severe hypokalemia detected after anesthesia, central venous cannulation access for individualized rapid potassium supplementation is an effective approach to reverse the life-threatening arrhythmias caused by severe hypokalemia and ensure the safety of the patients.