[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.

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.

[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.

Hypokalaemia associated with hydrochlorothiazide used in the treatment of hypertension in NHANES 1999-2018.

Hydrochlorothiazide is the most common thiazide diuretic used for hypertension in the US. Yet, hypokalaemia is a well-recognised adverse effect. To evaluate the prevalence and factors associated with hypokalaemia (serum potassium < 3.5 mmol/L) among hydrochlorothiazide users, we included US adults aged ≥20 years in the 1999-2018 National Health and Nutrition Examination Survey. Participants were categorised according to the use of hydrochlorothiazide and other antihypertensive agents. Factors associated with hypokalaemia, including demographics and prescription patterns (monotherapy vs single-pill fixed-dose combination vs polytherapy) were studied using multivariable logistic regression. Hypokalaemia was present in 12.6% of the hydrochlorothiazide users, equivalent to ~2.0 million US adults. Women (adjusted OR, 2.22; 95% CI, 1.74-2.83), non-Hispanic blacks (adjusted OR, 1.65; 95% CI, 1.31-2.08), underweight (adjusted OR, 4.33; 95% CI, 1.34-13.95), and participants taking hydrochlorothiazide for five years or more (adjusted OR, 1.47; 95% CI, 1.06-2.04) had a higher risk of hypokalaemia. Compared to monotherapy, fixed-dose combination therapy (adjusted OR, 0.32; 95% CI, 0.21-0.48) was associated with the lowest risk. Among those taking potassium supplements, hypokalaemia was found in 27.2% of participants on monotherapy and 17.9% on polytherapy. The prevalence of hypokalaemia among hydrochlorothiazide users was considerable, even among participants who also took potassium supplements. Women, ethnic minorities, underweight, monotherapy, and participants with long-term therapy are more likely to have hypokalaemia. Regular monitoring of potassium and combination with potassium-sparing drugs are needed.

The Effects of Magnesium Coadminstration During Treatment of Hypokalemia in the Emergency Department.

BACKGROUND: Hypokalemia is a common disorder that can negatively affect organ function. Magnesium supplementation is frequently recommended despite limited evidence to support its use. OBJECTIVES: The purpose of this study was to evaluate the clinical effects of magnesium coadministration in patients treated for hypokalemia in the emergency department (ED). METHODS: This retrospective, single-center study evaluated adults treated with intravenous (i.v.) potassium for hypokalemia (serum potassium <3.5 mMol/L) in the ED between July 1, 2016 and June 30, 2020. Patients given magnesium supplementation within 4 h of potassium administration (MG+) were compared with those not given concurrent magnesium (MG-). The primary outcome was time to potassium normalization (≥ 3.5 mMol/L). Secondary outcomes included clinical effects, adverse effects, and dosing of magnesium and potassium. RESULTS: Two hundred patients were included (MG+ = 100; MG- = 100). Patients in the MG- group more frequently had history of myocardial infarction (16% vs. 6%; p = 0.02) and alcoholism (16% vs. 6%; p = 0.02). Patients in the MG+ group had higher incidence of symptomatic hypokalemia (34% vs. 19%; p = 0.02) and severe hypokalemia (serum potassium < 2.5 mMol/L) (15% vs. 8%; p = 0.03). There were no differences in time to serum potassium normalization, change in serum potassium after treatment, or incidence of potassium normalization within 24 h of treatment. MG+ patients required more potassium within 24 h of treatment and more frequently developed hypermagnesemia (serum magnesium >1.1 mMol/L). CONCLUSIONS: Magnesium coadministration during hypokalemia treatment did not affect time to serum potassium normalization but was associated with more hypermagnesemia.

Pairwise comparison of hydrochlorothiazide and chlorthalidone responses among hypertensive patients.

This study conducted a pairwise comparison of antihypertensive and metabolic effects of hydrochlorothiazide (HCTZ) and chlorthalidone (CTD) at 25 mg/day in the same individuals to address the clinical dilemma on preferred thiazide for hypertension (HTN) management. We included 15 African American (AA) and 35 European American (EA) patients with HTN treated with HCTZ and CTD as part of the Pharmacogenomic Evaluation of Antihypertensive Responses (PEAR) and PEAR-2 trials, respectively. Mean reduction in systolic/diastolic blood pressure (SBP/DBP) with HCTZ versus CTD was 8/5 versus 16/8 mmHg among EA patients (p < 1.0e-5 SBP, p = 0.002 DBP) and 11/8 versus 20/11 mmHg among AA patients (p = 0.03 SBP, p = 0.22 DBP). While CTD showed clinically meaningful benefit over HCTZ in two-thirds of participants with respect to SBP reduction and half of EA patients with respect to DBP reduction, a majority of AA patients (53%) showed similar DBP reduction with both thiazides. Sixty percent of AA patients and 29% of EA patients attained blood pressure (BP) <140/90 mmHg with both thiazides. Mean potassium (K+) reduction was greater with CTD compared to HCTZ both in EA patients (mean difference = 0.35, p = 0.0002) and AA patients (0.49, p = 0.043). While 31% of AA patients developed severe hypokalemia on CTD, <5% of others developed severe hypokalemia. Although 46% of AA patients on CTD required K+ supplementation, only 6%-11% of others required supplementation. Overall, in the majority of EA patients, CTD was superior to HCTZ, whereas among AA patients, it was superior in a minority, and was associated with significant potassium-related risk, suggesting that guideline preferences for CTD over HCTZ are reasonable in EA patients but may be less reasonable in AA patients, particularly if the target is <140/90 mmHg.

[A case of arrhythmia caused by barium carbonate poisoning].

Barium carbonate poisoning is mostly caused by mistaken ingestion in clinical cases, and self-administration of poisoning is rare. In November 2020, Tianjin Occupational Disease Prevention Hospital admitted a patient with severe hypokalemia complicated with arrhythmia after taking poison. It is very important to take timely and effective potassium supplementation, symptomatic and detoxification treatment in the course of treatment. At the same time, closely observing the changes of vital signs and taking quick and accurate rescue measures in the event of malignant arrhythmia are the keys to ensuring the success of rescue. In this paper, the clinical data of the case were retrospectively analyzed, providing reference for the diagnosis and treatment of similar clinical cases.

Hypokalemic Paresis in a 26-Year-Old Man After Recreational Cannabis Use.

BACKGROUND Hypokalemia (serum potassium level below 3.5 mmol/L) is present in approximately 11% of patients admitted to emergency departments. Hypokalemia can be a manifestation of many underlying causes and if untreated can be fatal. A careful approach to work-up and management is required in hypokalemic patients. CASE REPORT Here we report a 26-year-old previously healthy male patient who was admitted to the Emergency Department with rapidly progressing paresis of the lower and upper extremities. Initial laboratory results revealed severe hypokalemia of 2.1 mmol/l, which aggravated to 1.6 mmol/l before receiving treatment with intravenous potassium chloride supplementation. In addition, the patient developed rhabdomyolysis secondary to prolonged paralysis and immobilization induced by hypokalemia. Following this treatment, the patient's symptoms eased rapidly, and his potassium concentration was normalized. The patient admitted to smoking cannabis the day before admission. In this case report, we systematically elaborate and exclude the causes of hypokalemia in this otherwise healthy young adult, including medication, gastrointestinal symptoms, licorice consumption, and genetical testing. Cannabis has been associated with hypokalemia, proposedly through activation of the cannabinoid receptor 1 (CB1)-mediated activation of G protein-coupled inwardly rectifying potassium (GIRK) channels. CONCLUSIONS This case report emphasizes that hypokalemia can cause paralysis and cannabis should be included in the diagnostic mindset.

Hypomagnesemia and Hypokalemia: Considerations for Cancer Care.

Electrolyte imbalances can frequently occur among patients with cancer. Hypomagnesemia and hypokalemia are side effects of certain chemotherapies, including cisplatin, cetuximab, eribulin, and ifosfamide. When patients concurrently receive chemotherapy and take medications that cause hypomagnesemia or hypokalemia, electrolyte imbalances are amplified. Provider and patient education are vital to identifying and treating these conditions in a timely manner. If medication usage depletes electrolytes, repletion through diet and supplements is essential. In symptomatic cases of electrolyte deficiency, oral and IV formulations of potassium and magnesium are options for treatment. This article discusses the importance of identifying and understanding the etiologies, symptoms, and treatment modalities of hypomagnesemia and hypokalemia.

Capecitabine-induced severe diabetes and hypokalemia: a case report.

BACKGROUND: Capecitabine is widely used in chemotherapy for breast, colorectal, and gastric cancers. The frequent adverse reactions of capecitabine mainly include gastrointestinal side effects, anemia, and cardiovascular toxicity. Here, we report a rare case of severe hyperglycemia and hypokalemia during long-term treatment with capecitabine. CASE PRESENTATION: A 48-year-old Chinese female was hospitalized with the complaint of breathlessness and weakness after activity, for 1 month. Her past history is significant for a diagnosis of right-sided breast cancer 7 years ago. She underwent right mastectomy, following which capecitabine was started 1.5 years prior to the current admission as part of her primary treatment at the discovery of systemic osseous metastasis. Her fasting plasma glucose and hemoglobin A1c levels were quite normal 7 months ago but increased to 15.3 mmol/L and 11.2%, respectively, at the present admission. Her serum potassium level was as low as 2.5 mmol/L. Plasma autoantibodies related to islets and insulin were all negative. Capecitabine was discontinued, and an insulin pump and potassium supplement were given after admission. Her blood sugar and potassium levels returned to their normal ranges soon. Self-injection of insulin was withdrawn completely at 2 months after discharge, and no oral hypoglycemic agents were added. Her plasma glucose and electrolyte levels were at normal levels at her 1-year follow-up. CONCLUSION: Glucose intolerance and hypokalemia may be rare but serious adverse effects during long-term chemotherapy with capecitabine.

A Comprehensive Review of the Pharmacologic Perspective on Loop Diuretic Drug Interactions with Therapeutically Used Drugs.

BACKGROUND: Loop diuretics help to manage the patients with edema associated with congestive heart failure, liver cirrhosis, and renal disease and hypertension. The patients taking loop diuretics may receive other medications to treat comorbidities leading to drug interactions. METHODS: The literature was searched in databases such as Medline/PMC/PubMed, Google Scholar, Cochrane Library, Science Direct, EMBASE, Web of science, Ebsco, Directory of open access journals (DOAJ) and reference lists were used to spot relevant articles using keywords Drug interactions, Pharmacodynamic interactions, Loop diuretics, Bumetanide, Ethacrynic acid, Furosemide, and Torsemide. RESULTS: Loop diuretics are associated with hypokalemia, ototoxicity and other adverse effects. The drugs affected by hypokalemia and having the potential of inducing ototoxicity could interact with loop diuretics pharmacodynamically. Loop diuretics can interact with drugs such as amphotericin B, digoxin, angiotensin-converting enzyme inhibitors (ACE inhibitors), antidiabetic drugs, antifungal agents, dobutamine, gossypoland sotalol due to diuretic associated hypokalemia. In addition, the risk of ototoxicity could be enhanced by the concomitant use of loop diuretics and cisplatin, aminoglycoside antibiotics or phosphodiesterase 5 (PDE 5) inhibitors. Loop diuretics may also interact pharmacodynamically with drugs like cephalosporins, ceritinib, levothyroxine, pixantrone, probenecid, lithium, nonsteroidal anti-inflammatory drugs (NSAIDs), sulfonylureas and herbal drugs. CONCLUSION: Clinicians, pharmacists and other health care providers should take responsibility for the safe use of medications. In addition, they are required to be aware of the drugs interacting with loop diuretics to prevent adverse drug interactions.

Retrospective evaluation of acute salbutamol (albuterol) exposure in dogs: 501 cases.

OBJECTIVE: To determine the common clinical signs, with onset and duration, treatments given, and outcome in dogs with acute, accidental exposure to salbutamol. DESIGN: Retrospective study. ANIMALS: Five hundred and one canine cases reported to the UK's Veterinary Poisons Information Service (VPIS). MEASUREMENTS AND MAIN RESULTS: A review of all records in the VPIS database for dogs exposed to salbutamol was carried out. After applying inclusion and exclusion criteria, the records of 501 dogs were further analyzed. The most common clinical signs were tachycardia (80.6%), tachypnea (32.9%), depression (21.0%), and vomiting (19.2%). The dose was unknown in most cases as the dogs typically pierced a salbutamol inhaler. The blood potassium concentration was measured in at least 142 dogs and hypokalemia was reported in 21.2% (106/501), 18 (17%) of which had associated weakness, twitching, or collapse. Three dogs had paralysis probably as a result of hypokalemia, although no potassium concentration was reported in these cases. Arrhythmias occurred in 17 dogs (3.4%), and 7 required pharmacological intervention. There were no reports of persistent cardiac injury or thermal injury from the compressed gas present in some salbutamol products. Signs were rapid in onset, generally within 1-3 h, and, where time to outcome was recorded (n = 172), 78% of dogs recovered within 24 h. Of the 501 dogs, no treatment was required in 27.9%. Beta-blockers were used in 39.5%, intravenous fluids in 28.7%, and potassium supplementation in 15.8%. Overall, 30 dogs remained asymptomatic (6.0%), 469 recovered (93.6%), and 2 dogs (0.4%) died. CONCLUSIONS: Most dogs exposed to salbutamol rapidly develop clinical signs; these were commonly increased heart and respiration rates. Hypokalemia and arrhythmias (particularly ventricular arrhythmias) are potential complications. Any dog that chews a salbutamol inhaler should be assessed promptly for signs of toxicosis. Prognosis in dogs with acute salbutamol exposure is good, but more guarded in those with severe tachycardia and at risk of cardiac injury.

Dyskalemia risk associated with fixed-dose anti-hypertensive medication combinations.

A model-based meta-analysis quantified comparative dyskalemia risk (hyper- or hypo-kalemia) in hypertensive patients treated with angiotensin receptor blockers (ARBs), a calcium channel blocker (CCB) and/or a thiazide diuretic (hydrochlorothiazide; HCTZ) as monotherapy or as fixed-dose combinations. Among 15 randomized controlled trials in a US Food and Drug Administration regulatory review database, dyskalemia events were reported by five trials (24 treatment arms, 11,030 subjects, 8-week median follow up time). The five trials evaluated monotherapy (ARB or HCTZ) alongside dual (ARB + HCTZ, ARB + CCB, or HCTZ + CCB) or triple fixed-dose combinations (ARB + CCB + HCTZ). Hypo- and hyper-kalemia rates were analyzed jointly to account for correlation. Significant drug class, drug, or dose effects were included in the final model. Effect on various drug- and dose combinations on dyskalemia risk were simulated and compared with model-estimated placebo arm dyskalemia risk. After a typical follow-up of 8 weeks, fixed-dose combinations of ARB with a high dose (25 mg) of HCTZ were associated with a higher hypokalemia risk difference (RD) from placebo (e.g.,Valsartan + HCTZ: 2.52%[95%CIs:1.17, 4.38%]). However, when ARB was combined with a lower, 12.5 mg dose of HCTZ, hypokalemia RD from placebo was not significant (Valsartan + HCTZ: -0.03%[-0.80, 0.71%]). ARB monotherapy raised hyperkalemia RD from placebo (1.3%[0.3, 3.6%]). Hyperkalemia risk was not appreciably higher than placebo for any FDC that combined ARB with HCTZ (Valsartan + HCTZ: 0.06%[-1.48, 1.64%]). In uncomplicated hypertensive patients, ARB + 12.5 mg HCTZ fixed-dose combinations are safer with respect to dyskalemia than either ARB or HCTZ monotherapy for initial antihypertensive treatment.

Diuretic-induced hypokalaemia: an updated review.

Diuretic-induced hypokalaemia is a common and potentially life-threatening adverse drug reaction in clinical practice. Previous studies revealed a prevalence of 7%-56% of hypokalaemia in patients taking thiazide diuretics. The clinical manifestations of hypokalaemia due to diuretics are non-specific, varying from asymptomatic to fatal arrhythmia. Diagnosis of hypokalaemia is based on the level of serum potassium. ECG is useful in identifying the more severe consequences. A high dosage of diuretics and concomitant use of other drugs that increase the risk of potassium depletion or cardiac arrhythmias can increase the risk of cardiovascular events and mortality. Thiazide-induced potassium depletion may cause dysglycaemia. The risk of thiazide-induced hypokalaemia is higher in women and in black people. Reducing diuretic dose and potassium supplementation are the most direct and effective therapies for hypokalaemia. Combining with a potassium-sparing diuretic or blocker of the renin-angiotensin system also reduces the risk of hypokalaemia. Lowering salt intake and increasing intake of vegetables and fruits help to reduce blood pressure as well as prevent hypokalaemia.

Association between potassium supplementation and the occurrence of acute kidney injury in patients with hypokalemia administered liposomal amphotericin B: a nationwide observational study.

BACKGROUND: Hypokalemia and acute kidney injury (AKI) occur in patients administered liposomal amphotericin B (L-AMB), a wide-spectrum anti-fungicidal drug. However, the association between potassium supplementation and the occurrence of AKI in patients with hypokalemia who were administered L-AMB is not well understood. METHODS: Using nationwide claims data and laboratory data, the occurrence of AKI during L-AMB treatment was retrospectively compared between patients with hypokalemia who were or were not supplemented with potassium and between those adequately or inadequately supplemented with potassium (serum potassium levels corrected to ≥3.5 mEq/L or remained < 3.5 mEq/L, respectively) before or after L-AMB treatment initiation. RESULTS: We identified 118 patients who developed hypokalemia before L-AMB treatment initiation (43 received potassium supplementation [25 adequate and 18 inadequate supplementation] and 75 did not receive potassium supplementation), and 117 patients who developed hypokalemia after L-AMB initiation (79 received potassium supplementation [including 23 adequate and 15 inadequate supplementation] and 38 did not receive potassium supplementation). The occurrence of any stage of AKI was similar between patients with hypokalemia, regardless of potassium supplementation (i.e., before L-AMB treatment initiation [supplementation, 51%; non-supplementation, 45%; P = 0.570] or after L-AMB initiation [supplementation, 28%; non-supplementation, 32%; P = 0.671]). After adjusting for confounding factors, we found that the occurrence of any stage of AKI was not associated with potassium supplementation before L-AMB initiation (odds ratio [OR]: 1.291, 95% confidence interval [CI]: 0.584-2.852, P = 0.528) or after L-AMB initiation (OR: 0.954, 95% CI: 0.400-2.275, P = 0.915). The occurrence of any stage of AKI tended to decline in patients with hypokalemia who were adequately supplemented with potassium (44%) before, but not after, L-AMB initiation relative to that in patients inadequately supplemented with potassium (61%), however this result was not significant (P = 0.358). CONCLUSION: Potassium supplementation was not associated with any stage of AKI in patients with hypokalemia who were administered L-AMB.

Prevalence of hypokalemia in older persons: results from the PolSenior national survey.

PURPOSE: Hypokalemia is one of the most common electrolyte disturbances in clinical practice. There are only a few epidemiological studies analyzing the occurrence of hypokalemia in older persons. The aim of the study was to determine the prevalence of hypokalemia in the Polish older population. METHODS: Serum potassium concentration was estimated in 4654 participants (2270 females and 2384 males, mean age 76.5 [11.0] years), who participated in the PolSenior study. Hypokalemia was defined as serum potassium concentration below 3.5 mmol/L. Hypokalemia was found in 39 participants (0.84%) and was significantly more frequent among females (28 females = 1.23% and 11 males = 0.46%; p = 0.003). The prevalence of hypokalemia was not related to age. Among 3303 participants suffering from arterial hypertension, 1093 were treated with potassium-losing diuretics. RESULTS: Hypokalemia was significantly more frequent among hypertensive than normotensive older participants (1.06 vs. 0.30% respectively; p = 0.007) and among hypertensive participants treated with potassium losing diuretics than ones untreated with these drugs (1.96 vs. 0.46% respectively; p < 0.001). In hypertensive participants, the prevalence of hypokalemia did not depend significantly on oral supplementation of potassium (1.92 and 0.98% respectively, NS). None of 81 participants using laxative agents presented hypokalemia. CONCLUSIONS: This study demonstrates that: older age seems not to appear to be a significant risk factor of hypokalemia. Hypokalemia is more often found in the older hypertensive patients treated with potassium losing diuretics, and prevention of diuretic-induced hypokalemia with oral supplementation of potassium seems to be insufficient.

[Pseudohyperaldosteronism with severe hypokalaemia and focal paresis triggered by licorice tea].

An excessive consumption of licorice can cause pseudohyperaldosteronism, which can lead to severe hypokalaemia and hypertension. Glycyrrhizin in licorice root activates the renal mineralocorticoid receptor increasing sodium reabsorption and potassium excretion. In this case report, an otherwise healthy 43-year-old woman presented with severe hypokalaemia, rhabdomyolysis, electrocardiogram changes and focal paresis after having consumed 2-2,5 litres of licorice tea daily for approximately eight weeks.

Acute Trimethyltin Poisoning Caused by Exposure to Polyvinyl Chloride Production: 8 Cases.

This manuscript aimed to describe and analyze acute trimethyltin poisoning caused by exposure to polyvinyl chloride production and review the literature. Combined with an analysis of occupational hygiene survey data, the clinical data of 8 cases of acute trimethyltin poisoning were analyzed retrospectively. The clinical manifestations of acute trimethyltin poisoning are mainly related to central nervous system damage, hypokalemia and metabolic acidosis in patients with severe poisoning. Early positive potassium supplementation and symptomatic treatment are beneficial to the improvement of the condition. The early recognition of central nervous system manifestations and hypokalemia is beneficial for early diagnosis and correct treatment.

Acute Kidney Injury Impacts on Hypokalemia Associated with Yokukansan Preparation: A Retrospective Observational Study.

The time course of acute kidney injury and hypokalemia remains unelucidated. We investigated whether altered renal function impacts hypokalemia and clinical predictors for acute kidney injury in patients who used Yokukansan preparation. We performed a secondary analysis of retrospective observational cohort data from adult patients who started Yokukansan preparation. The study was conducted from June 2015 to May 2019 at Tokyo Women's Medical University, Medical Center East. The effect of acute kidney injury (>1.5-fold increase from baseline serum creatinine level) or renal function recovery on hypokalemia (serum potassium level <3.0 mEq/L) was investigated. The clinical predictors for acute kidney injury were determined using a multivariate Cox proportional hazard analysis. Out of 258 patients, 12 patients had both outcomes, and all but one patient experienced in the order of acute kidney injury and hypokalemia. Excluding one patient, hypokalemia occurred in 11/34 (32%) patients after acute kidney injury and 27/223 (12%) patients without acute kidney injury (p = 0.005). Hypokalemia occurred in 9/25 (36%) of acute kidney injury with recovery, 2/9 (22%) of acute kidney injury without recovery, and 27/223 (12%) of no acute kidney injury (p = 0.014). Patients with acute kidney injury showed a late onset of hypokalemia compared with those without acute kidney injury (p = 0.001). In 258 patients, multivariate Cox proportional hazard analysis showed that high systolic blood pressure and mean arterial pressure increased the risk of acute kidney injury. Clinicians should remember that hypokalemia developed after acute kidney injury while Yokukansan preparation treatment.

An unusual complication of quadriparesis after trigger point injection: a case report.

ABSTRACT: Quadriparesis after intramuscular trigger point injections for myofascial pain syndrome has been rarely reported in the literature. A 37-year-old male patient presented with myofascial pain syndrome and was given trigger point injections in trapezius muscles under ultrasound guidance. The patient noticed weakness in all the 4 limbs at approximately 12 hours after the procedure, which gradually progressed to functional quadriplegia at the time of presentation to the emergency department. On examination, he had quadriparesis with no sensory involvement and superficial reflexes were normal. MRI screening of the whole spine was unremarkable, and MRI brain suggested an incidental granuloma, which could not explain his symptoms. Blood tests revealed severe hypokalemia (2.2 mEq/L) and deranged thyroid function tests. Immediate potassium correction with intravenous and oral potassium chloride was initiated, and the patient showed improvement within 6 hours of initiating correction. Stress of the procedure, use of steroids with mineralocorticoid effects such as methylprednisolone, or deranged thyroid function tests may have acted as triggers to precipitate hypokalemic paralysis in the patient. Knowledge of this complication is essential as prompt diagnosis and timely management of hypokalemia can result in complete resolution of the symptoms.