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.

[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.

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.

Hyperkalaemia and hypokalaemia outpatient management: a survey of 500 French general practitioners.

AIMS: How general practitioners (GPs) manage dyskalaemia is currently unknown. This study aimed at describing GP practices regarding hypokalaemia or hyperkalaemia diagnosis and management in their outpatients. METHODS AND RESULTS: A telephone survey was conducted among French GPs with a 20-item questionnaire (16 closed-ended questions and 12 open-ended questions) regarding their usual management of hypokalaemia or hyperkalaemia patients, both broadly and more specifically in patients with heart failure and/or chronic kidney disease and/or in patients treated with angiotensin-converting enzyme/angiotensin receptor blockers or mineralocorticoid receptor antagonists. We aimed to interview 500 GPs spread geographically throughout France. This descriptive survey results are presented as mean ± standard deviation (if normally distributed or as median and inter-quartile range if the distribution was skewed). Categorical variables are expressed as frequencies and proportions (%). A total of 500 GPs participated in the study. Dyskalaemia thresholds (for diagnosis and intervention) and management patterns were highly heterogeneous. The mean ± SD (range) potassium level leading to 'intervene' was 5.32 ± 0.34 mmol/L (4.5-6.5) for hyperkalaemia and 3.23 ± 0.34 mmol/L (2.0-6.5) for hypokalaemia. Potassium levels leading to refer the patient to the emergency department (ED) were 6.14 ± 0.55 (4.5-10) and 2.69 ± 0.42 mmol/L (1-4), respectively. Potassium binders (51-65%) or potassium supplements (67-74%) were frequently used to manage hyperkalaemia or hypokalaemia. GPs uncommonly referred their dyskalaemic patients to cardiologists or nephrologists (or to the emergency department, if the latter was deemed necessary owing to the severity of the dyskalaemia). We identified an association between the close vicinity of GP office from an ED and 'referring a heart failure patient' (19.2% with ED vs. 8.6% without ED) and referring a heart failure and chronic kidney disease patient on mineralocorticoid receptor antagonist (16.7% with ED vs. 9.3% without ED). Although the majority (67%) of GPs had an electrocardiogram on hand, it was rarely used (14%) in dyskalaemic patients. Subgroup analyses considering gender, age of the participating GPs, and high-income/low-income regions did not identify specific patterns regarding the multidimensional aspect of dyskalaemia management. CONCLUSIONS: Owing to the considerable heterogeneity of French GP practices toward dyskalaemia diagnosis and management approaches, there is a likely need to standardize (potentially enabled by therapeutic algorithms) practices.

A complicated chinese herbal medicine nephrotoxicity.

Chinese herbal medicine is widely used globally. In many instances, it is associated with severe adverse outcomes. We report case of a Chinese herbal nephropathy occurring in a 43-year-old woman showing renal impairment, metabolic acidosis, Stokes - Adams syndrome, hypernatremia, and hypokalemia, characteristics not usually encountered in published cases.

Intralipid and haemodialysis in caffeine overdose.

A 26-year-old woman presented after an intentional ingestion of 20 g of caffeine. She suffered a profound respiratory alkalosis with metabolic acidosis, hypokalaemia and sustained polymorphic ventricular tachycardia. She was treated with intravenous intralipid and haemodialysis, and her arrhythmia was controlled using magnesium sulphate. Once invasively ventilated and unable to hyperventilate the patient became acidotic and required intravenous bicarbonate to correct her acid-base status. Two days following the overdose the patient was extubated, haemodialysis was stopped and norepinephrine was weaned off. The patient was discharged after a further 7 days. Serial caffeine levels were taken during this patient's care; the highest measured caffeine concentration 7 hours after ingestion was 147.1 mg/L. The known lethal dose of caffeine is 80 mg/L. Intralipid and haemodialysis represent a new and viable treatment in life-threatening caffeine overdose. Intravenous magnesium may terminate unstable arrhythmias in caffeine-poisoned patients.

Safety, Efficacy, and Timeliness of Intravenous Potassium Chloride Replacement Protocols in a Pediatric Cardiothoracic Intensive Care Unit.

OBJECTIVE: Hypokalemia in children following cardiac surgery occurs frequently, placing them at risk of life-threatening arrhythmias. However, renal insufficiency after cardiopulmonary bypass warrants careful administration of potassium (K+). Two different nurse-driven protocols (high dose and tiered dosing) were implemented to identify an optimal K+ replacement regimen, compared to an historical low-dose protocol. Our objective was to evaluate the safety, efficacy, and timeliness of these protocols. DESIGN: A retrospective cohort review of pediatric patients placed on intravenous K+ replacement protocols over 1 year was used to determine efficacy and safety of the protocols. A prospective single-blinded review of K+ repletion was used to determine timeliness. PATIENTS: Pediatric patients with congenital or acquired cardiac disease. SETTING: Twenty-four-bed cardiothoracic intensive care unit in a tertiary children's hospital. INTERVENTIONS: Efficacy was defined as fewer supplemental potassium chloride (KCl) doses, as well as a higher protocol to total doses ratio per patient. Safety was defined as a lower percentage of serum K+ levels ≥4.8 mEq/L after a dose of KCl. Between-group differences were assessed by nonparametric univariate analysis. RESULTS: There were 138 patients with a median age of 3.0 (interquartile range: 0.23-10.0) months. The incidence of K+ levels ≥4.8 mEq/L after a protocol dose was higher in the high-dose protocol versus the tiered-dosing protocol but not different between the low-dose and tiered-dosing protocols (high dose = 2.2% vs tiered dosing = 0.5%, P = .05). The ratio of protocol doses to total doses per patient was lower in the low-dose protocol compared to the tiered-dosing protocol (P < .05). Protocol doses were administered 45 minutes faster (P < .001). CONCLUSION: The tiered-dosed, nurse-driven K+ replacement protocol was associated with decreased supplemental K+ doses without increased risk of hyperkalemia, administering doses faster than individually ordered doses; the protocol was effective, safe, and timely in the treatment of hypokalemia in pediatric patients after cardiac surgery.

[Management of Gitelman syndrome during pregnancy reporting 12 cases]. / Prise en charge de la grossesse chez des patientes atteintes de syndrome de Gitelman : série de 12 cas.

INTRODUCTION: Gitelman syndrome is a rare hereditary renal tubulopathy, responsable of hypokalemia and hypomagnesaemia-related ionic disorders, which management is poorly codified during pregnancy. We report 12 cases of pregnancies with Gitelman syndrome and we compare our data with those of literature. MATERIAL AND METHODS: It is a report of 12 pregnancies in 5 patients with Gitelman syndrome between 2002 and 2016. Follow up and outcome of pregnancy, delivery modalities and maternal-fetal prognosis have been collected. RESULTS: In our serie, maximum kaliemie observed was 3.4mmol/L, with an average potassium, over all pregnancies of 2.3mmol/L. Oral potassium and magnesium supplementation at the end of pregnancy were 8900mg/day and 460mg/day, respectively. There were no serious maternal complications. Two pregnancies were complicated by intrauterine growth retardation in a context of preeclampsia. There is a large disparity in the methods of anesthetic management of these patients. Materno-fetal prognosis at 1 month post-partum is good. CONCLUSION: Gitelman syndrome is a rare pathology where there is a lack of homogeneity in management of pregnancy. Monitoring of monthly ionogram is necessary. The goal is to obtain stable, non-symptomatic kaliemias, which will never be standardized even in increasing treatment. The most important is to inform and detect situations at risk of decompensation, including vomiting or the use of certain anesthetics. In agreement with literature data, monitoring of fetal growth and the amount of amniotic fluid in the third trimester is still warranted. These pregnancies require the development of a common care in multidisciplinary consultation meeting.

Refractory hypokalemia while weaning off bypass.

Hypokalemia is defined as serum potassium level less than 3.5 mEq/L. When the serum level of potassium is less than 3 mEq/L, intravenous potassium supplementation is warranted. A 23 yr old adult female with complaints of dyspnoea (NYHA II) since 6 yrs, dyspnoea (NYHA III) and paroxysmal nocturnal dyspnoea on and off since 2 months, diagnosed with severe mitral stenosis, was posted for mitral valve replacement. After the release of ACC, ECG revealed sine wave pattern, Transesophageal echocardiographic examination revealed global hypokinesia and ABG showed potassium of 2.3 mEq/L. Hypokalemia in cardiac patients can occur due to the effect of poor oral intake, increased renal loss by the secondary hyperaldosteronism in congestive heart failure, loss due to use of digoxin and diuretics like thiazide diuretics, loop diuretics etc. Hypokalemia should be avoided while weaning off cardiopulmonary support as it can lead to atrial and ventricular arrhythmias. Potassium ion is very important for the normal contractility of the heart. Hypokalemia if refractory to intravenous potassium supplementation, concomitant magnesium deficiency should be suspected and treated.

Peptide Receptor Radionuclide Therapy-Induced Gitelman-like Syndrome.

Peptide receptor radionuclide therapy (PRRT) is a molecular-targeted therapy in which a somatostatin analogue (a small peptide) is coupled with a radioligand so that the radiation dose is selectively administered to somatostatin receptor-expressing metastasized neuroendocrine tumors, particularly gastroenteropancreatic. Reported toxicities include myelotoxicity and nephrotoxicity, the latter manifesting as decreased kidney function, often developing months to years after treatment completion. We present a case of PRRT-induced kidney toxicity manifesting as a severe Gitelman-like tubulopathy with preserved kidney function. Because profound hypokalemia and hypocalcemia can lead to life-threatening arrhythmias, we highlight the necessity for careful monitoring of serum and urine electrolytes in patients receiving PRRT.

Diospyros rhodocalyx (Tako-Na), a Thai folk medicine, associated with hypokalemia and generalized muscle weakness: a case series.

INTRODUCTION: Diospyros rhodocalyx (Tako-Na) is a Thai folk medicine purported to promote longevity, treat impotence, etc. We present patients with hypokalemia, weakness and hypertension after consuming Tako-Na tea. CASE SERIES: Case 1: A 61-year-old man was brought in nine hours after drinking 400-500 mL of Tako-Na tea. One handful of Tako-Na bark was boiled in water to make tea. He had vomiting and watery diarrhea six hours after drinking it. He took no medications and had no history of hypertension. The only remarkable vital sign was BP 167/90 mmHg. Physical examination revealed generalized muscle weakness. Laboratory findings were potassium 2.7 mmol/L, bicarbonate 24 mmol/L, and transtubular potassium gradient (TTKG) 5.6. He was discharged the next day with a BP 140/90 mmHg and potassium 4.2 mmol/L. Case 2: A 78-year-old man, a friend of case 1, also drank Tako-Na tea from the same pot at the same time as case 1. He also had vomiting and diarrhea six hours later. He took no medications despite past history of hypertension (baseline SBP 140-160). Initial BP was 230/70 mmHg. He also had muscle weakness. Laboratory findings were potassium 3.3 mmol/L, bicarbonate 24 mmol/L, TTKG 7.37 and normal thyroid function. He was also discharged the next day with a BP 148/70 mmHg and potassium 4.2 mmol/L. Case 3-7: These were patients reported to a poison center and their potassium concentrations were 1.4, 1.4, 3.3, 1.3 and 1.2 mmol/L, respectively. Three of them were intubated and case 3 died. CONCLUSIONS: Tako-Na contains betulin, betulinic acid, taraxerone, lupeol, and lupenone. Their structures are similar to glycyrrhetic acid, the active metabolite of glycyrrhizic acid found in licorice which is well known to cause pseudoaldosteronism. Glycyrrhetic acid is potent in inhibiting 11-beta-hydroxysteroid dehydrogenase, and causes pseudoaldosteronism. We hypothesize that the compounds in Tako-Na act in the same way as glycyrrhetic acid in producing pseudoaldosteronism.

Secretory diarrhea and hypokalemia associated with colonic pseudo-obstruction: A case study and systematic analysis of the literature.

BACKGROUND: Colonic pseudo-obstruction (CPO) is characterized by colonic distention in the absence of mechanical obstruction or toxic megacolon. Concomitant secretory diarrhea (SD) with hypokalemia (SD-CPO) due to gastrointestinal (GI) loss requires further characterization. AIM: To perform a systematic review of SD-CPO, report a case study, and compare SD-CPO with classical CPO (C-CPO). METHODS: We performed a search of MEDLINE, EMBASE, Cochrane, and Scopus for reports based on a priori criteria for CPO, SD and GI loss of potassium. An additional case at Mayo Clinic was included. RESULTS: Nine publications met inclusion criteria, with a total of 14 cases. Six studies had high, three moderate, and our case high methodological quality. Median age was 74 years (66-97), with 2:1 male/female ratio. Kidney disease was present in 6/14 patients. Diarrhea was described as profuse, watery, or viscous in 10 patients. Median serum, stool, and urine potassium concentrations (mmol/L) were 2.4 (range: 1.9-3.1), 137 (100-180), and 17 (8-40), respectively. Maximal diameter of colon and cecum (median) were 10.2 cm and 10.5 cm, respectively. Conservative therapy alone was effective in five out of 14 patients. Median potassium supplementation was 124 mEq/d (40-300). Colonic decompression was effective in three out of six patients; one had a total colectomy; three out of 14 had died. The main differences between SD-CPO and C-CPO were lower responses to treatments: conservative measures (35.7% vs 73.6%, P=.01), neostigmine (17% vs 89.2%, P<.001), and colonic decompression (50% vs 82.4%, P=.02). CONCLUSION: SD-CPO is a rare phenotype associated with increased fecal potassium and is more difficult to treat than C-CPO.

Insight into specific pro-arrhythmic triggers in Brugada and early repolarization syndromes: results of long-term follow-up.

The pro-arrhythmic triggers in Brugada and early repolarization syndromes (BrS, ERS) have not been analyzed systematically except for case reports. We clinically investigated the circumstances which precede/predispose to arrhythmic events in these syndromes during long-term follow-up. A detailed history from the patients/witnesses was taken to investigate the antecedent events in the last few hours that preceded syncope/ventricular fibrillation (VF); medical records, ECG and blood test from the emergency room (ER) were reviewed. 19 patients that fulfilled the investigation criteria were followed up for 71 ± 49 months (34-190 months). Prior to the event (syncope/VF), the patients were partaking different activities in the following decreasing order; drinking alcoholic beverage, having meal, and getting up from sleep, exercise. 3 patients reported mental/physical stress prior to the event and 2 patients developed VF several days after starting oral steroid for treatment of bronchial asthma. In the ER, elevated J-wave amplitude (0.27 ± 0.15 mV) was found with 58 % of the patients having hypokalemia. After electrolyte correction and cessation of steroids, the following day plasma K+ (4.2 ± 0.3 mEq/L, P < 0.001) was significantly increased and J-wave amplitude (0.13 ± 0.1 mV, P < 0.001) was remarkably reduced. Three patients were kept on oral spironolactone/potassium supplements. During follow-up for 71 ± 49 (34-190) months, among 4 patients with VF recurrence, one patient developed VF after taking oral steroid. In ERS and BrS, hypokalemia and corticosteroid therapy add substantial pro-arrhythmic effects, but potentially treatable. Stopping steroid therapy and avoiding hypokalemia had excellent long-term outcome.

Clinical perspectives on the rationale for potassium supplementation.

Hypokalemia is a common electrolyte disturbance, observed in > 20% of hospitalized patients. Hypokalemia, although not formally defined, is generally considered to be when serum potassium levels fall below the normal value of 3.6 mmol/L. In contrast to other electrolytes, potassium is primarily an intracellular ion: only 2% of all potassium in the body is present in the extracellular fluid, so a small decrease in serum potassium may represent a significant decrease in intracellular potassium. Individuals with mildly decreased potassium levels (3.0-3.5 mmol/L) may be asymptomatic, but patients with more pronounced decreases may report symptoms including muscle weakness, fatigue, and constipation. Very low serum potassium levels (≤ 2.5 mmol/L) can lead to muscle necrosis, paralysis, cardiac arrhythmias, and impaired respiration, which can be life-threatening. Absent comprehensive and robust treatment guidelines, strategies for the prevention or treatment of hypokalemia, such as how to diagnose hypokalemia, when to treat patients, what dosage regimen of potassium supplementation to use and for how long, are often based on the experience of the physician and empirical evidence. However, proper evaluation and treatment of hypokalemia in patients is essential because of associated morbidities. Because small potassium deficits in serum represent large body losses, potassium repletion requires substantial and prolonged supplementation. For patients with known risk factors for hypokalemia (e.g. hypertension, heart failure, or diabetes), careful monitoring is crucial to avoid the adverse sequelae associated with potassium deficits and to ensure that adequate and timely preventive measures can be taken. In this review, we provide practical insights into the etiology, differential diagnosis, and treatment of hypokalemia, including treatment strategies for patients with known risk factors.

Etiologic and therapeutic analysis in patients with hypokalemic nonperiodic paralysis.

BACKGROUND: Hypokalemic nonperiodic paralysis represents a group of heterogeneous disorders with a large potassium (K(+)) deficit. Rapid diagnosis of curable causes with appropriate treatment is challenging to avoid the sequelae of hypokalemia. We prospectively analyzed the etiologies and therapeutic characteristics of hypokalemic nonperiodic paralysis. METHODS: Over an 8-year period, patients with hypokalemic nonperiodic paralysis were enrolled by excluding those with hypokalemic periodic paralysis due to acute shift of K(+) into cells. Blood and spot urine samples were collected for the measurements of electrolytes, pH, and biochemistries. Intravenous potassium chloride (KCl) at a rate of 10-20 mmol/h was administered until muscle strength recovered. RESULTS: We had identified 58 patients with hypokalemic nonperiodic paralysis from 208 consecutive patients with hypokalemic paralysis, and their average K(+) concentration was 1.8 ± 0.2 mmol/L. Among patients with low urinary K(+) excretion (n = 17), chronic alcoholism, remote diuretic use, and anorexia/bulimia nervosa were the most common causes. Among patients with high urinary K(+) excretion (n = 41) and metabolic acidosis, renal tubular acidosis and chronic toluene abuse were the main causes, while primary aldosteronism, Gitelman syndrome, and diuretics were the leading diagnoses with metabolic alkalosis. The average KCl dose needed to restore muscle strength was 3.8 ± 0.8 mmol/kg. Initial lower plasma K(+), volume depletion, and high urinary K(+) excretion were associated with higher recovery KCl dosage. During therapy, patients with paradoxical hypokalemia (n = 32) who required more KCl supplementation than patients without (4.1 ± 0.7 vs 3.4 ± 0.7 mmol/kg, P < 0.001) often exhibited significantly higher plasma renin activity and received a higher volume of normal saline before its appearance. CONCLUSIONS: Understanding the common etiologies of hypokalemic nonperiodic paralysis may aid in early diagnosis. Patients with initial lower plasma K(+), renal K(+) wasting, and hypovolemia required higher recovery K(+) dosage. Paradoxical hypokalemia is prone to develop in hypovolemic patients even during K(+) supplementation with volume repletion.

Hypokalemia syndrome in cattle.

This article describes hypokalemia syndrome. Lactating dairy cows seem to be at the highest risk, but younger animals may also develop the disease. At present, except for animals treated with repeated isoflupredone acetate administration, the exact determinants causing hypokalemia syndrome remain uncertain. Affected animals are anorexic, weak to recumbent, and most often show signs of gastrointestinal stasis. Treatment is directed toward supportive care and oral potassium supplementation.

Significance of serum potassium level monitoring during the course of post-operative rehabilitation in patients with hypokalemia.

OBJECTIVE: Our objective was to evaluate the significance of pre-hospital and post-operative serum potassium level monitoring and hypokalemia intervention in laparotomy patients with hypokalemia. METHOD: A total of 118 laparotomy patients with hypokalemia were randomly divided into an intervention group (N = 60) and a control group (N = 58). Blood samples were collected for measurement of potassium levels at various time points (pre-admission, admission, 24 h and 48 h post-operation) for both groups. Hypokalemia interventions were administered to patients in the intervention group in the pre-admission period and the post-operative period. Visceral dynamics were assessed after laparotomy in both groups. RESULT: Average serum potassium levels at admission, time period of drinking, and time of first bowel sound after laparotomy differed significantly (p < 0.001) between the two groups. Average serum potassium levels, first time of defecation, urination, and ambulation at 24 h and 48 h post-operation differed significantly (p < 0.05) between the two groups. CONCLUSION: An optimal pathway of serum potassium monitoring not only saves limited ward space but also allows for early correction of hypokalemia in patients undergoing laparotomy.

Hypokalemic periodic paralysis: a case series, review of the literature and update of management.

The objective of this study was to present a case series of patients with hypokalemic periodic paralysis. We described all patients with diagnosis of hypokalemic periodic paralysis admitted to the Al Ain Hospital (UAE) during the year 2006. Seventeen patients, all males and mostly Asians, were presented to the Al Ain Hospital over a 12-month period. The majority were admitted during the summer months. Four were thyrotoxic. All of the 17 patients received oral potassium supplements and recovered well without any major complications. In conclusion, clinicians should have a high index of suspicion, especially among Asians presenting with flaccid paralysis and hypokalemia. The main steps in the management include exclusion of other causes of hypokalemia, potassium replacement, hydration and close monitoring of the cardiac rhythm and serum potassium levels. When possible, the underlying cause must be adequately addressed to prevent the persistence or recurrence of paralysis.