Normal Potassium Levels Research Articles

Indication and functional outcome of orthotopic neo-bladder reconstruction following radical cystectomy for bladder cancers in a specialist hospital in north-west Cameroon

BackgroundRadical cystectomy (RC) and urinary diversion are treatment modalities for muscle invasive bladder cancer (MIBC). However, in Cameroon, there is little information on orthotopic neo-bladder (ONB) reconstruction in the literature.ObjectiveWe aimed to share our indications for ONB reconstruction, evaluate the functional outcomes, and enumerate the surgical complications. By sharing our experience with ONB reconstruction, we hope to broaden the understanding of this procedure and aid in anticipating its various outcomes.MethodsA retrospective assessment of medical records was conducted for all patients who underwent ONB reconstruction after RC for bladder cancer from January 2020 to April 2023 at Nkwen Baptist Hospital. Data collected included socio-demographic details, clinical and pathological data, indications for surgery, voiding, and metabolic outcomes at 6 and 12 months postoperatively. Data analysis was performed using IBM-SPSS version 26.0.ResultsEighteen patients (66.7% male) with a mean age of 60.50 (± 6.90) years were included. Indications for ONB were 56% for pT2b, 23% for pT2a, and 23% for multifocal T1 disease without ureteral, urethral, or bladder neck extension. At 12 months, 77.8% had acceptable diurnal continence, and 72.2% had acceptable nocturnal continence. Peak urinary flow rates and post-void residual volumes were acceptable in 77.8% and 83.3% of patients, respectively. Additionally, 88.9% had normal sodium levels, 94.4% had normal potassium levels, and 94.4% had normal chloride levels at 12 months post-ONB creation.ConclusionsONB reconstruction provides satisfactory continence and minimal rates of electrolyte derangement, contributing valuable insights into the functional outcomes of this procedure.

Comparison of sodium zirconium cyclosilicate and sodium polystyrene sulfonate in the treatment of acute hyperkalaemia

ObjectiveSodium polystyrene sulfonate (SPS) and sodium zirconium cyclosilicate (SZC) have been used for treating acute hyperkalaemia. The pharmacodynamic properties of SZC suggest greater theoretical utility in the acute setting than...

Hyperkalemia or Not? A Diagnostic Pitfall in the Emergency Department

Introduction: Hyperkalemia, a potentially life-threatening electrolyte disturbance, is commonly encountered in the Emergency Department (ED). However, the frequency of factitious hyperkalemia, an artificially elevated potassium level in hyperkalemic ED patients, is unknown. This study aims to detect the rate of factitious hyperkalemia among patients with a potassium concentration of ≥5.0 mmol/l in an all-comer ED population. Methods: This retrospective, monocentric chart review analyzed data of 2,440 ED patients who presented with a potassium concentration of ≥5.0 mmol/L in their initial whole blood or plasma sample, who also underwent a repeat potassium measurement on the same day. Two groups were established based on potassium levels in the initial and repeat blood tests: 1) True hyperkalemia, characterized by consistently elevated potassium levels in both the initial and repeat samples; and 2) Factitious hyperkalemia, defined by an elevated initial potassium level while the repeat blood test showed a normal potassium level. A subset of factitious hyperkalemia was spurious hyperkalemia. In spurious hyperkalemia, the initial blood sample showed an elevated potassium level with evidence of hemolysis, but a repeat test revealed a normal potassium level without evidence of hemolysis. Results: Of the 2,440 patients, 1,576 (65%) had true hyperkalemia and 864 (35%) factitious hyperkalemia. Among the 864 patients with factitious hyperkalemia, 597 (69%) displayed hemolysis in their initial blood sample, indicating spurious hyperkalemia due to in-vitro hemolysis. Conclusion: These data show that about one third of all hyperkalemic blood samples drawn in the ED were due to factitious hyperkalemia. The leading cause of factitious hyperkalemia was spurious hyperkalemia due to in-vitro hemolysis.

Severe Hyperkalemia in a Child with Vomiting and Diarrhea.

A 13-month-old child with past medical history of congenital adrenal insufficiency presented to the emergency department with vomiting and diarrhea. Initially the child was noticed to have bradycardia with normal blood pressure. An electrocardiogram (ECG) showed tall T waves, broad QRS complex, and widened PR interval suggestive of severe hyperkalemia. The initial blood gas showed potassium of 10.7 millimoles per liter. The patient was started on calcium gluconate with immediate resolution of ECG changes. Further management with insulin, dextrose, and sodium polystyrene sulfonate led to normal potassium levels. Hyperkalemia is a life-threatening condition in children, especially in those with congenital adrenal insufficiency. The ECG showed different changes as the levels of serum potassium levels increased ranging from tall T waves, wide QRS complex, increased PR interval to arrythmias. Immediate treatment with calcium gluconate in such cases has significant cardioprotective effect. It is important to recognize the ECG changes manifested by changes in serum potassium levels. Our patient had classic ECG changes manifested in severe hyperkalemia.

Comparative analysis of renin-angiotensin system inhibitors/angiotensin receptor neprilysin inhibitor and mineralocorticoid receptor antagonists in heart failure with mildly reduced ejection fraction

Abstract Background Apart from sodium-glucose co-transporter 2 inhibitors, the efficacy of renin–angiotensin system inhibitors/angiotensin receptor neprilysin inhibitors (RASI/ARNI)j8788 as well as mineralocorticoid receptor antagonist (MRA) in patients with heart failure with mildly reduced ejection fraction remains uncertain. We assessed the association between these medications and outcomes in patients with heart failure with mildly reduced ejection fraction (HFmrEF). Methods Patients with HFmrEF from our university hospital-integrated Medical Database were included. Associations between the medications and cardiovascular mortality/heart failure hospitalization were evaluated using Cox regressions in a 1:1 propensity score-matched cohort. Inverse probability of treatment weighting was employed to balance baseline patient characteristics. Results Of 2584 patients with HFmrEF, 17% received MRA and 43% received RASI/ARNI. Predictors of MRA use included older age, slightly higher ejection fraction, lower NT-proBNP level, and eGFR >60 mL/min/1.73 m^2. Predictors of RASI/ARNI use included higher body mass index, lower NT-proBNP level, normal uric acid level, normal potassium level, and eGFR >60 mL/min/1.73 m^2. MRA use was not associated with a lower risk of cardiovascular death and hospitalization for heart failure (hazard ratio [HR] = 0.89, 95% confidence interval [CI]: 0.78–1.02 and HR = 1.01, 95% CI: 0.94–1.09, respectively). Conversely, RASI/ARNI use was associated with a lower risk of cardiovascular death but not hospitalization for heart failure (HR = 0.82, 95% CI: 0.71–0.94 and HR = 0.995, 95% CI: 0.924–1.07, respectively). Notably, landmark analysis revealed no significant difference in the risk of outcomes when the follow-up duration exceeded two years. Conclusions The effect of MRA on cardiovascular death and hospitalization for heart failure was neutral, whereas RASI/ARNI was associated with a lower risk of cardiovascular death. Our findings suggest that RASi use may be more beneficial than MRA use in patients with HFmrEF.

Optimizing aldosterone receptor antagonist therapy by sodium zirconium cyclosilicate in heart failure - OPRA-HF trial

Abstract Background Heart failure remains a significant health burden, characterized by disabling symptoms and mortality rates comparable to cancer. Mineralocorticoid antagonists (MRAs), pivotal in treating heart failure with reduced ejection fraction (HFrEF), are underutilized due to concerns of hyperkalemia. Sodium Zirconium Cyclosilicate (SZC) enables optimized MRA therapy by reducing hyperkalemia. However, prospective studies on the efficacy and safety of SZC in patients with HFrEF and high hyperkalemia risk are lacking, particularly in the context of contemporary heart failure quadruple-therapy including angiotensin receptor neprilysin inhibitor (ARNI) and Sodium-Glucose Transport Protein 2 (SGLT2) Inhibitors. Purpose The OPRA-HF trial aims to assess the efficacy and safety of SZC in optimizing MRA treatment in symptomatic patients with HFrEF with risk for hyperkalemia on top of optimal guideline-directed medical therapy including ARNI and SGLT2 Inhibitors. Methods This investigator-initiated multicentred, randomized, placebo-controlled, and double-blinded trial include patients with HFrEF on suboptimal MRA treatment due to (1) history of hyperkalemia due to MRA, or (2) risk of hyperkalemia due to reduced renal function (eGFR 30-45 ml/min/m2) and current potassium 4.5-5-0 mmol/L. Patients undergo a Run-In phase with SZC, initiating or up-titrating MRA to target doses for 4-7 weeks and SZC was initiated in those patients that became hyperkalemic (K+>5 mEq/L. Those normokalemic and tolerating MRA ≥ 25 mg daily or at least 25 mg dose increase vs before run-in were randomized to SZC (5g or 10g) or placebo for 6 months. Study is powered to randomize 110 patients. Primary outcomes include maintaining daily MRA dose ≥ 25 mg or dose increase by 25 mg with normal potassium levels without rescue therapy. Secondary outcomes include evaluating the safety and tolerability of SZC as well as impact of SZC on quality of life. Results In this ongoing trial, so far 40 patients have been randomized. Of these, mean age was 74.3 years, 88.9% men. Most patients had ischemic etiology (54.2%), 36.1% had diabetes mellitus, 52.8% had hypertension.n. At screening 94.4% had beta-blockers, 35% ACEI/ARB, 60% ARNI and 72.2% had SGLT2 inhibitors, 33.3% had no MRAs and 35,6% of patients had less than 25 mg MRA daily,62,2% had 25 mg MRA daily, mean p-potassium was 4.7+0.4 mmol/L, and eGFR was 57.3 ml/min/1.73m². After run-in, 85.2% were on 50 mg MRA daily. A substantial number (51.2%) of eligible patients with previous hyperkalemia had Run-In failure as they now successfully tolerated target dose of MRA at 50 mg daily without recurrent hyperkalemia. SZC dosing was 5g once daily in 78.9% of patients. Conclusion This ongoing trial will provide evidence for the use of SZC to optimize MRA treatment in contemporary HFrEF patients. Preliminary findings suggest SZC effectively maintains normokalemia, enabling MRA optimization, potentially improving patients’ otcome.

Impact of hypokalemia on Brugada syndrome: case report unveiling mechanisms beyond QT interval prolongation.

Brugada syndrome (BrS) is associated with an increased risk of sudden death caused by ventricular arrhythmias. The characteristic electrocardiographic appearance of ST-segment elevation of more than 2mm with coved-type morphology in more than 1 right precordial lead is seen. Hypokalemia is known to unmask the Brugada type-1 pattern, but its exact role and mechanisms in this context are not well understood. We report a case of first-time diagnosis of BrS in a 51-year-old man with hypokalemia 2.8mmol/L. Despite the normalization of potassium levels with potassium chloride (KCL), the Brugada type-1 pattern persisted on ECG. Interestingly, the corrected QT interval was shorter during hypokalemia (QTc 390ms) compared to when potassium levels were normal (QTc 432ms). This case highlights that hypokalemia can unmask the Brugada type-1 electrocardiographic pattern, but does not alter it once unmasked. The observed shorter QT interval during hypokalemia challenges the assumption that QT prolongation is the sole mechanism by which hypokalemia influences Brugada syndrome. This underscores the need for further research into additional mechanisms by which hypokalemia might trigger ventricular arrhythmias in Brugada syndrome.

Respiratory failure and rhabdomyolysis caused by severe hypokalemia in a young female with hypertension: a rare critical condition in primary aldosteronism

BackgroundThe two classic manifestations of primary aldosteronism are hypertension and hypokalemia. However, acute respiratory failure due to hypokalemia in primary hyperaldosteronism is rare.Case presentationThe patient was a 27-year-old female who presented with drowsiness and weakness in all extremities. She had been diagnosed with hypertension three years prior, with irregular follow-up, and had a history of preeclampsia one year later. She exhibited high blood pressure and severe hypokalemia (2 mEq/L), leading to respiratory depression and impending respiratory arrest. Consequently, the patient was intubated and transferred to the intensive care unit (ICU). She also developed rhabdomyolysis. Blood pressure tests, including hormonal tests (aldosterone: 13.2 ng/dL, plasma renin activity: 0.32 ng/mL/h), were conducted. Due to the high aldosterone-renin ratio, an abdominopelvic computed tomography (CT) scan was performed. The CT scan revealed a 14 × 12 mm round mass with a washout value above 60%, consistent with an adrenal adenoma, leading to a diagnosis of primary aldosteronism. The patient was discharged after stabilization, and one and a half months after ICU admission, a laparoscopic left adrenalectomy was successfully performed without post-operative complications. Histopathology showed encapsulated hypertrophy of the adrenal cortex with a predominance of large clear cells, confirming the diagnosis of adrenal adenoma. At the most recent follow-up, the patient had normal potassium levels, was normotensive without any medications, and exhibited no alarming signs or symptoms.ConclusionRespiratory depression to the extent of impending respiratory failure and rhabdomyolysis as a result of hypokalemia in primary aldosteronism are extremely rare. In this patient, who developed respiratory depression due to resistant hypokalemia, timely investigation of secondary causes and diagnosis of adrenal adenoma were crucial. The surgery provided definitive treatment for the patient’s blood pressure and prevented the recurrence of life-threatening complications.

12616 Pembrolizumab-induced Autoimmune Adrenal Insufficiency: A Case Report And Literature Review

Abstract Disclosure: A. Calderon: None. E. Calderon-Martinez: None. J. Shakil, MD: None. A. Kansara: None. Immunechekpoint inhibitors (ICI)-related Primary Adrenal Insufficiency (PAI) is an uncommon entity. Compared to other endocrine-related adverse effects (irAES), antibody detection is less consistent. TPO and GAD65 antibodies are usually present in about 40-80% of the cases with hypothyroidism, hyperthyroidism, and diabetes. On the contrary, case reports and series for PAI seldom report the presence or absence of 21OH antibodies. We present a case and perform a literature review of PAI, in a patient who received pembrolizumab and developed PAI with 21 hydroxylase antibodies. A 62-year-old man with history HIV on ART (last CD4 count 590 cells/mm3) and locally advanced urothelial cancer on Pembrolizumab, presented with nausea, vomiting, abdominal pain, and decreased urine output. He was noted to be confused, and in hypoactive delirium. On admission, his chemistry panel he was noticed to have normal sodium and potassium levels. The CT scan of the abdomen revealed regional enteritis and was started on IV fluid therapy. His adrenal glands were described as normal on imaging. On the 16th day of hospitalization, the patient became unresponsive and hypotensive. He was transferred to the ICU. His sodium level was 132 mEq/L and potassium level was 6.1 mEq/L, bicarbonate level was 18 mEq/L, calcium of 10.3 mg/dl, and eosinophils of 15%. Random cortisol levels measured before administration of steroids were undetectable twice, 9 hours apart, with an ACTH level of 94. He underwent an ACTH stimulation test with cosyntropin 250 mcg IV with resulting undetectable cortisol levels after 30 and 60 minutes. CT and MRI of the brain showed no signs of hypophysitis. He was started on high-dose hydrocortisone with improvements in his mental status, hypotension, and gastrointestinal symptoms. He was discharged on hydrocortisone. His 21-Hydroxylase antibody was later found out to be positive. After combination immunotherapy regimens, CTLA-4 inhibitors are the most common to cause any irAE, however endocrine irAE particularly are mostly associated with PD-1 inhibitors. Among these, thyroid and pituitary disorders are the most common ones. Reports show that about 10% of patients receiving immunotherapy will develop endocrinopathy. ICI-induced PAI has been reported to occur in 7.6% of patients receiving combination therapy, and 2% of patients receiving Pembrolizumab. It has been reported that only 15% of patients will recover adrenal function. A meta-analysis that gathered 15 cases of ICI-induced PAI, found that only 2 cases had positive 21-hydroxylase antibodies. In our presented case, we have robust biochemical confirmation of PAI, with positive 21 hydroxylase antibody, after being on pembrolizumab for 9 months. Further information is needed to establish the pathophysiology, presentation, and prognosis of ICI-related PAI when anti adrenal antibodies are positive. Presentation: 6/1/2024

7658 A Case of Recurrent Cardiac Tamponade as Initial Presentation of Primary Adrenal Insufficiency

Abstract Disclosure: A. Farooq: None. A. Ghumatkar: None. J. Snitzer: None. Introduction:Cardiac tamponade, a life-threatening emergency, can be associated with primary adrenal insufficiency (Addison Disease), and accurate diagnosis requires a high degree of clinical suspicion in patients with uncertain etiology and nonspecific signs and symptoms. Case Presentation:A 58-year-old female with a history of Hashimoto thyroiditis was evaluated in the hospital for two episodes of cardiac tamponade requiring emergent pericardiocentesis within one month. The patient had been experiencing symptoms of fatigue, nausea, lightheadedness, dizziness, hiccups, and tanned skin for the past year. She also had a recent flu-like illness with nausea and vomiting four months before her current presentation. Her vitals were notable for hypotension during these episodes. Her lab work showed hyponatremia (128 mEq/L, reference range: 136-145 mEq/L) with normal potassium and glucose levels. Her thyroid function tests were within normal limits on her home levothyroxine dosage (TSH 4.588 IU/ml, reference range: 0.5-8.9 IU/ml). An ACTH stimulation test was performed based on the patient's clinical presentation, consistent with adrenal insufficiency. Her baseline cortisol level was 5.9 mcg/dL (reference range: 6.7-22 mcg/dL), a post-ACTH stimulation level of 6.7 mcg/dL after 30 minutes, and 6.0 mcg/dL after 60 minutes. Her 21 alpha-hydroxylase antibody titer was also positive for Addison Disease (231U/mL, reference range <1 IU/mL). A CT scan of the abdomen with intravenous contrast was done, which revealed no abnormality of the adrenal glands. She was treated with stress doses of hydrocortisone during hospitalization and discharged with maintenance dosage and follow-up with endocrinology. She had another episode of acute adrenal crisis about a month later but had no pericardial effusion this time and responded well to the treatment with stress doses of steroids. She has remained healthy at 14 years of follow-up. Conclusion: This case emphasizes the need to consider adrenal insufficiency in the evaluation of cardiac tamponade or pericardial effusions, especially in patients with existing autoimmune glandular disorders. This patient may have autoimmune polyglandular syndrome type 2 (APS-2), which is a cluster of two or more endocrine glandular disorders primarily diagnosed in adulthood and predominant in females. The risk of adrenal crisis is more than twofold in Addison disease due to APS-2. Lastly, this case highlights that hiccups can be related to adrenal insufficiency, with pathophysiology possibly involving diaphragmatic irritation due to adrenal inflammation that resolves with treatment. Presentation: 6/3/2024

Clinical, myopathological, and genetic features of two Chinese families with Andersen-Tawil syndrome.

To explore the clinical, muscle pathological, and pathogenic gene mutation characteristics of Andersen-Tawil Syndrome (ATS) and enhance the understanding of ATS among clinical practitioners. Retrospective analysis of clinical data and muscle pathology of two ATS families, along with genetic testing for probands and some family members. In Family 1, spanning four generations, four individuals were affected, while Family 2 had two affected individuals across four generations. All six patients in both families experienced onset in childhood, presenting with periodic paralysis, arrhythmias, and craniofacial skeletal abnormalities. In Family 1, the proband's periodic paralysis was more triggered by low temperature and exercise, occurring several times a year, lasting 4-7 days. All three adult patients in Family 1 had a history of hypokalemia, and the frequency and severity of attacks were reduced after regular oral potassium supplement therapy. Two adult females in Family 1 experienced limb weakness triggered by stress, exertion, and premenstrual period, with milder symptoms than the proband. In Family 2, the proband's periodic paralysis typically occurred the day after excessive exertion, with a frequency of approximately 2-3 months. Two years prior, the proband developed arrhythmias without palpitations or chest tightness. The proband's brother experienced intermittent limb weakness during adolescence, remained untreated, and had sudden death at age 40. Physical examination revealed characteristic features in Family 1 and both probands: small mandible, wide eye spacing, and fifth-digit clinodactyly. Four adult patients were shorter in stature, while the growth status of a pediatric patient was indeterminate. Supplementary tests showed a history of hypokalemia during muscle weakness episodes in Family 1, while Family 2 patients had normal potassium levels during episodes. The long exercise tests were positive in both probands. Muscle MRI showed no significant abnormalities, but muscle pathology revealed rimmed vacuoles and tubular aggregates. Genetic testing identified KCNJ2 gene mutations in two probands and some of their family members, with c.407C > T (p.S136F) heterozygous mutation in Family 1 and c.652C > T (p.R218W) heterozygous mutation in Family 2. Among the clinical symptoms of the patients with Andersen-Tawil Syndrome in this study, not everyone exhibits the full triad of signs: periodic paralysis is the most common initial symptom, craniofacial and digit skeletal abnormalities are characteristic signs, and ventricular arrhythmias pose the most serious potential risk. Given that these typical symptoms were observed in 5 out of 6 patients, clinicians should pay special attention to these typical symptoms, and patients with these symptoms should be followed up over time. Muscle biopsy May reveal pathological changes such as tubular aggregates, but genetic testing for KCNJ gene mutations remains a crucial diagnostic criterion for this syndrome.

Serum Electrolytes and Calcium Levels in Neonates Receiving Phototherapy for Neonatal Jaundice

Background: Neonatal Jaundice (NJ) is one of the most common causes of neonatal admission. Phototherapy is an important treatment modality for NJ. However, this treatment modality may itself result in changes of different biochemical parameters. The study aimed to evaluate the changes in serum electrolytes (Sodium, potassium and chloride) and calcium in neonates receiving phototherapy for NJ. Materials and methods: One hundred and two term neonates admitted to the Special Care Newborn Unit, Chattogram Medical College Hospital for the management of NJ by phototherapy were enrolled in this prospective observational study. Serum bilirubin, sodium, potassium, chloride and calcium were measured before and after 48 hours of phototherapy and compared. Results: The mean gestational age and mean age of admission of the neonates were 38.6±0.6 weeks and 6.42 ± .67 day respectively. The mean sodium, potassium and calcium level before therapy was respectively, 138.4±1.8 mmol/L, 4.1±0.3 mmol/L and 8.8±0.3 mg/dl. There was significant decrease in the level of mean sodium (136.4±1.6 mmol/L), potassium (3.8 ± 0.3 mmol/L) and calcium (8.4±0.4 mg/dL) after phototherapy. All neonates had normal level of serum calcium, sodium, potassium and chloride before phototherapy. After 48 hours of phototherapy, 46 (45.1%) of them had abnormal values with the incidence hypocalcaemia, hyponatraemia and hypokalemia respectively in 21.6%, 25.5% and 10.8% of the neonates. Conclusion: Neonates undergoing phototherapy are at risk of developing hyponatraemia, hypokalaemia and hypocalcaemia. Closed monitoring is essential to observe the changes in sodium, potassium and calcium and should be managed accordingly. IAHS Medical Journal Volume 6(2) December 2023; 83-86

A Rare Compound Heterozygous Mutation of TRPM6 Gene in Hereditary Hypomagnesemia with Secondary Hypocalcemia: A Cause of Refractory Seizures in an Infant

Background: Hypomagnesemia is an important cause of refractory hypocalcemic seizures. Among the causes of hypomagnesemia, genetic defects are rare. Clinical Description: A 20-month-old boy presented with a history of repeated hypocalcemic convulsions since 1 month of age. Besides seizures, the infant was thriving well and otherwise asymptomatic. Management and Outcome: On investigation, he had low serum calcium, normal vitamin D, low parathormone, and very low serum magnesium (0.5 mg/dl) levels, with normal sodium, potassium levels, and renal functions. The child was initiated on parenteral magnesium supplementation and subsequently discharged on high-dose oral magnesium supplementation. As further investigations ruled out common causes of hypomagnesemia, clinical exome sequencing was done, which revealed a compound heterozygous state with two variants in the TRPM6 gene NM_017662.5, one being a missense variant (chr9: c.5614T>C, [p.Trp1872Arg]/Heterozygous) and the other being a frameshift deletion (chr9: c.1939_1946delGCAATGGC, [p.Ala647Profs*2]/Heterozygous). The child maintained normal serum magnesium levels at follow-up and was seizure-free. Conclusion: Hereditary hypomagnesemia with secondary hypocalcemia is a rare cause of refractory seizures with onset since early infancy. Here, a compound heterozygous variant of the TRPM6 gene was identified as the cause of this condition.

The impact of hyperkalemia on ICU admission and mortality: a retrospective study of Chinese emergency department data

ObjectiveThis study assesses the influence of hyperkalemia on both disease severity and the risk of mortality among patients admitted to the emergency room.MethodsThis retrospective observational study utilized data from the Chinese Emergency Triage Assessment and Treatment database (CETAT, version 2.0), which was designed to evaluate and optimize management strategies for emergency room (ER) patients. Patients were systematically categorized based on serum potassium levels. Relationships between serum potassium levels, risk of mortality, and the severity of illness were then analyzed using multifactorial logistic regression and through Receiver Operating Characteristic (ROC) analysis. The effectiveness of various treatments at lowering potassium levels was also investigated.Results12,799 emergency patients were enrolled, of whom 20.1% (n = 2,577) were hypokalemic and 2.98% (n = 381) were hyperkalemic. Among hyperkalemic patients, the leading reasons for visiting the ER were altered consciousness 23.88% (n = 91), cardiovascular symptoms 22.31% (n = 85), and gastrointestinal symptoms 20.47% (n = 78). Comparative analysis with patients exhibiting normal potassium levels revealed hyperkalemia as an independent factor associated with mortality in the ER. Mortality risk appears to positively correlate with increasing potassium levels, reaching peaks when blood potassium levels ranged between 6.5 and 7.0. Hyperkalemia emerged as a strong predictor of death in the ER, with an Area Under the Curve (AUC) of 0.89. The most frequently prescribed treatment for hyperkalemia patients was diuretics (57.32%, n = 188), followed by intravenous sodium bicarbonate (50.91%, n = 167), IV calcium (37.2%, n = 122), insulin combined with high glucose (27.74%, n = 91), and Continuous Renal Replacement Therapy (CRRT) for 19.82% (n = 65). Among these, CRRT appeared to be the most efficacious at reducing potassium levels. Diuretics appeared relatively ineffective, while high-glucose insulin, sodium bicarbonate, and calcium preparations having no significant effect on the rate of potassium decline.ConclusionHyperkalemia is common in emergency situations, especially among patients with altered consciousness. There is a strong positive correlation between the severity of hyperkalemia and mortality risk. CRRT appears to be the most effective potassium reducting strategy, while the use of diuretics should be approached with caution.

Atrial fibrillation induced by carbon monoxide poisoning: Case report

Background: Carbon monoxide (CO) poisoning is known to have direct toxic effects on the cardiovascular system, including the potential to cause arrhythmias by prolonging the QTc interval. The arrhythmogenic properties of CO are believed to be attributed to its impact on cardiac membranes. Case Presentation: This case report presents the clinical course and management of a 21-year-old male who presented to the Emergency Department (ED) with an altered level of consciousness following exposure to carbon monoxide while cooking on a gas cylinder in a closed room. The patient had no history of chronic medical illness and was a non-smoker. Physical examination revealed stable vital signs, clear breath sounds, and a lax, soft, and non-tender abdomen. Laboratory investigations showed elevated troponin levels indicative of cardiac muscle injury but normal potassium levels. ECG revealed atrial fibrillation with a fast ventricular rate and transient ST elevation. The patient received high flow oxygen. The carboxyhemoglobin level decreased significantly after high-flow oxygen administration, confirming the successful treatment of carbon monoxide poisoning. Echocardiography and coronary angiography demonstrated normal cardiac function and ruled out coronary artery disease, respectively. The patient received high-flow oxygen therapy, continuous cardiac monitoring, and supportive care during hospitalization. Following stabilization and restoration of sinus rhythm, the patient was discharged in stable condition. Conclusion: This case highlights the importance of prompt recognition and management of carbon monoxide poisoning, as well as the need for careful evaluation of cardiac function in such cases. The patient responded well to high-flow oxygen therapy, leading to a decrease in the carboxy hemoglobin level and resolution of symptoms. Timely recognition and appropriate management of carbon monoxide poisoning are crucial in preventing adverse cardiac events and ensuring a favorable outcome for the patient.

High Dose Sesbania Grandiflora Extract Alters Rat Kidney Electrolytes based on Insights from Indonesia

This study investigates the acute toxicity of white turi flower extract (Sesbania grandiflora) on kidney electrolyte levels in rats (Rattus norvegicus). Conducted at Muhammadiyah University of Sidoarjo, male Wistar rats were divided into control and treatment groups, receiving 10,000, 15,000, and 20,000 mg/kgBW doses. Symptoms of toxicity included lethargy and hair loss, but no deaths occurred. Despite normal macroscopic kidney observations, sodium and potassium levels significantly increased with higher doses (p=0.000). These findings suggest that high doses of white turi flower extract can affect kidney electrolytes, indicating potential toxicity. Further research is needed to assess long-term safety for medicinal use. Highlights: 1. High doses increase sodium and potassium in rat kidneys.2. Symptoms: lethargy, hair loss, no fatalities.3. Requires further research for long-term safety. Keywords: Sesbania grandiflora, acute toxicity, kidney electrolytes, sodium, potassium

Potential medical impact of unrecognized invitro hypokalemia due to hemolysis: a case series.

The destruction of red cells during blood collection or with the processing of the sample continues to occur at a high rate, especially among emergency department (ED) patients. This can produce pre-analytical laboratory errors, particularly for potassium. We determined the incidence of hemolyzed samples and discuss the potential medical impact for hypokalemic patients who potassium level is artificially normal (pseudoeukalemia). Potassium results were obtained for a 6-month period. Using a measured hemolysis index (HI), hemolysis was present in 3.1 % for all potassium ordered (n=94,783) and 7.5 % for ED orders (n=22,770). Most of these samples were reported as having high normal result or were hyperkalemic. There were 22 hemolytic samples with a potassium of <3.5 mmol/L, and 57 hemolytic samples with a potassium in lower limit of normal (3.5-3.8 mmol/L). From this group, we examined the medical histories of 8 selected patients whose initially normal potassium levels were subsequently confirmed to have a potassium values that were below, at, or just above the lower limit of normal due to hemolysis. The primary complaint for these patients were: necrotizing soft tissue infection, pancreatitis, volume overload from heart failure with reduced ejection fraction, hypertension treated with hydrochlorothiazide, and presence of a short bowel syndrome. A subsequent non-hemolyzed sample was collected demonstrating hypokalemia in all of these patients. Within these cases, there was a potential for harm had hemolysis detection not been performed. We demonstrate the medical importance of detecting hemolysis for patients who have pseudoeukalemia. This is relevant because the HI cannot be obtained when electrolytes are tested using whole blood samples, and a normal potassium may lead to inappropriate patient management.

The effect of potassium levels on electrocardiographic data in calves with neonatal diarrhea

Objective: The objective of the current study was to assess the potassium levels and electrocardiographic (ECG) data in a cohort of 40 calves (age &lt; 30 days) diagnosed with newborn diarrhea, originating from dairy farms located in Ankara, Turkey.&#x0D; Materials and Methods: This study was conducted on a dairy farm located in Ankara, involving a population of 500 dairy animals. The calves were divided into two groups: one group with normal potassium levels (n=24) and another group with hyperkalemia (n=16) due to neonatal diarrhea. After the initial clinical examination was conducted on the farm, electrocardiographic investigations were carried out utilizing an ECG equipment. The biochemical analysis of blood samples that were collected in red and dry collecting tubes was carried out with the assistance of an automated analyzing machine &#x0D; Results: The findings indicate that there were no statistically significant differences observed across all ECG variables between the two groups.&#x0D; Conclusion: Acidemia and metabolic acidosis are commonly observed in calves suffering from hyperkalemic diarrhea, as documented in previous investigations, often accompanied by heart rhythm problems. In contrast, the current investigation revealed that neonatal calves with diarrhea and hyperkalemia had just a deepening of the T wave, without any additional abnormalities. Nevertheless, it is important to note that acidemia and metabolic acidosis were not of a severe nature. The implementation of Holter monitoring is indicated for calves experiencing hyperkalemia in conjunction with diarrhea.

Pseudohyperkalemia in myotonic dystrophy type 1: A case report

AbstractMyotonic dystrophy type 1 (DM1) is an autosomal dominant familial muscular dystrophy caused by abnormal CTG repeat expansion in the myotonic dystrophy protein kinase (DMPK) gene. The cardinal features of DM1 patients are muscular weakness, myotonia, and arrhythmia. DM1 patients with electrolyte imbalance caused by endocrinological alterations have also been reported. Herein, we report a female patient with DM1 and hyperkalemia, which fluctuated depending on the blood collection methods. We revealed that cold stimulation of red blood cells was associated with hyperkalemia, whereas blood examination immediately after collection showed normal potassium levels. She was, therefore, diagnosed with pseudohyperkalemia. Several previous reports have described DM1 patients with pseudohyperkalemia, similar to ours. Neurologists should be aware that some patients with DM1 may have pseudohyperkalemia. Thus, consider retesting with prompt measurement after blood collection to rule out pseudohyperkalemia when a patient shows hyperkalemia. If confirmed, evaluate for DM1 as a potential differential diagnosis.

Unexpected Hyperkalemia During Kawasaki Disease

Pseudohyperkalemia is defined as a markedly elevated serum potassium level with a normal plasma potassium concentration. It is mainly caused by leucocytosis and thrombocytosis. Here we report an infant treated with aspirin for Kawasaki disease who developed hyperkalemia during follow-up. He was finally diagnosed with pseudohyperkalemia based on a normal whole blood potassium level measured with a blood gas analyser.